The main objective in the clinical management of patients suffering from an acute malaria attack is the prompt elimination of the parasite form responsible for the symptoms, that is, the asexual erythrocytic form. Drugs that are particularly effective in this regard are called schizonticidal, or suppressive, agents. They include such compounds as amodiaquine, chloroguanide, chloroquine, hydroxychloroquine, pyrimethamine, quinine, and tetracycline. These drugs have the potential (excluding any drug resistance) for effecting a clinical cure; that is, they can reduce the parasitemia to zero. The term radical cure also has been used, and it, in contrast to clinical cure, implies the elimination of all parasite forms from the body.
Once the primary therapeutic objective has been achieved, attention can be focused on such additional considerations as elimination of the gametocytes and the tissue forms of the parasite. Success in these areas would help to ensure that relapses do not occur. Since no latent liver forms are associated with mosquito-induced, drug-sensitive P. falciparum malaria, administration of chloroquine for up to 3 months after the patient leaves a malarious area will usually bring about a complete or radical cure unless the organism is resistant to chloroquine.
The emergence of parasites resistant to chloroquine is an increasingly important problem. Several strains of chloroquine-resistant P. falciparum have been identified. This resistance would lead to the reappearance of overt symptoms of P. falciparum malaria.
P. falciparum malaria may be accompanied by an infection caused by one of the other three plasmodial forms (mixed infection). As long as all of the parasites are drug sensitive, the parasitemia can be eliminated. However, it must be remembered that even though P. falciparum malaria may be ameliorated or eliminated, relapses due to P. vivax and P. ovale still can occur.
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