Jett B D, Huycke M M, Gilmore M S
Division of Laboratory Medicine, Washington University Medical Center, St. Louis, Missouri 63110.
Clin Microbiol Rev. 1994 Oct;7(4):462-78. doi: 10.1128/CMR.7.4.462.
Enterococci are commensal organisms well suited to survival in intestinal and vaginal tracts and the oral cavity. However, as for most bacteria described as causing human disease, enterococci also possess properties that can be ascribed roles in pathogenesis. The natural ability of enterococci to readily acquire, accumulate, and share extrachromosomal elements encoding virulence traits or antibiotic resistance genes lends advantages to their survival under unusual environmental stresses and in part explains their increasing importance as nosocomial pathogens. This review discusses the current understanding of enterococcal virulence relating to (i) adherence to host tissues, (ii) invasion and abscess formation, (iii) factors potentially relevant to modulation of host inflammatory responses, and (iv) potentially toxic secreted products. Aggregation substance, surface carbohydrates, or fibronectin-binding moieties may facilitate adherence to host tissues. Enterococcus faecalis appears to have the capacity to translocate across intact intestinal mucosa in models of antibiotic-induced superinfection. Extracellular toxins such as cytolysin can induce tissue damage as shown in an endophthalmitis model, increase mortality in combination with aggregation substance in an endocarditis model, and cause systemic toxicity in a murine peritonitis model. Finally, lipoteichoic acid, superoxide production, or pheromones and corresponding peptide inhibitors each may modulate local inflammatory reactions.
肠球菌是共生生物，非常适合在肠道、阴道和口腔中生存。然而，与大多数被描述为可导致人类疾病的细菌一样，肠球菌也具有一些可在发病机制中发挥作用的特性。肠球菌易于获取、积累和共享编码毒力特征或抗生素耐药基因的染色体外元件的天然能力，使其在异常环境压力下具有生存优势，这也部分解释了它们作为医院病原体的重要性日益增加的原因。本综述讨论了目前对肠球菌毒力的理解，涉及（i）对宿主组织的粘附、（ii）侵袭和脓肿形成、（iii）可能与调节宿主炎症反应相关的因素以及（iv）潜在有毒的分泌产物。聚集物质、表面碳水化合物或纤连蛋白结合部分可能促进对宿主组织的粘附。在抗生素诱导的二重感染模型中，粪肠球菌似乎有能力穿过完整的肠粘膜。细胞溶素等细胞外毒素可导致组织损伤，如在眼内炎模型中所示；在心内膜炎模型中，与聚集物质联合使用时可增加死亡率；在小鼠腹膜炎模型中可导致全身毒性。最后，脂磷壁酸、超氧化物产生或信息素及相应的肽抑制剂各自可能调节局部炎症反应。
