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

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, HCO3, H2O ! 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

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 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 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

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 1st & 2nd 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

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

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

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 ! O2 & glycogen consumption ! heat, acid production, potassium, CO2 & 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

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.