Folate deficiency is assoc. with all except
a. Chloroquine does not produce folate deficiency, while rest of them do. Chloroquine has been found to be active against the asexual erythrocytic forms of all species of malaria parasites; P. vivax, P. ovale, P. malariae and susceptible strains of P. falciparum. It is a rapid acting blood schizontocide with some gametocytocidal activity against P. ovale, P. vivax, P. malariae and immature gametocytes of P. falciparum.
b. The mechanism of plasmodicidal action of chloroquine is. Its effect from its interaction with DNA. It acts mainly on the large ring form and mature trophozoite stages of the parasite.
c. In suppressive treatment, chloroquine inhibits the erythrocytic stage of development of plasmodia.
d. In acute attacks of malaria, chloroquine interrupts erythrocytic schizogony of the parasite. Its ability to concentrate in parasitized erythrocytes may account for its selective toxicity against the erythrocytic stages of plasmodial infection.
i. Chloroquine may cause blood dyscrasias, including agranulocytosis, aplastic anemia, neutropenia, or thrombocytopenia. Discontinuance of the drug should be considered, if any severe blood severe blood disorder appears which is not attributable to the disease under treatment. Complete blood cell counts should be made periodically if patients are given prolonged therapy.
ii. Chloroquine may cause hemolytic anemia in G6PD deficient patients.
iii. Caution is advised in cases of porphyria, renal disease, severe gastrointestinal and neurological disorders and in patients with myasthenia gravis.
iv. Chloroquine has a temporary effect on visual accommodation (BG Katzung’ 10th Edition, pp-848-49).