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The pathology and pathogenesis of canine cerebral babesiosis

Dissertation (MSc)--University of Pretoria, 2000.

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Other Authors: Kriek, N.P.J.
Format: Thesis
Published: University of Pretoria 2013
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access_status_str Open Access
author2 Kriek, N.P.J.
author_browse Kriek, N.P.J.
author_facet Kriek, N.P.J.
collection Thesis
dc_rights_str_mv © 2000 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.
description Dissertation (MSc)--University of Pretoria, 2000.
format Thesis
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institution University of Pretoria (South Africa)
last_indexed 2026-06-10T12:39:54.964Z
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provenance_str_mv Harvested via OAI-PMH from UPSpace — University of Pretoria Institutional Repository
publishDate 2013
publishDateRange 2013
publishDateSort 2013
publisher University of Pretoria
publisherStr University of Pretoria
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source_str UPSpace — University of Pretoria Institutional Repository
spelling oai:repository.up.ac.za:2263/27842 The pathology and pathogenesis of canine cerebral babesiosis Kriek, N.P.J. Pardini, Anne Dale Babesiosis Dogs -- Diseases Tick-borne diseases in animals Pathology Protozoa pathogenic UCTD Dissertation (MSc)--University of Pretoria, 2000. The pathology of canine cerebral babesiosis was examined at the gross, histological and ultrastructural levels. Gross lesions could be categorised as either global or regional. Congestive brain swelling , diffuse cerebral congestion and diffuse cerebral pallor were classified as global lesions. Multifocal haemorrhage and malacia were classified as regional lesions. Oedema was inconsistently present and could be either focal or diffuse. The majority of histological changes were observed in both cerebral babesiosis and control cases. Regional lesions were unique to cerebral babesiosis and had specific histological features. Highly localised endothelial injury was the primary lesion. Early lesions were multifocal and strictly associated with the microvasculature. Intermediate lesions, with perivascular haemorrhage and neutrophil infiltration, were suggestive of reperfusion injury. Advanced lesions were locally extensive and similar in appearance to haemorrhagic infarction. It is likely that the pathogenesis of regional lesions is by a process of microvascular infarction, as venous thrombosis could not be demonstrated. Ultrastructural evidence for adherent contact between erythrocytes and capillary endothelium was demonstrated. Endothelial cell necrosis occurred early in the development of lesions, before neuronal and glial injury. It is postulated that endothelial injury is the primary event in the development of regional lesions and secondary lesions develop as a consequence of microvascular infarction. Die patologie van die serebrale vorm van bosluiskoors in honde is ondersoek. Die letsels is makroskopies, histologies en elektronmikroskopies beskryf. Letsels kon makroskopies in twee groepe verdeel word: Globale letsels en gelokaliseerde letsels. Kongestiewe brein swelling, diffuse serebrale kongestie en serebrale anemie kom voor as globale letsels in serebrale babesiose. Multifokale bloeding en nekrose kom voor as gelokaliseerde letsels. Edeem was nie konsekwent teenwoordig nie, en was algemeen of verspreid. Die meeste algemene histologiese veranderinge was in beide serebrale en kontrole gevalle teenwoordig. Gelokaliseerde letsels waarin spesifieke hisotpatologiese veranderinge voorgekom het, was kenmerkend van serebrale babesiose. Die primere letsel is hoogs gelokaliseerde beskadiging van endoteelselle. Beskadiging van die kapillere bloedvate ontstaan vroeg in die ontwikkeling van letsels. Verdere ontwikkeling van die letsel word gekenmerk deur peri-vaskulere bloeding en neutrofiel infiltrasie wat aanduidend is van reperfusie beskadiging. Volontwikkelde letsels is plaaslik-ekstensief en het die voorkoms van hemoragiese infarkte Dit is waarskynlik dat mikrovaskulere infarksie 'n rol speel in die patogenese van die letsels, aangesien veneuse trombose nie ontstaan nie. Noue kontak tussen rooibloedselle en kapillere endoteel is elektronmikroskopies bevestig. Endoteelselnekrose ontstaan voordat tekens van beskadiging geidentifiseer kan word in neurone of gliaselle. Dit blyk dat kapillere endoteelselbeskadiging die primere letsel by die ontstaan van gelokaliseerde lese Is is, en dat sekondere lesels ontwikkel as gevolg van mikrovaskulere infarksie. Paraclinical Sciences Unrestricted 2013-09-07T12:29:00Z 2010-09-13 2013-09-07T12:29:00Z 2000-04-01 2010-09-13 2010-09-09 Dissertation Pardini AD, 2000, The pathology and pathogenesis of canine cerebral babesiosis, MSc dissertation, University of Pretoria, Pretoria, viewed yymmdd < http://hdl.handle.net/2263/27842 > H1058/th http://hdl.handle.net/2263/27842 http://upetd.up.ac.za/thesis/available/etd-09092010-173128/ © 2000 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. application/pdf application/pdf application/pdf application/pdf University of Pretoria
spellingShingle Babesiosis
Dogs -- Diseases
Tick-borne diseases in animals
Pathology
Protozoa pathogenic
UCTD
The pathology and pathogenesis of canine cerebral babesiosis
title The pathology and pathogenesis of canine cerebral babesiosis
title_full The pathology and pathogenesis of canine cerebral babesiosis
title_fullStr The pathology and pathogenesis of canine cerebral babesiosis
title_full_unstemmed The pathology and pathogenesis of canine cerebral babesiosis
title_short The pathology and pathogenesis of canine cerebral babesiosis
title_sort pathology and pathogenesis of canine cerebral babesiosis
topic Babesiosis
Dogs -- Diseases
Tick-borne diseases in animals
Pathology
Protozoa pathogenic
UCTD
url http://hdl.handle.net/2263/27842
http://upetd.up.ac.za/thesis/available/etd-09092010-173128/