Y. Nishikawa et al., EPIDEMIOLOGY AND PROPERTIES OF HEAT-STABLE ENTEROTOXIN-PRODUCING ESCHERICHIA-COLI SEROTYPE O169-H41, Epidemiology and infection, 121(1), 1998, pp. 31-42
Enterotoxigenic Escherichia coil (ETEC) serotype O169:H41 organisms ha
ve 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, enter
otoxigenicity, protein banding pattern, lipopolysaccharide banding pat
tern, plasmid analysis, and ribotyping. Further, the strains were exam
ined by haemagglutination, surface hydrophobicity, and the ability to
adhere to HEp-2 cells. The present study suggests that the outbreaks w
ere caused by multiple clones of STp-producing O169:H41 since they sho
wed differences in ribotype and outer membrane protein banding pattern
s. 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 re
sembling 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 strain
s expressed CS6, no structure for CS6 was identified. A strain that th
e anti-CS6 MAbs did not react with could adhere to HEp-2 cells in mann
ose resistant manner; thus, it is unlikely that CS6 play an important
role in the adhesion to the cells. Electron microscopy studies of the
O169:H41 strains suggested that curly fimbriae, a possible new coloniz
ation 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.