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 (Mayo Clinic, 2006); however, hepatitis A infection can still lead to acute liver failure and death.
Hepatitis A is relatively uncommon in nations with developed sanitation systems such as the United States. Nevertheless, it continues to occur here, and approximately one-third of the United States population has been previously infected with hepatitis A (Fiore, 2004).
Viral hepatitis is a major public health concern in the United States, and a source of significant morbidity and mortality. Each year, approximately 30 – 50,000 cases of hepatitis A occur in the United States. Direct and indirect costs of these illnesses exceed $300 million, including wage loss and medical expenses. Adults who become ill miss an average of 27 work days per illness. Eleven to 12 percent of persons infected are hospitalized, and 100 people die as a result of acute liver failure annually in the United States due to hepatitis A (CDC, 2007). The unfortunate aspect of these statistics is that with 21st Century medicine, hepatitis A is totally preventable and cases—especially outbreaks relegated to food consumption—need not occur.
The hepatitis A virus or “HAV” is relatively stable and will survive for up to a month at ambient temperatures in the environment, but can be inactivated by heating to 185°F (85°C) or higher, or exposure to formalin or chlorine.
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. Outbreaks associated with food have been increasingly implicated as a significant source of hepatitis A infection. Such “outbreaks are usually associated with contamination of food during preparation by an HAV-infected food handler.” (CDC, 2007; Francis & Maynard, 1983).
Food contaminated with the virus is a common vehicle transmitting hepatitis A. The food preparer or cook is the individual most often contaminating the food. He or she is generally not ill: the peak time of infectivity (i.e., when the most virus is present in the stool of an infectious individual) is during the 2 weeks before illness begins. Indeed, “viral gastroenteritis was reported as the most common food-borne illness in Minnesota from 1984 to 1991, predominantly associated with poor personal hygiene of infected food handlers.” (Jaykus, 1997).
In addition to infected food workers, 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).
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, by the ingestion of raw or undercooked fruits and vegetables 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.
Hepatitis A is much more common in countries with under-developed 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. Within the United States, Native American reservations also experience a greatly increased rate of disease (MMWR Reccom. Rep., 1999).
How is Hepatitis A Infection Diagnosed?
At onset, the various human hepatitis viruses cause very similar illnesses. Therefore, neither patient nor doctor can tell by symptoms or signs if a given individual is suffering from hepatitis A.
Fortunately, we now have excellent blood tests, which are widely available, to accurately diagnose hepatitis A.
These are tests for antibodies, or the patient’s immune response to hepatitis A proteins, which are called capsid proteins. Antibodies of the IgM variety, which indicated acute disease, and antibodies of the IgG variety, which stay positive for life, should both be measured. Following is the interpretation of the results:
* IgM negative / IgG negative: Most persons with these results have never contracted hepatitis A. Antibodies of the IgM variety develop five to ten days prior to the onset of symptoms.
* IgM positive / IgG negative: This result indicates acute hepatitis A.
* IgM positive / IgG positive: This result indicates that acute hepatitis A occurred within the last six months. By six months, the IgM reverts to negative.
* IgM negative / IgG positive: The person with this result is immune to hepatitis A. They have either been infected with the virus months or years in the past (with or without symptoms), or they have been vaccinated for hepatitis A. However, if they are currently ill, it is not likely to be due to hepatitis A.
Treatment for Hepatitis A Infection (Viral Hepatitis)
There is no specific treatment for hepatitis A. Patients generally suffer from loss of appetite, so the main concern is ensuring a patient receives adequate nutrition and avoids permanent liver damage (Mayo Clinic, 2006).
A patient’s perception of the severity of fatigue or malaise is the best determinant of the need for rest. Most patients show complete clinical and biochemical recovery within three to six months of the onset of illness (Koff, 1998; Wilner, 1998; Schiff, 1992).
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).
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.
Responsible restaurant managers will exclude ill food-handlers from work, with pay. Food-handlers must also be taught to always wash their hands with soap and water after using the bathroom, changing a diaper, and certainly before preparing food.
After a known exposure to the hepatitis A virus, administration of a shot of Immune Globulin (IG) should be considered. IG is 80%-90% effective in preventing hepatitis A infection if it is administered within 2 weeks of the exposure.
Cooking foods to a temperature of 185°F or higher will inactivate hepatitis A virus.
Hepatitis A Vaccine
Hepatitis A vaccine, which first became available in 1995, is the best protection from hepatitis A. After the first dose of hepatitis A vaccine, 94 – 100 percent of recipients are protected, and after the second dose nearly all are (CDC, 2007).
In 2005, the Advisory Committee on Immunization Practices (ACIP) recommended routine hepatitis A vaccination for all children ages 12-23 months. ACIP recommended 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 (Fiore, Wasley & Bell, 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
The vaccine may also help protect household contacts of those persons infected with hepatitis A (CDC, 2007; 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. Hepatitis A vaccine is licensed for individuals aged 2 and older; however, there is good evidence that the vaccine is safe and effective at 1 year of age (Piazza, et al., 1999).
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, 2007; Piazza, et al., 1999).
Outbreaks
* Carl’s Jr. Hepatitis A Outbreak
* Chi-Chi’s 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
* Quizno’s Hepatitis A Exposure
* Silver Grill Catering Hepatitis A Outbreak
* Subway Hepatitis A Outbreak
References
- 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.