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Epidemiology and properties of heat-stable enterotoxin-producing Escherichia coli serotype O169[ratio ]H41

Published online by Cambridge University Press:  01 August 1998

Y. NISHIKAWA
Affiliation:
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tojo-cho, Tennoji, Osaka 543-0026, Japan
A. HELANDER
Affiliation:
Department of Medical Microbiology and Immunology, Göteborg University, Sweden
J. OGASAWARA
Affiliation:
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tojo-cho, Tennoji, Osaka 543-0026, Japan
N. P. MOYER
Affiliation:
Hygienic Laboratory, The University of Iowa, Iowa City, Iowa, 52242–5002, USA
M. HANAOKA
Affiliation:
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tojo-cho, Tennoji, Osaka 543-0026, Japan
A. HASE
Affiliation:
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tojo-cho, Tennoji, Osaka 543-0026, Japan
A. YASUKAWA
Affiliation:
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tojo-cho, Tennoji, Osaka 543-0026, Japan
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Abstract

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Enterotoxigenic Escherichia coli (ETEC) serotype O169[ratio ]H41 organisms have become the most prevalent ETEC in Japan since the first outbreak in 1991. It was assumed that the outbreaks were due to clonal spread of this new ETEC serotype. The relationship of 32 strains isolated from 6 outbreaks were examined for biotype, antibiotic susceptibility, enterotoxigenicity, protein banding pattern, lipopolysaccharide banding pattern, plasmid analysis, and ribotyping. Further, the strains were examined by haemagglutination, surface hydrophobicity, and the ability to adhere to HEp-2 cells. The present study suggests that the outbreaks were caused by multiple clones of STp-producing O169[ratio ]H41 since they showed differences in ribotype and outer membrane protein banding patterns. The strains did not agglutinate human or bovine red blood cells in a mannose-resistant manner. They adhered to HEp-2 cells in a manner resembling enteroaggregative E. coli. Five strains were examined by dot-blot tests for the colonization factor antigens CFA/I, CS1, CS2, CS3, CS4, CS5, CS6, CS7, PCFO159, PCFO166 and CFA/III. Although four strains expressed CS6, no structure for CS6 was identified. A strain that the anti-CS6 MAbs did not react with could adhere to HEp-2 cells in mannose resistant manner; thus, it is unlikely that CS6 play an important role in the adhesion to the cells. Electron microscopy studies of the O169[ratio ]H41 strains suggested that curly fimbriae, a possible new colonization factor, may be playing an important role in the adhesion of the bacteria to HEp-2 cells. In conclusion, outbreaks due to ETEC O169: H41 were caused by multiple clones, and the strains should be examined in detail for a possible new colonization factor.

Type
Research Article
Copyright
© 1998 Cambridge University Press