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Resource Packages: Hepatitis C

Historical Overview

Belief in a third hepatitis virus was first expressed during 1970 by American scientists who found that cases of hepatitis still occurred in recipients after transfusion of blood which had been screened for hepatitis B.  These cases lacked any of the markers of hepatitis A or B infection and the key question at the time was whether the liver damage was caused by a transmissible agent or by some toxic chemical or drug. Little is known of the hepatitis C virus (HCV) pathogenesis as it has still not been isolated or cultured, although the entire genome has been identified. An antibody test for HCV became available in 1990. 

HCV has been known as parenterally transmitted hepatitis, non-A non-B hepatitis and post transfusion hepatitis.   

Recent Developments

Currently diagnosis depends on demonstration of an antibody to HCV using a second-generation assay. This method has been established as a screening test for HCV presence amongst blood donors. The majority of acute infections go unnoticed and up to 50% to 70% of acute infections in otherwise healthy adults may lead to chronic liver disease. HCV ribonucleic acid (RNA) can be detected in serum using polymerase chain reaction (PCR).  

Studies of HCV risk factors in Australia indicate that around 80% of people diagnosed with HCV were exposed through injecting drug use. A small proportion, 5% to 10% have been exposed through receipt of blood and blood products prior to 1990, whilst 10% to 15% were exposed and infected by other routes such as needlestick injuries in health care workers or via use of contaminated equipment for tattooing.  

It has been estimated that of all people with antibodies to HCV, around 8% would develop cirrhosis twenty years after exposure and 20% would do so after forty years. HCV may lie dormant for decades before causing symptoms such as portal hypertension, liver failure and liver cancers. In most countries HCV is now the major cause of liver disease that requires liver transplantation among adults. In America, the Center for Disease Control and Prevention (CDC) has estimated that HCV can cause eight to ten thousand deaths each year. CDC has also predicted that this number will triple in the next two decades.   

A number of HCV genotypes have been identified throughout the world. Genotypes 1a, 1b, 2a, 2b, and 3a are the most prevalent in blood donors and patients with chronic HCV. In Europe type 3a is more common in young adults with a history of injecting drug use. Type 1b is seen in most infections in people aged 50 years or older. In Australia types 1 and 3 are most common.            

The precise mechanism of community acquired disease is uncertain but transmission by injection, medical treatment(s), dental treatment(s), transmission in saliva or saliva containing blood and by human bite have been reported. The risk of HCV transmission by household contact and sexual activity has not been well defined but appears to be low. Transmission from mother to child appears to be uncommon. Simple precautions to prevent inadvertent parenteral transmission include avoiding sharing safety razors and toothbrushes and careful handling of bleeding cuts and wounds. 

Incubation Period ranges from two weeks to six months, most commonly within six to nine weeks. 

Standard Precautions should be practiced at all times.  A single room is not required unless there is uncontrolled bleeding. 

Notification to the Public Health Unit – Laboratories are responsible for notifying Public Health Units of HCV positive antibody tests.

References

Australian National Council on AIDS and Related Diseases. Hepatitis C Sub-Committee Hepatitis C Virus Projections Working Group: Estimates and Projections of the Hepatitis C Virus Epidemic in Australia. 1998.

Benenson, A.S. ed, 1995, Control of Communicable Diseases in Man.  An official report of the American Public Health Association.16th ed, American Public Health Association, Washington.

Bennett, Brachman, P S and Sandford J P eds, 1992 3rd ed, Hospital Infections. Little, Brown and Company, Boston.

Christie, A B 4th ed, 1987, Infectious Disease.  Churchill Livingstone.

Di Bisceglie, A.M. Hepatitis C. Lancet, 1998, 351: 351-55.

Dusheiko, G.M. Smith, M. Scheuer, P.J. Hepatitis C transmitted by a human bite. Lancet, 1990; 336: 503-4.

Dusheiko, G. M. Khakoo, Somi, P. Grellier, L. A Rational Approach to the Management of Hepatitis C Infection. British Medical Journal 1996, 312: 357-64.

Heathcote, J.L. Wong, D.K. Pathogenesis and efficacy of modulation of host response in hep B and C. Current Opinion in Infectious Diseases 1994;7:333-340. 

Hepatitis C Council of NSW. Hepatitis C What You Need To Know. 2nd ed,1996, Sydney.

National Health and Medical Research Council’s (NHMRC) and the Australian National Council on AIDS, 1996, Infection Control in the Health Care Setting. Guidelines for the Prevention of Transmission of Infectious Diseases. 

NSW Health Department, 1999. Infection Control Policy. 99/87, AIDS/Infectious Diseases Branch, Sydney.

Tortora, A.G. Funke, B. Case, C. Microbiology An Introduction. 5th ed, 1994,The Benjamin/ Cummings Publishing Company Inc, California.

Watson, K. Hep C infection in Australia. Modern Medicine of Australia. 1991; 1: 2-11.

Wenzel R.P. Prevention and Control of Nosocomial Infection.  2nd edition, 1993, WilliamsandWilkins, Baltimore.              

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