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Delta Hepatitis -- Massachusetts

An outbreak of hepatitis B (HB) that began in September 1983 is continuing in Worcester, Massachusetts, primarily involving parenteral drug abusers (PDAs) and their sexual contacts. As of August 1, 1984, 75 cases of acute HB have been identified, 50 of which are considered outbreak-related. Fulminant hepatitis has been a prominent feature of this outbreak. Six deaths have occurred, for an outbreak-related case fatality ratio of 12%.

Patients meeting all the following criteria were considered outbreak-related HB cases: (1) an acute clinical illness compatible with HB; (2) elevated serum glutamic-oxaloacetic transaminase (SGOT) or serum glutamic-pyruvic transaminase (SGPT) two or more times greater than the upper limit of normal (when such results were available); (3) positive serology for hepatitis B surface antigen (HBsAg); (4) residence and/or primary diagnosis and treatment within the city of Worcester; and (5) a PDA or a direct contact of a PDA.

Patients with acute HB who could be located were interviewed regarding their drug and alcohol use, as well as risk factors for HB. Serum samples were obtained to test for markers of hepatitis B virus (HBV) infection and delta virus infection.

Of the 50 outbreak-related case patients, 35 were male. Twenty-nine were white, non-Hispanic; 17 were Hispanic; two were black; and two were of unknown race. Ages ranged from 15 years to 43 years (median 25 years). Forty-three patients used needles; six were sexual contacts of PDAs; and one had direct contact with open wounds of a person with hepatitis. Of the six patients who died, three were male; five were white, non-Hispanic, and one was Hispanic. Ages ranged from 19 years to 34 years of age (median 27 years). Five were PDAs, and one was a sexual contact of a known PDA.

Drugs that were self-injected were primarily heroin and cocaine. No 3,4-methylene diamphetamine (MDA), a drug implicated in fulminant HB/PDA deaths in North Carolina in 1979, was used (1). The only potential hepatotoxin identified was alcohol.

Testing for HB markers confirmed HB in all cases. Serum specimens were available from four patients who died; three had immunoglobulin M (IgM) anti-delta virus antibodies. IgM anti-delta virus antibodies were also present in four of 22 PDAs with nonfulminant acute HB, one of seven PDA contacts with nonfulminant acute HB, and none of 11 nonoutbreak-related patients with acute HB. In addition, two of 13 non-ill HBsAg-positive PDAs had serologic markers of delta virus infection (one with IgG antibodies and one with IgM). Reported by T Ukena, MD, Worcester Hahnemann Hospital, LJ Morse, MD, A Gurwitz, MD, WG Irvine, JG McCarthy, EM Macewicz, M Smith, Worcester Dept of Public Health, R Bessette, MD, C Pelletier, St. Vincent Hospital, A Decelles, Worcester City Hospital, M Bemis, R Glew, MD, Memorial Hospital, S Weinstein, H Kotilainen, University of Massachusetts Hospital, GF Grady, MD, Acting Director, Communicable Diseases and Venereal Diseases, Massachusetts Dept of Public Health; Hepatitis Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Previous clusters of fulminant HB deaths among PDAs have been reported in this country (1,2); however, this is the first outbreak of fulminant HB in the United States in which the delta virus has clearly been shown to have contributed to the severity of the illness.

Delta virus is composed of a protein antigen (delta antigen) and a ribonucleic acid of low molecular weight. Although transmissible as an independent infectious agent, delta virus can only infect and cause illness in the presence of active HBV infection. To be infectious, this incomplete virus requires a coat of HBsAg (3). Delta virus and HBV may simultaneously infect a host (coprimary infection with HBV/delta virus), or delta virus may superinfect an existing HBV carrier. Either coprimary infection or superinfection may cause acute hepatitis; both types of infection have been associated with fulminant HB in Europe (4).

Delta virus infection is endemic in southern Italy. Based on limited serosurveys, it has also been found in the Middle East and in certain parts of South America and Western Africa. Superinfection with delta virus was implicated as the major cause of an exceptionally severe hepatitis epidemic among Venezuelan Indians in which 34 of 149 patients died (5). Delta virus infection has been limited to hemophilia patients and PDA populations in the rest of Western Europe, North America, and Australia (7,8). Fulminant coprimary HBV/delta virus infections among PDAs have occurred sporadically in Los Angeles (6).

Although delta virus is transmitted in a manner similar to HBV, to date, delta virus infection has not been reported in this country in health-care workers or male homosexuals, the other major groups at risk for HB. Because delta virus infections have never been found in the absence of infection with HBV, there appears to be little risk of spread outside of groups known to be at risk of acquiring HB. Testing for delta virus is indicated in the setting of fulminant HB infection or acute hepatitis occurring in a known HB carrier.

Control of HB outbreaks among PDAs is difficult. Efforts to control the current outbreak have focused on educating PDAs on the modes of transmission of HB and on updating physicians regarding serodiagnosis and reporting of HB and recommended prophylaxis of needle, sexual, and familial contacts of patients (9). Since HB vaccine will prevent both HB and delta virus infections, a program to vaccinate PDAs in Worcester is currently under development as a control measure.

References

  1. CDC. Hepatitis B--New Bern, North Carolina. MMWR 1979;28:373-4.

  2. CDC. Fulminant hepatitis B among parenteral drug abusers--Kentucky, California. MMWR 1984;33:70, 76-7.

  3. Rizzetto M, Canese MG, Gerin JL, London WT, Sly DL, Purcell RH. Transmission of the hepatitis B virus-associated delta antigen to chimpanzees. J Infect Dis 1980;141:590-602.

  4. Smedile A, Farci P, Verme G, et al. Influence of delta infection on severity of hepatitis B. Lancet 1982;II:945-7.

  5. Hadler S, Monzon M. Ponzetto A, et al. Delta virus infection and severe hepatitis: an epidemic in the Yucpa Indians of Venezuela. Ann Intern Med 1984;100:339-44.

  6. Govindarajan S, Chin KP, Redeker AG, Peters RL. Fulminant B viral hepatitis: role of delta agent. Gastroenterology 1984;86:1417-20.

  7. Rizzetto M, Shih JW-K, Gocke DJ, Purcell RH, Verme G, Gerin JL. Incidence and significance of antibodies to delta antigen in hepatitis B virus infection. Lancet 1979;II:986-90.

  8. Williams GV, Cossart YE. Delta associated hepatitis in Australia. Aust NZ J Med 1983;13:231-5.

  9. ACIP. Postexposure prophylaxis of hepatitis B. MMWR 1984;33:285-90.



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