Hepatitis B infection is caused by hepatitis B virus (HBV) which replicates in the liver and causes hepatic dysfunction. Infection with HBV causes a broad spectrum of liver disease, including subclinical infection, acute self-limited hepatitis and fulminant hepatitis, with some of those infected developing chronic infection leading to chronic liver disease and death from cirrhosis or hepatocellular carcinoma. The main burden of disease is related to chronic HBV infection. The risk of developing chronic HBV infection varies with age; approximately 90% of infected infants, 30% of infected children 1–4 years of age and <5% of those infected as adults will develop chronic disease.3 The analysis in this report is restricted to acute hepatitis B.

Relevant vaccine history

1980s

  • Hepatitis B vaccination funded for high-risk infants, including Aboriginal and Torres Strait Islander infants, in some jurisdictions then nationally in 1988.

1990

  • Neonatal hepatitis B vaccination funded for all infants in the Northern Territory (3-dose schedule: birth, 1 month and 6 months).

1997

  • Hepatitis B vaccination recommended and funded for all adolescents aged 11–12 years (initially 3-dose schedule using the paediatric formulation; changed to 2 doses of adult formulation at various times since 2001 in different jurisdictions).

2000

  • Universal infant vaccination included in childhood schedule with a birth dose of monovalent paediatric hepatitis B vaccine, followed by 3 doses of hepatitis B-containing combination vaccine.

Key points

Since the introduction of hepatitis B vaccination there has been a substantial reduction in HBV infection rates in Australia, although the rates are still higher in Aboriginal and Torres Strait Islander people than in other Australians. Consideration of further booster or catch-up vaccination may be necessary.

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Disease trends

Notification data (only for cases recorded as acute) are presented for all jurisdictions for the period 2007–2010. Hospitalisation data (principle cause of admission only) are presented for six jurisdictions (all except Tasmania and the Australian Capital Territory) by financial year for the period July 2005 to June 2010.

A total of 1,023 notifications and 711 hospitalisations for acute hepatitis B were recorded during these reporting periods; of these, 72 (7%) notifications and 31 (4.4%) hospitalisations were reported in Aboriginal and Torres Strait Islander people (Table 2.3.1 and Table 2.3.2).

No notifications or hospitalisations were recorded during this reporting period for Aboriginal and Torres Strait Islander children aged 0–4 years. For all other age groups, higher rates were recorded among Aboriginal and Torres Strait Islander people than among other people. Both notification and hospitalisation rates increased with age, peaking in the 25–49 years age group for both Aboriginal and Torres Strait Islander and other people.

Table 2.3.1: Hepatitis B* notifications, all Australian states, 2007 to 2010, by age group and Indigenous status
Age group
(years)
Indigenous status Notifications (2007–2010)
n Rate Rate ratio

* Recorded as acute only.

† Notifications where the date of diagnosis was between 1 January 2007 and 31 December 2010.

‡ Average annual age-specific rate per 100,000 population.

§ Includes cases with age unknown. Rates for all ages combined are age-standardised to the Australian Bureau of Statistics Australian population estimates for 2006.

|| Indicates statistically significant, 95% confidence intervals do not overlap 1.0.

0–4
Indigenous
0
0.0
0.0
Other
9
0.2
5–14
Indigenous
2
0.4
4.5
Other
9
0.1
15–24
Indigenous
24
5.4
4.6||
Other
138
1.2
25–49
Indigenous
42
6.1
3.0||
Other
625
2.1
>50
Indigenous
4
1.5
2.3
Other
170
0.6
All ages§
Indigenous
72
3.5
3.1||
Other
951
1.1

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Table 2.3.2: Hepatitis B* hospitalisations, selected Australian states, 2005 to 2010, by age group and Indigenous status
Age group
(years)
Indigenous status Hospitalisations (2005–2010)
n Rate Rate ratio

* Principal cause of admission only.

† Hospitalisations (New South Wales, Northern Territory, Queensland, South Australia, Victoria, Western Australia only) where the date of separation was between 1 July 2005 and 30 June 2010.

‡ Average annual age-specific rate per 100,000 population.

§ Includes cases with age unknown. Rates for all ages combined are age-standardised to the Australian Bureau of Statistics Australian population estimates for 2006.

|| Indicates statistically significant, 95% confidence intervals do not overlap 1.0.

0–4
Indigenous
0
0.0
0.0
Other
1
0.0
5–14
Indigenous
1
0.2
6.8
Other
3
0.0
15-24
Indigenous
6
1.2
2.2
Other
77
0.6
25-49
Indigenous
19
2.4
1.9||
Other
447
1.3
>50
Indigenous
5
1.7
3.4||
Other
152
0.5
All ages§
Indigenous
31
1.6
2.2||
Other
680
0.7

The overall Indigenous to non-Indigenous rate ratios were 3.1:1 for notifications and 2.2:1 for hospitalisations, both of which were statistically significantly different to 1:1. The biggest difference in notification rates was in the 15–24 years age group (rate ratio 4.6:1), while for hospitalisations the greatest difference was in the 5–14 years age group (rate ratio 6.8:1, not statistically significantly different to 1:1).

There were 32 deaths reported from the five jurisdictions (New South Wales, the Northern Territory, Queensland, South Australia and Western Australia) for the period 2006–2010 with hepatitis B as the underlying cause, of which 6 to 9 were reported in Aboriginal and Torres Strait Islander people (the ABS provides ranges when absolute numbers of deaths are low). None of the deaths in Aboriginal and Torres Strait Islander people were in children <5 years of age. There were 179 deaths reported with hepatitis B as either the underlying or a contributing cause, of which 25 (14%) were reported in Aboriginal and Torres Strait Islander people; none of these deaths were in children <5 years of age.

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Comment

Australia is generally regarded as a country with low risk for hepatitis B virus infection. This has been achieved by securing a safe blood supply, implementing a national hepatitis B vaccination program, and providing treatment for people with chronic hepatitis B through the Pharmaceutical Benefits Scheme. However, hepatitis B has been common in some Aboriginal and Torres Strait Islander communities, with the highest rates reported in the Northern Territory,19 including a death rate from hepatic cancer 10 times that in other people.20 Surveillance data such as those presented here have serious limitations; they are unlikely to include asymptomatic infections and so may underestimate acute hepatitis B disease, especially in children in whom most infection is asymptomatic. Moreover, they do not reflect the disease burden from chronic hepatitis B or later complications such as liver cirrhosis and hepatocellular carcinoma. The highest notification and hospitalisation rates were in the 25–49 years age group, which suggest continued horizontal transmission of infection.

Studies of markers of infection in Northern Territory Aboriginal and Torres Strait Islander adolescents and young adults who were targeted in the early years of the vaccination program show evidence of substantially lower levels of infection and chronic infection compared to the pre-immunisation period;21 however, levels are still higher than in non-Indigenous people of the same age.22 Some studies in some Aboriginal communities have suggested that immune responses to the early hepatitis B vaccines may have been suboptimal.23 An audit conducted in East Arnhem Land in the Northern Territory concluded that HBV infection was an ongoing public health problem in some Aboriginal communities for all age groups; reasons for this included the existence of a large cohort of susceptible people born before 1990, incomplete immunisation, ongoing vertical transmission despite the use of hepatitis B immunoglobulin, and a poor response to vaccination among Aboriginal children.22 There may also be a need for booster doses for those vaccinated as infants.21

Internationally, Alaska reported a decline in infection rates in both Alaskan Native and non-Native people after 1984, when universal infant vaccination commenced followed by a catch-up program from 1984–1988 for Alaskan Native people. The decline was further helped by ongoing high rates of immunisation.18

Substantial impacts of universal hepatitis B vaccination on the earlier manifestations of hepatitis B infection have been demonstrated in Aboriginal and Torres Strait Islander and other Australians,24,25 and these are likely to be reflected in lower rates of the serious long-term sequelae in coming years. However, there is evidence that infection continues to occur in Aboriginal and Torres Strait Islander communities that suffered from high levels of disease in the pre-vaccine era. The Australian Immunisation Handbook 10th edition recommends that all Aboriginal and Torres Strait Islander people have their risks and vaccination status reviewed, be offered testing and be vaccinated if non-immune.26