Phenotypic and molecular characterization of antimicrobial resistant Escherichia coli from urinary tract infections in Port-Harcourt, Nigeria.

INTRODUCTION

Multidrug resistance among Escherichia coli causing Urinary Tract Infections (UTIs) is a major public health problem, threatening the effective treatment of UTIs. This study investigated the phenotypic and molecular characteristics of E. coli associated with UTIs in Port-Harcourt, Nigeria.

METHODS

Twenty-five non-duplicate isolates of E. coli from UTIs patients at the University of Port-Harcourt Teaching Hospital, Nigeria were identified using Matrix-Assisted Laser Desorption Ionization Time-of-Flight (MALDI-TOF) Mass Spectrometry. The antimicrobial susceptibility patterns were determined using Kirby-Bauer disc diffusion technique. Phenotypic expression of Extended Spectrum Beta Lactamases (ESBLs) and AmpC beta-lactamase were determined using standard laboratory methods and polymerase chain reaction (PCR) was used to detect ESBLs, AmpC, Quinolones and Aminoglycosides resistance genes.

RESULTS

The isolates exhibited high rates of resistance to co-trimoxazole (76%), nalidixic acid (68%), ciprofloxacin (60%), gentamicin (44%) and low resistance to cefotaxime (20%) but were fully susceptible to cefoperazone/sulbactam, amikacin, nitrofurantoin, colistin and carbapenems. Phenotypic expression of ESBLs was recorded in 6(24%) isolates while genotypic detection revealed the highest prevalence of blaTEM 22(88%), followed by blaCTX-M-15 16(64%), blaSHV 7(28%) and blaOXA-1 6(24%) while AmpC (blaCMY-2) gene was detected in 8(32%) isolates. Amongst the quinolone resistant isolates, qnr variants (qnrB, qnrD and qnrS) and aac(6')-Ib genes were detected in 7(28%) and 3(12%) isolates respectively while all gentamicin resistant isolates possessed the aacC2 gene. The co-expression of blaCTX-M-15 with quinolones and aminoglycoside genes were 20% and 40% respectively. The prevalence of multiple drug resistance was 52%.

CONCLUSION

A high proportion of the studied E. coli isolates co-expressed ESBLs, quinolones and aminoglycosides resistance genes which call for prompt antibiotic stewardship and preventive strategies to limit the spread of these genes.