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.

Clustering of cases of Mycobacterium fortuitum infection investigated by molecular typing

Organisms of the Mycobacterium fortuitum complex are recognised but uncommon causes of pulmonary disease, primary cutaneous disease and a wide spectrum of nosocomial infections. M fortuitum was isolated from 20 patients over a 15 month period, with an apparent clustering of isolates occurring from January to March 1994. The molecular epidemiology of this clustering was investigated using an arbitrary primer polymerase chain reaction method (AP-PCR). 21 isolates were studied, which yielded 13 distinct profiles. Multiple isolates from a single patient yielded identical profiles. All of seven isolates recovered during the six week period from January to March 1994 shared a common profile which was distinct from all other isolates, suggesting that a single strain was isolated from specimens from all seven patients. The source of this cluster is uncertain. We can find no epidemiological basis for an episode of cross-infection within the hospital environment, and it is assumed that contamination of the specimens during collection, transport or processing was responsible for the [quot ]pseudo-outbreak[quot ] of M fortuitum.