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Journal of Clinical Microbiology, January 2003, p. 337-345, Vol. 41, No. 1
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.1.337-345.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Identification of Urovirulence Traits in Escherichia coli by Comparison of Urinary and Rectal E. coli Isolates from Dogs with Urinary Tract Infection

James R. Johnson,1,2* Nicholas Kaster,1,2 Michael A. Kuskowski,3,4 and Gerald V. Ling5

Medical Service,1 Geriatric Research, Education, and Clinical Center, VA Medical Center,3 Departments of Medicine,2 Psychiatry, University of Minnesota, Minneapolis, Minnesota,4 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, California5

Received 8 July 2002/ Returned for modification 18 August 2002/ Accepted 20 September 2002

Spontaneously occurring urinary tract infection (UTI) in dogs was exploited as an experiment of nature to gain insights into UTI pathogenesis in humans. Concurrent urinary and rectal Escherichia coli isolates from 37 dogs with UTI were compared with respect to phylogenetic background, O antigens, and extended virulence genotype. In 54% of the UTI episodes, the dog's urinary and rectal isolates represented the same strain. Urinary isolates differed dramatically from rectal-only isolates in that they derived predominantly from E. coli phylogenetic group B2, expressed typical (human) UTI-associated O antigens, and possessed many virulence-associated genes, most notably pap elements (P fimbriae), papG (adhesin) allele III, sfa/foc and sfaS (S fimbriae), hly (hemolysin), fyuA (yersiniabactin), iroN (siderophore), and ompT (outer membrane protease T). The 20 urinary isolates that corresponded with the host's predominant rectal strain were no less virulent according to the markers analyzed than were the 17 urinary isolates that differed from the host's predominant rectal strain. These findings suggest that UTI pathogenesis is similar in dogs and humans, provide added support for the special-pathogenicity over the prevalence hypothesis of UTI pathogenesis, and identify numerous specific virulence-associated factors as significant correlates of urovirulence.

* Corresponding author. Mailing address: Infectious Diseases (111F), VA Medical Center, One Veterans Drive, Minneapolis, MN 55417. Phone: (612) 725-2000, ext. 4185. Fax: (612) 727-5995. E-mail: johns007{at}umn.edu.

Journal of Clinical Microbiology, January 2003, p. 337-345, Vol. 41, No. 1
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.1.337-345.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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