Risk factors for acquisition of multidrug-resistant Escherichia coli and development of community-acquired urinary tract infections.

We examined risk factors associated with the intestinal acquisition of antimicrobial-resistant extraintestinal pathogenic Escherichia coli (ExPEC) and development of community-acquired urinary tract infection (UTI) in a case-control study of young women across Canada. A total of 399 women were recruited; 164 women had a UTI caused by E. coli resistant to ⩾1 antimicrobial classes and 98 had a UTI caused by E. coli resistant to ⩾3 antimicrobial classes. After adjustment for age, student health service (region of Canada) and either prior antibiotic use or UTI history, consumption of processed or ground chicken, cooked or raw shellfish, street foods and any organic fruit; as well as, contact with chickens, dogs and pet treats; and travel to Asia, were associated with an increased risk of UTI caused by antimicrobial resistant E. coli. A decreased risk of antimicrobial resistant UTI was associated with consumption of apples, nectarines, peppers, fresh herbs, peanuts and cooked beef. Drug-resistant UTI linked to foodborne and environmental exposures may be a significant public health concern and understanding the risk factors for intestinal acquisition of existing or newly emerging lineages of drug-resistant ExPEC is important for epidemiology, antimicrobial stewardship and prevention efforts.

Escherichia coli and urinary tract infections: the role of poultry-meat.

Extraintestinal pathogenic Escherichia coli (ExPEC) is the most common cause of community-acquired and hospital-acquired extraintestinal infections. The hypothesis that human ExPEC may have a food animal reservoir has been a topic of investigation by multiple groups around the world. Experimental studies showing the shared pathogenic potential of human ExPEC and avian pathogenic E. coli suggest that these extraintestinal E. coli may be derived from the same bacterial lineages or share common evolutionary roots. The consistent observation of specific human ExPEC lineages in poultry or poultry products, and rarely in other meat commodities, supports the hypothesis that there may be a poultry reservoir for human ExPEC. The time lag between human ExPEC acquisition (in the intestine) and infection is the fundamental challenge facing studies attempting to attribute ExPEC transmission to poultry or other environmental sources. Even whole genome sequencing efforts to address attribution will struggle with defining meaningful genetic relationships outside of a discrete food-borne outbreak setting. However, if even a fraction of all human ExPEC infections, especially antimicrobial-resistant ExPEC infections, is attributable to the introduction of multidrug-resistant ExPEC lineages through contaminated food product(s), the relevance to public health, food animal production and food safety will be significant.

Measuring antimicrobial use in hospitalized patients: a systematic review of available measures applicable to paediatrics.

OBJECTIVES: The optimal measure to use for surveillance of antimicrobial usage in hospital settings, especially when including paediatric populations, is unknown. This systematic review of literature aims to list, define and compare existing measures of antimicrobial use that have been applied in settings that included paediatric inpatients, to complement surveillance of resistance. METHODS: We identified cohort studies and repeated point-prevalence studies presenting data on antimicrobial use in populations of inpatients or validations/comparisons of antimicrobial measures through a systematic search of literature using MEDLINE, EMBASE, CINAHL and LILACS (1975-2011) and citation tracking. Study populations needed to include hospitalized paediatric patients. Two reviewers independently extracted data on study characteristics and results. RESULTS: Overall, 3878 records were screened and 79 studies met selection criteria. Twenty-six distinct measures were found, the most frequently used being defined daily doses (DDD)/patient-days and exposed patients/patients. Only two studies compared different measures quantitatively, showing (i) a positive correlation between proportion of exposed patients and antimicrobial-days/patient-days and (ii) a strong correlation between doses/patient-days and agent-days/patient-days (r = 0.98), with doses/patient-days correlating more with resistance rates (r = 0.80 versus 0.55). CONCLUSIONS: The measure of antimicrobial use that best predicts antimicrobial resistance prevalence and rates, for surveillance purposes, has still not been identified; additional evidence on this topic is a necessity.

A systematic review of outbreak and non-outbreak studies of extraintestinal pathogenic Escherichia coli causing community-acquired infections.

A systematic review of outbreak and non-outbreak studies of infections caused by extraintestinal pathogenic Escherichia coli (ExPEC) was conducted. This review examines the epidemiology, seasonality, source or mode of transmission, and temporal changes, based on E. coli serogroup, in ExPEC causing sporadic vs. outbreak-associated infections. Twelve outbreak and 28 non-outbreak studies were identified. The existence of ExPEC outbreaks was well supported. Three of four outbreak reports indicated peak periods during the winter months. Serogroups associated with outbreak infections ranged from 1% to 26% (average 11·4%) vs. (range 1-15%, average 3·5%) for serogroups associated with sporadic infections; the distribution of serogroups also differed for outbreak and non-outbreak infections. Study authors indicated that the outbreaks may have resulted from foodborne transmission, but direct evidence was unavailable. This review provides evidence that the epidemiology of endemic vs. epidemic ExPEC infections differs; however, study reporting quality limited epidemiological inferences.

The changing prevalence of drug-resistant Escherichia coli clonal groups in a community: evidence for community outbreaks of urinary tract infections.

A multidrug-resistant clonal group (CgA) of Escherichia coli was shown to cause half of all trimethoprim-sulphamethoxazole (TMP-SMZ)-resistant urinary tract infections (UTIs) in a college community between October 1999 and January 2000. This second study was conducted to determine the fate of CgA. Urine E. coli isolates from women with UTI, collected between October 2000 and January 2001, were tested for antibiotic susceptibility, O serogroup, ERIC2 PCR and DNA macrorestriction patterns using pulsed-field gel electrophoresis. The proportion of UTIs caused by CgA declined by 38% (P<0.001) but the prevalence of resistance to TMP-SMZ did not change. Six additional clonal groups were identified and these were responsible for 32% of TMP-SMZ-resistant UTIs. The temporal decline in the proportion of UTIs caused by CgA provides evidence that CgA caused a community outbreak of UTI. The fluctuation and occurrence of other E. coli clonal groups in this community suggest that a proportion of community-acquired UTIs may be caused by E. coli disseminated from one or more point sources.

Widespread distribution of urinary tract infections caused by a multidrug-resistant Escherichia coli clonal group.

BACKGROUND: The management of urinary tract infections is complicated by the increasing prevalence of antibiotic-resistant strains of Escherichia coli. We studied the clonal composition of E. coli isolates that were resistant to trimethoprim-sulfamethoxazole from women with community-acquired urinary tract infections. METHODS: Prospectively collected E. coli isolates from women with urinary tract infections in a university community in California were evaluated for antibiotic susceptibility, O:H serotype, DNA fingerprinting, pulsed-field gel electrophoretic pattern, and virulence factors. The prevalence and characteristics of an antibiotic-resistant clone were evaluated in this group of isolates and in those from comparison cohorts in Michigan and Minnesota. RESULTS: Fifty-five of the 255 E. coli isolates (22 percent) from the California cohort were resistant to trimethoprim-sulfamethoxazole as well as other antibiotics. There was a common pattern of DNA fingerprinting, suggesting that the isolates belonged to the same clonal group (clonal group A), in 28 of 55 isolates with trimethoprim-sulfamethoxazole resistance (51 percent) and in 2 of 50 randomly selected isolates that were susceptible to trimethoprim-sulfamethoxazole (4 percent, P<0.001). In addition, 11 of 29 resistant isolates (38 percent) from the Michigan cohort and 7 of 18 (39 percent) from the Minnesota cohort belonged to clonal group A. Most of the clonal group A isolates were serotype O11:H(nt) or O77:H(nt), with similar patterns of virulence factors, antibiotic susceptibility, and electrophoretic features. CONCLUSIONS: In three geographically diverse communities, a single clonal group accounted for nearly half of community-acquired urinary tract infections in women that were caused by E. coli strains with resistance to trimethoprim-sulfamethoxazole. The widespread distribution and high prevalence of E. coli clonal group A has major public health implications.

Analysis of virulence of clinical isolates of Salmonella enteritidis in vivo and in vitro.

Salmonella enterica serotype Enteritidis (S. enteritidis) is a major food-borne pathogen, and its incidence among all Salmonella serotypes has increased dramatically in the last two decades. To study the virulence characteristics of clinical isolates of S. enteritidis, we determined the 50% lethal doses (LD(50)) in mice of isolates of two major phage types (4 and 8). Isolates of both phage types showed a wide range of LD(50) after oral inoculation, varying from under 10(2) organisms to over 10(8) organisms. No significant difference in LD(50) was observed between the phage types. These observations indicated that clinical isolates of S. enteritidis are highly heterogeneous in their ability to cause death in mice. We compared the LD(50)s of these isolates to the results observed from in vitro pathogenicity assays. We also analyzed these isolates for recognized Salmonella virulence loci (spv, sodCI, sopE, and sef). The in vitro phenotypes of the isolates showed no obvious correlation with their LD(50) in any given assay, and the virulence genes tested were present in all isolates. However, the isolate with the lowest LD(50) (isolate 97A 2472) was resistant to acidified sodium nitrite (ASN). Moreover, the most acid-susceptible, macrophage-susceptible, and ASN-susceptible isolates were attenuated for virulence in mice. These results, based on extensive analysis of clinical isolates of S. enteritidis, demonstrate the complex nature of Salmonella pathogenesis in mice. Our results also indicate the limitation of in vitro assays in predicting in vivo virulence.