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Foodborne Hepatitis A -- Missouri, Wisconsin, and Alaska, 1990-1992

Person-to-person spread is the predominant mode of transmission of hepatitis A virus (HAV) infection. However, based on findings for national surveillance for viral hepatitis, since 1983, 3%-8% of reported hepatitis A cases have been associated with suspected or confirmed foodborne or waterborne outbreaks (1). This report summarizes three recent foodborne outbreaks of hepatitis A and addresses the prevention of this problem. Missouri

On November 26, 1990, hepatitis A was diagnosed in an employee of a restaurant in Cass County, Missouri. The employee's duties involved washing pots and pans in the restaurant. From December 7, 1990, through January 9, 1991, hepatitis A was diagnosed in 110 persons, including four waitresses, who had eaten at the restaurant; two persons died as a result of fulminant hepatitis.

To identify risk factors for hepatitis A in restaurant patrons, CDC, in collaboration with the Missouri Department of Health (MDH), conducted a case-control study. A case was defined as an anti-HAV immunoglobulin M (IgM)-positive diagnosis in a person who had eaten at the restaurant three or more times during the 6-week period before onset of illness. Eating companions of case-patients were selected as controls. Twenty-three case-patients and 31 controls were included. Case-patients were asked about risk factors for hepatitis A (including contact {i.e., sexual, household, or other} with a person with hepatitis A, employment as a food handler, injecting-drug use, recent international travel, association with child care centers, consumption of raw shellfish, and eating at other restaurants in town) during the 2-6 weeks before onset of illness. Foods at the restaurant that were either uncooked or were handled after cooking were included in a food-history questionnaire.

Case-patients were more likely than controls to have consumed a salad (odds ratio {OR}=8.6; 95% confidence interval {CI}=2.0- 40.6). In addition, case-patients (100%) were more likely than controls (48%) to have eaten lettuce, either in a salad or as a garnish for a sandwich (OR=undefined; lower 95% confidence limit=6.2). On follow-up interview, the index case-patient reported that he occasionally helped unpack fresh produce and prepare lettuce for salads. From December 1990 through January 1991, immune globulin (IG) was administered to 22 restaurant employees and approximately 3000 potentially exposed restaurant patrons. No cases of hepatitis A were reported among restaurant patrons after January 9, 1991. Wisconsin

On April 10, 1991, a food handler employed at sandwich shops in downtown Milwaukee and at a university campus sought medical attention following onset of fatigue, loss of appetite, diarrhea, and fever. He was jaundiced and excluded from work. Acute hepatitis A was diagnosed serologically, and the case was reported to the Milwaukee Health Department (MHD).

Inspection by the MHD of the downtown shop found no health-code violations, and medical histories and serologies obtained from other employees were negative for evidence of hepatitis A. The case-patient reported his hygiene to be good, although this report could not be confirmed by his supervisor. His coworkers received prophylaxis with IG. Because of the report of good hygiene and a good report following inspection of the facility, the risk to patrons was considered minimal. Because 2 weeks had elapsed since the employee had last worked in the campus sandwich shop, this shop was not inspected, and IG was not administered to other employees.

On April 27, eight students presented to the student health service of a university in Milwaukee with symptoms of hepatitis. On April 28, 60 additional persons with hepatitis A were reported to local public health agencies. Review of food histories from these patients suggested both the downtown and university sandwich shops as probable sources. Because no new cases were identified among food handlers, and because a 2-week period had passed between the food handler's last working at the campus sandwich shop and recognition of the outbreak, IG was not offered to restaurant patrons.

The two sandwich shops were owned by the same person and received some produce from the same commercial suppliers; no other common links were identified. Although the infected food handler reported his personal hygiene to be good, one coworker and several customers reported his hygiene was poor. To prevent secondary transmission of hepatitis from shop customers who might be food handlers, more than 350 centrally located restaurants were visited by MHD inspectors and advised on proper precautions.

Overall, outbreak-related hepatitis A was diagnosed in 230 persons: 50 reported eating at the university sandwich shop and 180 reported eating at the downtown sandwich shop during April 17-May 29, 1992. The 2-week peak period for onset of jaundice (in 85% of cases) occurred approximately 1 month after the 2-week period in which the infected food handler staffed both shops. Because 228 of the 230 case-patients ate exclusively at one of the two shops and because no prepared food was shared between them, food was considered to have been contaminated independently at each site. Through July 15, one second generation case (in a household contact of a sandwich shop patron) was documented. Alaska

On May 4, 1992, a food handler who routinely prepared uncooked sandwiches at a fast-food restaurant in Juneau, Alaska, had onset of nausea, vomiting, and diarrhea. Although his employer instructed him not to handle food, he was allowed to continue work. On May 8, he sought medical attention and was jaundiced; IgM anti-HAV was negative. On May 18, repeat testing was positive for IgM anti-HAV. The case-patient reported his hygiene to be good, and this was confirmed by his supervisor and coworkers.

From June 1 through June 11, 11 cases of acute hepatitis A were diagnosed in residents of or visitors to Juneau. To identify risk factors for infection, the Alaska Department of Health and Social Services conducted a case-control study. A case was defined as an anti-HAV IgM-positive diagnosis in a Juneau resident or visitor with onset of illness during June 1-11. Twenty-four controls were selected from among coworkers of case-patients. Case-patients were asked about risk factors for hepatitis A, including contact (i.e., sexual, household, or other) with a person with hepatitis A, employment as a food handler, injecting-drug use, recent international travel, association with child care centers, consumption of raw shellfish, and eating at restaurants in town. All case-patients, compared with six (25%) controls, ate at least once during May 4-8 at the fast-food restaurant where the index case-patient worked (OR= undefined; lower 95% confidence limit=5.1). Because 2 weeks had elapsed between the index case-patient's onset of illness and serologic confirmation of HAV infection, IG was not administered to coworkers or restaurant patrons.

Reported by: M Skala, C Collier, CJ Hinkle, HD Donnell, Jr, MD, State Epidemiologist, Missouri Dept of Health. T Schlenker, MD, K Fessler, M Hotelling, Milwaukee Health Dept; D Hopfensperger, Div of Health, Wisconsin Dept of Health and Social Svcs. M Schloss, JP Middaugh, MD, State Epidemiologist, Alaska Dept of Health and Social Svcs. Div of Field Epidemiology, Epidemiology Program Office; Hepatitis Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Foodborne hepatitis A outbreaks are most often caused by contamination of food during preparation by an infected food handler. An important method of prevention is attention to personal hygiene, including frequent handwashing during all phases of food preparation. In addition, when hepatitis A is diagnosed in a food handler, IG should be administered to all other food handlers at the establishment. Administration of IG to patrons should be considered if 1) the infected person is directly involved in handling, without gloves, foods that will not be cooked before they are eaten; 2) the hygienic practices of the food handler are deficient or the food handler has had diarrhea; and 3) patrons can be identified and treated within 2 weeks of exposure (2,3).

The outbreaks in this report highlight several important aspects concerning recognition and reporting of persons with hepatitis A and decisions on the use of IG. Restaurant employees other than food handlers may handle food and, if infected with hepatitis A virus, pose a risk for foodborne transmission. Therefore, regardless of their job description and duties, restaurant employees with hepatitis A should be asked about any handling of uncooked food during the period that they may have been infectious.

In the Milwaukee outbreak, despite the self-reported good hygienic practices of the food handler, criteria were sufficient to recommend IG to restaurant patrons. Without the presence of diarrhea in a food handler with hepatitis A, a self-report of good hygienic practice may be inadequate to assess the level of risk to patrons. Evaluation of the hygienic practices of an infected food handler should include interviews with supervisors and coworkers.

In the outbreak in Alaska, all criteria were met for the consideration of administration of IG to restaurant customers. However, because the food handler was initially IgM anti-HAV negative at the time of jaundice, diagnosis was delayed beyond the 2-week interval for recommended use of IG. Even though specific antibody is almost always present at the time of the onset of symptoms (4-8), in food handlers with acute onset of jaundice and no identified cause, retesting for IgM anti-HAV is recommended.

Factors that are essential in the prevention and control of foodborne hepatitis A include accurate assessment of the hygienic status of food handlers; identification of food handlers and other restaurant employees with hepatitis A; and rapid diagnosis and reporting of cases in food handlers. Because IG must be administered within 2 weeks of exposure to HAV to be effective, health-care providers should promptly evaluate food handlers with symptoms of hepatitis and report food handlers with hepatitis A to appropriate public health agencies.


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  2. CDC. Protection against viral hepatitis: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1990;39(no. RR-2):2-5.

  3. Carl M, Francis DP, Maynard JE. Food-borne hepatitis A: recommendations for control. J Infect Dis 1983;148:1133-5.

  4. Lemon SM. Type A viral hepatitis: new developments in an old disease. N Engl J Med 1985;313:1059-67.

  5. Decker RH, Overby LR, Ling CM, Frosner C, Deinhardt F, Boggs J. Serologic studies of transmission of hepatitis A in humans. J Infect Dis 1979;139:74-82.

  6. Bradley DW, Fields HA, McCaustland KA, et al. Serodiagnosis of viral hepatitis A by a modified competitive binding radioimmunoassay for immunoglobulin M anti-hepatitis A virus. J Clin Microbiol 1979;9:120-7.

  7. Lemon SM, Brown CD, Brooks DS, Simms TE, Bancroft WH. Specific immunoglobulin M response to hepatitis A virus determined by solid-phase radioimmunoassay. Infect Immun 1980;28:927-36.

  8. Locarnini SA, Ferris AA, Lehmann NI, Gust ID. The antibody response following hepatitis A infection. Intervirology 1977;8:309-

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