BACKGROUND: In early 1996 an outbreak of hepatitis B was detected among patients who attended an electroencephalogram (EEG) clinic in Toronto operated by a neurologist. In this article we report the results of an investigation conducted to determine the extent and source of the outbreak. METHODS: Notifications were sent to 18 567 patients who had attended any of 6 EEG clinics operated by the neurologist between 1990 and 1996 asking them to see their physician to be tested for hepatitis B virus (HBV) infection; 2957 envelopes were returned. Of the remaining 15 610 patients, results of laboratory tests were available for 10 244 (65.6%). A detailed follow-up of patients with newly acquired hepatitis B and those with chronic infection (carriers) was conducted. Viral DNA sequencing was used to compare strains of available HBV isolates. RESULTS: A total of 75 patients were identified in whom hepatitis B developed between 1991 and 1996; all of them had had at least one EEG performed in which reusable subdermal electrodes had been used. No cases were detected among patients who participated only in sleep studies, for which disk electrodes had been used. The peak rate of HBV infection (18.2 cases per 1000 person-EEGs) occurred in 1995. One technician performed all of the EEGs at the clinics and was found to be positive for hepatitis B e antigen. DNA sequencing confirmed that the virus isolated from the technician was identical to the virus isolated in 4 cases of hepatitis B tested. Infection control procedures were found to be inadequate. INTERPRETATION: The hepatitis B outbreak was a result of a common source of infection, the technologist, and inadequate infection control practices. Reusable subdermal EEG electrodes were the likely vehicles of transmission. Health care workers should follow recommended infection control practices and be vaccinated against hepatitis B.
BACKGROUND: In early 1996 an outbreak of hepatitis B was detected among patients who attended an electroencephalogram (EEG) clinic in Toronto operated by a neurologist. In this article we report the results of an investigation conducted to determine the extent and source of the outbreak. METHODS: Notifications were sent to 18 567 patients who had attended any of 6 EEG clinics operated by the neurologist between 1990 and 1996 asking them to see their physician to be tested for hepatitis B virus (HBV) infection; 2957 envelopes were returned. Of the remaining 15 610 patients, results of laboratory tests were available for 10 244 (65.6%). A detailed follow-up of patients with newly acquired hepatitis B and those with chronic infection (carriers) was conducted. Viral DNA sequencing was used to compare strains of available HBV isolates. RESULTS: A total of 75 patients were identified in whom hepatitis B developed between 1991 and 1996; all of them had had at least one EEG performed in which reusable subdermal electrodes had been used. No cases were detected among patients who participated only in sleep studies, for which disk electrodes had been used. The peak rate of HBV infection (18.2 cases per 1000 person-EEGs) occurred in 1995. One technician performed all of the EEGs at the clinics and was found to be positive for hepatitis B e antigen. DNA sequencing confirmed that the virus isolated from the technician was identical to the virus isolated in 4 cases of hepatitis B tested. Infection control procedures were found to be inadequate. INTERPRETATION: The hepatitis B outbreak was a result of a common source of infection, the technologist, and inadequate infection control practices. Reusable subdermal EEG electrodes were the likely vehicles of transmission. Health care workers should follow recommended infection control practices and be vaccinated against hepatitis B.
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