Kayser F H
Institute of Medical Microbiology, University of Zürich, Gloriastrasse 30/32, PO Box CH-8028 Zurich, Switzerland.
Int J Food Microbiol. 2003 Dec 1;88(2-3):255-62. doi: 10.1016/s0168-1605(03)00188-0.
Enterococci occur in a remarkable array of environments. They can be found in soil, food, and water, and make up a significant portion of the normal gut flora of humans (10(5)-10(7)/g of stool) and animals. As other bacteria of the gut flora, enterococci can also cause infectious diseases. Most clinical isolates are Enterocococus faecalis, which account for 80-90% of clinical strains. Enterocococus faecium accounts for 5-10% of such isolates. Typical enterococcal infections occur in hospitalised patients with underlying conditions representing a wide spectrum of severity of illness and immune modulation. Enterococci today rank second to third in frequency among bacteria isolated from hospitalised patients. They are isolated from urinary tract infections, intra-abdominal and pelvic infections, bacteremias, wound and tissue infections, and endocarditis--often as part of a polymicrobial flora. Surprisingly, little is known about the factors that contribute to the ability of enterococci to cause infections. Many strains of E. faecalis produce a cytolysin (haemolysin) exhibiting tissue-damaging capacity. Further extracellular products often observed in clinical isolates are a proteinase (gelatinase), hyaluronidase, and extracellular superoxide. Furthermore, many of the clinical isolates possess the aggregation substance on the surface and an extracellular surface protein, both contributing to the adherence to eucaryotic cells. Some strains of E. faecalis, and many E. faecium strains are resistant to multiple antimicrobials. The ultimate role of all these factors in enterococcal pathogenicity remains to be determined. It was previously thought that enterococcal infections were endogenously acquired from the patient's own gut flora. A rather new concept that has emerged is that enterococcal disease is a two-stage process. There is an initial colonisation of the gastrointestinal tract by enterococcal strains possessing virulence traits and/or antibiotic resistance. Subsequently, this population spreads, often facilitated by antibiotic elimination of competitors. For a selected number of patients, there is subsequent tissue invasion from the gastrointestinal tract reservoir. From this concept, it can be deduced that enterococcal strains without virulence traits and antibiotic resistances exogenously transferred into the human gut via food products or probiotics will not represent any risk for immunocompetent individuals. In very severely immunocompromised patients, however, a risk for enterococcal disease by such strains cannot completely be excluded.
肠球菌存在于各种各样的环境中。它们可在土壤、食物和水中被发现，并且在人类（每克粪便中有10⁵ - 10⁷个）和动物的正常肠道菌群中占很大比例。作为肠道菌群的其他细菌，肠球菌也可引起传染病。大多数临床分离株是粪肠球菌，占临床菌株的80 - 90%。屎肠球菌占此类分离株的5 - 10%。典型的肠球菌感染发生在患有各种严重程度疾病和免疫调节异常的住院患者中。如今，在从住院患者中分离出的细菌中，肠球菌的出现频率排名第二至第三。它们可从尿路感染、腹腔和盆腔感染、菌血症、伤口和组织感染以及心内膜炎中分离出来——通常是作为混合菌群的一部分。令人惊讶的是，对于促成肠球菌感染能力的因素了解甚少。许多粪肠球菌菌株产生一种具有组织损伤能力的细胞溶素（溶血素）。在临床分离株中经常观察到的其他细胞外产物有蛋白酶（明胶酶）、透明质酸酶和细胞外超氧化物。此外，许多临床分离株在表面具有聚集物质和一种细胞外表面蛋白，这两者都有助于其黏附到真核细胞上。一些粪肠球菌菌株以及许多屎肠球菌菌株对多种抗菌药物耐药。所有这些因素在肠球菌致病性中的最终作用仍有待确定。以前认为肠球菌感染是从患者自身的肠道菌群内源性获得的。一个新出现的概念是，肠球菌疾病是一个两阶段过程。具有毒力特征和/或抗生素耐药性的肠球菌菌株首先在胃肠道定植。随后，这个菌群扩散，通常是由于抗生素清除了竞争者而得以促进。对于一些特定患者，随后会从胃肠道储库发生组织侵袭。从这个概念可以推断，通过食品或益生菌外源性转移到人类肠道中的没有毒力特征和抗生素耐药性的肠球菌菌株，对于免疫功能正常的个体不会构成任何风险。然而，在非常严重的免疫受损患者中，不能完全排除此类菌株导致肠球菌疾病的风险。
