Feline babesiosis is caused by the small intra-erythrocytic haemoprotozoan parasite, Babesia felis. Only in South Africa does it cause a significant clinical disease among domestic cats. A study was undertaken to further describe signalment and clinico-pathological changes and to identify concurrent infections. Fifty-six cats with naturally occurring B. felis infection, presented to private veterinarians for examination and treatment, were studied. An age predisposition seemed to be present, as most affected cats were young adults of less than three years of age. Although no breed or sex predisposition was evident, Siamese cats seemed to be over-represented amongst purebred cats. Typical clinical signs included anorexia, listlessness and anaemia. Less common signs included icterus, weakness, weight loss, constipation and pica. Feline babesiosis was diagnosed by identification of parasites on stained, thin blood smears. Parasitaemias were variable and ranged between very low (0.3%) and extremely high (42.3%). A strong correlation existed between central and peripheral parasitaemias, indicating that sequestration does not occur. Macrocytic, hypochromic, regenerative anaemia was the most consistent haematological finding; this became quite severe in advanced cases of disease. The anaemia was further classified as haemolytic, presumably resulting from both intravascular and extravascular erythrocyte destruction. Almost half the cats (43%) were not anaemic. No characteristic changes were seen in total or differential leukocyte counts; when abnormal values were present they were often accompanied by concurrent illness or infection. Thrombocyte counts were variable and thrombocytopaenia was an inconsistent finding. In-saline agglutination tests were positive in a number of cases, indicating that secondary immune-mediated haemolytic anaemia could also be a feature of this disease. The most remarkable clinico-pathological changes were elevation of hepatic cytosol enzyme activities and total bilirubin concentrations. Serum alanine transaminase was significantly elevated in the majority of cases, whereas alkaline phosphatase and gamma glutamyltransferase were generally within normal limits. This provides evidence of primary hepatocellular injury or inflammation in feline babesiosis. The hyperbilirubinaemia was most likely a result of haemolysis, but secondary hepatocellular injury was probably an additional contributing factor. No characteristic changes in renal parameters were observed and serum urea and creatinine levels were mostly within normal limits, indicating that gross renal damage was not a consistent feature of the disease. No characteristic pattern of changes in serum electrolytes (sodium and potassium) was seen, although a variety of electrolyte disturbances occurred in a number of cases. Serum protein values were mostly normal, but elevations were seen in some cases. Hyperalbuminaemia was considered indicative of patient dehydration. Polyclonal gammopathies were observed in all cats with hyperglobulinaemia and were ascribed to a combination of acute- and chronic-phase proteins produced in response to the Babesia antigens. Concurrent infections with Haemobartonella felis, feline leukemia virus and/or feline immunodeficiency virus were identified in a number of cats in this study and seemed to have profound effects on response to treatment and outcome of the disease. / Dissertation (MMedVet (Med))--University of Pretoria, 2001. / Companion Animal Clinical Studies / unrestricted
| Identifer | oai:union.ndltd.org:netd.ac.za/oai:union.ndltd.org:up/oai:repository.up.ac.za:2263/23372 |
| Date | 23 March 2005 |
| Creators | Schoeman, Tanya |
| Contributors | Lobetti, R.G. (Remo Giuseppe), upetd@ais.up.ac.za |
| Publisher | University of Pretoria |
| Source Sets | South African National ETD Portal |
| Detected Language | English |
| Type | Dissertation |
| Rights | © 2001, University of Pretoria. All rights reserved. The copyright in this work vests in the University of Pretoria. No part of this work may be reproduced or transmitted in any form or by any means, without the prior written permission of the University of Pretoria. |
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