Co-resistance to Aminoglycosides and Fluoroquinolones in Carbapenemase-Producing Bacteria from Nigerian Hospital Sewage

Abstract

Background: Hospital sewage systems function as high-kinetic biological reactors that accelerate the convergence of diverse resistance determinants. This study investigated the phenotypic and genotypic landscapes of carbapenemase-producing bacteria (CPB) in effluent from a Nigerian tertiary hospital, focusing on the critical co-resistance between aminoglycosides and fluoroquinolones.

Methods: Environmental surveillance at the University of Ilorin Teaching Hospital (UITH) yielded 196 isolates. Identification and susceptibility profiling were conducted via VITEK® 2 and Kirby-Bauer methods. Carbapenemase activity was confirmed using the Modified Carbapenem Inactivation Method (mCIM). Molecular characterization of resistance genes (bla NDM, bla OXA−48, bla VIM, bla KPC, bla IMP) and the colistin-resistance marker (mcr−1) was achieved through multiplex PCR and genomic sequencing.

Results: While Enterobacteriaceae predominated (81.6%), significant carbapenem-resistant non-fermenters, including Burkholderia cepacia and Stenotrophomonas maltophilia, were recovered. A defining finding was the extensive co-resistance to fluoroquinolones and aminoglycosides; ciprofloxacin resistance was rampant (up to 50.0%), whereas amikacin efficacy remained robustly preserved (>90%), identifying a narrow therapeutic window. Genotypically, bla NDM (64.0%) was the primary driver. Notably, the co-carriage of bla NDM and mcr−1 in E. coli signaled a transition toward total-drug resistance (TDR). Genomic analysis established 100% clonal synteny between ICU clinical strains and environmental isolates.

Conclusion: Hospital sewage acts as a stable gateway for the dissemination of co-resistant "superbugs." The convergence of carbapenemase and fluoroquinolone resistance markers proves that clinical pathogens are actively seeding the environmental interface.