Bacterial Diseases of Turkeys and Ducks

Dr Wafaa Abd El-GhanyAssistant Professor of Poultry Diseases

Poultry Diseases DepartmentFac Vet Med

Cairo Univ

Bacterial diseases of Turkeys 1 Mycoplasma gallisepticum (MG)2 Mycoplasma meleagridis (MM)3 Maycoplasma synoviae (MS)4 Mycoplasma iowae (MI)5 Turkey coryza (Bordetellosis)6 Ornithobacterium rhinotracheal (ORT)7 Erysiplas infection8 Avian chlamydiosis9 Fowl cholera10 Avian salmonellosis (Paratyphoid infection Arizona disease and

Pullorum disease)11 Ecoli infection12 Clostridial infections13 Staphylococcus and Streptococcus infections14 Avian Tuberculosis

Bacterial diseases of Ducks

1 Rimerella anatipestifer

2 Botulism (Western duck sickness Limber neck)

3 Paratyphoid infection

4 Avian chlamydiosis

5 Fowl cholera

6 Mycoplasma immitans amp ansaris

7 Avian spiroketosis

8 Ecoli infection

9 Staphylococcus and Streptococcus infections

MYCOPLASMA GALLISEPTICUM

(MG)

(Infectious sinusitis of turkeys)

[Chronic respiratory disease (CRD) of chickens]

Mycoplasma gallisepticum (MG)

MG infections are Respiratory affections ofslow development and long coursecharacterized by Respiratory ralescoughing nasal discharge andconjunctivitis in chickens Swolleninfraorbital sinus is frequently occurred inturkeys

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Bacterial diseases of Turkeys 1 Mycoplasma gallisepticum (MG)2 Mycoplasma meleagridis (MM)3 Maycoplasma synoviae (MS)4 Mycoplasma iowae (MI)5 Turkey coryza (Bordetellosis)6 Ornithobacterium rhinotracheal (ORT)7 Erysiplas infection8 Avian chlamydiosis9 Fowl cholera10 Avian salmonellosis (Paratyphoid infection Arizona disease and

Pullorum disease)11 Ecoli infection12 Clostridial infections13 Staphylococcus and Streptococcus infections14 Avian Tuberculosis

Bacterial diseases of Ducks

1 Rimerella anatipestifer

2 Botulism (Western duck sickness Limber neck)

3 Paratyphoid infection

4 Avian chlamydiosis

5 Fowl cholera

6 Mycoplasma immitans amp ansaris

7 Avian spiroketosis

8 Ecoli infection

9 Staphylococcus and Streptococcus infections

MYCOPLASMA GALLISEPTICUM

(MG)

(Infectious sinusitis of turkeys)

[Chronic respiratory disease (CRD) of chickens]

Mycoplasma gallisepticum (MG)

MG infections are Respiratory affections ofslow development and long coursecharacterized by Respiratory ralescoughing nasal discharge andconjunctivitis in chickens Swolleninfraorbital sinus is frequently occurred inturkeys

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Bacterial diseases of Ducks

1 Rimerella anatipestifer

2 Botulism (Western duck sickness Limber neck)

3 Paratyphoid infection

4 Avian chlamydiosis

5 Fowl cholera

6 Mycoplasma immitans amp ansaris

7 Avian spiroketosis

8 Ecoli infection

9 Staphylococcus and Streptococcus infections

MYCOPLASMA GALLISEPTICUM

(MG)

(Infectious sinusitis of turkeys)

[Chronic respiratory disease (CRD) of chickens]

Mycoplasma gallisepticum (MG)

MG infections are Respiratory affections ofslow development and long coursecharacterized by Respiratory ralescoughing nasal discharge andconjunctivitis in chickens Swolleninfraorbital sinus is frequently occurred inturkeys

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

MYCOPLASMA GALLISEPTICUM

(MG)

(Infectious sinusitis of turkeys)

[Chronic respiratory disease (CRD) of chickens]

Mycoplasma gallisepticum (MG)

MG infections are Respiratory affections ofslow development and long coursecharacterized by Respiratory ralescoughing nasal discharge andconjunctivitis in chickens Swolleninfraorbital sinus is frequently occurred inturkeys

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Mycoplasma gallisepticum (MG)

MG infections are Respiratory affections ofslow development and long coursecharacterized by Respiratory ralescoughing nasal discharge andconjunctivitis in chickens Swolleninfraorbital sinus is frequently occurred inturkeys

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

MOI amp Transmission of MG

Vertical infectionFrom infected hens to the embryos causing

embryonic mortalities or infection of day old chicks

Horizontal infectionThrough aerosol (air born) droplet infectionDirect or indirect contact of susceptible birds to

clinical or subclinical infected birds Mechanical (Fomites)workers free living birds utensils visitors cars

feed bags etchellip

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Signs of MG

In turkeys (Infectious sinusitis)

1) Unilateral or bilateral swelling of theinfraorbital sinuses with facial swelling

2) Partial or complete closure of eye fromsevere sinus swelling

3) Nasal discharge with foamy eye secretion

4) Tracheal rales coughing and laboredbreathing

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Signs of MG

5) Decreased feed intake and weight loss

6) MG can induce encephalitic form in 12-16 weeks old commercial meat turkeywith torticollis and opithotenous

7) Breeder flocks show drop in eggproduction

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Lesions of MG

MG without complications

1) Catarrhal rhinitis sinusitis (turkeys)conjunctivitis tracheitis and broncheitis

2) Lung congestion and pneumonia

3) Mild pericarditis perihepatitis andairsacculitis

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Lesions of MG

MG with complications

1) Seofibrinous or fibrinous (casous orpurulent) pericarditis perihepatitis andairsacculitis

2) Peritonitis

3) Salpingitis

4) Lung congestion and pneumonia

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Swelling of the

infraorbital sinuses

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Mild tracheitis with a small amount of mucoid exudate in the tracheal lumen

Congestion of the trachea and catarrhal exudate

Plugs of exudate in the lumen of the

trachea and bronchi

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Mild airsacculitis with light presence of

foamAirsacculitis with caseous exudate

Severe airsacculitis with abundant foam and aggregates

of caseous exudate

Severe perihepatitis and

pericarditis

Fibrinous pericarditis and peritonitis

Severe perihepatitis and pericarditis

pericarditis and fibrinous pneumonia

Fibrinous pericarditis

Pneumonia

MYCOPLASMA

MELEAGRIDIS

(MM)

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Fibrinous pericarditis and peritonitis

Severe perihepatitis and pericarditis

pericarditis and fibrinous pneumonia

Fibrinous pericarditis

Pneumonia

MYCOPLASMA

MELEAGRIDIS

(MM)

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

pericarditis and fibrinous pneumonia

Fibrinous pericarditis

Pneumonia

MYCOPLASMA

MELEAGRIDIS

(MM)

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Pneumonia

MYCOPLASMA

MELEAGRIDIS

(MM)

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

MYCOPLASMA

MELEAGRIDIS

(MM)

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Mycoplasma meleagridis (MM)

It is a specific pathogen of turkeys causingegg transmitted disease (venereal) withprimary lesions in air sacs with decreasehatchability skeletal abnormalities andpoor performance

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Airsaculitis deficiency syndrome (TS-65)1) Bowing2) Twisting and shortening of the tarsometatarsal

bone3) Hock joint swelling4) Deformity of the cervical vertebrate5) Lameness 6) Stunting and abnormal feathering 7) Retardation in growth8) Late embryonic mortality9) Respiratory signs

Signs of MM

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Lesions of MM

1) Skeletal deformities (tibial dyschondroplasia and chondrodystrophy)

2) Sternal bursitis and synovitis

3) Airsacculitis (thickening of air sac walls with adherence of yellow exudates)

4) Sinusitis

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

MYCOPLASMA SYNOVIAE

(MS)

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Mycoplasma synoviae (MS)

MS induces acute or chronic infectioussynovitis in chickens and turkeys which ischaracterized by exudative synovitis andtenovaginitis or sternal bursitis (breastblister)

MS can also induce upper respiratoryinfection (air sac disease)

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Signs of MS

1) Swellings around joints especially hocks footpad and the sternal bursa is enlarged (turkeys) (breast blister)

2) Lameness3) Mild respiratory signs4) Slight drop egg production and egg quality

Retardation in growth5) Pale comb6) Greenish discoloration of dropping with large

amount of ureates7) Mortality 10

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Lesions of MS

1) The synovial membranes of tendon sheaths of affected joints and keel bursa have a viscous yellow exudates (fibrinopurelent in turkeys)

2) Articular surfaces become eroded3) Sternal bursitis (breast blister) in turkeys4) Caseous exudates may be found in air

sacs5) Enlarged liver and spleen kidneys usually

swollen mottled and pale

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

ORGAN Leg of bird

LESIONS Arthritis

SUSPDIS Viral Arthritis (REO)

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Swollen hock with yellow exudate

Airsacculitis

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Sternal bursitis

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Diagnosis of Mycoplasmosis Swabs organs are taken from the respiratory system joint

exudate Samples could be taken from the semen or fertile eggs from

adult suspected breeder flocks Mycoplasma species are fastidious organisms due to that

they difficult to grow and need long time for growth Mycoplasma species need enriched media like PPLO (pleuro-

pneumonia like organism) media or modified Freyrsquos FMmedia

Positive agar culture appears as a characteristic Fried eggshaped appearance (tiny smooth rounded colourlesstranslucent mass dense dark rough central area surroundedby flat translucent hallow zone) colonies under dissecting orsteromicroscope

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Serum plate agglutination (SPA) test

On the clean porcelain or glass plate add one drop of MG or MS specific coloured (stained) antigen then add on drop of the serum of the bird

Mix well and rotate the plate in a circular manner

Positive reaction appears with in 2 minutes as the form of agglutination (flocculation or granulation) suspected cases should be confirmed using HI test

flock test

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Prevention of Mycoplasmosis

Adopt all biosecurity measures

Egg sanitation and hatchery sanitation

Regular serological flock monitoring

II In case of MM

Examination of the phallus and cloacae ofadult male turkeys for MM serologicallybacteriologically and molecularly before thebreeding season

Using non-infected (non genetically carriers)birds for breeding (mating)

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Prevention of Mycoplasmosis

Vaccination1 Moderately virulent strain (F) strain2 685 strain3 Ts-11 strain4 New K 5054 strain5 Naturally occurring virulent strains (S6)6 Inactivated vaccines (bacterins) Vaccination with live MG vaccine between 12

and 16 weeks of age Vaccination can be carried out a 2-4 weeks of

age

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Control of mycoplasmosis

1 Separate diseased from healthy birds

2 Hygienic disposal of dead birds (burning or burring)

3 Thorough cleaning and disinfection

4 Treatment of birds Medication helps only to controlclinical signs and lesions and slow the spread ofinfection but it doesnt eliminate the infection

Complete elimination of mycoplasmas from all birds inthe infected flocks using medication is not expected asthe treatment is regarded as a method of short-termamelioration of the disease rather than as long termsolution of the problem

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Control of mycoplasmosis

use Teteracyclines Macroilds (erythromycin tylosinspiramycin lincomycin kitasamycin) Pleuromulins(tiamulin) and fluoroquinolones (norfloxacinenrofloxacin and danofloxacin)

Egg treatment

A) Egg inoculation Any antimycoplasmal antibiotics isinjected into the egg cell this method may kill theembryo

B) Egg dipping the eggs are warmed to 37-38C thenimmersed in cold antibiotic solution (1-4C) for 20minutes Due to the temperature differences cooling ofthe egg contents and the antibiotic is pulled throughthe egg shell

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Control of mycoplasmosis

C) Pressure differential vacuum (system) by decreasingthe pressure above the egg 25 Cm Hg by vacuumpump then the pressure return slowly to theatmospheric one This method is not completelyeliminate the organism but not affect on thehatchability

D) Heat forced incubator the eggs are heated inforced air incubator for 40C then putted at roomtemperature for cooling at 256C It is the mosteffective method but it reduces the hatchability to 8-12 with high embryonic mortalities

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

BORDETELLOSIS

(Turkey coryza)

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Bordetellosis(Turkey coryza)

It is a highly contagious upper-respiratory tractdisease affect young turkeys caused by Bordetellaavium and is characterized by inflammation anddistortion of the respiratory mucosa

The economic importance including impairedgrowth Mortalities and the losses are resultingfrom Colisepticemia secondary or complicatedinfections and stressors

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Transmission of B Avium

Close contact with infected poults or throughexposure to litter or water

Infection is transmitted by aerosol transmission

The severity of bordetellosis is exacerbated byadverse environmental and infectious factors(Temp humidity litter quality Ecoli)

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Signs of B Avium

An abrupt onset of sneezing (snick) in a high percentage of 2-6 week-old turkeys over the course of a week

Older turkeys may also develop a dry cough

A clear nasal discharge

During the first 2 weeks of disease the nares and feathers of the head and wings become crusted with wet tenacious brownish exudate and some birds develop submaxillary edema

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Signs of B Avium

Foamy exudate at the medial canthus of the eye

Open-mouth breathing and dyspnea and altered vocalization in the second week of clinical signs result when the nasal cavity and upper trachea become partially occluded with mucoid exudate

Poor weight gains In turkeys 2-6 weeks of age morbidity 80-100

whereas the mortality rate is less than 10 High mortality rates (gt40) in young turkeys

frequently are associated with concurrent isolation of Escherichia coli

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Lesions of B Avium

Nasal and tracheal exudates varies from serous initially to tenacious and mucoid during the course of disease

Generalized softening and distortion of the cartilaginous rings of the trachea dorsal-ventral compression

In cross-section tracheal rings appear to have thick walls and a diminished lumen

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Diagnosis of B Avium

Samples collected from the choanal opening and nostril or by passing a swab into the trachea through the larynx

Isolation and identification of bacterial agent isolation is accomplished on MacConkey agar

Serologic testing has proven to be useful a microagglutination test (MAT)

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Prevention of B Avium

Strict biosecurity measures are required toprevent infection of clean flocks

Vaccines available commercially for theprevention of bordetellosis are (ts) mutant of Bavium and a whole cell bacterin

Vaccination of breeder hens with killed bacterinsdelayed the onset and severity of clinicaldisease in challenge-exposed poults

Passive immunization of 3-week-old poults withconvalescent serum

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Control of B Avium

Treatment of bordetellosis with antibioticsadministered in the water by injection orby aerosol has produced minimal clinicalimprovement in most cases

Treatment of an infected breeder flockwith tetracycline-HCl and potassiumpenicillin-G for 3 days produced clinicalimprovement within 24 hours

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

ORNITHOBACTERIUM RIHINOTRACHEAL

(ORT)

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

ORT Infection amp Transmission

It is a contagious bacterial disease affectschickens and turkeys characterized by respiratorysigns variable mortality and decrease in eggproduction with change in egg quality

The infection occurred by the horizontal routes bycontact through aerosol or drinking water

The vertical transmission occurs by transovarianand oviduct

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Signs of ORTIn turkeysA Poults Turkey poults aged 2-8 weeks show mortality

up to 50 Respiratory signs coughing sneezing nasal

discharge and sinusitis Decrease in feed and water intakeB Breeders Decrease in egg production Increase in the number of unhatched eggs

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Lesions of ORT

Uni or bilateral pneumonia

Yoghurt like airsaculitis

Pleuritris

Subcutaneous edema of the head

Enlarged liver and spleen with degeneration of heart muscles are additionally seen in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Thickened opaque air sacs with

profuse foamy white to yellow ldquoyogurt-

likerdquo

Pneumonia and pleuritis in turkeys

Prevention amp control of ORT

1) Application of good sanitary measures especially separation of different ages and species

2) Vaccination

a Inactivated vaccine considered as serotype specific vaccine

b Live vaccine can induce cross protection between some serotypes

Amoxicillin and chlortetracycline in water

Tetracycline and penicillins by injection

ERYSIPELAS

Erysipelas

Erysipelas (Red Skin) occurs in growing turkeys geese chickens quail and Peafowl between 47 months

This acute to chronic disease is caused by the Gram-positive rod shaped bacterium Erysipelothrix rhusiopathiae It is non-spore forming non-acid fast and non-motile

Infection amp transmission of Erysipelas

It can be transmitted through a break in the skin or mucous membranes or fighting between males

It is a soil-borne organism and can also be spread by cannibalism or biting flies

Contaminated fish-meal is also a source of infection

Signsamp lesions of Erysipelas

Signs The incubation period is 2-3 days Swollen snoods (turkeys) and

shock Diarrhea emaciation weakness anemia skin haemorrhage and necrosis can be seen

Fever cyanotic toes and head drop in egg production and or fertility and embryonic mortality can occur

Post mortem lesions Enlarged friable purple-black spleen breast muscle haemorrhage

oral mucous Haemorrhage in muscles spleen lungs fat and small intestine and endocarditis may be seen

Fibrinopurulent Exudate in the joints Thickening of walls or proventriculus or gizzard ulceration and

yellow nodules can occur in the caeca

ERYSIPELAS

Erysipelas

Erysipelas (Red Skin) occurs in growing turkeys geese chickens quail and Peafowl between 47 months

This acute to chronic disease is caused by the Gram-positive rod shaped bacterium Erysipelothrix rhusiopathiae It is non-spore forming non-acid fast and non-motile

Infection amp transmission of Erysipelas

It can be transmitted through a break in the skin or mucous membranes or fighting between males

It is a soil-borne organism and can also be spread by cannibalism or biting flies

Contaminated fish-meal is also a source of infection

Signsamp lesions of Erysipelas

Signs The incubation period is 2-3 days Swollen snoods (turkeys) and

shock Diarrhea emaciation weakness anemia skin haemorrhage and necrosis can be seen

Fever cyanotic toes and head drop in egg production and or fertility and embryonic mortality can occur

Post mortem lesions Enlarged friable purple-black spleen breast muscle haemorrhage

oral mucous Haemorrhage in muscles spleen lungs fat and small intestine and endocarditis may be seen

Fibrinopurulent Exudate in the joints Thickening of walls or proventriculus or gizzard ulceration and

yellow nodules can occur in the caeca

Erysipelas

Erysipelas (Red Skin) occurs in growing turkeys geese chickens quail and Peafowl between 47 months

This acute to chronic disease is caused by the Gram-positive rod shaped bacterium Erysipelothrix rhusiopathiae It is non-spore forming non-acid fast and non-motile

Infection amp transmission of Erysipelas

It can be transmitted through a break in the skin or mucous membranes or fighting between males

It is a soil-borne organism and can also be spread by cannibalism or biting flies

Contaminated fish-meal is also a source of infection

Signsamp lesions of Erysipelas

Signs The incubation period is 2-3 days Swollen snoods (turkeys) and

shock Diarrhea emaciation weakness anemia skin haemorrhage and necrosis can be seen

Fever cyanotic toes and head drop in egg production and or fertility and embryonic mortality can occur

Post mortem lesions Enlarged friable purple-black spleen breast muscle haemorrhage

oral mucous Haemorrhage in muscles spleen lungs fat and small intestine and endocarditis may be seen

Fibrinopurulent Exudate in the joints Thickening of walls or proventriculus or gizzard ulceration and

yellow nodules can occur in the caeca

Infection amp transmission of Erysipelas

It can be transmitted through a break in the skin or mucous membranes or fighting between males

It is a soil-borne organism and can also be spread by cannibalism or biting flies

Contaminated fish-meal is also a source of infection

Signsamp lesions of Erysipelas

Signs The incubation period is 2-3 days Swollen snoods (turkeys) and

shock Diarrhea emaciation weakness anemia skin haemorrhage and necrosis can be seen

Fever cyanotic toes and head drop in egg production and or fertility and embryonic mortality can occur

Post mortem lesions Enlarged friable purple-black spleen breast muscle haemorrhage

oral mucous Haemorrhage in muscles spleen lungs fat and small intestine and endocarditis may be seen

Fibrinopurulent Exudate in the joints Thickening of walls or proventriculus or gizzard ulceration and

yellow nodules can occur in the caeca

Signsamp lesions of Erysipelas

Signs The incubation period is 2-3 days Swollen snoods (turkeys) and

shock Diarrhea emaciation weakness anemia skin haemorrhage and necrosis can be seen

Fever cyanotic toes and head drop in egg production and or fertility and embryonic mortality can occur

Post mortem lesions Enlarged friable purple-black spleen breast muscle haemorrhage

oral mucous Haemorrhage in muscles spleen lungs fat and small intestine and endocarditis may be seen

Fibrinopurulent Exudate in the joints Thickening of walls or proventriculus or gizzard ulceration and

yellow nodules can occur in the caeca

Swollen snood Turgid snood

Enlarged and mottled spleen (marbled spleen) )

Endocarditis inflammatory process around valves

Diagnosis of Erysipelas

Laboratory isolation from lesions is important and can show smooth colonies colorless to a bluish gray or pin-point size with smooth edges Haemorrhagic swollen spleen and wicked red lesions are diagnosed

It Simulates cholera Salmonella gangrenous dermatitis aspergillosis and E coli

Blood agar tiny pinpoint colonies round and translucent

Prevention and Control of Erysipelas

Prevention Vaccinate birds twice one at 1012 weeks and again at

14-16 weeks Debeak at day one and pooling is done if necessary to

prevent fighting No pigs should be reared near poultry and rotation of

the turkey range to reduce bacteria

Treatment Gallimycin and penicillin can reduce signs Disinfect premises with aerosol phenols or iodine

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Enlarged and mottled spleen (marbled spleen) )

Endocarditis inflammatory process around valves

Diagnosis of Erysipelas

Laboratory isolation from lesions is important and can show smooth colonies colorless to a bluish gray or pin-point size with smooth edges Haemorrhagic swollen spleen and wicked red lesions are diagnosed

It Simulates cholera Salmonella gangrenous dermatitis aspergillosis and E coli

Blood agar tiny pinpoint colonies round and translucent

Prevention and Control of Erysipelas

Prevention Vaccinate birds twice one at 1012 weeks and again at

14-16 weeks Debeak at day one and pooling is done if necessary to

prevent fighting No pigs should be reared near poultry and rotation of

the turkey range to reduce bacteria

Treatment Gallimycin and penicillin can reduce signs Disinfect premises with aerosol phenols or iodine

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Diagnosis of Erysipelas

Laboratory isolation from lesions is important and can show smooth colonies colorless to a bluish gray or pin-point size with smooth edges Haemorrhagic swollen spleen and wicked red lesions are diagnosed

It Simulates cholera Salmonella gangrenous dermatitis aspergillosis and E coli

Blood agar tiny pinpoint colonies round and translucent

Prevention and Control of Erysipelas

Prevention Vaccinate birds twice one at 1012 weeks and again at

14-16 weeks Debeak at day one and pooling is done if necessary to

prevent fighting No pigs should be reared near poultry and rotation of

the turkey range to reduce bacteria

Treatment Gallimycin and penicillin can reduce signs Disinfect premises with aerosol phenols or iodine

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Blood agar tiny pinpoint colonies round and translucent

Prevention and Control of Erysipelas

Prevention Vaccinate birds twice one at 1012 weeks and again at

14-16 weeks Debeak at day one and pooling is done if necessary to

prevent fighting No pigs should be reared near poultry and rotation of

the turkey range to reduce bacteria

Treatment Gallimycin and penicillin can reduce signs Disinfect premises with aerosol phenols or iodine

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Prevention and Control of Erysipelas

Prevention Vaccinate birds twice one at 1012 weeks and again at

14-16 weeks Debeak at day one and pooling is done if necessary to

prevent fighting No pigs should be reared near poultry and rotation of

the turkey range to reduce bacteria

Treatment Gallimycin and penicillin can reduce signs Disinfect premises with aerosol phenols or iodine

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

ARIZONOSIS

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Arizonoses

Arizonosis occurs young turkeys It is caused by Bacterium-Salmonella Arizona Gram negative flagellate bacterium Salmonella

Arizona

The effects are the same as for other Salmonella infections- Diarrhoea lameness somnolence (sleepiness) laboured breathing blindness and mortality Mortality up to 100 peaking at 7-10 days Tremors convulsions and twisted necks may also be seen

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Infection amp transmission of Arizona

The disease is transmitted in the same way as other salmonella species ie from bird to bird and between farms

Common vectors include birds rodents and sometimes reptiles

Spread via the transovarian route can also occur

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs and lesions of Arizona

Signs are the same as for other Salmonella Opaque eyes (blindness) tremors convulsions and twisted necks may be seen

Postmortem lesions

Lesions are the same as for Salmonella pullorum which include bacteria septicaemia peritonitis and retained yolk sacs

Congested (filled with blood) duodenum mottled (white necrotic spots) liver caseous plugs in caeca and caseous air sacs can be seen

Round heart (Characteristic)

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Diagnosis of Arizona

The organisms must be cultured from post mortem lesions egg yolk etc on brilliant green agar for a definitive diagnosis

Agglutination or ELISA tests using sera from breeders can confirm the presences of S Arizona

It simulates pullorum E coli and typhoid

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Prevention amp Control of Arizona

Prevention Biosecurity measures Bacterin for turkey breeders prevents egg transmission Egg and hatchery sanitation are important Breeders should be tested and those that are serologically

positive should be slaughtered Vector control helps control spread of the organismTreatment Treatments will reduce clinical problems but birds will

remain carriers SQ and Ormetoprin in the water and furazolidone in the feed are effective treatments Gentamicin and spectinomycin can be given to day-old-chicks by injection

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

RIMERELLA (PASTEURELLA) ANATIPESTIFER

(RA)

(DUCK SEPTICAEMIA INFECTIOUS SEROSITIS NEW DUCK SYNDROM)

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Riemerella anatipestifer (RA)

It is an acute septicaemic or chroniccontagious disease of growingduckling characterized byserofibrinous pericarditisperihepatitis and airsacculitiscaseous salpingitis and meningitisand high mortality in ducklings(75)

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Susceptibility amp Infection of RA

Ducklings aged 1-8 weeks are highly susceptible

The disease in laying birds is rare

Inhalation of infected droplets

Wound infection

Direct and indirect contact

Carrier birds

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs of RA

Respiratory signs (nasal and ocular discharges sneezing and coughing)

Nervous signs (Ataxia tremors of the head and neck and coma)

Greenish diarrhea

Survival ducks may stunted

Mortality ranged from 5 to75 in relation to other factors as age route of infection and the strain virulence

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Lesions of RA

Fibrinous pericarditis Fibrinous perihepatitis Fibrinous airsacculitis Caseous salpingitis fibrinopurulant pneumonia Arthritis Fibrinous meningitis Enlarged and mottled spleen In the chronic form the most predominant lesions in the

skin in the form of necrotic dermatitis on the lower back or around vent with yellowish exudates between skin and the fat layer

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Central nervous system infection

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Caseous exudate located in the head

region (subcutis)

Submandibulare oedema

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Spinal cord compression Vertebral osteomyelitis

(spondylitis)

perihepatitis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Diagnosis of RA

Samples from heart blood brain pericardial exudates air sacs lungs liver and oviduct

Detection of bipolar organism in blood or tissue smear stained by Gimsa

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Prevention amp Control of RA Sanitary measures

Avoid stress factors

Prevent contact of the birds with different species sources and ages

Inactivated vaccine must be containing a serotype specific to that cause endemic infection or frequent infection in the farm

Live RA vaccine given by drinking water or spray to day old birds can induces protection till 42 days of age

Sulfamethazine (02 -025) in water or feed sulfaquinoxaline (0025-005) in feed and lincomycin (0011-0022 ) in water are effective

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

BOTULISM (LIMBER NECK)

WESTERN DUCK SICKNESS

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Botulism

Cause

Age group affected

Transmission

Clostridium botulinum

Most avian esp ducks

Ingestion of toxin

Insects or maggots

Feeding on dead decayed carcass

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

signs of botulism Paralysis of legs wings neck and eye lids are

predominant Paralysis progressed cranially fromlegs to eye lids

Affected bird appear firstly sitting on hocksreluctant to move or appear lame droopedwings extended neck ruffled feathers andfallout with handling

Broiler chickens are showing diarrhea withexcess ureates in the loose droppings

Mortality and morbidity are related to theamount of ingested toxin

Death 12-24 hours

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Lesions of botulism

There is no gross or microscopic lesions

Maggots of fly blown carcasses or feathers can be found in crop of dead or affected birds

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Control of botulism

No treatment but rapid withdrawal of thetoxicated food

Episons salt as purgative to removedecomposed food from the intestine

use sodium selenite and vitamin AD3E Antibiotics including Bacitracin 100gton in

feed streptomycin 1 gl of water may be ofvalue

Also Inoculation of antitoxin neutralizes onlyfree and extracellular bound toxin and can beused for treatment of valuable birds

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

MYCOPLASMA IMMITANS

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Mycoplasma immitans

Infection with Mycoplasma immitans is seen in ducks and geese

Signs

Swollen sinuses

Post-mortem lesions

Sinusitis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

PARATYPHOID

INFECTION (PT)

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Paratyphoid (PT) Infection

It is infection of turkeys and duckswith motile salmonella serotypesrather than Salmonella gallinarumpullorum (S Typhimurium Senteritidis S anatum etchellip) resultingin relatively asymptomatic intestinalcarrier or inducing clinical diseaseThe disease in ducks is caused by S

anatum

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

MOI amp Transmission of PT

Egg shell contamination (false egg bornedisease)

Direct contact

Ingestion of contaminated food and water

Rodents animals wild birds and flies

Human

Contaminated animal protein supplements(Bone meal meet meal and fish meal)

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs of PT in Ducks

1) Arthritis

2) The bird is unable to move or stand

3) Diarrhea

4) Nervous manifestation

Trembling or shivering

Kicking and violent movement

Move in circle

Keeling over backward with leg paddling (Keeldisease)

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

1) Necrotic foci on the liver

2) Distended gall bladder

3) Enteritis

4) The ureter is distended with ureates

5) Enlargement and congestion of the internalorgans

6) Pericarditis and perihepatitis

7) Degeneration of the ovary

Lesions of PT in Ducks

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Prevention of PT

Sanitation and sound measures in poultryhouses egg store and hatcheries

Administrations of probiotics are exhibitingactivity against various PT salmonellae inthat diminish both intestinal colonizationand subsequent invasion to internal tissues(Competitive Exclusion)

Trials for preparation of killed or livevaccines

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

AVIAN CHLAMYDIOSIS

(ORNITHOSIS)

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Avian chlamydiosis

Avian chlamydiosis is acute fatal or chronic infectiouszonootic respiratory disease of domestic wild andmigratory birds

The disease is characterized by nasal and oculardischarge diarrhea loss of weight drop in eggproduction and the mortality rate reached to 5-30

Presence of intracytoplasmic elementary bodies (LCL)is characteristic to the organism

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Giemsa stain intracellular chlamydial inclusion

(reddish-purple)

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Infection amp Transmission of Chlamydiosis

Chlamydia Psittaci infection occur horizontally either by inhalation of infected dust or droplet or by ingestion of contaminated feed and water with infected droppings

There is an evidence of low percentage of vertical transmission through eggs (transoverian) in ducks and sea gulls

Chronic carriers transmit the organism without signs

Biting of insects as ticks lice and mites

Wild birds are important in transmission

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs of chlamydiosis

In turkeysI Acute epidemic Form (toxigenic highly virulent strain)Clinical signs appear as systemic fatal infection with1 Sudden death of 5-302 Fever and anorexia3 Nasal and ocular discharge swollen eye lids

conjunctivitis and sinusitis4 Off food and loss of weight (emaciation)5 Yellow green gelatinous diarrhea6 Rapid drop in egg production (40-50 decline)7 Morbidity rate may be reach 50-80

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

In ducks and geese (water fowl)

In duckling there are tremors trembling and staggered gait (incoordination)

Ocular and nasal discharge

Greenish watery Diarrhea

Inappetance

Emaciation convulsion and death

Morbidity rate 10-80

Mortality rate 1-30 (depending on the age health status and secondary infection with salmonella species)

Signs of chlamydiosis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Lesions of chlamydiosis

Congestion of the visceral organs

Congestion and pneumonia of the lungs

All the body cavities are filed with fibrinous exudates

Fibrinous pericarditis perihepatitis and airsacculitis and peritonitis

Catarrhal enteritis

Liver and spleen are enlarged dark and covered with gray white foci

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Liver necrosisFibrinous pericarditis

liver hepatomegaly and congestion

fibrinous pericarditis

Fibrinous pericarditis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Caseous pericarditisLungs congested and fibrinous exudate

in the pleural cavity

Necrosis and congestion of

spleen

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Enlarged congested

liver

Prehepatitis

Airsacculitis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

A Thickened

abdominal airsacs

totally covered

with fibrin plaques

B Serous fluid

and fibrin in the

pericardial sac

C Severe

hepatomegaly

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Diagnosis of chlamydiosis1 Detection of dark purple blue or pink (acc To the

stain) ICytoplasmic inclusion (LCL) bodies in stained smear (from nasal or ocular exudates serous membranes trachea lungs pancreas liver spleen heart faecal and cloacal swabs) in different stages of elementary body

2 Tissue culture3 Embryonated chicken eggs4 Laboratory animal inoculation Intra peritoneal or intra

cranial or intra nasal inoculation of 3-4 weeks old mice (3-6 mice) could resulted in death of mice after 5-7 days post inoculation Intra peritoneal inoculation resulted in peritonitis with accumulation of fibrinous exudate in the peritoneal cavity with splenomegaly

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Prevention of chlamydiosis1 Different avian species and ages must be reared away

from each other2 Newly purchased (imported) birds especially pets must

be quarantined for 35 days (if positive discarded ortreated with tetracyclines till recovery)

3 Prevent the introduction of birds from the enzootic areas4 Avoid the contact with the free living wild birds5 Thorough cleaning and disinfection (iodophors or

formaldhydes)6 Regular testing of the birds using serological tests7 Restrict the movement of people and visitors8 Trials for vaccine preparation

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Control of chlamydiosis

1 Oxytetracyclin (15mgkg bwt) in the drinking water for a period for 5 days

2 Chlorotetracyclin

(treatment may be extended to 15-45 days in severe infection)

3 Usage of combined antibiotics to control other associated infections as Salmonellae and Ecoli(quinolones like cipro enro and danofloxacin) for 3-5 days in the drinking water

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

AVIAN PASTEURELLOSIS

FOWL CHOLERA (FC)

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

FC

Peracute acute and chronic highly contagious bacterial disease of domestic and wild birds caused by Pasteurella multocida

In the acute form the disease is characterized by rapid course high morbidity and mortality and septicaemic picture while the chronic form is localized and follows the acute form or occur independently due to low virulent mo

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Susceptibility of FC

1 Natural hosts are water fowl (ducks and geese) turkeys and chickens

2 Water fowl are the most susceptible birds

3 Turkeys are more susceptible than chickens

4 Adult chickens (more than 16 weeks old) while young turkeys are the most susceptible ages

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Infection and transmission of FC

1 Inhalation of infected droplets

2 Ingestion of contaminated food and water by the infected excretions from the mouth and nostrils of diseased or carriers

3 Mechanically clothes feet or hands of workers contaminated equipments feed bags etchellip

4 Wild birds rodents and pets

5 Cannibalism of diseased or dead birds

6 Wound infection

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs of FC

1 Per acute form

Sudden death without clinical signs

No characteristic post mortem lesions

2 Acute form

High morbidity and mortality rates

Septicaemia (cyanosis of the comb and wattle)

Mucous discharge from the mouth and nostrils

Watery white or greenish mucoid diarrhea

Respiratory manifestations

Drop in egg production

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Lesions of FC

Acute form Petechial or echymotic hemorrhages on the

lungs proventriculus abdominal and coronary fats and on serosal membranes as peritoneum and subepicardium and haemorrhagic enteritis

Tracheitis bronchitis and pneumonia (TURKEYS) Oophoritis flaccid regressed or ruptured ova Free yolk material in the abdominal cavity Serofibrinous pericarditis and peritonitis Large amount of viscous mucous in the larynx

crop and intestine

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Edematous cyanotic comb and wattles

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Mucous excretion

from mouth

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Fibrinous pericarditis and perihepatitisEnlarged liver

Small areas of necrosis in the liver (corn meal liver)

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Subepicardial hemorrhages and petechiae

on the heart and coronary fat

The left lung has a severe

accumulation of fibrinous exudate on

its pleural surface In turkeys

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Hemorrhagic mucosal and serosal lesions

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs amp lesions of FC

3 Chronic forms

A Wattle form

Unilateral or bilateral swelling of wattle

Caseous exudates in the wattles cut sections

B Otitis media form

Nervous signs as torticollis

Caseous exudates in the middle ears and air spaces of cranial bones

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs amp lesions of FC

C Arthritic form Swelling of the joints and lameness Caseous exudates in the joints Inflammation of the tendon sheet Hemorrhages and erosions on the articular

cartilageD Ovarian form Drop in egg production Cheesy material around the ovary and

peritoneal cavity

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Signs amp lesions of FC

E Roup or catarrhal form

Respiratory signs (rals and dyspnea)

Mucous discharge from the mouth

Nasal discharge

Swelling of the sinuses and facial oedema

Conjunctivitis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Swelling of wattle

Swelling of the wattles

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

Swelling of the ear canal (middle ear)

Torticollis

Torticollis

strenal

bursitis

Arthritis

Caseous exudate over the hock region and

food pad

Swelling of the sternal bursae

Hyperemia and flaccid mature follicles

Egg-yolk peritonitis

Sinusitis and facial oedema

Yellow caseous exudate in the air spaces of the cranial bones

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Hyperemia and flaccid mature follicles

Egg-yolk peritonitis

Sinusitis and facial oedema

Yellow caseous exudate in the air spaces of the cranial bones

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Egg-yolk peritonitis

Sinusitis and facial oedema

Yellow caseous exudate in the air spaces of the cranial bones

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Sinusitis and facial oedema

Yellow caseous exudate in the air spaces of the cranial bones

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Yellow caseous exudate in the air spaces of the cranial bones

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Diagnosis of FC

Demonstration of bipolar P multocida mo

either from the blood film in acute stage afterstaining with Giemsa Leishmanrsquos stains andseen under microscope

or take impression smear from organs (liver)stain and examine microscopically

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Bipolar Pmultocida in between nucleated RBCS in acute infection

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Rough colony on the right and a smooth colony on the left

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Diagnosis of FC

Laboratory animal inoculationIntraperitoneal or SC inoculation of rabbit or mice

or hamster with blood of infected bird orsuspected material (liver supernatant) (02 ml)induces death of these animals within 24-48 hourspost inoculation with septicaemic pictureImpression smear from blood or tissues (liver)shows bipolar organism

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Prevention of FC Adopt all biosecurity measures

Vaccination

P multocida antigen vaccine should be homologous tothat cause fowl cholera or use of autogenous localprepared vaccine in endemic area or when commercialones are not protective

There are many types of vaccines against FC

Whole cell bactrine

Live attenuated vaccine

a CU- vaccine

b Mutants of CU-vaccine as M-9 MN and PM-1 strainsto avoid post vaccinal reaction of the CU

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Prevention of FC

In turkeys

Meat type 6-8 weeks bactrine injection or CU via drinking water and repeated every 4-6 weeks till marketing

Breeder flocks must be vaccinated first at 6- 8 weeks and revaccinated 2-5 times till start of egg production according to epidemiology of FC in the area and farm

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Control of FC

In chicken and turkeys sulfamerazine 02 in water or 04 in feed or Sulfaquinoxaline 001 ndash005 in water for 3-5 days to stop deaths in 2 days

Streptomycin (150 mg) for IlM injection in turkeys

Chloro- or oxytetracycline 40 mgkgbw by IlM

Chloramphenicol 20 mgkgbw via IlM

Enrofloxacin hellipetc

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

AVIAN SPIROKETOSIS

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Avian spiroketosis

The bacterium Borrelia anserina infects chickens turkey geese ducks pheasants grouse and canaries with morbidity and mortality up to 100

It is transmitted by arthropods eg Argas persicus and occasionally by infected faeces The bacterium is poorly resistant outside host but may be carried by Argas persicus for 430 days

Brachyspira pilosicoli previously known as Serpulina pilosicoli is an intestinal spirochaete that can be associated with inflammation of the large intestine in a broad range of mammals and birds

It has been associated with typhilitis diarrhoea reduced egg production and egg soiling in chickens

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Signs amp lesions of avian spiroketosis

Depression and thirst Cyanosis Often diarrhoea with excessive urates Weakness and progressive paralysis Drops in egg production may be seen in both systemic

and intestinal forms Post-mortem lesions Marked splenomegaly Spleen mottled with ecchymotic haemorrhages Liver enlarged with small haemorrhages Necrotic foci Mucoid enteritis

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Prevention amp Control of avian spiroketosis

Treatment

Various antibiotics including penicillin

Prevention

Control vectors

Vaccines in some countries

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Cause

Age group affected

Transmission

Forms of the disease

Escherichia coli

All types of avian and all ages

Fecal oral route transovarial contamination of the egg shell via fecal material from hen

Colisepticaemia

Airsac disease

Chronic forms (arthritis omphalitis panophthalmitis salpingitis enteritis coligranuloma and SHS)

E coli

Severely congested liver

Foci of necrosis on liver

Severely congested liver

Foci of necrosis on liver

GANGARINOUS

DERMATITIS

(GD)

GAS OEDEMA DISEASE

WING ROT

Gangrenous dermatitis

Gangrenous (necrotic) dermatitis in broilers and turkeys between 3-7 weeks old

It is caused by a bacteria- Clostridium septicum Escherichia coli Staphylococcus aureus

Disease often occurs in birds which are already immunosuppressed due to a prior infection (Chicken anaemia Infectious Bursal Disease) or mycotoxin ingestion

Transmission is by contact with infected wet caked litter The disease often occurs in immunosuppressed birds

Signs of GD

Loss of feathers

Pale combs and wattles depression

Incoordination

Leg weakness and ataxia (canrsquot move) can be seen

Mortality is low but dead birds decompose quickly

Lesions of GD

Congestion haemorrhage and necrosis of skin with intro lesion bacteria under the microscope

In turkeys with cellulitis of the tail (bubbly tail) edema and vesicle-like lesions were present laterally and ventrally around the tail

Tail feathers were soft blood-filled and broken

Dark and moist skin of the breast

Necrosis of the abdomen skinAffected leg and toes

Necrosis of the wattle

Ulceration and gangrenous formation of skin

Gangrenous dermatitis

Gangrenous (necrotic) dermatitis in broilers and turkeys between 3-7 weeks old

It is caused by a bacteria- Clostridium septicum Escherichia coli Staphylococcus aureus

Disease often occurs in birds which are already immunosuppressed due to a prior infection (Chicken anaemia Infectious Bursal Disease) or mycotoxin ingestion

Transmission is by contact with infected wet caked litter The disease often occurs in immunosuppressed birds

Signs of GD

Loss of feathers

Pale combs and wattles depression

Incoordination

Leg weakness and ataxia (canrsquot move) can be seen

Mortality is low but dead birds decompose quickly

Lesions of GD

Congestion haemorrhage and necrosis of skin with intro lesion bacteria under the microscope

In turkeys with cellulitis of the tail (bubbly tail) edema and vesicle-like lesions were present laterally and ventrally around the tail

Tail feathers were soft blood-filled and broken

Dark and moist skin of the breast

Necrosis of the abdomen skinAffected leg and toes

Necrosis of the wattle

Ulceration and gangrenous formation of skin

Signs of GD

Loss of feathers

Pale combs and wattles depression

Incoordination

Leg weakness and ataxia (canrsquot move) can be seen

Mortality is low but dead birds decompose quickly

Lesions of GD

Congestion haemorrhage and necrosis of skin with intro lesion bacteria under the microscope

In turkeys with cellulitis of the tail (bubbly tail) edema and vesicle-like lesions were present laterally and ventrally around the tail

Tail feathers were soft blood-filled and broken

Dark and moist skin of the breast

Necrosis of the abdomen skinAffected leg and toes

Necrosis of the wattle

Ulceration and gangrenous formation of skin

Lesions of GD

Congestion haemorrhage and necrosis of skin with intro lesion bacteria under the microscope

In turkeys with cellulitis of the tail (bubbly tail) edema and vesicle-like lesions were present laterally and ventrally around the tail

Tail feathers were soft blood-filled and broken

Dark and moist skin of the breast

Necrosis of the abdomen skinAffected leg and toes

Necrosis of the wattle

Ulceration and gangrenous formation of skin

Dark and moist skin of the breast

Necrosis of the abdomen skinAffected leg and toes

Necrosis of the wattle

Ulceration and gangrenous formation of skin

Ulceration and gangrenous formation of skin

Prevention amp Control of GD

Prevention Clean out house and add new litter to prevent the

disease Medicate in starter feed Flavomycin Virginamyciin

Bacitrcin and CTC can reduce bacteria Proper vaccination against IBDV CAV and MDV prevent

mycotoxin formation in the feed and eliminate ALV in the breeders to prevent immunosuppression

Treatment Erythromycin penicillin in the feed to treat signs

Chlortetracycine oxytetracycline copper sulphate can be added to the water to reduce morbidity

ULCERATIVE ENERITIS

(UE)

Ulcerative Enteritis

Turkeys of 6-14 weeks are susceptible to this acute to chronic disease

The agent involved in the aetiology of this disease is clostridium colinum which is spore-forming gram-positive aerobic and non-motile

Mode of transmission

Vectors are faeces soil and litter containing the bacteria

It often accompanies coccidiosis in broilers

Signs amp lesions of UE

High mortality watery diarrhoea ruffled feathers dull listlessness increased thirst emaciation and atrophy of pectoral muscles can occur

Postmortem lesions Yellow irregular ulcers on small intestine and

caeca hemorrhagic enteritis are seen Enlarged haemorrhagic necrotic spleen light

yellow mottling of liver and crop filled with water may occur

Prevention amp Control of UE

Prevention Improved sanitation Adding salt to the soil (500

lbs of salthouse) may kill spores Raising birds on wire andor feeding bacitracin at 50-100 gt will prevent the disease

Treatment NF-180 (50-100 gt) strephomycin (60 gt) and

chlortetracycline vitamins and minerals in water andor lincomycin 2 gt will reduce the signs

Remove dead birds and feed bacitracin (200 gt)

Thank you

ANY QUESTIONS

ULCERATIVE ENERITIS

(UE)

Ulcerative Enteritis

Turkeys of 6-14 weeks are susceptible to this acute to chronic disease

The agent involved in the aetiology of this disease is clostridium colinum which is spore-forming gram-positive aerobic and non-motile

Mode of transmission

Vectors are faeces soil and litter containing the bacteria

It often accompanies coccidiosis in broilers

Signs amp lesions of UE

High mortality watery diarrhoea ruffled feathers dull listlessness increased thirst emaciation and atrophy of pectoral muscles can occur

Postmortem lesions Yellow irregular ulcers on small intestine and

caeca hemorrhagic enteritis are seen Enlarged haemorrhagic necrotic spleen light

yellow mottling of liver and crop filled with water may occur

Prevention amp Control of UE

Prevention Improved sanitation Adding salt to the soil (500

lbs of salthouse) may kill spores Raising birds on wire andor feeding bacitracin at 50-100 gt will prevent the disease

Treatment NF-180 (50-100 gt) strephomycin (60 gt) and

chlortetracycline vitamins and minerals in water andor lincomycin 2 gt will reduce the signs

Remove dead birds and feed bacitracin (200 gt)

Thank you

ANY QUESTIONS

Ulcerative Enteritis

Turkeys of 6-14 weeks are susceptible to this acute to chronic disease

The agent involved in the aetiology of this disease is clostridium colinum which is spore-forming gram-positive aerobic and non-motile

Mode of transmission

Vectors are faeces soil and litter containing the bacteria

It often accompanies coccidiosis in broilers

Signs amp lesions of UE

High mortality watery diarrhoea ruffled feathers dull listlessness increased thirst emaciation and atrophy of pectoral muscles can occur

Postmortem lesions Yellow irregular ulcers on small intestine and

caeca hemorrhagic enteritis are seen Enlarged haemorrhagic necrotic spleen light

yellow mottling of liver and crop filled with water may occur

Prevention amp Control of UE

Prevention Improved sanitation Adding salt to the soil (500

lbs of salthouse) may kill spores Raising birds on wire andor feeding bacitracin at 50-100 gt will prevent the disease

Treatment NF-180 (50-100 gt) strephomycin (60 gt) and

chlortetracycline vitamins and minerals in water andor lincomycin 2 gt will reduce the signs

Remove dead birds and feed bacitracin (200 gt)

Thank you

ANY QUESTIONS

Signs amp lesions of UE

High mortality watery diarrhoea ruffled feathers dull listlessness increased thirst emaciation and atrophy of pectoral muscles can occur

Postmortem lesions Yellow irregular ulcers on small intestine and

caeca hemorrhagic enteritis are seen Enlarged haemorrhagic necrotic spleen light

yellow mottling of liver and crop filled with water may occur

Prevention amp Control of UE

Prevention Improved sanitation Adding salt to the soil (500

lbs of salthouse) may kill spores Raising birds on wire andor feeding bacitracin at 50-100 gt will prevent the disease

Treatment NF-180 (50-100 gt) strephomycin (60 gt) and

chlortetracycline vitamins and minerals in water andor lincomycin 2 gt will reduce the signs

Remove dead birds and feed bacitracin (200 gt)

Thank you

ANY QUESTIONS

Prevention amp Control of UE

Prevention Improved sanitation Adding salt to the soil (500

lbs of salthouse) may kill spores Raising birds on wire andor feeding bacitracin at 50-100 gt will prevent the disease

Treatment NF-180 (50-100 gt) strephomycin (60 gt) and

chlortetracycline vitamins and minerals in water andor lincomycin 2 gt will reduce the signs

Remove dead birds and feed bacitracin (200 gt)

Thank you

ANY QUESTIONS

Thank you

ANY QUESTIONS

ANY QUESTIONS