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The emergence of antimicrobial resistance, especially to the β-lactam group, which is the most commonly used antibiotic to treat various infectious diseases, is particularly important because it limits the therapeutic options, thereby increasing the morbidity and mortality rates [1, 2]. In Enterobacteriaceae, antibiotic resistance is linked to different mechanisms, for example the production of a certain type of enzymes named as extended-spectrum β-lactamases (ESBLs). ESBLs are plasmid-mediated and efficiently hydrolyze penicillins, third-generation cephalosporins, and aztreonam, which are commonly used to treat infections [3, 4]. In addition, antibiotic resistance due to AmpC β-lactamases, 16S rRNA methylases, aminoglycoside-modifying enzymes, and carbapenemases has also been reported [5]. ESBL-producing bacteria remain susceptible to carbapenems, and the activity of these enzymes is inhibited by clavulanic acid [6, 7]. In K. pneumoniae, AmpC beta-lactamases are located on plasmids, while in other Enterobacteriaceae spp., these enzymes are either plasmid or chromosomally encoded [8, 9]. AmpC β-lactamases confer resistance to cephamycins (e.g., cefoxitin and cefotetan) and β-lactamase inhibitor combinations [6]. Moreover, K. pneumoniae has also been found to harbor carbapenemase enzyme (KPC), which confers resistance to carbapenems such as imipenem and meropenem [10]. The emergence of carbapenem-resistant Enterobacteriaceae spp. in general and K. pneumoniae, in particular, has become a major public health problem due to lack of effective antibiotics [11], increasing the morbidity ABSTRACT

Emergence of AmpC β-Lactamase– and Metallo-β-Lactamase–producing Klebsiella pneumoniae in Sebha, Libya