Abstract

The urinary tract is among the most common sites of both community-acquired and nosocomial infections, and Escherichia coli is the most common etiologic agent of these infections. Infections by uropathogenic E. coli (UPEC) can range from asymptomatic bacteriuria to cystitis and acute pyelonephritis to bacteremia and sepsis [1]. There is ample evidence that UPEC differs from most E. coli strains isolated from the feces of healthy individuals. Numerous epidemiologic studies have suggested a role for P and other fimbriae, afimbrial adhesins, hemolysin, aerobactin, capsule, and cytotoxic necrotizing factor in the pathogenesis of urinary tract infections (UTIs) [2]. However, many of these factors have not been proven to be involved in disease. UPEC and other pathogenic E. coli harbor pathogenicity islands (PAIs) and possess genomes that are 20% larger than E. coli K-12 and other nonpathogenic fecal strains [3], suggesting the presence of many pathogenesis genes that have yet to be discovered. In the present study, we employed a genomic approach to discover genes that are present in a very potent UPEC strain but absent from an E. coli laboratory strain.

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