JMI Laboratories, 345 Beaver Kreek Centre, Suite A, North Liberty, IA 52317, USA.
Antimicrob Agents Chemother. 2010 Sep;54(9):3614-7. doi: 10.1128/AAC.01390-09. Epub 2010 Jun 21.
Among 4,167 Staphylococcus aureus and 790 coagulase-negative Staphylococcus (CoNS; not S. saprophyticus) isolates collected consecutively from North American and Australian hospitals, only 87 (1.7% overall) isolates displayed a fusidic acid (FA; also known as CEM-102) MIC of > or = 2 microg/ml (FA resistance). These strains were further evaluated with a multiplex PCR to amplify the acquired resistance genes fusB, fusC, and fusD. Mutations in fusA and fusE were evaluated in all isolates showing an absence of acquired resistance genes and/or showing FA MIC values of > or = 64 microg/ml. S. aureus resistance rates were very low in the United States (0.3%) and were higher in Canada and Australia (7.0% for both countries). Among CoNS isolates, FA resistance rates were significantly more elevated than that for S. aureus (7.2 to 20.0%; the highest rates were in Canada). All 52 (41 CoNS) FA-resistant isolates from the United States showed FA MIC results of < or = 64 microg/ml, and 7 of 11 S. aureus isolates carried fusC. CoNS strains from the United States carried fusB or fusC. In Canada, fusB and fusC occurrences were similar among S. aureus and CoNS isolates, and modestly elevated FA MIC values were observed (all MIC results were < or = 32 microg/ml). Isolates from Australia showed MIC values ranging from 2 to 32 microg/ml, and S. aureus isolates were predominantly fusC positive. fusA mutations were detected in only three S. aureus isolates, conferring FA MIC values of 2 to 8 microg/ml. Target mutations have been considered the primary FA resistance mechanism among Staphylococcus spp.; however, acquired resistance genes appear to have a dominant role in resistance against this older antimicrobial agent. In summary, this study shows that acquired genes are highly prevalent among FA-resistant strains (>90%) in three nations with distinct or absence (United States) of fusidic acid clinical use.
在北美和澳大利亚医院连续采集的 4167 株金黄色葡萄球菌和 790 株凝固酶阴性葡萄球菌（不包括腐生葡萄球菌）中，只有 87 株（总体为 1.7%）分离株对夫西地酸（FA；也称为 CEM-102）的 MIC 大于等于 2μg/ml（FA 耐药）。这些菌株进一步用多重 PCR 进行评估，以扩增获得的耐药基因 fusB、fusC 和 fusD。在所有显示不存在获得性耐药基因和/或 FA MIC 值大于等于 64μg/ml 的菌株中评估 fusA 和 fusE 的突变。美国金黄色葡萄球菌的耐药率非常低（0.3%），而加拿大和澳大利亚的耐药率较高（两国均为 7.0%）。凝固酶阴性葡萄球菌的 FA 耐药率明显高于金黄色葡萄球菌（7.2%至 20.0%；最高耐药率见于加拿大）。来自美国的 52 株（41 株凝固酶阴性葡萄球菌）FA 耐药分离株的 FA MIC 结果均小于等于 64μg/ml，11 株金黄色葡萄球菌分离株中有 7 株携带 fusC。来自美国的凝固酶阴性葡萄球菌菌株携带 fusB 或 fusC。在加拿大，金黄色葡萄球菌和凝固酶阴性葡萄球菌分离株的 fusB 和 fusC 发生率相似，并且观察到适度升高的 FA MIC 值（所有 MIC 结果均小于等于 32μg/ml）。来自澳大利亚的分离株的 MIC 值范围为 2 至 32μg/ml，金黄色葡萄球菌分离株主要 fusC 阳性。仅在 3 株金黄色葡萄球菌分离株中检测到 fusA 突变，导致 FA MIC 值为 2 至 8μg/ml。靶基因突变被认为是金黄色葡萄球菌属中 FA 耐药的主要机制；然而，获得性耐药基因在对抗这种较老的抗菌药物方面似乎起着主导作用。总之，这项研究表明，在三个国家（具有明显或不存在夫西地酸临床应用的美国）中，获得性基因在 FA 耐药株中高度流行（>90%）。
