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Pathogenesis of liver lesions in mice following a primary infection with Ascaris suum
Abstract:
The development of liver lesions in mice infected with Ascaris suum is described and compared to the lesions in pigs. The findings suggest that liver necroses in mice are initially periacinar (centrilobular), caused by anoxia resulting from a vascular obstruction by the A. suum larvae located in the sinusoids; and that the lesions in pigs following a primary infection have a different pathogenesis. It is concluded that mice are unsuitable models for studying the pathogenesis of A. suum-induced liver lesions in pigs.
Insights
Mice infected with Ascaris suum develop liver lesions different from pigs. The study concludes mice are unsuitable models for studying pig liver diseases caused by this parasite.
Area of Science:
- Veterinary Pathology
- Parasitology
- Comparative Medicine
Background:
- Ascaris suum is a significant helminth parasite affecting pigs.
- Understanding parasite-induced pathology is crucial for animal health.
- Rodent models are often used to study parasitic infections, but their suitability requires validation.
Purpose of the Study:
- To describe and compare liver lesions in mice infected with Ascaris suum.
- To evaluate the suitability of mice as a model for studying Ascaris suum-induced liver lesions in pigs.
Main Methods:
- Histopathological examination of liver tissues from infected mice.
- Comparison of observed lesions with known pathology in pigs.
Main Results:
- Liver necrosis in mice was primarily periacinar (centrilobular).
- Lesions in mice were attributed to anoxia from larval vascular obstruction.
- Pathogenesis of lesions in pigs following primary infection differs significantly.
Conclusions:
- Mice develop distinct liver lesions compared to pigs after Ascaris suum infection.
- Mice are not an appropriate model for studying the pathogenesis of Ascaris suum-induced liver lesions in pigs.