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 virulenceassociated 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. Dogs spontaneously develop urinary tract infection (UTI)due to strains of Escherichia coli similar to those that cause UTI in humans (4, 6, 7, 15, 18, 25, 30, 42, 45-47, 50, 51). In both host groups, the urinary pathogens typically derive from specific clonal groups within virulence-associated E. coli phylogenetic group B2, express one of several UTI-associated O antigens, and possess specialized virulence-associated factors (VFs) that directly contribute to, or are markers for, an enhanced ability to overcome host defenses and cause extraintestinal disease (15,18,25,41). In both dogs (18, 30) and humans (8,40,49) at the time of a UTI episode, the infecting urinary strain is often the host's predominant rectal E. coli strain, consistent with the fecal reservoir as the proximate source from which pathogens enter the urinary tract. Even healthy dogs are frequently intestinally colonized with uropathogenic E. coli and shed these organisms in their feces (23,50,51).These observations are potentially relevant to human health because they suggest that dogs may pose an infectious threat to humans by providing a reservoir of "human" uropathogenic E. coli for acquisition by susceptible human hosts (15,18,23,25,30,45). In addition, they suggest that the pathogenesis of UTI is similar in dogs and humans, so that dogs might serve as a pathogenetically relevant model system for observational or experimental studies of UTI pathogenesis (15,25).Accordingly, in the present study we took advantage of spontaneously occurring UTI in dogs to address several questions regarding the pathogenesis of UTI in humans. In 37 dogs with UTI, which served as their own controls, we compared concurre...

P fimbriae of extraintestinal pathogenic Escherichia coli mediate digalactoside-specific adherence via the tip adhesin molecule PapG, which occurs in three known variants (I to III), which are encoded by the corresponding three alleles of papG. In the present study, newly discovered variants of papG allele I and the respective wild-type source strains were characterized. One of the new papG allele I variants conferred a unique agglutination phenotype that combined the phenotypes associated with papG alleles I, II, and III. Comparative hydrophilicity analysis of predicted PapG peptides revealed regions that might explain the observed phenotypic similarities and differences between the PapG variants. The new papG allele I variants occurred either as the sole papG allele or together with both papG alleles II and III, rather than with only papG allele III, as in archetypal strains J96 and CP9. They also occurred in the absence of the usual F13 papA allele. One of the new papG allele I variants occurred in a serogroup O6 strain that, according to random amplified polymorphic DNA analysis, was phylogenetically distant from the "J96-like" clonal group of E. coli O4:H5, which includes all previously identified examples of papG allele I. Cluster analysis of nucleotide and predicted peptide sequences suggested that papG allele I represents the earliest evolutionary branch from a common papG ancestor. These results demonstrate unexpected diversity within papG allele I and, together with previous findings, suggest that the J96-like clonal group of E. coli O4:H5 may represent the original source of papG within the species.

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