Melbourne School of Population and Global Health - Research Publications
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ItemNo Preview AvailableSchistosomiasis in Australian travellers to Africa(AUSTRALASIAN MED PUBL CO LTD, 1998-01-05)
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ItemNo Preview AvailableSchistosomiasis in Australian travellers to Africa(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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ItemNo Preview AvailableChemoprophylaxis and treatment of malaria.( 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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ItemNo Preview AvailableAGE AND STRAIN TRANSCENDING IMMUNITY TO PLASMODIUM-FALCIPARUM - REPLY(ELSEVIER SCI LTD, 1994-08)
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ItemNo Preview AvailableCLINICAL IMMUNITY TO PLASMODIUM-FALCIPARUM - REPLY(ELSEVIER SCI LTD, 1994-02)
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ItemNo Preview AvailablePROTECTION, PATHOGENESIS AND PHENOTYPIC PLASTICITY IN PLASMODIUM-FALCIPARUM MALARIA(ELSEVIER SCI LTD, 1993-08)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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ItemNo Preview AvailableADHERENCE OF INFECTED ERYTHROCYTES TO VENULAR ENDOTHELIUM SELECTS FOR ANTIGENIC VARIANTS OF PLASMODIUM-FALCIPARUM(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.
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ItemANTIGENIC VARIATION IN PLASMODIUM-FALCIPARUM(NATL ACAD SCIENCES, 1991-10)Antigenic variation of infectious organisms is a major factor in evasion of the host immune response. However, there has been no definitive demonstration of this phenomenon in the malaria parasite Plasmodium falciparum. In this study, cloned parasites were examined serologically and biochemically for the expression of erythrocyte surface antigens. A cloned line of P. falciparum gave rise to progeny that expressed antigenically distinct forms of an erythrocyte surface antigen but were otherwise identical. This demonstrates that antigenic differences on the surface of P. falciparum-infected erythrocytes can arise by antigenic variation of clonal parasite populations. The antigenic differences were shown to result from antigenic variation of the parasite-encoded protein, the P. falciparum erythrocyte membrane protein 1.
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ItemNo Preview AvailableChromosome 9 from independent clones and isolates of Plasmodium falciparum undergoes subtelomeric deletions with similar breakpoints in vitro(Elsevier, 1990-04-01)We show that chromosome 9 in all isolates and clones of Plasmodium falciparum examined so far exists as one of two distinctly different forms, a large form about 1.9 megabases long or a smaller form about 25% shorter. Physical maps of chromosome 9 from independent clones with large and small forms of chromosome 9, and from an isolate with the large form and 3 derived clones with the small form reveal the underlying structural basis of this size polymorphism. The small form differs from the large only in that there are subtelomeric deletions at each end, one of these deletions involving about 0.45 megabases. Remarkably, the breakpoints map within about +/- 1% of the total chromosome length for each of these populations. We discuss some possible mechanisms for this.
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ItemNo Preview AvailablePlasmodium Falciparum: Cytoadherence occurring in the absence of knobs uses the thrombospondin receptor (CD36)(Elsevier BV, 1990)P. falciparum is the cause of the lethal form of malaria which results in thousands of deaths each year. The primary cause of death, cerebral malaria, is associated with the sequestration of erythrocytes infected with the mature stages of P. falciparum (trophozoites and schizonts) in the post capillary venules of the brain. The identification of the parasite protein(s) involved in this process will provide important vaccine candidate molecules and knowledge about the pathological processes involved in cell-cell adhesion in general. The mechanism of cytoadherence is studied in vitro using cultured lines of P. falciparum which bind to umbilical vein endothelial cells and C32 amelanotic melanoma cells. Mature stages of the parasite may induce knob-like protrusions in the erythrocyte membrane, and it was previously thought that ‘knobs’ were necessary although not sufficient for cytoadherence to occur both in vitro and during natural infection. We have derived a clone of the Brazilian isolate of P. falciparum, ITG2F6, and selected for cytoadherence by repeated passage over amelanotic melanoma cells. Chromosome analysis using pulsed-field gradient electrophoresis and DNA amplification using the polymerase chain reaction reveal that this clone has deleted the gene coding for knobs. Furthermore, cytoadherence which is independent of knobs occurs via the receptor for the platelet protein, thrombospondin.