Professional Documents
Culture Documents
Pig Board Review PDF
Pig Board Review PDF
Dr Nicola Parry
Large Animal Pathology, NBC (610) 925-6451
GI DISEASES
(A) PIGLETS UP TO 3weeks TGE (Any age of pig)
Rotavirus
Colibacillosis (E. coli)
Clostridiosis
Coccidiosis
Rotavirus
Etiology: Rotavirus (A,C,B)
Pathogenesis: Villous epithelial cells are damaged & subsequently lost
Clinically: Similar to TGE but less severe. Transient diarrhea & dehydration
Histopath: Villous atrophy; Necrosis of epithelial cells at tips of villi
E. coli can also have endotoxins in their outer membrane that have a role in mastitis, septicemia & urinary
tract infections, amongst others. It is also a cause of polyserositis. Fimbriae are another type of virulence
factor – required for adhesion to mucous membranes.
COLIFORM DISEASES
Edema Disease
Etiology: E. coli (can be Multifactorial).
Pathogenesis: E. coli infects pig ! multiplies & colonizes intestine, adhering via fimbriae ! produce SLT-
IIe, an angiotoxin ! toxin enters blood ! damages vessel walls (especially brain, skin, small
intestine) ! leaky vessels ! edema & neurologic signs.
Clinically: Often a disease of the “best”, fastest growing animals immediately after weaning. Eyelid
edema, ataxia, convulsions & paralysis.
Grossly: Edema of stomach wall, mesocolon, subcutaneous tissue, gall bladder.
Histopath: Vascular fibrinoid necrosis of small arteries & arterioles in the brain (especially brainstem).
Also encephalomalacia.
Remember, however, that E. coli is always in the GI tract – so isolating it does not necessarily
mean it is the etiology of the intestinal disease. Typing is important to perform when E. coli is
identified ! E. coli isolation is considered significant if typing demonstrates the isolate is
positive for any of F4 F5 F6 F41 F18, if more than 107 colony forming units/ml are present or
if the isolate adheres to cultured porcine epithelial cells.
CLOSTRIDIOSIS
Several Clostridial species cause disease in young pigs.
Clostridium difficile
Pathogenesis: Little known. Spores normally present in large intestine proliferate when normal flora is
upset ! toxin production (essential to disease). The toxins are the largest known – type A
is enterotoxic & causes fluid accumulation in the intestine. Type B is cytotoxic (cytopathic
for cultured cells).
Clinically: Piglets 1-7 days old with yellow diarrhea – can begin soon after birth.
Grossly: Mesocolonic edema, ascites, hydrothorax.
Histopath: Restricted to large intestine.. Mesocolonic edema. Erosive, fibrinosuppurative enteritis.
Coccidiosis
Etiology: Isospora suis
Clinically: Disease 7-11 days old, therefore can rule out this as a cause of early onset diarrhea.
Source of protozoal oocysts is unclear, but they do not originate from the dam.
Grossly: Catarrhal to Fibrinonecrotic, pseudomembranous enteritis in many cases.
Histopath: Villus atrophy or fusion. Erosive or necrotic enteritis. Parasites in vacuoles in enterocytes.
Other organisms can cause diarrhea in young pigs, including cryptosporidium, adenovirus,
calicivirus, parvovirus & Chlamydia, although are uncommon.
Intestinal Spirochetosis
Etiology: Brachyspira pilosicoli (Weakly β-hemolytic)
Clinically: Mild colitis.
Grossly: Mild catarrhal to fibrinous colitis with a loose “wet-cement-like” stool.
Histopath: Mild superficial erosive colitis with goblet cell hyperplasia & mats of serpentine spirochetes
in crypts.
Salmonellosis
Mostly caused by S. typhimurium & S. choleraesuis. Typhimurium causes enteric disease &
choleraesuis causes septicemia, often with subsequent pneumonia, enterocolitis, hepatitis &
meningoencephalitis. Both tend to occur in grower & finisher pigs. Seen in younger pigs these
days too, due to diseases like PRRS.
Enteric Salmonellosis
Etiology: Salmonella typhimurium
Pathogenesis: More than 200 virulence factors (see septicemia section)
Grossly: SI & LI. Fibrinonecrotic enterocolitis. Enlarged mesenteric LNs. Chronic disease can lead
to rectal prolapse, rectal stricture & pot belly.
Histopath: Necrosis of mucosal epithelium. Vasculitis & thrombi. Ulcers.
Can differentiate this disease from swine dysentery because of involvement of SI as well as LI.
Also pigs are usually sick with enlarged LNs, which tends not to occur in swine dysentery.
Lawsonia enteropathies are also often talked about as “Regional Ileitis” which involves
proliferative change & mucosal ulceration & necrosis in addition. Another term used is
“Necrotic Enteritis” in which there is coagulation necrosis in addition to the proliferative lesion.
Gastric Ulcers
Etiology: Multifactorial – Risk factors include: Gender (barrows) / Genotype / Season (summer) /
Stress / Food particle size / Anorexia (concurrent disease) / Vit E-Se deficiency / Cu
toxicity / Zn deficiency / ?Helicobacter role. Costly problem in the pig industry.
Pathogenesis: Unclear
Clinically: Severe disease can cause massive hemorrhage into the gastric lumen & sudden death.
Subclinical disease can produce tarry feces & anemia.
Grossly: Blood in the stomach or intestine. Anemia. Ulcers in the pars oesophagea.
Histopath: Mucosal ulcers, sometimes with secondary invaders.
Trichuriasis
Etiology: Trichuris suis (whipworm)
Clinically: Growers & finishers. Secondary infection with Balantidium coli often occurs.
Grossly: Cecum & colon mainly. Fibrinohemorrhagic colitis with worms in mucosa +/- ulcers.
Ascariasis
Etiology: Ascaris suum.
Life Cycle: DIRECT – Egg ! Intestine ! L1 in egg ! L2 in egg ! L2 ingested & invades SI wall ! into
portal vein ! reaches liver ! L3 ! goes to lung ! coughed up & swallowed ! intestine !
L4 ! L5 ! egg (Females can produce 2 million eggs each day!)
Grossly: Liver & lung hemorrhage. Liver fibrosis – Milk Spot Liver. Lung edema.
NON-HEMORRHAGIC HEMORRHAGIC
RESPIRATORY DISEASES
Most common in weaner – finisher groups, & mostly infectious, but often exacerbated by or
predisposed to by environmental factors - high ammonia/dust levels, poor ventilation, overcrowing.
Infectious agents - primary or secondary / Viral or bacterial / Parasitic pneumonia possible.
Classified as bronchopneumonia or interstitial pneumonia.
Pleuropneumonia
Etiology: Actinobacillus pleuropneumoniae (APP)
Pathogenesis: Produces toxins (Apx I,II,III) which are perforins that make holes in cell membranes.
Toxins kill & inhibit macrophages ! predisposing to secondary infection. Toxins are also
toxic to alveolar epithelial cells & endothelial cells.
Clinically: Usually 6-8wo, but all ages can be affected. Peracute-acute forms can appear like shock &
result in sudden death (especially in grower/finisher pigs). Most commonly the subacute
form is seen at the slaughterhouse.
Grossly: Peracute Sudden death with no premonitory signs. Well demarcated areas of
hemorrhage & necrosis – lesions more scattered, unlike EPP.
(Fulminant necrohemorrhagic pneumonia)
Acute Bilateral, all lobes: dark red & solid. Fibrinous, hemorrhagic, necrotic
Chronic Subclinical disease usually. See fibrosis, fibrosing pleuritis with adhesions
to the pleura of the thoracic wall. Cavitation & abscesses.
Histopath: Necrosis, hemorrhage, suppurative inflammation, thrombosis, edema & fibrin
deposition. When chronic, difficult to differentiate from other chronic pneumonias
Bordetellosis
Etiology: Bordetella bronchiseptica
Clinically: Not a common cause of respiratory disease. Usually affects suckling piglets.
Grossly: Hemorrhage & necrosis in lungs. Suppurative bronchopneumonia.
Histopath: Suppurative inflammation. May see necrosis of alveolar septa.
Streptococcal pneumonia
Etiology: Streptococcus suis
Pathogenesis: Not fully known. Most serotypes are secondary pathogens - type 1 can be primary.
Clinically: Becoming important as a secondary agent in PRRS cases. Type 1 ! Meningitis in baby pigs /
Type 2 ! Any age – This tends to be the predominant serotype.
Grossly: Suppurative bronchopneumonia with fibrinous pleuritis. See interstitial pneumonia with
septicemic cases.
Histopath: Suppurative bronchopneumonia. Possibly alveolar necrosis.
Arcanobacterium pyogenes
Etiology: Arcanobacterium pyogenes
Pathogenesis: Common secondary invader.
Grossly: Abscesses & chronic pneumonia.
Glassers Disease
Etiology: Haemophilus parasuis
Pathogenesis: As a primary pathogen ! polyserositis. Rarely it can be associated with septicemia. As a
secondary pathogen ! bronchopneumonia.
Clinically: Different manifestations – Respiratory disease is an important one – dyspnea, cyanosis,
fever. Polyarthritis can also occur ! lameness & swollen joints. May also present as
neurologic disease – incoordination seen - causes acute, usually fatal fibrinosuppurative
leptomeningitis in young adult breeding stock after entering a new herd, or in pigs mixed
from different herds. A big problem, especially in high health herds. May see polyserositis
at necropsy.
Grossly: Fibrinous Polyserositis (pericarditis, pleuritis, peritonitis). Meningitis. Otitis media &
eustachitis. Arthritis & vegetative endocarditis.
DDx: Strep suis / Erysipelas / E. coli / Actinobacillus suis / Salmonella / Myco hyorhinis
(C) Primary Viral Agents
Porcine Reproductive & Respiratory Syndrome (PRRS)
Etiology: Arterivirus
Pathogenesis: Replicates in macrophages ! inhibits their function ! predisposes to secondary infection,
especially in lung ! Porcine Respiratory Disease Complex (PRDC).
Clinically: a) Respiratory Syndrome Most severe lesions in piglets <3wo, also in weaners.
Can also see conjunctivitis, depression, dyspnea.
b) Reproductive Syndrome In adults – rolling inappetance, abortion,premature
farrowing, stillbirth, neonatal death, weak piglets,
infertility. Virus can survive for months in boar semen & also
persists in the herd.
Grossly: Aborted fetuses may have interstitial pneumonia. Pure PRRS virus infection rare
(tan consolidated dorsal lung). Mostly see Dz with concurrent secondary infections which
dominate the clinical picture & lesion. Enlarged LNs frequently seen.
Histopath: Interstitial pneumonia. Hallmark - alveolar macrophage necrosis. Lymphoid necrosis then
lymphoid hyperplasia. Myocarditis. Lymphoplasmacytic encephalitis.
Dx: Serology, VI.
Swine Influenza
Etiology: Type A swine influenza virus (orthomyxovirus) H1N1 more common in USA.
Pathogenesis: An enveloped virus with hemagglutinin (H) & Neuraminidase (N) spikes. Its viral RNA is
segmented which allows reassortment required for antigenic shift/drift. H facilitates
attachment to the cell & N facilitates elution from the cell.
Clinically: Most common form of viral pneumonia in pigs. Classically a herd disease with sudden onset &
rapid progression. Explosive cough, fever, dyspnea, prostration & rapid recovery. More
common in growers/weaners but all ages affected. 100% morbidity / <1% mortality. SIV
pneumonia potentiated by concurrent infection with PRRSV & possibly PCV2 – but
Mycoplasma hyopneumonia does not potentiate disease. Zoonotic – transmission of new
pandemic strains to humans – seen in pig farmers. Controversial association with pig
abortion.
Grossly: Fetuses Interstitial pneumonia – dark red, heavy wet lungs
Postnatal Lungs dark red, consolidated/atelectatic – checkerboard pattern.
Histopath: Necrotizing bronchiolitis & Type II pneumocyte proliferation.
(E) Rhinitis
Atrophic Rhinitis
Etiology: Pasteurella multocida & Bordetella bronchiseptica
Pathogenesis: P. multocida ! Type D cytotoxin (dermonecrotoxin) – central to lesion development.
Bacterial colonization of nasal cavity aided by injury (chemical, infectious
Clinically: Sneezes & snuffles in piglets 3-4wo.
Grossly: Nasal turbinate atrophy with nasal septal deviation. Take the section of snout between the
upper 1st & 2nd premolars to check for this lesion.
Histopath: Epithelial hyperplasia; Mucosal gland atrophy; Osteolysis & mesenchymal cell proliferation.
Classical Swine Fever (Hog Cholera) REPORTABLE Dz – Not currently in North America
Etiology: Pestivirus
Pathogenesis: Tonsil ! LN ! Blood ! Spleen ! Endothelial cells ! Results in endothelial cell
degeneration & reduced platelet number ! Hemorrhage
Clinically: Acute, Subacute & Chronic forms.
Acute form High fever, depression, anorexia, hemorrhage, high mortality.
Sick drowsy pigs. Conjunctivitis (DDx – Chlamydophila suis / Porcine
paramyxovirus). Purple skin.
Subacute form Often little to see clinically.
Chronic form Less severe depression, anorexia & fever, with recovery.
See prolonged & intermittent disease periods with anorexia, fever,
diarrhea, constipation. Quickly lose weight.
Congenital Dz Abortion, stillbirth, “shaker” pigs with congenital tremors.
Grossly: Acute form Tonsillar necrosis (DDx Aujesky’s Dz). Multiorgan
hemorrhage – usually LNs & kidneys (“Turkey-egg” kidney).
Purple skin. Splenic infarcts – considered pathognomonic by some
but they can occur with salmonellosis – due to thrombi.
Chronic form Intestinal tract button-ulcers (DDx Salmonellosis) – due to
secondary infection.
Congenital Dz Cerebellar hypoplasia ! Congenital tremors (DDx PCV-2).
Dx: Early Dx is imperative. Can base Dx on history such as - recent pig purchase, neighboring
farms with disease, visitors in contact with pigs, gross lesions, clinical signs & high mortality
within 1-2w of start of disease, rapid disease spread & leulopenia. Important to obtain
laboratory confirmation since it can appear similar to other diseases like pasteurellosis,
salmonellosis, erysipelas.
SEPTICEMIAS
Many bacteria can cause septicemia: The presence of circulating bacteria in the blood. Clinically,
all present similarly & organisms tend to localize in similar sites – especially heart valves, lungs,
meninges, skin, joints. Some bacteria (G-ve) may produce endotoxins that can damage blood
vessels ! Hemorrhage, Infarcts, Ulceration & Necrosis. Affected animals are usually inappetant
& pyrexic & frequently may have cyanosis of extremities (ears, feet, tail, ventral abdomen).
Abortion may occur in sows. The classic septicemic disease is that caused by S. choleraesuis.
Salmonella Septicemia
Etiology: Salmonella choleraesuis
Pathogenesis: Different virulence factors involved: Important ones are those for adhesion (pili) & invasion
(flagella), & others that act as toxins or confer resistance to phagocytosis.
Clinically: Severe septicemia +/- concurrent pneumonia or enterocolitis in weaned/grower pigs
Multifocal hepatic necrosis (paratyphoid nodules) is a fairly consistent lesion.
Replicates in macrophages & extracellularly in lymphoid tissues (causing necrosis) &
elsewhere. Large amounts of systemic endotoxin activate cytokines & induce vascular
damage (hemorrhage, interstitial pneumonia & edema, glomerulonephritis, gastric mucosal
venous thrombosis & arterial thrombosis (skin of extremities & colon → ulcers).
Ochratoxins may increase susceptibility to infection with S. choleraesuis. Innumerable
sources of infection - most important are carrier pigs, infected littermates or visitors from
infected farms, infected food, vermin, birds.
Grossly: Acute disease more frequently produces - Cyanotic extremities, LN Hemorrhage,
Splenomegaly, Renal petechiae & Infarcts, Interstitial Pneumonia, Meningitis, Tonsil
Abscesses. Chronic disease – Fibrinonecrotic enteritis, DIC, Button Ulcers.
Histopath: Button ulcers (Necrosis of Peyer’s patches). Paratyphoid nodules in liver (foci of hepatic
necrosis surrounded by a zone of macrophages). Thrombi especially in blood vessels of skin,
kidneys, stomach.
Dx: Must culture for definitive Dx.
Dermatosis Vegetans
Etiology: Hereditary – often congenital (Landrace)
Clinically: Usually starts in first few weeks of life if not present at birth. See lesions over abdomen,
inner thighs – raised pink swellings that rapidly enlarge & extend over flanks & back.
Affected pigs have concurrent Giant Cell Pneumonia ! Develop pneumonia & die around 6wo
Grossly: Grey-brown, proliferative & papilliferous, vegetative lesions on hooves – brittle, fissured,
thick & hard – almost like horn. Hooves may be deformed & ridged with exudate along the
coronary band.
Histopath: Pustular dermatitis. Granulomatous (giant cell) pneumonia
Dx: Characterisitc gross lesions, histopath, concurrent pneumonia, specific breeds.
Ectoparasites
(a) Pediculosis Haematopinus suis louse – big enough to see.
Associated with Pox virus, ASFV, Eperythrozoonosis, alopecia, abrasions.
Ringworm
Hyperkeratotic dermatitis & alopecia. Microsporum parvum or Trichophyton verrucosum most
common. Zoonotic.
Nutritional
Zinc Deficiency is the major problem.
Parakeratosis – fissuring & cracking of skin, especially on hindlimbs.
Histopathology is diagnostic. Analyze feeds / serum for zinc levels.
Neoplastic
Melanomas Occur in young pigs
Congenital in Duroc breed
Similar in Sinclair mini pigs – used as a model for human disease
Typical raised black skin masses – rarely metastasize.
Benign & can spontaneously regress.
Vesicular Skin Diseases
Diseases: Foot & Mouth Disease (FMD)
Swine Vesicular Disease (SVDV)
Vesicular Exanthema of Swine (VES)
Vesicular Stomatitis (VS)
Pathogenesis: Viral replication in epidermal or mucosal epithelium.
Clinically: 1-5 days post-exposure ! blanching of mucous membranes with resultant vesicles &
subsequent erosions when vesicles burst – on snout, tongue, palate, coronary band, heel
bulbs, interdigital clefts, teats. Secondary bacterial invasion can lead to endotoxemia. May
also see abortion. Non are fatal – problem lies in rapid spread & economic losses due to poor
weight gain & abortion.
Grossly: Vesicles & erosions. Salivation, lameness, inappetance.
Histopath: Edema & necrosis of epithelial cells, erosions, ulcers, vesicles.
Dx: Imperative to confirm a definitive diagnosis. CF, ELISA, VI, EM – sample of vesicular tissue
or fluid.
NEUROLOGIC DISEASES
Genetic Diseases
Meningoencephalocele: Piglets born with cranioschisis (congenital failure of skull bones to fuse) may
have a meningoencephalocele – a protrusion of meninges & brain through the
skull. Its pathogenesis involves a neural tube defect due to an insult
between days 12-14 of gestation.
Infectious Diseases
(1) PCV-2: Epidemic tremors. Tremors stop when sleeping. Piglets that reach 3wo tend
to survive. The condition is due to retarded myelin deposition, so no gross
lesions seen.
(2) CSF: Congenital tremors.
(3) Bacterial Meningitis: Streptococcus suis & Haemophilus parasuis mostly. Usually affects several
piglets – collapse, leg paddling, opisthotonus. Chcek for other lesions like
polyserositis. Remember Strep suis is zoonotic.
(4) Aujesky’s Disease: Nervous signs in baby pigs / Respiratory disease in adults. 100% mortality.
See multi-organ necrosis. Tonsil - primary replication site.
Metabolic Disease
Mainly see Hypoglycemia. - if they fail to suck, or due to mastitis/agalactiae in the sow.
Salt Poisoning
Etiology: Usually due to lack of water - usually accidental - due to water system failure, or freezing
temperatures. Excessive dietary salt can also be a cause, as can adding antibiotics that may
make water unpalatable.
Pathogenesis: Unclear.
Clinically: Pigs appear thirsty, deaf, blind, wander aimlessly & have convulsions. Rehydration can
exacerbate signs.
Histopath: Pathognomonic lesion is an eosinophilic meningoencephalitis.
Aujesky’s Disease
Etiology: Porcine herpesvirus-1 (alpha-herpesvirus)
Clinically: Nervous signs. 100% mortality. Multi-organ necrosis.
Grossly: Tonsillar necrosis.
Histopath: Multi-organ necrosis.
Dx: VI from tonsil.
Rabies
Pigs are one of the more resistant species to rabies virus, but needs to be considered.
Fibrocartilaginous Embolism IVDDz ! Disk material enters blood ! blocks spinal blood vessels !
spinal cord infarcts. Heavy pigs, often after a period of activity
such as loading pigs into a truck. Hindlimb paresis or paralysis.
Ruptured Hamstring Selection for muscular growth may favor metabolic dysbalances in
the muscle & subsequent degeneration.
Arsenic Toxicity Nervous disease – convulsions, paraparesis & paraplegia. Myelin &
axonal degeneration in the white matter of the SC.
Bacterial Leptospirosis
Listeriosis
Salmonellosis
Brucellosis
Erysipelas
Chlamydiosis
Any Septicemic Disease
Stress
ABORTION WORK-UP
FF = 2 sections of each tissue – one fresh in a clean bag & the other in 10% formalin
HP = Histopath/FA = Fluorescent Antibody Test/VN = Virus Neutralization/VI = Virus Isolation
Zearalenone Toxicity
Etiology: Fungus Fusarium roseum produces F1 toxin – an estrogenic mycotoxin.
Clinically: Produces follicular cysts, uterine hypertrophy, anestrus, vulval swelling
Grossly: Classic gross lesion is vulval swelling.
Metritis
Causes include Actinobacillus suis, Clostridia, Staphylococcus aureus, Aujesky’s Disease
Mastitis
Causes include A. pyogenes, E. coli, Leptospira, Staphylococcus aureus.
Brucellosis
B. suis causes necrotizing orchitis & abscesses, although is rare.
MUSCULOSKELETAL DISEASES
Infectious Arthritis
Etiology: Mycoplasma hyorhinis
Mycoplasma hyosynoviae (usually >10wo)
Streptococcus suis
Haemophilus parasuis (Glasser’s Disease)
E. coli
Erysipelothrix rhusiopathiae
Arcanobacterium pyogenes
Grossly: Most cause fibrinous polyserositis (hence fibrinous polyarthritis), except for M.
hyosynoviae. Strep suis also tends to be more suppurative than fibrinous. Swollen joints.
Thin synovial fluid with fibrin, pus, debris.
M. hyosynoviae ! milder & more chronic disease, & also includes meningitis, in 10-20wo pigs.
The lesion tends to be more proliferative - synovial villous hypertrophy.
Osteochondrosis
An umbrella term – encompasses diseases in which the primary defect involves defective
endochondral ossification ! retained cartilage cores ! weakened physis. Rapidly growing pigs in
grower/weaner stages are most affected. All major joints can be involved, especially
coxofemoral joints. Most domestic pigs have some microscopic lesions typical of this disease
category. Various manifestations:
Chronic Zinc Toxicity Joint & bone lesions like osteochondrosis have been documented in pigs with
chronic Zn toxicity. (Also pancreatic necrosis)
Lactogenic Osteoporosis Osteopenia due to ↓ activity & ↑ bone resorption during lactation.
Infectious Myositis
Clostridium novyi Can cause sudden death, mostly in large breeding stock, usually sows.
The pathogenesis lies in production of an alpha toxin. Dx is difficult
as this is a common postmortem invading organism – best to examine
freshly dead animals.
Clostridium perfringens type A Can invade wounds (such as those due to piglet iron injections). Fatal
– causes liver necrosis & gas bubble production.
Clostridium chauvoei Blackleg – few definitive reports in pigs.
Myofibrillar Hypoplasia
Splayleg – a genetic defect in piglets. Landrace predisposed.
Parasitic
Trichinella spiralis – larval stages may encyst in porcine muscle. Zoonotic ! larval release into
intestines of people eating undercooked pork.
Neoplastic
Lymphoma All ages. Multicentric or thymic.
Nephroblastoma Pigs <1yr old. A poorly differentiated neoplasm but most common in pigs.
Parasitic
Stephanurus edentatus – the kidney worm. Ova are shed in urine. Causes fibrosis & abscesses in the
kidney. Can also damage the liver during its larval migration stages.
NUTRITIONAL DISEASE Vitamin E / Selenium Deficiency
Selenium Toxicity
Zinc Deficiency
Salt Poisoning
Selenium Toxicity
Poliomyelomalacia ! Paresis / Paralysis
Zinc Deficiency
Parakeratosis – fissuring & cracking of skin, especially on hindlimbs.
Salt Poisoning
Due to lack of water / Excess salt / Unpalatable water. Pigs are thirsty, deaf, blind, wander
aimlessly, convulsions. Rehydration can exacerbate signs. Eosinophilic meningoencephalitis.
Porcine juvenile pustular psoriasiform dermatitis Ventral abdomen, benign, self limiting.
Landrace.
Epitheliogenesis Imperfecta Autosomal recessive inheritance. See areas of skin & mucous
membranes devoid of epidermal / mucosal covering. May
affect tongue. Can have concurrent hydroureter & hydronephrosis.
Anal Atresia Male > females. Fatal in 2-3 weeks. Rectum ends blindly. Secondary
megacolon.
Toxic Hepatopathies
Etiology: Coal Tar
Gossypol
Aflatoxins
Pyrrolizidine Alkaloids
Iron Dextran
Grossly: Hepatic necrosis & hemorrhage. Depending on the toxin, other lesions may also be seen,
such as pulmonary edema with gossypol toxicity.
Histopath: Hepatic necrosis & hemorrhage. Megalocytosis & bile duct hyperplasia is classic with
pyrrolizidine alkaloids.
Toxic Nephropathies
Etiology: Plants such as pigweed (Amaranthus retroflexus)
Mycotoxins – Fumonisin produced by Fusarium species
Antibiotics (Aminoglycosides / Tetracyclines)
Heavy Metals
Ethylene Glycol
Clinically: Pigweed ! CNS signs, paralysis & death
Mycotoxins like ochratoxin A (Aspergillus ochraceus) & citrinin can contaminate grain !
acute nephrotoxicity, but more usually cause chronic wasting.