Investigates the genetic location and coexistence of resistance genes in E. coli isolates, suggesting a need for enhanced antibiotic monitoring.
Introduction: Escherichia coli resistance to aminoglycosides is a major obstacle to the treatment of nosocomial infections. This resistance is often promoted by aminoglycoside-modifying enzymes (AMEs) encoded by genes such as aac(6′)-II, aac(3)-II, aph(3′)-VI, and ant(3″)-I. Objective: To study the coexistence and genetic localization of aac(6′)-II, aac(3)-II, aph(3′)-VI, and ant(3″)-I genes in clinical isolates of E. coli obtained at Saint-Camille Hospital in Ouagadougou and exhibiting a phenotype resistant to at least one of the aminoglycosides tested. Methodology: E. coli isolates were identified using standard microbiological methods and tested for susceptibility to aminoglycosides according to CA-SFM recommendations. Resistance genes were detected using conventional PCR, and their genetic support was evaluated by plasmid extraction and targeted amplification. Results: E. coli accounted for 191/300 (63.66%) of the isolates analyzed. The resistance rates observed were 91 (47.6%) for streptomycin, 42 (22.0%) for kanamycin, 36 (18.8%) for gentamicin, and 3 (1.6%) for amikacin. The presence of the aac(6′)-II, aac(3)-II, ant(3″)-I, and aph(3′)-VI genes was observed in 89 (87.3%), 38 (37.3%), 33 (32.4%), and 2 (2.0%) of E. coli isolates, respectively. In addition, the aac(6’)-II and ant(3”)-I genes coexisted in 21 (20.58%) of isolates, while the aac(3)-II and aph(3’)-VI genes were simultaneously present in 2 (2.0%) of isolates. A significant correlation was observed between aac(3)-II and resistance to various aminoglycosides, as well as between aph(3’)-VI and resistance to neomycin and netilmicin (p < 0.05). The majority of aac(6’)-II genes 88 (98.88%) were located on chromosomes, while 26 (68.42%) of the aac(3)-II genes identified were found on plasmids. Conclusion: These results highlight the importance of monitoring the evolution of antibiotic resistance and promoting the judicious use of antibiotics to limit the spread of such resistance.
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