In 1987, 93 Escherichia coli O157:H7 isolates were collected during routine surveillance for this pathogen in the state of Washington. Toxin genotypes and plasmid profiles were correlated with the clinical sequelae of illness in 88 of the 93 patients from whom these strains were isolated. Thirteen plasmid patterns were observed among the 88 tested isolates; four patterns accounted for 82% of the isolates. Genetic probing for Shiga-like toxins (SLT) I and II demonstrated the presence of both genes in 67 (76%), SLT I alone in three (3%), and SLT II alone in 18 (20%). The hemolytic uremic syndrome or thrombotic thrombocytopenic purpura developed in seven (39%) of 18 patients infected with isolates having only the SLT II gene, while these complications occurred in only four (6%) of 70 patients infected with isolates having the other two genotypes (relative risk, 6.8; 95% confidence interval, 1.9, 26.4). This study shows that E. coli O157:H7 isolates systematically collected from a single geographic region over a defined time period exhibit considerable diversity in plasmid content and toxin genotype and that the toxin genotype of the infecting strain may influence the risk of developing microangiopathic sequelae.

Standard procedures at a state-of-the-art plant that produced unpasteurized juices were inadequate to eliminate contamination with E. coli O157:H7. This outbreak demonstrated that unpasteurized juices must be considered a potentially hazardous food and led to widespread changes in the fresh juice industry.

ABSTRACT. Objective. To evaluate risk factors for progression of Escherichia coli O157:H7 infection to the hemolytic uremic syndrome (HUS).Study Design. We conducted a retrospective cohort study among 278 Washington State children <16 years old who developed symptomatic culture-confirmed E coli O157:H7 infection during a large 1993 outbreak. The purpose of the study was to determine the relative risk (RR) of developing HUS according to demographic characteristics, symptoms, laboratory test results, and medication use in the first 3 days of illness.Results. Thirty-seven (14%) children developed HUS. In univariate analysis, no associations were observed between HUS risk and any demographic characteristic, the presence of bloody diarrhea or of fever, or medication use. In multivariate analysis, HUS risk was associated with, in the first 3 days of illness, use of antimotility agents (odds ratio [OR] ‫؍‬ 2.9; 95% confidence interval [CI] 1.2-7.5) and, among children <5.5 years old, vomiting (OR ‫؍‬ 4.2; 95% CI 1.4 -12.7). Among the 128 children tested, those whose white blood cell (WBC) count was 13 000/L in the first 3 days of illness had a 7-fold increased risk of developing HUS (RR 7.2; 95% CI 2.8 -18.5). Thirteen (38%) of the 34 patients with a WBC count 13 000/L developed HUS, but only 5 (5%) of the 94 children whose initial WBC count was <13 000/L progressed to HUS. Among children who did not develop HUS, use of antimotility agents in the first 3 days of illness was associated with longer duration of bloody diarrhea.Conclusions. Prospective studies are needed to further evaluate measures to prevent the progression of E coli O157:H7 infection to HUS and to assess further clinical and laboratory risk factors. These data argue against the use of antimotility agents in acute childhood diarrhea. Our finding that no intervention decreased HUS risk underscores the importance of preventing E coli O157:H7 infections. Pediatrics 1997;100(1). URL: http:// www.pediatrics.org/cgi/content/full/100/1/e12; antibiotics, antimotility agents, Escherichia coli O157:H7, kidney failure, leukocytosis.ABBREVIATIONS. HUS, hemolytic uremic syndrome; BUN, blood urea nitrogen; RR, relative risk; CI, confidence interval; TMP/SMZ, trimethoprim/sulfamethoxazole; OR, odds ratio; WBC, white blood cell; Stx, Shiga toxin. E scherichia coli O157:H7 causes bloody and nonbloody diarrhea that progresses to hemolytic uremic syndrome (HUS) in a subset of patients.1,2 Though the gastrointestinal manifestations of infection with E coli O157:H7 can be severe, HUS accounts for the major acute and chronic morbidity and mortality caused by this organism.Associations between certain host-specific factors and the risk of progression of enteric infection with E coli O157:H7 to HUS have been reported. In population-based studies of HUS, age-specific incidence was highest among children Ͻ5 years of age, but these studies did not evaluate risk factors for progression of diarrhea or hemorrhagic colitis to HUS. [3][4][5][6] In some studies of children with E coli O...

WA1 is morphologically indistinguishable but antigenically and genotypically distinct from B. microti. Some patients elsewhere who were assumed to have been infected with B. microti may have been infected with WA1. Improved serodiagnostic and molecular techniques are needed for characterizing Babesia species and elucidating the epidemiology of babesiosis, an emergent zoonosis.

No abstract

In November 1986, a statewide outbreak of Escherichia coli O157:H7 infections in Washington State was identified after a physician in an eastern Washington community hospitalized three patients with hemorrhagic colitis which progressed to thrombotic thrombocytopenic purpura. Epidemiologic investigation identified 37 cases in this community and linked the illnesses to a local restaurant which had served ground beef that was the suspected initial vehicle of transmission. The plasmid profile and toxin production pattern (Shiga-like toxin II alone) of the outbreak strain provided a unique strain marker. E. coli O157:H7 infections caused by this strain were simultaneously seen in other parts of the state among nursing home residents and in patients with the hemolytic-uremic syndrome, and an increase in sporadic cases of hemorrhagic colitis was noted at a Seattle health maintenance organization. It is suspected that a contaminated product, probably ground beef distributed statewide, was the common source. Tracing of this meat led to farms where rectal swabs from six (1%) of 539 cattle tested yielded E. coli O157:H7, although the plasmids and toxin production patterns of these isolates differed from the human outbreak strain. Introduction of a single strain of E. coli O157:H7 has the potential to cause widespread concurrent outbreaks. Such outbreaks are likely to escape recognition until heightened screening and surveillance for E. coli O157:H7 is established.

To analyze the association between the results of routine inspections and foodborne outbreaks in restaurants, we conducted a matched case-control study using available data from Seattle-King County, Washington. Case restaurants were facilities with a reported foodborne outbreak between January 1, 1986 and March 31, 1987 (N=28). Two control restaurants with no reported outbreaks during this period were matched to each case restaurant on county health district and date of routine inspection (N=56). Data from the routine inspection that preceded the outbreak (for case restaurants) or the date-matched routine inspection (for control restaurants) were abstracted from computerized inspection records.

The resistance of Escherichia coli O157:H7 to amoxicillin/clavulanic acid, ampicillin, ceftazidime, ceftriaxone, cefuroxime, cephalothin, chloramphenicol, ciprofloxacin, gentamicin, streptomycin, sulfisoxazole, tetracycline, ticarcillin, tobramycin, and trimethoprim-sulfamethoxazole was examined, and resistant strains were characterized. All 56 isolates collected between 1984 and 1987 were susceptible to all antibiotics tested; 13 (7.4%) of 176 strains isolated between 1989 and 1991 were resistant to streptomycin, sulfisoxazole, and tetracycline. lambda-restriction fragment length polymorphism analysis suggested that the 13 resistant strains belonged to nine different clones. The emerging resistance of E. coli O157:H7 to antibiotics could portend an increased prevalence of this pathogen in food animals that receive antibiotics. Antimicrobial resistance of E. coli O157:H7 could be useful as a rapid epidemiologic marker and as a way to select this pathogen from suspected vehicles of transmission, but this resistance could also complicate therapeutic trials with sulfa-containing antibiotics.