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Infection and Immunity, July 2008, p. 3281-3292, Vol. 76, No. 7
0019-9567/08/$08.00+0     doi:10.1128/IAI.01646-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

New Adhesin of Enteroaggregative Escherichia coli Related to the Afa/Dr/AAF Family

Statens Serum Institut, Department of Bacteriology, Mycology and Parasitology, Copenhagen, Denmark,¹ Center for Vaccine Development, Departments of Pediatrics and Medicine, University of Maryland School of Medicine, Baltimore, Maryland²

Received 11 December 2007/ Returned for modification 7 January 2008/ Accepted 17 April 2008

Enteroaggregative Escherichia coli (EAEC) is an important cause of diarrhea worldwide. We analyzed 17 Danish EAEC strains, isolated in the course of a case control study, for phenotypic and genotypic properties. The strains belonged to at least 14 different serotypes. Using PCR to investigate the prevalence of various putative virulence genes, we found that all but two strains were typical EAEC, as they harbored all or part of the previously described AggR regulon. The majority of the strains harbored genes encoding aggregative adherence fimbriae (AAF). The most common was AAF/I, found in nine strains; eight strains carried no known AAF-related genes. We utilized TnphoA mutagenesis to localize the aggregative adherence (AA) adhesin from one typical EAEC strain, C1010-00, which lacked a known AAF. We identified a TnphoA insertion in a hypothetical Dr-related pilin deposited in GenBank as HdaA. Four additional Danish strains harbored HdaA, and all but one displayed AA to HEp-2 cells. By using PCR primers derived from the pilins and ushers from the three AAF and Hda, we found that 16 of 17 strains exhibited evidence of one of these factors; importantly, the one negative strain also lacked the aggR gene. Cloning of the complete Hda gene cluster and expression in E. coli DH5 resulted in AA and complementation of the C1010-00 nonadherent mutant. Four related adhesins have now been found to confer AA in typical EAEC strains; our data suggest that, together, these variants may account for AA in the large majority of strains.

Published ahead of print on 28 April 2008.

Editor: A. J. Bäumler