Hepatitis A
From Wikipedia, the free encyclopedia
| 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 |
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| ICD-10 | B15.- |
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| ICD-9 | 070.1 |
| DiseasesDB | 5757 |
| MedlinePlus | 000278 |
| eMedicine | med/991 ped/977 |
| MeSH | D006506 |
Hepatitis A, (formerly known as infectious hepatitis), is an acute infectious disease of the liver caused by Hepatitis A virus,[1] which is most commonly transmitted by the fecal-oral route via contaminated food or drinking water. Every year, approximately 10 million people worldwide are infected with the virus.[2] 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.[3]
In developing countries, and in regions with poor hygiene standards, the incidence of infection with this virus approaches 100% and the illness is usually contracted in early childhood. Hepatitis A infection causes no clinical signs and symptoms in over 90% of these children and since the infection confers lifelong immunity, the disease is of no special significance to the indigenous population. In Europe, the United States and other industrialised 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.[3]
Hepatitis A does not have a chronic stage and does not cause permanent liver damage. Following infection, the immune system makes antibodies against the hepatitis A virus that confer immunity against future infection. The disease can be prevented by vaccination and hepatitis A vaccine has been proved effective in controlling outbreaks worldwide.[3]
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[edit] Virus
The Hepatitis virus (HAV) is a Picornavirus; it is non-enveloped and contains a single-stranded RNA packaged in a protein shell. There is only one type of the virus.
[edit] Pathogenesis
Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestine.[4] The blood carries the virus to its target, the liver, where it lives and multiplies within hepatocytes and Kupffer cells (i.e., liver macrophages). There is no apparent virus-mediated cytotoxicity, and liver pathology is likely immune-mediated. Virions are secreted into the bile and released in stool. HAV is excreted in large quantities approximately 11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15-50 days, and mortality is less than 0.5%.
[edit] 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,[5] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[6] Approximately 40% of all acute viral hepatitis is caused by HAV.[7] 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).
[edit] Symptoms
Early symptoms of hepatitis A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks, (the incubation period ), after the initial infection.[8]
Symptoms can return over the following 6-9 months which include:[9]
- 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
[edit] Diagnosis
Although the virus is excreted in the feces towards the end of the incubation period, specific diagnosis is made by the detection of Hepatitis A virus specific IgM antibodies in the blood.[10] IgM antibody is only present in the blood following an acute hepatitis A infection. It is detectable from one to two weeks after the initial infection and persists for up to 14 weeks. The presence of IgG antibody in the blood means that the acute stage of the illness is past and the person is immune to further infection. IgG antibody to HAV is also found in the blood following vaccination and tests for immunity to the virus are based on the detection of this antibody.[10]
During the acute stage of the infection, the liver enzyme alanine transferase (ALT) is present in the blood at levels much higher than is normal. The enzyme comes from the liver cells that have been damaged by the virus.[11]
Hepatitis A virus is present in the blood, (viremia), and feces of infected people up to two weeks before clinical illness develops.[11]
[edit] Epidemiology
HAV is found in the feces of infected persons and those who are at higher risk include travelers to developing countries where there is a higher incidence rate,[12] and those having sexual contact or drug use with infected persons.[13] There were 30,000 cases of Hepatitis A reported to the CDC in the U.S. in 1997. The agency estimates that there were as many as 270,000 cases each year from 1980 through 1999.[14]
HAV outbreaks still occur in and caused by poor hand hygiene among infected, sometimes symptomatic restaurant employees failing to wash their hands after toilet breaks.
[edit] Epidemics
The most widespread hepatitis A outbreak in America afflicted at least 640 people (killing four) in north-eastern Ohio and south-western Pennsylvania in late 2003. The outbreak was blamed on tainted green onions at a restaurant in Monaca, Pennsylvania.[15] In 1988, 300,000 people in Shanghai, China were infected with HAV after eating clams from a contaminated river.[16]
[edit] See also
[edit] References
- ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, 541–4. ISBN 0838585299.
- ^ Thiel TK (1998). "Hepatitis A vaccination". Am Fam Physician 57 (7): 1500. PMID 9556642.
- ^ a b c Connor BA (2005). "Hepatitis A vaccine in the last-minute traveler". Am. J. Med. 118 Suppl 10A: 58S–62S. doi:. PMID 16271543.
- ^ Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.
- ^ Brundage SC, Fitzpatrick AN (2006). "Hepatitis A". Am Fam Physician 73 (12): 2162–8. PMID 16848078.
- ^ Lees D (2000). "Viruses and bivalve shellfish". Int. J. Food Microbiol. 59 (1-2): 81–116. doi:. PMID 10946842.
- ^ Insert footnote text Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.
- ^ Hepatitis A Symptoms. eMedicineHealth (2007-05-17). Retrieved on 2007-05-18.
- ^ Hepatitis A : Fact Sheet. Center for Disease Control (2007-08-09). Retrieved on 2007-12-07.
- ^ a b Stapleton JT (1995). "Host immune response to hepatitis A virus". J. Infect. Dis. 171 Suppl 1: S9–14. PMID 7876654.
- ^ a b Musana KA, Yale SH, Abdulkarim AS (2004). "Tests of liver injury". Clin Med Res 2 (2): 129–31. PMID 15931347.
- ^ Chapter 4 - Hepatitis, Viral, Type A - Yellow Book | CDC Travelers' Health
- ^ Hepatitis A: Fact Sheet | CDC Viral Hepatitis
- ^ http://www.cdc.gov/Ncidod/diseases/hepatitis/a/global_hepA_epi.pdf
- ^ http://www.cdc.gov/mmwR/preview/mmwrhtml/mm5247a5.htm
- ^ Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.
[edit] External links
- NIAID Bioinformatics Resource Center)
- CDC's hepatitis A links
- CDC's hepatitis A Fact Sheet
- MeSH Hepatitis+A
- MeSH Hepatitis+A+virus
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