Reversion of the glycopeptide resistance phenotype in Staphylococcus aureus clinical isolates
Reversion of the glycopeptide resistance phenotype in Staphylococcus aureus clinical isolates
复制标题
DOI：
10.1128/aac.44.2.272-277.2000
复制
发表时间：
2000-02-01
影响因子：
4.9
通讯作者：
Daum, RS
中科院分区：
文献类型：
--
作者：
Boyle-Vavra, S;Berke, SK;Daum, RS
最近鉴定的糖肽中间耐药金黄色葡萄球菌（GISA）的临床分离株提供了一个机会，以评估非选择性连续传代的糖肽耐药表型的稳定性，并评估逆转相关的细胞表面变化。在添加或不添加万古霉素的营养琼脂上每日传代3株来自美国的GISA分离株（万古霉素MIC = g μ g/ml）和2株来自日本的GISA分离株（万古霉素MIC = 8和2 μ g/ml）。在非选择性培养基上传代15天后，通过肉汤稀释法测定，从各GISA分离株中获得万古霉素和替考拉宁敏感回复突变体。比较回复突变菌株与亲本菌株在万古霉素异源耐药性、荚膜产生、溶血表型、凝固酶活性和溶葡萄球菌酶敏感性方面的变化。几个回复突变体失去了中间万古霉素耐药的亚群，而两个回复突变体保持它们。此外，尽管所有亲本GISA分离株均产生5型荚膜（CP 5），但除一个回复突变体外，所有检测的回复突变体均不再产生CP 5。相比之下，在含万古霉素的培养基上传代产生的分离株对万古霉素仍具有中等耐药性，替考拉宁的MIC未降低，并产生可检测的CP 5，未观察到回复突变体在溶血表型、溶葡萄球菌酶敏感性或凝固酶活性方面的一致变化。这些数据表明万古霉素耐药表型在临床GISA分离株中不稳定。万古霉素耐药表型的逆转可能解释了从万古霉素治疗失败的患者血液中分离万古霉素耐药临床分离株的困难，并且可能解释了临床实验室中鉴定GISA分离株的一些困难。
The recent identification of glycopeptide intermediate-resistant Staphylococcus aureus (GISA) clinical isolates has provided an opportunity to assess the stability of the glycopeptide resistance phenotype by nonselective serial passage and to evaluate reversion-associated cell surface changes. Three GISA isolates from the United States (MIC of vancomycin = g mu g/ml) and two from Japan (MICs of vancomycin = 8 and 2 mu g/ml) were passaged daily on nutrient agar with or without vancomycin supplementation, After 15 days of passage on nonselective medium, vancomycin- and teicoplanin-susceptible revertants were obtained from each GISA isolate as determined by broth dilution MIG. Revertant isolates were compared,vith parent isolates for changes in vancomycin heteroresistance, capsule production, hemolysis phenotype, coagulase activity, and lysostaphin susceptibility. Several revertants lost the subpopulations with intermediate vancomycin resistance, whereas two revertants maintained them. Furthermore, although all of the parent GISA isolates produced capsule type 5 (CP5), all but one revertant tested no longer produced CP5. In contrast, passage on medium containing vancomycin yielded isolates that were still intermediately resistant to vancomycin, had no decrease in the MIC of teicoplanin, and produced detectable CP5, No consistent changes in the revertants in hemolysis phenotype, lysostaphin susceptibility, or coagulase activities were discerned. These data indicate that the vancomycin resistance phenotype is unstable in clinical GISA isolates. Reversion of the vancomycin resistance phenotype might explain the difficulty in isolating vancomycin-resistant clinical isolates from the blood of patients who fail vancomycin therapy and, possibly, may account for some of the difficulties in identifying GISA isolates in the clinical laboratory.