The Hepatitis A Blog supplements Marler Clark’s Web site www.about-hepatitis.com, a site that provides information about hepatitis A, the symptoms and risks of infection, hepatitis A testing/detection, and how to prevent the spread of the hepatitis A virus.
While about-hepatitis.com is informational in purpose, the hepatitis A blog is intended to be a forum for discussion among the site’s authors and users. The authors of the hepatitis A blog conduct surveillance on matters related to hepatitis A’s impact on individuals and families in different cities, states, and regions.
Please join us in a conversation about hepatitis A that includes subjects such as outbreaks, recalls, and legal cases by commenting on posts that you find interesting
About hepatitis A (HAV)
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. 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.
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). 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 Infection 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 (Butot et al., 2008; Calder et al., 2003; Fiore, 2004; Hutin, et al., 1999; Wheeler, et al., 2005).
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.
What are the 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. 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 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).
How is Hepatitis A Infection Diagnosed?
At onset, the various human hepatitis viruses cause very similar illnesses. Therefore, neither the individual nor the healthcare provider can tell by symptoms or signs if a given individual is suffering from hepatitis A.
Fortunately, blood tests are widely available to accurately diagnose hepatitis A. These are tests for antibodies, or the affected person’s immune response to hepatitis A proteins. Immunoglobulin M (IgM) antibodies, which indicate acute disease, and immunoglobulin G (IgG) antibodies, 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: Persons with this result are 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) 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 developed brain complications, like encephalopathy or cerebral edema, generally undergo an intense course of supportive treatment. But for those whose liver failure is so complete that it has led to these complications, 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. 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
* 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
Advisory Committee on Immunization Practices (ACIP), Fiore AE, Wasley A, Bell BP. (2006). Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP).
MMWR Recomm Rep.55(RR-7):1-23. 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.