To define more exactly the epidemiology of delta virus infection and confirm its role in causing fulminant Labrea hepatitis in the Amazon Basin, we studied the prevalence of delta virus infection among persons with acute and chronic hepatitis B virus infection in the Boca do Acre district of the southern Amazon Basin. Delta virus infection was found in 24% of asymptomatic hepatitis B virus carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. Chronic delta virus infection occurred primarily in older children and adults, while acute and fulminant delta virus infection occurred in young children as well. In fulminant hepatitis cases, delta virus superinfection of hepatitis B virus carriers was the most common serological pattern; histopathologic examination showed features identical to those described in fulminant hepatitis cases of similar etiology in Colombia and Venezuela. Delta virus infection is highly endemic in the southern Amazon Basin and is the principal cause of Labrea hepatitis.

Hepatitis has been identified as a major cause of morbidity and mortality in the Amazon Basin. Hepatitis morbidity may exceed 90 cases per 100,000 inhabitants per year in some parts of this region, and monality from acute hepatitis on the order of four deaths per 100,000 inhabitants per year has been reported-a rate five to 10 times the average reponed in the rest of the hemisphere (1). Monality due to cirrhosis is also reponed as being high in some parts of the region. Funhermore, in rural pans of the southern Amazon tributaries an unusual type of severe hepatitis, known as labrea hepatitis or black fever, has been recognized for 40 years (2-5). This entity is characterized by rapid progression of acute hepatitis with hematemesis and / or encephalopathy developing within days of the onset of illness, together with a characteristic histologic picture of microvesicular fatty infiltration and eosinophilic necrosis of the liver (5-6). It occurs in young adults and children, and often clusters in families. Recent studies have suggested combined hepatitis B virus (HBV) and delta virus infection as a possible cause of this illness (7-8). Several studies have indicated that both hepatitis A virus (HAV) and HBV infection are highly endemic throughout the Amazon region (9-11). In addition, delta virus infection also appears to be endemic and to be a major cause of chronic hepatitis in this area (8, 11). Nevertheless, studies to date have not focused upon the frequency and causes of acute and fulminant hepatitis in the Amazon region.

Yupik Eskimos of southwestern Alaska have the highest known prevalence of hepatitis B virus infection of any general population in the United States. Prospective serological surveys of 1,280 seronegative Yupik Eskimos, performed between 1971 and 1976, identified 189 (14.8%) who developed serological evidence of hepatitis B virus infection. Twenty-six (13.8%) developed clinical hepatitis during the interval when seroconversion occurred. The proportion of patients with clinically apparent hepatitis increased with age (P less than .01), ranging from 9.5% of infections in patients who were four years of age or less to 33.3% of infections in patients who were 30 years of age or older. Twenty-five (13.3%) of the 188 individuals who were studied became chronic carriers of hepatitis B surface antigen. The risk of becoming a carrier was inversely related to the age of the patient at the time of infection (P = .02). Among patients who were four years of age or less when infected, 28.8% became chronic carriers of hepatitis B, as compared with 7.7% of those who were 30 years of age or older.

Sera collected in 1973-1975 from 3053 residents of 12 selected Alaskan Eskimo villages were tested for evidence of hepatitis B virus infection. Overall, hepatitis B surface antigen (HBsAg) was found in 6.4% of those tested. Evidence of hepatitis B infection (positive for HBsAg or antibody to hepatitis B surface antigen (anti-HBs] varied considerably by village, from 4.6% to 69.9%, and increased with advancing age. The proportion with HBsAg was significantly higher in those under the age of 13 years, and the male/female ratio varied from 0.9 to 1.5 to 1.5 in the prepubertal, postpubertal-premenopausal, and postmenopausal age groups, respectively. The prevalence of hepatitis B e antigen (HBeAg) in HBsAg-positive persons decreased with advancing age, and conversely, the prevalence of antibody to hepatitis B e antigen (anti-HBe) increased with age. Hepatitis B infection was found to be sporadically distributed, with great village-to-village variation and further variation by household within most villages. The high HBsAg and HBeAg seropositivity observed in children suggests that children are both more recently infected with hepatitis B and are more involved in hepatitis B transmission in these villages.