Antibiotic resistance profiles and co-occurrence of ESBL and AmpC β-lactamase genes in ESBL-producing Gram-negative bacteria of clinical origin

Abstract

Abstract The hospital setting provides a critical environment for understanding the public health implications of antibiotic resistance, given the diversity of clinical samples and bacteria encountered. This study investigated the resistotyping and detection of ESBL and AmpC β-lactamases in clinical Gram-negative bacteria. Bacteria were obtained from the laboratory benches of a Teaching Hospital in Nigeria for three months, and identified. Antibiotic susceptibility was carried out using the disc diffusion method, while detection of ESBL production was done using the Double Disc Synergy Test (DDST). Biofilm formation by the isolates was detected using the Tissue Culture Plate method. Screening for hypermucoviscosity in Klebsiella pneumoniae isolates was done using the string test. Genotyping of the ESBL-producing isolates for ESBL and AmpC β-lactamases was done using primer-specific PCR. Seventy-two isolates [( Klebsiella (38), Pseudomonas (14), Escherichia (12), Enterobacter (5), Hafnia (1), Acinetobacter (1) and Morganella (1)] were identified. The resistance of the isolates to the antibiotics was: amoxicillin-clavulanate (69.4%), cefepime (59.7%), ceftriaxone and azithromycin (56.9% each), aztreonam 54.2%, gentamicin (52.8%), ampicillin-sulbactam (48.6%), ciprofloxacin (45.8), ceftazidime (38.9%), cefoxitin (36.1%) and cefuroxime (19.4%). Fifty-three isolates (73.6%) had multidrug-resistant phenotypes and 21 were ESBL producers. Thirty-five of the total isolates were biofilm producers, while 21.1% of the Klebsiella pneumoniae were hypermucoviscous. The frequency of genes in the 21 ESBL producers was bla TEM (35.3%), bla CTX−M (29.4%), bla SHV (23.5%) and bla CMY (11.8%). The occurrence of MDR and ESBL-producing bacteria from clinics raises alarm on the need to further educate people on the consequences of indiscriminate usage of antibiotics without prescription.