Abstract
Extended spectrum beta-lactamases (ESBLs) are enzymes produced by bacteria, mostly members of the family Enterobacteriaceae commonly Escherichia coli and Klebsiella pneumoniae. ESBLs hydrolyze the beta-lactam ring of beta-lactam antibiotics making these antibiotics ineffective therefore rendering the bacteria resistance against beta-lactam antibiotics. The global upsurge of ESBLs producing bacteria causing both hospital and community acquired infections mostly urinary tract infections, pneumonia and bloodstream infections, threatens the effectiveness of infectious diseases treatment. ESBL families; TEM, SHV and CTX-M are globally disseminated and frequently detected in clinical isolates as well as colonization and contamination isolates. Various laboratory detection methods of ESBLs producing Gram negative bacteria are available. These methods; phenotypic methods, automated methods and molecular-based methods are varying in sensitivity and specificity, need of technical expertise, and rapidness. Therefore, they should be clearly understood before being employed for routine or research use for detection of ESBLs production among Enterobacteriaceae. In addition, understanding the mode of action and mechanisms of resistance to beta-lactam antibiotics, and the epidemiology of ESBLs producing bacteria is of paramount.
Highlights
Production of these enzymes is encoded by genes which may be found on bacterial chromosome or cytoplasmic mobile genetic elements (MGEs) e.g., harboring of conjugative plasmids is common
In developed countries the proportion of extended spectrum beta-lactamases (ESBLs) producing bacteria causing infections is below 14% whereby in developing countries the proportion of ESBLs producing bacteria causing diseases is above 50% [23]
Clinical and Laboratory Standards Institute (CLSI) screening methods Method I: CLSI disc diffusion method The CLSI is recommending on the use of beta-lactam antibiotics by disc diffusion method in screening for ESBLs production among gram negative bacteria, E. coli, K. pneumoniae, K. oxytoca and P. mirabilis [32]
Summary
Beta-lactam antibiotics namely penicillins e.g., ampicillin, amoxycillin, and piperacillin; cephalosporins: first generation (e.g., cefazolin and cephalexin), second generation (e.g., cefotetan, cefoxitin and cefuroxime), third generation (e.g., ceftriaxone, cefotaxime and cefixime), fourth generation (e.g., cefepime) and fifth generation (e.g., ceftaroline); monobactams e.g., aztreonam; and carbapenems e.g., meropenem and imipenem, have a beta-lactam ring in their molecular structure [1,2,3]. Betalactam ring in beta-lactam antibiotics resemble D-alanyl-D-alanine competitively acts as substrate and covalently binds to peptidoglycan transpeptidase enzyme [5]. This enzymatic reaction is irreversible resulting to bacteriolysis and cell death [4, 6, 7]. Production of these enzymes is encoded by genes which may be found on bacterial chromosome or cytoplasmic mobile genetic elements (MGEs) e.g., harboring of conjugative plasmids is common. ESBLs are effective in hydrolyzing penicillins, cephalosporins (1st, 2nd and 3rd generations) and monobactams but have poor or no effect against methoxy-cephalosporins (i.e., cephamycins) and carbapenems They are inhibited by beta-lactamase inhibitors such as sulbactam, tazobactam and clavulanic acid [11]. The resistant bacteria and their ARGs are transmitted locally (between health-care facilities and communities within the same region or country) and internationally between countries by geographical migrations of carriers e.g., humans and animals colonized with ESBL producing bacteria
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