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Molecular surveillance of drug resistance through imported isolates of Plasmodium falciparum in Europe

DOI: 10.1186/1475-2875-1-11

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Abstract:

337 isolates have been tested so far. Prevalence of mutations that are associated with resistance to chloroquine on the pfcrt and pfmdr genes of P. falciparum was demonstrated at high levels. However, the prevalence of mutations associated with resistance to antifolates at the DHFR and DHPS genes was unexpectedly low, rarely exceeding 60% in endemic areas.Constant screening of imported isolates will enable TropNetEurop to establish a screening tool for emerging resistance in endemic areas.In an increasing number of countries where malaria is endemic, the effectiveness of routinely administered antimalarials like chloroquine and sulfadoxine/pyrimethamine is severely reduced because of the multi-drug resistance of Plasmodium falciparum. This poses a serious problem in terms of treatment and prophylaxis. Yet, mainly for financial reasons, chloroquine remains the first-line drug for treatment of malaria in these countries.On the other hand, travelers from Europe and other industrialised countries, who have contracted Falciparum malaria, are commonly treated, on their return home, with highly effective antimalarials (usually mefloquine, halofantrine or quinine) that are frequently not freely available for routine treatment in endemic areas. Therefore, drug resistance is as yet not a frequent problem in the treatment of Falciparum malaria in hospitals of industrialized countries. Infected European travelers and immigrants carry a wide variety of P. falciparum strains from all endemic areas. Data and parasite material gained from this population, if properly used, can help to predict the development of drug resistance in endemic areas.Point mutations at several codons of Plasmodium falciparum genes have been associated with emergence of drug resistance to commonly used antimalarial drugs. In particular, resistance to antifolates (e.g. pyrimethamine/sulfadoxine) and chloroquine depends on point mutations at the Dihydrofolate Reductase (DHFR) and Dihydropteroate Synthetase (

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