The hepatitis C virus (HCV) is a member of the flavivirus family and is an enveloped virus that contains single-stranded RNA. HCV is considered to be a bloodborne pathogen. Onset of disease is usually insidious, with a 1- to 5-month incubation. Mortality associated with acute infection is uncommon. However, chronicity is common with potentially life-threatening sequelae. Additional characteristics of HCV and the other 4 human hepatitis viruses shown to cause disease are presented in the table accompanying this article.1
EPIDEMIOLOGY
Chronic HCV infection is a major cause of chronic liver disease and death throughout the world. More than 170 million people worldwide are chronically infected with HCV. Infection kills almost 300,000 individuals throughout the world each year.2
HCV infection is the most common chronic bloodborne infection in the United States. In 1985, the Centers for Disease Control and Prevention (CDC) estimated that 242,000 new cases of HCV occurred each year. Since 1989, the annual number of new infections declined by more than 80% to less than 25,000 by 2001. Effective methods to screen blood for transfusions were made commercially available in May 1990. An estimated 3.9 million people have been infected, of whom 2.7 million are chronically infected.3
HCV occurs among persons of all ages, but the highest incidence of acute infection is found among persons aged 20 to 39 years. Males predominate. African Americans have the highest overall incidence rate. The highest prevalence rates are among persons with hemophilia treated with products made before 1987 and current injecting-drug users.3,4
Table. Comparison of Hepatitis Viruses*
Modified from references 1 through 4. |
Historically, HCV transmission has been highest among blood transfusion and transplant recipients. By the mid-1980s, HCV (then called non-A, non-B hepatitis) declined 50% because donors with HIV infection and/or surrogate HCV markers were excluded. More sensitive multi-antigen tests for HCV were implemented in July 1992. Current risk for transfusion-associated HCV is 1 in 100,000 units transfused. Approximately 50% of HCV cases are associated with intravenous drug abuse; 10% are associated with sexual activity; 3% with blood transfusions; and 1% with occupational exposure in healthcare workers (HCWs). The remaining cases have unidentified routes of transmission.1-5
NATURAL HISTORY
Persons with acute HCV infection typically are either asymptomatic (60% to 70%) or have a mild clinical illness. Twenty percent to 30% might have jaundice, while 10% to 20% might have nonspecific symptoms (eg, anorexia, malaise, fatigue, dark urine, nausea, or abdominal pain). In some patients, symptoms may start before anti-HCV seroconversion has occurred. The average time period from exposure to symptoms is 6 to 7 weeks, while the average time period from exposure to seroconversion is 8 to 9 weeks. Anti-HCV can be detected in 80% of patients within 15 weeks of exposure; in 90% within 5 months after exposure; and 97% by 6 months of exposure. The course of acute infection is variable. Fluctuating elevations of serum ALT levels is the most common characteristic. Fulminant hepatic failure following acute HCV is rare.1-5
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| Figure 1. Sequelae of the HCV Hepatitis |
Chronic HCV infection develops in most persons (70% to 85%), with persistent or fluctuating ALT elevations (Figure 1). However, ALT levels can in some cases remain normal through the entire infection process.4-6
The course of chronic liver disease is usually insidious, progressing at a slow rate without symptoms or physical signs in the majority of patients during the first 2 or more decades after infection. Chronic HCV infection is most often detected after a blood donation or routine physical examination; 15% to 30% of persons appear to resolve their infection without sequelae as defined by the sustained absence of HCV RNA in serum and normalization of ALT levels.1-6 Chronic HCV infection develops from most acute infections. Fluctuating ALT levels, which indicate active liver disease, occur in 60% to 70% of chronically infected persons. No clinical or epidemiologic features among persons with acute infection have been found to be predictive of either persistent infection or chronic liver disease. Oddly, persons chronically infected may experience extended periods of normal ATL activity. Long-term monitoring is required in order to determine clinical outcome or prognosis. It is assumed that chronically infected persons are infectious to some extent during the course of their disease.1-6
Most studies have reported that cirrhosis develops in 10% to 20% of chronic cases over a 20- to 25-year period (Figure 1). Hepatocellular carcinoma might develop in 1% to 5% with marked geographic variations in rates. However, when cirrhosis is already established, the rate of development of hepatocellular carcinoma may be as high as 1% to 4% per year. There are questions regarding the lifetime consequences of chronic HCV infection, especially among those infected while relatively young. However, several factors seemed to be related to severity of liver disease. These include (1) increased alcohol consumption, (2) being aged ≥ 40 years at infection, and (3) being male. Disease progress is rapid when alcohol abuse is present.1-6
OCCUPATIONAL TRANSMISSION OF HCV
HCV is not as easily transmitted as HBV through occupational exposure. However, studies of HCWs exposed to HCV-positive body fluids (especially blood) indicate seroconversion rates that ranged from 0% to 7% with an average of 1.8%.7-9 Greater risk has been associated with exposure to hollow-bore needles.10 Most cases of occupational disease transmission have involved needlesticks, but 3 cases of mucous membrane spread have been documented.11-13 There has been one case of dual HCV-HIV infection via non-intact skin.14
Prevalence of HCV infection among dental personnel approaches that of the general American population: about 1% to 2%.7,15-17 Prospective studies indicate similar attack rates. Unless contradictory data emerge, the risk of occupational acquisition by HCWs, including dental personnel, is not zero but fortunately is rather low.
Post-Exposure Procedures for HCV
Again, no vaccine is currently available to prevent HCV infection. Studies indicate that immune globulin is not effective for post-exposure prophylaxis.3,4,18 There is little information that has assessed the effect of antiviral agents such as interferon to prevent HCV infection. Mechanisms of the effect of interferon in treating patients with HCV are not well understood, and an established infection might need to be present for interferon to be an effective treatment.3,4
Testing for the presence of HCV after an occupational exposure is now a standard procedure. Ideally, the source patient is known and is amenable to serological screening for antibodies. A number of activities should be performed on the exposed HCW if the source patient is shown to be HCV-positive.3.4,7,18 These include the following:
•Baseline serologic testing for HCV antibodies and liver enzyme activity (ALT).
•If no diagnosis is made, the 2 tests are repeated 4 to 6 months after the exposure.
•If an early diagnosis is sought, testing for the presence of HCV RNA can be conducted 4 to 6 weeks after exposure.
•All anti-HCV results made though enzyme immunoassay methods should be confirmed through supplemental testing (eg, recombinant immune blot assay).
•Refer infected HCWs to a gastroenterologist for further medical evaluation and management.
References
1. Miller CH, Palenik CJ. Infection Control and Management of Hazardous Materials for the Dental Team. 3rd ed. St Louis, Mo: Mosby; 2004:87-96.
2. Poynard T, Yuen MF, Ratziu V, et al. Viral hepatitis C. Lancet. 2003;362:2095-2100.
3. Centers for Disease Control and Prevention. Hepatitis C slide set. Available at: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_c/hep_c.pdf. Accessed April 2004.
4. Centers for Disease Control and Prevention. Hepatitis C: what clinicians and other health professionals need to know [on-line training course]. Available at: http://www.cdc.gov/ncidod/diseases/hepatitis/c_training/edu/default.htm. Accessed April 2004.
5. Strader DB, Wright T, Thomas DL, et al. Diagnosis, management, and treatment of hepatitis C. Hepatology. 2004;39:1147-1171.
6. Centers for Disease Control and Prevention. Hepatitis C fact sheet. Available at: http://www.cdc.gov/ncidod/diseases/hepatitis/c/cfact.pdf. Accessed April 2004.
7. Cleveland JL, Cardo DM. Occupational exposures to human immunodeficiency virus, hepatitis B virus, and hepatitis C virus: risk, prevention, and management. Dent Clin North Am. 2003;47:681-696.
8. Puro V, Petrosillo N, Ippolito G. Risk of hepatitis C seroconversion after occupational exposures in health care workers. Italian Study Group on Occupational Risk of HIV and Other Bloodborne Infections. Am J Infect Control. 1995:23:273-277.
9. Mitsui T, Iwano K, Masuko K, et al. Hepatitis C virus infection in medical personnel after needlestick accident. Hepatology. 1992;16:1109-1114.
10. Lanphear BP, Linnemann CC Jr, Cannon CG, et al. Hepatitis C virus infection in healthcare workers: risk of exposure and infection. Infect Control Hosp Epidemiol. 1994;15:745-750.
11. Hosoglu S, Celen MK, Akalin S, et al. Transmission of hepatitis C by blood splash into conjunctiva in a nurse. Am J Infect Control. 2003;31:502-504.
12. Sartori M, La Terra G, Aglietta M, et al. Transmission of hepatitis C via blood splash into conjunctiva. Scand J Infect Dis. 1993;25:270-271.
13. Polish LB, Tong MJ, Co RL, et al. Risk factors for hepatitis C virus infection among health care personnel in a community hospital. Am J Infect Control. 1993;21:196-200.
14. Ippolito G, Puro V, Petrosillo N, et al. Simultaneous infection with HIV and hepatitis C virus following occupational conjunctival blood exposure. JAMA. 1998;280:28.
15. Cooper BW, Krusell A, Tilton RC, et al. Seroprevalence of antibodies to hepatitis C virus in high-risk hospital personnel. Infect Control Hosp Epidemiol. 1992;13:82-85.
16. Gerberding JL. Incidence and prevalence of human immunodeficiency virus, hepatitis B virus, hepatitis C virus, and cytomegalovirus among health care personnel at risk for blood exposure: final report from a longitudinal study. J Infect Dis. 1994;170:1410-1417.
17. Klein RS, Freeman K, Taylor PE, et al. Occupational risk for hepatitis C virus infection among New York City dentists. Lancet. 1991;338:1539-1542.
18. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR Recomm Rep. 1998:47(RR-19):1-39.
Dr. Palenik has held over the last 25 years a number of academic and administrative positions at Indiana University School of Dentistry. These include professor of oral microbiology, director of human health and safety, director of central sterilization services, and chairman of infection control and hazardous materials management committees. Currently, he is director of infection control research and services. Dr. Palenik has published 125 articles, more than 290 monographs, 3 books, and 7 book chapters, the majority of which involve infection control and human safety and health. Also, he has instructed more than 100 continuing education courses throughout the United States and 8 foreign countries. All questions should be directed to OSAP by e-mailing office@osap.org.
