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     Tropical Diseases

Malaria   |   Dengue Infection   |   Japanese Encephalitis   |   Diarrhea   |   Filariasis   |   Viral Hepatitis

Viral Hepatitis

Hepatitis A

Acute hepatitis A continues to be a public health problem in developing countries especially in Asia, Africa and Latin America. Hepatitis A virus (HAV) is a single-stranded RNA virus from the genus Hepatovirus and is a member of the Picornaviridae family. There are seven genotypes of HAV (I–VII) which can be easily acquired via the fecal-oral route through contaminated food or water and physical contact with infected individuals. Some infected adults do not exhibit any symptoms whereas others may experience mild flu-like illness, fulminant hepatitis or severe acute liver failure.

Acute HAV is diagnosed by detecting the presence of HAV-specific antibodies and antigens. Molecular epidemiology studies can identify the strain/genotype, extent, route of transmission and source of infection.

In Thailand, before 1981, more than 97% of adults were anti-HAV positive. This data indicated that HAV was prevalent throughout the country. When campaigns to improve sanitation and hygiene were enforced, this dramatically reduced the number of HAV outbreaks.

Reference: Pathog Glob Health. 2013 Oct;107(7):367-72.

Hepatitis B

The hepatitis B virus (HBV) is one of the most common causes of chronic hepatitis B (CHB), liver cirrhosis and hepatocellular carcinoma (HCC). Globally more than 2 billion people have been infected with HBV and 378 million are suffering from chronic hepatitis. Over 600,000 people die each year because of HBV infection.

In high prevalence areas such as the central Asian republics, Southeast Asia, Sub-Saharan Africa and the Amazon basin over 8% of the population may be HBV carriers. The main route of HBV infection is vertical transmission from mother to infant and horizontal transmission between children, whereby 90% will develop chronic hepatitis as infants or in early childhood and never clear the virus. In contrast, 15% of HBV infections in adulthood develop into chronic hepatitis with viral persistence.

Medications for treatment of chronic hepatitis B are Interferon therapy and antiviral medications. Long term follow-up and surveillance for hepatocellular carcinoma are necessary for all individual with chronic hepatitis B infection.

Reference: PLoS One. 2014 Jan 23;9(1):e86007.

Hepatitis C

Hepatitis C virus infection is an important worldwide public health problem. Most HCV cases become chronic hepatitis C, which may advance to liver fibrosis, cirrhosis, and hepatocellular carcinoma. The global prevalence of HCV infection is estimated at more than 170 million people.

Hepatitis C virus is a member of the Flaviviridae family and belongs to the genus Hepacivirus. HCV is classified into six major genotypes (1-6) and subdivided into various subtypes named in alphabetical order from a to z. The prevalence of HCV genotypes varies geographically: HCV-1 is found worldwide including developed regions such as North America and Europe. HCV-2 has high prevalence in Central and West Africa as well as some western countries, while HCV-3 is predominantly found in the Far Eastern countries and the Indian subcontinent. Meanwhile, HCV genotypes 4, 5 and 6 are endemic to specific geographical areas: HCV-4 is mainly found in Egypt and Sub-Saharan Africa, HCV-5 in South Africa, and HCV-6 in South China and South-East Asian countries.

In the past 10 years, the standard treatment of HCV patients has been a combination of pegylated interferon (PEG-IFN) and ribavirin (RBV) with a 24 to 48 wk regimen depending on the viral genotype of each infected individual. However recently a newer agents known as direct-acting antivirals (DAA) were approved for use in the treatment of HCV.

Reference: World J Gastroenterol. 2014 Mar 21;20(11):2927-40.

Hepatitis D

Hepatitis D or delta hepatitis is caused by the hepatitis delta virus (HDV), a defective RNA virus. HDV requires the help of a hepadnavirus like hepatitis B virus (HBV) for its own replication. HDV is transmitted percutaneously or sexually through contact with infected blood or blood products.

Chronic HBV carriers are at risk for infection with HDV. Individuals who are not infected with HBV, and have not been immunized against HBV, are at risk of infection with HBV with simultaneous or subsequent infection with HDV. Since HDV absolutely requires the support of a hepadnavirus for its own replication, inoculation with HDV in the absence of HBV will not cause hepatitis D. Alone, the viral genome indeed replicates in a helper-independent manner, but virus particles are not released.

The hepatitis delta virus is present worldwide and in all age groups. Its distribution parallels that of HBV infection, although with different prevalence rates (highest in parts of Russia, Romania, Southern Italy and the Mediterranean countries, Africa and South America). In some HBV-prevalent countries such as China, HDV infection is disproportionately low.

The diagnosis of acute hepatitis D is made after evaluation of serologic tests for the virus. Total anti-HDV are detected by commercially available radioimmunoassay (RIA) or enzyme immunoassay (EIA) kits. The method of choice for the diagnosis of ongoing HDV infection should be RT-PCR, which can detect 10 to 100 copies of the HDV genome in infected serum.

Reference: World Health Organization, http://www.who.int/csr/disease/hepatitis/ HepatitisD_whocdscsrncs2001_1.pdf

Hepatitis E

Hepatitis E virus (HEV), a member of the genus Hepevirus in the family Hepeviridae is a small RNA virus. HEV infection occurs in mammals, including humans, domestic pigs, wild boar, deer and rodents. HEV has been classified into four major genotypes by molecular characterization and HEV genotype 3 has been identified almost worldwide. Hepatitis E virus (HEV) is an emerging pathogen worldwide. In Thailand, seroprevalence of HEV ranges from 9% to 22% in adult subjects and increases with age. This prevalence is comparable with the data from east Asia. In occupational risk groups such as pig and poultry farmers who have worked in farms for more than 2 years, HEV prevalence amounted to 27.9 %. HEV has been known to be transmitted via contaminated water in endemic areas and recent data have demonstrated animal to human transmission in almost every part of the world.

The majority of patients with acute HEV infection remain asymptomatic. Clinical manifestations of acute hepatitis E can range from asymptomatic to fulminant with ensuing liver failure. The risk of acute or subacute liver failure from acute HEV infection is exacerbated by pre-existing chronic liver disease. In case of liver cirrhosis, HEV infection can induce rapid liver decompensation and death.

Acute HEV infection can be detected by laboratory tests for anti-HEV IgM with sensitivities and specificities of close to 90% and 100%, respectively. Molecular techniques appear to be complementary for diagnosing HEV infection during early acute infection and in immunosuppressed patients.

Reference: Asian Pac J Trop Med. 2014



Last updated: July 28, 2014
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