Zorgani Abdulaziz, Daw Hiyam, Sufya Najib, Bashein Abdullah, Elahmer Omar, Chouchani Chedly
Medical Microbiology and Immunology Department, Faculty of Medicine, University of Tripoli, Tripoli, Libya.
National Centre for Disease Control, Tripoli, Libya.
Open Microbiol J. 2017 Sep 26;11:195-202. doi: 10.2174/1874285801711010195. eCollection 2017.
Extended-spectrum β-lactamases (ESBLs), including the AmpC type, are important mechanisms of resistance among and isolates.
The aim of the study was to investigate the occurrence of AmpC-type β-lactamase producers isolated from two hospitals in Tripoli, Libya.
All clinical isolates (76 and 75 ) collected over two years (2013-2014) were evaluated for susceptibility to a panel of antimicrobials and were analyzed phenotypically for the ESBL and AmpC phenotype using E-test and ESBL and AmpC screen disc test. Both ESBL and AmpC-positive isolates were then screened for the presence of genes encoding plasmid-mediated AmpC β-lactamases by polymerase chain reaction (PCR).
Of the and tested, 75% and 16% were resistant to gentamicin, 74% and 1.3% to imipenem, 71% and 12% to cefoxitin, 80% and 12% to cefepime, 69% and 22.6% to ciprofloxacin, respectively. None of the isolates were multidrug resistant compared with (65.8%). ESBL producers were significantly higher (85.5%) compared with (17.3%) isolates (P <0.0001, OR=4.93). Plasmid-mediated AmpC genes were detected in 7.9% of , and 4% isolates. There was low agreement between phenotypic and genotypic methods, phenotypic testing underestimated detection of AmpC enzyme and did not correlate well with molecular results. The gene encoding CMY enzyme was the most prevalent (66.6%) of AmpC positive isolates followed by MOX, DHA and EBC. Only one AmpC gene was detected in 5/9 isolates, i.e, (n=3), (n=1), (n=1). However, co-occurrence of AmpC genes were evident in 3/9 isolates with the following distribution: and (n=1), and and (n=2). Neither nor was detected in all tested isolates. All AmpC positive strains were resistant to cefoxitin and isolated from patients admitted to intensive care units.
Further studies are needed for detection of other AmpC variant enzyme production among such isolates. Continued surveillance and judicious antibiotic usage together with the implementation of efficient infection control measures are absolutely required.
超广谱β-内酰胺酶（ESBLs），包括AmpC型，是革兰氏阴性菌和革兰氏阳性菌分离株耐药的重要机制。
本研究旨在调查从利比亚的黎波里两家医院分离出的AmpC型β-内酰胺酶产生菌的发生率。
对两年（2013 - 2014年）收集的所有临床分离株（76株革兰氏阴性菌和75株革兰氏阳性菌）进行一组抗菌药物的敏感性评估，并使用E-test以及ESBL和AmpC筛选纸片法对ESBL和AmpC表型进行表型分析。然后，通过聚合酶链反应（PCR）对ESBL和AmpC阳性分离株进行编码质粒介导的AmpCβ-内酰胺酶基因的筛选。
在所测试的革兰氏阴性菌和革兰氏阳性菌中，分别有75%和16%对庆大霉素耐药，74%和1.3%对亚胺培南耐药，71%和12%对头孢西丁耐药，80%和12%对头孢吡肟耐药，69%和22.6%对环丙沙星耐药。与革兰氏阳性菌（65.8%）相比，革兰氏阴性菌分离株均无多重耐药。革兰氏阴性菌ESBL产生菌（85.5%）显著高于革兰氏阳性菌（17.3%）分离株（P<0.0001，OR = 4.93）。在7.9%的革兰氏阴性菌和4%的革兰氏阳性菌分离株中检测到质粒介导的AmpC基因。表型和基因型方法之间的一致性较低，表型检测低估了AmpC酶的检测，且与分子结果相关性不佳。编码CMY酶的基因是AmpC阳性分离株中最常见的（66.6%），其次是MOX、DHA和EBC。在5/9的分离株中仅检测到一个AmpC基因，即阴沟肠杆菌（n = 3）、肺炎克雷伯菌（n = 1）、产气肠杆菌（n = 1）。然而，在3/9的分离株中明显存在AmpC基因共现情况，分布如下：阴沟肠杆菌和肺炎克雷伯菌（n = 1），以及阴沟肠杆菌和产气肠杆菌（n = 2）。在所有测试分离株中均未检测到DHA和FOX。所有AmpC阳性菌株均对头孢西丁耐药，且均从入住重症监护病房的患者中分离得到。
需要进一步研究以检测此类分离株中其他AmpC变异酶的产生情况。绝对需要持续监测、合理使用抗生素以及实施有效的感染控制措施。
