Vaccine Preventable Diseases in Australia, 2005 to 2007

3.4 Hepatitis B

Page last updated: 24 December 2010

Acute infection with hepatitis B virus (HBV), a hepadnavirus, 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.1,2 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.1 Of people chronically infected with HBV, without therapeutic intervention 15%–40% develop cirrhosis of the liver and/or hepatocellular carcinoma.3,4

HBV transmission occurs by percutaneous or permucosal exposure to infective body fluids such as blood, semen and vaginal secretions.1 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.1 The summary below is restricted to acute, or newly acquired, hepatitis B. Reviews of the burden of disease related to chronic hepatitis B infection in Australia have been published elsewhere.3,5–7

Case definitions

Notifications

See Appendix 6.6 for pre-2004 definition

National definition* for newly acquired hepatitis B from January 2004:8

Only confirmed cases are notifiable.

  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 (anti-HBc IgM), 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 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 2 years from January 2006 to December 2007, there were 580 notifications (average annual rate 1.4 per 100,000) with a median of 24.5 notifications per month (range 16–38) (Figure 3.4.1; Table 3.4.1). The national annual notification rate had an upward trend between 1997 and 2001, peaked in 2001 at 2.2 per 100,000, before declining to 1.2 per 100,000 in 2005 and 1.4 per 100,000 in 2007 (Appendix 6.2).

Figure 3.4.1: Acute hepatitis B notifications, and hospitalisations with a principal diagnosis of acute hepatitis B, Australia, 1996 to 2007,*,† by month of diagnosis or admission

Figure 3.4.1:  Acute hepatitis B notifications, and hospitalisations with a principal diagnosis of acute hepatitis B, Australia, 1996 to 2007, by month of diagnosis or admission

* In contrast to previous reports, this figure only includes data from 1996 onwards as, prior to July 1994, hospitalisations for acute hepatitis B could not be distinguished from hospitalisations for chronic hepatitis B infection, and it was not until 1996 that 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.

† Notifications where the date of diagnosis was between January 1996 and December 2007; hospitalisations where the date of admission was between January 1996 and June 2007.

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In the period from July 2005 to June 2007, there were 315 hospitalisations with a principal diagnosis of acute hepatitis B (average annual rate 0.77 per 100,000) with a median of 13 hospitalisations per month (range 9–19). Nearly all (98%; 310/315) of these hospitalisations were coded as ‘acute hepatitis B without delta-agent and without hepatic coma’ (ICD-10-AM code B16.9). Hospitalisations have generally declined since 1993, stabilising at a national rate of 0.7–0.8 per 100,000 since 2003 (Appendix 6.3).

Table 3.4.1: Acute hepatitis B notifications, hospitalisations and deaths, Australia, 2005 to 2007,* by age group

Age group
(years)
Notifications
2 years
(2006–2007)
Hospitalisations
2 years
(July 2005–June 2007)
LOS per admission
(days)
Deaths
2 years
(2005–2006)
n Rate§ n Rate§ Median n Rate§
0–4
5
0.19
0
0
5–14
8
0.15
2
0.04
n.p.
0
15–24
120
2.06
43
0.75
4.0
0
25–59
419
2.07
248
1.24
4.0
21
0.10
60+
28
0.37
22
0.30
8.0
18
0.25
All ages
580
1.39
315
0.77
4.0
39
0.09

* 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.

† 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.

n.p. Not published.

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Severe morbidity and mortality

For patients with a principal diagnosis of acute hepatitis B, 1,843 hospital bed days were recorded over the 2-year reporting period between July 2005 and June 2007 (916 in 2005/2006 and 927 in 2006/2007). The median length of stay was 4 days, with longer stays for adults aged ≥60 years (Table 3.4.1). There was only one case of hepatic coma, aged 25–59 years, recorded in 2006/2007, among hospitalisations with a principal diagnosis of acute hepatitis B.

There were 39 deaths from acute hepatitis B recorded in the AIHW National Mortality Database in the 2 years between January 2005 and December 2006, 30 in males and 9 in females. All deaths occurred in those aged ≥25 years. Approximately half occurred in those aged 25–59 years and half in those aged ≥60 years. The number of deaths in 2006 was almost double that in 2005 (25 vs 14 by date of recording, and 23 vs 16 by actual date of death). The underlying cause of death in 2 of these 39 cases was acute hepatitis B (without delta agent) with hepatic coma (ICD-10 code B16.2); both these deaths were recorded in 2006. The remaining 37 cases were without hepatic coma (ICD-10 code B16.9). In contrast, only 4 deaths in notified cases were recorded during 2005 and 2006 and none in 2007.

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Age and sex distribution

In 2006–2007, the peak acute hepatitis B notification rate was in the 25–29 years age group (average annual rate 3.7 per 100,000), followed by the 20–24 years age group (average annual rate 2.8 per 100,000) (Figure 3.4.2). Historically, notification rates have consistently been highest in older adolescents and young adults aged 15–29 years. Between 2001 and 2005, notification rates declined in this age group, particularly among persons 15–19 years of age, where, for the first time in 2005, rates fell below 1 per 100,000. Since 2005, there has been a continued decline in the rates among persons 20–24 years of age, but not among persons 15–19 and 25–29 years of age, with notification rates of 1.2 per 100,000 and 3.8 per 100,000, respectively, in 2007. Rates have remained fairly stable in the other age groups. As in previous years, there were more male than female notifications in almost all age groups in 2006 and 2007, with an overall male:female ratio of 1.7:1.

Figure 3.4.2: Acute hepatitis B notification rates, Australia, 1996 to 2007,* by age group and year of diagnosis

Figure 3.4.2:  Acute hepatitis B notification rates, Australia, 1996 to 2007, by age group and year of diagnosis

* Notifications where the date of diagnosis was between January 1996 and December 2007.

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As in previous years, during the period July 2005 to June 2007, rates for hospitalisations with a principal diagnosis of acute hepatitis B varied between males and females (Figure 3.4.3). Males had almost double the hospitalisation rate of females (an overall male:female ratio of 1.9:1). Among males, hospitalisation rates were highest in the 25–29 years age group (2.1 per 100,000). Among females, the rates were highest in the 35–39 years age group (1.1 per 100,000). Among persons 15–24 years of age there was little gender disparity in hospitalisation rates.

Figure 3.4.3: Acute hepatitis B hospitalisation rates, Australia, 2005/2006 to 2006/2007,* by age group and sex

Figure 3.4.3:  Acute hepatitis B hospitalisation rates, Australia, 2005/2006 to 2006/2007, by age group and sex

* Hospitalisations where the principal diagnosis was acute hepatitis B and the date of separation was between July 2005 and June 2007.

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Geographical distribution

During the period January 2006 to December 2007, Victoria recorded the highest number of notifications (n=191; 33% of total notifications), followed by Queensland (n=114; 20% of total notifications), with the Northern Territory having the highest average annual notification rate at 4.5 per 100,000. The Australian Capital Territory and Western Australia had the next highest notification rates (2.8 and 2.2 per 100,000, respectively), while rates were 1.8 per 100,000 or less in the other jurisdictions (Appendix 6.2). Rates in the Australian Capital Territory doubled from 1.8 per 100,000 (n=6 cases) in 2006 to 3.8 per 100,000 (n=13 cases) in 2007. For the   years 2005/2006 to 2006/2007, the Northern Territory had the highest annual average hospitalisation rate for acute hepatitis B (1.4 per 100,000), followed by Victoria (1.0 per 100,000) (Appendix 6.3).

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Vaccination status

Universal infant hepatitis B immunisation was introduced in Australia in May 2000, and high school programs of hepatitis B immunisation for older children and adolescents were introduced at varying times in different jurisdictions. Over the review period, there were 14 cases of acute hepatitis B in children born since 1 May 2000, with 5 cases notified in 2006–2007. One, which was notified in 2005, was recorded as Indigenous. One of the 5 cases notified in 2006–2007 had received 4 doses of vaccine (validated); the vaccination status was recorded as “unknown” or “missing” in the remaining 13 of these 14 cases on NNDSS.

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Comment

Since 2004, only confirmed cases of newly acquired hepatitis B have been notified. This change in requiring the absence of prior evidence of hepatitis B infection in a confirmed case could have partially contributed to less notifications since 2004; however, the declining trend of notifications started before this change.9 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 years age group. The decline in notifications in those aged 15–29 years since 2001 is consistent with the marked reduction in injecting drug use since the heroin drought and estimated declines in hepatitis C incidence.10 The rapid decline in notifications from 2003 to 2005 seems to have plateaued in 2006 and 2007. The slight increase in notifications in this reporting period may partly be due to more complete case follow-up; as a result, cases that were previously reported as unspecified hepatitis B were able to be confirmed as newly acquired.11 Several reports note high rates of chronic hepatitis B carriage in immigrants and refugees from both Asia–Pacific countries and sub-Saharan Africa.12,13 However, notification data from Victoria since 2006 report that approximately 70%–80% of newly acquired notifications were from those born in Australia, and only a few cases were notified in Aboriginal and Torres Strait Islander people.14–18

The source of exposure for hepatitis B in 2006 was reported in South Australia, Victoria and the Australian Capital Territory. The proportion of incident hepatitis B notifications associated with injecting drug use has not increased, remaining stable at approximately 51% from 2002 to 2006.11 Injecting drug use was the main risk factor identified in notification data from Victoria in 2006–2007.14–18

The first Australian children received hepatitis B vaccines as infants in the late 1980s. Adolescent hepatitis B catch-up immunisation programs for children aged 10–13 years were introduced from 1997 and implemented at different times by jurisdictions (New South Wales 1999, the Northern Territory 1998 [catch-up program only], Tasmania 1998, Victoria 1998, South Australia 1999, Western Australia 2002, and the Australian Capital Territory 1999).19 This program may be responsible for the continuing low rates in those aged <25 years. In a national serosurvey in 2002, the prevalence of hepatitis B surface antibody detection among those aged 12–17 years was 45.5%, nearly 2-fold higher than the prevalence seen in the serosurvey of 1996–1999 (28.5%). Prevalence of hepatitis B surface antibody detection was significantly higher in those states and territories that had implemented school-based programs.20 This cohort was aged 17–22 years in 2006–2007 and their vaccine-induced immunity to hepatitis B is likely to account for some of the recent decrease in notifications in adolescents.

The effect of the universal infant hepatitis B immunisation policy on the reported incidence of acute hepatitis B in the 15–25 years age group will start to become apparent from 2015 onwards (which is 15 years after the universal program started). In countries with a high burden of hepatitis B, such as Taiwan and Italy, universal hepatitis B vaccination programs have had a profound impact on the incidence of chronic infection and hepatocellular carcinoma.21,22 Fourteen cases of hepatitis B were notified to NNDSS for children born since 1 May 2000, with 5 cases in 2006–2007, and nearly all (93%; 13/14) had vaccination status recorded as “unknown”. Reporting of cases according to age and vaccination status will become more important as the vaccinated cohort ages, and will assist in measuring the impact of vaccination and the duration of immunity. Data on the duration of immunity following infant vaccination in low endemic countries is sparse.

Notification rates were substantially higher than hospitalisation rates in all age groups in 2006–2007. The 39 deaths recorded in 2005 and 2006, all aged ≥25 years, increased from an annual average of approximately 10 since 2001. Misclassification remains a potential problem, as only 2 of the 39 deaths recorded for 2005 and 2006 had acute hepatitis B with hepatic coma (ICD-10 codes B16.0 [with delta agent] or B16.2 [without delta agent]) recorded as the underlying cause of death. This is probably due to misclassification of some chronic hepatitis B cases, particularly those with hepatic flare who had detectable anti-hepatitis B core immunoglobulin M antibodies (anti-HBc IgM), as acute hepatitis B infection. The mortality rate in those aged 25–59 years has more than doubled from 0.04 per 100,000 in 2003–20049 to 0.10 per 100,000 in 2005–2006, notwithstanding limitations of the data and possible misclassifications of chronic HBV deaths.

The current prevalence of chronic HBV infection reflects historical transmission patterns and possibly the recent arrival of immigrants from high endemic countries. Data from Victoria on the country of birth of persons with newly acquired hepatitis B infection suggests approximately 20% of cases were born outside Australia. Over the next decade the full impact of immunisation policies implemented from the 1990s should be reflected in trends in chronic infection and reductions in hepatitis B related complications, such as liver cirrhosis and hepatocellular carcinoma.5,6,23

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References

1. Hepatitis, viral. 11. Viral hepatitis B. In: Heymann DL, ed. Control of Communicable Diseases Manual. 19th edn. Washington, DC: American Public Health Association, 2008.

2. Kaldor JM, Plant AJ, Thompson SC, Longbottom H, Rowbottom J. The incidence of hepatitis B infection in Australia: an epidemiological review. Med J Aust 1996;165(6):322–326.

3. Ryder SD, Beckingham IJ. ABC of diseases of liver, pancreas, and biliary system: chronic viral hepatitis. BMJ 2001;322(7280):219–221.

4. O’Sullivan BG, Gidding HF, Law M, Kaldor JM, Gilbert GL, Dore GJ. Estimates of chronic hepatitis B virus infection in Australia, 2000. Aust N Z J Public Health 2004;28(3):212–216.

5. Law MG, Roberts SK, Dore GJ, Kaldor JM. Primary hepatocellular carcinoma in Australia, 1978–1997: increasing incidence and mortality. Med J Aust 2000;173(8):403–405.

6. Williams A. Reduction in the hepatitis B related burden of disease—measuring the success of universal immunisation programs. Commun Dis Intell 2002;26(4):458–460.

7. Amin J, Law MG, Bartlett M, Kaldor JM, Dore GJ. Causes of death after diagnosis of hepatitis B or hepatitis C infection: a large community-based linkage study. Lancet 2006;368(9539):938–945.

8. Communicable Diseases Network Australia. Surveillance case definitions for the Australian National Notifiable Diseases Surveillance System. 2004. Available from: http://www.health.gov.au/internet/main/publishing.nsf/Content/cdna-casedefinitions.htm Accessed on 24 August 2009.

9. Brotherton J, Wang H, Schaffer A, Quinn H, Menzies R, Hull B, et al. Vaccine Preventable Diseases and Vaccination Coverage in Australia, 2003 to 2005. Commun Dis Intell 2007;31(Suppl):S1–S152.

10. Razali K, Thein HH, Bell J, Cooper-Stanbury M, Dolan K, Dore G, et al. Modelling the hepatitis C virus epidemic in Australia. Drug Alcohol Depend 2007;91(2–3):228–235.

11. Begg K, Roche P, Owen R, Liu C, Kaczmarek M, Hii A, et al. Australia’s notifiable diseases status, 2006: annual report of the National Notifiable Diseases Surveillance System. Commun Dis Intell 2008;32(2):139–207.

12. Martin JA, Mak DB. Changing faces: a review of infectious disease screening of refugees by the Migrant Health Unit, Western Australia in 2003 and 2004. Med J Aust 2006;185(11–12):607–610.

13. Gibney KB, Torresi J, Lemoh C, Biggs BA. Isolated core antibody hepatitis B in sub-Saharan African immigrants. J Med Virol 2008;80(9):1565–1569.

14. Public Health Branch, Department of Human Services Victoria. Surveillance of notifiable infectious diseases in Victoria, 2006. Victoria: Department of Human Services, 2008.

15. Higgins N. Surveillance report. Blood borne viruses: hepatitis B – acute. Victorian Infectious Diseases Bulletin 2007;10(2):43.

16. Higgins N. Surveillance report. Blood borne viruses: hepatitis B – newly acquired. Victorian Infectious Diseases Bulletin 2007;10(3):68.

17. Higgins N. Surveillance report. Blood borne viruses: hepatitis B – newly acquired. Victorian Infectious Diseases Bulletin 2007;10(4):102.

18. Higgins N. Surveillance report. Blood borne viruses: hepatitis B – newly acquired infections. Victorian Infectious Diseases Bulletin 2008;11(1):19.

19. Skinner R, Nolan T. Adolescent hepatitis B immunisation – should it be the law? Aust N Z J Public Health 2001;25(3):230–233.

20. Gidding HF, Warlow M, MacIntyre CR, Backhouse J, Gilbert GL, Quinn HE, et al. The impact of a new universal infant and school-based adolescent hepatitis B vaccination program in Australia. Vaccine 2007;25(51):8637–8641.

21. Shepard CW, Simard EP, Finelli L, Fiore AE, Bell BP. Hepatitis B virus infection: epidemiology and vaccination. Epidemiol Rev 2006;28:112–125.

22. Mele A, Tosti ME, Mariano A, Pizzuti R, Ferro A, Borrini B, et al. Acute hepatitis B 14 years after the implementation of universal vaccination in Italy: areas of improvement and emerging challenges. Clin Infect Dis 2008;46(6):868–875.

23. Condon JR, Barnes T, Cunningham J, Armstrong BK. Long-term trends in cancer mortality for Indigenous Australians in the Northern Territory. Med J Aust 2004;180(10):504–507.

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