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. 1967 Feb;93(2):531–537. doi: 10.1128/jb.93.2.531-537.1967

Mechanisms of Pathogenesis in Listeria monocytogenes Infection II. Characterization of Listeriosis in the CD-1 Mouse and Survey of Biochemical Lesions

Martin S Wilder a,1, C P Sword a
PMCID: PMC276472  PMID: 4960178

Abstract

Several physiological and biochemical changes which occur in CD-1 pathogen-free mice during the course of infection with Listeria monocytogenes strain A4413 have been examined. Mice injected with 104 to 106 organisms by the intraperitoneal route displayed a significant depression in weight gain. In contrast, at 24 hr after infection an increment in total liver weight averaging 0.1 g was observed. The ratios of liver to body weight increased throughout the observation period. As the severity of the infection increased, food intake, as well as total liver protein and nitrogen, showed a corresponding decrease, with the diminution being most evident immediately prior to the death of the animals. Blood urea nitrogen remained relatively constant for 24 hr and then increased continuously as the infection progressed to the acute stage. Total liver lipid increased until the death of the animals. At 72 hr postinfection, a significant decrease in oxidative phosphorylation was observed. Xanthine dehydrogenase activity increased, with maximal values obtained 72 hr after infection. Uric acid levels remained constant for 24 hr, diminished at 48 hr, and then increased until the death of the animals. After 24 hr, uricase activity showed a slight increase. This activity returned to within normal ranges at 48 hr and decreased as the infection progressed to the acute stage at 72 hr. The results support the hypothesis that at least a part of the cause of death is a derangement in hepatic purine and carbohydrate metabolism. The data are also consistent with the possibility of changes in iron transport in the infected mice.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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