Vaccine Preventable Diseases in Australia, 2005 to 2007

3.3 Hepatitis A

Page last updated: 24 December 2010

Hepatitis A is caused by the hepatitis A virus (HAV), an RNA virus classified within the genus hepatovirus of the picornavirus family. There is only one human HAV serotype.1–3 Hepatitis A infection causes an acute inflammatory disease of the liver and can produce either asymptomatic or symptomatic infection. Clinical manifestations of symptomatic infection vary from mild anicteric illness to fulminant hepatic failure. Severity tends to increase with age and case fatality is normally low (0.1%–0.3%).4 HAV infection typically has a sudden onset of symptoms that can include fever, anorexia, malaise, nausea, and abdominal discomfort followed by jaundice and dark urine.5,6 The likelihood of having symptoms with HAV is related to age. Only 10%–50% of infections acquired before the age of 5 years are symptomatic, while 70%–95% of infected adults show clinical symptoms.6

Case definitions


See Appendix 6.6 for pre-2004 definition

National definition from January 2004:7

Both confirmed and probable cases are notifiable.

  1. Detection of anti-hepatitis A virus IgM antibody, in the absence of recent vaccination (confirmed case); or
  2. Detection of hepatitis A virus by nucleic acid testing (confirmed case); or
  3. Clinical hepatitis (jaundice and/or bilirubin in urine) without a non-infectious cause and an epidemiological link to a laboratory-confirmed case (probable case).

Hospitalisations and deaths

The ICD-10-AM/ICD-10 code B15 (hepatitis A) was used to identify hospitalisations and deaths.

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Secular trends

There were 445 hepatitis A notifications in the period January 2006 to December 2007 (average annual notification rate 1.1 per 100,000) (Table 3.3.1). Of these 445 notifications, 428 (96%) were confirmed cases, and 17 (4%) were probable cases. A median of 18 cases (range 7–37) were notified per month. There were 408 hospitalisations in the period July 2005 to June 2007 (average annual hospitalisation rate 1.0 per 100,000) with a median of 17 admissions (range 9–25) per month. The notification rate for hepatitis A infection in Australia has declined over recent years, from 1.8 per 100,000 population reported in 2003–20058 to 1.1 per 100,000 population in 2006–2007, the lowest levels recorded since national data have been collated for notifications in the NNDSS (January 1991) and for hospitalisations (July 1993) (Figure 3.3.1). The large point source and community epidemics documented in the 1990s have not returned.

There was no apparent seasonality in notifications or hospitalisations.

Figure 3.3.1: Hepatitis A notifications and hospitalisations, Australia, 1993 to 2007,* by month of diagnosis or admission

Figure 3.3.1:  Hepatitis A notifications and hospitalisations, Australia, 1993 to 2007, by month of diagnosis or admission

* Notifications where the date of diagnosis was between January 1993 and December 2007; hospitalisations where the date of admission was between July 1993 and June 2007.

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Table 3.3.1: Hepatitis A notifications, hospitalisations and deaths, Australia, 2005 to 2007,* by age group

Age group
2 years
2 years
(July 2005–June 2007)
LOS per
2 years
n Rate n (§) Rate (§) Median (§) n Rate
All ages

* Notifications where the date of diagnosis was between January 2006 and December 2007; hospitalisations where the date of separation was between July 2005 and June 2007; deaths where the death was recorded between January 2005 and December 2006.

† LOS = length of stay in hospital.

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

§ Principal diagnosis (hospitalisations).

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Severe morbidity and mortality

In the review period July 2005 to June 2007, there were 2,617 hospital bed days (average 1,309 per year) recorded for patients with an ICD-10-AM code for hepatitis A. Overall, hepatitis A was the principal diagnosis in 55% of hospitalisations where hepatitis A was recorded (224 cases, average annual rate 0.5 per 100,000), declining from 95% in those aged 5–14 years to 42% in those aged ≥60 years. The median length of stay was longer for hospitalisations in those aged ≥60 years than for younger age groups (Table 3.3.1). There were no admissions recorded as hepatic coma (ICD-10-AM code B15.0) in the period of this report. In 2005–2006, hepatitis A was recorded as the underlying cause of 3 deaths (Table 3.3.1), 2 of them in people aged >80 years and 1 in a person aged 44 years.

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Age and sex distribution

Notification and hospitalisation rates for all age and sex groups continued to fall compared with previous years (Figures 3.3.2 and 3.3.3). In particular, the notification rate for males 15–34 years of age continued to decrease from the high rates in the latter part of the 1990s (Figure 3.3.2). For notifications, decreased rates in 2006–2007 occurred predominantly among people aged <20 years and 50–59 years. For hospitalisations, the decrease was most marked in the 0–9 years age group.

Figure 3.3.2: Hepatitis A notification rates, Australia, 1993 to 2007,* by age group, sex and year of diagnosis

Figure 3.3.2:  Hepatitis A notification rates, Australia, 1993 to 2007, by age group, sex and year of diagnosis

* Notifications where the date of diagnosis was between January 1993 and December 2007.

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Figure 3.3.3: Hepatitis A hospitalisation rates, Australia, 1993/1994 to 2006/2007,* by age group, sex and year of separation

Figure 3.3.3:  Hepatitis A hospitalisation rates, Australia, 1993/1994 to 2006/2007, by age group, sex and year of separation

* Hospitalisations where the date of separation was between July 1993 and June 2007.

Notification rates tended to be lower in older age groups, while the reverse was true for hospitalisation rates. The highest notification rate was seen in males and females aged 5–9 years and the highest hospitalisation rate in males and females aged 50–59 years. Among persons aged <40 years, notifications exceeded hospitalisations, whereas the reverse was true in those ≥40 years of age and was particularly pronounced in the ≥60 years age group (Figure 3.3.4).

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Figure 3.3.4: Hepatitis A notification rates, Australia,* 2006 to 2007 and hospitalisation rates, 2005/2006 to 2006/2007, by age group

Figure 3.3.4:  Hepatitis A notification rates,  Australia, 2006 to 2007 and hospitalisation rates, 2005/2006 to 2006/2007, by age group

* Notifications where the date of diagnosis was between January 2006 and December 2007; hospitalisations where the date of separation was between July 2005 and June 2007.

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The sex ratio differed between age groups (Figure 3.3.2), with a marked male excess for those aged 15–59 years in earlier years, not seen in those aged <15 years or ≥60 years. For the two reporting years, the overall male:female ratio was 1.2:1 for both notifications and hospitalisations. Male predominance was reported mainly in those aged 15–59 years for notifications, and in those aged 35–59 years for hospitalisations. Two of the three reported deaths were in males.

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Geographical distribution

Notification and hospitalisation rates for hepatitis A infection varied by jurisdiction, being higher in the Northern Territory, New South Wales and Western Australia than elsewhere during the respective reporting periods. The highest notification and hospitalisation rates were reported in the Northern Territory (8.2 per 100,000 population and 6.5 per 100,000 population, respectively). Rates in the other jurisdictions ranged from 0.4 to 2.1 per 100,000 for notifications and 0.5 to 1.1 per 100,000 for hospitalisations (see also Appendices 6.2 and 6.3).

There were decreasing notification rates in all jurisdictions from 2003–2005 to 2006–2007 (Figure 3.3.5), particularly notable in the Northern Territory (Appendix 6.2). There were also decreasing hospitalisation rates in the Northern Territory, South Australia, Victoria and Western Australia from 2005/2006 to 2006/2007 (Appendix 6.3).

Figure 3.3.5: Hepatitis A notification rates, Australia, 2006–2007* compared with 2003–2005, by state or territory

Figure 3.3.5:  Hepatitis A notification rates, Australia, 2006-2007 compared with 2003-2005, by state or territory

* Notifications where the date of diagnosis was between January 2006 and December 2007.

† Notifications where the date of diagnosis was between January 2003 and December 2005.

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Vaccination status

Vaccination status was reported for 169 (38%) of the 445 notifications on the NNDSS in 2006–2007. There were 162 (36% of 445) who were unvaccinated, and 7 (2% of 445) who were partially vaccinated. No notified cases were fully vaccinated, and none of the partially vaccinated cases were <7 years of age. The vaccination status was unknown in 36 (57%) of 63 notified cases who were aged <7 years, and was unknown or missing in 226 (59%) of the 382 notified cases aged ≥7 years in the current reporting period; the vaccination status of 14 (4% of 382) cases was categorised as ‘not applicable’.

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Hepatitis A infection is a worldwide problem associated with low levels of personal hygiene and sanitation.2 Australia and other developed countries have low endemicity of hepatitis A infection; cases occur sporadically with epidemic peaks associated with outbreaks.9 Hepatitis A notification and hospitalisation rates over the last 5 years have been low with a downward trend. Prior to that, there were substantial declines in notifications and hospitalisations, from the peaks observed during the 1990s which were due to a large outbreak associated with consumption of contaminated oysters in February 199710 and large community-wide epidemics, mainly among men who have sex with men (MSM) and injecting drug users (IDUs).11,12 The decrease in numbers of notifications and hospitalisations following these large outbreaks may have been due to a combination of a reduction in the number of people in high-risk groups who were susceptible to hepatitis A virus infection, and the promotion by local health authorities of vaccination and improved hygiene in target groups.13

In recent years, an increasing proportion of cases with hepatitis A infection have reported travel to countries where hepatitis A is endemic.14–16 The promotion of vaccination of travellers is the most efficient way to prevent secondary cases and reduce the burden of disease in Australia.17 Although there are currently limited data on the vaccination status of notified cases, none was fully vaccinated, with most being unvaccinated. Given the high vaccine efficacy reported, it is reasonable to assume that the majority of notified cases with unknown vaccination status were unvaccinated.

Higher risk of hepatitis A infection has been reported for various population groups, including household contacts of a case, MSM, sewage workers, IDUs, those attending child care centres, homeless individuals and Indigenous Australians.2,11,13,15,16,18–27 The epidemiology of hepatitis A differs significantly for the Aboriginal and Torres Strait Islander population, in whom it has been endemic. Among non-Indigenous Australians, as in other developed countries, adolescents and young adults have a lower seroprevalence than older adults.11 In contrast, hospitalisation and notification rates are higher among Indigenous Australians, with rates in Indigenous children aged <5 years over 20 times as high as those of non-Indigenous children in the same age group.28 The rate of hospitalisation is likely to be underestimated, due to the known under-identification of Indigenous Australians in the hospitalisation data. This greater disease burden in Indigenous children has been particularly pronounced in more remote areas.18,19,29 During 2003–2006, there was 1 death due to hepatitis A in a person aged >50 years identified as Indigenous.28

Prevention of hepatitis A infection is effectively achieved by hepatitis A vaccination.30–32 In Australia, vaccination is recommended for selected at-risk groups and occupations.30 In 1999, an immunisation program commenced for Indigenous children aged 18 months living in north Queensland, with catch-up vaccination up to the 6th birthday. Data indicated that this program had a significant impact on reducing hepatitis A across the community.18 This program was expanded in 2005 to include all Indigenous children aged ≤5 years in the Northern Territory, Queensland, South Australia and Western Australia.33 In the expanded program, children aged <2 years received the vaccine in the primary program and children aged 2–5 years in the catch-up program which finished in 2007.34 As the hepatitis A vaccination program has been running in north Queensland since 1999, most Indigenous children >2 years of age have now been immunised against hepatitis A in this region. Therefore, children ≤2 years of age in this region are currently provided with the free vaccine. This program appears to have contributed to the declining trend in notifications from these regions in the current reporting period (Figure 3.3.5). Similar trends have been observed in the USA where the number of hepatitis A cases decreased substantially following the staged implementation of vaccination of all infants and children in the country.14,35

More hospitalisations and deaths due to complications of hepatitis A infection have been reported in the elderly compared with younger adults,36,37 but the hospitalisation data for people aged ≥60 years in the current report should be interpreted with caution. The majority of hospitalisations in this age group had principal diagnoses unlikely to be related to hepatitis A and, therefore, may reflect the high prevalence of co-morbidities in the elderly and incidental hepatitis A infection. A recent report from the USA of false positive IgM anti-hepatitis A virus tests in those without clinical hepatitis found this to be particularly common in the elderly.38 In contrast, among the hepatitis A hospitalisations in young children aged 5–14 years (95%), there was a high proportion with hepatitis A as the principal diagnosis; this emphasises that hepatitis A infection in young children, although regarded as generally asymptomatic, can require hospitalisation.

Enhanced surveillance (including more complete case information, such as risk factors and vaccination status) is needed to fully evaluate the hepatitis A vaccination program in Australia, to assess both the impact of new vaccination initiatives and the need for expansion of vaccination programs.

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16. Ward K, McAnulty J. Hepatitis A: who in NSW is most at risk of infection? N S W Public Health Bull 2008;19(1–2):32–35.

17. Zwar N, Streeton CL. Pretravel advice and hepatitis A immunization among Australian travelers. J Travel Med 2007;14(1):31–36.

18. Hanna JN, Hills SL, Humphreys JL. Impact of hepatitis A vaccination of Indigenous children on notifications of hepatitis A in north Queensland. Med J Aust 2004;181(9):482–485.

19. Adams L, Johnson G. Hepatitis A virus infection, immunisation and the Kimberley [letter]. Kimberley Public Health Bulletin 2003;May:13.

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20. O’Donovan D, Cooke RP, Joce R, Eastbury A, Waite J, Stene-Johansen K. An outbreak of hepatitis A amongst injecting drug users. Epidemiol Infect 2001;127(3):469–473.

21. MacIntyre CR, Burgess MA, Hull B, McIntyre PB. Hepatitis A vaccination options for Australia. J Paediatr Child Health 2003;39(2):83–87.

22. MacIntyre CR, Burgess M, Isaacs D, McIntyre PB, Menzies R, Hull B. Epidemiology of severe hepatitis A in Indigenous Australian children. J Paediatr Child Health 2007;43(5):383–387.

23. Poulos R, Ferson M, Orr K, Lucy A, Botham S, McCarthy M, et al. Risk factors and seroprevalence of markers for hepatitis A, B and C in persons subject to homelessness in inner Sydney. Aust N Z J Public Health 2007;31(3):247–251.

24. Sunthornchart S, Linkins RW, Natephisarnwanish V, Levine WC, Maneesinthu K, Lolekha R, et al. Prevalence of hepatitis B, tetanus, hepatitis A, human immunodeficiency virus and feasibility of vaccine delivery among injecting drug users in Bangkok, Thailand, 2003–2005. Addiction 2008;103(10):1687–1695.

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29. Bowden FJ, Currie BJ, Miller NC, Locarnini SA, Krause VL. Should Aboriginals in the “Top End” of the Northern Territory be vaccinated against hepatitis A? Med J Aust 1994;161(6):372–373.

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30. National Health and Medical Research Council. The Australian Immunisation Handbook. 9th edn. Canberra: Australian Government Department of Health and Ageing, 2008.

31. André FE. Universal mass vaccination against hepatitis A. Curr Top Microbiol Immunol 2006;304:95–114.

32. Wasley A, Fiore A, Bell BP. Hepatitis A in the era of vaccination. Epidemiol Rev 2006;28:101–111.

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34. Government of South Australia, Department of Health. Questions and answers about the new Hepatitis A Vaccination Program: information for immunisation providers. 2005. Available from: Accessed on 22 October 2009.

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36. Koslap-Petraco MB, Shub M, Judelsohn R. Hepatitis A: disease burden and current childhood vaccination strategies in the United States. J Pediatr Health Care 2008;22(1):3–11.

37. Brown GR, Persley K. Hepatitis A epidemic in the elderly. South Med J 2002;95(8):826–833.

38. Centers for Disease Control and Prevention. Positive test results for acute hepatitis A virus infection among persons with no recent history of acute hepatitis—United States, 2002–2004. MMWR Morb Mortal Wkly Rep 2005;54(18):453–456.

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