Department of Medicine, Division of Infectious Diseases, Washington University in St Louis, School of Medicine, St Louis, Missouri, USA.
Infectious Disease Section, Medicine Service, St Louis Veterans Affairs Health Care System, St Louis, Missouri, USA.
J Infect Dis. 2021 Dec 20;224(12 Suppl 2):S813-S820. doi: 10.1093/infdis/jiab359.
Enterotoxigenic Escherichia coli (ETEC) are ubiquitous diarrheal pathogens that thrive in areas lacking basic human needs of clean water and sanitation. These genetically plastic organisms cause tremendous morbidity among disadvantaged young children, in the form of both acute diarrheal illness and sequelae of malnutrition and growth impairment. The recent discovery of additional plasmid-encoded virulence factors and elucidation of their critical role in the molecular pathogenesis of ETEC may inform new approaches to the development of broadly protective vaccines. Although the pathogens have been closely linked epidemiologically with nondiarrheal sequelae, these conditions remain very poorly understood. Similarly, while canonical effects of ETEC toxins on cellular signaling promoting diarrhea are clear, emerging data suggest that these toxins may also drive changes in intestinal architecture and associated sequelae. Elucidation of molecular events underlying these changes could inform optimal approaches to vaccines that prevent acute diarrhea and ETEC-associated sequelae.
肠产毒性大肠杆菌(ETEC)是普遍存在的腹泻病原体,在缺乏清洁水和卫生等基本人类需求的地区茁壮成长。这些遗传可塑性生物体在贫困的幼儿中引起巨大的发病率,以急性腹泻病和营养不良及生长障碍的后遗症的形式出现。最近发现了其他质粒编码的毒力因子,并阐明了它们在 ETEC 分子发病机制中的关键作用,这可能为开发广泛保护的疫苗提供新的方法。尽管病原体在流行病学上与非腹泻后遗症密切相关,但这些情况仍知之甚少。同样,虽然 ETEC 毒素对促进腹泻的细胞信号传导的典型作用是明确的,但新出现的数据表明,这些毒素也可能导致肠道结构和相关后遗症的变化。阐明这些变化背后的分子事件可以为预防急性腹泻和 ETEC 相关后遗症的疫苗提供最佳方法。