QUININE RESISTANT FALCIPARUM-MALARIA ACQUIRED IN EAST-AFRICA

A 43 year old man with falciparum malaria acquired in East Africa was treated with quinine intravenously at a loading dose of 500 mg and sub sequently 500 mg tid. Within 42 hours after initiation of treatment th e parasitaemia increased from 2 % to 16 %. A RIII-resistance against q uinine was suspected and therapy was switched to oral administration o f halofantrine (500 mg at 6 hourly intervals) which led to complete re covery. Blood samples were cultured for malaria parasites 42 hours aft er start of therapy with quinine but before initiation of therapy with halofantrine. In vitro resistance testing was performed with samples directly derived from the patient and after 24 and 48 hours of culturi ng. In repeated tests an in vitro resistance to quinine could be confi rmed (IC 50: 25.6 x 10(-6) mol/l, IC 99: > 51.2 x 10(-6) mol/l) while the strain was fully susceptible to chloroquine (IC 50: < 0.4 x 10(-6) mol/l, IC 99: 1.6 x 10(-6) mol/l), mefloquine (IC 50: < 0.4 x 10(-6) mol/l, IC 99: 3.2 x 10(-6) mol/l), tetracycline (IC 50: 0.16 x 10(-6) mol/l, IC 99: 0.32 x 10(-6) mol/l) and halofantrine (IC 50: 0.02 x 10( -6) mol/l, IC 99: 0.04 x 10(-6) mol/l). Increased susceptibility to qu inine after addition of verapamil was noted. The presence of a specifi c mutation, on the pfmdr1-gene on chromosome 5, previously associated with chloroquine drug resistance, could be confirmed by polymerase cha in reaction. To our knowledge it R III- in vivo and in vitro resistanc e of Plasmodium falciparum to quinine has not been described yet in Ea st Africa. P. falciparum strains with isolated resistance to quinine l ike the strain described here might have been overlooked previously du e to their full susceptibility to other commonly used antimalarial dru gs.