Biomedical subjects
Publications and source records attributed to S Iwarson.
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Eight women with chronic hepatitis C virus (HCV) infection during pregnancy gave birth to 11 children. Five of these children had elevated ALT, but only two had increased levels in more than one sample. All children tested before 6 months of age were positive for anti-HCV at most up to 7 months of age and then became negative. One child with a maximum ALT level of 8.4 mukat/l however, regained anti-HCV positivity at 12 months of age, and a liver biopsy at 21 months of age showed resolving hepatitis. Passively acquired HCV antibodies are obviously found in newborns of anti-HCV-positive mothers with chronic hepatitis. In 1 of 11 children, active anti-HCV production and concomitant liver disease suggested mother to infant transmission of hepatitis C virus infection.
Since the surveillance of salmonellosis in Sweden is primarily passive, it can be assumed that most of the asymptomatic salmonella infections are never identified. We here report the proportion of asymptomatic and symptomatic salmonella infections in Swedish travellers to different geographic areas as well as in "contacts" to index cases with salmonellosis. In the 346 travellers studied Salmonellae were isolated equally often among those who remained healthy (10/216; 4.6%) as in those with intestinal symptoms (7/130; 5.4%). Similarly, most of the salmonella-infected "contacts" to index cases (11/15; 73%) had an asymptomatic infection. No difference in the mean duration of excreting Salmonella in the stool was found between carriers with symptomatic and asymptomatic infection. The literature concerning transmission of nontyphi Salmonellae from carriers was reviewed. Since person to person transmission is rarely noted, screening for carriers may be limited to food handlers and hospital personnel taking care of patients susceptible to low infective doses of Salmonella. Similarly, follow-up faecal cultures in individuals with notified salmonella infection may be restricted to these groups.
After exposure to hepatitis B (HB) virus, passive immunisation with HB immune globulin is widely used for protection while active immunity is induced by conventional vaccination regimens. Protective antibody titres can be achieved much more quickly with accelerated vaccination, and the role of passive immunisation may need to be reconsidered.
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To study experimentally the protective effect of post-exposure prophylaxis against hepatitis B (HB), a special preparation of hepatitis B immune globulin (HBIG) was injected intravenously (i.v.) into three chimpanzees simultaneously with, or at different time intervals after, intravenous injection of a titred inoculum of hepatitis B virus (HBV). The HBIG was given either simultaneously with the HBV inoculum, at 4 hours after, or at both 4 hours and 4 weeks after the HBV injection. A fourth chimpanzee received a standard preparation of HBIG intramuscularly (i.m.) at both 4 hours and 4 weeks after receiving the HBV injection. A fifth animal received HBIG i.v. 4 hours after the HBV inoculum and at the same time received its first of three HB vaccine injections. All chimpanzees were followed for 1 year. The animals which received HBIG simultaneously with HBV or received HBIG plus vaccine had no serological or biochemical sign of HB during follow-up. The three animals which received HBIG after HBV inoculation all developed HBs-antigenemia and serum aminotransferase (ALT) elevations. HBsAg did however appear in serum several weeks later than expected for the HBV inoculum used. Post-exposure prophylaxis with HBIG did protect the HBV-exposed chimpanzees, only if HBIG was combined with HB-vaccination or if HBIG was given simultaneously with the HBV inoculum.
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To study the effect of postexposure vaccination, four chimpanzees were vaccinated with hepatitis B (HB) vaccine 4, 8, 48, and 72 hr, respectively, after intravenous injection of an infectious hepatitis B virus (HBV) inoculum. The second and third vaccine inoculations were given 2 and 6 weeks later, i.e., at considerably shorter intervals than recommended either for ordinary prophylactic vaccination or for postexposure vaccination in combination with hepatitis B immune globulin (HBIG). The chimpanzees were followed for 1 year. None showed HBs-antigenemia, liver enzyme elevation (ALT), or histopathological alterations in liver biopsies. Late appearance of anti-HBc was observed only in the serum of the animal whose series of vaccination started 72 hr after HBV inoculation. An unvaccinated control chimpanzee, which received the HBV inoculum only, developed clinical hepatitis B with ALT-elevations and HBs-antigenemia within 2 months of the experimental HBV inoculation. These results indicate that postexposure vaccination against hepatitis B begun within 48 hr after HBV exposure, with short intervals between the vaccine injections, can protect against hepatitis B infection also when concomitant HBIG-prophylaxis is not given.
Non-A, non-B of hepatitis (NANBH) may occur following blood transfusions or administration of blood products. The causative agent(s) is still not identified and the symptoms are usually mild. The only indication of infection may be increased serum alanine transferase levels. The incidence of posttransfusion NANBH has been reported as high as 4-12% in the US (average 7%) while in Sweden it is according to recent studies on the average 2%. An estimated 2-3% of Swedish blood donors are probably carriers of the NANBH agent(s). Of patients acquiring posttransfusion NANBH, 40-60% will develop chronic hepatitis which in 15-20% will progrediate to cirrhosis.
Serological responses to relevant enterotoxinogenic Escherichia coli (ETEC) antigens were studied in 85 Swedish travellers to subtropical and tropical areas. Serum samples were collected from the travellers before and then after 3-5 weeks, i.e. within a week after return to Sweden, when a faecal specimen was also taken. 40% of the participants had traveller's diarrhoea during their visit abroad, while 21% reported "loose stools" and 39% had no such problems. ETEC was rarely isolated from the stool of any of the travellers on their return to Sweden (6%). Salmonellae, Shigellae or Campylobacter jejuni were isolated from 13 (15%) of the travellers, 12 of whom were healthy when the specimens were collected and 4 of whom had been healthy during travel as well. Significant serum antibody responses to E. coli heat-labile enterotoxin (LT) and colonization factor antigens CFA I or II were seen in 33% and 20% of the travellers, respectively. Anti-LT responses were comparable in participants with traveller's diarrhoea or "loose stools" and in the healthy ones, whereas anti-CFA responses were more frequent in those with symptomatic infections. Of 34 Swedes in a non-travelling control group none responded to LT and one to CFA I or CFA II.