Treviño M, Martínez-Lamas L, Romero-Jung P A, Giráldez J M, Alvarez-Escudero J, Regueiro B J
University Hospital Complex of Santiago de Compostela, La Coruña, Spain.
Eur J Clin Microbiol Infect Dis. 2009 May;28(5):527-33. doi: 10.1007/s10096-008-0657-5. Epub 2008 Nov 5.
The aim of this article was to report the emergence of patient infections with linezolid-resistant Staphylococcus epidermidis (LRSE) in a tertiary university hospital. Our objectives were to determine the molecular mechanism of the resistance, set up the genetic relationship among isolates, and analyze the relations between linezolid usage, period of treatment, and emergence of resistance in the hospital. The emergence of infection with linezolid-resistant S. epidermidis affecting 20 patients in a tertiary university hospital was investigated using repetitive sequence-based PCR (rep-PCR, DiversiLab System; BioMérieux, Inc., France). The presence of the G2576T mutation of 23S rRNA was screened by pyrosequencing. We determined the pattern of linezolid usage in the hospital as a whole and in the critical care unit that was most affected. G2576T mutation of 23S rRNA was detected in all linezolid-resistant S. epidermidis studied. Of these, 90% were genetically related and had been recovered from patients admitted to the same critical care unit. There had been an increase in linezolid usage in the hospital and in the critical care unit in the 2 years prior to the emergence of resistant strains. More strict control measures in hand washing and linezolid prescription were subsequently established, but no reduction in LRSE rates have yet been observed. Linezolid-resistant S. epidermidis emerged at our hospital, probably from a single strain originating in the critical care unit. The most likely explanation is that person-to-person spread of linezolid-resistant S. epidermidis led to skin colonization and, after linezolid treatment, this resistant staphylococci became the dominant cutaneous flora causing infection in some critical patients. In order to preserve the usefulness of this antibiotic as a therapeutic agent and to avoid a situation similar to methicillin-resistant Staphylococcus aureus, judicious use of antibiotics is essential.
本文旨在报告在一所三级大学医院中出现的耐利奈唑胺表皮葡萄球菌(LRSE)导致的患者感染情况。我们的目标是确定耐药的分子机制,建立分离株之间的遗传关系,并分析医院中利奈唑胺的使用情况、治疗时间与耐药性出现之间的关系。我们使用基于重复序列的PCR(rep-PCR,DiversiLab系统;法国生物梅里埃公司)对一所三级大学医院中20例受耐利奈唑胺表皮葡萄球菌感染的患者进行了调查。通过焦磷酸测序筛选23S rRNA的G2576T突变情况。我们确定了整个医院以及受影响最严重的重症监护病房中利奈唑胺的使用模式。在所研究的所有耐利奈唑胺表皮葡萄球菌中均检测到23S rRNA的G2576T突变。其中,90%在基因上具有相关性,并且是从同一重症监护病房收治的患者中分离出来的。在耐药菌株出现前的两年里,医院和重症监护病房中利奈唑胺的使用量有所增加。随后制定了更严格的洗手和利奈唑胺处方控制措施,但尚未观察到LRSE发生率有所下降。耐利奈唑胺表皮葡萄球菌在我们医院出现,可能源自重症监护病房的单一菌株。最有可能的解释是,耐利奈唑胺表皮葡萄球菌的人际传播导致皮肤定植,在使用利奈唑胺治疗后,这种耐药葡萄球菌成为一些重症患者皮肤感染的主要菌群。为了保持这种抗生素作为治疗药物的有效性,并避免出现类似于耐甲氧西林金黄色葡萄球菌的情况,明智地使用抗生素至关重要。