Hepatitis A

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Overview

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Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
CT
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]

Overview

Hepatitis A (formerly known as infectious hepatitis and epidemical virus) is an acute infectious disease of the liver caused by the hepatitis A virus (Hep A), an RNA virus, usually spread the fecal-oral route; transmitted person-to-person by ingestion of contaminated food or water or through direct contact with an infectious person. Tens of millions of individuals worldwide are estimated to become infected with Hep A each year. The time between infection and the appearance of the symptoms (the incubation period) is between two and six weeks and the average incubation period is 28 days. In developing countries, and in regions with poor hygiene standards, the incidence of infection with this virus is high and the illness is usually contracted in early childhood. As incomes rise and access to clean water increases, the incidence of HAV decreases. Hepatitis A infection causes no clinical signs and symptoms in over 90% of infected children and since the infection confers lifelong immunity, the disease is of no special significance to those infected early in life. In Europe, the United States and other industrialized countries, on the other hand, the infection is contracted primarily by susceptible young adults, most of whom are infected with the virus during trips to countries with a high incidence of the disease or through contact with infectious persons.

Historical Perspective

Hepatitis A virus was first identified in 1973. It was classified as a separate disease from other types of hepatitis during World War II. However, its true prevalence and route of transmission would only be recognized later. During 1995-1996, the Food and Drug Administration (FDA) approved the inactivated hepatitis A vaccines. Consequently, hepatitis A became a disease that was not only common but also vaccine-preventable.

Pathophysiology

Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.

Causes

Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.

Differential Diagnosis

Hepatitis A must be differentiated from other diseases that cause fever, nausea, vomiting, jaundice, hepatomegaly, icteric sclera, elevated ALT, AST, and PCR such as other viral hepatitis, alcoholic hepatitis, and autoimmune hepatitis.

Epidemiology and Demographics

The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noted a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. In the United States, the incidence of hepatitis A in 2011 was 0.4 cases per 100,000 population. In recent years, the rates of hepatitis A have been similar among all age groups. After the introduction of the HAV vaccine, historic differences in rates of hepatitis A among racial/ethnic populations have also narrowed. In developed countries, elimination of historic geographic differences in incidence rates has also occurred. In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) are infected with the hepatitis A virus before the age of 10.

Risk Factors

Subjects who are not immunized against hepatitis A virus (HAV) and who travel to endemic areas where there is poor sanitation and lack of safe water are at increased risk of contracting HAV infection. Additional risk factors for HAV include intravenous drug injection, living in a household with an infected person, having a sexual partner with acute HAV infection, and attending childcare centers.

Screening

The detection of hepatitis A virus (HAV) antibodies in the blood is used to screen for hepatitis A. Anti-HAV IgG remains elevated after acute disease.

Natural History, Complications and Prognosis

Hepatitis A is caused by infection with hepatitis A virus (HAV) which has an incubation period of approximately 28 days. HAV infection produces a self-limited disease, rarely leading to acute liver failure. The risk for symptomatic infection is related to the age of the patient. While children most commonly have either asymptomatic or unrecognized infection, more than 80% of adults exhibit symptoms of acute viral hepatitis, such as fatigue, malaise, nausea, vomiting, and anorexia. Possible complications of hepatitis A include dehydration, electrolyte imbalance, bleeding, and rarely fulminant hepatitis. The prognosis depends on the age of the patient and the underlying liver condition. Approximately 10 to 15% of patients experience a relapse of symptoms during the 6 months following acute illness.

Diagnosis

History and Symptoms

Hepatitis A virus (HAV) infection can be either asymptomatic or symptomatic. Symptoms of hepatitis A include fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, and jaundice.

Physical Examination

Hepatitis A virus infection is commonly associated with fever, jaundice, icteric sclera, abdominal tenderness, and hepatomegaly on physical examination. Other pertinent findings include rash, cervical lymphadenopathy, abdominal distension, ascites, and altered mental status.

Laboratory Findings

Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Laboratory tests are required for its diagnosis. Serologic tests in hepatitis A virus (HAV) infection reveal elevated IgM anti-HAV in the acute phase (gold standard) in addition to an elevated IgG anti-HAV that remains elevated for the person's lifetime. Additional laboratory findings include the detection and sequencing of HAV RNA, an elevated direct bilirubin, and elevated liver enzymes. Liver biopsy has a minimal role in the diagnosis of HAV infection and it is only used when the diagnosis is unclear or when relapse is suspected.

CT

A CT scan is usually not indicated for the diagnosis of hepatitis A. However, it may be performed to exclude alternative diagnoses.

Ultrasound

An ultrasound of the abdomen may be performed in patients with hepatitis A to rule out other possible causes of hepatomegaly or chronic liver disease. Common ultrasound findings in acute hepatitis A include brightness of the portal vein walls and decreased echogenicity of the liver.

Treatment

Medical Therapy

There is no specific treatment for hepatitis A. Recovery from symptoms following infection may be slow and may take several weeks or months. Therapy is aimed at maintaining comfort and adequate nutritional balance, including replacement of fluids that are lost from vomiting and diarrhea.

Surgery

Patients who develop fulminant hepatitis may require aggressive supportive therapy, and be transferred to a center capable of performing liver transplantation.

Primary Prevention

Two products are available for the prevention of HAV infection: hepatitis A vaccine and immune globulin (IG) for intramuscular (IM) administration. Administered IM in a 2-dose series at 0 and 6--12 months, these vaccines induce protective antibody levels in virtually all adults. By 1 month after the first dose, 94%--100% of adults have protective antibody levels; 100% of adults develop protective antibody after a second dose. IG is a sterile solution of concentrated immunoglobulins which, when administered IM before or within 2 weeks after exposure to HAV, is >85% effective in preventing HAV infections. Vaccination is the most effective means of preventing HAV transmission among persons at risk for infection (e.g., MSM, illegal drug users, and persons with chronic liver disease). Because transmission of HAV during sexual activity probably results from fecal-oral contact, measures typically used to prevent the transmission of other sexually transmitted disease (e.g., use of condoms) do not prevent HAV transmission.

Secondary Prevention

Until recently, an injection of immune globulin (IG) was the only recommended way to protect people after they have been exposed to hepatitis A virus. In June 2007, U.S. guidelines were revised to allow for hepatitis A vaccine to be used after exposure to prevent infection in healthy persons aged 1–40 years. Persons who recently have been exposed to hepatitis A virus (HAV) and who previously have not received hepatitis A vaccine should be administered a single dose of single-antigen vaccine or immunoglobulin (IG) (0.02 mL/kg) as soon as possible. Information about the relative efficacy of vaccine compared with immunoglobulin postexposure is limited, and no data are available for persons aged more than 40 years or those with underlying medical conditions. Therefore, decisions to use vaccine or immunoglobulin should take into account patient characteristics associated with more severe manifestations of hepatitis A, including older age and chronic liver disease.

References

Pathophysiology

Hepatitis Main Page
Hepatitis A
Home
Patient Information
Overview
Historical Perspective
Pathophysiology
Causes
Differentiating Hepatitis A from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
CT
Ultrasound
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Case Studies
Case #1
Hepatitis A On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Hepatitis A All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Hepatitis A
CDC on Hepatitis A
Hepatitis A in the news
Blogs on Hepatitis A
Directions to Hospitals Treating Hepatitis A
Risk calculators and risk factors for Hepatitis A

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [6]

Overview

Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.

Pathogenesis

• Hepatitis A is a liver disease caused by the HAV that can affect anyone.

• HAV is acquired by mouth (through fecal-oral transmission) and replicates in the liver. After 10-12 days, the virus is present in blood and is excreted via the biliary system into the feces.

• Peak titers occur during the 2 weeks before onset of illness. Although virus is present in serum, its concentration is several orders of magnitude less than in feces. Virus excretion begins to decline at the onset of clinical illness, and has decreased significantly by 7–10 days after onset of symptoms.

• Peak infectivity occurs during the 2-week period before onset of jaundice, or elevation of liver enzymes, when the concentration of virus in stool is highest.

• The concentration of virus in stool declines after jaundice appears.

• Most infected persons no longer excrete virus in the feces by the third week of illness.

• Children may excrete virus longer than adults.

• Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness.

• The virus is resistant to detergent, acid, solvents, drying, and temperatures up to 60ºC. It can survive for months in salt water. Common-source outbreaks, such as water or restaurants are typical.

• HAV can be inactivated by chlorine treatment, formalin, peracetic acid, beta-propiolactone, and UV radiation.

Transmission

The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation. Hepatitis A can be transmitted by the parenteral route but very rarely by blood, and blood products. Today transmission of the virus through blood is rare, however, some risk groups such as IV drug users and their care takers are still infected by this route.

Food-borne outbreaks are not uncommon, and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.

Direct Transmission

• Eating food prepared by someone who has HAV and who did not properly wash their hands after using the bathroom
• Having anal or oral sex with someone who has HAV
• Not washing hands after changing a diaper (young children often are asymptomatic)

Indirect Transmission

• Eating uncooked food that is HAV-contaminated
• Eating cooked food that is not heated to 185°F (85°C) for 1 minute after being contaminated with HAV
• Drinking contaminated water: This is a common route of infection in underdeveloped countries. Chlorinated water, such as tap water in developed countries, kills HAV

Gross Pathology

Gross observation of the liver with acute hepatitis A may include:

• Enlarged liver
• Erythematous surface

Microscopic Pathology

Virus-induced cytopathology may not be responsible for the pathologic changes seen in HAV infection, as liver disease may result primarily from immune mechanisms. Antigen-specific T-lymphocytes are responsible for the destruction of infected hepatocytes.

Common histologic findings include:

• Inflammatory infiltrates (lymphocytes)
• Necrosis and apoptosis of hepatocytes
• The hepatocyte inflammation may have the following patterns:

• Multifocal
• Panacinar

• Inflammation of portal tracts

Rarely, patients with acute viral hepatitis A develop features of cholestasis.

Confluent hepatic necrosis may lead to fulminant hepatitis and death in 30-60% of cases. Death appears to be inevitable when necrosis involves more than 65-80% of the total hepatocyte fraction. In patients who survive an episode of acute fulminant hepatic failure, neither functional nor pathologic sequelae are common, despite the widespread necrosis.

During the recovery stage, cell regeneration is prominent. The damaged hepatic tissue is usually restored within 8 to 12 weeks.

Shown below is a video depicting the pathological findings in viral hepatitis. Click on the arrow to view the video. {{#ev:youtube|_hXvbpSxFZw}}

References

Epidemiology and Demographics

Hepatitis Main Page
Hepatitis A
Home
Patient Information
Overview
Historical Perspective
Pathophysiology
Causes
Differentiating Hepatitis A from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
CT
Ultrasound
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Case Studies
Case #1
Hepatitis A On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Hepatitis A All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Hepatitis A
CDC on Hepatitis A
Hepatitis A in the news
Blogs on Hepatitis A
Directions to Hospitals Treating Hepatitis A
Risk calculators and risk factors for Hepatitis A

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [7]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [8]

Overview

The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noted a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. In the United States, the incidence of hepatitis A in 2011 was 0.4 cases per 100,000 population. In recent years, the rates of hepatitis A have been similar among all age groups. After the introduction of the HAV vaccine, historic differences in rates of hepatitis A among racial/ethnic populations have also narrowed. In developed countries, elimination of historic geographic differences in incidence rates has also occurred. In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) are infected with the hepatitis A virus before the age of 10.

Incidence

Prevaccine Era

• Before vaccine licensure during 1995-1996, hepatitis A incidence was primarily cyclic, with peaks occurring every 10-15 years.

• In the United States, during 1980-1995, approximately 22,000-36,000 hepatitis A cases were reported annually to CDC (rate: 9.0-14.5 cases per 100,000 population), but incidence models indicate that the number of infections was substantially higher.

Postvaccine Era

• There were 1,398 reported cases of acute HAV in 2011, representing an estimated 2,700 (1,650- 4,370) actual acute cases.

• The number of acute hepatitis A cases reported in the United States declined by approximately 53%, from 2,979 in 2007 to 1,398 in 2011.

• Of the 50 states that reported hepatitis A cases in 2011, 24 states had rates below the national rate.

• The rate of acute hepatitis A in the United States declined from 1.0 case per 100,000 population in 2007 to 0.4 cases per 100,000 population in 2011.

• In 2011, the case rate ranged from no cases in New Hampshire and North Dakota to 1.2 cases per 100,000 population in Arizona.

Improvement in Sanitation

• The resistance of the virus allows it to survive in urban sewage. Accordingly, outbreaks of the disease occur in overcrowded areas where there is poor sanitation. Improvements made throughout the years have decreased the incidence of the infection in new infants, which has led to an increasing number of adults with hepatitis A.

Age

Prevaccine Era

• The reported incidence of hepatitis A was highest among children aged 5-14 years, with approximately one third of reported cases involving children aged <15 years.

• Because young children frequently have unrecognized or asymptomatic infection, a relatively smaller proportion of infections among children than adults are detected by routine disease surveillance. Incidence models indicate that during 1980-1999, the majority of HAV infections occurred among children aged <10 years, and the highest incidence was among those aged 0-4 years.

Postvaccine Era

• In recent years, rates of hepatitis A have been similar among all age groups.

Race

Prevaccine Era

• Hepatitis A rates among American Indians and Alaska Natives were more than five times higher than rates in other racial/ethnic populations, and rates among Hispanics were approximately three times higher than rates among non-Hispanics.

Postvaccine Era

• The historic differences in the rates of hepatitis A among racial/ethnic populations have narrowed in the vaccine era.

• Recent rates among American Indians and Alaska Natives represent a 99% decline compared with the prevaccine era and are now approximately the same or lower than those of other racial/ethnic populations.

• Rates among Hispanics also declined 87% during this period, from 20.6 cases per 100,000 population during 1990-1997 to 2.7 per 100,000 in 2004, but remain higher than those for non-Hispanics.

Developed Countries

Prevaccine Era

• Since the 1960s, the highest hepatitis A rates and the majority of cases occurred in a limited number of states and counties concentrated in the western and southwestern United States.

• Despite year-to-year fluctuations, rates in these areas consistently remained above the national average. In 11 states (Alaska, Arizona, California, Idaho, Nevada, New Mexico, Oklahoma, Oregon, South Dakota, Utah, and Washington) with consistently elevated rates, representing 22% of the U.S. population, average annual hepatitis A incidence was >20 cases per 100,000 during 1987-1997 (twice the national average of approximately 10 cases per 100,000 population); cases among residents of these states accounted for an average of 50% of reported cases.

• An additional 18% of cases occurred among residents of six states (Arkansas, Colorado, Missouri, Montana, Texas, and Wyoming) with average annual rates above (but less than twice) the national average during this time.

• The majority of U.S. cases of hepatitis A resulted from person-to-person transmission of HAV during communitywide outbreaks.

• The most frequently reported source of infection (in 12%-26% of cases) was household or sexual contact with a person with hepatitis A.

• For approximately 50% of persons with hepatitis A, no source was identified for their infection.

Postvaccine Era

• There has been an elimination of the historic geographic differences in the incidence rates of hepatitis A in the United States. Since 2001, rates of hepatitis A in states where vaccination was recommended, have been approximately equal to the rest of the United States. In recent years, counties with higher rates have varied from year to year and have been distributed throughout the country.

• In developed countries with good sanitary and hygienic conditions, infection rates are low. Disease may occur among adolescents and adults in high-risk groups, such as injecting-drug users, men who have sex with men, people traveling to areas of high endemicity, and in isolated populations such as closed religious communities.

Developing Countries

Areas with High Levels of Infection

• In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) have been infected with the hepatitis A virus before the age of 10. Those infected in childhood do not experience any noticeable symptoms.

• Epidemics are uncommon because older children and adults are generally immune. Symptomatic disease rates in these areas are low and outbreaks are rare.

Areas with Intermediate Levels of Infection

• In developing countries, countries with transitional economies and regions where sanitary conditions are variable, children often escape infection in early childhood. Ironically, these improved economic and sanitary conditions may lead to a higher susceptibility in older age groups and higher disease rates, as infections occur in adolescents and adults, and large outbreaks can occur.

References

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Natural History, Complications & Prognosis

Diagnosis

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Treatment

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