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Infection and Immunity, March 2003, p. 1434-1441, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1434-1441.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Intravenous Mouse Infection Model for Studying the Pathology of Enterococcus faecalis Infections

Claudia Gentry-Weeks,1* Monica Estay,1 Cindy Loui,1 and Dale Baker1,2

Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado 80523,1 Genentech, Inc., South San Francisco, California 94080-49902

Received 1 August 2002/ Returned for modification 3 September 2002/ Accepted 2 December 2002

An intravenous mouse infection model was used to compare the virulence of Enterococcus faecalis strains, to study bacterial localization and organ histopathology, and to examine the effects of Nramp1 and gamma interferon (IFN-{gamma}) on the course of infection. Infection of BALB/c mice with 5 x 108 CFU of E. faecalis JH2-2, MGH-2, 418, DS16C2, or OG1X revealed the following virulence ranking (from highest to lowest): MGH-2, 418, DS16C2, JH2-2, and OG1X. Discernible differences in the number of MGH-2 and JH2-2 bacteria were observed at 7 days (168 h) in the blood (P = 0.037), at 72 h in the liver (P = 0.002), and at 8 h in the spleen (P = 0.036). At these time points, the number of MGH-2 bacteria was higher in the blood and liver while the number of JH2-2 bacteria was higher in the spleen. At 72 h, livers from MGH-2-infected mice had higher numbers of coalescing aggregates of leukocytes and a greater degree of caseous necrosis than those from JH2-2-infected mice. These results indicate a correlation between the virulence of the E. faecalis strain, the number of bacteria in the liver, and the degree of histopathology of the liver at 72 h postinfection. IFN-{gamma} was important in E. faecalis infection, since IFN-{gamma} gene knockout mice had reduced mortality and massive coagulative necrosis was observed in wild-type mice. The contribution of Nramp1 was unclear, since Nramp1-/- mice and the respective control mice were innately resistant to E. faecalis. The mortality of mice in this model is probably due to induction of cytokine release and massive coagulative necrosis.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Pathology, Colorado State University, campus mail 1682, Fort Collins, CO 80523. Phone: (970) 491-5411. Fax: (970) 491-1815. E-mail: claudia.gentry-weeks{at}colostate.edu.

Editor: S. H. E. Kaufmann

Infection and Immunity, March 2003, p. 1434-1441, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1434-1441.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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