Drissi M, Ahmed Z Baba, Dehecq B, Bakour R, Plésiat P, Hocquet D
Laboratoire << Antibiotiques-Antifongiques >>, université Abou Bekr Belkaïd, B.P. 119, Tlemcen 13000, Algeria.
Med Mal Infect. 2008 Apr;38(4):187-91. doi: 10.1016/j.medmal.2008.01.009. Epub 2008 Apr 18.
Pseudomonas aeruginosa is a major causative agent of hospital infections. Studies on this subject being rare in Algeria, we determined the antibiotic susceptibility of P. aeruginosa and investigated the mechanisms of beta-lactam resistance and the spread of multidrug resistant strains in the university affiliated Hospital of Tlemcen (Algeria).
One hundred and ninety-nine consecutive strains of P. aeruginosa were collected between November 2005 and February 2007. MICs of antibiotics were measured by the agar dilution method. The resistance mechanisms to beta-lactams were identified phenotypically or by molecular methods (isoelectrofocusing, PCR and sequencing). Strains expressing a secondary beta-lactamase were serotyped and genotyped (Random Amplified Polymorphic DNA).
The proportion of susceptible isolates were: ticarcillin (56%), piperacillin-tazobactam (81%), ceftazidime (88%), cefepime (80%), aztreonam (64%), imipenem (65%), amikacin (83%), tobramycin (81%) and ciprofloxacin (97%) according to the French CASFM breakpoints. Resistance to beta-lactams was linked to the production of transferable beta-lactamases (16%), overproduction of cephalosporinase AmpC (12%) and/or non-enzymatic mechanisms such as the loss of porin OprD (35%) and overproduction of the active efflux system MexAB-OprM (24%). High level resistance to ticarcillin was due to the expression of beta- lactamase OXA-10 alone or associated with TEM-110. A genotypic analysis revealed the spread of a multidrug resistant epidemic clone expressing these two acquired beta-lactamases in the surgical ICU.
This study shows that resistance to antibiotics, in particular to imipenem of P. aeruginosa, is becoming a cause of concern in the Hospital of Tlemcen.
铜绿假单胞菌是医院感染的主要致病菌。鉴于阿尔及利亚关于该主题的研究较少，我们测定了铜绿假单胞菌的抗生素敏感性，研究了β-内酰胺耐药机制以及多重耐药菌株在特莱姆森大学附属医院（阿尔及利亚）的传播情况。
2005年11月至2007年2月期间收集了199株连续的铜绿假单胞菌菌株。采用琼脂稀释法测定抗生素的最低抑菌浓度（MIC）。通过表型或分子方法（等电聚焦、聚合酶链反应和测序）鉴定对β-内酰胺类抗生素的耐药机制。对表达二级β-内酰胺酶的菌株进行血清分型和基因分型（随机扩增多态性DNA）。
根据法国抗菌药物敏感性试验委员会（CASFM）的标准，敏感菌株的比例分别为：替卡西林（56%）、哌拉西林-他唑巴坦（81%）、头孢他啶（88%）、头孢吡肟（80%）、氨曲南（64%）、亚胺培南（65%）、阿米卡星（83%）、妥布霉素（81%）和环丙沙星（97%）。对β-内酰胺类抗生素的耐药与可转移β-内酰胺酶的产生（16%）、头孢菌素酶AmpC的过量产生（12%）和/或非酶机制有关，如孔蛋白OprD的缺失（35%）和主动外排系统MexAB-OprM的过量产生（24%）。对替卡西林的高水平耐药是由于单独表达β-内酰胺酶OXA-10或与TEM-110相关。基因分析显示，在外科重症监护病房中，一种表达这两种获得性β-内酰胺酶的多重耐药流行克隆正在传播。
本研究表明，铜绿假单胞菌对抗生素尤其是亚胺培南的耐药性在特莱姆森医院正成为一个令人担忧的问题。
