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Epidemiologic Notes and Reports Outbreak of Food-borne Hepatitis A -- New Jersey

An increase in the number of hepatitis cases in Monmouth County, New Jersey, was reported to the New Jersey Department of Health on June 15, 1981. Investigation by state and local area health departments revealed that 56 cases of hepatitis had occurred during the first 3 weeks of June in an area of Monmouth County where the usual average is 3-4 cases/ month. Patients for whom appropriate laboratory tests had been done were confirmed to have hepatitis A.

Detailed food histories revealed that, within the appropriate incubation period for hepatitis A, 55 of the 56 patients had eaten at a Mexican style restaurant (Figure 1). Interviews of a control group matched for age, sex, and neighborhood of residence, showed that 10% of the controls ate food from this restaurant over a time period comparable with that for 98% of the patients. The restaurant agreed to close voluntarily pending further investigation.

Of the patients whose illness was related to the Mexican restaurant, 71% were male, 68% were between the ages of 15 and 29 years, and 4 were children under 15 years. A case-control study using 46 non-ill patrons revealed that patients were more likely to have eaten nachos, beans, and jalapeno peppers. Both beans and jalapeno peppers were used in preparing nachos.

Ten individuals including the 2 owners worked in the restaurant; all handled food at one time or another. Interviews on June 18 revealed that 1 employee who frequently ate food from the restaurant was ill with hepatitis at the time of the interview. Another employee had symptoms compatible with hepatitis on May 9. He had worked all day May 9, but felt too ill to work thereafter; the diagnosis of hepatitis A was confirmed for him on May 16. This employee prepared food--including grating cheese, shredding lettuce, and occasionally cutting meat--measured portions of meat, beans, jalapeno peppers, onions, cheeses, and lettuce into shells, and served the customers.

Because a food handler was recently ill with hepatitis and because the restaurant was implicated in the spread of hepatitis, immune globulin was offered to all individuals who ate in the restaurant from June 5 until it closed. A total of 1,430 people were immunized at a 2-day clinic held June 19 and 20. Reported by R Hary, Matawan Borough, S McKee, Middletown Township, S Scapricio, Hazlet Township, L. Jargowski, Monmouth County Health Dept, F Richart, Red Bank, R Altman, MD, P Marzinsky, B Mojica, MD, WE Parkin, DVM, State Epidemiologist, New Jersey State Dept of Health; Field Svcs Br, Hepatitis Laboratory Div, Center for Infectious Diseases, Field Svcs Div, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: Hepatitis A virus (HAV) can be transmitted by food contaminated with feces from an infected food handler. If acute hepatitis A has been confirmed in a food handler by testing for IgM-specific HAV antibody, immunoglobulin prophylaxis (IG, gamma globulin) may be considered for patrons, depending on the probability of transmission of infectious virus and the probability of successful intervention in transmission by using IG. However, few food handlers actually appear to transmit disease via food, and IG prophylaxis of patrons is seldom warranted. Although for the past few years approximately 1,000 food handlers with non-B hepatitis have been reported annually to CDC, an average of 4 outbreaks of food-borne hepatitis A have been reported each year.

Transmission of HAV is affected by the amount of virus excreted by the food handler, the type of food handled, and the food handler's hygiene practices. Because the amount of virus excreted peaks 7-10 days before onset of symptoms and declines rapidly thereafter (1), food-borne outbreaks of hepatitis commonly originate from foods prepared before the food handler has clinical symptoms (2,3). As in this outbreak, most reported outbreaks have been traced to symptomatic rather than asymptomatic excreters. Uncooked foods have most frequently been associated with food-borne hepatitis because normal cooking temperatures inactivate HAV (4). However, cooked foods that were handled after cooling and foods that were contaminated and then cooked with insufficiently high internal temperature to inactivate HAV have also been implicated (2,5). Although poor hygiene practices among food handlers increase the chance of transmission of virus, outbreaks have occurred even when food handlers' personal hygiene practices were described as "acceptable" and "generally good" (3). Hygiene practices should be assessed by interviewing the ill food handler, coworkers, and employer. If deficiencies occurred and the ill food handler did not wear gloves, prophylaxis may be considered for patrons who ate implicated food items during the appropriate time period. Successful intervention in disease transmission depends on identifying persons at risk and administering IG within 2 weeks after exposure (6).

Other employees who have been regularly exposed to the index case are at risk of acquiring infection. If they do become infected, they may serve as additional sources of infection for future food consumers. These employees should be extremely conscientious in their hygiene practices, and those who handle high-risk foods should be given IG. Screening of coworkers for elevated liver enzymes or antibodies to HAV does not appear justified because the enzymes are not specific for hepatitis A, and both enzymes and antibodies appear after most virus excretion has occurred.


  1. Bradley DW, Gravelle CR, Cook EM, Fields RM, Maynard JE. Cyclic excretion of hepatitis A virus in experimentally infected chimpanzees: biophysical characterization of the associated HAV particles. J Med Virol 1977;1:133-8.

  2. Leger RT, Boyer KM, Pattison CP, Maynard JE. Hepatitis A: report of a common-source outbreak with recovery of a possible etiologic agent. I. Epidemiologic studies. J Infect Dis 1975;131:163-6.

  3. Denes AE, Smith JL, Hindman SM, et al. Foodborne hepatitis A infection: a report of two urban restaurant-associated outbreaks. Am J Epidemiol 1977;105:156-62.

  4. Krugman S, Gocke DJ. Viral hepatitis. Philadelphia: WB Saunders Company, 1978.

  5. Peterson DA, Wolfe LG, Larkin EP, Deinhardt FW. Thermal treatment and infectivity of hepatitis A virus in human feces. J Med Virol 1978;2:201-6.

  6. Brachott D, Lifschitz I, Mosley JW, Kendrick MA, Sgouris JT. Potency of fragmented IgG: two studies of postexposure prophylaxis in Type A hepatitis. J Lab Clin Med 1975;85:281-6.

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