Swine diseases

Neonates 0-3 weeks (birth: 3-4 lbs)

<4 kg (8.8 lbs) Weanlings/nursery 3-10 weeks (~ 25 lbs)

4-25 kg (8.8 – 55 lbs) Growers/finisher 10-26 weeks (~ 50

lbs)

25-120 kg (55 – 264 lbs) Breeders/adults >6-8 months (~ 220 - 240 lbs)

>120 kg (> 264 lbs)

Multisystemic Diseases Respiratory Diseases Gastrointestinal Diseases Neurologic Diseases Musculoskeletal Diseases Reproductive Diseases Dermatology Miscellaneous

Nutritional◦ Vitamin E / selenium deficiency

Infectious◦ Erysipelas (Erysipelothrix rhusiopathiae): gram +

rod◦ Glasser’s disease (Haemophilus parasuis): gram -

coccobacillus◦ Salmonella: gram negative◦ PRRS (arterivirus)◦ Pseudorabies virus (herpes virus)

Erysipelothrix rhusiopathiae Gram positive rod

Environmental contaminant most herds have carriers

Septicemia diamond skin, arthritis, endocarditis, necrosis

acute septicemia ◦ fever, prostration,

anorexia, vomiting, reluctance to walk

◦ Hemorrhages may be present in multiple organs throughout the body.

◦ Mortality can be quite high.

chronic forms of infection include endocarditis and arthritis

"Diamond skin disease" erythematous skin lesions •These may be the classic diamond-shaped lesions or more diffuse edema and erythema. •The lesions are due to vasculitis and thromboembolism.

Treatment Penicillin Tetracyclins

Prevention and control Sanitation Vaccinate at weaning and

then q6 months Zoonotic: ‘erysipeloid’

occupational diseases for people such as veterinarians, abattoir workers and fisherman

Direct contact

Penicillin – first choice people and animals cephalosporins and clindamycin -people. Caution and hygiene are important to

prevent infection when working with potentially infected animals or in potentially contaminated environments

Haemophilus parasuis small, pleomorphic, and fastidious, Gram-negative

rod (coccobacillus) Endemic 3wk – 3 month (have no active/passive

immunity) initiated by stress

◦ weaning, changes in environment, commingling, or as coinfection with other disease agents

Also associated with PRRS or swine influenza

1931 an organism, presumably the same one, was isolated from swine with influenza and named Haemophilus influenzae suis.

1943 it was clear that the organism was a pathogen in its own right, not necessarily associated with swine influenza, and the name was shortened to Haemophilus suis.

1976, definitive taxonomic studies resulted in the present name, Haemophilus parasuis

Initially: fever, anorexia, depression Meningoencephalitis:

◦ tremors, incoordination, posterior paresis or lateral recumbency

Polyserositis Polyarthritis Mortality at any age Less common clinical signs:

◦ rhinitis, dyspnea, reddening of the conjunctiva, cyanosis of the extremities and edema of the eyelids or ears

Serosal surfaces: peritoneum, pleura, pericardium, joints, meninges

Polyserositis (serous membrane inflammation with effusion, fibrinous),

Pleuritis Pericarditis Peritonitis

Pig with Glässer’s disease. Noticeable presence of fibrin in the peritoneal cavity (fibrinous peritonitis) and pericardiac cavity (fibrinous pericarditis

red, multifocal, disseminated and suggestive of septicemia and hematogenous spread

Diagnosis Culture is difficult (but try it)

Brain, visceral pleura and other serosal exudates are preferred culture sites

Go with suspicion from gross lesions Molecular techniques for identifying H. parasuis

(research) Treatment: Antibiotics and sulphonamides

Penicillins Tetracyclins periodic evaluation of antibiograms is warranted. Mass: medicate, through the water (same age group)

Prevention and control Reduce stress Control of other diseases: PRRSV prophylactic antimicrobials Vaccine at weaning then again 3-4 weeks later

against one serovar of H. parasuis may not assure good protection against all serovars. (21 serovars)

2000 serotypes: small, hardy, ubiquitous, Gram-negative bacilli◦ Salmonella cholerasuis: mostly only in swine◦ Salmonella typhimurium

Zoonotic Contaminated pork products are not a primary

source of food-borne salmonellosis outbreaks in people but efforts to reduce salmonellae in the pork food chain are a high priority for the swine industry

disease in both people and swine include Salmonella serotypes typhimurium, enteritidis, agona and heidelberg

Microbiologist Brad Bearson analyzes cultures for the presence of Salmonella enterica serovar Typhimurium in swine feces.

“But S. Typhimurium’s success in swine isn’t just due to its increased motility when norepinephrine levels increase. It also has a mechanism for acquiring iron from its host to support its own growth and replication” 7/2009

In 1886 the organism now known as Salmonella serotype choleraesuis was erroneously reported to cause hog cholera

weaned or growing/finishing pigs

Low-level endemnicity, carriers

Septicemia pyrexia, anorexia purple discoloration of

the ears (infarction) Small or large intestinal

diarrhea (button ulcers) Pneumonia Rectal strictures

Pig, intestine. The intestinal lumen has reddened erosions and a fibrinonecrotic exudate. Credit: Dr. B. Inskeep, AFIP

Diagnosis Aerobic culture

Treatment Neomycin in the feed/water

for whole group Naxcel (ceftiofur) for

individual Prevention and control

Sanitation: inactivated by chlorine, iodine and phenol-based disinfectants

All in - all out operation Various vaccines (live

avirulent)Pig, mesenteric lymph node. The mesenteric lymph node is enlarged and edematous. This lymph node is good for obtaining cultures.Credit: Dr. B. Inskeep, AFIP

Porcine reproduction (sows and gilts) and respiratory syndrome (young growing pigs but also occurs in naïve finishing pigs and breeding stock)

Most important economic disease in USA (after eradication of classical swine fever)

Arterivirus: SS enveloped RNA Virus (high mutation rates)

persist in long-term carrier pigs (greater than 200 days) in reality stop shedding 60 days later

1987-88 in North Carolina, Iowa and Minnesota 1989 – 90: Several outbreaks in Indiana were reported During the subsequent decade, PRRS spread rapidly, both

in Europe and North America By the end of 1992 the disease was reported in Canada,

Great Britain and several European countries. Two distinct strains of virus, one in Europe and one in the

United States, were characterized as genetically different but are clinically similar in most respects. Both are now in the United States, along with a multitude of viral variants.

Old name: swine infertility and respiratory syndrome (SIRS)

Transmission: direct contact (very infectious): It is present in nasal secretions, urine, semen, mammary secretions and

feces. Clinical signs – neonates pulmonary intravascular macrophages (PIM) and

pulmonary alveolar macrophages (PAM); anorexia, lethargy, fever cyanosis of the ears, respiratory distress secondary bacterial pneumonia delayed or abnormal estrus cycle with increased

numbers of stillborns/mummies (3rd trimester)

Abortions, mummies and weak pigs

Lung affected with interstitial pneumonia of a pig with PMWS and co-infected with porcine reproductive and respiratory syndrome virus (PRRSV). This “infectious combination” is relatively frequent at field level; macroscopically it is not possible to distinguish between these two infections, so laboratory studies are required to confirm the etiologic diagnosis.

Diagnosis virus isolation (VI), detection of PRRS antigen by

fluorescent antibody tests (FAT) or immunohistochemistry (IHC), or detection of PRRS virus genome by polymerase chain reaction (PCR) and be coupled with presence of typical lesions.

serology provides indirect evidence of infection but does not determine if there is actual disease caused by PRRS virus.

Supportive care, treat secondary bacteria moderately resistant to environmental degradation,

the virus is easily inactivated by phenol, formaldehyde, and most common disinfectants

closed herds: ◦ replacements do not enter male or female replacements from

PRRSv positive herds outside the pyramid◦ Enter only PRRSv free replacement seedstock into a

production pyramid. semen:

◦ Do not use PRRSv positive semen from a stud outside the pyramid.

◦ Assure any outside semen is from a stud that is confirmed PRRSv free before entering it into a production pyramid.

commercial modified live vaccines◦ Live vaccines pose a dilemma as vaccine virus may act as a

foreign introduction Change feed with mycotoxins

Aujesky’s disease Type 1 Herpes virus: alphavirus The disease was eradicated from the US

commercial pig industry in 2004 but remains in some localized feral swine populations

Species: cattle, sheep, dogs, cats, and goats but not horses AND rats, mice, raccoons, opossums, rabbits, and several fur-bearing mammals◦ Close contact with infected swine

central nervous system (CNS), respiratory system or reproductive system

Not humans!

The disease is named after the Hungarian veterinarian Dr. Aladár Aujeszky who linked the disease in cattle, dogs, and cats in 1902.

Pseudorabies was not identified as a viral disease in swine until 1909

Prior to 1960, the disease in swine was important in Eastern Europe but major outbreaks did not occur in the US until the mid-1970s

In 1989, the US embarked on a 5-stage Federal/State/Industry program for eradication of PRV in swine; eradication of PRV from the commercial industry was achieved in 2004

Baby piglets up to 100% mortality high fever, depression, anorexia, tremors,

incoordination, dog-sitting position, vomiting, foaming at the mouth, blindness, paddling, coma and convulsions

Weanling/growers up to 60% mortality in weanlings, 0-15% in finishers pneumonia impt, neurologic dz, vomiting, extreme

pyrexia Adults - often inapparent

can cause stillbirth/abortion

Dead pigs (and a cat), a result of PseudorabiesMummified pigs, a

symptom of Pseudorabies

Lesions on post-mortemed lung

Lesions on nose of piglet

Reportable disease! Diagnosis

Necropsy - histologic lesions in brain, ulcers in gi tract

Serum neutralization is standard test ELISA can be used as a screening test

Treatment - none Prevention

closed herd! quarantine! restrict wildlife The virus can be destroyed by many disinfectants,

including orthophenylphenol, quarternary ammonium or iodine compounds, and 5% sodium hydroxide

vaccination

Regulation◦ use of vaccine regulated by states◦ federal regulations for monitoring

all animals over 6mo old must be tested 25% of herd tested q3months or... 10% of herd tested q1month

Nursery or grower pigs (few weeks – 4 months)

Vitamin E / Selenium deficiency Feeds high in the concentration of polyunsaturated

fatty acids, copper, vitamin A or mycotoxins can either destroy vitamin E or make it less bioavailable

Grains from soils deficient (midwest) in selenium, or selenium antagonists in mixed feeds, can result in feeds low in selenium.

Both vitamin E and selenium work as antioxidants.

Clinical signs acute death (mulberry heart disease) muscle weakness (white muscle disease)

more common in lambs, calves and chickens rather than swine

Diagnosis Necropsy - hydropericardium, fibrinous epicarditis,

myocardial hemorrhage Diffuse hepatic necrosis - hepatosis dietetica Liver selenium < 0.5 ug/g

The condition was named after the mottled appearance of the heart muscle in affected pigs. Typically, there are alternating areas of necrosis and hemorrhage throughout the myocardium.

Hepatosis dietetica consists in a degenerative lesion caused by vitamin E and selenium insufficiency.

prevention or treatment of a deficiency, pigs can be injected with vitamin E and/or selenium and tissue levels will be increased rapidly.

supplementation of feed or drinking water Sows injected in late gestation give birth to

pigs with increased levels of both compounds.

MHD is more responsive to vitamin E; HD more so to selenium

http://www.aphis.usda.gov/animal_health/animal_dis_spec/swine/

http://www.ncsu.edu/project/swine_extension/ncporkconf/2002/roberts.htm

http://www.vetmed.wisc.edu/pbs/zoonoses/Erysipelas/erysipelasindex.html

http://vetmed.iastate.edu/vdpam/new-vdpam-employees/food-supply-veterinary-medicine/swine/swine-diseases/haemophilus-parasuis-

http://vetpath.wordpress.com/category/necropsy-cases/

http://www.fmv.utl.pt/atlas/figado/pages_us/figad015_ing.htm