Chloroquine (CQ), the first cost-effective synthetic antimalarial, is rendered ineffective in malaria-endemic regions owing to the rise and spread of CQ-resistant Plasmodium falciparum.
Considering that primaquine (PQ) efficacy is highly dependent on concurrent administration of a blood schizontocidal agent and that PQ could not circumvent CQR, together with the fact that no pvmdr1 mutation should be expected in successfully cured patients, these findings seem to indicate that the pvmdr1 gene is not a reliable marker of CQR.
The current study revealed that CQ showed a high rate of efficacy (96.7 %) among the study participants even though some reports from previous studies elsewhere in Ethiopia showed an increase in CQR P. vivax.
The results indicate a significant [χ 2 test, P ≤ 0.05 (2006 vs 2013)] reversal to sensitivity by the P. falciparum population in the study site compared to the situation reported in 2006 at the same study site.
The present study demonstrates the presence of resistance to CQ in the treatment of malaria by P. vivax in the Amazon region of Bolivia.
High prevalence of mutations in candidate genes conferring CQR in P. vivax was identified.
This study does not provide evidence for a direct beneficial effect of CQ on the induction of sporozoite-induced immune responses and protection in P. berghei malaria models.
Amongst several communicable diseases (CDs), malaria is one of the deadliest parasitic disease all over the world, particularly in African and Asian countries.
The presence of an alkyne group and the size of the side chain affected anti-P. falciparum activity in vitro.
Among adults with symptomatic uncomplicated falciparum malaria in Africa, the combination of AZ 1,000 mg and CQ 600-mg base once daily for three days resulted in Day-28 PCR-corrected parasitological clearance rates of >=98% and was non-inferior to treatment with MQ. AZCQ was well tolerated.