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

Hepatitis B

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

The focus of this chapter is acute infection with hepatitis B virus (HBV), a hepadnavirus. It 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.44,84 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 an acute infection becoming chronic varies inversely with age: chronic HBV infection occurs in about 90% of infants infected at birth, 20%–50% of children infected at 1–5 years of age, and about 1%–10% of persons infected as older children and adults.44 Of people chronically infected with HBV, 15%–40% develop cirrhosis of the liver and/or hepatocellular carcinoma.85,86

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.44 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.44 The summary below is restricted to acute hepatitis B. Reviews of the burden of disease related to chronic hepatitis B infection in Australia have been published elsewhere.85,87–89

Case definitions

See Appendix 6 for pre 2004 definition

National definition* for newly acquired hepatitis B from January 2004:11

  1. Detection of hepatitis B surface antigen (HBsAg) in a patient shown to be negative within the last 24 months; or
  2. Detection of HBsAg and IgM to hepatitis B core antigen, in the absence of prior evidence of hepatitis B virus infection; or
  3. 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.

* Queensland implemented a consistent but less comprehensive definition for laboratory notification in December 2005 for ‘Hepatitis B (acute)’: HBsAg positive AND Anti-HBc IgM positive. However the public heath protocol for notification in Queensland accepts cases meeting the broader national case definitions for notification.

Hospitalisations

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

As in the previous reports, 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.

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Secular trends

In the three years from January 2003 to December 2005, there were 874 notifications (average annual rate 1.5 per 100,000) with a median of 23.5 notifications per month (range 15–40) (Figure 7, Table 5). The peak notification rate was in the 20–29 year age group (average annual rate 3.9 per 100,000). From 2002/2003 to 2004/2005, acute hepatitis B was the principal diagnosis in 35% of all hospitalisations with acute hepatitis B. There were 517 hospitalisations with a principal diagnosis of acute hepatitis B (average annual rate 0.9 per 100,000) with a median of 13 hospitalisations per month (range 7–28). Nearly all (97% (507/521)) of these hospitalisations were coded as ‘acute hepatitis B without delta-agent and without hepatic coma’ (ICD-10-AM B16.9). The national notification rate had an upward trend between 1997 and 2001, peaked in 2001 at 2.2 per 100,000 and is now in continuing decline from 1.7 per 100,000 in 2003, to 1.4 per 100,000 in 2004 and down to 1.2 per 100,000 in 2005 (Appendix 2). Hospitalisations have generally declined since 1993/1994 and, since 1999/2000, seem to have stabilised at a national hospitalisation rate of 0.8 per 100,000 (Appendix 3).

Figure 7. Acute hepatitis B notifications, and hospitalisations with a principal diagnosis of acute hepatitis B,* Australia, 1993 to 2005, by month of diagnosis or admission

Figure 7. Acute  hepatitis B notifications, and hospitalisations with a principal diagnosis of  acute hepatitis B, Australia,  1993 to 2005, by month of diagnosis or admission

* Prior to July 1994, hospitalisations for acute hepatitis B could not be distinguished from hospitalisations for chronic hepatitis B infection.

† 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. Note that the number of jurisdictions notifying acute hepatitis B increased over the review period until 1996 when acute hepatitis B became notifiable in all states and territories. The Australian Capital Territory did not report in 1994 and Western Australia did not report in 1994 and 1995.

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Severe morbidity and mortality

For patients with a principal diagnosis of acute hepatitis B, 2,408 hospital bed days (914, 829 and 665 bed days in 2002/2003, 2003/2004 and 2004/2005, respectively) were recorded. The median length of stay was three days, with longer stays for adults aged 60 years and over (Table 5). There were 22 deaths from acute hepatitis B recorded in the two years 2003 to 2004, 17 in males and five in females. All of the deaths occurred in those aged 25 years and over, and nearly two thirds (14/22) were aged over 60 years, in whom nine of the fourteen were males. In 2003, there were twice as many deaths (15/22) as in 2004 (7/22). There were four cases of hepatic coma recorded among hospitalisations with a principal diagnosis of acute hepatitis B, with none of these cases recorded as having delta co-infection (Table 6). There were three deaths reported to NNDSS in notified cases between 2003 and 2005.

Table 5. Acute hepatitis B notifications, hospitalisations and deaths, Australia, 2002 to 2005,* by age group

Age group
(years)
Notifications
3 years
(2003–2005)
Hospitalisations
3 years
(July 2002–June 2005)
LOS per admission
(days)
Deaths
2 years
(2003–2004)
n Rate§ n Rate§ Median n Rate§
0–4
6
0.2
0
0
0
0
0
5–14
16
0.2
12
0.2
1.5
0
0
15–24
229
2.8
98
1.2
3.0
0
0
25–59
586
2.0
360
1.2
3.0
8
0.04
60+
37
0.4
47
0.5
7.0
14
0.2
All ages
874
1.5
517
0.9
3.0
22
0.06

* 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.

† Hospitalisations with a principal diagnosis of acute hepatitis B.

‡ LOS = length of stay for hospitalisations with a principal diagnosis of acute hepatitis B.

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

Table 6. Hepatic coma* in hospitalised cases with principal diagnosis of acute hepatitis B

Age group
(years)
Hepatic coma
n Hospitalisations (%)
0–4
0
0
5–14
0
0
15–24
0
0
25–59
2
0.6
60+
2
4.3
All ages
4
0.8

* Measured using National Hospital Morbidity data where the month of hospital separation was between 1 July 2002 and 30 June 2005.

† ICD-10-AM codes B16.0 and B16.2.

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Age and sex distribution

Historically, notification rates have consistently been highest in young adults aged 15–19 years, 20–24 years and 25–29 years (Figure 8). Since 2001, notification rates in these three age groups have declined, particularly in 15–19 year olds, where for the first time in 2005 rates fell below 1 per 100,000 to 0.8 per 100,000. Rates have remained fairly stable in the other age groups from 1993 to 2005. As in previous years, there were more male than female notifications in almost all age groups in 2003, 2004 and 2005, with an overall male:female ratio of 1.7:1.

During the period 2002/2003 to 2004/2005, rates for hospitalisations with a principal diagnosis of acute hepatitis B were highest in adults aged 25–29 years (1.9 per 100,000) and 20–24 years (1.8 per 100,000) (Figure 9). Like notifications, and as in previous years, hospitalisations occurred predominantly in males with an overall male:female ratio of 1.8:1.

Figure 8. Acute hepatitis B notification rates, Australia, 1993 to 2005,* by age group

Figure 8. Acute  hepatitis B notification rates, Australia,  1993 to 2005, by age group

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

Figure 9. Acute hepatitis B hospitalisation rates, Australia, 2002/2003 to 2004/2005,* by age group and sex

Figure 9. Acute  hepatitis B hospitalisation rates, Australia, 2002/2003 to 2004/2005, by age group and sex

* Hospitalisations where the principal diagnosis was acute hepatitis B and the month of separation was between
1 July 2002 and 30 June 2005.

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Geographical distribution

During the period 2003–2005, Victoria recorded the highest number of notifications (n=340; 39%), followed by New South Wales (n = 185; 21%). The Northern Territory had the highest average annual notification rate at 4.7 per 100,000. Victoria and Tasmania were next at 2.3 and 2.1 per 100,000, respectively, while rates were 1.8 per 100,000 or less in the other jurisdictions (Appendix 2). Rates in jurisdictions other than New South Wales, Queensland, South Australia, and Western Australia, declined between 2004 and 2005. (Appendix 2)

For the same period, Victoria also had the highest number of hospitalisations (n = 198; 198/517, 38%) followed by New South Wales (n = 148; 148/517, 29%).

Vaccination status

There were six cases of acute hepatitis B in children aged 0–4 years notified between 2003 and 2005 and their vaccination status was recorded as “unknown” on NNDSS.

Comment

The national notification rate for newly acquired hepatitis B appears to have peaked in 2001 at 2.2 per 100,000, mirrored by corresponding peaks in incidence in the 15–24 year old age groups. The decrease in the national acute hepatitis B notification rate observed between 2003 and 2005 is largely confined to young adults aged 15–24 years, and, in particular, young adults aged 15–19 years. Notification rates in the latter group have fallen by 75%, from 3.1 per 100,000 in 2002 to 0.8 per 100,000 in 2005, while rates in 20–24 year olds have almost halved from 5.9 per 100,000 in 2002 to 3.1 per 100,000 in 2005. Rates of unspecified hepatitis B notifications* in 2000–2004 have also fallen by nearly 50% in the 15–19 year old age group.12 This is important as this age group are not likely to meet NNDSS incident hepatitis B notification criteria (because development of a clinical illness consistent with acute viral hepatitis occurs infrequently and they are unlikely to meet “absence of prior evidence of hepatitis B virus infection” criteria). The downward trend in notifications is not likely to be due to under-reporting of notifications as rates in other age groups, under 14 years and over 25 years, have remained unchanged. The change in national notification case definitions for newly acquired hepatitis B in January 2004 to include absence of prior evidence of hepatitis B infection may have resulted in reduced notifications since 2004; however, there was a trend to reduced notifications prior to this change. In addition, notification rates increased or remained the same from 2004 to 2005 in New South Wales, South Australia, Western Australia and Queensland, despite the change in notification definitions in 2004. One potential reason for the considerable reduction in notifications, particularly in 15–24 year olds, is the declining rates of intravenous drug use since 2000, consistent with trends in hepatitis C virus notifications.90 The first Australian children received hepatitis B vaccines as infants in the late 1980s. In a national serosurvey in 2002, the prevalence of hepatitis B surface antibody detection amongst those aged 12–17 years was 45.5%, suggesting that catch-up programs have had some impact (Helen Quinn, NCIRS, personal communication).

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. In the rest of Australia, at-risk infants have been given hepatitis B vaccine since 1987 (except in South Australia, which began in 1996), while universal infant hepatitis B immunisation was introduced in May 2000. Since 1997, most jurisdictions (New South Wales 2004, Northern Territory 1998 (catch-up program only), Tasmania 1998, Victoria 1998, South Australia 1999, Western Australia 2002 and Australian Capital Territory 1999) have also implemented hepatitis B catch-up immunisation school-based programs for adolescents in school years 6, 7 or 8 (aged 11–14 years).91 The effect of this policy on the reported incidence of acute hepatitis B is not expected to become apparent until the first cohort of vaccinated infants, part of the universal program, reaches adolescence. In countries with a high burden of hepatitis B, such as Taiwan, universal hepatitis B vaccination programs have had a profound impact on the incidence of chronic infection and hepatocellular carcinoma.88,92,93

At both national and jurisdictional levels, notifications increased between 1993 and 2001 and since then have declined, while hospitalisations have remained steady since 1999. Overall, there were more hospitalisations than would be expected given the number of notifications and the epidemiology of the disease, as usually less than half of infections are clinically recognised. From 1999 to 2002, the notification rate was twice the hospitalisation rate. However, from 2003 to 2005, the ratio of notifications to hospitalisations fell to less than twofold higher.

The stabilisation in hospitalisations is likely to be a reflection of changes to coding practices, as well as misclassification of hospitalisations due to chronic infection as acute infection. In 1998/1999, ICD-10-AM, which can differentiate between acute and unspecified hepatitis B, replaced the four ICD-9-CM codes. These coding changes, more specific for acute HBV disease, are therefore likely to have been responsible for the initial reduction in hospitalisation rates from 1998/1999 and, once established, have led to the stabilisation observed nationally since 1999/2000. Improved coding practices are also likely to be responsible for the significant decrease in deaths related to acute hepatitis B from an average 50 per year for the period 1993–1997 to a sustained number of approximately 10 per year since 2001. Misclassification is likely to still be a problem, as only one of the 22 deaths recorded for 2003 and 2004 had acute hepatitis B with hepatic coma (B16.0 or B16.2) as the underlying cause of death, when it would be expected to be more frequent for acute hepatitis B deaths. This is essentially unchanged from 2001 and 2002, when one out of 20 deaths had acute hepatitis B with hepatic coma. The age distribution of deaths (nearly two thirds over 60 years old) suggests that many of these cases may have been misclassified chronic HBV deaths.

The variation in notification rates between states and territories may be due to differences in surveillance methods, but could also be a real difference resulting from differences in the proportion of the population at increased risk of hepatitis B infection. The Australian Capital Territory and Victoria instituted enhanced surveillance of acute hepatitis B in January 2000 and July 2001, respectively, and this can be expected to influence notification rates in these jurisdictions. Enhanced surveillance was instituted in Victoria in 2001, for six months, due to recognition that an outbreak of acute hepatitis B infections was occurring in injecting drug users.94 This outbreak contributed to increased rates reported nationally in 200113 and has since ended.94

Only six cases of hepatitis B were notified to NNDSS for children born after 1 May 2000 (when universal infant hepatitis B vaccination commenced) and all had vaccination status recorded as “unknown”. As this cohort (born after 1 May 2000) ages and increases in size, reporting of vaccination status will become increasingly important. Reporting of cases according to age and vaccination status will add evidence to measure the impact of vaccination. Data on the longevity of immunity following infant vaccination in low endemic countries is sparse. After 2015, nearly all children will have received hepatitis B vaccines in infancy, and notification and hospitalisation rates in 15–19 year olds are likely to reflect the impact of the universal program, as well as the longevity of immunity.

Acute hepatitis B is only one measure of the burden of disease caused by HBV. The current prevalence of chronic HBV infection reflects historical transmission patterns and, in the longer term, the impact of immunisation policies will be reflected in trends in chronic infection and its complications, such as liver cirrhosis and hepatocellular carcinoma, as seen in Taiwan.87,88,95 The recent reduction in hepatitis B notifications, particularly among the 15–24 year olds, may be due to declining intravenous drug use, as has also been seen in hepatitis C notifications. It is likely that the impact of both the targeted infant and catch-up adolescent vaccination programs will become more evident in the next 5–10 years.

* Unspecified hepatitis B notifications – detection of hepatitis B surface antigen or hepatitis B virus by nucleic acid testing in cases who do not meet any of the criteria for a newly acquired case.

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