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Viral hepatitis, caused by one of five different viruses, is an important cause of illness in tropical countries and a significant cause of death. Vaccines against hepatitis A and B are now available and, if used widely, have the potential virtually to eliminate both these diseases (and also hepatitis D). Vaccines against hepatitis C and E are being developed.

The prevalence of infection with human T lymphotropic virus type I (HTLV-I) in 19,975 blood samples from Australia and the western Pacific was determined by measuring the presence of specific antibody (anti-HTLV-I) by enzyme-linked immunosorbent assay (ELISA) with confirmation by western blot and/or radioimmunoprecipitation techniques. In Australia no evidence of HTLV-I infection was found in injecting drug users, patients with the acquired immunodeficiency syndrome (AIDS), subjects attending a sexually transmitted diseases clinic, female prostitutes, or transfusion recipients. A low prevalence of infection was detected in people with haemophilia (0.5%) and in male homosexuals (0.5%-1%). No antibody was detected in sera from Vanuatu, Kiribati, American Samoa, the Cook Islands, New Caledonia, the Federated States of Micronesia, French Polynesia and Fiji, but a low frequency of anti-HTLV-I was detected in sera from the Solomon Islands (1.2%) and Nauru (0.6%).

Objective: To elucidate the seroepidemiology of hepatitis C in patients with clotting disorders in comparison with other blood borne infections; to examine the effects of hepatitis C on liver function; and to assess the effectiveness of current screening and inactivation procedures used in preventing the transmission of blood borne viruses by clotting factor preparations., Design: A retrospective analysis of the prevalence of antibodies to hepatitis C virus (HCV), hepatitis B virus (HBV) and human immunodeficiency virus (HIV) by means of commercially available enzyme immunoassays (for antibodies to HCV and HIV) or radioimmunoassays (for HBV antibodies and surface antigen). An analysis was made of serum transaminase levels where such information was available and this was correlated with HCV status., Patients and Setting: Panels of sera were collected from adults and children with clotting disorders attending two Melbourne haemophilia treatment centres in 1973 (n = 33), 1980 (n = 33), 1984-1985 (n = 111) and 1987-1990 (n = 217) and tested for antibodies to HCV, HBV and HIV., Results: The prevalence of antibodies to HCV in the four panels tested was 45%, 74%, 75% and 76%, and the prevalence of markers of infection with HBV was 66%, 74%, 62% and 65% respectively. No antibodies to HIV were found in sera in Panels I and II but the prevalence in Panels III and IV was 23% and 36% respectively. In subjects in whom liver function test results were available, there was a significant association between the presence of antibodies to HCV and raised transaminase levels. Since heat inactivation of clotting factors was commenced in Australia in 1984, no new cases of transmission of HIV by clotting factors has been detected, but transmission of HCV in 19 subjects and HBV in one subject could not be excluded., Conclusions: Hepatitis C infection in haemophiliacs has been a very frequent event, and the presence of antibodies to HCV is associated with an increased incidence of raised transaminase levels. Screening and heat inactivation of clotting factors has prevented further HIV transmission, but exposure to HBV and HCV has not been eliminated.

Objective: To determine the relationship between the development of hepatitis C antibody (anti-HCV) and the clinical symptoms in acute hepatitis C., Design: Retrospective analysis of sera from patients with acute non-A non-B hepatitis., Setting and Patients: Patients admitted to Fairfield Hospital with the diagnosis of acute non-A non-B hepatitis between 1979 and 1989. Inclusion criteria included a typical clinical illness, accompanied by an alanine aminotransferase level of more than 2.5 times the upper limit of normal (normal, less than or equal to 40 U/L) and negative serological test results for acute hepatitis A and B., Main Outcome Measure: Time to develop anti-HCV after the onset of symptoms in patients with acute hepatitis C., Results: Seroconversion was demonstrated in 26 of the 128 patients who fulfilled the inclusion criteria. In these patients, antibody was detected between one week and 32 weeks after the onset of dark urine; more than half the patients (54%) had seroconverted by four weeks and a third (34%) developed antibodies within two weeks. Of 20 patients who had sera collected within four weeks of the onset of dark urine, 14 (70%) had developed antibody., Conclusion: These results suggest that in patients with community-acquired hepatitis C, seroconversion occurs significantly earlier than is observed in patients who have been infected by blood transfusion. Sera taken shortly after the onset of symptomatic hepatitis C may be useful in the diagnosis of this condition.

Parenterally transmitted non-A, non-B (NANB) hepatitis virus or hepatitis C virus is a common cause of both acute and chronic hepatitis. Using a recently developed enzyme-linked immunosorbent assay we looked at the prevalence of antibodies to hepatis C virus (anti-HCV) in a number of groups. People with haemophilia (75.6%) and intravenous drug users (61.9%) had the highest prevalence, while homosexual men attending a sauna (34.1%) and prisoners (30.8%) had a moderately high prevalence of anti-HCV. A lower prevalence of antibody was detected in female prostitutes (10.4%), institutionalised mentally retarded subjects (9.5%), homosexual men requesting human immunodeficiency virus (HIV) testing through their local doctor (8.8%), dialysis patients (5.9%), renal transplant patients (6.9%), and patients referred from a sexually transmitted diseases clinic (6.2%). The lowest prevalence of anti-HCV was recorded in women attending a provincial hospital for antenatal care (0.4%). The predominance of anti-HCV in groups of people exposed to blood-borne and sexually transmitted infections suggests that these routes may be primarily involved in the spread of hepatitis C virus infection.

Haemodialysis of patients who were acutely or chronically infected with hepatitis B virus has been undertaken at Fairfield Hospital for Communicable Diseases for the past 10 years. Over this period, only one staff member has shown serological evidence of infection. The procedures taken to prevent the spread of infection, and the results of an ongoing serological survey of all persons associated with the haemodialysis unit are presented.

Sera collected from a group of 1053 Victorians were tested for antibody to hepatitis A virus by solid phase radioimmunoassay. The group comprised approximately equal numbers of males and females of all ages, 488 of whom lived in Melbourne and 565 in six provincial cities. In both the metropolitan and provincial groups, the prevalence of antibody to hepatitis. A virus was independent of sex and increased steadily with age. Antibody was detected in approximately 20% of children by the age of 10 years, in 40% at 40 years and in excess of 95% above the age of 60 years.

Faecal specimens were obtained from 92 Aboriginal infants admitted to Alice Springs Hospital during an extensive outbreak of gastroenteritis in the surrounding area in July, 1976. Specimens were examined for potentially pathogenic viruses, bacteria and parasites. Rotavirus proved to be by far the most common potential pathogen, being detected in 54% of specimens.

Some aspects of the 1976 influenza epidemic are described and compared with findings in previous years. Rapid diagnostic techniques gave encouraging results, but were less sensitive than conventional techniques. A higher rate of virus isolation was obtained from nasopharyngeal aspirates than from pooled nose and throat swabs.

In early 1984, five patients who were undergoing plasmapheresis at a Melbourne hospital developed a transient hepatitis B surface antigenaemia. A common batch of stabilized plasma-protein solution (SPPS) that was included in the replacement therapy for each patient was found to contain hepatitis B surface antigen (HBsAg). A follow-up study was undertaken of these patients and others who were known to have received SPPS from the same batch (in total, 10 patients were followed for a median of 46.5 weeks). No patient developed evidence of hepatitis, although one patient developed antibody to surface antigen. It was concluded that the manufacturing process was effective in destroying the infectivity of the HBsAg-positive plasma that was used in this batch of SPPS and that the final product was poorly immunogenic in these patients.

During November and December 1982, a persistent outbreak of gastroenteritis took place in an isolated guest house. An estimated 26% of the changing population of guests and staff developed symptoms. Laboratory studies implicated Norwalk agent as the cause of illness, although the original source of the outbreak could not be established. Information on clinical features of the illness, its mode of spread, and eventual control is presented.

The prevalence of delta infection was studied in 3986 individuals seropositive for hepatitis B surface antigen (HBsAg), who were seen in Melbourne between 1971 and 1985. The group comprised 2004 patients with acute hepatitis B, 1820 asymptomatic HBsAg carriers, 139 HBsAg carriers with evidence of chronic liver disease, and 23 carriers who had suffered more than two separate attacks of acute hepatitis. Markers of delta infection were found almost exclusively among intravenous drug abusers and their close contacts. Studies of stored sera suggest that delta infection was introduced into this group about 1970. In carriers with no evidence of chronic liver disease, the prevalence of delta infection was highest among intravenous drug abusers (19.2%). In carriers with evidence of chronic liver disease, delta markers were present in 20.1% and all 23 carriers with recurrent acute hepatitis had evidence of infection with the delta virus.

In the period from January 1971 to June 1983, 46 of 5477 patients (0.84%) admitted to Fairfield Hospital, Melbourne, with acute viral hepatitis died of fulminant hepatic failure. The case-fatality rate for patients with hepatitis A was 0.14%; for patients with hepatitis B, 0.84%; and for patients with non-A non-B (NANB) hepatitis, 2.29%. The highest case-fatality rates were observed in patients with post-transfusion hepatitis B (18.8%), and in patients with NANB hepatitis aged less than 5 years (50%) and 40 years and over (10%).

Murray Valley encephalitis virus was isolated from the brains of three patients who died from encephalitis during the 1974 epidemic. Isolation of the virus from autopsy material was successful when death occurred within two weeks of the onset of illness; however, no isolations were made from specimens collected before death or from autopsy material obtained from patients who died more than two weeks after the onset of symptoms. The virus was recovered most frequently in embryonated eggs, but two strains were isolated in cell culture.

Hepatitis B surface antigen was detected by radioimmunoassay in the saliva of 11 of 25 patients with hepatitis B, for periods of up to 23 days after the onset of illness. It was also detected in the saliva of three of five chronic carriers. The presence of this antigen in the saliva may be an important factor in non-parenteral transmission of hepatitis B.

In a group of 126 Australian patients with haemophilia, who were receiving lyophilized clotting-factor concentrates prepared from locally collected plasma, a high prevalence of antibody to human T-cell lymphotropic virus III (HTLV-III) was demonstrated in those with severe disease. Patients with moderate or mild disease had a much lower prevalence of HTLV-III antibody. After heat treatment of lyophilized factor VIII and factor IX concentrates (60 degrees C for 72 hours) to inactivate the virus, the losses of activity of an intermediate-purity and of a fibrinogen-poor factor VIII concentrate, and of the coagulant activity of a factor IX concentrate, were within acceptable limits. The solubility of the intermediate-purity factor VIII concentrate was markedly decreased; the fibrinogen-poor factor VIII concentrate and the factor IX concentrate were readily soluble. In-vivo recovery and survival of heated concentrates were equivalent to those of the unheated products, and they were effective in the treatment of spontaneous and traumatic haemorrhages.