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Details on all cases of hepatitis A notified in North Queensland in 1996 and 1997 were prospectively collected. There were two substantial outbreaks and a total of 225 cases during this period. The total incidence rate (per 100,000) was 11.0 in 1996 and 27.0 in 1997. Aborigines and Torres Strait Islanders constituted 29% of cases and had incidence rates of 75.2 and 62.7 per 100,000 for 1996 and 1997 respectively. Thirty-nine cases (17.3%) were admitted to hospital for a total of 202 bed-days and a 4 year old died with fulminating hepatitis. A probable source of infection was identified for 69% of cases. The common risk categories for infection were: living in or visiting a rural Aboriginal or Torres Strait Islander community, injecting drug use, contact with a known case of hepatitis A, and travel to countries with endemic hepatitis A. Commun Dis Intell 1999;23:120-124.

Introduction

Infection with the hepatitis A virus (HAV) causes considerable morbidity in North Queensland. (Figure 1 illustrates the geographical extent of Far North Queensland and the North Queensland Public Health Zone.) For example, Far North Queensland was subjected to a prolonged community-wide epidemic from 1992 to 1994 (Figure 2). During this epidemic numerous episodes of transmission in child day-care centres were documented and many occupational exposures were identified.^1,2,3

An inactivated hepatitis A vaccine was first licensed in Australia in 1993 and recommendations for its use were subsequently published by the National Health and Medical Research Council (NHMRC).⁴ The Tropical Public Health Unit (TPHU) promoted vaccination of at-risk groups, including staff at child day-care centres and some health care providers, in response to the Far North Queensland epidemic.

This prospective study was undertaken to describe the current epidemiology of hepatitis A in North Queensland, and to reassess the risk factors for what is now a vaccine preventable disease.

Figure 1. Map of North Queensland



Figure 2. Notifications of hepatitis A in Far North Queensland, quarter of year



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Methods

The TPHU collected details on all notified cases of hepatitis A in the North Queensland Public Health Zone for 1996 and 1997 (Figure 1). The Zone has a population of 592,000, 8.1% of whom are Aborigines or Torres Strait Islanders.⁵ Acute hepatitis A is a notifiable disease in Queensland and all public and private laboratories in North Queensland are therefore required to notify the TPHU when IgM antibodies to hepatitis A (anti-HAV IgM) are detected in serum. In addition, clinicians are requested to report any clinical case of acute hepatitis, regardless of whether confirmatory serology is available. All cases in this report were thus confirmed by the presence of anti-HAV IgM in the absence of recent vaccination, or had an illness consistent with hepatitis and an epidemiological link to a serologically confirmed case.⁶

The staff at TPHU contacted the treating doctor of each notified case and, when possible, interviewed the patient directly. The following details were sought: onset date of illness, age, sex, race, address, occupation, potential risk categories for infection,⁷ management, immediate health outcome and contacts eligible for hepatitis A prophylaxis. Normal human immunoglobulin (NHIG) was provided to contacts in conjunction with the treating doctor and further public health measures were instituted as required.

Incidence rates were calculated for the total and the indigenous population in North Queensland using denominator data from the 1996 Australian Bureau of Statistics Census.⁵

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Results

A total of 225 cases were notified; 65 in 1996 and 160 in 1997. Total incidence rates were thus 11.0 and 27.0 per 100,000 persons for 1996 and 1997 respectively. Only one case was not serologically confirmed. In addition to sporadic cases, there were two substantial outbreaks; one in the Torres Strait during 1996 (34 cases) and a second in Mackay during 1997 (72 cases) (Figure 3). There were also discrete clusters in two rural Aboriginal communities during 1997, both resulting in 9 notifications. The majority of cases were Caucasian (151), but Aboriginal and Torres Strait Islanders were clearly over-represented as they accounted for 29% (66) of all cases. Incidence rates for indigenous persons were 75.2 and 62.7 per 100,000 persons for 1996 and 1997 respectively.

Figure 3. Notifications of hepatitis A, North Queensland, 1996 to 1997



Hepatitis A was more common in children and young adults, and the mean age of Aboriginal and Torres Strait Islander cases (12.6 years) was significantly lower than that of non-indigenous cases (30.0 years, p<0.001) (Figure 4). There were more male than female cases (140 and 85 respectively).

Figure 4. Notifications of hepatitis A, North Queensland, 1996 to 1997, by age and indigenous status



Thirty-nine cases (17.3%) were admitted to hospital, for a total of 202 bed days (median length of hospital stay 4 days, range 1-18 days). Four people required transfer from a peripheral hospital to a regional base hospital and a 45 year old Australian resident was evacuated by air from Papua New Guinea (PNG) to Cairns acutely ill with hepatitis A.

There was one death during 1997. A 4 year old Aboriginal boy developed severe hepatic encephalopathy due to fulminating hepatitis A and died in the Royal Childrens Hospital in Brisbane before liver transplantation was possible.

Risk categories indicating a probable source of infection were identified for 69% of cases, a possible source for a further 2%, and for 29% the source was unknown. Some cases had more than one risk factor identified (Table 1). For example, among those who had contact with a known case, 17 were also identified as injecting drug users, 7 were in the rural indigenous group, 2 had travelled overseas to HAV endemic areas and 1 had child day-care contact. Only a few cases in other groups had multiple risk factors. People were allocated to risk categories on the basis of available information and misclassification may have occurred for some cases. For example, it is likely that some cases had unrecognised contact with an HAV-infected person and that not all injecting drug users (IDUs) were identified.

Table 1. Risk category for source of hepatitis A infection, North Queensland, 1996-97

Probable source of infection	Number	Per cent
Rural indigenous community resident or visitor	59	26
Contact with a known case	43	19
Injecting Drug Use	41	18
Overseas travel to an endemic country	17	8
Urban indigenous community resident	10	4
Child day-care contact (children, staff and parents)	10	4
Homosexual male	4	2
Oysters (Wallis Lake outbreak)	4	2
Sewage exposure	1	0
Total cases with one or more probable risk categories	155	69
Possible source of infection
Cleaner	5	2
Unknown source	65	29
Total notified cases	225	100

The most common risk category indicating a probable source of infection was either living in or visiting a rural Aboriginal or Torres Strait Islander community. The majority of people infected in these communities were local indigenous residents, but two non-indigenous residents (a doctor and a hospital clerk) and three visitors also acquired HAV infection. Other common risk categories were injecting drug use (IDU), contact with a known case of hepatitis A, and travel to overseas countries with endemic hepatitis A.

A total of 41 cases were identified as IDUs, 34 of whom were involved in the Mackay outbreak. A variety of different drugs, including amphetamines and heroin, were injected by the affected IDUs and no common drug source was identified. Very few cases reported sharing needles, but many described sharing other objects such as cigarettes and bongs. Many lived in houses with other IDUs. During 1997 several other outbreaks of HAV infection in IDUs were identified in southern Queensland but no epidemiological links with the Mackay outbreak were established.

Seventeen cases probably acquired their infection overseas. None had received HAV vaccination or NHIG prior to travel. The most common regions implicated were Papua New Guinea (9 cases) and South East Asia (3 cases).

Other risk categories accounting for small numbers of cases included urban indigenous residents, association with child day-care centres, homosexual males, eating oysters implicated in an outbreak ⁸ and exposure to sewage. Cleaners could feasibly be exposed to HAV in their workplace and were over-represented as an occupational group among cases; they were included as a possible risk category.

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Discussion

Hepatitis A results in considerable morbidity and expense for the North Queensland community. The death of a 4 year old child during this period also indicates how serious this infection can be. While the reported case fatality rate for HAV infection is low (<1/1000), higher rates have been reported in children under the age of 5 years (1.5/1000) and adults over the age of 50 years (27/1000).⁹ As a safe and effective vaccine is available, there is a need to consider whether more can be done to prevent HAV infection in north Queensland.

This report identifies a number of key population groups that continue to be at increased risk of contracting HAV infection. These include rural and urban indigenous community residents and visitors, IDUs and people travelling to endemic regions overseas.

Many rural Aboriginal and Torres Strait Islander communities have endemic HAV infection. Nearly all residents (98.5%) from a sample of remote Aboriginal communities in the Northern Territory (NT) were immune to HAV by the age of 10 years when assessed in 1994.¹⁰ In such endemic circumstances HAV infection is usually acquired in early childhood and confers lifelong immunity. Acute infection at this early age is often mild and anicteric, thus the disease may be largely invisible despite very high real incidence rates. Clinical notifications will considerably underestimate infection in such communities.

Paradoxically, hepatitis A initially becomes a more obvious problem as communities experience lower incidence rates in response to changes such as improved sewage disposal, housing and water supply. Fewer early childhood infections result in a susceptible pool of older children, adolescents and adults, and infection in this older group is more likely to be clinically apparent. The outbreak that occurred in the Torres Strait during 1996 and the clusters of cases seen in several rural communities during 1997 probably reflect this transitional process. Further outbreaks and clusters can be expected as this transition continues.

The hepatitis A vaccine has been used to interrupt transmission in communities with high incidence rates but its use needs to be tailored to specific situations. Following the NT seroprevalence study noted above, it was concluded that vaccination was not indicated in those communities as only 1.5% of people over the age of 10 years of age were susceptible to HAV.¹⁰

There is thus a need for appropriate seroprevalence studies before considering an immunisation program in indigenous communities in North Queensland. Other issues such as the expense of the vaccine and the logistics involved in maintaining such a program would also need to be considered. Community-wide HAV vaccination programs often target young children (aged 3 to 5 years) on the basis that they are a vulnerable group, and because they are recognised as key transmitters of disease within a community.¹¹

Non-indigenous staff employed in indigenous communities are also at risk of HAV infection. The NHMRC currently recommends HAV vaccination for teachers and health staff in remote indigenous communities,¹² and this should be arranged prior to their arrival in the community.

Injecting drug use is well recognised as a risk category for HAV infection^7,13 but had not previously been associated with an outbreak in North Queensland. The exact mechanism by which infection is acquired is unclear, but is likely to involve the associated lifestyle and possibly the use of shared equipment such as bongs. Although the NHMRC recommends that IDUs be considered for HAV vaccination,¹² they are likely to be a difficult group to access.

The number of cases in travellers to endemic areas is of concern. Hepatitis A is the most frequent infection in travellers that can be prevented by immunisation,¹⁴ and it should be possible to more readily identify and target this group for vaccination prior to travel.

Ten cases were associated with child day-care centres; 4 were children in care, 1 was a day-care staff member and 5 were parents of children in care. All were isolated cases and all but four had another risk factor. There were no outbreaks in child day-care centres, which is in marked contrast to the 1992-94 epidemic in Far North Queensland.^1,2

There were 4 cases attributed to oysters from the Wallis Lakes in New South Wales, but no other foodborne cases were identified.

In conclusion, we have identified a number of important risk factors for HAV infection in North Queensland. There is a need for greater use of the HAV vaccine to protect at risk groups identified in the current NHMRC guidelines including IDUs and travellers to endemic areas. Vaccination also needs to be further considered for some indigenous groups.

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Acknowledgements

We thank Dr Jeffrey Hanna, Public Health Physician, TPHU for his supervision of the surveillance program and for assisting with the preparation of this report.

Author affiliations

1. Public Health Registrar, Tropical Public Health Unit, Cairns, Queensland Health, PO Box 1103, Cairns, Queensland, 4870.

2. Tropical Public Health Unit, Mackay, Queensland Health, PO Box 688, Mackay, Queensland, 4740.

3. Torres Strait and Northern Peninsula Area District Health Service, Queensland Health, PO Box 39, Thursday Island Queensland, 4875.

Corresponding author: PO Box 2651, Cairns, Queensland, 4870, E-mail: tmerritt@medeserv.com.au

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References

1. Hanna J. Hepatitis A in a child day-care centre. Commun Dis Intell 1993;17:73-75.

2. Hanna J, Brookes D. Some occupational exposures to hepatitis A. Commun Dis Intell 1994;18:3-5.

3. Hanna JN, Loewenthal MR, Negel P, Wenck DJ. An outbreak of hepatitis A in an intensive care unit. Anaesth Intens Care 1996;24:440-444.

4. National Health and Medical Research Council. The Australian Immunisation Procedures handbook. 5^th ed. Canberra: Australian Government Publishing Service, 1994:56-60.

5. Australian Bureau of Statistics. 1996 Census of population and housing. Canberra: Australian Government Publishing Service, 1997.

6. National Health and Medical Research Council. Surveillance case definitions. Canberra: Australian Government Publishing Service, 1994:3.

7. Advisory Committee on Immunization Practices. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices. MMWR 1996;45:1-30.

8. Hepatitis A outbreak in New South Wales. Commun Dis Intell 1997;21:46.

9. Benenson AS, ed. Control of communicable diseases. 16th ed. Washington: American Public Health Association, 1995:217.

10. 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;161:372-373.

11. Smith PF, Grabau JC, Werzberger A, Gunn RA, Rolka HR, Kondracki SF et al. The role of young children in a community-wide outbreak of hepatitis A. Epidemiol Infect 1997;118:243-252.

12. National Health and Medical Research Council. The Australian Immunisation Handbook. 6th ed. Canberra: Australian Government Publishing Service, 1997.

13. Harkess J, Gildon B, Istre GR. Outbreaks of hepatitis A among illicit drug users, Oklahoma, 1984-87. Am J Public Health 1989;79:463-466.

14. Steffen R, Kane MA, Shapiro CN, Billo N, Schoellhorn KJ, van Damme P. Epidemiology and prevention of hepatitis A in travellers, JAMA 1994;272:885-889.


This article was published in Communicable Diseases Intelligence Volume 23, No 5, 13 May 1999.