Hepatitis B infection of children in a mixed-race community in western New South Wales.

A seroprevalence survey of markers of hepatitis B virus (HBV) infection in children aged 0-16 years was conducted in a mixed-race township in western New South Wales. A total of 408 children were screened representing 95% of the total 0-16-year-old population. Of the Aboriginal subjects, 69% had seromarkers which indicated previous infection with HBV and 14% were hepatitis B surface antigen (HBsAg) seropositive. In the non-Aboriginal subjects the prevalence of seromarkers was 10% with no subjects HBsAg positive. The township provided an ideal setting for studying possible crossinfection from children in a high risk (Aboriginal) population group to children in a low-risk (non-Aboriginal) group. The ratio of children in the high-risk group for HBV infection to those in the low-risk group was approximately 2.7:1. Although HBsAg was highly endemic in the Aboriginal population, the data indicate that little crossinfection has occurred. We conclude that in this and similar mixed-race communities action should be taken to accelerate vaccination programmes aimed at reducing HBV infection among neonates and children in the high-risk groups. This will provide an immediate overall reduction of potential risk to both high-risk and low-risk groups while the issue of universal vaccination is considered further.

The prevalence of markers of infection with hepatitis B virus in a mixed-race Australian community.

A seroepidemiological study of markers of infection with hepatitis B virus was conducted in Brewarrina, a mixed-race township in north-western New South Wales. Six hundred and forty-three subjects, who represented 41.5% of the town's population, were screened for a range of serological markers of hepatitis B virus infection. Of the Aboriginal subjects, 72% had markers which indicated previous infection with hepatitis B virus, with 19.2% of subjects being identified as hepatitis B surface antigen (HBsAg)-seropositive. In the non-Aboriginal subjects, the prevalence of infection with markers of hepatitis B virus was 13.1%, with 2.2% of subjects being HBsAg-seropositive. The marker prevalences for Aboriginal and non-Aboriginal subjects in the 15- to 19-year-old age-group were 86.7% and 28%, respectively. The prevalence of hepatitis B virus infection in the total non-Aboriginal sample was higher than it is in the general Australian blood-donor population. The extent to which hepatitis B virus infection may result from cross-infection between coexisting "high-risk" and "low-risk" population groups is speculative. Furthermore, the risk of infection to non-Aborigines is unlikely to be spread evenly across the non-Aboriginal community. The cost of vaccine remains high, and until further data become available, mass vaccination of the population probably is not warranted. Initially, control measures should concentrate on the reduction of hepatitis B virus infection in the Aboriginal population and in non-Aboriginal households which contain a HBsAg-seropositive member.