Hepatitis A
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Overview
| Hepatitis A | ||||||
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 Electron micrograph of hepatitis A virions.
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| Virus classification | ||||||
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| Type species | ||||||
| Hepatitis A virus |
| Hepatitis A Classification and external resources | |
| ICD-10 | B15.- |
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| ICD-9 | 070.1 |
| DiseasesDB | 5757 |
| MedlinePlus | 000278 |
| eMedicine | med/991 ped/977 |
| MeSH | D006506 |
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Hepatitis A (formerly known as infectious hepatitis) is an acute infectious disease of the liver caused by the hepatovirus hepatitis A virus.[1] Most commonly transmitted by the fecal-oral route, such as contaminated food, hepatitis A does not typically have a chronic stage and does not cause permanent liver damage. The patient's immune system makes antibodies against the hepatitis A virus that confer immunity against future infection. A vaccine is available that will prevent infection from hepatitis A for at least ten years.[3] In the United States, viral hepatitis is an important public health problem because it causes serious illness, it affects millions, and it has a close connection with HIV.
References
http://www.cdc.gov/idu/hepatitis/index.htm
Virus
Hepatitis virus (HAV) is a non-enveloped ssRNA virus with a single serovar.[1]
Epidemiology and Demographics
Person-to-person transmission through the fecal-oral route is the primary means of HAV transmission in the United States. Transmission occurs most frequently among close contacts, especially in households and extended family settings. Because the majority of children have asymptomatic or unrecognized infections, they play a key role in HAV transmission and serve as a source of infection for others. In one study of adults without an identified source, 52% of their households included a child aged <6 years, and the presence of a young child was associated with HAV transmission in the household. In studies in which serologic testing of the household contacts of adults without an identified source of infection was performed, 25%-40% of contacts aged <6 years had serologic evidence of acute HAV infection (IgM anti-HAV).
Common-source outbreaks and sporadic cases also can occur from exposure to fecally contaminated food or water. Uncooked foods have been recognized frequently as a source of outbreaks. Cooked foods also can transmit HAV if cooking is inadequate to kill the virus or if food is contaminated after cooking, as occurs commonly in outbreaks associated with infected food handlers. Waterborne outbreaks of hepatitis A are infrequent in developed countries with well-maintained sanitation and water supplies. The majority of waterborne outbreaks are associated with sewage-contaminated or inadequately treated water. Outbreaks in the context of floods or other natural disasters (e.g., hurricanes) have not been reported in the United States.
Depending on conditions, HAV can be stable in the environment for months. Heating foods at temperatures >185°F (>85°C) for 1 minute or disinfecting surfaces with a 1:100 dilution of sodium hypochlorite (i.e., household bleach) in tap water is necessary to inactivate HAV.
On rare occasions, HAV infection has been transmitted by transfusion of blood or blood products collected from donors during the viremic phase of their infection. Since 2002, nucleic acid amplification tests such as polymerase chain reaction (PCR) have been applied to the screening of source plasma used for the manufacture of plasma-derived products.
In experimentally infected nonhuman primates, HAV has been detected in saliva during the incubation period. However, transmission by saliva has not been demonstrated.
Can I get viral hepatitis from an animal?
No. Hepatitis viruses are not zoonotic meaning that they cannot be transmitted between, or be shared by, animals and humans. No natural animal or insect hosts or vectors are known to exist. While humans are the only natural hosts, some non-human primates can be experimentally infected for research purposes.
Prevalence:
In the U.S. population, the overall age-adjusted prevalence of HBV infection (including persons with chronic infection and those with previous infection) was 4.9% in the third National Health and Nutrition Examination Survey (NHANES III, 1988--1994). Foreign-born persons (particularly Asian/Pacific Islanders) who have emigrated from countries in which HBV is endemic contribute disproportionately to the burden of chronic HBV infection in the United States. The prevalence of chronic HBV infection among foreign-born persons immigrating to the United States from Central and Southeast Asia, the Middle East, and Africa varies (range: 5%--15%) and reflects the patterns of HBV infection in the countries and regions of origin for these persons. During 1994--2003, approximately 40,000 immigrants with chronic HBV infection were admitted annually to the United States for permanent residence (78; CDC, unpublished data, 2005).
During 1990-2004, overall incidence of reported acute hepatitis B declined 75%, from 8.5 to 2.1 per 100,000 population. The most dramatic declines occurred in the cohort of children to whom recommendations for routine infant and adolescent vaccination have applied. Incidence among children aged <12 years and adolescents aged 12--19 years declined 94%, from 1.1 to 0.36 and 6.1 to 2.8 per 100,000 population, respectively (Figure 2). Since implementation of routine childhood immunization, an estimated 6,800 perinatal infections and an additional 18,700 infections during the first 10 years of life have been prevented annually in the United States.
Although infections in infants and children aged <10 years represented <10% of all HBV infections before implementation of childhood immunization programs, childhood infections resulted in an estimated 30%-40% of the chronic HBV infections among persons who acquired their infections in the United States. In two population-based studies conducted among Asian/Pacific Islander children who were born in the United States before perinatal hepatitis B prevention programs were widely implemented, 61%-66% of the chronic HBV infections occurred in children born to HBsAg-negative mothers. A substantial proportion of these chronic infections would not have been prevented by a selective program of identification and immunization of only infants born to HBsAg-positive mothers.
In addition to declines in incidence among all age groups, racial disparities in hepatitis B incidence among children have been substantially reduced. The reduction of the disparity between Asian/Pacific Islander and other children is consistent with recent observations noting a decline in seroprevalence of HBV infection after successful implementation of routine hepatitis B vaccination among Asians who have recently immigrated to the United States. However, as hepatitis B incidence has declined among U.S.-born children, unvaccinated foreign-born children account for a high proportion of infections. During 2001--2002, of 19 children born after 1991 in whom acute hepatitis B had been verified, eight (42%) were foreign born.
Pathophysiology & Etiology
Is a liver disease caused by the hepatitis A virus (HAV). Hepatitis A can affect anyone. In the United States, hepatitis A can occur in situations ranging from isolated cases of disease to widespread epidemics.
HAV, a 27-nm RNA agent classified as a picornavirus, can produce either asymptomatic or symptomatic infection in humans after an average incubation period of 28 days (range: 15--50 days).
References
http://www.cdc.gov/ncidod/diseases/hepatitis/index.htm
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm
Transmission
The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. Food-borne outbreaks are not uncommon,[1] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[1] Approximately 40% of all acute viral hepatitis is caused by HAV.[1] Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60oC. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection there is life-long immunity. HAV can be inactivated by: chlorine treatment (drinking water), formalin (0.35%, 37oC, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm2/min).
Risk Factors
Travelers:
Persons from developed countries who travel to developing countries are at substantial risk for acquiring hepatitis A. Such persons include tourists, immigrants and their children returning to their country of origin to visit friends or relatives, military personnel, missionaries, and others who work or study abroad in countries that have high or intermediate endemicity of hepatitis A. Hepatitis A remains one of the most common vaccine-preventable diseases acquired during travel. One study estimated the risk among persons who did not receive IG or vaccine before departure to be four to 30 cases per 100,000 months of stay in developing countries. The risk might be higher among travelers staying in areas with poor hygienic conditions, varies according to the region and the length of stay, and appears to be increased even among travelers who reported observing protective measures and staying in urban areas or luxury hotels (CDC, unpublished data, 2005). In the United States, children account for approximately 50% of reported travel-related cases. In one study of Hispanic children in San Diego with hepatitis A, two thirds reported international travel (to Mexico) during the incubation period; travel was the only exposure associated with infection in a case-control study. Travelers who acquire hepatitis A during their trips also might transmit to others on their return.
MSM:
Hepatitis A outbreaks among MSM have been reported frequently. Cyclic outbreaks have occurred in urban areas in the United States, Canada, Europe, and Australia and can occur in the context of an outbreak in the larger community. Seroprevalence surveys have not consistently demonstrated an elevated prevalence of anti-HAV compared with a similarly aged general population. Certain studies have identified specific sex practices associated with illness, whereas others have not demonstrated such associations. Since 1996, ACIP has recommended hepatitis A vaccination of MSM. Although precise data are lacking, vaccine coverage appears to be low.
Users of Injection and Noninjection Drugs:
During the preceeding 2 decades, outbreaks have been reported with increasing frequency among users of injection and noninjection drugs in Australia, Europe, and North America. In the United States, outbreaks have frequently involved users of injected and noninjected methamphetamine, who have accounted for up to 48% of reported cases during outbreaks. Cross-sectional serologic surveys have demonstrated that injection-drug users have a higher prevalence of anti-HAV than the general U.S. population. Transmission among injection-drug users probably occurs through both percutaneous and fecal-oral routes. Since 1996, ACIP has recommended hepatitis A vaccination of users of illicit drugs, but vaccine coverage data are not available.
Persons with Clotting-Factor Disorders:
During 1992-1993, outbreaks of hepatitis A were reported in Europe among persons with clotting-factor disorders who had been administered solvent-detergent-treated, "high-purity" factor VIII concentrates that presumably had been contaminated from plasma donors incubating hepatitis A. In the United States, data from one serologic study suggested that persons with hemophilia might be at increased risk for HAV infection. HAV is resistant to solvent-detergent treatment, and during 1995-1996, one study identified six patients with clotting-factor disorders who had hepatitis A after having been administered solvent-detergent-treated factor VIII and factor IX concentrates. However, changes in viral inactivation procedures, high hepatitis A vaccine coverage, and improved donor screening have decreased the risk for HAV transmission from clotting factors. During May 1998-July 2002, no new cases of HAV infection attributed to blood products were identified in an analysis of serosurveillance data from 140 participating hemophilia treatment centers.
Persons Working with Nonhuman Primates:
Outbreaks of hepatitis A have been reported among persons working with nonhuman primates that are susceptible to HAV infection, including Old and New World species. Primates that were infected were those that had been born in the wild, not those born and raised in captivity.
Risk for Severe Adverse Consequences of Hepatitis A Among Persons with Chronic Liver Disease:
Although not at increased risk for HAV infection, persons with chronic liver disease are at increased risk for fulminant hepatitis A. Death certificate data indicate a higher prevalence of chronic liver disease among persons who died of fulminant hepatitis A compared with persons who died of other causes.
Risk for Hepatitis A in Other Groups and Settings:
- Food-Service Establishments and Food Handlers:
Foodborne hepatitis A outbreaks are recognized relatively infrequently in the United States. Outbreaks typically are associated with contamination of food during preparation by an HAV-infected food handler; a single infected food handler can transmit HAV to dozens or even hundreds of persons. However, the majority of food handlers with hepatitis A do not transmit HAV. Food handlers are not at increased risk for hepatitis A because of their occupation. However, among the approximately 40,000 adults with hepatitis A reported during 1992--2000 for whom an occupation was known, 8% were identified as food handlers, reflecting the large number of persons employed in the food service industry. Evaluating HAV-infected food handlers is a common and labor-intensive task for public health departments. In a 1992 common-source outbreak involving 43 persons, the estimated total medical and disease control cost was approximately $800,000.
Outbreaks associated with food, especially green onions and other raw produce, that has been contaminated before reaching a food-service establishment have been recognized increasingly in recent years. Low attack rates are common, and outbreaks often have been recognized in association with a single restaurant in which no infected food handler was identified on subsequent investigation.
Child Care Centers:
Outbreaks among children attending child care centers and persons employed at these centers have been recognized since the 1970s, but their frequency has decreased as overall hepatitis A incidence among children has declined in recent years. Because infection among children is typically mild or asymptomatic, outbreaks often are identified only when adult contacts (typically parents) become ill. Poor hygiene among children who wear diapers and the handling and changing of diapers by staff contribute to the spread of HAV infection; outbreaks rarely occur in child care centers in which care is provided only to children who are toilet trained.
Although child care centers might have been the source of outbreaks of hepatitis A in certain communities, disease in child care centers more commonly reflects extended transmission from the community. Despite the occurrence of outbreaks when HAV is introduced into child care centers, results of serologic surveys do not indicate a substantially increased prevalence of HAV infection among staff at child care centers compared with prevalence among control populations.
Health-Care Institutions:
Nosocomial HAV transmission is rare. Outbreaks have occasionally been observed in neonatal intensive-care units because of infants acquiring infection from transfused blood and subsequently transmitting hepatitis A to other infants and staff. Outbreaks of hepatitis A caused by transmission from adult patients to health-care workers are typically associated with fecal incontinence, although the majority of hospitalized patients who have hepatitis A are admitted after onset of jaundice, when they are beyond the point of peak infectivity. Data from serologic surveys of health-care workers have not indicated an increased prevalence of HAV infection in these groups compared with that in control populations.
Institutions for Persons with Developmental Disabilities:
Historically, HAV infection was highly endemic in institutions for persons with developmental disabilities. As fewer children have been institutionalized and as conditions in institutions have improved, the incidence and prevalence of HAV infection have decreased, although outbreaks can occur in these settings.
Schools:
In the United States, the occurrence of cases of hepatitis A in elementary or secondary schools typically reflects disease acquisition in the community. Child-to-child disease transmission in the school setting is uncommon; if multiple cases occur among children at a school, the possibility of a common source of infection should be investigated.
Workers Exposed to Sewage:
Data from serologic studies conducted outside the United States indicate that workers who had been exposed to sewage had a possible elevated risk for HAV infection; however, these analyses did not control for other risk factors (e.g., socioeconomic status). In published reports of three serologic surveys conducted among U.S. wastewater workers and appropriate comparison populations, no substantial or consistent increase in the prevalence of anti-HAV was identified among wastewater workers. No work-related instances of HAV transmission have been reported among wastewater workers in the United States.
Diagnosis
Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. Sensitive tests for IgM and immunoglobulin G (IgG) anti-HAV in saliva have been developed but are not licensed in the United States. In the majority of persons, serum IgM anti-HAV becomes detectable 5--10 days before onset of symptoms. IgG anti-HAV, which appears early in the course of infection, remains detectable for the person's lifetime and provides lifelong protection against the disease. Two serologic tests are licensed for the detection of antibodies to HAV: 1) IgM anti-HAV and 2) total anti-HAV (i.e., IgM and IgG anti-HAV, referred to in this report as anti-HAV). In the majority of patients, IgM anti-HAV declines to undetectable levels <6 months after infection. However, persons who test positive for IgM anti-HAV >1 year after infection have been reported, as have likely false-positive tests in persons without evidence of recent HAV infection. Total anti-HAV testing is used in epidemiologic studies to measure the prevalence of previous infection or by clinicians to determine whether a person with an indication for pre-exposure prophylaxis is already immune.
HAV RNA can be detected in the blood and stool of the majority of persons during the acute phase of infection by using nucleic acid amplification methods, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates for epidemiologic investigations. However, only a limited number of research laboratories have the capacity to use these methods.
History and Symptoms
Persons with hepatitis A virus infection may not have any signs or symptoms of the disease. Older persons are more likely to have symptoms than children. If symptoms are present, they usually occur abruptly and may include fever, tiredness, loss of appetite, nausea, abdominal discomfort, dark urine, and jaundice (yellowing of the skin and eyes). Symptoms usually last less than 2 months; a few persons are ill for as long as 6 months. The average incubation period for hepatitis A is 28 days (range: 15–50 days).
Symptoms of hepatitis A may be mistaken for flu. Some sufferers, especially children, may exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks after start of infection. [1]
Symptoms may return over the following 36 months and may include [1]:
- Fatigue
- Fever
- Abdominal pain
- Nausea
- Diarrhea
- Appetite loss
- Depression
- Jaundice, a yellowing of the skin or whites of the eyes
- Sharp pains in the right-upper quadrant of the abdomen
- Weight loss
References
http://www.cdc.gov/ncidod/diseases/hepatitis/a/faqa.htm
Physical Examination
Appearance of the Patient
Pathology
Click on the arrow to view the pathologic findings in viral hepatitis:
Differential Diagnosis
Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. [1] [1]
References
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm
Treatment
There is no specific treatment for hepatitis A. Sufferers are advised to rest, avoid fatty foods and alcohol (these may be poorly tolerated for some additional months during the recovery phase and cause minor relapses), eat a well-balanced diet, and stay hydrated. Approximately 15% of people diagnosed with hepatitis A may experience one or more symptomatic relapse(s) for up to 24 months after contracting this disease.
Prognosis
The United States Centers for Disease Control and Prevention (CDC) in 1991 reported a low mortality rate of 4 deaths per 1000 cases for the general population but a higher rate of 17.5 per 1000 in those aged 50 and over.
Young children who are infected with hepatitis A typically have a milder form of the disease, usually lasting from 1-3 weeks, whereas adults tend to experience a much more severe form of the disease. They are often confined to bed and minimal activity for about 4 weeks and have to stop their work for one to three months or longer. Many adults take up to 36 months and occasionally longer to recover entirely. Symptoms that may be experienced after the first month or two are low immunity: It is much easier to catch minor infections and for these infections to linger longer than they normally would. Many people experience a slow but sure improvement, over this later period. They are generally able to function fairly normally, still needing more sleep and reduced athletic activity. It is common for recovering patients to experience occasional "off" days, during which they need to rest more. Hepatitis A can be sexually transmitted, especially during oral-anal contact, but not after the patient has recovered.
Prevention
Hepatitis A can be prevented by good hygiene and sanitation. Vaccination is also available, and is reconmended in areas where the prevalence of hepatitis A is high. To prevent it, use your own towels and toothbrushes, eating utensils, and other personal products. Always wash your hands after and before eating and more importantly after using the toilet.
Primary Prevention
Always wash your hands after using the bathroom, changing a diaper, or before preparing or eating food.
Two products are used to prevent hepatitis A virus infection: immune globulin and hepatitis A vaccine.
1. Immune globulin is a preparation of antibodies that can be given before exposure for short-term protection against hepatitis A and for persons who have already been exposed to hepatitis A virus. Immune globulin must be given within 2 weeks after exposure to hepatitis A virus for maximum protection.
2. Hepatitis A vaccine has been licensed in the United States for use in persons 12 months of age and older. The vaccine is recommended (before exposure to hepatitis A virus) for persons who are more likely to get hepatitis A virus infection or are more likely to get seriously ill if they do get hepatitis A. The vaccines currently licensed in the United States are HAVRIX® (manufactured by GlaxoSmithKline) and VAQTA® (manufactured by Merck & Co., Inc).
Hepatitis A Vaccine:
Inactivated and attenuated hepatitis A vaccines have been developed and evaluated in human clinical trials and in nonhuman primate models of HAV infection; however, only vaccines made from inactivated HAV have been evaluated for efficacy in controlled clinical trials. The vaccines containing HAV antigen that are currently licensed in the United States are the single-antigen vaccines HAVRIX® (manufactured by GlaxoSmithKline, Rixensart, Belgium) and VAQTA® (manufactured by Merck & Co., Inc., Whitehouse Station, New Jersey) and the combination vaccine TWINRIX® (containing both HAV and HBV antigens; manufactured by GlaxoSmithKline). All are inactivated vaccines.
- http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm
- http://www.cdc.gov/ncidod/diseases/hepatitis/a/faqa.htm
Vaccine
Main article Hepatitis A vaccine
The Hepatitis A vaccine, Avaxim, protects against the virus in more than 95% of cases and provides protection from the virus for ten years. The vaccine contains inactivated Hepatitis A virus providing active immunity against a future infection.[1]
See also
References
External links
- CDC's hepatitis A links
- CDC's hepatitis A Fact Sheet
- [4]
- [5]
- [6]
- Merck's product sheet for VAQTA, their hepatitis A vaccine
- Hepatitis A - General Information about Hepatitis A
- GlaxoSmithKline's product sheet for HAVRIX, their hepatitis A vaccine
- Medical article: review summary at medstudents.com
- Hepatitis A Exams & Tests at aboutinfections.com
- MeSH Hepatitis+A
- MeSH Hepatitis+A+virus
Acknowledgements
- The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
- List of contributors: Pilar Almonacid
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
