Vaccine Preventable Diseases and Vaccination Coverage in Australia, 2003 to 2005

Hepatitis A

Disclaimer: This is the fourth report on vaccine preventable disease and vaccination coverage in Australia, and is 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 31, June 2007.

Page last updated: 20 July 2007

Acute infection with the hepatitis A virus (HAV), a picornavirus, presents a clinical spectrum from malaise and diarrhoea to acute hepatitis with jaundice to fulminant liver failure. Onset of symptoms is usually abrupt with fever, anorexia, malaise, nausea and abdominal discomfort followed by jaundice and dark urine.44 The single most important factor in determining the clinical presentation and outcome of HAV infection is age. Whilst only 10% to 50% of infections acquired before the age of 5 years are symptomatic, 70% to 95% of infected adults will show symptoms.43

Case definitions

See Appendix 6 for pre 2004 definition

National definition from January 2004:11

a) Detection of anti-hepatitis A virus IgM antibody, in the absence of recent vaccination;


b) Detection of hepatitis A virus by nucleic acid testing;


c) Clinical hepatitis (jaundice and/or bilirubin in urine) without a non-infectious cause
and an epidemiological link to a laboratory-confirmed case.

Hospitalisations and deaths

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

Secular trends

There were 1,075 hepatitis A notifications in the period January 2003 to December 2005 (average annual notification rate 1.8 per 100,000) (Table 4). A median of 27 cases (range 18–56) were notified per month. There were 755 hospitalisations (average annual hospitalisation rate 1.3 per 100,000) with a median of 20 admissions (range 10–36) per month.

Notification and hospitalisation rates continued to decline from 2003 to 2005 (Figure 4).These were the lowest levels recorded since national data have been collated on NNDSS from 1991 and hospitalisations from 1993, following large point-source and community epidemics in the 1990s.

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Severe morbidity and mortality

In the review period July 2002 to June 2005, there were 4,557 hospital bed days (average 1,519 per year) recorded for patients with an ICD-10-AM code for hepatitis A. Hepatitis A was the principal diagnosis in 49% of hospitalisations where hepatitis A was recorded (371 cases, average annual rate 0.6 per 100,000). This proportion was highest in those aged 0–4 years (88%), decreasing with increasing age to 24% in those aged 60 years and over. In this age group, more than 50% of hospitalisations had a principal diagnosis that was unlikely to be associated with hepatitis A infection, such as cancer, respiratory, ocular, or cardiac conditions or fractures. The median length of stay was longer for those aged 60 years and over than for younger age groups (Table 4). Hepatitis A with hepatic coma (ICD-10-AM B15.0) was recorded for six hospital admissions, one aged less than five years.

In 2003 to 2004, hepatitis A was recorded as the underlying cause of four deaths, all in people aged over 70 years. One of the cases notified to NNDSS between 2003 and 2005 was reported to have died from hepatitis A.

Figure 4. Hepatitis A notifications and hospitalisations, Australia, 1993 to 2005,* by month of diagnosis or admission

Figure 4. Hepatitis  A notifications and hospitalisations, Australia, 1993 to 2005, by month  of diagnosis or admission

* Notifications where the month of diagnosis was between January 1993 and December 2005; hospitalisations where the month of admission was between 1 July 1993 and 30 June 2005.

Table 4. Hepatitis A notifications, hospitalisations and deaths, Australia, 2002 to 2005,* by age group

Age group
3 years
3 years
(July 2002–June 2005)
LOS† per admission
2 years
n Rate n (§) Rate‡ (§) Median (§) n Rate
3.0 (3.5)
2.0 (2.0)
3.0 (3.0)
3.0 (3.0)
6.0 (6.0)
All ages
3.0 (3.0)

* Notifications where the month of diagnosis was between January 2003 and December 2005; hospitalisations where the month of separation was between 1 July 2002 and 30 June 2005; deaths where the death was recorded in 2003 or 2004.

† LOS = length of stay in hospital.

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

§ Principal diagnosis.

|| Principal diagnosis.

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Age and sex distribution

The overall male to female ratio was 1.4:1 for notifications and 1.2:1 for hospitalisations. Three of four reported deaths were in females. The sex ratio was highest in those aged less than five years (notifications 2.5, hospitalisations 2.3) and lowest in those aged five to 24 years (1.2 and 0.9, respectively).

Notification and hospitalisation rates for all age and sex groups continued to fall compared with previous years (Figures 5 and 6). The previously high rates in males aged 15–34 years declined so that from 2003 to 2005 the highest notification rate occurred among males and females aged 0–14 years (average annual rate, 2.7 per 100,000), while the highest hospitalisation rates occurred in two age groups: males aged 34–59 years and males and females aged 60 years and over (average annual rates of 1.7 per 100,000).

Notification rates tended to decrease with increasing age, while the reverse was true for hospitalisation rates. The 5–14 year age group had the highest notification rate and the lowest hospitalisation rate. Those aged 60 years and over had the lowest notification rate and the highest hospitalisation rate, and there were nearly twice as many reported hospitalisations with hepatitis A than there were notified cases in that age group.

Figure 5. Hepatitis A notification rates, Australia, 1993 to 2005,* by age group, sex and year of diagnosis

Figure 5. Hepatitis  A notification rates, Australia,  1993 to 2005, by age group, sex and year of diagnosis

* Notifications where the month of diagnosis was between January 1993 and December 2005.

Figure 6. Hepatitis A hospitalisation rates, Australia, 1993 to 2005,* by age group, sex and year of separation

Figure 6. Hepatitis A hospitalisation rates, Australia, 1993 to 2005, by age  group, sex and year of separation

* Hospitalisations where the month of separation was between 1 July 1993 and 30 June 2005.

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Geographical distribution

The highest rates were reported from the Northern Territory (average annual rates 20 per 100,000 for notifications and 8 per 100,000 for hospitalisations, Appendices 2 and 3). The jurisdiction with the next highest rates was Western Australia with 3.5 for notifications and 1.5 for hospitalisations, and there was comparatively little difference between the other jurisdictions, which ranged from 0.7 to 1.7 for notifications and 0.7 to 1.4 for hospitalisations (Appendices 2 and 3). There were no clear trends over time in any jurisdiction in the last three years of data.

Vaccination status

Vaccination status was reported for 244 (23%) of the 1,075 notifications on NNDSS from 2003 to 2005. Three of those were recorded as fully vaccinated, all adults, and there was no information on whether these were verified by written records or what the length of time was between vaccination and disease.


In Australia, as in other industrialised countries, hepatitis A occurs sporadically with periodic epidemic peaks related to point-source and community-wide outbreaks. The overall patterns are evident in hepatitis A notification and hospitalisation rates over the 13 years 1993–2005. Peaks in total hepatitis cases during the 1990s were due to a large outbreak associated with consumption of contaminated oysters in February 199765 and large community-wide epidemics mainly among men who have sex with men and injecting drug users.66–69 The decline 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.66 Notification and hospitalisation rates remained low during the last three years, with minor peaks associated with two outbreaks in Alice Springs – a food-borne outbreak in 2003 at an interstate gathering,70 and a community outbreak in 2005 for which no source was identified.71

Infection in the elderly has been reported as much more likely to lead to hospitalisation with hepatitis A as the principal cause, to involve complications or to result in death, compared with that in younger adults.72,73 However, the low proportion of hospitalisations in the elderly with hepatitis A as the principal diagnosis (24%) in these data suggests caution in interpreting hospitalisations with hepatitis A as a contributing cause in this age group. The majority of hospitalisations in this age group had principal causes 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.74 The contrastingly high proportion with a principal diagnosis in young children (88%) emphasises that hepatitis A infection, although regarded as usually asymptomatic in young children, can require hospitalisation. The total number of hospitalisations recorded here was 70% of the total notifications for a similar period. A US study has estimated that 13% of cases resulted in hospitalisation,72 suggesting substantial under-notification of hepatitis A in Australia over this period.

The most commonly reported risk exposures for notified hepatitis A cases in recent years have been travel to countries where hepatitis A is endemic, household contact with a case and attendance at child care centres.12,13,75 Others at higher risk include sewage workers, men who have sex with men, injecting drug users and Indigenous Australians.76

The epidemiology of hepatitis A differs significantly for the Indigenous population, where it has been endemic. Among non-Indigenous Australians, as in other developed countries, adolescents and young adults have a lower seroprevalence than older adults.68 In contrast, hospitalisation and notification rates are higher among Indigenous Australians, with rates in Indigenous children aged less than five years over twenty times as high as those of non-Indigenous children in the same age group.77 The rate of hospitalisation is likely to be underestimated due to the known under-identification of Indigenous people in the hospitalisation data. This greater disease burden in Indigenous children has been particularly pronounced in more remote areas.67,78,79 During 1999–2002, there were three deaths due to hepatitis A among children aged less than five years; all were Indigenous.67,77

Hepatitis A vaccines are effective in preventing disease in individuals76 and in controlling outbreaks in some settings.76,80 In Australia, vaccination is recommended for selected at-risk groups and occupations.76 In 1999, an immunisation program commenced for Indigenous children aged 18 months to 6 years living in north Queensland. Data indicate that this program has had a significant impact on reducing hepatitis A across the community.81 This was expanded in 2005 to include all Indigenous children aged 12 to 24 months in the Northern Territory, Queensland, South Australia and Western Australia.82 In the United States, hepatitis A cases decreased substantially following the recommendation of vaccination of children in communities with high rates of disease in 1996, and for states and counties with high hepatitis A notification rates in 1999. In 2006, this was expanded to include all US infants, as part of a staged implementation of progressively expanded vaccination.83 Continued monitoring should be a priority in Australia, both to assess the impact of these recent changes, and the need for any further expansion of vaccination.

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