Infectious Diseases - Research Publications

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End date: 1998 × Type: Journal Article ×

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Now showing 1 - 10 of 31
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    Schistosomiasis in Australian travellers to Africa
    Davis, TME ; Beaman, MH ; McCarthy, JS (AUSTRALASIAN MED PUBL CO LTD, 1998-01-05)
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    Integration of hepatitis B vaccination into the expanded programme on immunization in Chonburi and Chiangmai provinces, Thailand
    Chunsuttiwat, S ; Biggs, BA ; Maynard, J ; Thamapalo, S ; Laoboripat, S ; Bovornsin, S ; Charanasri, U ; Pinyowiwat, W ; Kunasol, P (ELSEVIER SCI LTD, 1997-04-01)
    Hepatitis B (HB) immunization was introduced as part of the expanded programme on immunization (EPI) in two provinces in Thailand and evaluated over a four year period. Three doses of HB vaccine were offered to 60,980 newborns at birth, 2 and 6 months of age. The overall coverage for complete HB immunization was 90.4%. Serosurveys of randomly selected children under the age of 5 years were undertaken before and at the end of the project. Levels of HBsAg positivity were reduced by 85%, and there was a corresponding 70% increase in protective immunity. These findings demonstrate that HB immunization can be successfully integrated into EPI without adverse effect on coverage rates of other antigens, and results in a marked reduction in the rate of chronic carriage of HB virus in preschool age children.
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    Schistosomiasis in Australian travellers to Africa
    Hipgrave, DB ; Leydon, JA ; Walker, J ; Biggs, BA (WILEY, 1997-03-17)
    OBJECTIVE: To determine the proportion of Australian travellers to Africa at risk of Schistosoma infection, and the proportion of those infected. DESIGN AND PARTICIPANTS: Retrospective postal survey of 360 patients who had attended Fairfield Hospital travel clinic in 1994 and stated an intention to travel to Malawi, Zimbabwe or Botswana. MAIN OUTCOME MEASURES: Self-reported risk status for Schistosoma infection. For those at risk, results of an indirect haemagglutination assay (IHA). For those with IHA titres > or = 1:32, results of enzyme-linked immunosorbent assay, urine microscopy and eosinophil count. RESULTS: 360 letters were sent; 35 were returned to sender. Of the 325 remaining, 250 (77%) either responded or had an IHA test; 19 of these were still overseas or did not travel. 117/231 (51%) returned travellers considered themselves at risk of infection. Significantly fewer older patients reported exposure (chi 2 = 66.6; P < 0.001). 109/117 (93%) of those at risk had IHA tests and 18 had titres > or = 1:32. Subsequent testing indicated infection in 10/117 travellers (8.5%; 95% CI, 4.2%-15.2%). CONCLUSION: Our findings indicate that a considerable number of Australian travellers to Africa are at risk of schistosomiasis, and some are infected. As complications can be serious, screening is recommended for individuals with any risk of infection, and treatment should be offered to those infected.
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    HIV-1 INFECTION OF HUMAN MACROPHAGES IMPAIRS PHAGOCYTOSIS AND KILLING OF TOXOPLASMA-GONDII
    BIGGS, BA ; HEWISH, M ; KENT, S ; HAYES, K ; CROWE, SM (AMER ASSOC IMMUNOLOGISTS, 1995-06-01)
    The susceptibility of patients with AIDS to certain opportunistic infections is due to defective cell-mediated immunity. The contribution of direct infection of macrophages with HIV-1 to this defect is unknown. To address this issue, we infected normal human monocyte-derived macrophages with a monocytotropic strain of HIV-1 and examined their ability to phagocytose and kill the opportunistic pathogen, Toxoplasma gondii. Phagocytosis of heat-killed T. gondii was reduced in HIV-infected macrophages compared with mock-infected controls. Opsonization of heat-killed T. gondii increased phagocytosis by both mock- and HIV-infected macrophages, but phagocytosis in HIV-infected cultures remained lower than in controls. Internalization of live T. gondii by macrophages was unaffected by HIV infection. Intracellular replication of live T. gondii was enhanced by HIV infection, as shown in four experiments, each using monocyte-derived macrophages from a different donor. Treatment of HIV-infected macrophages with IFN-gamma decreased parasite replication but not to control levels. These findings suggest that infection of macrophages by HIV may be a contributing factor to the reactivation of T. gondii infection in patients with AIDS.
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    Chemoprophylaxis and treatment of malaria.
    Rogerson, SJ ; Biggs, BA ; Brown, GV ( 1994-09)
    Prevention of malaria morbidity relies on the use of personal protection from mosquito bites, appropriate chemoprophylactic drugs, and early investigation of symptoms in returning travellers. Malaria chemoprophylaxis must be tailored to the individual patient's travel and personal needs, and no chemoprophylaxis is completely effective. Chloroquine alone is adequate for those areas with P vivax, or sensitive P falciparum but in most circumstances the choice will be between mefloquine and doxycycline. The specific area visited, the time spent there and the individual's medical history will help determine the final choice.
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    AGE AND STRAIN TRANSCENDING IMMUNITY TO PLASMODIUM-FALCIPARUM - REPLY
    ROBERTS, DJ ; NEWBOLD, CI ; BIGGS, BA ; BROWN, G (ELSEVIER SCI LTD, 1994-08-01)
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    CLINICAL IMMUNITY TO PLASMODIUM-FALCIPARUM - REPLY
    ROBERTS, DJ ; NEWBOLD, CI ; BIGGS, BA ; BROWN, G (ELSEVIER SCI LTD, 1994-02-01)
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    PROTECTION, PATHOGENESIS AND PHENOTYPIC PLASTICITY IN PLASMODIUM-FALCIPARUM MALARIA
    ROBERTS, DJ ; BIGGS, BA ; BROWN, G ; NEWBOLD, CI (ELSEVIER SCI LTD, 1993-08-01)
    Why does Plasmodium falciparum cause severe illness in some but not all infections? How is clinical immunity acquired? These questions have intrigued investigators since the clinical epidemiology of malaria was first described. The search for answers to both questions has highlighted the changes that take place at the surface of infected red blood cells during the last half of the erythrocytic cycle. These changes specify the antigenic and adhesive or cytoadherence phenotypes for the infected cell. Now the antigenic and adhesive phenotypes appear to be linked and together undergo clonal variation. In this article David Roberts, Beverley-Ann Biggs, Graham Brown and Christopher Newbold explain how clonal phenotypic variation and the linkage between adhesive and antigenic types contribute to our understanding of naturally acquired immunity and of pathogenesis of severe malaria.
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    Erratum: Protection, pathogenesis and phenotypic plasticity in Plasmodium falciparum malaria (Parasitology Today 9, (1993) (281-286))
    Roberts, DJ ; Biggs, BA ; Brown, G ; Newbold, CI (Elsevier BV, 1993-01-01)
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    ADHERENCE OF INFECTED ERYTHROCYTES TO VENULAR ENDOTHELIUM SELECTS FOR ANTIGENIC VARIANTS OF PLASMODIUM-FALCIPARUM
    BIGGS, BA ; ANDERS, RF ; DILLON, HE ; DAVERN, KM ; MARTIN, M ; PETERSEN, C ; BROWN, GV (AMER ASSOC IMMUNOLOGISTS, 1992-09-15)
    Erythrocytes (E) infected with asexual forms of malaria parasites exhibit surface antigenic variation. In Plasmodium falciparum infections, the variant Ag is the P. falciparum E membrane protein 1 (PfEMP1). This molecule may also mediate the adherence of infected E to host venular endothelium. We show here that parasite lines selected for increased adherence to endothelial cells have undergone antigenic variation. Three adherent lines selected from the same P. falciparum clone reacted with the same agglutinating antiserum that failed to agglutinate the parental clone. Immunoprecipitation experiments with the agglutinating anti-serum demonstrated that the selected lines expressed cross-reactive forms of PfEMP1 that were of higher m.w. and antigenically distinct from PfEMP1 of the parental clone. When one of the adherent lines was cloned in the absence of selection, a range of variant antigenic types emerged with differing cytoadherence phenotypes. These findings show that selection for cytoadherence in vitro favors the emergence of antigenic variants of P. falciparum and suggest that the requirement for cytoadherence in vivo may restrict the range of antigenic variants of P. falciparum in natural infections.