Histopathological changes and oxidative stress associated with Fascioliasis in bovines.
Trop Anim Health Prod
; 56(2): 48, 2024 Jan 18.
Article
em En
| MEDLINE
| ID: mdl-38236357
ABSTRACT
Fascioliasis, a prevalent disease in livestock globally, is primarily caused by the trematode parasites Fasciola hepatica and Fasciola gigantica. This parasitic infection leads to significant economic repercussions. In this study, our objective was to gain insight into the pathophysiological consequences of Fascioliasis in cattle through the evaluation of metabolic, oxidative stress, and histological parameters. A thorough investigation was carried out on the liver of 197 bovines after their slaughter, which unveiled the occurrence of Fascioliasis, with a prevalence rate of 13.2% observed. The bovine that were infected exhibited notable increase in serum transaminases (ALT, AST, and ALP) and malondialdehyde (MDA) and catalase (CAT) while the decrease in glutathione (GSH) and superoxide dismutase (SOD) levels. The lipid profile analysis of infected cattle revealed alterations in the cholesterol and triglyceride levels. Moreover, the histopathological examination revealed a range of hepatic lesions associated with Fascioliasis, including necrosis, inflammation, fibrosis, and proliferative alterations. The bile ducts also displayed distinct pathological changes, including hyperplasia, thickening, and edema, and harbored various developmental stages of Fasciola spp. highlighting the parasitic infestation's effects on the biliary system. These results highlight the serious effects of Fascioliasis on lipid metabolism and the oxidative damage that is induced in the livers of cattle. Thus, Fasciola infestation in bovine causes alteration in biochemical and antioxidant activities, which are considered as important factors in the diagnosis of Fascioliasis.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Doenças dos Bovinos
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Fasciola
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Fasciola hepatica
/
Fasciolíase
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article