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OBJECTIVE: To define the epidemiology and clinical manifestations of hepatitis D virus infection in an institutionalized population. DESIGN: A case-control study of hepatitis B carriers with and without serologic evidence of hepatitis D virus infection. Demographic, institutional, and medical data were obtained through questionnaires and chart review. Clinical status was assessed by liver function assays. SETTING: Thirteen Illinois state facilities for the developmentally disabled. PARTICIPANTS: Clients (238) who were hepatitis B carriers. RESULTS: Antibody to hepatitis D virus (anti-HDV) was detected in 71 of 238 (30%) hepatitis B carriers. Nine of thirteen facilities housed positive clients. Previous residence at one facility, designated B, was the strongest correlate of anti-HDV positivity; 85% of positive persons had lived there compared with 16% of negative controls (odds ratio 28.3 [95% CI, 13.2 to 60.7], P less than 0.001). Past hepatitis episodes were more common among anti-HDV-positive clients (37% compared with 7%) (odds ratio, 7.5 [95% CI, 3.0 to 19.1], P less than 0.001) and occurred mainly at facility B from 1950 to 1975. Liver function tests were infrequently abnormal among anti-HDV-positive clients. CONCLUSIONS: Results show widespread hepatitis D virus infection in our institutionalized population and suggest that transmission occurred mainly in the past at the overcrowded facility B. The low prevalence of laboratory evidence of chronic liver disease in the anti-HDV-positive clients may be explained by increased mortality among those originally infected from 1950 to 1975.

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A substantial proportion of the lymphomas in HIV-carriers are EBV positive. Together with the fact that there are multiple signs of EBV-activation in AIDS-patients and patients with ARC or PGL, this suggests that these virus carrying tumors develop as results of the immunosuppression, and that EBV has an important role in their pathogenesis.

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The density of HLA Class I antigen on peripheral blood mononuclear cells was evaluated by flow cytometry in the following groups of patients: 41 HBsAg carriers; 12 individuals with chronic non-A, non-B hepatitis, and 4 with acute hepatitis B. Fourteen of the carriers were positive for antibody to human immunodeficiency virus, and all were negative for antibody to delta agent. Elevated levels of Class I antigen were observed in only 19% of patients with chronic hepatitis B virus infection alone. In contrast, 86% of HBsAg carriers with coexistent human immunodeficiency virus infection demonstrated increased expression. These data suggest that HBsAg carriers are capable of sustaining a systemic interferon response to another chronic viral infection and further supports the hypothesis that a defective interferon response exists in chronic hepatitis B virus infection.

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The epidemiology and clinical outcome of hepatitis D viral infection in HBsAg-positive acute hepatitis, chronic liver disease, primary hepatocellular carcinoma and the symptomless carrier state was studied in Jordan. The prevalence of hepatitis D viral infection was significantly higher in patients with chronic liver disease (18/79, 23%) and acute hepatitis (17/108, 16%) than in symptomless HBsAg carriers (2/136, 2%). The highest prevalence of hepatitis D viral infection was found in patients with primary hepatocellular carcinoma (10/15, 67%) who were also significantly older than such patients without hepatitis D viral infection. Antihepatitis D virus IgM was detected persistently in 83% of patients with antihepatitis D virus-positive chronic liver disease and transiently in 41% of patients with acute hepatitis. A trend to increased mortality was observed in acute hepatitis D viral superinfection (25%) compared to hepatitis D viral coinfection (0%) and to antihepatitis D virus-negative HBsAg-positive acute hepatitis (4%). In patients with established chronic liver disease, however, neither survival nor histological parameters of disease activity were significantly different in the antihepatitis D virus-positive and antihepatitis D virus-negative groups. While the early stage of hepatitis D viral superinfection is associated with increased mortality, it appears that in patients with late-stage chronic liver disease, severe histological activity subsides, and survival is no longer influenced by the factor of hepatitis D viral infection. However, primary hepatocellular carcinoma appears to complicate the course of those antihepatitis D virus-positive patients surviving beyond this stage.

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Knowledge about hepatitis B virus (HBV) has expanded vastly over the past 20 years, elucidating not only the spectrum of clinical illnesses it causes but also its biologic characteristics. HBV is an important cause of both acute and chronic liver disease in the United States. The most serious outcome of hepatitis B infection is chronic liver disease, which can range from chronic hepatitis eventuating in cirrhosis to primary hepatocellular carcinoma. Molecular biologic studies have shown that HBV-DNA can be integrated into the genome of hepatocytes. This integration may be part of the natural history of chronic hepatitis B infection and may transform normal hepatocytes into neoplastic cells. Immunization with hepatitis B vaccine (Heptavax-B) of persons at high or intermediate risk is an essential means for preventing transmission of hepatitis B. Use of the vaccine after recent exposure to hepatitis B breaks the chain of transmission--an exciting capability. Postexposure immunization of neonates born of HBsAg-positive mothers is particularly important in preventing vertical, or perinatal, transmission of infection.

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The increased incidence of Salmonella osteomyelitis in patients with sickle cell disease has never been entirely explained. Problems such as cholelithiasis, intestinal infarction, and frequent antibiotic use in this population could possibly result in prolonged or chronic intestinal carriage of Salmonella after acute gastroenteritis. If prolonged carriage were a factor in the pathogenesis of osteomyelitis, attempts to eliminate the Salmonella with antibiotics would be indicated. We did a stool culture survey of 71 patients attending our pediatric sickle cell clinic to determine the incidence of asymptomatic Salmonella carriage. At least two rectal swab cultures were obtained from each patient; 69% of patients also mailed in a stool sample for culture. No Salmonella was isolated. It therefore appears unlikely that prolonged intestinal Salmonella carriage is an important mechanism in the development of Salmonella osteomyelitis in patients with major sickle hemoglobinopathies.

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HBV exposure and HBsAg positivity rate were examined in 561 residents of an area endemic for S. japonicum and 22 additional cases with severe HSS japonica were also included. The differences in HBV exposure and HBsAg positivity rates among the groups without the parasitism, with schistosomiasis japonica and with HSS (53 cases) were not statistically significant. Comparison of the same parameters between those with and without S. japonicum infection according to sex and age groupings did not also show significant differences. Increasing intensity of S. japonicum infection was not associated with either increasing or decreasing HBV exposure and HBsAg positivity. It is postulated that HBV infection does not contribute to the production of HSS japonica mainly because HBV infection occurs at a much earlier age than S. japonicum infection.

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Sera of thirty-five hepatitis B surface antigen (HBsAg) positive hemodialysis patients and fifty-three asymptomatic HBsAg chronic carrier were studied to assess the relationship between markers of virus activity (hepatitis B e antigen and core-associated DNA polymerase activity) and titers of HBsAg and of antibody to hepatitis B core antigen (anti-HBc). All sera were tested by solid-phase radioimmunoassay methods. HBeAg was detected in 20 (51%) hemodialysis patients and in 14 (26%) asymptomatic carriers, whereas DNA P activity was present in sera of 21 (60%) and 17 (32%) respectively. The highest titers of HBsAg and anti-HBc expressed as P/N ratio between positive and negative controls, were detected in the majority of hemodialysis patients, whereas asymptomatic carriers showed low titers of these markers. These data suggest that in HBsAg positive hemodialysis patients a more active viral replication occurs and further underline the difference between these patients and other categories of HBsAg carriers in terms of infectivity.

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The frequency of hepatitis B surface antigen (HBsAg) has been studied in the sera and renal biopsies of 276 patients with various forms of glomerulonephritis (GN), the nephrotic syndrome and other nephropathies. Using a modified Hepanosticon method, HBs antigenemia was detected in 32 of 196 patients (16.3%) with immune complex (IC) GN and the nephrotic syndrome. Indirect immunofluorescence revealed HBsAg in 33 renal biopsy tissue specimens (16.8%). HBsAg was found in the sera of four of the 80 remaining patients with other renal diseases (5%), and in the renal biopsy tissues of another four (5%). Antibody against HBsAg could only be demonstrated in the serum of one glomerulonephritic patient. The sera of 18,799 normal blood donors were used as controls; of these 186 (0.99%) had positive tests for HBsAg. It is concluded that, in some patients with GN and the nephrotic syndrome, HBsAg-containing IC may be implicated in the development and/or progression of the disease.

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Forty-two episodes of culture-proved salmonellosis were found retrospectively among 2,262 patients treated for malignant diseases at St Jude Children's Research Hospital, Memphis. These cases were reviewed in an effort to determine whether Salmonella infections in childhood cancer patients are associated with an increased frequency of septicemia and death, as has been reported for adults with cancer. Septicemia occurred in only 10% of the patients studied, consistent with the frequency established in general populations. There were no deaths attributable to Salmonella infection. Most of the patients (57%) with salmonellosis had gastroenteritis, and the clinical course of this syndrome was no more severe or prolonged than that seen in otherwise normal children. We recommend that management of Salmonella infections in children with cancer follow presently accepted guidelines for normal hosts.

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