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A Program to Control an Outbreak of Hepatitis A in Alaska by Using an Inactivated Hepatitis A Vaccine
Brian J. McMahon, MD;
Michael Beller, MD, MPH;
James Williams, RN, ANP;
Mindy Schloss, RN, MPH;
Harvey Tanttila;
Lisa Bulkow, MS
Arch Pediatr Adolesc Med. 1996;150(7):733-739.
Abstract
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Objective
To stop an epidemic of hepatitis A in rural Alaska by mass immunization of susceptible persons with 1 dose of an inactivated hepatitis A vaccine.
Design
Nonrandomized, uncontrolled trial. Hepatitis A vaccine was offered to all persons in susceptible age groups in villages with documented cases of hepatitis A. Immune globulin was not offered at the time of vaccination.
Setting
Twenty-five rural communities located in interior Alaska and along the northwest coast of the Bering Sea and Arctic Ocean.
Participants
Persons without a history of acute hepatitis A in age groups selected by applying results of a previous serosurvey conducted on serum collected before the epidemic.
Intervention
One dose of a formalin-inactivated hepatitis A vaccine was given to each participant. Adults 20 years of age and older received 1440 enzyme-linked immunosorbent assay units and persons younger than 20 years received 720 enzyme-linked immunosorbent assay units. Prevaccination and postvaccination levels of antibody to hepatitis A IgG were obtained from 136 participants.
Main Outcome Measures
An active surveillance system was established to detect persons with symptomatic illnesses compatible with hepatitis A; persons who met the illness criteria were tested for antibody to hepatitis A IgM. One area (the Kotzebue region), where all communities were offered vaccine, was selected for intensive surveillance and analysis.
Results
During the 12-month period before the vaccine trial, 529 cases of icteric hepatitis A were reported, and 443 were confirmed to be positive for antibody to hepatitis A IgM. Hepatitis A vaccine was administered to 4930 persons, 3517 of whom were younger than 20 years. After vaccination began, 237 persons positive for antibody to hepatitis A IgM were identified during a 60-week surveillance period; 46 were vaccinees and 191 were unvaccinated susceptible persons. In the Kotzebue region, in communities in which more than 80% of persons considered susceptible were vaccinated, the outbreak ceased in 4 to 8 weeks, whereas in 1 large community in which less than 50% of susceptible persons were vaccinated, the outbreak continued for more than 50 weeks. More than 90% of seronegative persons developed antibody to hepatitis A IgG 3 to 4 weeks after vaccination.
Conclusion
This trial suggested that by providing both short-term and long-term protection, hepatitis A vaccine used without immune globulin halted an established epidemic of hepatitis A in rural Alaska.
Arch Pediatr Adolesc Med. 1996;150:733-739
Author Affiliations
From the Alaska Native Medical Center, Alaska Area Native Health Services, Indian Health Service (Dr McMahon and Messrs Williams and Tanttila); Section of Epidemiology, Division of Public Health, Department of Health and Social Services, State of Alaska (Dr Beller and Ms Schloss); and Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention (Ms Bulkow), Anchorage, Alaska.
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