The value of biomedical research training for veterinary anatomic and clinical pathologists.

Veterinary pathologists traditionally have been actively engaged in research as principal investigators and as collaborators. Pathologists frequently obtain advanced training in research; however, it appears that in the last 10 years there has been a reversal of a previous trend toward increasing numbers of pathologists obtaining PhD degrees. This has arisen despite an established shortage of veterinarians engaged in research. This article evaluates the benefits of research training for individual pathologists, including a wide spectrum of professional opportunities and additional skill development beyond that usually provided by diagnostic pathology training alone. Various training models are discussed, including combined and sequential diagnostic residency and research degree training as well as the nondegree research fellowship programs more commonly pursued in human medicine. Best-practice recommendations for program infrastructure, mentorship, time management, and a team approach to research and research training are advocated to facilitate the development of successful programs and to encourage a continued emphasis on integrated training for pathologists as both clinical diagnosticians and experimentalists. This article is intended to help prospective and active pathology trainees, their mentors, and educational administrators optimize opportunities to ensure the future vitality of veterinary pathologists, and their contributions, in basic and applied research.

Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis).

Pituitary adenomas were identified in 14 of 491 (2.9%) cynomolgus macaques evaluated from 1994 to 2004. Cases included male (8) and female (6) cynomolgus macaques ranging from 18 to 32 years of age. Seven of the pituitary adenomas caused gross enlargement of the pituitary gland that was visible on postmortem examination, whereas the remaining 7 were multifocal microadenomas identified on histologic examination. A total of 35 adenomas were identified in the 14 macaques, 6 of which were being treated for diabetes mellitus. Mean (+/- SD) pituitary weight was 0.31 +/- 0.42 g, compared with 0.07 +/- 0.02 g for 430 historical control animals (P < 0.0001). Immunohistochemical staining for follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone, thyroid-stimulating hormone, and adrenocorticotropic hormone was applied to pituitary tissue from all cases. Immunostaining revealed 22 of 35 (62.9%) lactotroph adenomas, 5 of 35 (14.3%) plurihormonal cell adenomas, 3 of 35 (8.6%) corticotroph adenomas, 2 of 35 (5.7%) null cell adenomas, 1 of 35 (2.9%) somatotroph adenomas, 1 of 35 (2.9%) mixed corticotroph-somatotroph adenomas, 1 of 35 (2.9%) mixed lactotroph-corticotroph adenomas, 0 of 35 gonadotroph adenomas, and 0 of 35 thyrotroph adenomas. This study represents the first extensive retrospective case series performed to evaluate the histologic and immunohistochemical characteristics of pituitary adenomas in cynomolgus macaques. Our findings indicated that macaque pituitary adenomas frequently had mixed histologic appearance and hormone expression, and that, similar to human pituitary adenomas, prolactin-secreting neoplasms were the most prevalent type.

Rinderpest epidemic in wild ruminants in Kenya 1993-97.

A severe epidemic of rinderpest, affecting mainly wild ruminants, occurred between 1993 and 1997 in East Africa. Buffalo (Syncerus caffer), eland (Taurotragus oryx) and lesser kudu (Tragelaphus imberbis) were highly susceptible. The histopathological changes, notably individual epithelial cell necrosis with syncytia formation, were consistent with an infection with an epitheliotrophic virus. Serology, the polymerase chain reaction, and virus isolation confirmed the diagnosis and provided epidemiological information. The virus was related to a strain which was prevalent in Kenya in the 1960s, of a second lineage (II), and distinct from isolations of rinderpest virus in the region since 1986. The source of the virus was presumed to be infected cattle from the Eastern region of Kenya and Somalia. The pathogenicity of the virus varied during the epidemic. The mortality in buffalo populations was estimated to be up to 80 per cent, and population data suggested that the virus had an adverse effect on a wide range of species. The virus caused only a mild disease in cattle, with minimal mortality. The results confirmed the importance of wildlife as sentinels of the disease, but although wildlife were important in the spread of the virus, they did not appear to act as reservoirs of infection.

Mycobacterium avium-related epizootic in free-ranging lesser flamingos in Kenya.

An epizootic in free-ranging lesser flamingos (Phoeniconaias minor) in Kenya resulted in more than 18,500 deaths from August through mid-November 1993. Disease was concentrated along the shores of Rift Valley Lakes Bogoria and Nakuru (Kenya) and did not involve any of the other avian or mammalian species frequenting the lakes. Coincidental to the outbreak was a bloom of algae on Lake Bogoria, toxins from which were first suspected to be causative. Discrete necrotic and granulomatous lesions were often noted in spleen and liver, and Mycobacterium avium serovar I was isolated from both organs. Escherichia coli and Pseudomonas aeruginosa also were often recovered in pure culture from liver. Gross and histopathological evaluation of the cases disclosed signs of acute sepsis and also chronic, potentially life-threatening lesions of mycobacteriosis, primarily involving the spleen and liver. Lesions typical for algae toxicosis were not seen in any birds. Deaths were attributed to septicemia complicated in those affected, by mycobacteriosis.

Myocardial Purkinje degeneration and necrosis with fibrosis in free-ranging black rhinoceroses (Diceros bicornis) in Zimbabwe.

Degeneration and necrosis of Purkinje fibers with fibrosis around Purkinje fibers were found in the hearts of three adult black rhinoceroses (Diceros bicornis) in Zimbabwe in 1989 and 1990, among 38 animals examined from 1988 to 1994. Causes of death were not apparently related to these changes, nor was there evidence of heart failure. The etiology of these changes is unknown.

Detection of Cowdria ruminantium in blood and bone marrow samples from clinically normal, free-ranging Zimbabwean wild ungulates.

Cowdria ruminantium causes severe, often fatal disease in domestic ruminants, whereas wildlife species usually are not affected. Blood and bone marrow samples from healthy, free-ranging Zimbabwean ungulates were taken during translocation from areas harboring Amblyomma ticks and tested for the presence of C. ruminantium, using a PCR assay based on the C. ruminantium map1 gene. Positive reactions were obtained in tsessebe (Damaliscus lunatus), waterbuck (Kobus ellipsiprymnus), and impala (Aepyceros melampus). Wildlife species may therefore be a reservoir for C. ruminantium thus contributing to the spread of cowdriosis.

Flaccid trunk paralysis in free-ranging elephants (Loxodonta africana) in Zimbabwe.

An epizootic of flaccid trunk paralysis began in free-ranging Zimbabwean elephants (Loxodonta africana) on the southern shore of Lake Kariba in 1989. It involved a selective neuropathy of peripheral nerves supplying the trunk, with axon and myelin degeneration, muscle atrophy, compensatory hypertrophy, and fine endomyseal fibrosis, without inflammatory changes.

Variation in clinical disease and species susceptibility to psittacine beak and feather disease in Zimbabwean lovebirds.

While psittacine beak and feather disease has caused 100% mortality in captive flocks of 2 species of native Zimbabwean lovebirds (Agapornis nigrigensis and A. lilianae), other lovebird species in close contact with the sick birds have been only transiently affected or not at all. The clinical course of the disease in affected lovebirds may differ from that reported elsewhere, with recovery in some cases. These differences, along with ultrastructural differences may suggest a different virus or different strain of virus underlying disease in Zimbabwe.

An outbreak of haemorrhagic septicaemia (septicaemic pasteurellosis) in cattle in Zimbabwe.

An outbreak of haemorrhagic septicaemia caused by Pasteurella multocida in beef cattle in Zimbabwe grazing effluent-irrigated pastures, is described. The outbreak occurred during the wet summer months and predisposing stress factors included excessive rainfall and unusual cold weather during the preceding month. History, clinical features and post-mortem findings were consistent with reports of the disease from other countries, except that meningitis was also a constant feature. Morbidity approached 77% and mortality 5 per cent. Prophylactic treatment and vaccination with a killed bacterin together with a return of warmer and drier weather were probably important in halting the outbreak.

Concurrent systemic cryptococcosis and haemangiosarcoma in a dog.

A young dog with progressive neurological signs was humanely killed by the injection of barbiturate for postmortem examination. Lesions in the nose, lung, pancreas, lymph nodes, kidneys and the meninges were heavily infiltrated with Cryptococcus neoformans. In addition, haemangiosarcoma was detected in the right atrium. The finding of systemic mycosis and neoplasia together in a young dog suggests an immunosuppressed state.