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Outbreaks of Gastrointestinal Illness of Unknown Etiology Associated with Eating Burritos -- United States, October 1997-October 1998

From October 1997 through October 1998, 16 outbreaks of gastrointestinal illness associated with eating burritos occurred in Florida, Georgia, Illinois, Indiana, Kansas, North Dakota, and Pennsylvania. All but one outbreak occurred in schools, and most of the approximately 1700 persons affected were children. This report summarizes investigations of two of these outbreaks and describes the collaborative efforts of CDC, the U.S. Department of Agriculture (USDA), and the Food and Drug Administration (FDA) to identify the etiologic agent(s); these outbreaks may have been caused by an undetected toxin or a new agent not previously associated with illness.


On March 23, 1998, the Hall County Health Department received a report that students in an elementary school became ill after eating lunch. Health officials obtained food and illness histories from 452 (77%) of the 584 students. A case was defined as nausea, abdominal cramps, vomiting, or diarrhea within 24 hours in a person after eating the school lunch on March 23. Of the 452 students, 155 (34%) had illnesses meeting the case definition. Symptoms most commonly reported were nausea (89%), headache (65%), abdominal cramps (53%), vomiting (29%), and diarrhea (17%). The median incubation period was approximately 15 minutes (range: 5-25 minutes), and median duration of illness was 4.5 hours (range: 10 minutes-8 hours).

The children had access to nine foods during lunch. One hundred forty-five (48%) of 304 who ate burritos, and 10 (7%) of 148 who did not eat burritos became ill (relative risk {RR}=7.1; 95% confidence interval {CI}=3.8-13.0). The burritos were produced by company A; the main ingredients were beef, chicken, pinto beans, seasoning, textured vegetable protein, and tortillas.


On October 8, 1998, the Hillsborough County Health Department was notified that students at 12 elementary schools became ill after eating lunch. Health officials conducted investigations at two schools. A case was defined as nausea, abdominal cramps, or vomiting in a person after eating the school lunch on October 8. In both schools, students who initially reported illness and classmates in the three classes with the highest number of cases were interviewed. Twenty-seven cases were identified. The predominant symptoms of the 14 ill children identified in one school were abdominal cramps (88%), vomiting (62%), headache (62%), and nausea (39%). In the other school, symptoms among the 13 identified ill children were abdominal cramps (82%), vomiting (55%), headache (27%), nausea (18%), and dizziness (18%).

In a case-control study at one school, eight (57%) of 14 case-patients and five (13%) of 38 well children ate burritos (odds ratio {OR}=8.8; 95% CI=1.8-47.6). In the other school, 11 (85%) of 13 case-patients and 11 (33%) of 33 well children ate burritos (OR=11.0; 95% CI=1.8-87.6). The tortillas used to make the burritos were supplied by company B; the fillings, beef at one school and beef and pinto beans at the other, were made in the two school kitchens.

Summary Findings

During October 1997-March 1998, burritos from three outbreaks of gastrointestinal illness were traced to company A, and during May-October 1998, burritos from another 13 outbreaks were traced to company B. Three outbreaks were linked to chicken and bean burritos, pork-sausage and egg burritos, and beef burritos; the other 13 were linked to beef and pinto bean burritos. All burritos used tortillas made with wheat flour. The burritos were distributed frozen and prepackaged except in Florida, where the filling was prepared locally.

The major symptoms were nausea, headache, abdominal cramps, and vomiting, typically beginning within 60 minutes after eating a burrito and lasting less than 24 hours. No one was hospitalized.

USDA requested that both companies A and B initiate timely national recalls, and approximately 2 million lbs of burritos were recalled or withheld from distribution. Company A and its tortilla supplier were unrelated to company B and its supplier.

Reported by: G Holcomb, Jr, PL Lacey, Hall County Environmental Health, Hall County Health Dept, Gainesville; TW McCoy, MA Stancil, MD, Health District 2; JA Benson, LL Cobb, ML Ray, MM Park, PhD, EA Franko, DrPH, MF Scarborough, PA Blake, MD, State Epidemiologist, Div of Public Health, Georgia Dept of Human Resources. MM Simons, L Dauphinais, Aberdeen Area Indian Health Svc, Minot; PJ Vukelic, MS, KJ Kruger, LA Shireley, MS, State Epidemiologist, North Dakota Dept of Health. E Gregos, Hillsborough County Health Dept, Tampa; M Friedman, MPH, N Richey, R Hammond, PhD, Bur of Environmental Epidemiology, Florida Dept of Health. T Monroe, MD, Kansas Dept of Health and Environment. J Cheek, MD, Indian Health Svc Headquarters, Albuquerque, New Mexico. Center for Food Safety and Applied Nutrition and Office of Regional Operations, Food and Drug Administration. Office of Public Health and Science, Food Safety and Inspection Svc, US Dept of Agriculture. Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health; Foodborne and Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; and EIS officers, CDC.

Editorial Note

Editorial Note: Data from the two outbreaks described in this report and the other 14 outbreaks indicate that the symptoms, incubation period, and duration of illness were similar. The variations in symptoms in the outbreaks in Florida and Georgia could be associated with differences in case finding methods. Epidemiologic investigations in several of the other outbreaks also have implicated burritos, which consisted of meat or vegetable filling wrapped in a tortilla. Data from the Florida outbreak suggest that the etiologic agent was in the tortillas because the filling was made locally. Outbreaks associated with products made by two unrelated companies that used different tortilla suppliers suggest that the agent was an ingredient common to the products made by both companies. No common first-line suppliers were identified; however, whether the source of any ingredients was shared has not been determined.

The short incubation periods suggest that a preformed toxin or other short-acting agent was the cause of illness. Possible agents include bacterial toxins (e.g., Staphylococcus aureus enterotoxin and Bacillus cereus emetic toxin); mycotoxins (e.g., deoxynivalenol {DON}, acetyl-deoxynivalenol, and other tricothecenes), trace metals, nonmetal ions (e.g., fluorine, bromine, and iodine), plant toxins (e.g., alkaloids such as solanines, opiates, ipecac, and ergot; lectins such as phytohemagglutinin; and glycosides), pesticides (e.g., pyrethrins, organophosphates, and chlorinated hydrocarbons), food additives (e.g., bromate, glutamate, nitrite, salicylate, sorbate, and sulfite), detergents (e.g., anionic detergents and quaternary amines), fat-soluble vitamins, spoilage factors (e.g., biogenic amines, putrefaction, and free fatty acids), or an unknown toxin. Mass sociogenic illness is an unlikely explanation based on the number of different sites where outbreaks have been reported over a short interval and the link to only two companies.

B. cereus emetic toxin and S. aureus enterotoxin are common causes of food poisoning, but headache is not usually a prominent feature, and most outbreaks traced to these toxins have incubation periods of 2-4 hours, which is longer than observed in these outbreaks (1,2). Food samples from five outbreaks were negative for B. cereus and S. aureus by culture and toxin analysis; testing from these same outbreaks for alkaloids, biogenic amines, and pesticides also did not identify the causative agent.

Some metals, such as cadmium, copper, tin, and zinc, can irritate mucosal membranes and cause gastrointestinal illness after short incubation periods; however, only elemental aluminum was mildly elevated in the burrito samples, and there is no evidence that it causes these symptoms (3,4). Several plant toxins, such as phytohemagglutinin, may survive cooking and cause gastrointestinal symptoms; however, previous outbreaks associated with phytohemagglutinin have been linked to red kidney beans and not pinto beans (5).

Outbreaks with symptoms and incubation periods similar to those described in this report have occurred in China and India, where illness has been linked to consumption of products made with grains contaminated with fungi. These fungi produce heat-stable tricothecene mycotoxins called vomitoxin (6). In China, 35 outbreaks affecting 7818 persons during 1961-1985 were attributed to consumption of foods made with moldy grain (7). Corn and wheat samples collected during two outbreaks had higher levels of DON than those collected at other times. In India in 1987, 97 persons consumed wheat products following heavy rains (8). DON and other tricothecene mycotoxins were detected in the implicated wheat products, and extracted toxins caused vomiting in laboratory tests on puppies (8). High doses of DON are known to cause vomiting in pigs (9). Laboratory testing from burrito samples from some of the U.S. outbreaks in this report detected DON within the acceptable FDA advisory level of 1 ppm for finished wheat products (10). However, the possibility remains that a mycotoxin is the cause.

To facilitate coordination of outbreak investigation and traceback activities, local health departments are encouraged to report immediately any outbreaks characterized by an incubation period of less than 1 hour, duration of less than 1 day, and symptoms including nausea, headache, abdominal cramps, and vomiting regardless of the suspected vehicle through state health departments to CDC. CDC recommends that vomitus, serum, stool, and urine specimens be obtained from at least 10 ill persons, if possible, in each outbreak and that any leftover food samples and shipping containers be saved.

In addition to testing food specimens for specific toxins and agents, laboratories at USDA, FDA, and CDC are examining these specimens by cell culture assays, biologic toxicity assays, and chemical analyses for toxins. The interagency investigating team seeks to collaborate with groups capable of analyzing suspect burritos and tortillas to identify the etiologic agent. Additional information is available from CDC's Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, telephone (404) 639-2206.


  1. Lund BM. Foodborne disease due to Bacillus and Clostridium species. Lancet 1990;336:982-6.

  2. Holmberg SD, Blake PA. Staphylococcal food poisoning in the United States: new facts and old misconceptions. JAMA 1984;251:487-9.

  3. Robertson WO. Arsenic and other heavy metals. In: Haddad M, Winchester Jl, eds. Clinical management of poisoning and drug overdose. Philadelphia, Pennsylvania: WB Saunders Co, 1983.

  4. Agency for Toxic Substances and Disease Registry. Toxicological profile for aluminum. Atlanta, Georgia: US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, 1997:21-32.

  5. Noah ND, Bender AE, Reaidi GB, Gilbert RJ. Food poisoning from raw red kidney beans. BMJ 1980;281:236-7.

  6. Bullerman L. Fusaria and toxigenic molds other than aspergilli and penicillia. In: Doyle MP, Beuchat LR, Montville TJ, eds. Food microbiology: fundamentals and frontiers. Washington, DC: ASM Press, 1997:419-34.

  7. Luo XY. Outbreaks of moldy cereal poisonings in China. In: Toxicology Forum and the Chinese Academy of Preventive Medicine. Issues in food safety. Washington, DC: Toxicology Forum, 1988:56-63.

  8. Bhat RV, Beedu SR, Ramakrishna Y, Munshi KL. Outbreak of trichothecene mycotoxicosis associated with consumption of mould-damaged wheat products in Kashmir Valley, India. Lancet 1989;1:35-7.

  9. Food and Drug Administration. Industry advisory regarding deoxynivalenol (DON) in wheat: letter to state agricultural directors, et al. Rockville, Maryland: Associate Commissioner for Regulatory Affairs, Food and Drug Administration, 1993.

  10. Rotter BA, Prelusky DB, Pestka JJ. Toxicology of deoxynivalenol (vomitoxin). J Toxicol Environ Health 1996;48:1-34.

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