Equine Pathology PDF

Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Clostridium piliforme - diffusely enlarged with - diarrhoea - equine herpes virus 1 Typical...

Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Clostridium piliforme - diffusely enlarged with - diarrhoea - equine herpes virus 1 Typical gross findings (Tyzzers disease) miliary grey foci - Joint lesions - Salmonella sp. Or E.coli - icterus - Infectious aetiology - Pneumonia septicaemia - Liver- hepatic enlargement - Multiple milary lesions - Meningitis - Actinobacillus equuli (sleepy foal with multiple pinpoint to miliary with small amount of disease) grey foci normal tissue between - Listeria monocytogenese - Intestine- necrotising - Multifocal to coalescing - enterocolitis with marked irregular areas of - transmission via fecal matter oedema + congestion Pyogranulomatous + - fecal matter ingested +carried by - Heart- occasional white linear necrotising hepatitis normal peristaltic activities through bands in myocardium with haemorrhage the oral pharynx, oesophagus + - Lymph nodes- Haemorrhagic stomach to small intestine + oedematous lymph nodes - Gain access to the intestinal mucosal epithelium Typical microscopic findings - Bacteria spread via the portal - liver- multifocal to coalescing circulation to the liver irregular areas of hepatic - Colonisation of hepatic necrosis, often surrounded by parenchyma haemorrhage, macrophages + - Causes multifocal necrosis neutrophils (Pyogranulomatous hepatitis) - Intestine- enterocolitis, often necrotising, described in foals + other species - bundles of bacteria within enterocytes - crypt abscesses - Heart- foci of myocardial necrosis Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Strongyles vulgaris - Segmental (Focally - cholic signs - Strongylus vulgaris (large - cranial mesentery artery extensive) Transmural - Asymptomatic unless strongyles, aberrant larval - Chronic, multifocal proliferative necrosis of the large thrombosis or vascular migrans, verminous arteritis) + necrotising, Transmural, colon damage comprises bowel - Horses ingest L3 larvae form arteritis with mural thrombosis - Chronic, severe Focally perfusion contaminated grass, hay or water + numerous larval strongyles extensive prolifersastive - Peak pasture egg counts from + necrotising, July to September Transmural arteritis with - Worms have predilection for mural thrombosis + cranial mesenteric artery + its numerous intralesional extensions due to the random- nematode larvae walk there - follow vessel curvature - most larvae won’t enter the aorta due to the perpendicular connection with the aorta - Causes cholic signs Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Coccobacilli - lung - multifocal to - lethargy - Rhodococcus equi - radiographic and/or coalescing, white to - Fever - normally inhabits soil + GIT of ultrasonographic evidence of yellow, semi-soft to firm - Cough herbivores lung abscesses nodules - Increased respiration - Airborne way of infection - - Bacterial culture and/or PCR - Mesenteric lymph nodes contaminated dust - amplification combines with - diffuse enlargement, Pyogranulomatous pneumonia cytological examination of mutlifocal ulcerative most common, single or combines transtracheal aspiration colitis finding seen in 95% of examined - Pyogranulomatous foals necrosis central core - Young foals at risk due to waning - Multifocal to coalescing passive humoural immunity + an Pyogranulomatous, underdeveloped cell mediated lymphoplasmacytic immune response- most infected pneumonia with by 2 weeks of age numerous - Failure of passive transfer of intrahistiocytic colostral immunoglobulins is a coccobacilli predisposing factor, hyper immune plasma protects against development of disease Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Actinobacillus equuli - multifocal small white - unwillingness to move - most common cause of emboli - Diagnose by isolation of milary lesions in the - Diarrhoea suppurative nephritis of foals bacteria by culture cortex of the kidney - Hypernea - Normal inhabitant of adult horse - In live foals = blood for blood - blue areas of multi-focal - Dehydration respiratory, alimentary + culture collected directly into lesions of inflammatory - Inflammation of genitourinary tracts blood culture bottles degenerate neutrophils conjunctivae - Transmission can occur in utero - In dead foals = PM kidney + - multifocal embolism or partuition, but postnatal lung biopsy suppurative necrotising infection is most common (via the - In adult horses = primary nephritis with large umbilicus) target of organ of the disease colonies of coccobacili, - Bacilli may persist as endogenous tubular degeneration + non-systematic focus + cause necrosis successive abortion in mares - bacteremia results in showers of septic emboli that frequently lodge in small capillaries, in glomeruli - Causes multiple microabscesses through the renal cortex, necrosis often obliterates the glomeruli; microabscesses in other organs such as liver, adrenal glands = joints causing polyarthritis - Failure of passive transfer, dam malnutrition, unsanitary birthing conditions + environmental stress can be predisposing factors to septicaemia + death Disease What does it look like Lesions Clinical signs Pathogenesis/causes Diagnosis Grass sickness/ - cranial cervical ganglion - weight loss - cause: clostridium botulinum type - Histology: neuronal equine dysautonomia - Check eosinophillic - Cholic C and/or type C neurotoxin degradation of intestinal + colour - Tachycardia - Affects the nerves + stops them extra intestinal ganglia- - Reddened neurones - Sweating from moving food through the minimal infection show neurological - Tucked abdomen large intestine - Cytological examination of damage - Acute clinical presentation as cranial cervical ganglion is a - Degeneration of cluster colic, tympani + drooling with relatable method for rapid post of neurones rapid progression + nearly always mortem diagnosis - Plexia can also be fatal within 7 days affected