In June 1999, the Tarrant County Health Department reported to the Texas Department of Health (TDH) that a group of teenagers attending a cheerleading camp during June 9--11 became ill with nausea, vomiting, severe abdominal cramps, and diarrhea, some of which was bloody. Two teenagers were hospitalized with hemolytic uremic syndrome (HUS), and two others underwent appendectomies. Routine stool cultures from eight ill persons failed to yield a pathogen. Stools subsequently were sent to laboratories at the Texas Department of Health and CDC, where Escherichia coli O111:H8 was isolated from two specimens. This report summarizes the investigation of this outbreak.

To identify additional cases, surveillance for non-O157 Shiga toxin-producing E. coli (STEC) illnesses in Texas was enhanced by alerting all local health departments, hospitals, clinical laboratories, and physicians about the outbreak. A cohort study of all campers attending the 3-day camp was conducted to identify the source of the outbreak and to collect data describing the clinical illness. Illness was defined as either diarrhea (three or more loose stools during any 24-hour period) accompanied by abdominal cramps or bloody diarrhea alone, occurring within 14 days after the start of the camp. Campers were interviewed for demographic information, medical histories, and symptoms and about their food and beverage consumption during the camp. Sanitarians inspected the cafeteria where meals were prepared and served to campers and the plumbing system in the dormitory where campers resided. Foodhandlers and other kitchen staff were interviewed about food preparation practices, menus, and the delivery schedules and suppliers for food items served to campers. Foodhandlers submitted stool specimens and rectal swabs for testing. Several food items from the cafeteria were cultured.

Of the 650 campers composing the cohort, 521 (80%) were interviewed. Of these, 58 (11%) had illnesses that met the case definition. The median age of the 58 ill persons was 16 years (range: 12--53 years), and 95% were female. The median length of illness was 5 days; four (7%) persons were hospitalized. Two persons developed HUS. In addition to diarrhea, reported symptoms included abdominal cramping (100%), nausea (62%), headache (56%), vomiting (38%), bloody diarrhea (37%), and fever with a median temperature of 100 F (38 C) (29%).

Illnesses peaked on the third and final day of camp (Figure 1). Illnesses with bloody diarrhea peaked on the day after the camp ended. No campers reported having a diarrheal illness or contact with a person with diarrhea during the 2 weeks before the start of camp.

One meal (supper on the first day of camp) and 21 other exposures were significantly associated with risk for developing illness. Of these 21 exposures, 19 were specific food items from among 202 foods and beverages served in the cafeteria during the camp and two were more general exposures. Only the two general exposures were significantly and independently associated with illness: consuming any ice from large trash can-style lined barrels that the camp provided in the dormitory lobby for filling water bottles (73% of ill persons versus 43% of nonill persons) (adjusted odds ratio [AOR]=3.4; 95% confidence interval [CI]=1.8--6.3; p=0.0001) and eating any salad from the cafeteria salad bar on at least one occasion (93% of ill persons versus 79% of nonill persons; AOR=3.5; 95% CI=1.4--11.8; p=0.02).

Inspection of the camp's water systems showed no evidence of plumbing cross-connections or failures that might have led to exposures to contaminated water or waste. Coliform testing of ice from the ice machines used to fill the barrels was negative. Campers reported dipping their drink containers and arms, hands, and heads into the ice. They also reported observing floating debris in the ice barrels. Inspection of the cafeteria and kitchen indicated that kitchen staff may have improperly followed cooking times and temperatures recommendations when preparing meals.

The laboratory investigation of stools specimens submitted by 11 ill persons yielded E. coli O111:H8 from two specimens. Three enrichment broths prepared from these 11 specimens had detectable Shiga toxin when screened with a commercial enzyme immunoassay (EIA). Two of these three EIA-positive stool specimens yielded colonies of Shiga toxin-producing E. coli, which were serotyped as E. coli O111:H8. Both isolates contained gene sequences for Shiga toxins 1 and 2 by polymerase chain reaction. E. coli O157:H7 was not isolated from any camper, foodhandler, or food or water sample. Samples of the implicated ice and salad items served during the camp were not available for testing.

Reported by: D Bergmire-Sweat, MPH, L Marengo, MS, P Pendergrass, MD, K Hendricks, MD, M Garcia, R Drumgoole, T Baldwin, K Kingsley, B Walsh, MPH, S Lang, L Prine, T Busby, L Trujillo, D Perrotta, PhD, Texas Dept of Health. A Hathaway, MD, B Jones, DVM, A Jaiyeola, MBBS, Tarrant County Health Dept, Fort Worth, Texas. S Bengtson, DVM, Food Safety Inspection Svc, US Dept of Agriculture. Foodborne and Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; and an EIS Officer, CDC.

Editorial Note:

  This was the first community outbreak of infections attributable to Shiga toxin-producing E. coli O111 reported in the United States. The findings of the investigation suggest a point-source outbreak. Although primary infection from eating a contaminated salad item and then secondary spread through the barrel ice is a plausible hypothesis, the original source of contamination and its means of spread are unknown.

Identification of non-O157 STEC requires techniques not used routinely by clinical laboratories. In this outbreak, a commercially available EIA kit was used to detect and isolate STEC in stool specimens; isolates were then serotyped at CDC.

STEC cause illness in otherwise healthy persons, including severe abdominal cramping (sometimes confused for appendicitis), bloody diarrhea, and HUS. E. coli O111 was the second most common non-O157 STEC (after E. coli O26) isolated from specimens submitted to CDC for serotyping during 1983--1998 and among isolates from persons with diarrhea collected for an ongoing survey in Minnesota initiated in 1995 (Minnesota Department of Public Health, unpublished data, 2000). STEC cause an estimated 110,000 illnesses each year in the United States, of which >30% may be attributable to non-O157 serotypes such as O111 (1); the burden of disease attributable to non-O157 STEC is unknown.

Most STEC outbreaks in North America have resulted from infection with E. coli O157. A household cluster of E. coli 0111 infection was reported in 1990 from Ohio (2), and outbreaks have occurred in Australia, Europe, and Japan (3--7). Despite investigations involving large numbers of persons in well-defined settings, the vehicle of transmission has been epidemiologically implicated and microbiologically confirmed in only one 1995 outbreak in South Australia, which was attributable to mettwurst, a dried fermented sausage (3).

As demonstrated by this outbreak, a commercially available kit could be used to screen stool specimens for Shiga toxin and potential STEC. However, culturing and serotyping the causative organism is critical to identify and better understand these emerging pathogens. To facilitate diagnosis of STEC infections, clinicians should inform health departments about clusters of suspected illnesses that could be attributable to STEC (e.g., bloody diarrhea and HUS). Clinical laboratories should screen stool specimens from persons with either bloody diarrhea or HUS for STEC, routinely or when E. coli O157 is not isolated, and attempt to isolate STEC from stools that are positive by the screening test and refer isolates to public health laboratories for serotyping. States should consider adding STEC infections to their notifiable disease lists.

References

1. Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Emerg Infect Dis 1999;5:60.
2. Banatvala N, Debeaukelaer MM, Griffin PM, et al. Shiga-like toxin-producing Escherichia coli O111 and associated hemolytic-uremic syndrome: a family outbreak. Pediatr Infect Dis J 1996;15:1008--11.
3. CDC. Community outbreak of hemolytic uremic syndrome attributable to Escherichia coli O111:NM---South Australia, 1995. MMWR 1995;44:550--1,557--8.
4. Tanaka H, Ohseto M, Yamashita Y, et al. Bacteriological investigation on an outbreak of acute enteritis associated with verotoxin-producing Escherichia coli O111:H [Japanese]. Kansenshogaku Zasshi Journal of the Japanese Association for Infectious Diseases 1989;63:1187--94.
5. Viljanen MK, Peltola T, Junnila SYT, et al. Outbreak of diarrhea due to Escherchia coli O111:B4 in schoolchildren and adults: association of Vi antigen-like reactivity. Lancet 1990;336:831--4.
6. Caprioli A, Luzzi I, Rosmini F, et al. Community-wide outbreak of hemolytic-uremic syndrome associated with non-O157 verocytotoxin-producing Escherichia coli. J Infect Dis 1994;169:208--11.
7. Wright JP, Rhodes P, Chapman PA, et al. Outbreaks of food poisoning in adults due to Escherichia coli O111 and campylobacter associated with coach trips to northern France. Epidemiology & Infection 1997;119:9--25.

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