烧伤病房细菌耐药性的分析

目的　分析笔者单位烧伤病房近 4年来的细菌耐药性。　方法　从本院 1996年～ 1999年烧伤患者血培养阳性及创面分离出的细菌 ,其中 5 0株以上者 5种 ,用纸片琼脂扩散法进行药敏试验。并以美国国家临床实验室标准委员会 (NCCLS)公布的数值作为判断耐药标准。应用双纸片协同试验检测 45株肺炎克雷伯菌的超广谱 -内酰胺酶 (ESBLs)。　结果　仅万古霉素对金黄色葡萄球菌有效。亚胺培南对大肠埃希菌、阴沟肠杆菌、肺炎克雷伯菌有效 ,而仅多粘菌素 -B对铜绿假单胞杆菌有效。 45株肺炎克雷伯菌中ESBLs阳性者有 38株 ,ESBLs的发生率为 84.4%。　结论笔者医院烧伤病房的细菌耐药率甚高 ,这可能是由于 β -内酰胺酶的产生 ,特别是ESBLs发生率甚高所致 ,亚胺培南依然对ES BLs稳定 ,抗菌效能佳 ;但复合 β-内酰胺酶抑制剂的抗生素作用已日趋减弱。铜绿假单胞菌对亚胺培南的耐药率正逐年增高 ,可能是由于大量使用该药 ,引起菌株产生一种新的由质粒传递的金属 β -内酰胺酶 ,细菌外膜蛋白产生减少与通透性的改变 ,从而导致细菌耐药性增加

Analysis of bacterial resistance to antibiotics in a burn ward

OBJECTIVE: To analyze the bacterial resistance to antibiotics in a burn ward in the past 4 years. METHODS: Six hundred and fifty strains of bacteria were isolated from the wounds and blood of burn patients admitted to our hospital in recent 4 years. Slip agar diffusion method was employed to carry out antibiotic sensitivity test, and the results were interpreted according to the NCCLS criteria. Extended spectrum beta -- lactamases (ESBLs) were detected by double slips synergic test in 45 strains of Klebsiella Pneumoniae. RESULTS: Only vancomycin was effective for staphylococcus aureus, and Imipenem was effective for E. coli, E. cloacae and K. pneumoniae. But P. aeruginosa was only susceptible to polymyxin -- B. In addition, Thirty -- eight out of 45 strains of K. pneumoniae were ESBLs positive with the incidence of 84.4%. CONCLUSION: The high resistance of the bacteria to most antibiotics in our burn ward might be related to the high production of beta -- lactamases and especially ESBLs. Imipenem remained stable to ESBLs and remained highly effective for most bacteria. But antibiotics with beta -- lactamases inhibitor became less effective in recent years. The resistance rate of P. aeruginosa to Imipenem increased gradually in recent years. This might be due to the abuse of Tienam in burn patients, which stimulated the bacteria to produce a new metallic beta -- lactamases transfected by plasmid, decreasing the production of bacterial outer membrane proteins and inducing a change in membranous permeability.