泛耐药鲍曼不动杆菌耐药机制及所涉感染诱因探讨

Drug resistance mechanism and clinical infection factors of pandrug-resistant Acinetobacter baumannii

目的探讨泛耐药鲍曼不动杆菌(PDR-AB)耐药机制及所涉感染诱因。方法收集鲍曼不动杆菌感染者分离菌株104株,PCR检测PDR-AB组和非PDR-AB组菌株16S rRNA甲基化酶基因、碳青霉烯类耐药基因和生物膜相关基因,微量半定量法检测菌株生物膜形成能力,微量肉汤稀释法测定菌株的最低抑菌浓度(MIC),并回顾性分析感染者的临床诱因。结果 104株菌株分为PDR-AB 28株和非PDR-AB 76株;PDR-AB组blaOXA-23、blaVIM、aba I和csu E基因携带率均高于非PDR-AB组(P<0.05),两组生物膜形成能力差异无统计学意义(P>0.05);PDR-AB组患者平均住院日、侵入性治疗(大于48 h)发生率、菌株分离前3种及以上抗菌药物使用率及抗菌药物暴露时间均高于非PDR-AB感染组患者(P<0.05)。结论 PDR-AB耐药与相关耐药基因携带有关,而PDR-AB感染与患者进行侵入性治疗、感染前抗菌药物暴露等临床诱因有关。

Objective To explore the drug resistance mechanism and clinical infection factors of pandrug-resistant Acinetobacter bau- mannii （PDR-AB）. Methods A total of 104 Acinetobacter baumannii （AB） strains were collected from the patients infected with AB in Longyan First Hospital, Fujian of China. 16S rRNA methylase-mediated gene, earbapenem-resistanee gene and biofilm-related genes of the 104 strains which were classified as PDR-AB and Non PDR-AB were analyzed by PCR. Trace semi-quantitative method was used to detect biofilm formation ability. The MIC method was used to determine the sensitivity of each strain to antibiotics. The clinical in- fection factors were retrospectively analyzed. Results The 104 strains were divided into 2 groups： PDR-AB （28 strains） and non PDR-AB （76 strains）. The detection rates of blaoxA_23, blaviM, abal and csuE genes in PDR-AB group were significantly higher than those of non PDR-AB group （ P 〈 0.05 ）, however there was no difference between the two groups in biofihn formation（ P 〉 0.05 ）. The average length of stay, invasive treatment time （ more than 48 hours） , combination use rate of three or more antibiotics and antibiotic exposure time in the patients of PDR-AB infection group were significantly higher than those in non PDR-AB infection group （P 〈 0.05 ）. Conclusion The drug resistance of PDR-AB may be related to drug resistant genes： The infection of PDR-AB may correlate to several clinical inducing factors, such as invasive treatment, antibiotic exposure, etc, before PDR-AB infection.