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Amplification of pfmdr1 in Plasmodium falciparum is linked to resistance to aryl-amino-alcohols and in reduced susceptibility to artemisinins. We demonstrate here that duplicated pfmdr1 genotypes circulate in West Africa. The monitoring of this prevalence in Africa appears essential for determining the antimalarial policy and to maintain the efficiency of artemisinin-based combination therapy (ACT) for as long as possible.

Hyperreactive malarial splenomegaly (HMS) is the chronic stage of a long-term stimulation of the immune system secondary to plasmodial infections, more frequently in genetically predisposed patients. HMS is a leading cause of large tropical splenomegaly in endemic zones but has been described in immigrants from Africa and in some European expatriates living in endemic countries. Diagnostic criteria include: long-term stay in a endemic zone, often large splenomegaly, high IgM titer, high antiplasmodial antibody titer, regression by at least 40% of splenomegaly six months after curative antimalarial treatment. In tropical settings, B-cell lymphoma and splenic lymphoma are the main differential diagnoses, which may be identified by a clonality analysis. Recent studies suggest that HMS can be treated by a short-term antimalarial therapy as long as the patient resides out of a malarial endemic country.

The atovaquone resistance of malaria parasites correlates with mutations in the cytochrome b gene. We sequenced the Plasmodium falciparum cytochrome b gene of 135 African isolates. Our data showed a high mutation rate (8.9%); however, the risk of emergence spreading of atovaquone-resistant P. falciparum strains could be limited.

The in vitro susceptibility of chloroquine and the genomic profile of dihydrofolate reductase (DHFR) codon 108 was determined against african isolates of P. falciparum (Pf) from imported malaria cases without previous drug intake by an isotopic microtest or PCR + RFLP. Pf resistance to chloroquine or to the DHFR inhibitor was present in 49% and 46% of isolates, respectively. Pf drug resistance was more frequent in permanent than in seasonal malarial transmission areas and chloroquine plus DHFR resistance reached 28% in years 1995-97. Updating the guidelines for the prevention of malaria in travellers to Africa is necessary.