Possible animal origin of human-associated, multidrug-resistant, uropathogenic Escherichia coli

Meena Ramchandani, Amee R. Manges, Chitrita DebRoy, Sherry P. Smith, James R. Johnson, Lee W. Riley

Research output: Contribution to journalArticlepeer-review

128 Scopus citations

Abstract

Background. The multistate occurrence of cases of urinary tract infection (UTI) caused by trimethoprimsulfamethoxazole (TMP-SMZ) - resistant Escherichia coli strains belonging to a single clonal group (designated as clonal group A [CgA]) in the United States has raised an intriguing hypothesis that these infections may have been spread by contaminated food products. The present study attempted to determine if CgA strains could be traced to food animals. Methods. A total of 495 animal and environmental E. coli isolates, which belonged to serogroups O11, O17, O73, and O77 and were collected between 1965 and 2002 by the Gastroenteric Disease Center at Pennsylvania State University (University Park, PA), were further subtyped by antimicrobial drug susceptibility, enterobacterial repetitive intergenic consensus (ERIC2) PCR, random amplified polymorphic DNA analysis, pulsed-field gel electrophoresis (PFGE), and virulence profile pattern. Results. Of 495 isolates, 128 (26%) had an ERIC2 PCR electrophoretic pattern indistinguishable from that of the human prototype CgA strain, and 14 CgA isolates were resistant to TMP-SMZ. Cluster analysis of PFGE patterns showed that 1 of these 14 isolates, obtained from a cow in 1988, was 94% similar to a CgA uropathogenic human-associated E. coli strain. The pattern for this isolate was included among a cluster of PFGE patterns for 5 human-associated UTI isolates that were >80% similar to each other. Conclusions. These observations suggest that drug-resistant, uropathogenic human-associated E. coli strains potentially have an animal origin. The possibility that human drug-resistant UTI could be a foodborne illness has serious public health implications.

Original languageEnglish (US)
Pages (from-to)251-257
Number of pages7
JournalClinical Infectious Diseases
Volume40
Issue number2
DOIs
StatePublished - Jan 15 2005

Bibliographical note

Funding Information:
We thank Peter Dietrich and the staff of Tang Health Center for their help, which enabled us to initiate this new study. Financial support. National Institutes of Health (grant RO3 AI053754) and US Department of Agriculture National Research Initiative Competitive Grants Program (grant 00–35212–9408). Potential conflicts of interest. All authors: no conflicts.

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