Nishikawa Y, Helander A, Ogasawara J, Moyer N P, Hanaoka M, Hase A, Yasukawa A
Department of Epidemiology, Osaka City Institute of Public Health and Environmental Sciences, Tennoji, Osaka, Japan.
Epidemiol Infect. 1998 Aug;121(1):31-42. doi: 10.1017/s0950268898001046.
Enterotoxigenic Escherichia coli (ETEC) serotype O169: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: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: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.
自1991年首次爆发以来，产肠毒素大肠杆菌（ETEC）O169:H41血清型菌株已成为日本最常见的ETEC。据推测，这些疫情是由这种新的ETEC血清型的克隆传播引起的。对从6次疫情中分离出的32株菌株进行了生物型、抗生素敏感性、产肠毒素性、蛋白条带模式、脂多糖条带模式、质粒分析和核糖体分型检查。此外，还通过血凝试验、表面疏水性以及黏附HEp-2细胞的能力对这些菌株进行了检测。本研究表明，这些疫情是由产STp的O169:H41的多个克隆引起的，因为它们在核糖体分型和外膜蛋白条带模式上存在差异。这些菌株不能以抗甘露糖的方式凝集人或牛红细胞。它们以类似于肠集聚性大肠杆菌的方式黏附于HEp-2细胞。通过斑点印迹试验对5株菌株检测了定植因子抗原CFA/I、CS1、CS2、CS3、CS4、CS5、CS6、CS7、PCFO159、PCFO166和CFA/III。尽管4株菌株表达了CS6，但未鉴定出CS6的结构。一株抗CS6单克隆抗体不与之反应的菌株能够以抗甘露糖的方式黏附于HEp-2细胞；因此，CS6不太可能在细菌黏附细胞过程中发挥重要作用。对O169:H41菌株的电子显微镜研究表明，卷曲菌毛（一种可能的新定植因子）可能在细菌黏附HEp-2细胞过程中发挥重要作用。总之，ETEC O169:H41引起的疫情是由多个克隆引起的，应对这些菌株详细检测可能存在的新定植因子。
