Leptospirosis is an infectious disease, caused by species of the Leptospiracae family, which has a worldwide distribution. Multiple species have been found to be affected by leptospirosis with many others considered to act as reservoirs for the bacteria; in the case of Leptospira icterohaemorrhagiae an important vector is the black rat (Rattus rattus).1 Although the common hippopotamus (Hippopotamus amphibus)2,3 has been recorded to have antibody titres to leptospires, little has been documented with regards to the pygmy hippopotamus’ (Choeropsis liberiensis) relationship with Leptospira titres nor clinical leptospirosis. This case report details a fatal leptospirosis infection attributed to Leptospira icterohemorrhagiae in a male, 10-year-old, 271 kg, pygmy hippopotamus.
Clinical signs started with non-specific lethargy and anorexia that was non-responsive to symptomatic therapy with Flunixin (Finadyne solution, Schering-Plough, 50 mg/ml) 350 mg IM and oxytetracycline (Duphacycline LA, Fort Dodge, 200 mg/ml) 6 g IM given via pole syringe. Examination under general anesthesia was undertaken. Induction was induced with medetomidine (medetomidine, Kyron Laboratories, 40 mg/ml) 25 mg and ketamine (ketamine, Kyron Laboratories, 200 mg/ml) 300 mg IM in the left neck using a carbon dioxide powered rifle (Daninject JM Special Rifle, Daninject). He was intubated with a 16 mm endotracheal tube and maintained with isoflurane, oxygen, and a small animal circle (CycloFlo, Burtons). Examination was unremarkable. Treatment consisted of oxytetracycline LA 5 g IM, flunixin 250 mg IV, lactated Ringer’s solution (Aqupharm 11, Animalcare) 3.5 litres IV via 20 g medial saphenous cannula, liquid paraffin 1 litre via stomach tube. The working differential diagnoses consisted of ileus, colic, systemic illness, neoplasia, or other. Biochemistry was indicative of early renal and hepatic failure. Serum was sent for L. icterohemorrhagiae antibody titres and the animal started on lactated Ringer’s solution 3.5 litres IV, procaine penicillin and dihydrostreptomycin sulphate (Penstrep injection, Norbrook, 200 mg/ml, 250 mg/ml respectively) 10 ml, and flunixin 250 mg IV. Leptospirosis titres were returned and were strongly positive for L. icterohemorrhagiae. By day eight of infection and little change in clinical signs the animal became jaundiced. Therapy was continued with two more repeat anesthetics for assessment, intravenous fluid therapy, repeat biochemistry, and CBC, which showed deterioration in renal and hepatic parameters. On day 13 the animal was found in distress and due to poor prognosis euthanasia was opted for on welfare grounds. Anesthesia was induced and he was euthanatized with 50 ml cinchocaine HCL and secobarbital sodium IV (Somulose, Arnolds, 25 mg/ml, 400 mg/ml respectively).
The oral mucous membranes, perineum, and skin were a bright yellow color. This continued throughout the postmortem with articular surfaces, larynx, trachea, mucous and peritoneal membranes, and visceral surfaces bright yellow in color. All body systems were grossly normal with little pathology to be noted. There were no transudates, and the lymph nodes were not enlarged. On the heart there were pericardial hemorrhages, but these were not organized and were thought to be associated with the method of euthanasia; the lungs had evidence of hypostatic congestion but again, little gross pathology. The liver was extremely friable but grossly normal, and the gall bladder had bile in but was not distended. The stomach was unusual in that it was full with grass and oats, yet the hippo had not been seen to eat for two weeks and had not been offered oats for that same period; the contents smelt fresh and not sour. The renal system was grossly normal with no evidence of polycystic kidney disease bilaterally; the cortex was slightly yellow in color and there were some streaks of hemorrhage in the medulla. The adrenals had a thick cortex and a thin medulla. The larynx had long vocal folds and the trachea was 19 mm in diameter.
The combination of histologic findings, particularly in the light of the positive titre for L. icterohemorrhagiae, was consistent with that of leptospirosis, consisting particularly of lesions in kidney, liver, and pancreas. There was significant non-suppurative tubulointerstitial nephritis with ongoing neutrophilic tubular inflammation and necrosis, and active epithelial regeneration that included occasional atypical multinucleated cells. There was also widespread precipitation of bile pigments in tubules consistent with the jaundice. In the liver, the changes were more subtle, but there was evidence of marked intrahepatic cholestasis, and hepatocyte cords were jumbled with loss of clear lobular architecture in some cases, suggesting earlier injury. Inflammation was not prominent, but there was widespread vacuolar change in hepatocytes. There was also evidence of an earlier episode of pancreatitis, with minimal active inflammation but multifocal interstitial fibrosis and replacement of acinar tissue with immature ductules. Pancreatitis has been noted to be a feature of leptospirosis in some species, including dogs and humans. Extramedullary hematopoiesis in the liver was likely to be a systemic reaction to inflammation and anemia.
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