School of Population Health

Hepatitis A – an ongoing cause of preventable illness

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Raina MacIntyre

February 18th 2015


The outbreak of hepatitis A due to contaminated frozen berries in Australia in February 2015 has caused an outcry about food security and food labeling. Managing the risks of imported food, however, is only one aspect of prevention for hepatitis A, and another aspect, vaccination, has gone unnoticed. 

Hepatitis A is a common cause of viral hepatitis, which causes more severe disease with increasing age.  Although most people recover, it can be fatal, and may cause a fulminant liver failure syndrome.  The elderly can also suffer severe complications. A proportion of people requiring liver transplant are those with acute liver failure as a result of hepatitis A.  It can often be asymptomatic or mild in children, who can shed virus in the stool and infect others, despite being asymptomatic. Close contacts of infected people are at risk of infection. Infection, once cleared, results in long-lasting antibodies and immunity to the infection. There is a safe and highly effective vaccine against hepatitis A, which requires 2 doses and confers long term immunity.

Transmission and incidence of hepatitis A

Hepatitis A is transmitted by the faecal-oral route, and may be sporadic, endemic or epidemic. It is endemic in low-income countries, with widespread incidence linked to poor sanitation. In countries such as Australia, epidemics or outbreaks may arise from contaminated foods, such as the frozen berry outbreak currently affecting Australia.  Frozen fruit has been implicated in past outbreaks.   Outbreaks also occur among men who have sex with men, in schools and child care centres. Sporadic cases in Australia and many other countries are imported by returning travellers who may acquire the infection overseas, most often due to poor food and water sanitation.

Public health response and post-exposure prophylaxis

The virus is transmitted through the faecal-oral route, so a single case can result in secondary infections in households and among other close contacts.  The public health response involves contact-tracing, and post-exposure prophylaxis (PEP). PEP used to be with human immunoglobulin, as normal human plasma contains high levels of antibodies to hepatitis A. However, over time, the hepatitis A vaccine has been used for post-exposure prophylaxis (PEP), with guidelines from 2009 onward recommending vaccine instead of immunoglobulin for PEP.  We have shown the vaccine effectiveness when hepatitis A vaccine is used as PEP to be over 95%, which provides confidence for the use of the vaccine in an outbreak. Surprisingly, the official advice to GPs during the current outbreak linked to frozen berries for people who have consumed affected berries, is to not vaccinate.  This vaccine is not recommended for Australians with no other indication for vaccine who have consumed the affected products. This is because of the low risk to an individual consumer, and because the vaccine is only effective if given soon after exposure to Hepatitis A virus. Also, a proportion of Australians (which increases with age) are already immune from previous infection, or Hepatitis A immunisation.”

Given the vaccine is safe, effective, and shown to be highly effective as post-exposure prophylaxis (and when official guidelines recommend vaccination as PEP), the risk-benefit equation for vaccinating people who have consumed affected berries would seem fairly heavily in favour of vaccination. Indeed, what are the risks of vaccinating in this situation? Why would we actively discourage anyone from seeking this vaccine, especially if they are willing to pay for it, and when it will protect against future exposures? The “low risk” to consumers is a subjective argument, given we cannot predict who among people who consume the berries will develop hepatitis A. Further, the level of risk of hepatitis A is higher in this situation than many other vaccine-preventable diseases we routinely vaccinate against. Is this actually inconsistent with the principles of the PEP guidelines which recommend vaccination? There are different means of exposure to hepatitis A. One is exposure to an infected individual; another is consumption of contaminated food. In neither case can we predict who among people exposed to infection will develop hepatitis A. In my view, PEP should be applied equally for any potential exposure.  The argument above about pre-existing immunity must be considered in the context of Australia being a country with much lower levels of immunity than developing countries.

Immunity or vulnerability to infection

Antibodies and immunity are conferred by natural infection or by vaccination. The incidence of infection correlates with poverty and socio-economic disadvantage, with the majority of adults showing evidence of past infection in developing countries.  The seroprevalence of antibodies to hepatitis A through natural infection, whilst high in developing countries, has declined in many developed countries. In wealthy countries with high standards of sanitation, a large proportion of the adult population remain susceptible to hepatitis A.  We have previously shown a decline in hepatitis A in Australia from 1993 to 2001.  However, more recently we have shown a surprising increase in serological immunity to Hepatitis A over a 30 year period from 1988 (when only 34% of people had immunity to hepatitis) to 2008 (55%). This may be due to increasing international travel and/or uptake of vaccination, but the reasons are unclear. In Australia, about half of adults are susceptible to hepatitis A, to me a level of vulnerability that would justify use of vaccine as PEP in an outbreak setting.

Vaccination for all children or only high risk groups?

Whilst some countries such as the USA have implemented universal childhood vaccination against hepatitis A, Australia only provides vaccination to Aboriginal and Torres Strait Islander children in the “top end” (NT, Qld, SA and WA). Otherwise, Australian guidelines recommend vaccination for high risk groups, such as travellers, high risk medical conditions, lifestyle and occupational risks.  The “top end” program arose after evidence of spectacular impact of a far north Queensland vaccination program for Indigenous children in 1999, where impressive herd immunity effects, including a significant reduction in child-care outbreaks, were seen, even in non-Indigenous children. The top end program was subsequently funded and commenced in 2005, and justified by the high burden of disease in Indigenous children

The US experience with hepatitis A vaccination

Almost 20 years ago in 1996, the US recommended the vaccine only for high risk groups, similar to current Australian recommendations. Plagued by outbreaks, a larger vaccination program in 11 states of the US was commenced in 1999, selected because the incidence of hepatitis A in these states was above a threshold value of >20/100,000. Similar to the far north Queensland experience, an impressive reduction in disease and herd immunity effect was seen.  This was followed by a universal recommendation for vaccination of all children between 1-2 years of age, with continued impact on the incidence of disease. Even the targeted program in 11 states was shown to be highly cost-effective

Time to ask questions about hepatitis A vaccination in Australia?

Whilst half the population are susceptible to hepatitis A, we will continue to see epidemics and sporadic cases in Australia. There have been much larger epidemics than the current berry outbreak in Australia during the era of vaccination. Hepatitis A is a vaccine-preventable disease, the vaccine is highly cost-effective because of herd immunity effects, the impact of universal vaccination has been demonstrated in the US, and we have already seen the dramatic benefit of it in the Top End. If we had rolled out universal childhood vaccination a decade ago, there would have been more protection against the infection in Australia. I never did understand why, after the success of the Top End program we did not expand the program for all of Australia, as they did in the US, who also started with a targeted high-risk program and expanded it as evidence of sucess was accumulated. It’s time to discuss universal hepatitis A vaccination in Australia.  


About the author:  Raina MacIntyre has researched prevention of hepatitis A since 1999.

Conflicts of interest: In the past, I have been on the Working Party for Hepatitis A for the Australian technical Advisory Group on Immunisation (ATAGI) prior to initiation of the Top End program, and did the background paper to inform that program for ATAGI. I have also in the past received funding for investigator-driven original research on vaccines and vaccine-preventable diseases from GSK and BioCSL (who manufacture hepatitis A vaccines).


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