journal article
LitStream Collection
doi: 10.1136/vr.158.4.113pmid: 16443836
Postmortem examinations were carried out on 379 otters found dead in southern and south‐west England between 1988 and 2003. Most (81 per cent) were road casualties, but many had open bite wounds and in some cases these had proved fatal. Mortality was strongly seasonal and was positively correlated with night length. Although numbers decreased in the summer months, the prevalence of bite wounds in adults was highest in late summer. The number of otters examined annually and the prevalence of bite wounds increased markedly during the study period, and in 2003 more than half the otters of both sexes had recent bite wounds. The majority of the bites were considered to have been caused by other otters, but some were thought to have been inflicted by American mink (Mustela vison). Bites to cubs were mostly caused by domestic dogs. The overall mortality due to bite wounds was approximately 10 per cent.
Kroeze, E. J. B. Veldhuis; Zentek, J.; Edixhoven‐Bosdijk, A.; Rothuizen, J.; Ingh, T. S. G. A. M.
doi: 10.1136/vr.158.4.120pmid: 16443837
Over the course of one year, slight jaundice and ascites suggestive of chronic liver disease occurred in 17 German shepherd dogs from one breeding colony. Blood analyses, performed twice with a six‐month interval, revealed elevated serum activities of liver enzymes in 13 dogs. In addition, four young adult German shepherd dogs that showed severe ascites, slight jaundice and increased serum liver enzyme activities were referred for further evaluation. Because of their poor prognosis these four dogs were euthanased. There were no signs of photosensitivity. Postmortem examinations revealed macronodular darkened livers, which were characterised histopathologically by cirrhosis associated with aggregates of brown pigments showing a striking orange birefringence in polarised light. Ultrastructurally, the crystalline pigments were typical of protoporphyrins. High‐performance liquid chromatographic analysis of liver samples revealed very high levels of protoporphyrins (mean 9550 nmol/g wet liver, reference value 0·41 nmol/g wet liver) and low activities of ferrochelatase (mean 0·274 mmol/mg protein/hour, reference value 0·684 nmol/mg protein/hour). Twenty‐six months after the onset of the hepatopathies, the clinical condition of the 13 surviving dogs had improved and their serum liver enzyme activities were normal. The clinical histories and pedigree analyses were not in concordance with an inherited form of protoporphyria. There was no known history of exposure to toxic substances or drugs. The findings are in accordance with a transient erythropoietic protoporphyria associated with hepatic complications, presumably caused by exposure to a porphyrinogenic, ferrochelatase‐inhibitory substance of unknown origin.
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