Stepwise selection for increased mefloquine resistance in a line of Plasmo dium falciparum in vitro resulted in increased resistance to halofantrine and quinine, in creased sensitivity to chloroquine, and amplification and overexpression of the P-glyco protein gene homolog (pfmdrl). A point mutation (tynosine to phenylalanine) noted at amino acid 86 in pfmdrl in the mefloquine-nesistant line W2mef was amplified in more resistant lines derived from it by in vitro selection pressure with mefloquine. Conversely, lines selected for increased chloroquine resistance exhibited a nevertant phenotype that was sensitive to mefloquine and halofantrine. These lines also demonstrated increased sensitiv ity to quinine, loss of amplification of pfindrl. loss of the mefloquine/halofantrine phe nylalanine-86 mutation, and selection for a tyrosine-86 mutation previously associated with chlonoquine resistance. These findings provide strong evidence for pfindrl mediating cross resistance to halofantrine and metloquine in P. falciparum in vitro.

DMPA use, but not OC use, appeared to be significantly associated with increased acquisition of cervical chlamydial and gonococcal infections.

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