By all outward appearances Jackson (not his real name) was a healthy 14-month-old infant. Recently adopted from abroad—one of more than 22,000 children adopted internationally in 2004¹—he was robust, and his initial medical examination was entirely normal. Routine laboratory tests were ordered and follow-up was planned. The positive anti-hepatitis A virus (HAV) immunoglobulin M (IgM) serology, reported 10 days later, identified another stealth vector of this highly contagious, infectious disease. Calls to the local public health agency followed, along with contact tracking and primary immunization and treatment with hepatitis A vaccine and immune globulin for numerous potential exposures at his day care and within his family. Fortunately, no fulminant secondary infections occurred.

The 1999 Advisory Committee on Immunization Practices (ACIP) recommendation for targeted immunization (i.e., immunizing groups at increased risk of HAV infection) was extremely effective, as noted by Brundage and Fitzpatrick in this issue of American Family Physician.² The American Academy of Family Physicians endorsed the 1999 recommendation and recommends universal immunization of children ages 12 to 23 months (seehttps://www.aafp.org/online/en/home/clinical/immunizations.html). Given its success, in October 2005 ACIP extended the recommendation for the two-dose series of hepatitis A vaccine to include all children ages 12 to 23 months.³ At first pass, one may question the wisdom of this recommendation because HAV infection has become fairly uncommon and causes little morbidity in children⁴; under the 1999 recommendation, reported cases of HAV infection fell by approximately 76 percent in the United States. However, an unexpected consequence of targeted childhood vaccination was an increase in the average age of patients infected with HAV and a greater severity of infection.⁵

The asymptomatic infection that generally occurs in young children provides a silent conduit for this virus to highly vulnerable individuals. Adults with chronic hepatitis C virus (HCV) infection have a substantial risk for fulminant hepatitis when superinfected with HAV. For example, in one series, 41 percent of persons with chronic HCV infection who also were infected with HAV developed fulminant liver failure; 86 percent of those persons died.⁶

Approximately 2.7 million Americans (0.9 percent) have chronic HCV infection.⁷ Despite clear recommendations for vaccination against HAV and hepatitis B virus (HBV) in patients with chronic liver disease,⁸ only 5 percent of these patients in primary care settings have completed the HAV series, and 14 percent have completed the HBV series.⁹ Universal HAV immunization of children not only will protect the vaccine recipients but also will quickly provide protection for persons with known or occult chronic liver disease while laying the groundwork for potential HAV elimination in the United States.

As long as endemic HAV is only an airline ticket away and nonimmune citizens travel abroad, as long as refugees and immigrants seek better lives in the United States, and as long as children are adopted from developing countries, this virus will continue to pose a threat. Breaking the chain of transmission requires heightened “herd” immunity. This can be achieved rapidly through the universal childhood vaccination recommendation.