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Histopathology of Listeria monocytogenes after oral feeding to mice
Abstract:
Ingestion by mice of Listeria monocytogenes in drinking water induced micro-abscesses of the liver and ulcerative enteritis. In pregnant mice, these lesions were larger and more extensive than in nonpregnant female and male mice. Pregnancy is interrupted by a purulent panmetritis and necrotizing placentitis. The early microabscess is unique in that it consists of monocytic cells with bizarre-shaped nuclei. The experimentally induced pathological changes in livers and intestines of mice used in this study are similar to those observed in listeric neonatal septicemia of human infants.
Insights
Listeria monocytogenes infection in mice caused liver micro-abscesses and intestinal lesions. Pregnant mice experienced more severe pathology, including uterine and placental inflammation, mirroring human infant septicemia.
Area of Science:
- Microbiology
- Pathology
- Immunology
Background:
- Listeria monocytogenes is a foodborne pathogen causing listeriosis.
- Neonatal listeriosis can lead to severe illness in human infants.
Purpose of the Study:
- To investigate the pathological effects of Listeria monocytogenes ingestion in mice.
- To compare lesion severity in pregnant versus non-pregnant mice.
- To characterize the cellular composition of early microabscesses.
Main Methods:
- Oral administration of Listeria monocytogenes to mice.
- Histopathological examination of liver, intestine, uterus, and placenta.
- Comparison of lesion severity between different groups of mice.
Main Results:
- Ingestion induced liver micro-abscesses and ulcerative enteritis.
- Pregnant mice exhibited larger and more extensive lesions.
- Pregnancy-specific pathology included purulent panmetritis and necrotizing placentitis.
- Early microabscesses contained unique monocytic cells with bizarre nuclei.
Conclusions:
- Experimentally induced murine listeriosis shares pathological similarities with human neonatal septicemia.
- Pregnancy exacerbates Listeria monocytogenes-induced pathology in mice.