Infection and Immunity, July 2001, p. 4366-4372, Vol. 69, No. 7
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.7.4366-4372.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Department of Pharmaceutical Sciences1 and Departments of Ophthalmology and Microbiology and Immunology,4 University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190, and Department of Veterans Affairs Medical Center5 and Department of Pathology,3 University of Maryland School of Medicine,2 Baltimore, Maryland 21201
Received 15 February 2001/Returned for modification 12 April 2001/Accepted 19 April 2001
Enterococcus faecalis bacteria isolated from patients with bacteremia, endocarditis, and urinary tract infections more frequently express the surface protein Esp than do fecal isolates. To assess the role of Esp in colonization and persistence of E. faecalis in an animal model of ascending urinary tract infection, we compared an Esp+ strain of E. faecalis to its isogenic Esp-deficient mutant. Groups of CBA/J mice were challenged transurethrally with 108 CFU of either the parent or mutant strain, and bacteria in the urine, bladder, and kidneys were enumerated 5 days postinfection. Significantly higher numbers of bacteria were recovered from the bladder and urine of mice challenged with the parent strain than from the bladder and urine of mice challenged with the mutant. Colonization of the kidney, however, was not significantly different between the parent and mutant strains. Histopathological evaluations of kidney and bladder tissue done at 5 days postinfection did not show marked histopathological changes consistent with inflammation, mucosal hyperplasia, or apoptosis, and there was no observable difference between the mice challenged with the parent and those challenged with the mutant. We conclude that, while Esp does not influence histopathological changes associated with acute urinary tract infections, it contributes to colonization and persistence of E. faecalis at this site.
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