Levine M M, Nataro J P, Karch H, Baldini M M, Kaper J B, Black R E, Clements M L, O'Brien A D
J Infect Dis. 1985 Sep;152(3):550-9. doi: 10.1093/infdis/152.3.550.
Isolates of the most common O serogroups of enteropathogenic Escherichia coli (EPEC) associated with infant diarrhea (designated class I) adhere to Hep-2 cells; the genes for this adhesin, termed EPEC adherence factor (EAF), are located on plasmids 50-70 MDa in size. Volunteers ingested 10(10) organisms of an O127:H6 Hep-2-adhesive class I strain (E2348/69) or its plasmid-minus, nonadhesive derivative. Diarrhea occurred in nine of 10 volunteers who ingested the parent strain (mean, 1,178 ml) but in only two of nine who took the plasmid-minus variant (mean, 433 ml; P less than .006). All volunteers ill from strain E2348/69 mounted serum IgA and IgG responses to a 94-kDa plasmid-associated outer membrane protein of E2348/69; this protein was found in other class I EPEC but not in enterotoxigenic or meningitic strains. The 50-70-MDa EAF plasmid seems necessary for full expression of pathogenicity in EPEC that exhibit Hep-2 adhesiveness. EPEC isolates of certain other, less common, O serogroups (O44, O86, and O114) are rarely Hep-2 adhesive. These EPEC, designated class II, possess distinct 50-70 MDa plasmids lacking EAF genes. Diarrhea was caused by 10(8) or 10(10) organisms of an O114:H2 class II EPEC strain (mean, 1,156 ml) in six of 11 volunteers. This result confirmed that class II EPEC are pathogenic by a mechanism not involving Hep-2 adhesiveness.
与婴儿腹泻相关的最常见的肠致病性大肠杆菌(EPEC)O血清群分离株(称为I类)可黏附于Hep-2细胞;这种黏附素的基因,称为EPEC黏附因子(EAF),位于大小为50 - 70 MDa的质粒上。志愿者摄入了10¹⁰个O127:H6 Hep-2黏附性I类菌株(E2348/69)或其无质粒、无黏附性的衍生物。摄入亲本菌株的10名志愿者中有9人出现腹泻(平均1178毫升),而摄入无质粒变体的9名志愿者中只有2人出现腹泻(平均433毫升;P < 0.006)。所有因E2348/69菌株患病的志愿者对E2348/69的一种94 kDa质粒相关外膜蛋白产生了血清IgA和IgG反应;这种蛋白在其他I类EPEC中存在,但在产肠毒素或脑膜炎菌株中不存在。50 - 70 MDa的EAF质粒似乎是表现出Hep-2黏附性的EPEC充分表达致病性所必需的。某些其他较不常见的O血清群(O44、O86和O114)的EPEC分离株很少有Hep-2黏附性。这些EPEC称为II类,拥有缺乏EAF基因的独特50 - 70 MDa质粒。11名志愿者中有6人因摄入10⁸或10¹⁰个O114:H2 II类EPEC菌株而出现腹泻(平均1156毫升)。这一结果证实II类EPEC通过一种不涉及Hep-2黏附性的机制致病。