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Background   Plasmodium falciparum  resistance to chloroquine (CQ) denied healthcare providers access to a cheap and effective anti-malarial drug. Resistance has been proven to be due to point mutations on the parasite’s  pfcrt  gene, particularly on codon 76, resulting in an amino acid change from lysine to threonine. This study sought to determine the prevalence of the  pfcrt  K76T mutation 13 years after CQ cessation in Msambweni, Kenya.    Methods  Finger-prick whole blood was collected on 3MM Whatman ®  filter paper from 99 falciparum malaria patients. Parasite DNA was extracted via the Chelex method from individual blood spots and used as template in nested PCR amplification of  pfcrt .  Apo 1 restriction enzyme was used to digest the amplified DNA to identify the samples as wild type or sensitive at codon 76. Prevalence figures of the mutant  pfcrt  76T gene were calculated by dividing the number of samples bearing the mutant gene with the total number of samples multiplied by 100 %. Chi square tests were used to test the significance of the findings against previous prevalence figures.    Results  Out of 99 clinical samples collected in 2013, prevalence of the mutant  pfcrt  76T gene stood at 41 %.    Conclusion  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. This could primarily be driven by diminished use of CQ in the study area in line with the official policy. Studies to establish prevalence of the  pfcrt  76T gene could be expanded countrywide to establish the CQ sensitivity status and predict a date when CQ may be re-introduced as part of malaria chemotherapy.

malaria journal

Chloroquine sensitivity: diminished prevalence of chloroquine-resistant gene marker pfcrt-76 13 years after cessation of chloroquine use in Msambweni, Kenya