Decoupling Genotype–Phenotype
Resistance type in MDR Klebsiella pneumoniae: Integrative Genomic and Structural
prudence into SULII, SULL and QnrB Determinants
Inas Sattar Abd
Res. J. Biotech.; Vol. 21(2); 271-285;
doi: https://doi.org/10.25303/212rjbt2710285; (2026)
Abstract
Antimicrobial resistance in Klebsiella pneumoniae stays to trial therapeutic efficacy,
predominantly when resistance genes contribute in complex cellular networks rather
than acting as isolated determinants. This study investigates interplay between
plasmid-mediated sulfonamide resistance genes (SULII, SULL) and quinolone resistance
(QnrB) in multidrug-resistant (MDR) clinical isolates, with a focus on how sequence
deviation translates or fails to translate into phenotypic resistance. Ten clinical
isolates were described using a collective phenotypic–genotypic framework, comprising
of antimicrobial susceptibility profiling, biofilm quantification, crystal violet
assay and Sanger sequencing of SULII, SULL and QnrB. Molecular docking was employed
to assess ciprofloxacin interface with the QnrB1 protein to further reveal structural
contributions to resistance.
All isolates accommodated the three target genes and demonstrated either moderate
or strong biofilm formation. Resistance phenotypes revealed no consistent association
with minor allelic variations. Structural modeling discovered an optimal ciprofloxacin–QnrB1
binding energy of −6.08 kcal/mol, supporting a protecting rather than catalytic
mechanism of resistance. Cooperatively, the findings emphasize that resistance in
K. pneumoniae emerges from a multifactorial, network-dependent architecture rather
than single-gene determinants. The study highpoints the limitations of conventional
genotypic markers for prophesy clinical consequences and affirm the need to integrate
whole-genome sequencing, transcriptomic data and structural biology to achieve resistance
that is more accurate in forecasting and amended antibiotic surveillance.
