dr khaled selim lecture 2011

In the Name of Allah,In the Name of Allah,

the Most Beneficent, the Most the Most Beneficent, the Most Merciful. Merciful.

Khaled M. Selim110509

Curriculum Vitae (C.V.)Dr: Khaled Mohamed Selim Mohamed Abd

ElrahmanLecturer of Fish Diseases and Management

Faculty of Veterinary MedicineZagazig University, Egypt

Academic Qualification : 1- Bachelor of Veterinary Medical Sciences (B.V.Sc) May, 1998 from

Zagazig University, Grade Very good.2- Master of Veterinary Medical Sciences (M.V.Sc), Fish diseases and

management since, July 27, 2002 from Zagazig University.Title: Studies on Some factors affecting health and survival of Ornamental

fish.3- Doctor philosophy of Science (Ph. D.), Reproductive biology of fish,

March 23, 2009 from Niigata University, Japan.Title: Effects of temperature and methyl testosterone on sex reversal of fish.4- Post-doctoral researcher for a year (2009 –2010), in Department of

Environmental Science, Fac. of Science, Niigata University, Japan.

Fish diseasesFish diseases

Parasitic Diseases

External or Ectoparasitic

Internal or Endoparasitic

Affect head, fins, skin, eye, opercula, buccal cavity, the surface of nasal epithelium or olfactory epithelium, crypts of the acoustolateralis system or gills.

internal organ- blood – swim bladder and deeper layer of muscles

Metazoal Diseases

ArgulosisErgasilosisLerneosis

Endoparasitic Metazoa

Digenetic trematode Cestode Nematode

Black spot disease

Yellow grub disease

Parasitic cataract

Blood fluke

Contracaecum

Diphylobothriasis

Ligulosis

Amplicaecum

Anasakiasis

Acanthocephala

1-Monogenetic trematodes• Diseases of bad water quality

• Affect external surface of fish

• Affect freshwater and marine water by direct contact

• direct life cycle

• All are hermaphrodites

• the attachment occurs by haptor ( Opisthaptor- Prohaptor)

• They mainly fed on tissue debris and blood

Etiology and suscebitability Dactylogyrus spp (gill fluke) up to

2mm Gyrodactylus spp (Skin fluke)

measure up to 0.4mm Benedenia and Neobenedenia spp

mainly affect marine fish (oral and cutaneous fluke) 5-12 mm

Dermophthrius spp mainly affect shark

•The identification of monogenea depends on

1. Haptor structure

2- Eye spots or pigments

3- Body size

4- Alimentary tract structure

5- Reproductive organ [oviparous or viviparous]

6- Site and mode of attachment

7- Feeding behavior

Benedenia and Neobenedenia spp

very small eye spots

8- Host specificity, geographical distribution and season

Life cycle

Life cycle

Dactylogyrus species at 24-28°C life cycle will be around 11-13 days

Mature eggs developed within 2-3 days

Post-oncho-miracidium is sexually matured in 4-5 days.

Epizootiology

Mechanical transmission by birds, reptile and amphibians

Nets and buckets are vehicle of transmission

Clinical signsI. General signs Affected fish appear

lethargic abnormal swimming

behaviors. Loss of reflexes Dark coloration

especially in heavy infection

Lower condition factor in long heavily infected fish

Abnormal swimming and movement

Loss of appetite

Remain at the side or bottom of the pond

Restlessness Listlessness Emaciation Hyperirritability

II. General signs of body surface affections

Irritation of skin Swim against

water current Scratching body

against any hard objects

Copious quantities of mucous

Loss of scales

• Minute abrasions or erosion

Sometimes small ulcer

hyperemia at the base of the fins

Sometimes secondary invaded by bacteria or fungi

III. General signs of gill affections

Aggregate on water inlet

Aggregate on water surface

Gasping of air Increase

opercula movement

Vertical swimming

Jump outside water

Die with open mouth

Infected gills sometimes appear pale or be covered by whitish patches

Economic importance Affect all types of fish Mechanical damage due to hooks Mechanical carrier for bacterial and

viral agent Secondary bacterial or fungal invasions Eye affections lead to blindness Decrease growth rate Individual Mortalities Aggregation of ration may lead to high

ammonia level

DiagnosisDiagnosis

• HistoryHistory

• clinical sign and PM lesionsclinical sign and PM lesions

• Parasitic examinationParasitic examination

• Molecular examinationMolecular examination

A) Prevention

Prophylactic measurements. predisposing cause source of infection

1 -Quarantine and restriction of movement of fish.2 -Good water quality.

3 -Reduction of over crowding of fish.4 -Proper nutrition of fish .

5 -Periodical disinfection of ponds by 120 kg quick lime/

hectar .6 -Control of aquatic plants .

7 -Control of organic matter.8 -All utensils such as nets, buckets, aereators,

must be disinfected.9 -Regular examination of fish for parasites.

B) Treatment and control

Prophylactic spray of chemical agents starting at mid-April up to end of July as dipterex. Ammonia can reduce infection so can be used in ammonia tolerant fish as Japanese eel (40 ppm)

Chemotherapy1. Dipterex: prepare 50% solution in xylene and

apply it to the pond at a dilution of 0.8ppm. 2. Potassium permanganate 20ppm with 4%

Nacl3. Methylene blue, Malachite green formalin,

Ammonium hydroxide, masotene….etc

Metazoal Diseases

Ectoparasitic Metazoa

Monogenetic trematode

Hirudinea or leech

Crustacean or Copepode


2- Hirudinea – leech – Annelid worm Parasites of fish,

amphibians and aquatic reptiles ( in both fresh and marine water)

blood suckling parasites affect body surface, fins, gill or mouth cavity.

Carried to the farm through contaminated water

Bisexual temporary parasites

Leave after the meal searching for

shelterLeave for cocoon

deposition

Can be seen by naked eye (2-4 cm) and swim actively to reach the prey

Body formed from several segments and has 2 suckers( anterior contains mouth and posterior contains suckers for attachment)

They are temporary or semi permanent

Etiology / susceptibility Class: Hirudinea

Phylum: AnnelidaSubphylum: Clitellataorder: Rhynchobdellida (Most important) 1) Family: Piscicolidae (Cylendrical

leech) – 4-8 cm 2) Family: Glossiphoniidae (flat leech)- 2-4 cm

The identification of leeches depends on

1. Body shape2. Length of the

body3. Pigmentation

colour and pattern

4. Numbers and arrangement of the eyes

5- Crescent form pigments on the body and caudal suckers.

6- Arrangement of papillae or tubercles.

It is better to examine the leech in fresh and relaxed state

• We can use alcohol or menthols crystals for short time in a Petri dish before the change of pigment colors

Male put sperms through spermatophore in female gonopore

Mating occures on or off the host fish

Fertilized egg will be attached to female body (within a special socket) or deposited on aquatic substrate (??) in the form of cocoons(1-5).

Off springs can survive for a week or more before their first blood meal

The period of nursing varies from 24 days – 4 months according to water temperature

After nursing leech need 3- 4 blood meals to reach maturity

Life cycle

Clinical signs and pathology

Leech as it is can be seen by naked eye

Site of affection appears well defined rounded and sometimes oozed blood

General sign of anemia especially in young fish ( thin body, emaciation, big head…)

HB content drop from 50 to 20%

RBCs count drop from 1.5 million to 300000/ml2.

Economic importance Affect all types of fish Young fishes are more seriously affected especially

that live in the bottom….lead to reduction in vitality and death ( so it will lead to great damage to hatcheries).

Mechanical damage to skin and scale pockets (sever epidermal erosions) due to suckers followed by Secondary bacterial or fungal invasions

Vector transmitter for haemoprotozoa Mechanical transmission of viral and bacterial

diseases Leech can suckle about 150 ml of blood within 2 days

leading to marked anemia Produce Hirudin enzyme that acts as anticoagulant

leading to oozing of blood from fish after leech leaving host

A predisposing cause for opportunistic pathogen Decrease growth rate Individual Mortalities

DiagnosisDiagnosis

• HistoryHistory

• clinical sign and pathologyclinical sign and pathology

• Parasitic examinationParasitic examination

• Molecular examinationMolecular examination

Treatment and control

Prophylactic: remove aquatic vegetations, apply net with small mesh size to prevent leech or gravels and stone entrance with water, summer drying season (chlorinated lime is able to destroy both live leech and cocoons),

Chemotherapy1. Dipterex: prepare 50% solution in xylene and apply it

to the pond at a dilution of 0.8 ppm. 2. Masotene: 0.5-1 ppm in fish pond but harmful to

zooplankton.3. Neguvon 1ppm for 5 days is effective against adult

leeches but not eggs4. We can use OPC or chlorine* Marine water leeches have very little trials for

treatment.

Metazoal Diseases

Ectoparasitic Metazoa

Monogenetic trematode

Hirudinea or leech

Crustacean or Copepode


III- Copepodes – Parasitic crustacea

Many of crustacean parasite are lethal under certain circumstances, other depilating and other of major importance to fish culture and the fishing industry

It showed exoskeleton with jointed appendages and segmented body.

Affect mainly external surface of body. Many of parasitic copepods burrow into the flesh

and cannot be dislodged by chemical treatment Treatment is directed toward killing larval forms.

Oviparous parasites with separate sex They have a complex life cycle which

involves mating of the parasites and attachment of the female to the fish with subsequent production of eggs which pass through several distinct larval stages.

The most important organisms are:1. Lernea2. Ergasilus.3. Argulus

General life cycles of Crustacean parasites

Mature male or female

napuliCopepode stages

Meta napuli

Fertilized egg

3- Lerneosis - Anchor worm Are the most harmful parasite of

cultured fresh water fishes They most commonly found in warm

water fish The destructive activity of lernea is

due to its relatively large size and its mode of attachment and feeding

The are long slender copepod give the appearance of soft strikes with two

eggs sacs attached at the end of the body the head is buried in the flesh by large horn-

like appendages ]anchors} that help in identification of the parasite

Etiology and suscebitability

• Affect mainly freshwater fishAffect mainly freshwater fish• There was two common species which There was two common species which

includeinclude

1.1. Lernea cyprinacea Lernea cyprinacea (host specific) affect carp (host specific) affect carp fish and accidentally other fish species fish and accidentally other fish species

2.2. Lernea elegans Lernea elegans (non host specific)(non host specific)

Life cycle

• infective stage id 3rd copepode stage• Mature stage is 5th • mating occures on 6th copepode stage• male will die after mating while female will die after production of 3 pairs of egg sacs or 20 days

The cycle will not be completed at the following1.Temperature lower than 15ºC2.Drying3.Salinity of 1.8%4.Lower pH 7

Epizootiology

Contaminated water, infected fish or carrier such as amphibians or birds.

1. Lernea itself can be seen by naked eye

2. They penetrate beneath scales and cause a lesion at the point of attachment (inflammation- hemorrhagic and erythematic lesion)


3- Irritation- fish rub itsbody against hard objects- excessive mucous secretion

4- General sign of fish diseases5. When affect gills lead to respiratory

manifestation6. When affect eye lead to blindness7. When affect fins lead to difficult

movement8. When large number of infestation

occures within the same fish lead to emaciation and thinning

Economic importance

Affect all types of freshwater fish Mechanical damage due to Anckors Secondary bacterial or fungal

invasions Eye affections lead to blindness Decrease growth rate Individual Mortalities

History Clinical sign Parasitic identification Wet mount of skin or gills

showing developing stages Molecular studies

Diagnosis

4- Ergasilosis- gill rot

crustacean parasite affect gill of fish.

Etiology and susceptibility Ergasilus spp most commonly found in warm water fish Affect freshwater and sometimes brackish

water fish Carp fish less affected and increase in fish

which live at the bottom Severity increase in high water

temperature and lower salinity. Cyclopoid in shape Female only is parasitic

• Cant be easily seen by naked eye. 2mm • The antennae will be transformed into hooks leading to damage of gill tissue……………..fed on blood and tissue

Life cycle• infective stage is 4th copepode stage• Mature stage is 5th • mating occures on 6th copepode stage• male will die after mating while female will die after production of 3 pairs of egg sacs or 20 days

EpizootiologyHooks penetrate gill tissue leads to hyperplasia

Interfere in blood supply of the squamous epithelium and respiration in fish

Different area of necrosis giving marbling appearance

Ended by sloughing of gill filaments


1.General sign of fish diseases

2.Respiratory signs3.Marbling appearance of gill4.Parasite can be seen by wet mount preparation

Economic importance

Highly significant epizootic of fish Mechanical gill damage due to hooks

Secondary fungal and rarely bacterial invasions

Decrease growth rate High Mortalities

History Clinical sign Parasitic identification under

the microscope Molecular studies

Diagnosis

5- Argulosis- Fish lice-Branchiurans of fish

Non specific Temporary parasites of skin, fins, gills or opercula mucosa

It called fish lice due to it ability to creep about over the surface of fish

Flattened against the side of the body

Can be seen by naked eye Heavy infestation may lead to

death even of large fish

Etiology and susceptibility Argulus spp affect

both fresh and marine water fish

Dorsal surface have a rigid or semi-rigid chitin exoskeleton

Ventral surface has 1.Two suction discs2.Four pairs of thoracic

legs3.Two respiratory area4.No egg sacs

pre-oral sting which injects digestive enzymes

Life cycleLife cycle

7 molts to reach the adult

• After mating female leave host and swim to aquatic plants or hard objects to put egg with sticky mucous material “sometimes mating occurs in water”.• life cycle take about 30-100 days according to water temperature.• water temperature must be above 16ºC for completion of life cycle.

1. Argulus feed by first inserting a pre-oral sting which injects digestive enzymes (or toxin produced from poisoning gland) into the body.

2.This toxin lead to tissue lysis, lymphocytic degeneration and break down of the skin.

3.They then suck out the liquidized body fluids with their proboscis-like mouth.

Epizootiology

4. This feeding activity causes intense irritation and localized inflammation

5. Transmitted via water supply, mechanically by birds and amphibians

Clinical signs and pathologyClinical signs and pathology1.Fish lice are one of the biggest

parasites (5-10 mm) and visible with the naked eye.

2. The site of bite appears as red circular depression with raised margin ( Button like lesion)

3. skin Hemorrhage and ulcer4. irritation and jump outside of

water to get rid of parasite5. general sign of fish disease

•They can cause significant morbidity and mortality• direct tissue damage• opportunistic bacteria such as Aeromonas or Pseudomonas sometimes infect these damaged areas leading to skin ulcers and gill disease. • It is also believed that the stylus may occasionally ‘inject’ viruses and bacteria into the fish.• all these lead to severe stress, which often leads to secondary parasite infestations such as white-spot and Costia.

Economic importanceEconomic importance

DiagnosisDiagnosis

HistoryClinical signParasitic identificationHistopathological section

Molecular studies

A) Prevention of crustacean A) Prevention of crustacean parasitesparasites

1. Summer drying season The parasites will die if dehydrated. If a

pond or tank is infected therefore, complete draining and leaving dry will kill off any parasites

2. copper sulphate as prphylactive treatment3. Quarantine and restriction of movement of fish.4. Good water quality .5. Reduction of over crowding of fish.6. Proper nutrition of fish. 7. Periodical disinfection of ponds by 120 kg quick lime /

hectar. 8. Control of aquatic plants. 9. Control of organic matter.10. All utensils such as nets, buckets, aereators, must be

disinfected.11. Regular examination of fish for parasites.

1. Chemicals interrupt life cyclea chitin inhibitor drugs such as Dimilin

will stop the juveniles developing as they moult their exoskeleton, most of the results have shown these compounds such as Lufenuron and Diflubenzuron to be entirely nontoxic to fish or other animals.

2. The most common treatments are organophosphates, Masoten and Malathion. Using three treatments over the estimated life cycle of the parasite. At typical summer pond temperatures of 20ºC or higher, treatments at 10-day intervals will kill existing adults and juveniles as well as emerging juveniles.

3. In small number reared fish mechanical removal of the parasites and dip in disinfectant (Potassium permanganate) and antibacterial drugs

4. Potassium permanganate is useful in Ergasilus

Treatment and controlTreatment and control



Black spot disease

Yellow grub disease

Parasitic cataract

white grub disease

Contracaecum

Diphylobothriasis

Ligulosis

Amplicaecum

Anasakiasis

Acanthocephala

Blood fluke

Metacercarial disease

1- Digenetic trematod• Trematodes that have a complex life cycle need one or more host• Most digenetic trematodes are not a serious threat to fish health; however, their presence often renders the fish undesirable by consumers.• There are 2 main groups1.Fish act as intermediate host: fish contain metacercaria or encysted metacercaria until will be eaten by final host such as:

a- Diplostomum spathaceum, parasitic cataract, eye fluke b- Clinostomum species, yellow grub disease c- Apophilus donicus, black spot disease2.Fish act as a final host: fish contain adult parasite and produce egg that leave fish to complete life cycle.

General life cycle of digenetic trematode

Die within hours

a- parasitic cataract - eye fluke

Diplostomum spathaceum Final host is aquatic birdsSite in the final host intestineFirst IH is snail as Limnia snailsSecond IH is FishSite in fish eye tissue

Etiology and Etiology and Life cycleLife cycle

Epizootiology•The usual route of transmission from snail to host fish is through water and active penetration of the cercria• Very rare the transmission is possible by fish feeding on snails containing cercariae.• This parasite lodges itself in the eye of a fish and induces cataract formation (from it's metabolic waste) this in turn increases predation on intermediate fish, because the fish is less able to get away from predator due to its new vision handicap.

• The fluke occurs in the lens and fluid portion of the fish’s eye. • A popeyed effect is sometimes created from accumulation of fluids in the eyeball. (Exophthalmia)

Clinical signs and pathologyClinical signs and pathology

• In advanced cases, the eye becomes opaque white and the fish becomes partially or totally blind.

This is a photo of a fish eye encysted with Diplostomum Spathaceum

B- yellow grub diseaseClinostomum marginatumEtiology and Life cycleEtiology and Life cycle

• Final host is aquatic birds• Site in the final 1. infected fish is eaten by a fish-eating bird2. the fish passes down into the stomach of the bird3.the cyst walls are digested by enzymes. 4.The freed grubs migrate up the esophagus to the trachea or the mouth cavity. Or drop with faeces5.the grubs attach themselves and become sexually mature adults. 6.the bird thrusts its beak into the water to feed, eggs laid by the adults are released into the water.

•

First IH is snail as HelisomaSecond IH is Fish (Cercaria burrow through the skin and encyst forming encysted metacercaria). Metacercaria released from their cysts are large and yellow in color , reaching up to 5-6 mm in length and 2 mm in widthSite in fish under the skin, gills and muscles sometimes in body cavity and internal organThe grubs can live for four years inindividual fish.

If the cyst is broken open, a yellowish or whitish parasite will be found


1- Yellowish vesicle can be seen in skin, muscles, gills and sometimes in internal organs2- when affect gills show respiratory manifestation3- general sign of fish sickness4- in human Inadequate cooking lead to haulzun disease

c- black spot disease- Apophilus donicus

Etiology and Life cycleEtiology and Life cycle

Final host is aquatic birdsSite in the final intestineFirst IH is snail as PlanorbellaSecond IH is FishSite in fish skin, tail base, fins, and musculature

1. Variable sized black spots (1 to 3 mm) in the skin, tail base, fins, and musculature.

• The metacercariae of the black grub become encapsulated by host tissue

• melanophores surround the outer layers• the dark color of the embedded grub causes

affected fish to have a “peppered” appearance2- Until the black grubs become encapsulated in the

host, the host loses lipids (fats) and their oxygen requirements increase.

• Heavily infected cold water fish often enter the winter months in lipid depleted (low fat) state; consequently, these fish have few energy reserves to last over winter and that would affect their ability to survive.


1. These parasites normally do not kill fish except in case of vital organ, but may reduce the growth rate if heavily infested.2. The presence of digenetic trematodes often renders the fish undesirable by consumers.3. It leads to sporadic mortalities4. Fish will be easily predated by enemy5. Proper cleaning and cooking will render the parasite harmless to man.


DiagnosisDiagnosis History Clinical sign Parasitic identification

1. identify the metacercaria2. cyst can be released by enzymatic

excystation using hatching solution or digestive solution

3.Complete the life cycle or developed in their natural host

Histopathological section Molecular studies

D- Blood fluke Sanguinicoloiasis

Etiology and Life cycleEtiology and Life cycle

Final host is fishSite in the final flukes of the vascular system of freshwater and marine fish.First IH is snail as Limniafound in cyprinid and salmonid fish in which it is a serious pathogen, especially in cultured carp.

Blood flukes (Sanguinicola) live as adults (in groups /solitary) in the arterioles of the bloodvessels of the mesenteries, hepatopancreas, pericardium,eye, gill, and caudal kidney of salmonoides and other fish species.

Etiology and life cycle

• These tiny worms lay eggs that become trapped in the capillary beds of the gills and other organs where they developed into meracidia • The ciliate miracidia burst from the gill to be eaten by the operculated snail, the only intermediat host.• Cercaria emerge from the snail and penetrate fish to complete the life cycle.

After Cercaria penetrate the skin pass to blood and then to internal organs cause inflammation and decrease the physiological and mechanical efficiency of these organs. In some cases, they kill the host.

Clinical sign and pathology1. Acute form occurs when heavy numbers of the parasites present in brachial BVS (Occlusion, thrombosis, rupture and necrosis) leading to respiratory manifestation and massive mortalities.

2. subacute form occures when heavy numbers of the parasites present in kidney Bvs (Glomerular occlusion- chronic nephritis) leading to general symptoms of ascites

3. Chronic form occures when small numbers of the parasites scattered in the different body organs leading to emaciation and anemia.

Economic importanceEconomic importance1- Massive mortalities when affect fish in acute form2- loss of fish flesh3- anemia and fish become predisposed for opportunistic pathogens3- Damaged kidney and spleen

DiagnosisDiagnosis History Clinical sign Parasitic identification Histopathological section Molecular studies

Prevention and controlPrevention and control All control measurements to

metacercaria are difficult because of the complexity of the life cycle, shortage of blood supply and disease condition.

There is no known control of digenetic trematodes in ponds, other than the possible control of the snails and the birds

The following will help in the reduction of the occurrence.1- Control of snailsA- Mechanical control1.aquatic vegetation act as a food and shade for snails so the reduction of aquatic vegetation will interrupt the life of snails.2.The water inlet should have a small mesh size to avoid introduction of snails to the pondB- Biological control1.Rearing of some snail eating fish such as snail carp2.Rearing of some duck and geese that fed on snails3.Some viruses and fungi that is fatal to snails and save to fish4.Snails that fed on snails but not act as IH for fish pathogeneC-Chemical control1.Copper Sulfate used to control both snails and algae but should not harm fish 2.OPC and CHC2- Aquatic bird control • control the disease in the surrounding birds• Deep water at the pond edge discourages birds that feed in shallow water3- Summer drying season

Monogenean infestations are more dangerous or digenean infestations

1. Have a direct life cycle.2. Mode of attachment.3. Rapid multiplication.



Black spot disease

Yellow grub disease

Parasitic cataract

white grub disease

Contracaecum

Diphylobothriasis

Ligulosis

Amplicaecum

Anasakiasis

Acanthocephala

Blood fluke

Metacercarial disease

Cestodes of fish

Ribbon like parasite, divided into scolex, neck and stroblia

Fish may be act as final host: present in the intestine and pyloric caeci of fish as sexually mature worm eg Proteocephalus

Fish may be act as IH: larval form (plerocercoid ) present outside intestine

1.vital organ ( Brain, heart ..)2.Less vital ( body cavity, visceral organs and

muscle) it will be dangerous in large numbers

Life cycle

1- Ligulosis Ligula intestinalis larvaFinal host is aquatic birdsSite in the final intestineFirst IH is copepodes as cyclopSecond IH fish body cavity (length

20-40 cm, width 0.5-1 cm and express 10% of body weight).

Perch, pike perch, numerous cyprinids and trout are susceptible

Clinical sign and PM lesions1. Reduced growth and emaciation2. Anemia and dark coloration3. Enlargement of the abdomen in post

cephalic region4. Peritonitis and atrophy of internal

organ5. internal organs showed

hemorrhage, necrotic white areas and ascites.

Diphylobothrium latum affect fresh water and marine water fishThis is the longest tapeworm found in man,

ranging from 3-10 meters with more than 3000 proglottids.

Final host are man sometimes fish eating mammals such as dog and cat

Site in the final intestine (3-10 m)First IH is copepodes as cyclop and

diatoms (500 um)

Second IH fish such as (pike, perch, salmon, trout and eel)

Site in fish body cavity (length 20-40 cm).

2- Diphylobothriasis

Hexacanth embryo

Eggs discharged from gravid proglottids in the small intestine of final host are passed in the feces.

The egg hatches in fresh water to produce a ciliated coracidium which needs to be ingested by a water flea (Cyclops) where it develops into a procercoid larva.

When infected Cyclops are ingested by the freshwater fish, the procercoid larva penetrates the intestinal wall and develops into a plerocercoid larva

Man and other animals are infected by eating uncooked fish, mature into adult worms in 3 to 5 weeks.

Etiology and Etiology and Life Life cyclecycle

Clinical signs

1. Plerocercoids are found encysted or lying in the viscera and musculature of marine and fresh water fishes.

2. migrating larvae can cause much damage with adhesions, sterility and even mortality

3. The presence of this cestode affect the market value of fish.

Economic importance of cestodes Migratory larval stages leads to peritoneal adhesions or damaged viscera because of pressure necrosis, other species may affect eye leading to blindness

Poor growth and chronic mortalities Sterility and stop spawning Miserable appearance of fish affect marketing (Diphyllobothrium latum) can have

hypochromic anaemia because it takes up vitamin B12, which is necessary for red blood cells to mature

Diagnosis

History Sign PM lesions Parasitic identification Molecular study

Prevent human being from infection by Freezing for 24 hours, thorough cooking or pickling of fish kills the larvae.

Fish reservoirs should be kept free of raw sewage

Treatment of adult worms in final host using suitable anthelmentic drugs

Prevention and controlPrevention and control

If fish act as final host, use:1. Di-N-butyl tin oxide 0.5- 0.6 %of

diet for 3 days2.Praziquantel bath 2 mg / liter

for 1 - 3 hours or oral 50 mg / kg body

weight / day Summer drying season for

copepode control

Nematodes of fish It is cylendrical parasites with separate sex Either oviparous or viviparous Fish may be act as a final host or

intermediate host or both at the same time The larval form in fish either uncapsulated

or capsulated by host CT When fish act as final host the mature

parasite will be found in the intestine When fish act as IH the parasite will be

found in the abdominal cavity or musculature

When fish act as IH it will be more dangerous than FH where it will usually affect a vital organ not intestine as well they infect the tissue and cause tissue damage during its migration

Nematodes are more noticeable than other endoparasites due to their cuticle are more resistant to the post mortem autolytic enzyme in the dead fish and remain alive.

The most common nematodes are1.Contracaecum2.Amplicaecum3.Anasakis

A- ContracaecumMesentry worm disease

• affect mainly freshwater fish, sometimes brackish• Final host fish-eating birds, marine mammals and sometimes carnivorous fish. • Site in the final intestine• First IH is copepodes as cyclop• Second IH fish • Site in fish in the body cavity and mesenteries• human act as a reservoir host if ate uncooked infected fish

B- AmplicaecumHeart worm disease

• affect mainly freshwater fish•Site in fish in the body cavity and mesenteries mainly in the pericardium and heart

Clinical sign and PM lesions1. encapsulated larval form of variable size in

tissues2. Round worms (red or white ) are found

within the encapsulation and the lesions3. Free, non-encapsulated worms also occur in

the abdominal and pericardial cavity and in sinus venosis (in case of heart worm disease)

4. necrotic lesion in the dermis, the sub dermis and visceral organs

5. deformed or atrophic gonads.

C- AnasakiasisHerring worm disease

• occur worldwide and all species of fish are susceptible.• common in marine mammals especially Herring fish.

The infected crustacean is subsequently eaten by a fish or squid, and the nematode burrows into the wall of the gut and encysts in a protective coat, usually on the outside of the visceral organs, but occasionally in the muscle or beneath the skin.

Clinical signs and PM lesions1. In the live fish larvae may be free or

coiled in capsule of host connective tissue

2. Distension of abdomen will be observed OR sometimes affected fish show no external signs

3. They can be found on or in the viscera, body cavity, skeletal muscles and mesenteries

If third stage larvae consumed in row or inadequately cooked fish, it will cause

1.serious gastrointestinal damage2.acute pain3.vomiting4.Diarrhea and blood in stools5.fever. 6.Larvae can penetrate the digestive

tract and enter the body cavity.


1. decrease the commercial value of affected fish

2. Cause many diseases in fish and man

3. Larval migrations lead to dangerous effect on vital organ

4. Poor growth and chronic mortalities

5. Sterility and stop spawning

Prevention and control of Prevention and control of NematodeNematode

1. Anisakiasis can be avoided by rapid evisceration and preparation fillets, deep freezing to -30 and sufficient marination or thorough cooking

2. Regular examination of fish for parasites.3. Mature parasite use:• Fenbendazole orally 25 mg / kg body

weight / day for 3 days or prolonged immersion 2 mg / liter

• Levamisole HCL orally 2.5 – 10 mg (8mg) / kg body weight / day for 7 days or prolonged immersion 10 mg / liter

dr khaled selim lecture 2011

Health & Medicine