Veterinary · Para-clinical · also MSVE VPP-221
Lesions organ system by organ system, plus the pathology of nutritional and production diseases.
In the exams: ICAR AICE-JRF core group 06; ICAR AIEEA-PG 13 (Pathology)
Systemic veterinary pathology describes the lesions of disease organ by organ: what the heart, lungs, gut, liver, kidneys, brain, muscles, bones, skin, reproductive tract and endocrine glands look like when diseased, in each domestic species, and what those lesions say about cause and outcome. It builds on general pathology (cell injury, inflammation, circulatory disturbance, growth disorders) and applies it. In India this is course VPP-221 of the Minimum Standards of Veterinary Education; elsewhere it is taught as 'systemic' or 'special' pathology within the pathology courses of a veterinary degree.
It matters in practice because the necropsy (post-mortem examination) is still the fastest and cheapest way to diagnose a herd or flock problem, and because clinicians must predict the lesion behind a clinical sign. A pattern of pneumonia seen at the abattoir, a pale streaked heart in a dead lamb, or a small pale kidney in an old cat each narrows the list of causes before any laboratory result arrives. Meat inspection, disease surveillance for notifiable diseases, forensic and welfare cases, and toxicology all depend on recognising lesions correctly.
Worldwide, the subject is examined as recall of named lesions and their causes (Indian ICAR and state service papers, China, Korea, Philippines, Nepal), as clinical-pathological reasoning from a case (NAVLE, BCSE, RCVS, Australasian and South African licensing exams), and as mechanism and precise morphology in specialist pathology boards. This manual covers each organ system, then nutritional and production pathology, and flags where disease distribution or legal handling differs by country.
Cardiac muscle cells (cardiomyocytes) are permanent cells: once lost they are replaced by fibrous tissue, not new muscle. The heart meets extra work by hypertrophy. Pressure overload, such as pulmonic or subaortic stenosis or systemic hypertension, produces concentric hypertrophy: a thick wall and a small lumen. Volume overload, such as valvular insufficiency or a left-to-right shunt, produces eccentric hypertrophy: a dilated chamber whose wall may look normal or thin. The pathologist judges ventricular size by the ratio of wall thicknesses or chamber weights against a laboratory reference, because eyeballing a dilated heart is unreliable. Heart failure is the state in which the heart cannot deliver enough blood for tissue needs. Left-sided failure causes pulmonary congestion and oedema; alveolar macrophages that have eaten red cells and hold haemosiderin are called heart failure cells. Right-sided failure causes chronic passive congestion of the liver (the cut surface shows dark centrilobular areas against pale periportal tissue, called nutmeg liver), subcutaneous oedema (the brisket in cattle), ascites and hydrothorax. In cattle, right-sided failure at high altitude from hypoxic pulmonary vasoconstriction is called brisket disease or high mountain disease; the same pulmonary hypertension mechanism underlies ascites in fast-growing broiler chickens. Hydropericardium is a clear transudate in the pericardial sac; haemopericardium is blood, often from a ruptured atrium or a bleeding right atrial haemangiosarcoma in dogs, and it kills by cardiac tamponade.
Fibrinous pericarditis gives the classic bread-and-butter heart. In cattle the commonest cause is traumatic reticulopericarditis: a swallowed wire penetrates the reticulum, diaphragm and pericardium and the sac fills with foul fibrinopurulent exudate. Fibrinous pericarditis is also seen in pigs with Glaesser's disease (Glaesserella parasuis) and with Streptococcus suis, and in poultry visceral gout coats the pericardium with chalky white urate. In starved or cachectic animals the epicardial fat of the coronary groove becomes grey, gelatinous and translucent, a change called serous atrophy of fat. Endocardiosis, better called myxomatous valve degeneration, is the commonest acquired heart disease of dogs: the mitral leaflets become thick, nodular and smooth, not ulcerated, in old small-breed dogs, and cause mitral regurgitation, left atrial dilation and jet lesions on the atrial wall. Valvular endocarditis is different: friable, cauliflower-like thrombotic vegetations containing bacteria. In cattle it most often affects the right atrioventricular (tricuspid) valve, frequently with Trueperella pyogenes, and it can shower septic emboli into the lungs. In pigs, Erysipelothrix rhusiopathiae and streptococci cause vegetative endocarditis, usually of the left-sided valves. Endocardial and arterial mineralisation (metastatic calcification) follows hypervitaminosis D, ingestion of calcinogenic plants such as Solanum malacoxylon and Cestrum diurnum, and, in cattle, advanced Johne's disease.
Myocardial necrosis with pale streaks and later mineralisation is seen in vitamin E and selenium deficiency (white muscle disease in calves and lambs; mulberry heart disease in pigs, with haemorrhage and oedema) and in ionophore poisoning, to which horses are especially sensitive. Foot-and-mouth disease kills young calves and lambs by myocardial necrosis that gives grey-white streaks, the tiger heart. Cardiomyopathies are primary heart muscle diseases. Hypertrophic cardiomyopathy is the commonest heart disease of cats; it predisposes to left atrial thrombosis and aortic thromboembolism at the iliac bifurcation (saddle thrombus), which causes painful hind-limb paralysis. Dilated cardiomyopathy occurs in large-breed dogs such as the Doberman, and historically in cats fed taurine-deficient diets. Boxers have arrhythmogenic right ventricular cardiomyopathy with fibro-fatty replacement of the right ventricle. Heart-base tumours (chemodectomas of the aortic body) favour brachycephalic dogs, and in cattle the right atrium is a common site of enzootic bovine leucosis lymphoma. Among congenital defects, patent ductus arteriosus is frequent in dogs, ventricular septal defect in cattle and horses, and subaortic stenosis in large breeds such as the Newfoundland. Tetralogy of Fallot combines pulmonic stenosis, ventricular septal defect, dextroposition of the aorta and right ventricular hypertrophy. A persistent right fourth aortic arch traps the oesophagus and causes megaoesophagus cranial to the heart. In vessels, Strongylus vulgaris larvae cause verminous arteritis and thrombosis of the cranial mesenteric artery of horses; Dirofilaria immitis causes proliferative (villous) endarteritis of the pulmonary arteries and right-sided heart failure in dogs; atherosclerosis in dogs is rare and linked to hypothyroidism with hypercholesterolaemia.
Because the circulation and the haemolymphatic organs are examined together at necropsy, a few splenic and nodal lesions belong here. A diffusely enlarged spleen that is dark and soft, with blood that fails to clot oozing from the orifices, in a ruminant found dead, suggests anthrax; such a carcass should not be opened, and a blood smear stained with polychrome methylene blue is examined for capsulated bacilli instead. Diffuse, firm, meaty enlargement suggests lymphoma or other infiltration; congested enlargement follows barbiturate euthanasia and splenic torsion, so a big spleen alone is not a lesion. Nodular splenic masses in old dogs are either nodular hyperplasia, which is benign, or haemangiosarcoma, which ruptures and bleeds; the two cannot be told apart reliably by eye, so the whole mass is sampled. Caseous lymphadenitis of sheep and goats, caused by Corynebacterium pseudotuberculosis, forms abscesses in superficial and internal lymph nodes; in sheep the caseous pus is often laid down in concentric onion-ring layers.
Atrophic rhinitis of pigs is the textbook upper-airway disease: toxigenic Pasteurella multocida, helped by Bordetella bronchiseptica, causes atrophy of the nasal turbinates, a twisted or shortened snout and poor growth. At slaughter the snout is sectioned transversely at the level of the first or second premolar tooth and turbinate loss is scored. Strangles, caused by Streptococcus equi subspecies equi, produces suppurative rhinitis and abscessation of the submandibular and retropharyngeal lymph nodes of horses; spread to other nodes is called bastard strangles. Guttural pouch mycosis, usually Aspergillus, erodes the internal carotid artery and can cause fatal epistaxis. Left recurrent laryngeal neuropathy, a distal axonopathy of the longest nerve in the body, causes atrophy of the left dorsal cricoarytenoid muscle and laryngeal hemiplegia (roaring) in tall horses. In sheep and goats, enzootic nasal tumour is a retrovirus-induced adenocarcinoma of the ethmoid mucosa; Oestrus ovis larvae cause catarrhal rhinitis and sinusitis. Infectious bovine rhinotracheitis (bovine herpesvirus 1) produces fibrinonecrotic rhinotracheitis with plaques that can be mistaken for diphtheria. In chickens, infectious laryngotracheitis causes haemorrhagic tracheitis with blood-stained mucus and intranuclear inclusions in the tracheal epithelium.
Pulmonary oedema makes lungs heavy and wet with froth in the airways. Emphysema is overdistension with rupture of alveolar walls. Cattle have thick, complete interlobular septa and little collateral ventilation, so air tracks into the septa and gives interstitial emphysema with bullae, a common agonal or secondary change. The pathologist classifies pneumonia by distribution and texture into four patterns. Bronchopneumonia is cranioventral, because inhaled organisms settle there; it is suppurative and lobular when the exudate is mainly neutrophils, or fibrinous and lobar when fibrin dominates. Interstitial pneumonia is diffuse, the lung fails to collapse, is rubbery and may bear rib impressions; injury arrives by blood or by toxic gas to the alveolar walls. Embolic pneumonia shows random multifocal lesions, often abscesses, seeded from septic foci such as a bovine tricuspid endocarditis or a liver abscess that has eroded the caudal vena cava. Granulomatous pneumonia gives firm nodules of different sizes, for example tuberculosis, systemic fungal infections and Rhodococcus equi pyogranulomatous pneumonia of foals. Recognising the pattern at necropsy narrows the list of causes before any culture result arrives.
Pneumonic mannheimiosis (shipping fever) of cattle, caused by Mannheimia haemolytica after stress and viral infection, is a fibrinous bronchopneumonia with pleuritis: the lobules are marbled by distended, fibrin-filled interlobular septa and areas of coagulation necrosis bordered by streaming, oat-shaped leucocytes. Contagious bovine pleuropneumonia (Mycoplasma mycoides subspecies mycoides) is also marbled and fibrinous and leaves encapsulated necrotic sequestra; it is a WOAH-listed disease. In pigs, enzootic pneumonia (Mycoplasma hyopneumoniae) causes purple-grey cranioventral consolidation with peribronchiolar lymphoid hyperplasia (cuffing), whereas porcine pleuropneumonia (Actinobacillus pleuropneumoniae) gives haemorrhagic necrotising lesions that often lie dorsally in the caudal lobes, with fibrinous pleuritis. Acute bovine pulmonary oedema and emphysema (fog fever) follows a move to lush pasture: rumen microbes convert L-tryptophan to 3-methylindole, which damages type I pneumocytes and club cells, giving diffuse interstitial pneumonia with oedema, emphysema and later type II pneumocyte hyperplasia. Maedi (ovine progressive pneumonia, a lentivirus) gives heavy, grey, non-collapsing lungs with lymphoid hyperplasia and smooth muscle hyperplasia. Ovine pulmonary adenocarcinoma (jaagsiekte, a betaretrovirus) produces masses of neoplastic type II pneumocytes and club cells; copious fluid pours from the nostrils when the hindquarters are raised. Dictyocaulus viviparus, the cattle lungworm, lies in the airways of the caudodorsal lobes. In poultry, airsacculitis with caseous exudate follows Mycoplasma gallisepticum and E. coli infection; aspergillosis produces yellow plaques and nodules in lungs and air sacs of chicks (brooder pneumonia).
Hydrothorax is a transudate in the pleural cavity, usually from heart failure or hypoproteinaemia. Haemothorax is blood; chylothorax is milky lymph rich in triglyceride from a damaged or obstructed thoracic duct, recognised in cats and dogs. Pyothorax (empyema) is pus; in cats it follows bite wounds and involves mixed anaerobes and Pasteurella, and in horses it is often an extension of pleuropneumonia. Fibrinous pleuritis accompanies the pneumonias of Mannheimia, Actinobacillus pleuropneumoniae, Glaesserella parasuis and Mycoplasma in pigs and cattle; at the abattoir, organised fibrous pleural adhesions are a common reason for trimming carcasses and a crude measure of herd respiratory disease. Mesothelioma is uncommon and seeds the pleura with numerous small nodules. In dogs and cats, neoplastic or cardiac effusions must be distinguished from inflammatory ones by cytology and protein content, because the gross appearance of the fluid alone can mislead, particularly with chylous and haemorrhagic effusions, which can look alike in a stored tube.
Oral lesions of ruminants and pigs are sorted by type, because type points to cause. Vesicles (fluid-filled blisters) are caused by foot-and-mouth disease, vesicular stomatitis, swine vesicular disease and vesicular exanthema of swine; they cannot be told apart by lesion alone, so any vesicular disease is a notifiable emergency. Erosions and ulcers without vesicles suggest bovine viral diarrhoea-mucosal disease, peste des petits ruminants, malignant catarrhal fever, bluetongue or rinderpest (eradicated in 2011, but still examined). Wooden tongue is actinobacillosis, a pyogranulomatous glossitis caused by Actinobacillus lignieresii in soft tissue; lumpy jaw is actinomycosis, a pyogranulomatous osteomyelitis of the mandible caused by Actinomyces bovis. Both show club colonies (sulphur granules) with Splendore-Hoeppli material. Choke is obstruction of the oesophagus by food or a foreign body. Megaoesophagus is dilation with loss of motility, congenital or acquired (for example myasthenia gravis in dogs). In the rumen, grain overload causes lactic acidosis and chemical rumenitis; bacteria such as Fusobacterium necrophorum then pass through the damaged wall to the portal vein and cause liver abscesses. Frothy bloat on legumes leaves congestion of the head and neck and a sharp bloat line in the cervical oesophagus, the line between congested cranial and pale caudal mucosa, which helps distinguish bloat from post-mortem gas production.
Abomasal displacement, usually to the left, is a periparturient disease of high-yielding dairy cows linked to reduced motility, hypocalcaemia and ketosis; right displacement can progress to abomasal volvulus with ischaemic necrosis. Abomasal ulcers may bleed or perforate and cause local or diffuse peritonitis. Haemonchus contortus causes blood-loss anaemia in sheep and goats with oedema of the abomasal folds; Ostertagia ostertagi causes nodular hyperplasia of the gastric glands that gives the abomasal mucosa a morocco-leather appearance and raises abomasal pH. In pigs, ulcers of the pars oesophagea, the non-glandular region around the oesophageal entry, are linked to finely ground or pelleted feed and stress; a pig may die from haemorrhage with pale carcass and blood in the stomach. Horses develop gastric ulcers mostly in the squamous mucosa near the margo plicatus. Gastric dilatation-volvulus in deep-chested dogs causes venous infarction of the stomach wall and spleen and shock. In horses, gastric rupture along the greater curvature is distinguished from post-mortem rupture by haemorrhage at the torn edges.
Diarrhoea arises by four mechanisms, each with its own lesion. Malabsorption follows villous atrophy: rotavirus and coronavirus infect the absorptive cells at the villus tips, so villi shorten and fuse while crypts survive; canine and feline parvovirus instead kill the dividing crypt cells, giving dilated crypts lined by flattened cells and collapse of villi, with lymphoid depletion. Hypersecretion without visible lesion is caused by enterotoxigenic E. coli, whose toxins drive chloride secretion. Inflammation and exudation follow invasive bacteria: Salmonella causes fibrinonecrotic enterocolitis with button ulcers in pigs; Brachyspira hyodysenteriae causes mucohaemorrhagic colitis (swine dysentery) confined to the large intestine; classical swine fever may leave button ulcers in the colon. Proliferation is typical of porcine proliferative enteropathy (Lawsonia intracellularis): the ileal mucosa thickens as crypt cells proliferate, and in the acute haemorrhagic form the ileum holds a blood clot. Johne's disease (Mycobacterium avium subspecies paratuberculosis) causes chronic granulomatous enteritis, most marked in the ileum, with a thick corrugated mucosa, lymphangitis and enlarged mesenteric nodes. Clostridium perfringens type C causes haemorrhagic necrotic enteritis in piglets and lambs; type D epsilon toxin causes enterotoxaemia (pulpy kidney) in sheep and goats; C. perfringens also causes necrotic enteritis in broiler chickens with a turkish-towel mucosa. Mechanical lesions include intussusception, volvulus and strangulation by a pedunculated lipoma in old horses; each causes venous infarction. Intestinal adenocarcinoma of sheep and alimentary lymphoma of cats are the tumours most often met. In the exocrine pancreas, acute pancreatitis in dogs, often in overweight animals after a fatty meal, causes pancreatic and peripancreatic necrosis with chalky white foci of fat necrosis in the mesentery. Pancreatic acinar atrophy in German shepherd dogs causes exocrine pancreatic insufficiency: a thin, translucent pancreas, weight loss and voluminous faeces. Peritonitis may be fibrinous, as in feline infectious peritonitis (pyogranulomatous serositis with a sticky, straw-coloured, protein-rich effusion) or in traumatic reticuloperitonitis of cattle.
The liver lobule has a blood gradient: the periportal zone (zone 1) receives the best-oxygenated blood, and the centrilobular zone (zone 3) around the central vein receives the least oxygen but holds most of the cytochrome P450 enzymes that turn many chemicals into toxic metabolites. Centrilobular necrosis therefore follows hypoxia (severe anaemia, heart failure) and many toxins, for example carbon tetrachloride, and paracetamol (acetaminophen) in cats and dogs. Periportal necrosis is less common and follows toxins that act before metabolism, such as white phosphorus. Midzonal necrosis is rare. Random multifocal necrosis, scattered foci without regard to lobular zone, indicates blood-borne infection: Salmonella, Tyzzer's disease (Clostridium piliforme) in foals and rodents, herpesvirus infections of neonates and fetuses (equine herpesvirus 1, bovine herpesvirus 1), and infectious canine hepatitis (canine adenovirus 1, with intranuclear inclusions in hepatocytes and a thickened, oedematous gall bladder). Massive necrosis involves whole lobules, as in hepatosis dietetica of pigs with vitamin E and selenium deficiency, where necrotic and haemorrhagic lobules alternate with normal ones. Hepatic lipidosis gives a large, yellow, greasy, friable liver whose slices float in formalin; it follows negative energy balance in dairy cows, anorexia in obese cats (feline hepatic lipidosis), and pregnancy toxaemia in ewes. Dogs treated with glucocorticoids, or with hyperadrenocorticism, develop steroid hepatopathy: vacuolated hepatocytes packed with glycogen.
Pyrrolizidine alkaloids from plants such as Senecio, Crotalaria and Heliotropium are converted in the liver to pyrroles that block hepatocyte division. Chronic intake causes megalocytosis (giant hepatocytes), bile duct hyperplasia and portal fibrosis, ending in a small, firm liver with hepatic encephalopathy in horses and cattle. Aflatoxins from Aspergillus flavus are hepatotoxic and carcinogenic; ducklings, turkey poults and young pigs are very sensitive, showing hepatocellular necrosis, lipidosis, bile duct proliferation and, with chronic exposure, liver tumours. Hepatogenous photosensitisation occurs when a damaged liver cannot excrete phylloerythrin, the chlorophyll breakdown product, as in facial eczema of sheep caused by sporidesmin from a pasture fungus. Copper accumulates in the liver of sheep, which tolerate copper poorly; release during stress causes an acute haemolytic crisis with jaundice, haemoglobinuria and gunmetal-blue kidneys. Bedlington terriers have an inherited copper-storage hepatitis (COMMD1 gene) leading to chronic hepatitis and cirrhosis. Cirrhosis is the end stage: fibrosis linking portal and central areas, regenerative nodules and loss of normal architecture. Portosystemic shunts are congenital vessels that bypass the liver; extrahepatic shunts are typical of small-breed dogs, intrahepatic shunts of large breeds. The liver is small from lack of portal blood flow, and ammonium urate uroliths may form in the bladder. Gall bladder mucocoele, a distended gall bladder full of immobile green mucus, is recognised in dogs and can rupture.
Fasciola hepatica has two forms of disease. Acute fasciolosis follows mass migration of immature flukes through the parenchyma, causing haemorrhagic tracks, peritonitis and sudden death in sheep; the migration tracks also let spores of Clostridium novyi type B germinate and cause black disease (infectious necrotic hepatitis). Chronic fasciolosis follows adult flukes in bile ducts: cholangitis, fibrosis and, in cattle, thick-walled calcified ducts described as pipestem liver. Larvae of Ascaris suum migrating through the pig liver leave white interlobular fibrous scars called milk spots, a common cause of liver condemnation. Hydatid cysts of Echinococcus granulosus and the thin-walled Cysticercus tenuicollis (larva of Taenia hydatigena) are also found at meat inspection. Liver abscesses in feedlot cattle, mostly Fusobacterium necrophorum with Trueperella pyogenes, follow ruminal acidosis and rumenitis. Among tumours, metastases are commoner than primary tumours; primary hepatocellular carcinoma occurs in dogs and in sheep, and cholangiocellular carcinoma in cats and dogs. Nodular hyperplasia is common in old dogs and must not be mistaken for neoplasia.
Renal agenesis, hypoplasia and dysplasia are congenital. Polycystic kidney disease of Persian and related cats is an autosomal dominant defect (PKD1) in which cysts gradually replace the parenchyma. Renal infarcts are wedge-shaped with the base at the capsule, red when fresh and pale later, and they follow emboli from valvular endocarditis. Glomerulonephritis in animals is mostly immune-complex disease: complexes of antigen and antibody lodge in glomerular capillary walls and trigger complement, so glomeruli become large, hypercellular or thickened. Chronic infections, pyometra, dirofilariasis, feline leukaemia virus and infectious canine hepatitis are recognised triggers. Damage to the filtration barrier causes protein-losing nephropathy, and severe protein loss gives the nephrotic syndrome of hypoalbuminaemia, oedema and hypercholesterolaemia. Renal amyloidosis is another cause of heavy proteinuria: in most dogs amyloid (AA type, from serum amyloid A in chronic inflammation) is deposited in glomeruli, whereas in Abyssinian cats and in Shar-Pei dogs it is mainly medullary interstitial, so these animals present with renal failure and less proteinuria. Amyloid stains with Congo red and shows green birefringence under polarised light.
Acute tubular injury (nephrosis) is either ischaemic, from shock or dehydration, or nephrotoxic. Nephrotoxins include aminoglycoside antibiotics, non-steroidal anti-inflammatory drugs (which reduce renal blood flow and cause papillary necrosis, notably in horses), oak leaves and acorns (tannins) in cattle, lilies in cats and grapes or raisins in dogs. Ethylene glycol (antifreeze) is metabolised to oxalate: the kidneys are swollen and pale, and birefringent calcium oxalate crystals fill tubules; the same crystals follow oxalate-rich plants in ruminants. Haemoglobin (from babesiosis, leptospirosis, chronic copper poisoning or red maple toxicity in horses) and myoglobin (from exertional rhabdomyolysis) stain the kidneys dark and cause pigment nephrosis. Tubulointerstitial nephritis is inflammation centred on the interstitium. Leptospirosis in dogs and pigs causes interstitial nephritis. Small white foci across the cortex of calves (white-spotted kidney) are foci of non-suppurative interstitial nephritis that follow bacteraemia. Pyelonephritis is ascending bacterial infection of the pelvis and medulla, favoured by urine stasis and reflux; in cows it is classically caused by Corynebacterium renale and in sows by Actinobaculum suis. Embolic suppurative nephritis follows bacteraemia: Actinobacillus equuli in foals produces pinpoint cortical abscesses, and Erysipelothrix in pigs does likewise. In the lamb or kid that died suddenly, a soft autolysed 'pulpy kidney' reflects epsilon toxin damage but is also partly post-mortem, so glucosuria and brain lesions are sought as well.
Chronic kidney disease ends in small, pale, firm kidneys with an irregular, pitted surface, thin cortex, cysts and fibrosis, whatever the original cause. Uraemia then causes lesions outside the kidney that the pathologist uses to confirm renal failure: ulcerative stomatitis and glossitis, uraemic gastritis with mineralisation of the gastric mucosa, mineralisation of the intercostal pleura and lungs, ulcerative endocarditis of the left atrium, non-regenerative anaemia, and renal secondary hyperparathyroidism with fibrous osteodystrophy of the skull ('rubber jaw' in dogs). Hydronephrosis is dilation of the pelvis with atrophy of the parenchyma behind a urinary obstruction. Urolithiasis depends on species, diet and urine pH. Struvite (magnesium ammonium phosphate) forms in alkaline urine, often with urease-producing bacterial infection in dogs; calcium oxalate stones are common in dogs and cats; urate stones form in Dalmatians, which have a defect in urate transport (SLC2A9), and in dogs with portosystemic shunts; silica stones occur in cattle and sheep grazing certain range grasses. In castrated male ruminants the calculi lodge at the sigmoid flexure or the urethral process, and urethral rupture causes 'water belly'. Enzootic bovine haematuria follows prolonged grazing of bracken fern (ptaquiloside), with chronic haemorrhagic cystitis and urinary bladder tumours, sometimes with bovine papillomavirus. The commonest bladder tumour of dogs is urothelial (transitional cell) carcinoma, often at the trigone; Scottish terriers are predisposed. Male cats form urethral plugs of matrix and struvite crystals within feline lower urinary tract disease.
Neurons are permanent cells. An irreversibly injured neuron shrinks, its cytoplasm turns bright pink and its nucleus dark, a change called red dead neuron, seen in ischaemia, hypoglycaemia and many toxicities. Central chromatolysis is swelling of the cell body with dispersal of Nissl substance after axonal injury. When an axon is cut, the distal part degenerates (Wallerian degeneration): axons fragment into spheroids, myelin breaks into ellipsoids in digestion chambers, and macrophages laden with lipid (gitter cells) clear the debris. Malacia means softening from necrosis; polioencephalomalacia affects grey matter, leukoencephalomalacia white matter. Astrocytes react by swelling and proliferation (gliosis), the scar of the brain. Microglia cluster around dying neurons (neuronophagia) or form glial nodules. Satellitosis is oligodendrocytes clustered around neurons. Perivascular cuffs of lymphocytes and plasma cells indicate non-suppurative encephalitis, typical of most viral infections, whereas neutrophils indicate bacterial infection. Oedema of the brain may raise intracranial pressure and cause herniation of the cerebellum through the foramen magnum.
Cerebellar hypoplasia follows infection of the fetus or neonate while the cerebellum is still developing: feline panleukopenia virus in kittens, bovine viral diarrhoea virus in calves and classical swine fever virus in piglets. Hydranencephaly (the cerebral hemispheres replaced by fluid-filled sacs) with arthrogryposis follows in utero infection with Akabane, Schmallenberg or bluetongue viruses in ruminants. Hydrocephalus may be congenital, common in toy and brachycephalic dogs, or acquired from obstruction. Inherited lysosomal storage diseases, such as alpha-mannosidosis in Angus cattle, fill neurons with vacuoles. Listeriosis in ruminants (Listeria monocytogenes, often from poor silage) enters through the trigeminal nerve and causes microabscesses and perivascular cuffing in the brainstem, with circling and unilateral facial paralysis. Thromboembolic meningoencephalitis (Histophilus somni) of feedlot cattle causes multifocal red haemorrhagic infarcts from vasculitis. Rabies gives mild non-suppurative encephalitis with intracytoplasmic eosinophilic Negri bodies, looked for in the hippocampus in carnivores and in the Purkinje cells of the cerebellum in ruminants; the brainstem is also sampled. Canine distemper virus causes demyelination and eosinophilic inclusions in astrocytes, neurons and epithelia. Equine herpesvirus 1 myeloencephalopathy is a vasculitis with thrombosis and infarction of the spinal cord. Transmissible spongiform encephalopathies (scrapie, bovine spongiform encephalopathy, chronic wasting disease) show bilaterally symmetrical vacuolation of grey matter neuropil and neurons without inflammation; the obex of the medulla is the standard sampling site. Parasites include Coenurus cerebralis (larva of Taenia multiceps), which forms a cyst in the brain of sheep and causes gid, and Sarcocystis neurona, which causes equine protozoal myeloencephalitis.
Polioencephalomalacia of ruminants is laminar necrosis of the cerebral cortex associated with thiamine deficiency or inhibition, excess dietary sulphur, and lead poisoning; affected cortex may fluoresce under ultraviolet light at 365 nm, and the animals are blind with head pressing. Salt poisoning with water deprivation in pigs causes cerebral oedema with eosinophilic perivascular cuffs. Clostridium perfringens type D epsilon toxin causes focal symmetrical encephalomalacia in sheep. Equine leukoencephalomalacia, liquefaction of cerebral white matter, follows fumonisin B1 from mouldy maize infected with Fusarium verticillioides. Nigropallidal encephalomalacia of horses follows prolonged grazing of yellow star thistle or Russian knapweed. Copper deficiency in pregnant ewes causes enzootic ataxia (swayback) in lambs, with cavitation of cerebral white matter in the congenital form and degeneration of spinal cord tracts. Intervertebral disc disease in dogs has two types: Hansen type I is extrusion of a degenerate calcified nucleus in chondrodystrophic breeds such as the dachshund, with acute compression and haemorrhage; type II is a slow protrusion of the annulus in older non-chondrodystrophic dogs. Cervical vertebral stenotic myelopathy (wobbler syndrome) occurs in young horses and in Great Danes and Dobermans. Degenerative myelopathy of German shepherd and other dogs, associated with SOD1 mutation, is an axonal and myelin degeneration of the thoracic cord. Fibrocartilaginous embolism causes sudden, non-progressive, often asymmetric infarction of the cord. Marek's disease of chickens enlarges peripheral nerves such as the sciatic nerve and brachial plexus with mixed lymphoid infiltrates. Meningioma is the commonest intracranial tumour of cats; gliomas favour brachycephalic dogs.
Muscle fibres respond to injury by segmental necrosis. Hyaline (Zenker's) necrosis gives swollen, glassy, hypereosinophilic fibre segments that later mineralise. If the basal lamina and satellite cells survive, as after a single toxic or nutritional insult, the fibre regenerates; if the insult is ischaemic or crushing, healing is by fibrosis. Grossly, necrotic muscle is pale, and mineralised necrotic muscle shows chalky white streaks. Nutritional myopathy from vitamin E and selenium deficiency (white muscle disease) affects rapidly growing calves, lambs and foals, often in the heavily used muscles of the limbs, diaphragm, tongue and heart, and is bilaterally symmetrical. Ionophores such as monensin and salinomycin cause myocardial and skeletal muscle necrosis; horses are most sensitive. Exertional rhabdomyolysis of horses causes swollen, dark muscle and myoglobinuria. Downer cows that lie on one side for hours develop ischaemic necrosis of the pelvic limb muscles from pressure. Capture myopathy in wild ruminants follows extreme exertion and stress. Blackleg (Clostridium chauvoei) produces dark red to black, dry, emphysematous muscle with a rancid odour in well-grown young cattle; malignant oedema (Clostridium septicum and others) follows wound contamination and is wetter and more oedematous. Eosinophilic myositis in cattle is associated with Sarcocystis and causes carcass trimming. Inherited myopathies include the porcine stress syndrome (RYR1 mutation) that causes malignant hyperthermia and pale, soft, exudative meat, hyperkalaemic periodic paralysis (SCN4A) and polysaccharide storage myopathy (GYS1) in Quarter Horses, and X-linked muscular dystrophy (dystrophin gene) in golden retrievers.
Bone disease is usually metabolic. Osteoporosis is too little bone that is normally mineralised, seen in starvation, copper deficiency and caged laying hens (cage layer fatigue). Rickets, in growing animals, is failure of mineralisation of cartilage and osteoid, caused by deficiency of vitamin D or phosphorus: the physes (growth plates) are wide and irregular, costochondral junctions enlarge (rachitic rosary) and long bones bend. Osteomalacia is the adult counterpart: excess unmineralised osteoid with soft bones and fractures. Fibrous osteodystrophy is resorption of bone and replacement by fibrous tissue driven by excess parathyroid hormone. Nutritional secondary hyperparathyroidism arises from diets low in calcium or high in phosphorus: horses fed bran or grazing oxalate-rich tropical grasses swell over the facial bones (big head), and puppies, kittens and reptiles fed all-meat diets fracture thin bones. Renal secondary hyperparathyroidism gives the rubber jaw of dogs. Hypervitaminosis A in cats fed mainly liver causes confluent exostoses of the cervical vertebrae with ankylosis. Chronic fluorosis mottles and pits the enamel of developing teeth and causes periosteal exostoses. Osteochondrosis is failure of endochondral ossification in the articular-epiphyseal cartilage complex of fast-growing pigs, horses and large-breed dogs; a flap of cartilage that separates gives osteochondritis dissecans. Hypertrophic osteopathy is periosteal new bone along the distal limbs secondary to a thoracic mass, and the bone lesion may regress when the mass is removed. Craniomandibular osteopathy affects the mandible of young terriers, especially West Highland white terriers. Osteosarcoma of large and giant-breed dogs arises in the metaphyses of long bones, classically distal radius, proximal humerus, distal femur and proximal tibia, and metastasises to the lungs.
Infectious arthritis in neonates follows bacteraemia from an infected umbilicus (joint ill or navel ill in calves and foals). Erysipelothrix rhusiopathiae causes chronic proliferative arthritis in pigs; Mycoplasma species cause arthritis in pigs, calves and poultry; caprine arthritis-encephalitis virus causes chronic carpal arthritis (big knee) in adult goats. Degenerative joint disease (osteoarthritis) shows fibrillation and erosion of articular cartilage, osteophytes at the joint margins, and eburnation (polished exposed subchondral bone); it follows instability, dysplasia and ageing, as in canine hip dysplasia and cranial cruciate ligament rupture. Articular gout in birds deposits urate crystals in joints; visceral gout on serosae follows kidney damage or dehydration. Manganese or choline deficiency in chicks causes perosis, slipping of the gastrocnemius tendon from its condyle. Chondrodysplastic dwarfism of Dexter cattle produces short-limbed 'bulldog' calves. Tendon and ligament injury, such as superficial digital flexor tendinitis in racehorses, heals slowly by fibrous scar that is weaker than the original tendon, which is why re-injury is common.
Skin pathology uses precise terms. Hyperkeratosis is a thickened stratum corneum: orthokeratotic when cells lack nuclei, parakeratotic when they keep nuclei (a sign of fast turnover, as in zinc-responsive dermatosis). Acanthosis is thickening of the living epidermis. Spongiosis is oedema between keratinocytes; ballooning degeneration is swelling within them, typical of poxviruses. Acantholysis is loss of cohesion between keratinocytes, producing rounded free cells in pustules, and is the hallmark of pemphigus. A vesicle is a small fluid-filled blister, a bulla a large one, and a pustule contains neutrophils. Photosensitisation is dermatitis of light-exposed, unpigmented skin caused by a photodynamic agent that absorbs ultraviolet light. Primary photosensitisation follows ingestion of a preformed photodynamic agent, such as hypericin from St John's wort or fagopyrin from buckwheat. Secondary (hepatogenous) photosensitisation, the most common type in livestock, follows liver damage that stops excretion of phylloerythrin. A third type is congenital porphyria, in which porphyrins accumulate, as in bovine congenital erythropoietic porphyria with reddish-brown teeth that fluoresce under ultraviolet light. Ergotism (Claviceps purpurea alkaloids) and fescue toxicosis cause vasoconstriction and dry gangrene of the extremities; chronic selenium poisoning causes hoof deformity and loss of long hair of the mane and tail in horses.
Dermatophilosis (Dermatophilus congolensis) causes crusted, matted tufts of hair (paintbrush lesions) in wet conditions; the organism forms branching filaments dividing into rows of cocci that look like railway tracks. Exudative epidermitis (greasy pig disease) of piglets is caused by Staphylococcus hyicus. Swine erysipelas produces raised, rhomboid, pink to purple diamond skin lesions. Dermatophytosis (ringworm) causes circular alopecia with scale; Trichophyton verrucosum is the main cattle species and Microsporum canis the main cat species, and ringworm is zoonotic. Poxviruses cause papules that become vesicles and pustules and then scabs, with ballooning degeneration and intracytoplasmic eosinophilic inclusion bodies (Bollinger bodies); examples are sheep and goat pox, lumpy skin disease with deep nodules in cattle, and contagious ecthyma (orf) of lips of lambs, which is zoonotic. Papillomaviruses cause warts. Sarcoptic mange causes intense pruritus, crusts and thickening; demodicosis in dogs is associated with follicular mites and furunculosis, often in young or immunosuppressed animals. Flea allergy dermatitis is the commonest allergic skin disease of dogs and cats in many regions; atopic dermatitis is inherited sensitivity to environmental allergens. Pemphigus foliaceus is the commonest autoimmune skin disease of dogs and cats: subcorneal pustules containing acantholytic keratinocytes on the face, ears and footpads. Endocrine alopecia is bilaterally symmetrical and non-pruritic; hyperadrenocorticism in dogs also causes thin skin, comedones and calcinosis cutis, mineral deposits in the dermis.
Mast cell tumour is the commonest malignant skin tumour of dogs; it varies from well differentiated to aggressive, is graded histologically, and its granules release histamine and heparin that can cause gastric ulcers and delayed wound healing. Cutaneous histiocytoma is a benign tumour of Langerhans cells in young dogs, a button-like dome on the head or limbs that often regresses spontaneously. Squamous cell carcinoma arises in unpigmented, sun-exposed skin: the ear tips and eyelids of white cats and the eyelid and third eyelid of cattle with unpigmented periocular skin (cancer eye). Equine sarcoid, the commonest skin tumour of horses, is a locally aggressive fibroblastic tumour associated with bovine papillomavirus types 1 and 2; it does not metastasise but recurs after incomplete removal. Melanomas are common in grey horses, often around the perineum and tail. Hepatoid (perianal) gland adenomas occur in older intact male dogs. Feline injection-site sarcoma is a fibrosarcoma associated with chronic inflammation at injection sites.
Cystic ovarian follicles in dairy cows are anovulatory follicles larger than a normal preovulatory follicle that persist; follicular cysts are thin-walled, luteal cysts have a lining of luteinised tissue. The granulosa cell tumour is the commonest ovarian tumour of mares: it is multicystic, may cause stallion-like behaviour or anoestrus, and the opposite ovary is small and inactive. Freemartinism is sterility of a heifer born twin to a bull: shared placental vessels exchange cells and hormones, producing an XX/XY chimera with a short vagina and hypoplastic gonads. The cystic endometrial hyperplasia-pyometra complex of older intact bitches develops under repeated progesterone exposure in dioestrus; the uterus fills with pus, commonly with E. coli, and endotoxaemia and immune-complex glomerulonephritis may follow. In cattle, postpartum metritis and pyometra are linked to retained placenta and a persistent corpus luteum. Fetal mummification (a sterile, dehydrated fetus in a closed cervix) differs from maceration (bacterial liquefaction leaving bones in an open uterus). Canine mammary tumours are common in intact bitches; roughly half are malignant, and spaying before the first or second oestrus greatly reduces risk. In cats most mammary tumours are malignant adenocarcinomas. Feline fibroadenomatous hyperplasia is a rapid, benign mammary enlargement in young cats under progesterone or progestin influence. Gangrenous mastitis of ewes and cows, mostly Staphylococcus aureus, makes the udder cold, blue-black and sloughing.
Aborted fetuses and placentas are examined together, because many lesions lie in the placenta. Brucella abortus causes necrotising placentitis of cows in late gestation: cotyledons are necrotic and the intercotyledonary placenta thick, leathery and yellow; the bacteria multiply in trophoblasts, and erythritol in the placenta favours their growth. Brucella melitensis affects goats and sheep and is the most important zoonotic Brucella. Mycotic abortion (often Aspergillus) also gives a thick leathery placenta, and the fetus may have raised grey ringworm-like skin plaques. Neospora caninum is a major cause of bovine abortion worldwide; the fetus shows multifocal non-suppurative encephalitis with necrosis and myocarditis. Toxoplasma gondii in ewes causes white foci of necrosis in the cotyledons. Chlamydia abortus causes enzootic abortion of ewes with necrotic cotyledons and a thick, reddish intercotyledonary placenta; it is zoonotic and dangerous to pregnant women. Bovine herpesvirus 1 and equine herpesvirus 1 cause late abortion with small foci of necrosis in the fetal liver and other organs and intranuclear inclusions. Campylobacter fetus venerealis causes early embryonic death and infertility in cattle. Porcine parvovirus causes stillbirths, mummified fetuses of different sizes, embryonic death and infertility in gilts (SMEDI). Leptospira, bovine viral diarrhoea virus and Coxiella burnetii are further causes. Most aborted fetuses are autolysed, and a cause is found in a minority of submissions, so pooled herd submissions and serology are used.
Testicular hypoplasia is congenital underdevelopment; testicular degeneration is acquired loss of germ cells from heat, fever, toxins or ageing, leaving a small, soft testis that may later be firm and fibrotic. Cryptorchidism, failure of testicular descent, is heritable in many species and the retained testis is at higher risk of neoplasia. In dogs, Sertoli cell tumours are more common in cryptorchid testes and may secrete oestrogen, causing feminisation, symmetrical alopecia, atrophy of the other testis and potentially fatal bone marrow suppression; seminomas and interstitial (Leydig) cell tumours are also common in old dogs. Orchitis and epididymitis in bulls follow Brucella abortus; Brucella ovis causes epididymitis in rams, with spermatic granulomas and palpably enlarged tails of the epididymis; Brucella canis causes epididymitis and abortion in dogs. Benign prostatic hyperplasia develops in most older intact dogs under the influence of dihydrotestosterone and regresses after castration; prostatic carcinoma, in contrast, also occurs in castrated dogs. Canine transmissible venereal tumour is transmitted as living tumour cells during mating and forms friable, cauliflower-like masses on the penis or vagina. Ulcerative posthitis (pizzle rot) of wethers and rams is associated with Corynebacterium renale and high-protein diets that raise urinary urea.
About 80 to 85 percent of spontaneous hyperadrenocorticism (Cushing's syndrome) in dogs is pituitary-dependent, caused by an adenoma or hyperplasia of corticotrophs secreting ACTH; both adrenal cortices are then enlarged by hyperplasia. The rest is caused by a functional adrenocortical adenoma or carcinoma, which suppresses ACTH, so the cortex of the opposite gland atrophies. The lesions of hyperadrenocorticism are steroid hepatopathy, thin skin, symmetrical alopecia, comedones, calcinosis cutis, a pendulous abdomen and muscle wasting; pulmonary thromboembolism is a recognised complication. Iatrogenic hyperadrenocorticism from glucocorticoid treatment produces the same lesions but with bilateral adrenocortical atrophy. Pituitary pars intermedia dysfunction of old horses is a hyperplasia or adenoma of the pars intermedia with a long, curly hair coat that fails to shed (hirsutism) and laminitis. Pituitary dwarfism of German shepherd dogs follows failure of pituitary development, often with cysts. Hypoadrenocorticism (Addison's disease) in dogs is usually immune-mediated destruction of the adrenal cortex, leaving small glands with a thin cortex; loss of mineralocorticoid causes hyponatraemia and hyperkalaemia. Phaeochromocytoma is a tumour of the adrenal medulla that secretes catecholamines and may invade the caudal vena cava.
Goitre is non-neoplastic enlargement of the thyroid. Iodine deficiency in pregnant animals causes neonatal goitre, hairlessness and stillbirth, still seen in iodine-deficient regions in many countries. Goitrogens include glucosinolates and thiocyanates of brassica crops. Hyperplastic goitre has tall follicular cells with little colloid; colloid goitre is the involuted phase with distended follicles. In dogs, hypothyroidism is mostly caused by lymphocytic thyroiditis (immune-mediated) or idiopathic follicular atrophy; it causes symmetrical alopecia, myxoedema of the face (a tragic expression), lethargy, hypercholesterolaemia and occasionally atherosclerosis. In old cats, hyperthyroidism is caused by adenomatous hyperplasia or adenoma of follicular cells, bilateral in the majority; carcinoma is uncommon. In dogs, thyroid tumours are more often carcinomas and usually non-functional. C-cell (parafollicular) tumours occur in old bulls. Primary hyperparathyroidism is usually a functional parathyroid adenoma causing hypercalcaemia; keeshonds are predisposed. In secondary hyperparathyroidism (nutritional or renal) the parathyroids are all enlarged by hyperplasia. Humoral hypercalcaemia of malignancy is caused by parathyroid hormone-related protein secreted by tumours such as apocrine gland adenocarcinoma of the anal sac and T-cell lymphoma in dogs; the parathyroid glands atrophy because calcium is high.
Diabetes mellitus in dogs is mostly insulin-deficient, from loss of beta cells linked to immune destruction or chronic pancreatitis. In cats, diabetes resembles human type 2 disease, with insulin resistance (obesity) and islet amyloidosis, in which islet amyloid polypeptide (amylin) forms amyloid that replaces islet cells. Lesions of diabetes include hepatic lipidosis, cataract in dogs (sorbitol accumulation in the lens), glycogen vacuolation of renal tubules and recurrent infections. Insulinoma, a beta-cell tumour, is usually malignant in dogs, secretes insulin regardless of blood glucose and causes hypoglycaemic weakness and seizures, which can leave neuronal necrosis in the cerebral cortex. Metastases go to regional lymph nodes and liver, so the pathologist examines these even when the pancreatic nodule is small. Diabetic dogs and cats also develop urinary tract infections and, in cats, a plantigrade stance from diabetic neuropathy with demyelination of peripheral nerves. Emaciation despite a good appetite is typical of untreated disease.
Vitamin E and selenium protect membranes against oxidation, selenium through glutathione peroxidase. Deficiency produces a range of species-specific diseases: white muscle disease (nutritional myopathy) of calves, lambs and foals; mulberry heart disease and hepatosis dietetica of young pigs; exudative diathesis (green-blue subcutaneous oedema from leaky capillaries) and nutritional encephalomalacia with cerebellar necrosis in chicks, the latter mainly vitamin E-dependent; and retained placenta in cows. Yellow fat disease (pansteatitis) of cats fed diets rich in unsaturated fish oils without enough vitamin E makes fat firm, yellow-orange and inflamed, with ceroid pigment. Vitamin A deficiency causes squamous metaplasia of glandular and mucous epithelia; in chickens this appears as white pustules in the oesophageal glands, and in calves compression of the optic nerve in narrowed optic canals causes blindness with papilloedema. Vitamin D deficiency with low phosphorus causes rickets and osteomalacia. Hypervitaminosis D, and ingestion of calcinogenic plants containing vitamin D-like glycosides (Solanum malacoxylon, Cestrum diurnum, Trisetum flavescens), cause metastatic mineralisation of the aorta, endocardium, lungs and kidneys. Vitamin K antagonism by coumarins, including dicoumarol from mouldy sweet clover, causes haemorrhage into body cavities and tissues.
Copper deficiency may be primary (low copper in soil and forage) or secondary, when molybdenum and sulphur in forage form thiomolybdates that bind copper in the rumen. The ratio of copper to molybdenum in the diet is therefore interpreted alongside sulphur, and the risk threshold used differs between advisory bodies and regions. Lesions include enzootic ataxia (swayback) in lambs, achromotrichia (loss of hair and wool pigment, with 'spectacle eye' around the eyes of cattle), steely wool in sheep, osteoporosis and fractures, anaemia, and in cattle falling disease, sudden death with myocardial fibrosis, as described in Western Australia. In pigs, copper deficiency weakens elastin and can cause aortic rupture. Cobalt deficiency is vitamin B12 deficiency in ruminants, because rumen microbes need cobalt to make the vitamin; it causes wasting (pine) and in sheep ovine white liver disease, a hepatic lipidosis. Iodine deficiency causes goitre. Zinc deficiency causes parakeratosis in pigs, especially when diets are high in calcium or phytate, with thick crusted skin over the limbs and belly; zinc-responsive dermatosis occurs in Siberian huskies and Alaskan malamutes. Manganese deficiency, and choline deficiency, cause perosis in chicks. Selenium excess causes chronic selenosis (hoof and hair lesions) and acute toxicity with myocardial necrosis and pulmonary oedema.
Thiamine deficiency in ruminants is usually induced, by thiaminase from rumen bacteria or plants such as bracken fern and horsetail, and is associated with polioencephalomalacia. Horses grazing bracken fern develop thiamine deficiency with ataxia. Carnivores fed raw fish containing thiaminase develop Chastek paralysis, with bilaterally symmetrical haemorrhagic necrosis in brainstem nuclei. Riboflavin deficiency in chicks causes curled toe paralysis from swelling and demyelination of peripheral nerves. Protein-energy malnutrition and starvation cause loss of body fat, serous atrophy of fat (gelatinous, translucent fat in the coronary groove, around the kidneys and in the bone marrow), muscle wasting, hypoproteinaemic oedema and atrophy of the thymus and lymphoid tissue. Finding serous atrophy of fat at necropsy is a key piece of evidence in animal welfare and neglect cases, and the pathologist should record body condition, fat stores and marrow fat carefully, since these changes take weeks to develop and help date the neglect.
Production diseases are disorders caused by the imbalance between the output demanded of an animal (milk, growth, eggs) and what its metabolism and management can supply. They are herd problems, and the pathologist's role is to prove the mechanism in individual animals and help quantify it in the group, using necropsy, slaughter findings and metabolic profiles. Their lesions are often subtle compared with infectious disease, so a negative necropsy with the right history is itself informative. Several production diseases interlock in the transition dairy cow, the three weeks before and after calving. Around calving, the energy demand of lactation exceeds intake, so non-esterified fatty acids are mobilised from adipose tissue. The liver takes them up faster than it can oxidise them or export them as lipoprotein, so triglyceride accumulates: fatty liver (hepatic lipidosis). Severe fatty liver gives a pale, yellow, greasy, friable liver; histologically hepatocytes are distended with lipid vacuoles. Ketosis is the linked excess of ketone bodies. Milk fever (parturient paresis) is acute hypocalcaemia with few specific lesions, but a cow down for hours develops ischaemic necrosis of the thigh muscles and damage to the sciatic and obturator nerves (the downer cow). Dietary cation-anion difference (DCAD) programmes prevent milk fever by making the prepartum diet acidogenic. Subacute and acute ruminal acidosis from rapidly fermentable diets leads to rumenitis, liver abscesses, caudal vena caval thrombosis with embolic pneumonia, and laminitis, whose claw lesions include sole haemorrhage, sole ulcer and white line disease. Left displaced abomasum and hypomagnesaemic tetany are further production diseases; grass tetany leaves little but agonal haemorrhage. Feedlot cattle and lambs suffer frothy bloat, polioencephalomalacia and obstructive urolithiasis.
Fast-growing broilers need high cardiac output, and lungs that cannot expand to match cause pulmonary hypertension. The right ventricle hypertrophies and dilates, the right atrioventricular valve becomes insufficient, and right heart failure causes ascites with fluid and fibrin clots in the abdomen and a congested liver. The weight ratio of right ventricle to total ventricles is used to confirm right ventricular hypertrophy; a ratio above about 0.28 is widely used in broiler research as a sign of pulmonary hypertension. Sudden death syndrome (flip-over) kills well-grown male broilers found on their backs with few lesions. Tibial dyschondroplasia is a plug of unmineralised cartilage in the proximal tibial physis causing lameness. Caged laying hens develop cage layer fatigue (osteoporosis, fractures) and fatty liver haemorrhagic syndrome, in which a fat-filled friable liver ruptures and the bird bleeds into the abdomen. In pigs, ulceration of the pars oesophagea follows finely ground feed; porcine stress syndrome in pigs carrying the RYR1 mutation causes sudden death during handling and pale, soft, exudative meat, whereas chronically stressed animals yield dark, firm, dry meat from depleted muscle glycogen. Tail-biting, rectal prolapse and splayleg in newborn piglets are further production problems.
Learn each organ system as a small set of lesion patterns, then attach causes to each pattern: for the lung, cranioventral bronchopneumonia versus diffuse interstitial pneumonia versus random embolic lesions versus nodular granulomas. At every necropsy class, describe before you diagnose: organ, distribution, colour, size, shape, consistency and cut surface, then write a morphological diagnosis such as 'severe, acute, cranioventral, fibrinous bronchopneumonia'. Link named lesions to their mechanism, not just to a name, so that a question phrased differently still makes sense. Practise sorting oral lesions of livestock into vesicular and erosive groups, because that decision triggers disease reporting.
In practice this subject decides what you do after an animal dies. A field necropsy on a dead calf, lamb or pig tells you whether to sample brain for rabies or a spongiform encephalopathy, heart and liver for vitamin E and selenium, kidney for ethylene glycol, or placenta and fetal stomach contents for abortion work-up. It also warns you when not to open a carcass, as with suspected anthrax. You choose fixed and fresh samples organ by organ, write a clear gross description for the laboratory, and explain to the owner what the lesion means for the rest of the herd: vaccination, feed changes, trace-element supplementation or culling.
After 25 years the value is in herd-level judgement and in handling difficult cases. You recognise production pathology patterns (fatty liver and displaced abomasum clusters in a transition group, liver abscess and laminitis rates in a feedlot, ascites mortality in a broiler flock) and link them to ration, housing or genetics. You use abattoir lesion data such as pleurisy, milk spots and liver condemnations as surveillance. You give evidence in welfare, insurance and toxicology disputes, where precise lesion descriptions and body-condition findings such as serous atrophy of fat carry legal weight, and you know when to send a case to a specialist pathologist.
At research level the subject becomes pathogenesis. Open questions include host genetics of susceptibility (RYR1, SOD1, COMMD1 and similar variants), mechanisms of toxic and nutritional injury, the biology of veterinary tumours as comparative models, and prion strain behaviour. Research design depends on standardised lesion scoring (turbinate atrophy scores, pneumonia scores, fatty liver grading, right ventricle to total ventricle ratio) with blinded, repeatable methods and validated reference ranges. A senior researcher also trains the next generation of diagnostic pathologists, contributes to board examinations and helps set surveillance case definitions with national authorities and WOAH.
This manual does not yet include images, which systemic pathology depends on, and it does not cover the eye and ear, the haemopoietic system in depth (bone marrow, lymphoma classification, spleen beyond necropsy basics), laboratory animals, fish or wildlife. Avian and infectious-disease pathology are treated only where they illustrate an organ lesion; they have their own subjects. Species-specific quantitative reference values (organ weights, wall-thickness ratios, liver trace-element concentrations) vary by laboratory, breed and method and are deliberately not listed; use your diagnostic laboratory's reference ranges. Plant toxicities are named by genus only where the association is standard, and local poisonous plants differ by country.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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