Viral hepatitis D is caused by the hepatitis delta virus (HDV). HDV infection occurs in persons with concurrent hepatitis B virus (HBV) infection who are hepatitis B surface antigen positive. Hepatitis D may occur concurrently with acute HBV infection or as an acute superinfection in a person with chronic HBV infection. Delta virus is a defective RNA virus that requires the helper function of HBV for replication.
Percutaneous spread among parenteral drug users is not unusual. HDV may also be transmitted via transfusion and from person to person among intimate or household contacts. The rate of infection is high in hepatitis B surface antigen (HBsAg)-positive prostitutes and in homosexual or bisexual men, as well as among parenteral drug users. About 5 percent of homosexual men are infected.
HDV infection is endemic in the general population in certain areas of the world, including parts of South America, Central Africa, southern Italy, and Middle Eastern countries. It is uncommon in China and Southeast Asia - areas where hepatitis B is common, except in high-risk groups, such as injection drug users.
In the United States and most of Western Europe, delta hepatitis is most prevalent among parenteral drug users and hemophiliacs. Epidemics of HDV infection have been reported in some communities of parenteral drug users.
The onset of symptoms of hepatitis D - similar to those of hepatitis B - is usually abrupt. As in other forms of hepatitis, jaundice usually develops after the disappearance of symptoms reflecting the initial acute infection. When a person is infected concurrently with hepatitis B and D, fulminant hepatitis is much more likely to occur than with infection with only hepatitis B, and some persons with fulminant hepatitis will die. In addition, patients with hepatitis D superinfection are more likely to progress to chronic liver disease than those patients with HBV infection alone.
Viral hepatitis D is of concern to drug treatment programs because of its association with hepatitis B, which affects up to 80 percent of injection drug users in some areas. The prevalence of HDV is estimated to be 20 to 53 percent among drug users who are HBsAg positive. HDV is clinically important because persons co-infected with hepatitis B and HDV are at increased risk of developing more severe liver disease. Hepatitis B vaccination will effectively prevent delta hepatitis. It is mandatory that persons infected with HBV who are HBsAg positive alter their risk-associated behavior to avoid infecting persons not previously exposed to hepatitis B with hepatitis B alone or with both hepatitis B and D if co-infection is present.
Drug treatment programs should screen all patients for immunity to hepatitis B. Routine screening for hepatitis D is not indicated in persons who are HBsAg positive but asymptomatic. However, the following screening and prevention procedures may be appropriate:
Patients known to be HBsAg positive who have acute or chronic hepatitis may be tested for hepatitis D. The followup care and counseling, however, of a person co-infected with hepatitis D is not different from that of a person who is HBsAg positive. Therefore, knowing if the patient is co-infected with hepatitis D is of limited clinical significance.
Patients with acute hepatitis B who are not yet HBsAg positive, but are immunoglobulin M (IgM) hepatitis B core antibody (anti-HBc) positive, may be tested for HDV; however, again, the presence of HDV antibody will not alter the care or counseling of such a patient.
Patients who are HBsAg positive and/or HDV antibody positive should be advised not to share razors, toilet articles, or drinking and eating utensils.
Patients who are not already immune to hepatitis B virus should be vaccinated against the virus.
Screening is not necessary in the general population at no risk for HBV or HDV.
Patients in drug treatment programs who refuse to be screened for hepatitis B and hepatitis D should be treated as potential risks for spreading these infections. However, they should not be excluded from treatment programs on the basis of real or suspected infection.
Special care should be taken in clinical settings to avoid accidental sticks with needles, syringes, and other sharp instruments and to follow proper sterilization or disposal procedures. Universal precautions apply for drawing blood or other medically related procedures.
When hepatitis D infection occurs concurrently with hepatitis B infection, the incubation period of between 6 weeks and 6 months is the same for both. When viral hepatitis D infection occurs as a superinfection in someone already infected with hepatitis B, who remains HBsAg positive, the incubation period is thought to be between 2 and 10 weeks, on the basis of experimental infections in chimpanzees. Hepatitis D is most contagious just before the onset of symptoms but may remain infectious indefinitely in the HBsAg-positive person.
Symptoms of hepatitis D are similar to those of hepatitis B. They include fever, malaise, abdominal pain, loss of appetite, pruritus, myalgias, arthralgias, and joint pain. The onset of symptoms is usually abrupt, and jaundice usually develops after the symptoms have disappeared.
The diagnosis of viral delta hepatitis is made by detecting both HBsAg and antibody to delta hepatitis (anti-HDV). In persons with acute HBV infection who have no detectable HBsAg, IgM anti-HBc with anti-HDV is diagnostic of acute co-infection. A liver biopsy is rarely indicated. Persons known to be HBsAg positive with acute or chronic hepatitis may be screened for HDV antibody, although the presence of HDV antibody does not alter the followup of such patients.
Exposure to hepatitis D may worsen the symptoms of hepatitis B. Patients with co-infection are more likely to have fulminant hepatitis than those patients with HBV infection alone.
When acute infection with HDV occurs in the face of an existing chronic HBV infection, especially in persons with progressive, symptomatic chronic disease, there is increased progression of hepatic cirrhosis and hepatic failure. Both co-infection of hepatitis D and hepatitis B, as well as superinfection of hepatitis D, have been associated with fulminant hepatitis. Hepatitis D results in death in between 2 and 20 percent of patients with acute icteric hepatitis.
There is no specific available treatment. For persons with severe hepatitis, only supportive care is given. The treatment of chronic active hepatitis B and coexistent hepatitis D infection with a-interferon would be done only after consultation and referral to a gastroenterologist.
Protection against hepatitis D among drug users can be accomplished by vaccinating against hepatitis B. Since HDV infection requires that the person be co-infected with HBV, vaccinating against hepatitis B also confers immunity to hepatitis D. Some 3 to 4 percent of healthy recipients have no response to the hepatitis B vaccine.
HIV-infected persons may not develop protective immunity after receiving hepatitis B vaccine. They therefore remain at risk for infection with HBV and HDV.
Pregnant women should be screened for hepatitis B infection. If the woman is at risk for HBV infection, she should be vaccinated. The current recommendations of the American College of Pediatrics and the Centers for Disease Control and Prevention are that all infants be immunized against hepatitis B.
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