2.2 Hepatitis A

Hepatitis A is caused by hepatitis A virus (HAV) which is a picornavirus.³ Infection may be inapparent, asymptomatic or symptomatic. Symptoms include fatigue, malaise, abdominal pain, nausea and vomiting. Features typical of hepatitis A include jaundice, dark urine and pale-coloured stools.³ Fulminant hepatitis A is the most severe form of the disease and the host factors associated with an increased risk of this complication include older age and chronic liver disease, with mortality as high as 60%. Infections acquired before the age of 5 years are asymptomatic in 50% to 90% of cases, so under-reporting may be an issue, whereas 70% to 90% of infected adults will have symptoms.³

Top of page

Disease trends

Notification rates for hepatitis A have dropped significantly over the period from 2000 to 2010, especially for Aboriginal and Torres Strait Islander people. The decline has been more marked since 2006/2007 which reflects the impact of the expanded hepatitis A vaccination program introduced in 2005 in areas of high incidence (the Northern Territory, Queensland, South Australia and Western Australia). There were no cases notified among Aboriginal and Torres Strait Islander people in 2007 or 2010 and only small numbers in 2008 and 2009. The small increase in 2009 (Figure 2.2.1) corresponds to the Australia-wide outbreak of hepatitis A which occurred mainly in non-Indigenous people.

Figure 2.2.1: Hepatitis A notification rates and 95% confidence intervals, selected Australian states,* 2000 to 2010,^† by Indigenous status

* Jurisdictions with satisfactory data quality over the whole time period; see Appendix A (New South Wales, Northern Territory, Queensland, South Australia, Victoria, Western Australia).

† Notifications where the date of diagnosis was between 1 January 2000 and 31 December 2010. Rates are age-standardised to the Australian Bureau of Statistics Australian population estimates for 2006.

Text description of Figure 2.2.1 (TXT 1 KB)

Top of page

Notification data are presented for all jurisdictions for the period 2007–2010. Hospitalisation data are presented for six jurisdictions (all except Tasmania and the Australian Capital Territory) by financial year for the period July 2006 to June 2010. This includes data from jurisdictions that were not included in the vaccination program because their disease rates were already low. The 2005/2006 year has been excluded from the hospitalisation data for hepatitis A to restrict the data to the post-vaccination period.

A total of 1,272 notifications and 869 hospitalisations for hepatitis A were recorded during their respective reporting periods; of these, 11 (0.9%) notifications and 19 (2.2%) hospitalisations were reported in Aboriginal and Torres Strait Islander people (Table 2.2.1 and Table 2.2.2). Both these numbers are much lower than in the previous reporting periods: 162 (14%) notifications (2003–2006) and 66 (11%) hospitalisations (2002/2003–2004/2005).

Table 2.2.1: Hepatitis A 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
* 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. § Indicates statistically significant, 95% confidence intervals greater than 1 (p<0.05).
0–4	Indigenous	1	0.4	0.3
	Other	70	1.3
5–14	Indigenous	5	1.0	0.5
	Other	194	1.8
15–24	Indigenous	3	0.7	0.3§
	Other	258	2.2
25–49	Indigenous	2	0.3	0.2§
	Other	500	1.7
>50	Indigenous	0	0.0	0.0§
	Other	239	0.9
All ages‡	Indigenous	11	0.5	0.3§
	Other	1,261	1.5

Top of page

Notification rate point estimates in Aboriginal and Torres Strait Islander people were lower than in other people across all age groups. The differences were statistically significant for age groups from 15 years and above. The highest rate in Aboriginal and Torres Strait Islander people was 1 per 100,000, in the 5–14 years age group, while the highest rate in others was 2.2 per 100,000, in the 15–24 years age group (Table 2.2.1). A similar pattern was seen in hospitalisation rates, with point estimates lower in Aboriginal and Torres Strait Islander people than in others across all age groups except 25–49 years (Table 2.2.2). The overall Indigenous to non-Indigenous rate ratios were 0.3:1 for notifications and 0.9:1 for hospitalisations.

No notifications or hospitalisations were recorded for Aboriginal and Torres Strait Islander people over 50 years of age during this reporting period. Among Aboriginal and Torres Strait Islander children aged 0–4 years, there were no notifications during 2008–2010 and no hospitalisations during 2006/2007–2009/2010 for the first time since 2000 (data not shown).

Table 2.2.2: Hepatitis A hospitalisations, selected Australian states, 2006 to 2010, by age group and Indigenous status

Age group (years)	Indigenous status	Hospitalisations* (2006–2010)
		n	Rate†	Rate ratio
* Hospitalisations (New South Wales, Northern Territory, Queensland, South Australia, Victoria, Western Australia only) where the date of separation was between 1 July 2006 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	13	0.3
5–14	Indigenous	2	0.4	0.8
	Other	48	0.5
15–24	Indigenous	3	0.7	0.6
	Other	129	1.2
25–49	Indigenous	14	2.2	1.8§
	Other	342	1.2
>50	Indigenous	0	0.0	0.0§
	Other	323	1.3
All ages‡	Indigenous	19	0.9	0.9
	Other	850	1.1

There were 6 deaths reported from the five reporting jurisdictions (New South Wales, the Northern Territory, Queensland, South Australia and Western Australia) for the period 2006–2010 with hepatitis A as the underlying cause and 12 deaths with hepatitis A as either the underlying or a contributing cause. None of these deaths were reported in Aboriginal or Torres Strait Islander people.

Top of page

Comment

In the immediate pre-vaccine period, notification and hospitalisation rates were significantly higher in Aboriginal and Torres Strait Islander people than in others in almost all age groups and in all ages combined.¹³ In Aboriginal and Torres Strait Islander children <5 years of age, notification rates were 24 times higher and hospitalisation rates were 150 times higher than rates in other infants. In the post-vaccination data presented here, point estimates were lower for Aboriginal and Torres Strait Islander than for other people within almost every age group. There were no significant differences in notification or hospitalisation rates for all ages combined between Aboriginal and Torres Strait Islander people and others. This, together with the trends shown in Figure 2.2.1, makes a compelling case for the success of the expanded hepatitis A vaccination program.

Since the introduction of the targeted vaccination program for Aboriginal and Torres Strait Islander children in high incidence jurisdictions, it appears that hepatitis A has almost disappeared from these areas and is now predominantly acquired outside the Northern Territory in the non-Indigenous population. This trend will have further implications in identifying and targeting non-Indigenous at-risk groups.

Prior to vaccination, in many remote Aboriginal and Torres Strait Islander communities, the probability of exposure to the hepatitis A virus was high, thus most infants became infected and immune at an early age. The Northern Territory and the Kimberley region had significantly higher rates of hepatitis A than the rest of Australia. It was thought that the disease was hyperendemic in Aboriginal and Torres Strait Islander communities in the Northern Territory.¹⁴ In the non-Indigenous population the probability of exposure was low, leaving the vast majority of the population non-immune and susceptible to more serious infection with increasing age.¹⁴ The difference in the epidemiology in the two population groups reflected different transmission dynamics arising from inequalities in housing, sanitation infrastructure, hygiene and education, and also illustrates the interaction between risk of exposure, population immunity and disease incidence.¹⁴

In recent years, however, most cases of hepatitis A in Australia have been imported via overseas travellers returning from countries where hepatitis A is endemic.^15,16 Outbreaks due to contaminated food or water have also been reported.^15,16 In 2009, an Australia-wide outbreak with 415, predominantly non-Indigenous, cases was associated with imported semi-dried tomatoes.¹⁷

Internationally, Indigenous populations like American Indian and Alaskan Native people have also suffered disproportionately from infectious diseases compared with the general population in the United States. Previously in the United States, hepatitis A recommendations targeted at-risk individuals and children living in states and communities with high hepatitis A rates, which included all Native American people. By 2004, hepatitis A disease had declined to such an extent in these populations that an epidemiological shift was noted, with approximately two-thirds of reported hepatitis A cases occurring in states with historically lower incidence and without childhood hepatitis A vaccination recommendations. Recent recommendations now call for routine hepatitis A vaccination of all children.¹⁸

Hepatitis A infection in Aboriginal and Torres Strait Islander people is now rare, and in fact possibly even less common than in non-Indigenous people, following the introduction of a targeted vaccination program. Continued surveillance and evaluation of the current vaccination program may help to identify if there is a need for future changes to the program. There is also a need to promote vaccination of travellers to prevent outbreaks and to further reduce the burden of disease in Australia.