Hepatitis A is spread person-to-person by the fecal-oral route and occurs when a person eats food or drinks a beverage contaminated by someone with the virus. Thorough hand washing after using the restroom, after changing diapers, and before touching or preparing food or drinks is the best way to control the spread of Hepatitis A.

The Vanderburgh County Health Department and the Indiana State Department of Health are investigating a case of Hepatitis A in a food worker at the Lone Star Restaurant located in the Eastland Place Shopping Center at 943 N. Green River Road Evansville IN, 47715-2418.

“We’ve been in contact with Lone Star and we wanted to let people know that they may have been exposed,” Dr. Ray Nicholson, Health Officer for the Health Department said.

Persons who were exposed and unvaccinated can receive a dose of Hepatitis A vaccine to help lessen the effects of the disease or prevent disease if given within 14 days of exposure. Persons who ate or drank at the Lone Star from April 20-April 26, 2012 could have been exposed to Hepatitis A, but should not receive vaccine because it is not effective for exposure past 14 days. Those people should seek medical care if they show symptoms of Hepatitis A.

Persons who ate at the Lone Star from April 27, 2012 to May 3, 2012 may also have been exposed to the Hepatitis A virus. The Vanderburgh County Health Department and Indiana State Department of Health are working to secure vaccine to offer to anyone who ate at the restaurant from April 27 to May 3, 2012. Information on immunization clinics will be released when the health department receives the vaccine. In the meantime, health officials say to remain on the alert.

1. Organism

Hepatitis A virus (HAV) particles are environmentally hardy organisms that can be transmitted by contaminated food, water, environmental surfaces (e.g., contaminated table tops, cooking utensils) and through direct or indirect person-to-person contact. Although HAV cannot grow in the environment, they are considered to be extremely stable under a wide range of environmental conditions, including freezing, heat, chemicals, and desiccation. Concentrations of disinfectants commonly used against pathogenic bacteria are not considered effective against these viruses.

There are six HAV genotypes (I-VI), as determined by RNA sequence analysis at the VP1-2A junction of the virus genome. Genotypes I, II, and III contain strains associated with human infections, with the majority of human strains grouped within genotypes I and III. Genotypes I-III have been further divided into sub-genotypes A and B for each genotype. Most non-human primate strains are grouped within genotypes IV, V, and VI. Despite the identification of multiple genotypes/strains, this is the only known serotype for HAV. Humans and several species of non-human primates are the only known natural hosts for HAV.

HAV is classified with the enterovirus
group of the Picornaviridae family, genus
Hepatovirus, and is comprised of single
positive-stranded RNA genome of
approximately 7.5 kilobases. This RNA molecule is protected from the environment by a protein capsid (“shell”) comprised of multiple copies of three or four proteins. HAV is a non-enveloped (i.e., no lipid-containing envelope), hydrophobic virus 22 to 30 nm in size, with icosahedral symmetry with 20 sides.

2. Disease

• Mortality: The overall death rate among people with hepatitis A (that is, liver involvement; the term “hepatitis A” is used to refer to the disease, not to the virus) is approximately 2.4%. Increased age (over 50 years old) slightly increases the death rate. Overall, hepatitis A accounts for < 0.001% of all foodborne-associated deaths. Although fulminant (severe, rapidly progressing) disease is rare, the mortality rate is much higher, at 70% to 80%, as noted in the Illness / complications section, below.

• Infective Dose: The infective dose of HAV is presumed to be low (10 to 100 viral particles), although the exact dose is unknown. The viral particles are excreted in the feces of ill people (symptomatic and asymptomatic) at high densities (106 to 108/gm) and have been demonstrated to be excreted at these levels for up to 36 days post-infection.

• Onset: In symptomatic patients, mean incubation phase is 30 days (range 15 to 50 days).

• Illness / complications: HAV infections can be asymptomatic or symptomatic. Infections usually are asymptomatic in children younger than age 6 and symptomatic in older children and adults. 
When disease does occur, it is usually mild and recovery is complete within 1 to 2 weeks, although it may last up to several months, in which case it is also generally self-limiting. HAV infection is not considered to be chronic; however, a prolonged or relapsing disease lasting up to 6 months in 10-15% of patients has been reported. Patients feel chronically tired during convalescence, and their inability to work can cause financial loss. 
An atypical, and rare, clinical outcome of acute HAV infection is fulminant hepatitis or fulminant hepatic disease, which occurs in less than 1% to 1.5% of cases. This more severe outcome of acute HAV infection and illness involves massive hepatic necrosis, with acute liver failure, and has a high case-fatality rate (70% to 80%). 
The reasons for progression to acute, severe, or fulminant hepatitis remain unclear; however, it is known that patients with an underlying chronic liver disease are at particularly high risk for fulminant disease or liver failure. Factors that may play a role in severe hepatic disease progression include the nature of the host response (e.g., genetic, immunologic, or physiologic), the viral pathogen (e.g., strain virulence), and/or viral dosage (e.g., viral inoculums, patient viral load, or levels of viral replication). 
A hepatitis A vaccine is available.

• Symptoms: Symptoms associated with HAV infection include fever, anorexia, nausea, vomiting, diarrhea, myalgia, hepatitis, and, often, jaundice. Jaundice generally occurs 5 to 7 days after onset of gastrointestinal symptoms; however, in 15% of reported jaundice cases, the jaundice was not preceded by gastrointestinal symptoms.

• Duration: Typically 1 to 2 weeks, although prolonged or relapsing cases may continue for up to 6 months in a minority of patients.

• Route of entry: HAV may cause infection through various routes. The route of entry for the foodborne infection is oral.

• Pathway: The exact mechanism of HAV pathogenesis is not fully understood. The route of entry for foodborne HAV typically is the gastrointestinal tract. From the intestinal tract, the virus is transported to the liver via the blood, where hepatocytes generally are thought to be the site of viral replication. The virus is thought to be excreted by the hepatocytes and transported to the intestinal tract via bile. However, some studies suggest that initial replication may occur in crypt cells of the small intestine.

3. Frequency

An estimated 1,566 cases of hepatitis A from consumption of contaminated food occur annually in the United States. This constitutes a small portion (1% to 1.5%) of the total number of patients infected with HAV. Overall, hepatitis A accounts for < 0.001% of all foodborne-associated hospitalizations in the U.S. Hepatitis A from any cause (i.e., not just the foodborne illness) has a worldwide distribution occurring in both epidemic and sporadic fashion. In the U.S., from 1980 through 2001, an average of 25,000 cases of hepatitis A was reported to the Centers for Disease Control and Prevention (CDC) annually. However, correcting for under-reporting and asymptomatic infections, CDC estimates that an average of 263,000 HAV infections, from all causes, occurred annually in the U.S. during this period.

Until 1995, the overall incidence of HAV infection in the U.S. was cyclic, with nationwide increases occurring every 10 to 15 years (Figure 1). Since 1995, the estimated overall number of reported HAV infections in the U.S. has been declining. This significant decrease (with the most significant decrease occurring in children) appears to coincide with the vaccination program, for children and adolescents 2 to 12 years old that began in the U.S. in 1996.

Incidence of Acute, Symptomatic Hepatitis A – United States, 1980-2008

Centers for Disease Control and Prevention. Accessed May 2011.

4. Sources

HAV is excreted in feces of infected people and can produce clinical disease when susceptible people consume contaminated water or foods. Cold cuts and sandwiches, fruits and fruit juices, milk and milk products, vegetables, salads, shellfish, and iced drinks are commonly implicated in outbreaks. Water, shellfish, and salads are the most frequent sources. Contamination of foods by infected workers in food-processing plants and restaurants also is common.

In the U.S., the estimated transmission rate of this virus by person-to person contact was 22%. Of that, 8% was associated with day-care settings, 5% with international travel, 5% with illegal injectable drug use, and 4% with consumption of common-source contaminated food or water. The transmission routes for 65% of cases are unknown. Low income, low education level, crowding, and lack of access to safe drinking water and sanitation facilities are associated with increased rates of HAV infection.

5. Diagnosis

Clinical diagnosis of an HAV infection can be achieved by performing the appropriate analytical tests on serum or stool specimens. HAV diagnosis is generally performed by immunoglobulin (Ig) anti-hepatitis A antibody tests, IgM or IgG, in which an increase in virus-specific serum antibody titers is indicative of a recent HAV infection. One notable limitation for these antibody- based tests is that they cannot readily distinguish a recent HAV infection from increased antibody titer due to immunization, which can lead to elevated IgG and/or IgM being elicited against HAV. In addition to antibody testing, which also includes the use of immunoelectron microscopy, the use of molecular tests premised on reverse transcription polymerase chain reaction (RT-PCR) can also be utilized. Commercial kits are available to assist in HAV diagnosis.

6. Target Populations

All people are considered susceptible to HAV infection. Immunity can be developed by exposure and/or immunization that elicit an immune response that confers long-term immunity. In the U.S., the percentage of adults with immunity increases with age (10% for those 18 to 19 years of age to 65% for those over 50 years old). The increased number of susceptible people allows common-source epidemics to evolve rapidly.

7. Food Analysis

Methods have been developed to detect HAV in the food commodities most often implicated in HAV-associated illnesses; most notably, produce and shellfish. The manner in which the food is analyzed is dependent on the presumed location of contamination. For example, produce methods generally use a method to wash the viruses from the surface, whereas shellfish methods extract the virus from the digestive tract. Following extraction, the viruses are concentrated to suitable levels, so that detection via RT-PCR can be performed. These methods currently used by specialized regulatory laboratories to analyze suspected food for HAV are undergoing rigorous validation to verify that they are suitable for routine analysis.

8. Examples of Outbreaks

Hepatitis A is endemic throughout much of the world. Major national epidemics occurred in 1954, 1961, and 1971. Foods continue to be implicated in HAV outbreaks, which continue to occur in the U.S. following consumption of contaminated produce and shellfish. The most notable recent HAV outbreaks, in the U.S., that were associated with foods include:

• 1987 - Louisville, Kentucky- lettuce (imported)

• 1998 - Ohio- green onions (Mexico/California)

• 2000 - Kentucky and Florida- green onions (from Mexico) or tomatoes (California)

• 2003 - Tennessee, North Carolina, Georgia, Pennsylvania – green onions (Mexico)

• 2005 - Tennessee, Alabama – oysters (Louisiana) 
Case Example: In August 2005, at least 10 clusters of hepatitis A illness, totaling 39 people, occurred in four states among restaurant patrons who ate oysters. Epidemiologic data indicated that oysters were the source of the outbreak. Trace-back information showed that the implicated oysters were harvested from a specific Gulf Coast shellfish-growing area. A voluntary recall of oysters was initiated in September. HAV was detected in multiple 25-gm portions in one of two recalled samples, indicating that as many as 1 of every 15 oysters from this source was contaminated (Shieh, 2007). 
Other examples include:

• CDC Morbidity and Mortality Weekly Report: Hepatitis A Virus
Provides a list of CDC Morbidity and Mortality Weekly Reports relating to this 
organism.

• NIH/PubMed: Hepatitis A Virus
Provides a list of research abstracts contained in the National Library of Medicine’s 
MEDLINE database for this organism.

• Agricola: Hepatitis A Virus
Provides a list of research abstracts contained in the National Agricultural Library 
database.

9. Other Resources

• Shieh YC, Khudyakov YE, Xia G, Ganova-Raeva LM, Khambaty FM, Wood JW, Veazey JE, Motes ML, Glatzer MB, Bialek SR, and Fiore AE. 2007. Molecular confirmation of oysters as the vector for hepatitis A in a 2005 multistate outbreak. J. Food Prot. 70:145-150.

• HAV Definition and MeSH headings from the National Library of Medicine

Hepatitis A is one of five human hepatitis viruses (hepatitis A, B, C, D, and E) that primarily infect the liver and cause illness. An estimated 80,000 cases occur each year in the U.S., although much higher estimates have been proposed based on mathematical modeling of the past incidence of infection. Each year, an estimated 100 persons die as a result of acute liver failure in the U.S. due to hepatitis A, but the rate of infection has dramatically decreased since the hepatitis A vaccine was licensed and became available in the U.S. in 1995.

Hepatitis A is a communicable (or contagious) disease that spreads from person-to-person. It is spread almost exclusively through fecal-oral contact, generally from person-to-person, or via contaminated food or water. Food contaminated with the virus is the most common vehicle transmitting hepatitis A. The food preparer or cook is the individual most often contaminating the food, although he or she is generally not ill at the time of food preparation. The peak time of infectivity, when the most virus is present in the stool of an infectious individual, is during the two weeks before illness begins. Although only a small percentage of hepatitis A infections are associated with foodborne transmission, foodborne outbreaks have been increasingly implicated as a significant source of hepatitis A infection.

Hepatitis A may also be spread by household contact among families or roommates, sexual contact, ingestion of contaminated water, ingestion of raw or undercooked fruits and vegetables or shellfish (like oysters), and from persons sharing illicit drugs. Children often have asymptomatic or unrecognized infections and can pass the virus through ordinary play to family members and other children and adults.

Symptoms of hepatitis A Infection

Hepatitis A infection 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 ñ you can only get hepatitis A once) by getting a blood test later in life. The incubation period (from exposure to onset of symptoms) is 15-50 days, with an average of 30 days. Many children and most adults will experience the sudden onset of flu-like symptoms. After a day or two of muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever and malaise, 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 turn dark with bile and the stool will be light or clay-colored from lack of bile. When jaundice sets in, the initial symptoms begin to subside.

In general, the period of acute illness lasts from 10 days to three weeks, at which time affected individuals tend to recapture some sense of wellness. It is not unusual for blood tests to remain abnormal for six months (or more), prolonging recovery for up to a year. Most affected individuals show complete recovery within three to six months of the onset of illness. Relapse is possible, and although more common in children, it does occur with some regularity in adults.

Diagnosis and treatment of hepatitis A

There are blood tests widely available to accurately diagnose hepatitis A; blood samples are tested for hepatitis antibodies, which are present when the immune system responds to the hepatitis virus. Antibodies of the immune globulin (Ig) M variety, which indicate acute disease, and IgG antibodies, which stay positive for life, should both be measured.

Hepatitis A infection is an acute self-limiting disease. There is no specific treatment; treatment and management is merely supportive. The liver function tests generally improve as the affected individual begins to feel better. It is therefore well accepted that the need for rest is best determined by the person’s own perception of the severity of fatigue or malaise.

Preventing hepatitis A Infection

Hepatitis A infection is totally preventable. Ill food-handlers should be excluded from work. Commercial food workers and other individuals who prepare food for others must always wash their hands with soap and water after using the bathroom, changing a diaper, and before preparing food. Cooking food to a temperature of 185∞F or higher will inactivate hepatitis A.

After a known exposure to hepatitis A, administration of a shot of immune globulin should be considered. If administered within two weeks of the exposure, it will usually be effective in preventing or at least ameliorating the disease.

Hepatitis A vaccine is the best protection from hepatitis A infection. The vaccine is recommended for persons traveling to areas with increased rates of hepatitis A, men who have sex with men, injecting and non-injecting drug users, persons with blood clotting factor disorders (such as hemophilia), persons with chronic liver disease, and children living in regions of the U.S. with increased rates of hepatitis A. The vaccine may also help protect household contacts of those with hepatitis A infection. Vaccination of food handlers would likely substantially diminish the incidence of hepatitis A outbreaks. The vaccine is licensed for individuals aged two and older, but there is good evidence that the vaccine is safe and effective at one year of age.

References

Bialek SR, Thoroughman DA, Hu D, Simard EP, Chattin J, Cheek J, Bell BP. (2004). Hepatitis A Incidence and Hepatitis A Vaccination Among American Indians and Alaska Natives, 1990–2001. Am J Public Health. 94(6):996-1001.

Bownds L, Lindekugel R, Stepak P. (2003). Economic impact of a hepatitis A epidemic in a mid-sized urban community: the case of Spokane, Washington. J Community Health. 28(4):233-246.

Butot S, Putallaz T, Sánchez G. (2008). Effects of sanitation, freezing and frozen storage on enteric viruses in berries and herbs. Int J Food Microbiol. 126(1-2):30-35.

Calder L, Simmons G, Thornley C, Taylor P, Pritchard K, Greening G, Bishop J. (2003). An outbreak of hepatitis A associated with consumption of raw blueberries. Epidemiol Infect. 131(1):745-751.

Centers for Disease Control and Prevention (2009a). Disease Burden from Viral Hepatitis A, B, and C in the United States. Available at http://www.cdc.gov/hepatitis/PDFs/disease_burden.pdf).

Centers for Disease Control and Prevention (2009b). Surveillance for Acute Viral Hepatitis—- United States, 2007. Surveillance Summaries. 58 (SS03):1-27.

Centers for Disease Control and Prevention (2009c). Hepatitis A. In: Epidemiology and Prevention of Vaccine-Preventable Diseases. Atkinson W, Wolfe S, Hamborsky J, McIntyre L, eds. 11th ed. Washington DC: Public Health Foundation, pp. 85-97.

Centers for Disease Control and Prevention (2009d). Updated recommendations from the Advisory Committee on Immunization Practices (ACIP) for use of hepatitis A vaccine in close contacts of newly arriving international adoptees. Centers for Disease Control and Prevention (CDC); Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 58(36):1006-7.

CDC (2007). Update: Prevention of Hepatitis A after Exposure to Hepatitis A Virus and in International Travelers. Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. 56(41);1080-1084.

Detry O, De Roover A, Honore P, Meurisse M. (2006). Brain edema and intracranial hypertension in fulminant hepatic failure: pathophysiology and management. World J Gastroenterol. 12: 7405-7412.

Feldman, M, Friedman, LS, Sleisenger, MH. (2002). Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 80: 1571.

Fiore, AE. ( 2004). “Hepatitis A Transmitted by Food.” Clinical Infectious Diseases. 38:705-715.

Gilkson M, Galun E, Oren R, Tur-Kaspa R, Shouval D. (1992). Relapsing hepatitis A. Review of 14 cases and literature survey. Medicine. 71:14-23.

Hutin YJF, Pool V, Cramer EH, et al. (1999). A multistate, foodborne outbreak of hepatitis A. N Engl J Med. 340:595–602.

Jaykus L. (1997). Epidemiology and Detection as Options for Control of Viral and Parasitic Foodborne Disease. Emerg Infect Dis. 3(4):529-539.

Mayo Clinic. (2009). Hepatitis A. Available at http://www.mayoclinic.com/health/hepatitis-a/DS00397.

Piazza M, Safary A, et al. (1999). Safety and immunogenicity of hepatitis A vaccine in infants: a candidate for inclusion in the childhood vaccination program. Vaccine. 17:585-588.

Rawls RA and Vega KJ (2005). Viral Hepatitis in Minority America. J Clin Gastroenterol. 39:144–151.

Sagliocca L, Amoroso P, et al. (1999). Efficacy of hepatitis A vaccine in prevention of secondary hepatitis A infection: A randomized trial. Lancet. 353:1136-39.

Scharff RL, McDowell J, Medeiros L. (2009). Economic Cost of Foodborne Illness in Ohio. J Food Prot. 72(1):128-136.

Schiff ER. (1992). Atypical Manifestations of hepatitis-A. Vaccine. 10(Suppl. Vol. 1): 18-20.

Taylor R, Davern T, Munoz S, Han S-H, McGuire B, Larson AM, et al. (2006). Fulminant hepatitis A virus infection in the United States: incidence, prognosis, and outcomes. Hepatology. 44:1589-1597.

Todd EC, Greig JD, Bartleson CA, Michaels BS. (2009). Outbreaks where food workers have been implicated in the spread of foodborne disease. Part 6. Transmission and survival of pathogens in the food processing and preparation environment. J Food Prot. 72(1):202-219.

Wheeler C, Vogt TM, Armstrong GL, et al. (2005). An Outbreak of Hepatitis A Associated with Green Onions. N Engl J Med. 353: 890-897.

Willner IR, Uhl MD, Howard SC, Williams EQ, Riely CA, Waters B. (1998). Serious hepatitis A: an analysis of patients hospitalized during an urban epidemic in the United States. Ann Intern Med. 128:111-114.

City health care workers will be on site administering shots until 7 p.m Friday.

The Lubbock Health Department is urging anyone who ate at Cheddar's Restaurant from Aug. 31 through Sept. 8 to come to the civic center for a precautionary vaccination.

Early lines were more than an hour long as concerned citizens said they'd rather be safe than sorry.

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).

Outbreaks

• 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

• CDC. (2007).  Epidemiology and Prevention of Vaccine-Preventable Diseases. Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. 10th ed. Washington DC: Public Health Foundation.  Chap. 14.
• Detry O, De Roover A, Honore P, Meurisse M.  (2006).  Brain edema and intracranial hypertension in fulminanth epatic failure:  pathophysiology and management.  World J Gastroenterol. 12: 7405-7412
• Feldman, M, Friedman, LS, Sleisenger, MH.  (2002).  Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 80: 1571
• Fiore, AE.  2004.  “Hepatitis A Transmitted by Food.” Clinical Infectious Diseases.  38:705-15.
• Fiore A, Wasley A, Bell BP. (2006, May 19).  Prevention of Hepatitis A Through Active or Passive Immunization.  MMWR Weekly.  55 (RR07);1-23)
• Francis, CM, Maynard JE.  (1983).  Foodborne hepatitis-A: Recommendations for Control.  J Infect Dis.  148:1133-5.
• Gilkson M, Galun E, Oren R, Tur-Kaspa R, Shouval D.  (1992).  Relapsing hepatitis A. Review of 14 cases and literature survey.  Medicine.  71:14-23.
• Hutin YJF, Pool V, Cramer EH, et al.  (1999).  A multistate, foodborne outbreak of hepatitis A.  N Engl J Med.  340:595–602.
• Jaykus L.  (1997).  Epidemiology and Detection as Options for Control of Viral and Parasitic Foodborne Disease.  Emerg Infect Dis.  3 (4).
• Koff, Raymond.  (1998).  hepatitis-A.  Lancet.  351 (9116).
• Mayo Clinic.  (2006, October 4).  Hepatitis A.  Retrieved August 8, 2007 from Mayo Clinic Web site:  http://www.mayoclinic.com/health/hepatitis-a/DS00397/DSECTION=1.
• MMWR Recomm. Rep.  (1999).  Prevention of Hepatitis A Through Active or Passive Immunization:  Recommendations of the Advisory Committee of Immunization Practices (ACIP).  October 9, 1999 / 48(RR-12):1-37.  Atlanta, GA:  Centers for Disease Control and Prevention.
• MMWR Weekly.  (2006, January 6). Recommended childhood and adolescent immunization schedule---United States, 2006. 54(52);Q1-Q4.  Atlanta, GA:  Centers for Disease Control and Prevention.
• Piazza M, Safary A, et al.  (1999).  Safety and immunogenicity of hepatitis A vaccine in infants: a candidate for inclusion in the childhood vaccination program.  Vaccine. 17:585-8.
• Sagliocca L, Amoroso P, et al.  (1999).  Efficacy of hepatitis A vaccine in prevention of secondary hepatitis A infection: A randomized trial.  Lancet. 353:1136-39.
• Schiff ER.  (1992).  Atypical Manifestations of hepatitis-A.  Vaccine. 10(Suppl. Vol. 1): 18-20.
• Wheeler C, Vogt TM, Armstrong GL, et al.  (2005).  An Outbreak of Hepatitis A Associated with Green Onions.  N Engl J Med. 353: 890-897
• Willner IR, Uhl MD, Howard SC, Williams EQ, Riely CA, Waters B. (1998).  Serious hepatitis A: an analysis of patients hospitalized during an urban epidemic in the United States.  Ann Intern Med.  128:111-4.

Hepatitis A is a communicable (or contagious) disease that spreads from person-to-person. It is spread almost exclusively through fecal-oral contact, generally from person-to-person, or via contaminated food or water. Food contaminated with the virus is the most common vehicle transmitting hepatitis A. The food preparer or cook is the individual most often contaminating the food, although he or she is generally not ill at the time of food preparation. The peak time of infectivity, when the most virus is present in the stool of an infectious individual, is during the two weeks before illness begins. Although only a small percentage of hepatitis A infections is associated with foodborne transmission, foodborne outbreaks have been increasingly implicated as a significant source of hepatitis A infection.

Hepatitis A may also be spread by household contact among families or roommates, sexual contact, ingestion of contaminated water, ingestion of raw or undercooked fruits and vegetables or shellfish (like oysters), and from persons sharing illicit drugs. Children often have asymptomatic or unrecognized infections and can pass the virus through ordinary play to family members and other children and adults.

Symptoms of hepatitis A infection

Hepatitis A infection 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. The incubation period (from exposure to onset of symptoms) is 15-50 days, with an average of 30 days. Many children and most adults will experience the sudden onset of flu-like symptoms. After a day or two of muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever and malaise, 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 turn dark with bile and the stool will be light or clay-colored from lack of bile. When jaundice sets in, the initial symptoms begin to subside.

In general, the period of acute illness lasts from 10 days to three weeks, at which time affected individuals tend to recapture some sense of wellness. It is not unusual for blood tests to remain abnormal for six months (or more), prolonging recovery for up to a year. Most affected individuals show complete recovery within three to six months of the onset of illness. Relapse is possible, and although more common in children, it does occur with some regularity in adults.

Diagnosis and treatment of hepatitis A

There are blood tests widely available to accurately diagnose hepatitis A; blood samples are tested for hepatitis antibodies, which are present when the immune system responds to the hepatitis virus. Antibodies of the immune globulin (Ig) M variety, which indicate acute disease, and IgG antibodies, which stay positive for life, should both be measured.

Hepatitis A infection is an acute self-limiting disease. There is no specific treatment; treatment and management is merely supportive. The liver function tests generally improve as the affected individual begins to feel better. It is therefore well-accepted that the need for rest is best determined by the person's own perception of the severity of fatigue or malaise.

Preventing hepatitis A infection

Hepatitis A infection is totally preventable. Ill food-handlers should be excluded from work. Commercial food workers and other individuals who prepare food for others must always wash their hands with soap and water after using the bathroom, changing a diaper, and before preparing food. Cooking food to a temperature of 185 degrees F or higher will inactivate hepatitis A.

After a known exposure to hepatitis A, administration of a shot of immune globulin should be considered. If administered within two weeks of the exposure, it will usually be effective in preventing or at least ameliorating the disease.

Hepatitis A vaccine is the best protection from hepatitis A infection. The vaccine is recommended for persons traveling to areas with increased rates of hepatitis A, men who have sex with men, injecting and non-injecting drug users, persons with blood clotting factor disorders (such as hemophilia), persons with chronic liver disease, and children living in regions of the U.S. with increased rates of hepatitis A. The vaccine may also help protect household contacts of those with hepatitis A infection. Vaccination of food handlers would likely substantially diminish the incidence of hepatitis A outbreaks. The vaccine is licensed for individuals aged two and older, but there is good evidence that the vaccine is safe and effective at one year of age.