Genotypic Characterization of Urinary Tract Infections causing bacteria isolates among Adults at Kiambu Level 5 Hospital, Kenya: Selected Extended Spectrum β-Lactamase genes and Biofilm Formation

Abstract

AbstractThe menace of antimicrobial resistance to public health is constantly arising globally. Many pathogenic bacteria use mechanisms such as mutations and biofilm formation, which significantly reduces efficacy of antimicrobial agents. In this cross-sectional study, we aimed at determining the prevalence of selected extended spectrum β-lactamase (ESβLs) genes and analyse the possible biofilm formation abilities of the isolated bacteria causing urinary tract infection among adult patients seeking medicare at Kiambu Level 5 hospital, Kenya. The double-disk synergy test was used for phenotypic identification of ESβLs producing isolates, while microtiter plate assays with some modifications were used to test biofilm formation analysis. A total of 10 isolates were bioassayed for ESβL genes presence out of 57 bacteria isolates obtained from urine samples. From this study, theblaTEMgenes were found to be the most prevalent ESβLs genes (100%), followed byblaOXAandblaSHVgenes at 40% and 30% respectively. In addition, the co-carriage ofblaTEMandblaSHVwas revealed at 50% lower than that ofblaTEM+ blaOXAgenes at 66.7% among the studyE. coliisolates. Biofilm formation finding disclosed that most of the isolates form biofilms 36 (63.2%), with Gram-negatives being the most biofilm formers 25 (69.4%) compared to the Gram-positive 11 (30.6%).E. coli15(41.7 %),Klebsiella sp. 7(19.4%) andS. aureus7(19.4%) were the most common biofilm formers. Further analysis showed no significant difference in biofilm formation among all tested isolates with a p-value of more than 0.05. However, overall Gram-positive isolates had a significant P-value of 0.056. Although biofilm formation’s impact on urinary tract infections is not fully recognized, the carriage of ESβLs resistance genes and the biofilm formation ability negatively impact effectiveness of UTI treatment. Therefore, we advocate for surveillance studies to map ESβLs distribution and biofilm formation genes among UTI etiological agents to halt UTI treatment failure.