4. Introduction Hepatitis Delta Virus Recognized in 1977 – co existent with HBV infection A defective RNA virus than need hepadnavirus (HBV) to replicate 1980 – noticed the dependency of HDV to HBV (need HBsAg to as virion coat) Associated with most severe form of acute and chronic HBsAg +
5. Epidemiology of Hepatitis D Spread worldwide Highest in Russia, Romania, Southern Italy, Mediterranean countries, Africa, South America Low in China, Taiwan, India Latest trends New foci in Okinawa, certain area of China, India, Albania Decreasing trend in Mediterranean
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7. Mode of Transmission Spread Percutaneous and sexually and through body fluid/blood Potentially infectious in whole phase People at risk HBV carrier, HBV unvaccinated person IVDU Unprotected sex Exposed to unscreen blood, body fluid People receiving blood, blood product
8. Hepatitis D Features IP – 5 to 64 days Super-infection* or co-infection with HBV Diagnosis Liver biopsy Serology – anti HDV, Ig M*, RNA* Lead to fulminant acute hepatitis, severe chronic active hepatitis – cirrhosis, hepatocellular carcinoma
11. Prevention and Control Hep B vaccination* Reduce risk behaviour May improve with α-interferon Epidemic measures Surveillance Screening Cases with common exposure – active case detection, investigate source and do appropriate action
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13. Introduction was not recognized as a distinct human disease until 1980 non-enveloped, positive-sense, single-stranded RNA virus. antibodies to HEV or closely related viruses have been detected in primates and several other animal species.
14. Epidemiology of Hepatitis E Central and South-East Asia, North and West Africa, and in Mexico Common in hot climate area sporadic cases of hepatitis E - south-east and central Asia, the Middle East, northern and western Africa, and North America
16. Mode of Transmission Spread faecal-oral route Food and waterborne disease possibility of zoonotic Risk factor poor sanitation
17. Hepatitis E Features IP - 15 to 60 days self-limiting viral infection prolonged viraemia or faecal shedding are unusual and chronic infection does not occur. Fulminant hepatitis rarely occur (mortality 0.5-4%) Higher in pregnant woman (mortality rate 20% in 3rd trimester) Diagnosis serology - hepatitis E antibody by RT-PCR
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19. Prevention and Control Surveillance and control procedures should include • provision of safe drinking water and proper disposal of sanitary waste • monitoring disease incidence • determination of source of infection and mode of transmission by epidemiologic investigation • detection of outbreaks • spread containment good personal hygiene, high quality standards for public water supplies and proper disposal of sanitary waste
20. References WHO. (2001). WHO Department of Communicable Disease Surveillance & Response Available: http:/www.who.int/emc Microbiology and Immunology Online, University of South Carolina Available: http://pathmicro.med.sc.edu/virol/hepatitis-disease.htm US CDC, Atlanta Available: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset
Editor's Notes
More than 10 million worldwide infected with HDV
Highly infectious before onset of acute disease
HepD should be considered in any individual who is HBsAg positive or has evidence of recent infectionIn one study involving 192 chronic carriers in Los Angeles, CAH or cirrhosis was found in 94% of patients who were HDV positive, compared to 61% of patients who were HDV negative. Fulminant HDV hepatitis carried a mortality rate of 70%. Coinfection is when someone is infected with HBV and HDV at the same time. Superinfection is when someone already has hepatitis B and then is infected with HDV. This may be acute or occasionally it can be picked up as chronic HDV.
Coinfection is usually acute, and will resolve by itself. Superinfection has the possibility of being more serious. With superinfections, mild cirrhosis from hepatitis B can become severe and become progressive cirrhosis. Some cases will lead to fulminant hepatitis.
The highest rates of infection occur in regions where low standards of sanitation promote the transmission of the virus. Epidemics of hepatitis E have been reported in Central and South-East Asia, North and West Africa, and in Mexico, especially where faecal contamination of drinking water is common. However, sporadic cases of hepatitis E have also been reported elsewhere and serological surveys suggest a global distribution of strains of hepatitis E of low pathogenicity. hepatitis E is responsible for up to 70% of acute hepatitis cases in countries such as Saudi Arabia, Vietnam, Indonesia, Malaysia, and Nepal.
Hepatitis E is a viral disease, and as such, antibiotics are of no value in the treatment of the infection. There is no hyperimmune E globulin available for pre- or post-exposure prophylaxis. HEV infections are usually self-limited, and hospitalization is generally not required. No available therapy is capable of altering the course of acute infection.As no specific therapy is capable of altering the course of acute hepatitis E infection, prevention is the most effective approach against the disease. Hospitalization is required for fulminant hepatitis and should be considered for infected pregnant women. For travelers to highly endemic areas, the usual elementary food hygiene precautions are recommended. These include avoiding drinking water and/or ice of unknown purity and eating uncooked shellfish, uncooked fruits or vegetables that are not peeled or prepared by the traveler.
