Risk Factors for Non-O157 Shiga Toxin-Producing Escherichia coli Infections, United States.

Shiga toxin-producing Escherichia coli (STEC) causes acute diarrheal illness. To determine risk factors for non-O157 STEC infection, we enrolled 939 patients and 2,464 healthy controls in a case-control study conducted in 10 US sites. The highest population-attributable fractions for domestically acquired infections were for eating lettuce (39%), tomatoes (21%), or at a fast-food restaurant (23%). Exposures with 10%-19% population attributable fractions included eating at a table service restaurant, eating watermelon, eating chicken, pork, beef, or iceberg lettuce prepared in a restaurant, eating exotic fruit, taking acid-reducing medication, and living or working on or visiting a farm. Significant exposures with high individual-level risk (odds ratio >10) among those >1 year of age who did not travel internationally were all from farm animal environments. To markedly decrease the number of STEC-related illnesses, prevention measures should focus on decreasing contamination of produce and improving the safety of foods prepared in restaurants.

Risk of Hemolytic Uremic Syndrome Related to Treatment of Escherichia coli O157 Infection with Different Antimicrobial Classes.

Treatment of Shiga toxin-producing Escherichia coli O157 (O157) diarrhea with antimicrobials might alter the risk of hemolytic uremic syndrome (HUS). However, full characterization of which antimicrobials might affect risk is lacking, particularly among adults. To inform clinical management, we conducted a case-control study of residents of the FoodNet surveillance areas with O157 diarrhea during a 4-year period to assess antimicrobial class-specific associations with HUS among persons with O157 diarrhea. We collected data from medical records and patient interviews. We measured associations between treatment with agents in specific antimicrobial classes during the first week of diarrhea and development of HUS, adjusting for age and illness severity. We enrolled 1308 patients; 102 (7.8%) developed confirmed HUS. Antimicrobial treatment varied by age: <5 years (12.6%), 5-14 (11.5%), 15-39 (45.4%), ≥40 (53.4%). Persons treated with a ß-lactam had higher odds of developing HUS (OR 2.80, CI 1.14-6.89). None of the few persons treated with a macrolide developed HUS, but the protective association was not statistically significant. Exposure to "any antimicrobial" was not associated with increased odds of HUS. Our findings confirm the risk of ß-lactams among children with O157 diarrhea and extends it to adults. We observed a high frequency of inappropriate antimicrobial treatment among adults. Our data suggest that antimicrobial classes differ in the magnitude of risk for persons with O157 diarrhea.

Genetic Susceptibility to Postdiarrheal Hemolytic-Uremic Syndrome After Shiga Toxin-Producing Escherichia coli Infection: A Centers for Disease Control and Prevention FoodNet Study.

Background: Postdiarrheal hemolytic-uremic syndrome (D+HUS) following Shiga toxin-producing Escherichia coli (STEC) infection is a serious condition lacking specific treatment. Host immune dysregulation and genetic susceptibility to complement hyperactivation are implicated in non-STEC-related HUS. However, genetic susceptibility to D+HUS remains largely uncharacterized. Methods: Patients with culture-confirmed STEC diarrhea, identified through the Centers for Disease Control and Prevention FoodNet surveillance system (2007-2012), were serotyped and classified by laboratory and/or clinical criteria as having suspected, probable, or confirmed D+HUS or as controls and underwent genotyping at 200 loci linked to nondiarrheal HUS or similar pathologies. Genetic associations with D+HUS were explored by multivariable regression, with adjustment for known risk factors. Results: Of 641 enrollees with STEC O157:H7, 80 had suspected D+HUS (41 with probable and 32 with confirmed D+HUS). Twelve genes related to cytokine signaling, complement pathways, platelet function, pathogen recognition, iron transport, and endothelial function were associated with D+HUS in multivariable-adjusted analyses (P ≤ .05). Of 12 significant single-nucleotide polymorphisms (SNPs), 5 were associated with all levels of D+HUS (intergenic SNP rs10874639, TFRC rs3804141, EDN1 rs5370, GP1BA rs121908064, and B2M rs16966334), and 7 SNPs (6 non-complement related) were associated with confirmed D+HUS (all P < .05). Conclusions: Polymorphisms in many non-complement-related genes may contribute to D+HUS susceptibility. These results require replication, but they suggest novel therapeutic targets in patients with D+HUS.

Infections in pediatric postdiarrheal hemolytic uremic syndrome: factors associated with identifying shiga toxin-producing Escherichia coli.

OBJECTIVE: To describe pathogens identified through routine clinical practice and factors associated with identifying Shiga toxin-producing Escherichia coli (STEC) infection in patients with postdiarrheal hemolytic uremic syndrome (DHUS). DESIGN: Population-based active surveillance. SETTING: Hospitals in the FoodNet surveillance areas from 2000 through 2010. PARTICIPANTS: Children younger than 18 years with DHUS. MAIN EXPOSURES: Testing for STEC and demographic and clinical characteristics. MAIN OUTCOME MEASURES: Percentage of patients with evidence of infection with likely HUS-causing agents and associations between exposures and evidence of STEC infection. RESULTS: Of 617 patients, 436 (70.7%) had evidence of infection with likely HUS-causing agents: STEC O157 (401 patients), non-O157 STEC (21 patients), O157 and non-O157 STEC (1 patient), Streptococcus pneumoniae (11 patients), and other pathogens (2 patients). Among patients without microbiological evidence of STEC, 76.9% of those tested had serologic evidence of STEC infection. Children more likely to have evidence of STEC infections included those patients tested for STEC less than 4 days after diarrhea onset, 12 months or older (71.6% vs 27.8% if <12 months of age), with infections as part of an outbreak (94.3% vs 67.3%), with bloody diarrhea (77.2% vs 40.4%), with onset during June through September (76.9% vs 60.1%), with a leukocyte count greater than 18 000/µL (to convert to ×10(9)/L, multiply by 0.001) (75.7% vs 65.3%), or with only moderate anemia (hemoglobin 7.0 g/dL [to convert to grams per liter, multiply by 10] or hematocrit greater than 20% [to convert to a proportion of 1, multiply by 0.01]) (75.1% vs 66.3%). However, many of these associations were weaker among children with thorough STEC testing. CONCLUSIONS: Early stool collection for E coli O157 culture and Shiga toxin testing of all children with possible bacterial enteric infection will increase detection of STEC strains causing HUS. In the absence of microbiological evidence of STEC, serologic testing should be performed.

Outbreak of salmonellosis linked to live poultry from a mail-order hatchery.

BACKGROUND: Outbreaks of human salmonella infections are increasingly associated with contact with live poultry, but effective control measures are elusive. In 2005, a cluster of human salmonella Montevideo infections with a rare pattern on pulsed-field gel electrophoresis (the outbreak strain) was identified by PulseNet, a national subtyping network. METHODS: In cooperation with public health and animal health agencies, we conducted multistate investigations involving patient interviews, trace-back investigations, and environmental testing at a mail-order hatchery linked to the outbreak in order to identify the source of infections and prevent additional illnesses. A case was defined as an infection with the outbreak strain between 2004 and 2011. RESULTS: From 2004 through 2011, we identified 316 cases in 43 states. The median age of the patient was 4 years. Interviews were completed with 156 patients (or their caretakers) (49%), and 36 of these patients (23%) were hospitalized. Among the 145 patients for whom information was available, 80 (55%) had bloody diarrhea. Information on contact with live young poultry was available for 159 patients, and 122 of these patients (77%) reported having such contact. A mail-order hatchery in the western United States was identified in 81% of the trace-back investigations, and the outbreak strain was isolated from samples collected at the hatchery. After interventions at the hatchery, the number of human infections declined, but transmission continued. CONCLUSIONS: We identified a prolonged multistate outbreak of salmonellosis, predominantly affecting young children and associated with contact with live young poultry from a mail-order hatchery. Interventions performed at the hatchery reduced, but did not eliminate, associated human infections, demonstrating the difficulty of eliminating salmonella transmission from live poultry.

Strategies for surveillance of pediatric hemolytic uremic syndrome: Foodborne Diseases Active Surveillance Network (FoodNet), 2000-2007.

BACKGROUND: Postdiarrheal hemolytic uremic syndrome (HUS) is the most common cause of acute kidney failure among US children. The Foodborne Diseases Active Surveillance Network (FoodNet) conducts population-based surveillance of pediatric HUS to measure the incidence of disease and to validate surveillance trends in associated Shiga toxin-producing Escherichia coli (STEC) O157 infection. METHODS: We report the incidence of pediatric HUS, which is defined as HUS in children <18 years. We compare the results from provider-based surveillance and hospital discharge data review and examine the impact of different case definitions on the findings of the surveillance system. RESULTS: During 2000-2007, 627 pediatric HUS cases were reported. Fifty-two percent of cases were classified as confirmed (diarrhea, anemia, microangiopathic changes, low platelet count, and acute renal impairment). The average annual crude incidence rate for all reported cases of pediatric HUS was 0.78 per 100,000 children <18 years. Regardless of the case definition used, the year-to-year pattern of incidence appeared similar. More cases were captured by provider-based surveillance (76%) than by hospital discharge data review (68%); only 49% were identified by both methods. CONCLUSIONS: The overall incidence of pediatric HUS was affected by key characteristics of the surveillance system, including the method of ascertainment and the case definitions. However, year-to-year patterns were similar for all methods examined, suggesting that several approaches to HUS surveillance can be used to track trends.

Outbreak of shiga toxin-producing Escherichia coli serotype O26: H11 infection at a child care center in Colorado.

BACKGROUND: Shiga toxin-producing Escherichia coli (STEC) O26:H11 is an emerging cause of disease with serious potential consequences in children. The epidemiology and clinical spectrum of O26:H11 are incompletely understood. We investigated an outbreak of O26:H11 infection among children younger than 48 months of age and employees at a child care center. METHODS: Every employee at the center (n = 20) and every child <48 months (n = 55) were tested for STEC and administered a questionnaire. Thirty environmental health inspections and site visits were conducted. A cohorting strategy for disease control was implemented. RESULTS: Eighteen confirmed and 27 suspect cases were detected. There were no hospitalizations. The illness rate was 60% for children and employees. The risk of being a case in children <36 months was twice the risk among children of 36 to 47 months (risk ratio: 2.10; 95% confidence interval: 1.00, 4.42). The median duration of shedding among symptomatic confirmed cases was 30.5 days (range: 14-52 days). Four (22%) confirmed cases were asymptomatic and 3 (17%) shed intermittently. Nearly half (49%) of the household contacts of confirmed cases developed a diarrheal illness. The outbreak was propagated by person-to-person transmission; cohorting was an effective disease control strategy. CONCLUSIONS: This was the largest reported outbreak of O26:H11 infection in the United States and the largest reported non-O157 STEC outbreak in a US child care center. Non-O157 STEC infection is a differential diagnosis for outbreaks of diarrhea in child care settings. Aggressive disease control measures were effective but should be evaluated for outbreaks in other settings.