Poster Presentation First Malaria World Congress 2018

Absence of Resistance-Associated Mutations in pfcrt and k13 genes of Plasmodium falciparum Isolates from Haiti (#494)

JEANNE PERPETUE VINCENT 1 2 , KANAKO KOMAKI-YASUDA 2 , ALEXANDRE EXISTE 3 , JACQUES BONCY 3 , SHIGEYUKI KANO 1 2
  1. Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan
  2. Research Institute National Center for Global Health and Medicine, Shinjuku, Tokyo, Japan
  3. Laboratoire National de Santé Publique, Port-au-Prince, Haiti

BACKGROUND

Haiti, located in the Caribbean Hispaniola island is a special case where malaria is mainly caused by Plasmodium falciparum (Pf) and despite chloroquine (CQ) being introduced since 1955, it is still the main drug in use for treatment of uncomplicated malaria.

This practice started to be questioned after the first publication about the presence of CQ-resistant haplotype in Haiti in 2009. We aimed at genotyping a CQ resistance marker, Pf chloroquine resistance transporter (pfcrt) and an artemisinin resistance marker, kelch 13 (k13) in Pf isolates from Haiti to continue molecular surveillance and provide recommendation for clinical practice in the wake of malaria elimination.

METHODOLOGY

Febrile patients were recruited in 3 departments of southern Haiti from August to September 2017. Pf positive samples were first selected by the Loop-Mediated Isothermal Amplification method as potentially eligible. Those confirmed by a nested-PCR targeting the 18s rRNA gene, were finally included for pfcrt and k13 analysis.

Using DNA extracted from dried blood spots, a segment including codons 72~76 of pfcrt and the propeller domain of k13 were amplified by nested-PCR followed by direct sequencing of secondary PCR products.

RESULTS

Seventy-eight (78) samples were finally included. All analyzed samples presented the wild type amino acid sequence CVMNK at positions 72~76 of pfcrt. None presented any resistance-associated polymorphism of k13. Five samples presented a synonymous mutation at nucleotide 1359 (bp: T1359A, codon: G453) of k13.

CONCLUSION

No drug resistance-associated mutation was detected for pfcrt and k13 in samples from highest transmission areas of Haiti. Indeed, the reported scant CQ-resistant haplotypes aren’t confirmed autochthonous. We can assert that CQ-resistant and artemisinin-resistant haplotypes are not consistently circulating in Haiti.

CQ still remains the treatment of choice for uncomplicated Plasmodium infection while achieving the target malaria elimination in Haiti. Artemisinin-based therapy can be an alternative for extraordinary cases.