blaCTX-M-G1 and blaNDM genes in ESBL bacilli isolated at Schiphra Protestant Hospital, Ouagadougou, Burkina Faso
- African Journal of Biotechnology , 25 (1) : 1-8
Résumé
Gram-negative bacilli producing extended-spectrum β-lactamases (ESBLs) are multidrug-resistant bacteria that pose significant therapeutic challenges. Their infections often necessitate the use of broad-spectrum antibiotics such as carbapenems, which has contributed to the emergence of metallo β-lactamases. Among these, New Delhi metallo-β-lactamase (NDM) is a relatively recent enzyme associated with resistance to multiple classes of antibiotics. The objective of this study was to characterize the blaCTX-M group 1 (blaCTX-M-G1) and blaNDM resistance genes in ESBL-producing Gramnegative bacilli. This study included 63 bacterial strains, mainly Escherichia coli and Klebsiella pneumoniae, isolated from clinical specimens collected at the Siphra Hospital Center in Ouagadougou. Antimicrobial susceptibility testing and ESBL phenotyping were performed using the Mueller–Hinton agar disk diffusion method. Detection of resistance genes was carried out using conventional polymerase chain reaction (PCR). Among the bacterial strains analyzed, 92.06% were confirmed ESBL producers. PCR analysis revealed that 89.66% of the isolates harbored at least one of the resistance genes investigated. The blaCTX-M-G1 gene was detected in 87.93% of the strains, while the blaNDM gene was present in 29.31%. Coexistence of blaCTX-M-G1 and blaNDM genes was observed in 27.59% of the isolates. A high proportion of the bacterial strains exhibited resistance mediated by CTX-M–type ESBL production. Notably, a substantial proportion of these strains also harbored the blaNDM gene. These findings highlight the urgent need to implement effective infection control and antimicrobial stewardship measures to slow the emergence and spread of ESBL-producing Gram-negative bacilli and to preserve the effectiveness of last-resort antibiotics.
Mots-clés
Gram-negative bacilli, extended-spectrum β-lactamases, blaCTX-M-G1, blaNDM.