Institute of Tropical Medicine Antwerp
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Malaria transmission intensity and the rate of spread of chloroquine resistant Plasmodium falciparum: why have theoretical models generated conflicting results?

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Show simple item record Talisuna, A. O. en_US Erhart, A. en_US Samarasinghe, S. en_US Van Overmeir, C. en_US Speybroeck, N. en_US D'Alessandro, U. en_US 2007-12-06T14:34:11Z 2007-12-06T14:34:11Z 2006 en_US
dc.identifier.issn 1567-1348 en_US
dc.identifier.other ITG-P1A en_US
dc.identifier.other ITG-P2A en_US
dc.identifier.other ITG-P4B en_US
dc.identifier.other ITG-A5A en_US
dc.identifier.other ITG-PLA en_US
dc.identifier.other PARAS en_US
dc.identifier.other U-MALAR en_US
dc.identifier.other ANIMAL en_US
dc.identifier.other U-ANIMAL en_US
dc.identifier.other JIF en_US
dc.identifier.other DOI en_US
dc.identifier.other MULTI en_US
dc.identifier.other ABSTRACT en_US
dc.description.abstract The rate at which falciparum resistant malaria spreads in different transmission settings is still a controversial subject. We have assessed the spread of mutant Plasmodium falciparum parasites in six Ugandan populations with varying prevalence of chloroquine resistance (CQR), malaria transmission intensity, multiplicity of parasite clones and prevalence of CQ use. For each population, we have determined the wild and mutant allele frequency at codons 76 and 86 of the pfcrt and pfmdr1 genes, respectively. The highest frequency (median = 16.3%, range: 0.0-70.4%) of infections with two pure mutants (no wild genotype in either gene), adjusted for clone multiplicity, was observed at the extremes of malaria transmission intensity. The wild/mutant (W/M) allele ratio (an index for tracking the progression of CQR) was less than one in all sites (median = 0.51, range: 0.09-0.98) for the pfcrt-76 gene, while it was greater than one in two of six sites (median = 0.75, range: 0.4-1.6) for the pfmdr1-86 gene, suggesting that the pfcrt-76 mutants were the predominant parasites at all sites. Furthermore, the pfmdr1-86 W/M allele ratio was consistently higher than that of the pfcrt-76. The spread of mutations linked to CQR in P. falciparum commences with the pfcrt-76 gene mutations, followed later by the pfmdr1-86 gene mutations that modulate higher CQR. Such spread occurs faster at the extremes of the transmission spectrum and could explain why mathematical models have previously generated conflicting results with respect to malaria transmission intensity and spread of CQR. en_US
dc.language English en_US
dc.subject Protozoal diseases en_US
dc.subject Malaria en_US
dc.subject Transmission intensity en_US
dc.subject Chloroquine en_US
dc.subject Drug resistance en_US
dc.subject Mutations en_US
dc.subject Pfcrt en_US
dc.subject Pfmdr-1 en_US
dc.subject Uganda en_US
dc.subject Africa, East en_US
dc.title Malaria transmission intensity and the rate of spread of chloroquine resistant Plasmodium falciparum: why have theoretical models generated conflicting results? en_US
dc.type Article en_US
dc.citation.issue 3 en_US
dc.citation.jtitle Infection, Genetics and Evolution en_US
dc.citation.volume 6 en_US
dc.citation.pages 241-248 en_US
dc.citation.jabbreviation Infect Genet Evol en_US

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