eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Hepatitis A

Author: Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Coauthor(s): Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University; Lisa C Turner, MD, Clinical Instructor, Departments of Pediatrics and Communicable Diseases, University of Michigan Medical Center
Contributor Information and Disclosures

Updated: Jun 2, 2009

Introduction

Background

The earliest description of an illness consistent with viral hepatitis dates back to the second century. During the centuries that followed, epidemics of jaundice were reported, and outbreaks plagued military campaigns, both ancient and modern. In the 1920s, a viral etiology was suggested for what was then known as infectious hepatitis. Various viral agents were isolated from urine, blood, and stool from patients with hepatitis in the first half of the 20th century; however, the 27 nm particles of the hepatitis A virus (HAV) were not described until 1973.1
This finding led to the development of serologic testing and, more recently, molecular techniques, such as polymerase chain reaction (PCR). This resulted in greater knowledge regarding the epidemiology, transmission, and infectivity of hepatitis A virus (HAV), as well as the development of prevention measures, including active and passive immunization. Hepatitis A is now the target of routine childhood immunizations, starting at age 1 year. See Recommendations Updated for Universal Administration of Hepatitis A Vaccination in US Children.

Pathophysiology

Hepatitis A virus infection is transmitted via the fecal-oral route and leads to hepatic injury. The entire liver exhibits necrosis, which is most marked in the centrilobular areas, as well as increased cellularity in the portal areas. The regional lymph nodes and spleen may become enlarged. Liver injury is represented in 3 ways:

  • Direct cellular injury that elevates serum liver enzyme levels
  • Cholestasis that causes jaundice and hyperbilirubinemia
  • Inadequate liver function that lowers serum albumin levels and prolongs the prothrombin time (PT)

Frequency

United States

In 2006, the national annual incidence in the United States was 1.2 cases per 100,000 population.2 Prior to widespread vaccination, rates were above 9 cases per 100,000 population.3  

Incidence of acute hepatitis A virus in the Unite...

Incidence of acute hepatitis A virus in the United States from 1982-2006. (Image from "Surveillance for Acute Viral Hepatitis --- United States, 2006." MMWR March 21, 2008. 57(SS02);1-24)

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Incidence of acute hepatitis A virus in the Unite...

Incidence of acute hepatitis A virus in the United States from 1982-2006. (Image from "Surveillance for Acute Viral Hepatitis --- United States, 2006." MMWR March 21, 2008. 57(SS02);1-24)


Nearly one third of adults have serologic evidence of prior hepatitis A virus infection. Higher rates are associated with lower socioeconomic status, crowding, and poor sanitation. Outbreaks may occur in association with poor food hygiene or undercooked food.

International

In developing countries, infection is highly endemic; nearly 100% of the population in some countries has serologic evidence of past hepatitis A virus disease during childhood.

Mortality/Morbidity

In most patients, hepatitis A virus infection is self-limited, and complete recovery occurs. In fact, many cases are asymptomatic. A chronic carrier state is not seen with hepatitis A virus infection. Fulminant hepatitis due to hepatitis A virus is rare and has a case-fatality rate of 0.4%.

Race

Prior to targeted vaccination programs, certain well-defined populations were considered high-risk groups, including Native Americans, Alaskan natives, and some Hispanic people. Epidemics occurred in these groups every 5-10 years, as susceptible people entered or were born into the population. In addition, overall rates of infection in nonepidemic years were also greater in these populations than in the United States as a whole.

Since 2003, racial and ethnic differences have virtually disappeared. For example, a nearly 99% decrease was noted in hepatitis A vaccine incidence among Native Americans due to a widespread targeted vaccination campaign among high-risk groups.

Sex

Hepatitis A virus infection has no sex predilection. Homosexual males may have a higher risk of infection than heterosexual males.

Age

In the United States, prior to targeted vaccination programs, the highest rate of infection occurred in children aged 5-14 years. In more recent years, as many as 80% of infections have been in adults. Interestingly, the classic symptoms of hepatitis are less likely in younger patients. Young children, especially those younger than 5 years, may be asymptomatic or have anicteric illness that appears to be a nonspecific viral infection.

Clinical

History

  • The incubation period from the time of exposure to hepatitis A virus (HAV) to the appearance of symptoms is around 28 days (range 2 wk to 6 mo).
  • The patient's initial symptoms during the prodromal period include low-grade fever, nausea, vomiting, decreased appetite, and abdominal pain.
  • Older children and adults are more likely to report pain in the right upper quadrant.
  • Diarrhea may occur in young children, whereas constipation is more common in adults.
  • If present, jaundice, dark urine, and light-colored stool develop several days to a week after the onset of systemic symptoms. Anicteric infections are common in young children.

Physical

  • The general appearance is that of mild-to-moderate illness. A patient who appears severely ill is likely to have hepatitis of another cause or an atypical course.
  • Mild hepatomegaly and right upper quadrant tenderness may be present.
  • Clinical jaundice is present in two thirds of symptomatic patients.
  • Splenomegaly may occur in 10-20% of patients.

Causes

  • Hepatitis A virus is a positive-sense, single-stranded, nonenveloped RNA virus that belongs to the picornavirus family and Hepadnavirus genus.
  • Transmission is via the fecal-oral route, and viral replication occurs in the liver. Hepatitis A virus is then excreted into the bile. Its concentration is highest in the stool, especially during the 2 weeks prior to the onset of jaundice. This correlates with the period of peak infectivity. Children and adults can be assumed to be noninfectious one week after the appearance of jaundice.
  • Common-source outbreaks from contaminated food or water may occur.
    • Hepatitis A virus is concentrated in filter-feeding shellfish, which may thrive close to sewage outlets, and widespread outbreaks can occur from a single contaminated source, such as uncooked vegetables that are disseminated to restaurants or grocery stores.
    • Statistically, eating out is actually less risky than home cooking.
  • Childcare centers may be sources of outbreaks from contaminated changing tables. These outbreaks may not be identified until an adult contact has a recognizable hepatitis A virus infection because young children are often asymptomatic or have anicteric illnesses.
  • Nosocomial outbreaks have occurred because of hepatitis A virus shedding.
  • Outbreaks of hepatitis A virus infection have been increasingly reported among illicit drug users.
  • International travel is another risk factor for hepatitis A virus infection.
  • Hepatitis A virus spread from nonhuman primates to humans has been reported.
  • Hepatitis A virus vertical transmission (mother to neonate) and transmission by means of blood transfusion are extremely rare.
  • Sexual transmission is possible, especially between homosexual men.

More on Hepatitis A

Overview: Hepatitis A
Differential Diagnoses & Workup: Hepatitis A
Treatment & Medication: Hepatitis A
Follow-up: Hepatitis A
Multimedia: Hepatitis A
References
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References

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  2. Wasley A, Grytdal S, Gallagher K. Surveillance for acute viral hepatitis--United States, 2006. MMWR Surveill Summ. Mar 21 2008;57(2):1-24. [Medline]. [Full Text].

  3. Wasley A, Samandari T, Bell BP. Incidence of hepatitis A in the United States in the era of vaccination. JAMA. Jul 13 2005;294(2):194-201. [Medline].

  4. Fiore AE, Wasley A, Bell BP. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. May 19 2006;55:1-23. [Medline]. [Full Text].

  5. Victor JC, Monto AS, Surdina TY, Suleimenova SZ, Vaughan G, Nainan OV, et al. Hepatitis A vaccine versus immune globulin for postexposure prophylaxis. N Engl J Med. Oct 25 2007;357(17):1685-94. [Medline]. [Full Text].

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  7. Ahmed M, Munshi SU, Nessa A, Ullah MS, Tabassum S, Islam MN. High prevalence of hepatitis A virus antibody among Bangladeshi children and young adults warrants pre-immunization screening of antibody in HAV vaccination strategy. Indian J Med Microbiol. Jan-Mar 2009;27(1):48-50. [Medline].

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  9. AAP. Hepatitis A. In: Red Book: Report of the Committee on Infectious Diseases. American Academy of Pediatrics; 2006:326-35.

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Further Reading

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Keywords

hepatitis A, hepatitis A virus, HAV, viral hepatitis, catarrhal jaundice, epidemic jaundice, infectious hepatitis, viral hepatitis type A, virus A hepatitis, Picornaviridae, picornavirus, cholestasis, fulminant hepatitis, splenomegaly, fulminant hepatitis, abdominal pain, diarrhea, treatment, diagnosis

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Contributor Information and Disclosures

Author

Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Nicholas John Bennett, MB, BCh, PhD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Lisa C Turner, MD, Clinical Instructor, Departments of Pediatrics and Communicable Diseases, University of Michigan Medical Center
Lisa C Turner, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Rosemary Johann-Liang, MD, Medical Officer, Infectious Diseases and Pediatrics, Division of Special Pathogens and Immunological Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration
Rosemary Johann-Liang, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine
Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; sanofi pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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