1 Medical Microbiology and Immunology Department, Faculty of Medicine, University of Tripoli, Tripoli, Libya
2 Medical Microbiology and Immunology Department, Faculty of Pharmacy, University of Tripoli, Tripoli, Libya
3 Biochemistry Department, Faculty of Medicine, University of Tripoli, Tripoli, Libya
4 National Centre for Disease Control, Tripoli, Libya
5 Faculty of Medical Technology, University of Tripoli, Tripoli, Libya
6 Laboratoire de Microorganismes et Biomolécules Actives Faculté des Sciences de Tunis, Université de Tunis El-Manar, 2098 El-Manar II, Tunisie.
7 Laboratoire de Recherche Sciences et Technologies de l’Environnement, Institut Supérieur des Sciences et Technologies de l’Environnement de Borj-Cedria, Université de Carthage, Technopôle de Borj-Cedria, BP-1003, Hammam-Lif 2050, Tunisie.
Extended-spectrum β-lactamases (ESBLs), including the AmpC type, are important mechanisms of resistance among Klebsiella pneumoniae and Escherichia coli 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 K. pneumoniae and 75 E. coli) 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 K. pneumoniae and E. coli 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 E. coli isolates were multidrug resistant compared with K. pneumoniae (65.8%). K. pneumoniae ESBL producers were significantly higher (85.5%) compared with (17.3%) E. coli isolates (P <0.0001, OR=4.93). Plasmid-mediated AmpC genes were detected in 7.9% of K. pneumoniae, and 4% E. coli 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, blaCMY (n=3), blaMOX (n=1), blaDHA (n=1). However, co-occurrence of AmpC genes were evident in 3/9 isolates with the following distribution:
blaCMY and blaEBC (n=1), and blaCMY and blaMOX (n=2). Neither blaFOX nor blaACC 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.
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