Epidemiology of Hepatitis A in Australia Research Paper

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Literature Review

Presently in Australia, an estimated 31% percentage of the population is infected with the hepatitis virus. The hepatitis A virus (HAV)-infected individuals are heterogeneous and encompass individuals infected through contaminated medical equipment particularly injection needles and eating food or drinking water contaminated with the virus through feces. A significant percentage of diagnosed cases involve vulnerable population subgroups such as the Aboriginal people and the immigrants. The management of viral hepatitis A involves various drug therapy measures, dietary management and interventions that reduce alcohol and substance abuse.

Hepatitis A: Treatment and Diagnosis

The hepatitis A virus is a major cause of the liver disease with an estimated 1.4 million people infected with the disease globally. In Australia, the prevalence rates of HAV among young children under the age of five in Queensland were 10 and 264 per 100 000 people in non-Indigenous and Indigenous populations respectively between 1999 and 2002. Hepatitis A is leading cause of hepatocellular carcinoma or liver failure especially among children in Indigenous Australian populations.

Diagnosis of hepatitis A is through serological tests. A blood test that confirms the presence of IgM anti-HAV in blood serum indicates the diagnosis of Hepatitis A infection. The IgM antibodies indicate recent HAV infection and can remain detectable in the blood for over 6 months. On the other hand, the occurrence of anti-HAV IgG antibodies in the blood serum confers prolonged immunity in the patient. Infection by HAV normally confers effects on the patient that range from absence of symptoms to fulminant hepatitis that is often fatal. The likelihood of developing these effects increases with age. In children below 6 years old, the majority of the new infections (>60%) do not show any symptoms. In adults, new infections are symptomatic, with the most common symptom being jaundice (>70% of patients). After a four-week incubation period, majority of the HAV-infected individuals develop initial non-specific symptoms such as nausea, anorexia, vomiting and fatigue, followed by gastrointestinal discomfort, jaundice and dark urine in adults. The onset of symptoms normally occurs within the first two months of infection and serves as an indication for diagnosis.

An immune response to HAV takes place in the asymptomatic phase of the infection. HAV immunoglobulin M antibodies (IgM anti-HAV) are elevated prior to the onset of symptoms, before declining to levels undetectable by most diagnostic tests (3 to 5 months). The HAV igG antibodies (igG anti-HAV) are elevated after the IgM anti-HAV and confer long-term immunity years after infection. Following a new infection, IgM and IgA anti-HAV are detectable in urine, feces, serum and saliva. These two antibodies (antibodies produced against capsid proteins) serve as primary markers of HAV infection.

Besides the serological tests, saliva tests are used as alternative diagnostic tests for anti-HAV due to ease of sample collection especially during epidemiological studies and outbreaks. However, the sensitivity of saliva tests is lower than that of serological tests. The serological tests include enzyme-linked immunisorbent assay, dot blot immunogold filtration and radioimmunoassay. The assays are able to detect total anti-HAV (IgM and IgG antibodies). The absence of IgM anti-HAV antibodies and the presence of total anti-HAV indicate current and past infections respectively. Molecular diagnostic methods that detect HAV RNA in the blood or stool are also used in diagnosis. Nucleic acid sequencing and nucleic acid amplification methods have been used to establish the level of relatedness of HAV strains during the acute phase of the disease.

Hepatitis A has no treatment; infected individuals normally recover without treatment, 2 to 3 weeks after infection. The prevention strategies against HAV involve vaccines that confer life-long protection against HAV infection. Vaccination significantly lowers the disease incidence and the transmission of the infection. Widespread childhood hepatitis A vaccination involving the indigenous populations has significantly reduced the hepatitis A incidence and changed its epidemiology. In addition, childhood vaccination appears to prevent the cyclical nature of hepatitis A among the Australian indigenous populations. Hepatitis A vaccination strategies target at-risk groups including travelers and children living in areas with high infection rates of the disease. Routine immunization of the children has been effective in reducing transmission and outbreaks of the disease.

Recent Epidemiology of Hepatitis A in Australia

The HAV virus is usually transmitted through contaminated drink or food. As such, the incidence rates are high in areas with poor hygiene, low standards of living and densely populated areas. The disease largely confined to young children as most adults are immune. In Australia, the infection is less common in children following the widespread and routine immunization. The HAV transmission occurs readily in childhood services and households; as the children, the primary source of the infection, are often asymptomatic while adult caregivers are symptomatic. Outbreaks of the infection in Australia arise from the consumption of contaminated foods and through nasocomial transmission. Widespread childhood vaccination programs introduced in Australia have significantly reduced the incidence rates of the disease. In north Queensland, the introduction of the HAV vaccine in 1999 targeting the indigenous populations nearly eliminated HAV in these communities and reduced the incidence rates by 92% in the larger community. In 2005, the Aboriginal and Torres Straight Islanders were also included in the childhood immunization program.

In Australia, the incidence rates of Hepatitis A has declined dramatically in the recent past; from about 13, 000 cases in 1960s to only 270 cases in 2008. In 1997, the incidence of HAV reported in the Northern Territory were among the highest (52 per 100, 000 persons). However, in 2006, following the immunization program, the rates declined to 1.4 per 100,000. In New South Wales, the incidence rate declined from a high of 46.7 % in 1991to 15.4% in 2005 while in Queensland the rate decreased from 25.1% to 15.4% over the same period. In 2009, the rates increased dramatically in South Australia and Victoria (200 cases); however, this has been associated with the consumption of contaminated dried tomatoes. Between 1998 and 2000, 8 fatalities associated with HAV infection were reported nationally and 236 cases were reported in eastern Sydney between 1997 and 1999, attributed to illicit drug use, homosexual contact and consumption of contaminated foods. Hepatitis A has been the leading cause of death of children of indigenous communities in northern Queensland. Severe HAV is common among indigenous children than non-indigenous children due to the disparity in living standards. Between 2003 and 2006, the incidence rates for indigenous and non-indigenous populations were 8.1% and 1.7% respectively.

Since most childhood cases are asymptomatic, children play a significant role in transmission of HAV and a source of infection to adults (4, 34). In a study involving newly infected adults, 57% of their households had a child below five years, associated with transmission of HAV in the households. Thus, most Australian HAV cases (11-16%) a rise from children-adult transmission during outbreaks. Another frequent source of transmission is sexual contact with HAV-infected person (9-12%). In the US, about 2% of cases are associated with contaminated food sources while 4-6% of new infections involve international travelers. Cyclic outbreaks occur among drug users using injections and through homosexual contact.

The HAV incidence rates in Australia vary depending on socioeconomic status and race. The highest rates involve the indigenous populations; the Aborigines and the Torres Straight Islanders, while the non-indigenous populations have the lowest incidence rates. The racial differences in incidence rates reflect the risk factors that predispose vulnerable groups to infection. Disparities in socioeconomic levels, low standards of living and contact with travelers from hepatitis-A endemic areas contribute to the high rates among these groups. Serologic evidence indicates that about a third of the Australian indigenous population have prior hepatitis A infections. Additionally, in Australia, the HAV infection patterns vary regionally based on epidemiological characteristics such as childhood infections and temporal infection patterns. Regions such as Northern Territory and Queensland predominantly occupied by indigenous communities have the highest incident rates nationally.

Communities with high incidence rates of HAV typically experience epidemics every six to ten years. Usually, peak incidence involves over 700 cases per 100,000 people with majority of the infections involving children less than six years of age. Sero-prevalence data indicate that, globally, about 40% of children below five years from vulnerable communities get infected with HAV. These communities are defined geographically and culturally and include indigenous, migrant and religious communities. In contrast, intermediate rates often involve populations in large metropolitan areas such as Sidney. In these populations, the infections are not age-specific; they involve adults, children and adolescents indicating widespread infections especially during outbreaks. Additionally, high rates during communitywide outbreaks may result from high infection rates among homosexuals and injecting drug users. Low incidence rates relate to international travels. It accounts for 10-12% of infected cases, which, however, do not contribute significantly to transmission within the community. HAV vaccination programs in high incidence rate communities target the children (school-age and pre-school children). The impact of vaccination in Australia has been modest; often targeting high risk age groups, who may not constitute the majority of the cases.

Public Health Measure/Control for HAV in Australia

Public health control measures in Australia involve vaccination and prophylaxis and HAV surveillance. The goals of HAV vaccination include:

  1. reducing the incidence rates;
  2. eliminating transmission;
  3. protecting individuals from new infections.

Highly effective vaccine Avaxim and Havrix are used in Australia to mitigate the risk of HAV infection. The risk of HAV infection is reduced through the promotion of childhood vaccination.

The Government of Western Australia Department of Health has issued guidelines for the management of Hepatitis A in HAV endemic areas such as the Northern Territory. The guidelines require an evaluation of water treatment plants and food processing facilities following an HAV outbreak. Another approach involves childhood vaccination by Hepatitis A vaccine (NHIG). Unvaccinated adults attending to the children in child care centers and family members also undergo vaccination during outbreaks. Additionally, the guidelines require the public health units to institute surveillance for hepatitis symptoms in households near the outbreak facility, 50 days after the outbreak.

The goal of HAV surveillance is to identify cases that may need post-exposure prophylaxis, to monitor the disease incidence rates, detect outbreaks and to assess the effectiveness of HAV vaccination. New HAV infections identified through surveillance are reported to local or state public health departments. HAV surveillance in Australia is maintained at local level to ensure that the various vaccination strategies are implemented accordingly and their effectiveness assessed both at local and national levels. Surveillance, involves the examination of food handling practices, drinking water and minimizing the risk of exposure to infection during social activities and international travels. To ensure a reduction in HAV incidence rates nationally, widespread and routine immunization of children is important. The surveillance data is used to assess the states or communities with elevated HAV rates for immunization and other control strategies.

Community Cost and Burden of Hepatitis A

Case investigation following an outbreak usually starts a day after notification of a confirmed case. In Australia, the public health unit (PHU) staff collaborates with other healthcare providers in the investigations. The doctors, laboratories and hospitals notify the local Public Health Unit of new HAV cases. The general practice (GP) visits involve the PHU practitioners who visit patient’s family and childcare centers to identify the contacts exposed to new infection. The GP personnel follow special guidelines when attending to HAV-infected cases at work or in a child care facility, and in food distribution sites. Their role involves case management, contact management and control of the environment. They identify the cause of HAV-outbreak and implement the appropriate control and preventive measures.

The response procedure following a confirmed HAV infection involves case investigation. The visits by the PHU staff are very important in case management and prevention of further spread of the infection; they confirm the symptoms and the onset of the infection, confirm the results from serological tests or recommend the tests to be conducted to determine the likely cause of the infection and assess the cases that require prophylaxis. Control of the environment involves the examination of the water supply, food facility and childcare centers. Specialist visits play a role in immunization (passive and active) and antibiotic prophylaxis. In active immunization, a single dose of hepatitis vaccine (NHIG) offers a two-week protection to patients. However, a two-dose course is important for an effective and long-term protection. Individuals given a single dose normally complete the course through their GP. Specialized visits also involve the interpretation of follow-up serologic results. In the US, vaccination encompasses persons with chronic liver disease and persons traveling or working in other countries.

The economic burden associated with HAV infection is huge due to the high mortality and morbidity caused by liver disease or cirrhosis. In the US, the cost-analysis of the HAV infection indicate that about 1.2 million people, with majority being immigrants from HAV endemic regions, carry the HAV virus. About a third of this population develops symptoms or clinical complications of the disease. In one study, the cost of healthcare for HAV-patients was higher compared to that of the control patients. The healthcare costs tend to escalate with the severity of the infection. In one study, the average cost of hospitalization was estimated at USD 8464 in 1999. The costs cover immunization and specialized treatment. Over 50% 0f HAV-infected persons in the US have no specified risk factor. In Australia, indigenous communities, age-specific factors and food-borne factors predispose individuals to infection. Additionally, in Australia, the sources of infections include injection-drug users, children centers and contaminated food. In developing countries, most HAV infections go unnoticed but are largely due to contaminated foods.

Mortality and morbidity arising from fulminant hepatitis A or liver failure has significant economic costs. In the US, about 100 people die from HAV-related liver failure. The CDC estimates that about 0.3% of adults above 50 years old with chronic liver disease are at a high risk of developing fulminant hepatitis A. In addition, the HAV infection economic costs are substantial; about 10-22% of HAV-infected cases are hospitalized. In case of adults, lost work days and wages may affect the living standards of the family and that of the larger community.

In Latin America, a region considered to be endemic to HAV, childhood infection is very high. An epidemiological study conducted recently in the region established the highest anti-HAV prevalence rates in Dominican Republic and Mexico. The same study established that 30% of children between 6 and 10 years in Chile are infected by the disease. The greatest risk factors for infection in Latin American and Africa relates to water and food contamination. In Asia, Japan, China and Taiwan have low endemicity of HAV while Pakistan, Philippines, Malaysia, Thailand amongst others have the highest endemicity. In Australia, over 3000 serum samples obtained in 1998, 41% tested positive for HAV. In Europe, countries such as Slovakia and the Czech Republic have intermediate endemicity while Poland, UK and Russia have the lowest endemicity.

Globally, the control measures for HAV infection include health education, proper HAV surveillance, management of outbreaks and improvement in personal hygiene. Other approaches used include prophylaxis immunization with vaccines and immune globulin serum. HAV vaccine is highly effective with regard to its immunogenic properties. However, countries usually consider the cost-effectiveness of a vaccination strategy prior to implementation. A study conducted in Germany to analyze the economic impacts of vaccination of HAV and HBV established that the vaccination of older children 11-15 years old is the most cost effective strategy. However, this strategy would leave a large proportion of at-risk individual unprotected. Most countries adopt an expensive hepatitis vaccination program to ensure maximum epidemiological impact. In the US, an analysis of cost-effectiveness of vaccination proved that vaccination strategy is cost-effective. In Israel, immunization program involving children nationally was found to be cost-effective with optimal medical outcomes.

The HAV screening and vaccination have an impact on the healthcare facilities and the community in general. Outbreaks in care facilities can result to infection of caregivers. HAV transmission through nasocomial means has been observed in intensive care units because of infected blood transfused to infants who in turn transmit it to hospital staff and other people. Hospitalization of HAV-infected patients occurs after the onset of jaundice because the patients at this point are not infective . HAV outbreaks and subsequent hospitalization/isolation disrupt the family/community’s way of life. In the US, the prevalence of HAV in elementary and secondary schools reflect the transmission rate of the infection within the community.

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