Previous Article | Next Article ![]()
Journal of Clinical Microbiology, 12 1995, 3174-3178, Vol 33, No. 12
S Franke, D Harmsen, A Caprioli, D Pierard, LH Wieler and H Karch
Shiga-like toxin (SLT)-producing Escherichia coli (SLTEC) O101 has recently
been associated with hemorrhagic colitis and hemolytic-uremic syndrome in
humans. In this study, SLTEC O101 strains from humans and pigs were
characterized for clonal relatedness by nucleotide sequence analysis of
their slt genes, DNA finger-printing of genomic DNA, and determination of
virulence factors. The slt genes of five E. coli O101 strains were cloned
and sequenced. For all strains, the deduced amino acid sequences of the B
subunits were identical to those of the SLT-IIe present in the classical
SLTEC O139 strains that cause edema disease in pigs. The A subunit revealed
more than 99% homology to that of SLT-IIe. DNA fingerprinting revealed a
high degree of genetic relatedness between the human and porcine O101
isolates. None of the O101 strains investigated had virulence factors
frequently found in porcine (F107 fimbriae or heat-stable or heat-labile
enterotoxins) or human SLTEC strains (eaeA or enterohemorrhagic E. coli
hemolysin). The absence of virulence factors typical of SLT-I- and
SLT-II-producing E. Coli together with the presence of SLT-IIe, a toxin
previously seen only in porcine E. coli, suggests a new pathogenic
mechanism for E. coli O101 infection of humans. For diagnostic purposes, we
recommend the use of PCR primers and DNA probes complementary to slt-IIe to
correctly identify such strains and to further evaluate their role in human
diseases.
Copyright © 1995 by the American Society for Microbiology. All rights reserved.
Clonal relatedness of Shiga-like toxin-producing Escherichia coli O101 strains of human and porcine origin
Institut fur Hygiene und Mikrobiology, Universitat Wurzburg, Germany.
This article has been cited by other articles:
| Antimicrob. Agents Chemother. | Clin. Microbiol. Rev. |
|---|---|
| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
|---|