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Epidemiologic Notes and Reports Hepatitis B among Dental Patients -- Indiana

Between April 1, and December 30, 1984, nine cases of clinical hepatitis B (HB) occurred in a rural Indiana county (population 35,000); this was nine times the normal yearly HB incidence for the past decade. Two of the cases resulted in fatal fulminant hepatitis; an additional case was complicated by polyarteritis nodosa, mononeuritis multiplex, and paralysis. All cases except one had been treated by a dentist in the county.

In mid-September, the dentist, who had practiced general family dentistry in the county for 20 years and saw between 100 and 150 patients per week, noted that all three of the cases to date had been his patients. Because of his possible involvement, he was tested for hepatitis B surface antigen (HBsAg) and found to be positive. He then voluntarily suspended his practice and notified health authorities. Initial investigation by the Indiana State Board of Health and CDC revealed that seven patients who had developed clinical HB between April 1 and October 1 were among the dentist's patients. All were positive for HBsAg, subtype ad, and all of six available sera were positive for the IgM fraction of hepatitis B core antibody (anti-HBc IgM), indicating probable recent infection. Although the dentist had no known history of HB infection, his serum was positive for HBsAg, subtype ad, and hepatitis e antigen (HBeAg) but negative for anti-HBc IgM.

The dentist did not routinely wear gloves when treating patients but denied lacerations or dermatitis on the hands. He gave no history of hepatitis and had no knowledge of HB carriers in his practice. Other than practicing dentistry, he denied all risk factors for HB. He was not a blood donor and had never been tested serologically for hepatitis. On April 25, and May 30, 1984, he had received his first two doses of HB vaccine.

Further investigation of the outbreak by CDC in late October concentrated on case-finding and interviews of the dentist, his assistants, and the known HB patients and their families. Appropriate blood specimens were also taken. A comparison of the dentist's 1984 patient list with reported HB cases in Indiana uncovered no new cases. However, a review of county residents rejected for blood donation because of HBsAg-positivity found one patient, who, asymptomatic at the time, had been treated by the dentist several times between May and July and was rejected for blood donation in August. Since she had donated blood in March, her HB infection was considered outbreak-related. Clinical disease, however, did not develop until November 13, nearly 3 months after she became antigen-positive.

The spouse of one HB patient was found to be HBsAg positive, serotype ad, HBeAg positive, and anti-HBc IgM negative. He had not been treated by the dentist within the last 2 years but had other risk factors for HB. No other patient's family member had positive HB markers. The patients had no histories of risk factors for HB except traumatic dental work (procedures that produced bleeding) by the dentist 3-5 months before onset of symptoms. None of the HB patients were taking hepatotoxic drugs. Antibody and antigen tests for delta virus were negative on the dentist and all seven of the HB patients tested.

In mid-December, a large seroprevalence study was carried out on the dentist's patients in an attempt to determine the degree of subclinical transmission; results of this study are pending. The dentist has not resumed his practice. Reported by RH Hamm, MD, RB Peare, MD, WL Painter, KC Allman, M Hamilton, K Cutting, CL Barrett, MD, State Epidemiologist, Indiana State Board of Health; Hepatitis Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: HB is a significant health risk for dental professionals (1,2) but is only rarely associated with transmission from dentist to patient. Seven HB outbreaks traced to dentists or oral surgeons have been reported. In each instance, the dental professional was a chronic carrier of HB virus and was HBeAg positive, indicating high titers of HB virus in blood. None used gloves when treating patients. Transmission of HB virus was thought to occur by transfer of infective serum from the dentist's hands into the patient's mouth through small abrasions, lacerations, or dermatitis. When subclinical transmission was studied, the overall rate of infection ranged from 1.5 infections per 100 patients screened to 11.1/100. The risk of transmission correlated with the amount of trauma involved in the dental procedure. For those dentists who remained carriers and returned to work, wearing gloves was usually successful in preventing further transmission (3).

The present outbreak illustrates again that HBsAg-positive dentists can unknowingly transmit infection to patients. Available epidemiologic and serologic data suggest that the Indiana dentist was infected before January 1984, too early to be affected by HB vaccine started in April, and that he probably obtained his infection while treating an HB-carrier patient. The dentist and the HB patients had matching antigenic subtypes. However, since ad subtype is extremely common in the United States, this does not prove that the dentist was the source of the outbreak as convincingly as the time/place clustering in his practice and the lack of other risk factors among the HB patients.

The 22% case-fatality rate in this outbreak is much higher than the usual rate of 1% of hospitalized HB patients. Furthermore, one patient suffered severe polyarteritis nodosa, a complication seen in no more than 1 of 500 cases. Neither coinfection with delta virus nor the use of hepatotoxic drugs explain the unusual amount of severe disease in this outbreak. CDC is continuing to investigate the possibility that a non-B hepatitis virus could be a cofactor in the outbreak.

This is the first reported outbreak of HB traceable to a dentist that has involved deaths. It illustrates an uncommon but serious consequence of HB infection in the dental profession. Outbreaks of this type should reinforce efforts to deliver HB vaccine to dental professionals early in their careers.


  1. Mosley JW, Edwards VM, Casey G, Redeker AG, White E. Hepatitis B virus infection in dentists. N Engl J Med 1975;293:729-34.

  2. Smith JL, Maynard JE, Berquist KR, Doto IL, Webster HM, Sheller MJ. From the Center for Disease Control. Comparative risk of hepatitis B among physicians and dentists. J Infect Dis 1976;133:705-6.

  3. Ahtone J, Goodman RA. Hepatitis B and dental personnel: transmission to patients and prevention issues. J Am Dent Assoc 1983;106:219-22.

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