Abstract
Chloroquine (CQ) is outmoded as an antimalarial drug in most of the malarial world because of the high resistance rate of parasites. The parasite resistance to CQ is attributed to pfcrt/pfmdr1 gene mutations. Recent studies showed that parasites with mutations of pfcrt/pfmdr1 genes are less virulent, and that those with dhfr/dhps mutations are more susceptible to host immune clearance; the former and latter mutations are linked. In the era of artemisinin-based combination therapy, the frequency of pfcrt/pfmdr1 wild variants is expected to rise. In areas of unstable malaria transmission, the unpredictable severe epidemics of malaria and epidemics of severe malaria could result in high mortality rate among the semi-immune population. With this in mind, the use of CQ for intermittent preventive treatment of adults (IPTa) is suggested as a feasible control measure to reduce malaria mortality in adults and older children without reducing uncomplicated malaria morbidity. The above is discussed in a multidisciplinary approach validating the deployment of molecular techniques in malaria control and showing a possible role for CQ as a rescue drug after being abandoned.
Acknowledgments
I am thankful to the patients and families involved in the series of our studies in different sites in Sudan. My thanks also go to the authors of our published work and our research teams. This review is based on research funded by different bodies, but principally the WHO: (1) the EMRO DCD/TDR Small Grants Scheme for Operational Research in Tropical and Other communicable Disease, project number SGS02/110; (2) UNDP/WORD BANK/WHO special programme for Research and Training in Tropical Diseases TDR and the Multilateral Initiative on Malaria in Africa (MIM), Project ID A00003.
Ethical approval
The study received ethical approval from the Ministry of Health, Sudan.
Notes
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