摘要
目的 了解临床分离金黄色葡萄球菌对常用抗菌药物耐药性及产生机制。方法 4 2株金黄色葡萄球菌先用PCR检测mecA基因 ,再用VITEK2高级专家系统 (AES)检测并分析对 2 0种抗菌药物耐药性及耐药机制。结果 19株金黄色葡萄球菌mecA基因检测阳性 ,2 3株阴性 ;VITEK2AES耐药机制分析 ,对 β 内酰胺类耐药涉及青霉素结合蛋白 (PBP)改变、获得性青霉素酶 ;氨基糖苷类耐药包括磷酸转移酶 (2”) +乙酰转移酶 (6 ')双功能酶、磷酸转移酶 (3') Ⅲ、腺苷转移酶 (4') (4”) ;大环内酯类 /林可霉胺类 /链阳菌素B(MLSB)与MLSB固有耐药或诱导耐药有关 ;对四环素类耐药包括TETK蛋白导致药物外排和 (或 )TETM蛋白导致靶位改变 ;利福霉素类耐药主要为高水平耐药 ;MRSA对喹诺酮类均耐药 ,而MSSA除 1株外均敏感 ;其余抗菌药物如呋喃妥因、糖肽类(万古霉素、替考拉宁 )、复方新诺明、夫西地酸等均敏感。结论 临床分离金黄色葡萄球菌 ,尤其是MRSA具有多种耐药机制 ,因而对常用抗菌药物产生多重耐药性 ,VITEK2AES能可靠推测分析耐药菌所具有的耐药机制 ,将为临床抗感染治疗提供更加准确的依据。
OBJECTIVE To investigate resistant mechanisms of clinical isolates of Staphylococcus aureus to 20 antimicrobial agents. METHODS The PCR was used to detect mecA gene for 42 S. aureus isolates. Mechanisms of resistance to 20 antimicrobial agents were inferred with VITEK2 Advanced Expert System(AES). RESULTS Nineteen S.aureus isolates were mecA positive. Mechanisms of resistance included modification of PBP- and acquired penicillinase-mediated beta-lactam resistance; heterogeneous APH(2')+ AAC(6'), APH(3')-Ⅲ and ANT(4')(4')-mediated aminoglycoside resistance; macrolides/lincosamides/streptogramin B (MLSB) constitutive and inducible-mediated MLSB resistance; partially resistant (Efflux TET K) and/or target modification (TET M) for tetracyclines and resistance(high-level) to rifamycins. S.aureus isolates tested were susceptible to other families of antimicrobial agents. CONCLUSIONS Clinical S. aureus isolates, especially MRSA are multiple-drug resistant because of resistant mechanisms. VITEK2 AES can be reliable to infer resistant mechanisms with resistance phenotype and species to be recognized.
出处
《中华医院感染学杂志》
CAS
CSCD
2003年第12期1107-1109,共3页
Chinese Journal of Nosocomiology
