What is Hepatitis A?
Hepatitis A is the only common vaccine-preventable foodborne disease in the United States (Fiore, 2004). It is one of five human hepatitis viruses that primarily infect the human liver and cause human illness. Unlike hepatitis B and C, hepatitis A doesn’t develop into chronic hepatitis or cirrhosis, which are both potentially fatal conditions; however, infection with the hepatitis A virus (HAV) can still lead to acute liver failure and death.
Hepatitis A is much more common in countries with underdeveloped sanitation systems. This includes most of the world: an increased transmission rate is seen in all countries other than the United States, Canada, Japan, Australia, New Zealand, and the countries of Western Europe. Nevertheless, it continues to occur in the United States; approximately one-third of the population has been previously infected with HAV (Fiore, 2004; Centers for Disease Control and Prevention [CDC], 2009a). Each year, approximately 30,000 to 50,000 cases of hepatitis A occur in the United States. Historically, acute hepatitis A rates have varied cyclically, with nationwide increases every 10 to 15 years. The national rate of HAV infections has declined steadily since the last peak in 1995. Although the national incidence (1.0 case per 100,000 population) of hepatitis A was the lowest ever recorded in 2007, it is estimated that 25,000 new infections occurred that year after asymptomatic infection and underreporting were taken into account. Although the rates of HAV infection have declined over the years, rates are twice as high among American Indians/Alaskan Natives (AIAN) and Hispanics compared to non-Hispanic Whites in the United States (Rawls & Vega, 2005). Rates among AIAN have decreased dramatically, though, coincident with the implementation of routine hepatitis A vaccination of AIAN children, both in urban and rural communities (Bialek et al., 2004).
In 2007, a total of 2,979 acute symptomatic cases of hepatitis A were reported (CDC, 2009b). Among the 1,047 cases with available information regarding foodborne or waterborne exposure, 6.5% were found to be foodborne or waterborne related, about one-third the proportion reported at the last peak in 2003. However, 2500 cases remained without known risk factors.
Estimates of the annual direct and indirect costs of hepatitis A in the United States have ranged from $300 million to $488.8 million in 1997 dollars (CDC, 2007). In a Spokane, Washington study, the combined direct and indirect costs for each case of hepatitis A from all sources ranged from $2892 to $3837 (Bownds et al., 2003). In an Ohio study, the estimated cost per case of foodborne illness due to HAV in 2007 was $10,000, including medical and drug costs, deaths, and quality of life (Scharff et al., 2009). Nationwide, adults who become ill miss an average of 27 work days per illness and 11 to 22 percent of those infected are hospitalized (CDC, 2009c). These are avoidable illnesses, since 21st Century medicine and the advent of hepatitis A vaccine have rendered hepatitis A infections totally preventable.
How is Hepatitis A transmitted?
Hepatitis A is a communicable (or contagious) disease that spreads from person to person. It is transmitted by the “fecal – oral route,” generally from person-to-person, or via contaminated food or water. Food-related outbreaks are usually associated with contamination of food during preparation by an HAV-infected food handler (CDC, 2009c). The food handler is generally not ill: the peak time of infectivity (that is, when the most virus is present in the stool of an infectious individual) occurs during the 2 weeks before illness begins. Fresh produce contaminated during cultivation, harvesting, processing, and distribution has also been a source of hepatitis A (Fiore, 2004). In 1997, frozen strawberries were determined to be the source of a hepatitis A outbreak in five states (Hutin, et al., 1999), and in 2003, fresh green onions were identified as the source of a hepatitis A outbreak traced to consumption of food at a Pennsylvania restaurant (Wheeler, et al., 2005). Other produce, such as blueberries and lettuce, has been associated with hepatitis A outbreaks in the U.S. as well as other developed countries (Butot et al., 2008; Calder et al., 2003).
HAV is relatively stable and can survive for several hours on fingertips and hands and up to two months on dry surfaces, but can be inactivated by heating to 185°F (85°C) or higher for one minute or disinfecting surfaces with a 1:100 dilution of sodium hypochlorite (household bleach) in tap water (Advisory Committee on Immunization Practices [ACIP], 2006; CDC, 2009c; Todd et al., 2009). However, HAV can still be spread from cooked food if it is contaminated after cooking.
Although ingestion of contaminated food is a common means of spread for hepatitis A, it may also be spread by household contact among families or roommates, sexual contact, by the ingestion of contaminated water or shellfish (like oysters), and by direct inoculation from persons sharing illicit drugs. Children often have asymptomatic or unrecognized infections and can pass the virus through ordinary play, unknown to their parents, who may later become infected from contact with their children.
Symptoms of Hepatitis A Infection
Hepatitis A may cause no symptoms at all when it is contracted, especially in children. Such individuals will only know they were infected (and have become immune – you can only get hepatitis A once) by getting a blood test later in life. Approximately 10 to 12 days after exposure, HAV is present in blood and is excreted via the biliary system into the feces (CDC, 2009c). Peak titers occur during the 2 weeks before onset of illness. Although virus is present in the blood, its concentration is much higher in feces. Virus excretion begins to decline at the onset of clinical illness, and decreases significantly by 7 to 10 days after onset of symptoms. Most infected persons no longer excrete virus in the feces by the third week of illness. Children may excrete virus longer than adults.
Seventy percent of hepatitis A infections in children younger than six years of age are asymptomatic; in older children and adults, infection tends to be symptomatic with more than 70% of those infected developing jaundice (CDC, 2009c). Symptoms typically begin about 28 days after contracting HAV, but can begin as early as 15 days or as late as 50 days after exposure and include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise. After a few days of the aforementioned symptoms, jaundice (also termed “icterus”) sets in. Jaundice is a yellowing of the skin, eyes and mucous membranes that occurs because bile flows poorly through the liver and backs up into the blood. The urine will also turn dark with bile and the stool light or clay-colored from lack of bile. When jaundice sets in, the initial systemic manifestations (such as fever and headache) begin to subside.
In general, symptoms usually last less than 2 months, although 10% to 15% of symptomatic persons have prolonged or relapsing disease for up to 6 months. It is not unusual, however, for blood tests to remain abnormal for six months or more. The jaundice so commonly associated with hepatitis A can linger for a prolonged period in some infected persons – sometimes as long as eight months. Additionally, pruritus, or severe “itchiness” of the skin, can also persist for several months after the onset of symptoms. These conditions are frequently accompanied by diarrhea, anorexia, and fatigue. Relapse is possible with hepatitis A, typically within three months of the initial onset of symptoms. Although relapse is more common in children, it does occur with some regularity in adults. The vast majority of persons who contract hepatitis A fully recover, and do not develop chronic hepatitis. Persons do not carry hepatitis A long-term as with hepatitis B and C.
Fulminant Hepatitis A
Fulminant hepatitis A is a rare but devastating complication of an HAV infection; as many as 50% of individuals with acute liver failure may die or require emergency liver transplantation (Taylor et al., 2006). Elderly patients and patients with chronic liver disease are at a higher risk of fulminant hepatitis A. In parallel with a declining incidence of acute HAV infection in the general population, however, the incidence of fulminant HAV appears to be decreasing (Taylor et al., 2006).
HAV infects the liver’s parenchymal cells (internal liver cells). Once a cell has been penetrated by the viral particles, the hepatitis A virus releases its own toxins that cause, in essence, a hostile takeover of the host cell’s system. The cell then produces new viral components that are released into the bile capillaries or tubes that run between the liver’s parenchymal cells. This process results in the death of liver cells, called hepatic necrosis. The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells – upwards of three-quarters of the liver’s total cell count – that the liver can no longer perform its job. Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema. Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function. Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure. Intracranial hypertension leading to brain stem death and sepsis with multiple organ failure are the leading causes of death in individuals with fulminant hepatic failure (Detry, 2006).
Treatment of those suffering from fulminant hepatic failure turns largely on the victim’s status. Those who have not become encephalopathic generally undergo an intense course of supportive treatment. But for those whose liver failure is so complete that it has lead to encephalopathy or cerebral edema, timely liver transplantation is often the only option. For these unlucky few, the process of necrosis has left their liver scarred and useless. Unfortunately, many patients with irreversible liver failure do not receive a transplant because of contraindications or the unavailability of donor livers (Feldman, 2002).
Persons most at risk of suffering fulminant hepatitis A include those with:
• Pre-existing chronic liver disease (Gilkson, et al., 1992)
• Chronic hepatitis B
• Chronic hepatitis C (there are 3.9 million such persons in the U.S. [MMWR, Oct. 9, 1999])
• Alcohol-induced chronic hepatitis or cirrhosis
• Older individuals, over the age of 50
Treatment for Hepatitis A Infection (Viral Hepatitis)
Once a clinical infection is established, there is no specific treatment for hepatitis A. Affected individuals generally suffer from loss of appetite, so the main concern is ensuring a patient receives adequate nutrition and avoids permanent liver damage (Mayo Clinic, 2009). An individual’s perception of the severity of fatigue or malaise is the best determinant of the need for rest.
Treatment of those suffering from fulminant hepatic failure depends largely on the affected person’s status. Those who have not become encephalopathic generally undergo an intense course of supportive treatment. But for those whose liver failure is so complete that it has lead to encephalopathy or cerebral edema, timely liver transplantation is often the only option. Unfortunately, many individuals with irreversible liver failure do not receive a transplant because of contraindications or the unavailability of donor livers (Feldman, 2002).
How to Prevent Hepatitis A Infection
Hepatitis A is TOTALLY PREVENTABLE. Although outbreaks continue to occur in the United States, outbreaks NEED NOT OCCUR if responsible preventive measures are taken. Food handlers must always wash their hands with soap and water after using the bathroom, changing a diaper, and certainly before preparing food. Food handlers should always wear gloves when handling or preparing ready-to-eat foods, although gloves are not a substitute for good hand washing. Ill food-handlers should be excluded from work.
After exposure, immune globulin (IG) is 80% to 90% effective in preventing clinical hepatitis A when administered within 2 weeks of last exposure (CDC, 2007). Efficacy is greatest when IG is administered early in the incubation period; when administered later in the incubation period, IG might only attenuate the clinical expression of HAV infection. Given the lack of appropriately designed studies comparing the postexposure efficacy of vaccine with that of IG, the Advisory Committee on Immunization Practices (ACIP) recommends IG exclusively for postexposure (CDC, 2007). Hepatitis A vaccine, if recommended for other reasons, could be given at the same time.
In 2006, the ACIP recommended routine hepatitis A vaccination for all children ages 12-23 months, that hepatitis A vaccination be integrated into the routine childhood vaccination schedule, and that children not vaccinated by two years of age be vaccinated subsequently (ACIP, 2006). The vaccine is recommended for the following persons:
• Travelers to areas with increased rates of hepatitis A
• Men who have sex with men
• Injecting and non-injecting drug users
• Persons with clotting-factor disorders (e.g. hemophilia)
• Persons with chronic liver disease
• Persons with occupational risk of infection (e.g. those who work with hepatitis A-infected primates or with hepatitis A virus in a laboratory setting)
• Children living in regions of the U.S. with increased rates of hepatitis A
• Household members and other close personal contacts (such as regular babysitters) of adopted children newly arriving from countries with high or intermediate rates of hepatitis A (CDC, 2009d)
The vaccine may also help protect household contacts of those persons infected with hepatitis A (CDC, 2009c; Sagliocca, et al., 1999). Although generally not a legal requirement at this time, vaccination of food handlers would be expected to substantially diminish the incidence of hepatitis A outbreaks. Persons traveling to a high-risk area less than four weeks after initial dose of hepatitis A vaccine, or travelers who choose not to be vaccinated against hepatitis A should receive a single dose of Immune Globulin, which provides protection against hepatitis A infection for up to three months (CDC, 2009c; Piazza, et al., 1999).
• Carl’s Jr. Hepatitis A Outbreak
• Chi-Chi’s Hepatitis A Outbreak
• Chipotle Grill Hepatitis A Outbreak
• D’Angelo’s Hepatitis A Outbreak
• Friendly’s Hepatitis A Exposure
• Maple Lawn Dairy Hepatitis A Outbreak
• McDonald’s Hepatitis A Outbreak
• McDonald’s Hepatitis A Outbreak (Quad-Cities, Illinois)
• Quizno’s Hepatitis A Exposure
• Silver Grill Catering Hepatitis A Outbreak
• Subway Hepatitis A Outbreak