DISEASES OF PIGS

Boards Review 2003

Dr Nicola Parry
Large Animal Pathology, NBC (610) 925-6451


Stages: Suckling < 2-3 weeks
Nursery !1-2 months
Grower/Finisher 3-6 months
Breeding /Adult > 6 months



GI DISEASES
(A) PIGLETS UP TO 3weeks TGE (Any age of pig)
Rotavirus
Colibacillosis (E. coli)
Clostridiosis
Coccidiosis

Transmissible Gastorenteritis (TGE)
Etiology: Porcine coronavirus
Pathogenesis: Damages epithelial cells in villi ! ! Absorptive capacity
Clinically: Profuse watery diarrhea, dehydration, cachexia. High mortality in piglets <2wo.
Can affect pigs of all ages
Grossly: Intestinal distension; Thin-walled SI; Severe villous atrophy; No lacteal chyle; Fecal pH is
acidic.
Histopath: Blunted villi ! Villi: Crypt ratio is ! to 1:1 (Normal is 7:1)


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


Escherichia coli ! Colibacillosis
E. coli: G-ve rod with flagellae
Various serotypes exist - grouped according to their antigens
Antigens are: Somatic (O) & Flagellar (H)`
To cause Dz, E. coli organisms must:
(1) Colonize intestine &
(2) Produce toxins
Fimbrial antigens: Promote colonization (thus are Virulence Factors)
Many types of Fimbrial antigens exist.
The most important ones are: F4 F5 F6 F41 F18
Toxins produced by E. coli include:
1) STa Heat stable
Activates cGMP ! inhibits Na/Cl transport ! ! electrolyte/water absorption
2) STb Heat stable
Unclear role in diarrhea
3) LT Heat labile
Activates cAMP ! " secretion of Na, Cl, HCO
3
, H
2
O ! Acidosis
4) SLT-IIe Shiga-like toxin
Causes Edema Disease

Grouping is based on virulence factors:
1) ETEC Enterotoxigenic ! releases toxin into gut ! triggers fluid secretion.
Hemolytic or non-hemolytic. SI only. Suckling & weaned piglets.
2) ETEEC Enterotoxemic ! produce systemic pathology
3) AEEC Enteropathogenic ! colonize GIT by attaching & effacing mechanism.
SI & LI. Uncommon in 1-6wo piglets.

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

Neonatal colibacillosis (0-4 days)
Etiology: ETEC
Pathogenesis: E. coli adheres to SI mucosa via fimbrial antigens F4 F5 F6 F41 ! releases enterotoxins
STa STb LT.
The type of fimbriae can dictate the level of intestine & age of pig affected brush border
fimbrial receptors are not present in all pigs some lack F4 receptors & are resistant to
infection.
In other pigs, F4 is present from birth to adult, while F18 is only expressed after 20 days
old, so pigs <20 days of age do not have disease with F18-expressing E. coli.
Recognition of these fimbrial antigens is important for vaccine design.
Clinically: Diarrhea & dehydration within hours of birth in one pig or whole litter. Colostrum is
important for protection. Low ambient temperature can be detrimental since it may reduce
peristalsis & increase time for bacteria to pass through intestine.
Grossly: Gross findings non-specific. Alkaline intestinal pH. Intestinal dilation.
Histopath: Villus atrophy. See bacteria adhering to mucosal surface.

Attaching & Effacing E. coli (AEEC)
Etiology: AEEC
Pathogenesis: Intimin is a specific virulence factor allows mucosal attachment. Some produce SLT-1 !
hemorrhage, necrosis, ischemia & vasculitis in the brain & intestine.
Clinically: Septicemia, arthritis, meningitis, serositis.


Edema Disease & Post-Weaning Diarrhea
Both of these coliform diseases share the same virulence factors & clear distinction is often not
possible. Both can occur in the same batch of pigs at the same time, & certain strains can cause
both conditions, so there is much room for confusion! The bacteria produce similar enterotoxins
in both diseases, but one main difference is that in edema disease, the toxins enter the
blood. E. coli expressing F4 & F18 factors are often associated with Post-Weaning Diarrhea.
Hemorrhagic Gastroenteritis is a distinct form of Edema Disease with bloody diarrhea &
hemorrhagic lesions in the gastric cardia, ileum & large intestine.

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 10
7
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 perfringens type C
Pathogenesis: Produces ! & " toxins. " toxin is necrotizing & lethal.
Clinically: Acute disease ! sudden death. Chronic forms ! nonhemorrhagic diarrhea.
Grossly: Intensely hemorrhagic, dilated small intestines with blood-stained fluid in the abdominal
cavity. Sometimes see gas bubbles.
Histopath: Fibrinonecrotic enteritis with large bacilli in intestine.


Clostridium perfringens type A
Pathogenesis: Produces ! & # toxins.
Clinically: High morbidity, low mortality. Less severe than type C. White scours. Can see in
combination with coccidiosis.
Grossly: Non-specific findings.
Histopath: Acute enteritis with villus atrophy or necrosis.


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.


(B) POSTWEANING TO ADULT TGE (Any age of pig)
Swine dysentery
Colonic spirochetosis
Salmonellosis
Porcine proliferative enteritis
Trichuriasis
Swine Dysentery
Etiology: Brachyspira hyodysenteriae (Strongly "-hemolytic)
Pathogenesis: Motility is a virulence factor. Attachment may or may not be a factor. Hemolysin &
endotoxin production. Diarrhea is due to malabsorption.
Clinically: Weaned pigs mainly growers & finishers. Hemorrhagic colitis.
Grossly: Lesions restricted to large intestine. Catarrhal to fibrinohemorrhagic colitis. May see
erosions.
Histopath: Erosive enteritis & crypt abscesses.

Intestinal Spirochetosis
Etiology: Brachyspira pilosicoli (Weakly "-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.

Porcine Proliferative Enteritis
Comprise two manifestations of enteric disease caused by Lawsonia intracellularis, an
obligate intracellular organism. Disease forms can be acute or chronic.
(a) Acute form: Proliferative Hemorrhagic Enteropathy (PHE)
Clinically: Hemorrhagic diarrhea & sudden death in pigs 4-6 months old often valuable breeding stock
about to enter the herd or have a first litter in which abortion may result may be due to
stress.
Grossly: Thickened ileal mucosa (+/- colon & terminal jejunum). See a corrugated mucosa (much like
Johnes Dz) & reduced lumen diameter. Blood clots found in terminal ileum.
Histopath: Severe proliferation of crypt enterocytes. Warthin Starry is a special stain that allows you
to see curved rod shaped bacteria in enterocyte cytoplasm.

(b) Chronic Form: Porcine Intestinal Adenomatosis (PIA)
Pathogenesis: Bacteria infect pig ! invade crypt enterocytes, mainly ileum ! enterocyte proliferation !
hyperplastic/proliferative enteritis by unknown mechanism.
Clinically: Chronic wasting & non-hemorrhagic diarrhea in weaners & growers (6-16wo). Disease is
transient but valuable growing time is lost. Animals dont usually die.
Grossly: Thickened ileal mucosa (+/- colon & terminal jejunum). See a corrugated mucosa (much like
Johnes Dz) & reduced lumen diameter.
Histopath: Severe proliferation of crypt enterocytes. Warthin Starry is a special stain that allows you
to see curved rod shaped bacteria in enterocyte cytoplasm.

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.

Other GIT parasites include:
Hyostrongylus rubidus Stomach worm
Oesophagostomum spp. & Strongyloides ransomi - SI.

DIARRHEA

NON-HEMORRHAGIC

HEMORRHAGIC

Colibacillosis Cl. perfringens type C
Cl. perfringens type A Salmonellosis (dark blood)
Coccidiosis PHE form of Proliferative enteritis
Viral enteritis (Rota, Corona) Swine dysentery
Proliferative enteritis (not PHE) Whipworms
Whipworms
Intestinal spirochetosis



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.

(A) Primary Bacterial Agents
Enzootic Pneumonia of Pigs (EPP)
Etiology: Mycoplasma hyopneumoniae
Pathogenesis: Bacteria adhere to bronchial/bronchiolar epithelium ! ciliostasis, ciliary loss, epithelial cell
loss, affects goblet cell metabolism ! ! mucociliary clearance ! predisposed to secondary
infection (especially Pasteurella multocida).
Clinically: 3-6mo age group. Mainly coughing. Most common respiratory disease of pigs.
Grossly: Well-demarcated, purple-red areas in cranioventral lobes. Plugging of airways with
mucopurulent exudate. LNs enlarged.
Histopath: Mainly suppurative inflammation in the airways with later peribronchial & peribronchiolar
lymphocytic cuffing.
Dx: Based on clinical signs of cough, slow onset, serology (ELISA), IFA. The organism has
fastidious growth requirements for culture.

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.

(B) Secondary Bacterial Agents
Pneumonic Pasteurellosis
Etiology: Pasteurella multocida
Pathogenesis: Usually secondary to enzootic pneumonia cant invade healthy lung.
Clinically: Most common secondary bacterial pathogen isolated from lung. A serious cause of economic
loss. Vaccination of pigs with classical swine fever or Aujeskys Disease vaccines can
predispose to this condition.
Grossly: Consolidated, dark red to grey cranioventral lung lobes (looks similar to EPP) an acute
bronchopneumonia. Purulent exudate in airways. Adhesions of lung to thoracic cavity, with
fibrinohemorrhagic or necrotic pneumonia & pleuritis. More of a dry lesion than APP which
is wetter.
Histopath: Exudative bronchopneumonia.

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.

Septicemic Interstitial Pneumonias
Etiology: Strep suis / E. coli / Salmonella. choleraesuis / Actinobacillus suis / Erysipelas

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.

Postweaning Multisystemic Wasting Syndrome (PMWS)
Etiology: Porcine Circovirus type 2 (circular single stranded DNA virus)
Pathogenesis: Virus is associated with macrophages in lung, small intestine, lymphoid tissue.
Clinically: 5-15% of weaned pigs are apparently affected, usually around 5-12 wo. Controversial as to
whether or not PCV-2 is a primary pathogen. Contributes to PRRS clinical signs. Causes
epidemic tremors in young piglets. See inappetance, weight loss, enlarged lymph nodes,
respiratory disease, Icterus.
Grossly: Interstitial pneumonia like PRRS heavy, rubbery, grey lungs. Enlarged LNs
Histopath: Interstitial pneumonia a consistent finding. LNs unique lesion of granulomatous
lymphadenitis with intracytoplasmic globular, basophilic inclusion bodies (often described as
botryoid). Hepatitis, nephritis, perivasculitis less common. Myocarditis in the very young.
Dx: VI, Histopathology, Immunohistochemistry.

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.


Porcine Respiratory Coronavirus
A mutant of the TGE virus. Aerosol transmission. Important secondary viral infection in PRDC.

Aujeskys Disease (Pseudorabies)
Etiology: Porcine Herpesvirus type 1 (an alpha-herpesvirus)
Pathogenesis: Some strains are neurotropic, others pneumotropic. The virus inhibits macrophage function.
Infections in aberrant hosts are fatal cat, dog, ruminant, horse.
Clinically: Classically see rapid virus spread - within a week.
Piglets Almost 100% mortality. CNS signs seizure, salivation, opisthotonus
Young pigs Grower/Finisher groups - Respiratory disease fever, depression, cough,
lower mortality. Secondary bacterial complications of pneumonia slow
groeth, ! feed conversion efficiency, death. May contribute as a
complicating factor to PRDC.
Adults Abortion.
Grossly: Ranges from no gross lesions to red lungs with necrosis & hemorrhage. Can also see pinpoint
white foci of necrosis in the liver (DDx Salmonella). Also tonsillar necrosis (An important
DDx here is Classical Swine Fever).
Histopath: Necrotizing bronchitis/alveolitis with hemorrhage & fibrin. Intranuclear inclusion bodies in
bronchial epithelium & hepatocytes. Multifocal splenic & hepatic necrosis. Necrotizing
tonsillitis. Nonsuppurative meningoencephalitis.



(D) Parasitic Agents
Lungworm
Etiology: Metastrongylus apri
Life Cycle: Larvated egg ! coughed up & swallowed ! out in poop ! earthworm eats egg ! L1
produced & enters earthworm heart ! pig eats earthworm ! L3 stage penetrates SI ! L4
invades mesenteric LN ! reaches right side of heart ! travels to lung ! moults to L5 !
becomes larvated egg.
Histopath: Mucoid bronchitis mainly in caudal lobes see adults & eggs.


(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 1
st
& 2
nd
premolars to check for this lesion.
Histopath: Epithelial hyperplasia; Mucosal gland atrophy; Osteolysis & mesenchymal cell proliferation.


Inclusion Body Rhinitis
Etiology: Cytomegalovirus
Pathogenesis: Important in causing nasal damage which predisposes to bacterial infection.
Clinically: Clinical signs in piglets <1wo older pigs generally asymptomatic.
Grossly: Mild rhinitis erosion & hyperemia
Histopath: Classic basophilic intranuclear inclusion bodies & cytomegaly of nasal mucous gland cells, and
acinar & duct epithelial cells of Harderian & lacrimal glands.



SYSTEMIC DISEASES PRRS
PMWS
Classical Swine Fever
African Swine Fever

Porcine Reproductive & Respiratory Syndrome (PRRS)
Etiology: Arterivirus
Pathogenesis: Replicates in macrophages ! inhibits their function ! predisposes to secondary infection,
especially in lung.
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: Consistent gross lesions in lungs & LNs only. Aborted fetuses may have interstitial
pneumonia. Pure PRRS virus infection is rare, but manifests as tan consolidation of the
doral lung surface. More usual to see disease with concurrent secondary infections which
dominate the clinical picture & lesion. Enlarged LNs frequently seen.
Histopath: Interstitial pneumonia with hallmark necrosis of alveolar macrophages. Lymphoid necrosis is
followed by lymphoid hyperplasia. Myocarditis. Lymphoplasmacytic encephalitis.
Dx: Serology, VI.

Postweaning Multisystemic Wasting Syndrome (PMWS)
Etiology: Porcine Circovirus type 2 (circular single stranded DNA virus)
Pathogenesis: Virus is associated with macrophages in lung, small intestine, lymphoid tissue.
Clinically: 5-15% of weaned pigs are apparently affected, usually around 5-12 wo. Controversial as to
whether or not PCV-2 is a primary pathogen. Contributes to PRRS clinical signs. Causes
epidemic tremors in young piglets. See inappetance, weight loss, enlarged lymph nodes,
respiratory disease, Icterus.
Grossly: Weaned pigs - Interstitial pneumonia similar to PRRS lungs are heavy, rubbery, grey.
Enlarged LNs can be very big. Icterus. Wasting.
Histopath: Hallmark is granulomatous inflammation. LNs unique lesion of granulomatous lymphadenitis
with intracytoplasmic globular, basophilic inclusion bodies. Interstitial pneumonia, hepatitis,
interstitial nephritis, perivasculitis often less common. Myocarditis in the very young.
Dx: VI, Histopathology, Immunohistochemistry.


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 Aujeskys 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.


African Swine Fever REPORTABLE Dz Not currently in North America
Etiology: Iridovirus
Pathogenesis: Consumptive coagulopathy ! Thrombocytopenia with Endothelial damage & Increased
vascular permeability ! Hemorrhage (DIC). Soft ticks are vectors. Cycle involving wild
boar keeps virus in circulation. Primary method of spread from country to country - feeding
of uncooked garbage containing ASFV-infected pork scraps to pigs. Once a pig is infected,
ASFV spreads by direct contact, & contaminated people, equipment, vehicles, and feed.
Clinically: In contrast to CSF no conjunctivitis or encephalitic disease.
Acute form High fever, terminal bloody diarrhea, death.
Subacute form Less fatal.
Grossly: Acute form Pigs dying peracutely minimal lesions. Those dying 7days post
infection or more, have classic lesions marked splenomegaly /
hemorrhagic & enlarged gastrohepatic & renal LNs. Other lesions
include serosal hemorrhage, renal cortical, medullary &
pelvic hemorrhage, hydropericardium & hydrothorax, perirenal
edema. Pigs normally remain in good condition, unlike CSF.
Subacute form Hemorrhage in LNs, spleen, kidneys. Abortion.
Chronic form Necrotic skin lesions, generalized lymphadenopathy,
consolidated lungs, swollen joints, fibrous pleuritis/pericarditis.
Dx: VI, FA, Histopathology




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 Peyers 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.


Other Types Of Septicemia
Etiology: Strep suis, Erysipelas, Arcanobacterium pyogenes, Actinobacillus suis, E. coli (Haemophilus
parasuis rarely)
Pathogenesis: Infection may be via: Ingestion, Wound, Aerogenous ! Bacterial replication in bloodstream
! +/- production of endotoxins / cytokines ! Bacteria localize in various sites ! Necrosis,
Vasculitis, Thrombi, Infarcts.
Grossly: Cyanosis. Petechial hemorrhage in organs. Infarcts kidney, spleen, stomach. Multi-organ
inflammation & necrosis liver & heart. Some cause polyserositis (Strep. suis, Haemophilus
parasuis). Arthritis. Meningitis. Interstitial/Bronchopneumonia. Splenomegaly &
Hepatomegaly.
Histopath: Streps ! more suppurative lesions. Haemophilus ! lesions are more fibrinous.
Dx: Culture use tissues like Bloos, Spleen, Liver, Lung, LN, Tonsil, Blood



Haemophilus parasuis Glassers Disease Fibrinous: Pleuropneumonia
Pericarditis
Peritonitis
Meningitis
Arthritis

Streptococcus suis Fibrinous: Pleuropneumonia
Meningitis
Arthritis

Actinobacillus pleuropneumoniae Fibrinous: Pleuropneumonia

Mycoplasma hyorhinis Fibrinous: Pleuropneumonia
Pericarditis
Pericarditis
Arthritis

Mycoplasma hyosynoviae Fibrinous: Arthritis
SKIN DISEASES Exudative Epidermitis
Porcine Juvenile Pustular & Psoriasiform Dermatitis
Dermatosis Vegetans
Porcine Dermatitis & Nephropathy Syndrome
Diamond Skin Disease
Porcine Pox
Ectoparasites
Ringworm
Nutritional
Neoplasia

Exudative Epidermitis (Greasy Pig Disease)
Etiology: Staphylococcus hyicus
Pathogenesis: Can penetrate intact skin but more usually is associated with trauma/abrasions especially
from milk teeth/poor flooring. Produces a toxin that induces separation of epidermal
keratinocytes, to aid invasion.
Clinically: Sporadic disease. Variable morbidity. High mortality possible. Usually after introduction
of carrier animals into a non-immune herd. Affects pigs from a few days old ! 6wo.
Grossly: Thickened, crusty skin with waxy, greasy brown sebum exudate. Usually involves head &
neck, but anywhere can be affected. Can begin as well circumscribed circular lesions & then
spread to involve extensive regions of skin.
Histopath: Severe epidermal hyperkeratosis, hyperplasia & coccal bacteria. Vesicles, pustules.
Dx: Culture skin or suprascapular LNs. Clinical signs highly suggestive.

Porcine Juvenile Pustular & Psoriasiform Dermatitis
Etiology: Genetic Landrace breed.
Clinically: 3-14wo pigs. Looks much like ringworm expansile, circular, red, raised lesions on ventral
abdomen & inner thighs. Not greasy. Benign & self limiting.
Grossly: Circular, red, raised lesions with central crater.
Histopath: Psoriasiform epidermal hyperplasia & parakeratosis.
Dx: Rule out ringworm & greasy pig Dz. Clinical features & histopathology.

Porcine Dermatitis & Nephropathy Syndrome
Etiology: Unknown. PRRSV +/- PCV2 have been implicated.
Pathogenesis: Underlying lesion is segmental (?immune-mediated) vasculitis +/- thrombosis.
Clinically: 20-65kg pigs affected. Skin lesions involve macules & papules with brown crusts on
hindlimbs (looks like skin has been dragged over rough ground), ears, scrotum, vulva & face.
Subcutaneous edema swollen legs, proteinuria, elevated urea/creatinine.
Grossly: Cutaneous infarcts, Pale brown kidneys with petechiae (Glomerulonephritis);
Lymphadenopathy. Fluid in body cavities. Skin & kidney tropism.
Histopath: Necrotizing & proliferative glomerulonephritis; Vasculitis, thrombi & cutaneous infarcts.

Diamond Skin Disease
Etiology: Erysipelothrix rhusiopathiae
Clinically: Infection via: Ingestion, Wound, Aerogenous ! Bacterial replication in bloodstream ! +/-
production of endotoxins / cytokines ! Bacteria localize in various sites ! Necrosis,
Vasculitis, Thrombi, Infarcts.
Grossly: Classic diamond shaped skin lesions due to vasculitis, thrombosis & infarcts.
Histopath: Vasculitis, thrombosis, infarcts.
Dx: Classic lesions suggestive (but can result from infection with other septicemia-inducing
bacteria). Culture is definitive.
Porcine Pox
Etiology: Porcine Pox Virus
Clinically: Young pigs. Virus vector is Haematopinus suis louse.
Grossly: Round, red papules on ventral & lateral skin, medial limbs, face. Lesions can become
umbilicated (central necrosis) but rarely get vesicles.
Histopath: Epidermal hyperplasia & necrosis & intracytoplasmic, eosinophilic inclusion bodies.
Dx: Rule out other vesicular diseases. EM, FA, Histopathology.


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.

(b) Mange Sarcoptes scabei var suis
Produces crusting skin lesions, especially on ears.
Extremely pruritic ! headshaking ! aural hematomas
Scraping from skin / ear material to diagnose.

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.




DISEASE ETIOLOGY RUMINANT PIG HORSE MORBIDITY TRANSMISSION
FMD Picornavirus + + - High Aerosol
VSV Rhabdovirus + (Not
SR)
+ + Low - Moderate Insect bite, Fomite
VES Calicivirus - + - Moderate Contaminated garbage
SVD Enterovirus - + - Moderate Contaminated food
SR = Small ruminants






NEUROLOGIC DISEASES

(A) Baby Pigs (< 3wo) Genetic Diseases
Infectious Diseases PCV-2
CSF
Bacterial meningitis
Aujeskys Disease
Metabolic Disease


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) Aujeskys 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.


(B) Weaners & Growers Infectious Diseases Bacterial Meningitis
Edema Disease
Aujeskys Disease
Salmonella choleraesuis
Salt poisoning
Infectious Diseases
(1) Bacterial Meningitis: Streptococcus suis & Haemophilus parasuis mostly.
(2) Edema Disease: E. coli. Produce Shiga-like toxin - an angiotoxin ! enters blood !
damages brain vessels ! leaky vessels ! edema & neurologic signs.
Often affects fastest growing animals after weaning. Eyelid edema, ataxia,
convulsions & paralysis.
(3) Aujeskys Disease: Nervous signs. 100% mortality. Multi-organ necrosis. Tonsil - primary
replication site.
(4) S. choleraesuis: Causes septicemia, with subsequent meningoencephalitis.

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.


(C) All ages of pigs Teschen-Talfan
Hemagglutinating Encephalomyocarditis
Aujeskys Disease
Rabies
Teschen-Talfan Disease
Etiology: Enterovirus
Clinically: Teschen & Talfan are just different manifestations of a spectrum of enterovirus disease.
Both involve polioencephalomyelitis. Talfan is a mild, benign form of disease with lower
morbidity & mortality than the more severe Teschen. See convulsions, paralysis & death
with Teschen high morbidity & mortality. Really only occurs in central Europe & Africa
Histopath: Polioencephalomalacia.
Hemagglutinating Encephalomyocarditis
Etiology: Coronavirus
Clinically: Vomiting & wasting disease in pigs <3wo. Most common signs are cachxia & abdominal
distension. Also causes Nonsuppurative encephalitis.
Grossly: Wasting, abdominal distension.
Histopath: Nonsuppurative encephalitis.
Dx: VI from tonsil, brain, lung.


Aujeskys 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.



(D) Finisher to Adult Posterior Paralysis or Paresis:
Spinal cord: Enteroviral poliomyelitis
Selenium toxicity
Fibrocartilagenous emboli
Contusions
Neoplasia
Spinal column: Osteomyelitis/Osteomalacia
Spinal Canal Abscesses
Bones & Muscles: Epiphysiolysis
Rupture of the hamstring
Fractures
Arthritis
Peripheral nerves: Arsenic Toxicity
Sciatic nerve damage

Enteroviral poliomyelitis Teschen-Talfan ! Paresis, Paralysis

Selenium Toxicity Bilateral poliomyelomalacia,! Paralysis

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.

Contusions Secondary to spinal fracture

Neoplasia Most frequently lymphoma

Osteomyelitis/Osteomalacia Fractures may be a sequel

Spinal Canal Abscesses Often Arcanobacterium pyogenes.

Epiphysiolysis Form of osteochondrosis in which there is traumatic separation of
the epiphysis along the weakened physis.

Ruptured Hamstring Selection for muscular growth may favor metabolic dysbalances in
the muscle & subsequent degeneration.

Vertebral Fractures Traumatic in origin / Secondary to osteomyelitis/osteomalacia.

Arthritis A sequel to any arthropathy.

Arsenic Toxicity Nervous disease convulsions, paraparesis & paraplegia. Myelin &
axonal degeneration in the white matter of the SC.

Sciatic Nerve Damage Secondary to injections.








REPRODUCTIVE DISEASES Viral PRRSV
Swine Influenza Virus
Porcine Parvovirus
(A) Abortion Aujeskys Disease
Classical Swine Fever
African Swine Fever

Bacterial Leptospirosis
Listeriosis
Salmonellosis
Brucellosis
Erysipelas
Chlamydiosis
Any Septicemic Disease

Other Agents Toxoplasmosis
Fungal

Stress








ABORTION WORK-UP

ETIOLOGY SAMPLES TO SUBMIT PROCEDURE USED BY LAB
AUJESKYS DISEASE At least 3 fetuses
FF tonsil, lung, brain, spleen
Placenta
Serum
HP / FA / VI


ELISA / VN
PORCINE PARVOVIRUS Mummified fetuses & placenta
FF lung, placenta
Serum fetal fluid, or acute &
convalescing serum from dam
HP / FA / VI
BRUCELLA SUIS Fetuses & placenta
FF lung
Stomach contents
Serum as above
Culture
LEPTOSPIRA Fetuses
FF kidney, liver
Serum as above
HP / FA / Microagglutination
OTHER BACTERIA Fetuses & placenta
FF kidney, liver, lung
Stomach contents
Serum as above
Culture

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


(B) Other Diseases of the Female Reproductive Tract


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, Aujeskys Disease

Mastitis
Causes include A. pyogenes, E. coli, Leptospira, Staphylococcus aureus.




(C) Male reproductive tract diseases

Brucellosis
B. suis causes necrotizing orchitis & abscesses, although is rare.


MUSCULOSKELETAL DISEASES


Lameness Infectious Arthritis
Osteochondrosis
Chronic Zinc Toxicity
Trauma
Lactogenic Osteoporosis
Spinal Canal Abscesses


Infectious Arthritis
Etiology: Mycoplasma hyorhinis
Mycoplasma hyosynoviae (usually >10wo)
Streptococcus suis
Haemophilus parasuis (Glassers 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:

(a) Osteochondritis Dissecans Involves necrosis of a superficial zone of defective articular
cartilage ! The cartilage becomes dissected along the necrotic
region
(b) Epiphysiolysis Traumatic separation of the epiphysis from the metaphysic through
the weakened physis (also in Shetland Sheepdogs)
(c) Degenerative Joint Disease A sequel to any of the above forms


Chronic Zinc Toxicity Joint & bone lesions like osteochondrosis have been documented in pigs with
chronic Zn toxicity. (Also pancreatic necrosis)

Trauma Vertebral fractures / Limb fractures / Sole abrasions / Cruciate
rupture / Overgrown hooves / Heel abscesses

Lactogenic Osteoporosis Osteopenia due to ! activity & " bone resorption during lactation.

Spinal Canal Abscesses Usually A. pyogenes

Myopathies Infectious Myositis
Porcine Stress Syndrome
Myofibrillar Hypoplasia
Parasitic

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.

Porcine Stress Syndrome
Etiology: Genetic (Pietrain, Landrace, Large White, Yorkshire)
Pathogenesis: Single point mutation in skeletal muscle ryanodine receptor ! excessive calcium release
from the sarcoplasmic reticulum ! excessive metabolism ! " O
2
& glycogen consumption !
" heat, acid production, potassium, CO
2
& muscle protein release into circulation ! muscle
degeneration & necrosis
Grossly: Pale, soft, exudative muscle (mostly sublumbar muscles)
Dx: PCR to detect mutant gene in blood sample

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.




URINARY TRACT DISEASES Infectious
Neoplastic
Parasitic
Infectious
Pyelonephritis Actinobaculum suis.
Leptospirosis Leptospira pomona. Chronic interstitial nephritis. Icterus, hemoglobinuria.
Embolic Nephritis A sequel to any septicemic disease. A. pyogenes, A. suis, E. coli
PDNS Glomerulonephritis. ?PRRSV +/- PCV2

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


Vitamin E / Selenium Deficiency
Pathogenesis: Vit E & Se are antioxidants protect against oxidative injury from free radical (FR)
production during normal metabolic processes ! FRs damage cell membranes
Grossly: Mulberry Heart Disease Myocardial necrosis & hemorrhage. Vascular fibrinoid
necrosis.
Hepatosis Dietetica Massive hepatic necrosis & hemorrhage.


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.




CONGENITAL / HEREDITARY DISEASES Hernia
Myofibrillar Hypoplasia
Arthrogryposis
Microphthalmia
Hyperostosis
Renal Cysts
Porcine juvenile pustular psoriasiform dermatitis
Dermatosis Vegetans
Epitheliogenesis Imperfecta
Anal Atresia
Meningoencephalocele

Hernia Inguinal/Scrotal Male>female, left>right (unilateral), Weakness of tunica
vaginalis. Occasionally associated with freemartinism
Umbilical Sequel to omphalitis. Less common than inguinal hernia

Myofibrillar Hypoplasia Splayleg. Landrace.

Arthrogryposis In-utero Vit. A or manganese deficiency, CSF infection,
exposure to tobacco stalk, jimsonweed (thorn apple), wild black
cherry (bark) or poison hemlock.

Microphthalmia Due to in utero CSF infection. Or heritable.
Hyperostosis Autosomal recessive inheritance. Grossly thickened forelimbs
Periosteal proliferation. Fatal in first few weeks of life.

Renal Cysts Mainly at pole of kidney. Can become confluent.

Porcine juvenile pustular psoriasiform dermatitis Ventral abdomen, benign, self limiting.
Landrace.

Dermatosis Vegetans Thick papillomatous crusts on skin often on feet as hyperkeratotic
pododermatitis. Associated with fatal giant cell pneumonia. Very
infrequent. All carriers originate from one Danish landrace sow.

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.

Meningoencephalocele Insult 12-14d gestation. Associated with cranioschisis.





INTOXICATIONS Toxic Hepatopathies
Toxic Nephropathies

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.