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Distribution of Putative Adhesins in Different Seropathotypes of Shiga Toxin-Producing Escherichia coli

Division of Bacterial Pathogenesis, Department of Microbiology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Okinawa,¹ Department of Bacteriology, National Institute of Infectious Diseases, Tokyo, Japan,³ Servicio Fisiopatogenia, Instituto Nacional de Enfermedades Infecciosas, ANLIS-Dr. Carlos G. Malbrán, Buenos Aires, Argentina²

Received 6 May 2004/ Returned for modification 17 June 2004/ Accepted 25 July 2004

The distribution of eight putative adhesins that are not encoded in the locus for enterocyte effacement (LEE) in 139 Shiga toxin-producing Escherichia coli (STEC) of different serotypes was investigated by PCR. Five of the adhesins (Iha, Efa1, LPF_O157/OI-141, LPF_O157/OI-154, and LPF_O113) are encoded in regions corresponding to genomic O islands of E. coli EDL933, while the other three adhesins have been reported to be encoded in the STEC megaplasmid of various serotypes (ToxB [O157:H7], Saa [O113:H21], and Sfp [O157:NM]). STEC strains were isolated from humans (n = 54), animals (n = 52), and food (n = 33). They were classified into five seropathotypes (A through E) based on the reported occurrence of STEC serotypes in human disease, in outbreaks, and in the hemolytic-uremic syndrome (M. A. Karmali, M. Mascarenhas, S. Shen, K. Ziebell, S. Johnson, R. Reid-Smith, J. Isaac-Renton, C. Clark, K. Rahn, and J. B. Kaper, J. Clin. Microbiol. 41:4930-4940, 2003). The most prevalent adhesin was that encoded by the iha gene (91%; 127 of 139 strains), which was distributed in all seropathotypes. toxB and efa1 were present mainly in strains of seropathotypes A and B, which were LEE positive. saa was present only in strains of seropathotypes C, D, and E, which were LEE negative. Two fimbrial genes, lpfA_O157/OI-141 and lpfA_O157/OI-154, were strongly associated with seropathotype A. The fimbrial gene lpfA_O113 was present in all seropathotypes except for seropathotype A, while sfpA was not present in any of the strains studied. The distribution of STEC adhesins depends mainly on serotypes and not on the source of isolation. Seropathotype A, which is associated with severe disease and frequently is involved in outbreaks, possesses a unique adhesin profile which is not present in the other seropathotypes. The wide distribution of iha in STEC strains suggested that it could be a candidate for vaccine development.

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