Coexistence and Genetic Location of Aminoglycoside-Modifying Enzyme Genes in Clinical Escherichia coli Isolates from a Tertiary Hospital in Ouagadougou.

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.