Distribution of virulence determinants among antimicrobial‑resistant and antimicrobial-susceptible Escherichia coli implicated in urinary tract infections.

Introduction: Uropathogenic Escherichia coli (UPEC) rely on the correlation of virulence expression with antimicrobial resistance to persist and cause severe urinary tract infections (UTIs). Objectives: We assessed the virulence pattern and prevalence among UPEC strains susceptible and resistant to multiple antimicrobial classes. Methods: A total of 174 non‑duplicate UPEC strains from patients with clinically significant UTIs were analysed for susceptibility to aminoglycoside, antifolate, cephalosporin, nitrofuran and quinolone antibiotics for the production of extended‑spectrum β‑lactamases and for the presence of six virulence determinants encoding adhesins (afimbrial, Type 1 fimbriae, P and S‑fimbriae) and toxins (cytotoxic necrotising factor and haemolysin). Results: Relatively high resistance rates to nalidixic acid, ciprofloxacin, cephalothin and trimethoprim‑sulfamethoxazole (82%, 78%, 62% and 59%, respectively) were observed. Fourteen distinct patterns were identified for the virulence determinants such as afaBC, cnfI, fimH, hylA, papEF and sfaDE. The toxin gene, cnfI (75.3%), was the second most prevalent marker to the adhesin, fimH (97.1%). The significant association of sfaDE/hylA (P < 0.01) among antimicrobial resistant and susceptible strains was also observed notwithstanding an overall greater occurrence of virulence factors among the latter. Conclusions: This study provides a snapshot of UPEC complexity in Jamaica and highlights the significant clonal heterogeneity among strains. Such outcomes emphasise the need for evidence‑based strategies in the effective management and control of UTIs.

The emergence of qnr-mediated quinolone resistance among Enterobacteriaceae in Jamaica / Surgimiento de la resistencia a las quinolonas mediada por qnr entre las Enterobacteriaceae en Jamaica

OBJECTIVE: Quinolone resistance is usually caused by various chromosomal mutations, but has been more recently associated with plasmids which carry the qnr determinant. The aim of this study is to investigate the prevalence of qnr genes in clinical isolates of Enterobacteriaceae in Jamaica. METHODS: A total of 255 non-duplicate fluoroquinolone-resistant Enterobacteriaceae clinical isolates, comprising 232 Escherichia coli, 20 Klebsiella species and three Enterobacter spp were collected between October 2007 and November 2008 from hospitalized patients in Jamaica. The presence of the qnr gene was screened by PCR using specific primers for qnrA, qnrB and qnrS in extracted plasmid DNA. RESULTS: Eighty-three (32.5%) of these isolates were qnr-positive, of which 47.0% housed the qnrA gene only, 1.2% qnrB and 9.6% qnrS only. Another 36.1% possessed both qnrA and qnrS genes. Approximately 30% of the quinolone-resistant E coli isolates harboured the qnr gene while 50% Klebsiella spp and all Enterobacter spp were positive. CONCLUSION: The emergence of qnr-mediated quinolone resistance among clinical Enterobacteriaceae isolates is described for the first time in Jamaica.

OBJETIVO: La resistencia a la quinolona es generalmente causada por varias mutaciones cromosomáticas, pero más recientemente ha sido asociada con plásmidos portadores del determinante qnr. El objetivo de este estudio fue investigar la prevalencia de genes qnr en los aislados clínicos de Enterobacteriaceae en Jamaica. MÉTODOS: Un total de 255 aislados clínicos no duplicados de Enterobacteriaceae resistentes a la fluoroquinolona, incluyendo 232 de Escherichia coli, 20 especies de Klebsiella y tres Enterobacter spp, fueron recogidos entre octubre de 2007 y noviembre de 2008, de pacientes hospitalizados en Jamaica. La presencia del gen qnr fue tamizada mediante marcadores PCR, usando primers específicos para qnrA, qnrB y qnrS en el ADN plásmido extraído. RESULTADOS: Ochenta y tres (32.5%) de éstos aislados fueron qnr-positivos. De ellos, 47.0% alojaban solamente el gen qnrA, 1.2% el qnrB y 9.6% el qnrS solamente. Otro 36.1% poseía tanto genes qnrA cuanto genes qnrS. Aproximadamente 30% de los aislados E. coli resistentes a la quinolona, albergaban el gen qnr mientras que 50% de Klebsiella spp y todas las Enterobacter spp fueron positivas. CONCLUSIÓN: Se describe por primera vez el surgimiento de la resistencia a las quinolonas mediada por qnr en Jamaica.

Prevalence of chronic renal failure in the diabetic population at the University Hospital of the West Indies

The prevalence of chronic renal failure (CRF) in 460 patients with diabetes mellitus attending the diabetic outpatient clinic at the University Hospital of the West Indies in Jamaica was determined from a review of medical records. The prevalence of CRF was 10 (39/386) in the diabetic clinic population. Significant positive associations with CRF were found with male gender (20/98, 20 vs 19/287, 7; odds ratio (OR), 3.24; p = 0.001); age 60 years and older (22/162; 14 vs 17/221, 8; OR, 2.01; p = 0.04); fasting blood glucose concentrations exceeding 8.0 mmol/L (22/162, 13 vs 12/182, 7; OR, 2.08; p = 0.05); the presence of significant proteinuria as a marker for outcome (13/39, 33 vs 48/346, 14; OR, 3.60; p = 0.02) and peripheral vascular disease (6/20, 30 vs 139/386, 10; OR, 4.75; p = 0.005). The prevalence of CRF did not differ significantly between patients with Type 1 and Type 2 diabetes mellitus. Also, the presence of CRF was not significantly associated with duration of diabetes mellitus, type of hypoglycaemic agents used, or history of hypertension. However, the presence of persistent proteinuria was significantly associated with duration of diabetes mellitus exceeding five years (46/255, 17 vs 11/149, 7; OR, 2.52; p = 0.005) and a history of hypertension (41/235, 17 vs 20/198, 10; OR, 1.88; p = 0.03) but not with age or gender. This study emphasizes the need to evaluate patients with diabetes mellitus for renal impairment so that intervention strategies may be adopted early to delay progression to endstage renal disease