Vaccine Preventable Diseases and Vaccination Coverage in Aboriginal and Torres Strait Islander People, Australia, 2003 to 2006

Hepatitis B (acute)

Disclaimer: Produced by the National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases and the Australian Institute of Health and Welfare on behalf of the Australian Government Department of Health and Ageing. Published as a supplement to the Communicable Diseases Intelligence journal Volume 32, June 2008.

Page last updated: 30 June 2008

Acute infection with hepatitis B virus (HBV) produces a range of conditions from subclinical infection to acute and, rarely, fulminant hepatitis. The majority of HBV infections are not clinically recognised, with less than 10% of children and 30%–50% of adults experiencing jaundice.36,47 When illness occurs, it is usually insidious, with anorexia, vague abdominal discomfort, nausea and vomiting, sometimes arthralgia and rash, often progressing to jaundice. The main burden of disease is related to chronic HBV infection. The risk of chronic infection is greatest in those infected as infants, particularly if infected in the perinatal period. Of people chronically infected with HBV, 15%–40% develop cirrhosis of the liver and/or hepatocellular carcinoma.48,49

HBV transmission occurs by percutaneous or permucosal exposure to infective body fluids such as blood, semen, vaginal secretions and any other body fluid containing blood.36 Major modes of transmission include sexual or close household contact with an infected person, perinatal transmission from mother to infant, injecting drug use and nosocomial exposure.36 The analysis in this report is restricted to acute hepatitis B.

Case definitions


Notifications

National definition for newly acquired hepatitis B from January 2004:10

Detection of hepatitis B surface antigen (HBsAg) in a patient shown to be negative within the last 24 months; or

Detection of HBsAg and IgM to hepatitis B core antigen, in the absence of prior evidence of hepatitis B virus infection; or

Detection of hepatitis B virus by nucleic acid testing, and IgM to hepatitis B core antigen, in the absence of prior evidence of hepatitis B virus infection.

(See Appendix D for pre-2004 definition)

Hospitalisations

The ICD-10-AM code used to identify hospitalisations was B16 (acute hepatitis B).

As in the previous report,1 hospitalisations were included only where the relevant ICD code was the principal diagnosis.

Deaths

The ICD-10 code B16 (acute hepatitis B) was used to select deaths from acute hepatitis B.

Distribution by Indigenous status and age

Of the total 916 notifications of acute hepatitis B recorded in New South Wales, the Northern Territory, South Australia, Victoria and Western Australia over the four years from 2003 to 2006, 56 (6%) were identified as occurring in Aboriginal and Torres Strait Islander people (Table 4). For hospitalisations, 27 (9%) of the total 296 cases were recorded as Aboriginal and Torres Strait Islander in the three-year period July 2002 to June 2005 in New South Wales, the Northern Territory Queensland, South Australia and Western Australia (Table 5).

Table 4. Hepatitis B notification rates, selected Australian states, 2003 to 2006, by age group and Indigenous status

Age group
(years)
Indigenous status
Notifications* (2003–2006)
n Rate Rate ratio
0–4 Indigenous
1
0.6
2.3
Other
10
0.3
5–14 Indigenous
3
0.9
8.1||
Other
9
0.1
15–24 Indigenous
22
8.3
3.6||
Other
191
2.3
25–49 Indigenous
26
6.0
2.4||
Other
559
2.5
50+ Indigenous
4
2.7
5.6||
Other
91
0.5
All ages Indigenous
56
4.3
3.1||
Other
860
1.4

* Notifications (New South Wales, the Northern Territory, South Australia, Victoria and Western Australia only) where the date of diagnosis was between 1 January 2003 and 31 December 2006.

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

‡ Rates for all ages combined are age-standardised to the Australian Bureau of Statistics Australian population estimates for 2005.

|| Shaded cells indicate statistically significant, 95% confidence intervals greater than 1 (p<0.5).

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Table 5. Hepatitis B hospitalisations and deaths, selected Australian states, 2002 to 2005, by age group and Indigenous status

Age group
(years)
Indigenous status
Hospitalisations*
(July 2002–June 2005)
Deaths
2003–2005
n Rate Rate ratio n
0–4 Indigenous
0
0.0
0
Other
0
0.0
0
5–14 Indigenous
3
0.9
5.6
0
Other
9
0.2
0
15–24 Indigenous
5
1.9
2.1
0
Other
52
0.9
0
25–49 Indigenous
16
3.8
3.8||
0
Other
151
1.0
5
50+ Indigenous
3
2.1
4.8
0
Other
57
0.4
9
All ages§ Indigenous
27
2.4
3.8||
0
Other
269
0.6
14

* Hospitalisations (New South Wales, the Northern Territory, Queensland, South Australia and Western Australia only) where the date of separation was between 1 July 2002 and 30 June 2005.

† Deaths (the Northern Territory, Queensland, South Australia and Western Australia only) where the death was recorded between 1 January 2003 and 31 December 2005.

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

§ Includes cases with unknown ages. Rates for all ages combined are age-standardised to the Australian Bureau of Statistics Australian population estimates for 2005.

|| Shaded cells indicate statistically significant, 95% confidence intervals greater than 1 (p<0.5).

No hospitalised cases of hepatitis B were recorded as Aboriginal and Torres Strait Islander among children 0–4 years of age. However, one Aboriginal and Torres Strait Islander child in the 0–4 year age group was recorded in the hepatitis B notification data. Notification rates for acute hepatitis B increased progressively with age, peaking at age 15–24 years in those recorded as Indigenous and 25–49 years in presumed non-Indigenous people (Figure 3). Hospitalisation rates peaked in the 25–49 year age group for both cases identified as Indigenous and those presumed non-Indigenous.

Figure 3. Hepatitis B notification rates, selected Australian states,* 2003 to 2006, by age group and Indigenous status

Figure 3. Hepatitis B notification rates, selected Australian states, 2003 to 2006, by age group and Indigenous status

* New South Wales, the Northern Territory, South Australia, Victoria and Western Australia.

† Notifications where the date of diagnosis was between 1 January 2003 and 31 December 2006.

The overall Indigenous to non-Indigenous rate ratio was 3.1:1 for notifications and 3.8:1 for hospitalisations and both ratios were statistically significantly above 1.0 (Table 4 and Table 5). The rate ratios for notifications were greater than 1.0 in all age groups, highest in those aged 5–14 years, and statistically significant in all age groups except 0–4 years. The rate ratios for hospitalisations were greater than 1.0 in all age groups except 0–4 years and statistically significant in the 25–49 year age group.

No time series analysis of hospitalisations was conducted due to small numbers.

There were no Aboriginal and Torres Strait Islander deaths from acute hepatitis B recorded in the Northern Territory, Queensland, South Australia and Western Australia between 2003 and 2005 and 14 in people presumed to be non-Indigenous.

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Comment

Hepatitis B immunisation efforts initially focused, in both Indigenous and non-Indigenous Australians, on preventing maternal-infant transmission. During the late 1980s and 1990s, programs targeted newborn Aboriginal and Torres Strait Islander infants as one of several groups at high risk. In the Northern Territory, hepatitis B vaccine has been routinely given at birth to Aboriginal and Torres Strait Islander infants since 1988 and to all infants since August 1990. Adolescent vaccination programs commenced from 1997 and the universal infant hepatitis B immunisation program was introduced in all jurisdictions in May 2000.20

In the pre-vaccine era, high rates of chronic infection (5%–40%) in Aboriginal and Torres Strait Islander Australians were associated with infection in early childhood, and reflected in a rate of hepatocellular carcinoma up to 10 times that in non-Indigenous people.47,50 In more recent years, there has been little reported infection in children and adolescents, the vast majority of reported disease occurring in those aged 15–49 years, and disproportionately high rates in Aboriginal and Torres Strait Islander people of all ages.1 That pattern continues in the data presented here.

These data underestimate acute hepatitis B disease as they are unlikely to include asymptomatic infections, and do not reflect the significant chronic disease burden from hepatitis B, and later complications such as liver cirrhosis and hepatocellular carcinoma. However, the substantial impact of universal hepatitis B vaccination on all these manifestations of hepatitis B infection, on both high and low risk populations and Aboriginal and Torres Strait Islander people, has been demonstrated in Australia and overseas.51–54

Aboriginal and Torres Strait Islander people used to have high rates of infection in children, resulting in high rates of liver disease in adults. As a result of universal hepatitis B vaccination, rates of acute hepatitis B are low in Indigenous and non-Indigenous children. However, the rates are still significantly higher amongst unvaccinated Aboriginal and Torres Strait Islander adults.