Antimalarial Drug Resistance: A Threat to Malaria Elimination

Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinin...

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Bibliographic Details
Published inCold Spring Harbor perspectives in medicine Vol. 7; no. 7; p. a025619
Main Authors Menard, Didier, Dondorp, Arjen
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 01.07.2017
Subjects
Antigens, Bacterial
Antigens, Bacterial - genetics
Antigens, Surface
Antigens, Surface - genetics
Antimalarials
Antimalarials - pharmacology
Artemisinins
Artemisinins - pharmacology
Drug Resistance
Drug Resistance - genetics
Drug Therapy, Combination
Human health and pathology
Humans
Infectious diseases
Life Sciences
Malaria, Falciparum
Malaria, Falciparum - drug therapy
Malaria, Vivax
Malaria, Vivax - drug therapy
Plasmodium
Plasmodium - drug effects
Plasmodium - genetics
Online AccessGet full text
ISSN2157-1422
2472-5412
DOI10.1101/cshperspect.a025619

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Abstract Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinins has emerged in the Greater Mekong Subregion. Concomitant emergence of partner drug resistance is now causing high ACT treatment failure rates in several areas. Genetic markers for artemisinin resistance and several of the partner drugs have been established, greatly facilitating surveillance. Single point mutations in the gene coding for the Kelch propeller domain of the K13 protein strongly correlate with artemisinin resistance. Novel regimens and strategies using existing antimalarial drugs will be needed until novel compounds can be deployed. Elimination of artemisinin resistance will imply elimination of all falciparum malaria from the same areas. In vivax malaria, chloroquine resistance is an increasing problem.
AbstractList Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinins has emerged in the Greater Mekong Subregion. Concomitant emergence of partner drug resistance is now causing high ACT treatment failure rates in several areas. Genetic markers for artemisinin resistance and several of the partner drugs have been established, greatly facilitating surveillance. Single point mutations in the gene coding for the Kelch propeller domain of the K13 protein strongly correlate with artemisinin resistance. Novel regimens and strategies using existing antimalarial drugs will be needed until novel compounds can be deployed. Elimination of artemisinin resistance will imply elimination of all falciparum malaria from the same areas. In vivax malaria, chloroquine resistance is an increasing problem.
Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinins has emerged in the Greater Mekong Subregion. Concomitant emergence of partner drug resistance is now causing high ACT treatment failure rates in several areas. Genetic markers for artemisinin resistance and several of the partner drugs have been established, greatly facilitating surveillance. Single point mutations in the gene coding for the Kelch propeller domain of the K13 protein strongly correlate with artemisinin resistance. Novel regimens and strategies using existing antimalarial drugs will be needed until novel compounds can be deployed. Elimination of artemisinin resistance will imply elimination of all falciparum malaria from the same areas. In vivax malaria, chloroquine resistance is an increasing problem. Resistance to antimalarial drugs (e.g., artemisinins) is an increasing problem, but molecular markers have helped with surveillance. Novel regimens and strategies will be needed until new drugs can be deployed.
Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinins has emerged in the Greater Mekong Subregion. Concomitant emergence of partner drug resistance is now causing high ACT treatment failure rates in several areas. Genetic markers for artemisinin resistance and several of the partner drugs have been established, greatly facilitating surveillance. Single point mutations in the gene coding for the Kelch propeller domain of the K13 protein strongly correlate with artemisinin resistance. Novel regimens and strategies using existing antimalarial drugs will be needed until novel compounds can be deployed. Elimination of artemisinin resistance will imply elimination of all falciparum malaria from the same areas. In vivax malaria, chloroquine resistance is an increasing problem.Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination therapies (ACTs) are first-line treatment for uncomplicated falciparum malaria in all endemic countries, yet partial resistance to artemisinins has emerged in the Greater Mekong Subregion. Concomitant emergence of partner drug resistance is now causing high ACT treatment failure rates in several areas. Genetic markers for artemisinin resistance and several of the partner drugs have been established, greatly facilitating surveillance. Single point mutations in the gene coding for the Kelch propeller domain of the K13 protein strongly correlate with artemisinin resistance. Novel regimens and strategies using existing antimalarial drugs will be needed until novel compounds can be deployed. Elimination of artemisinin resistance will imply elimination of all falciparum malaria from the same areas. In vivax malaria, chloroquine resistance is an increasing problem.
Author Dondorp, Arjen
Menard, Didier
AuthorAffiliation 1 Malaria Molecular Epidemiology Unit, Institut Pasteur in Cambodia, Phnom Penh 12201, Cambodia
2 Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok 73170, Thailand
AuthorAffiliation_xml – name: 2 Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok 73170, Thailand
– name: 1 Malaria Molecular Epidemiology Unit, Institut Pasteur in Cambodia, Phnom Penh 12201, Cambodia
Author_xml – sequence: 1
  givenname: Didier
  surname: Menard
  fullname: Menard, Didier
– sequence: 2
  givenname: Arjen
  surname: Dondorp
  fullname: Dondorp, Arjen
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28289248$$D View this record in MEDLINE/PubMed
https://hal.science/hal-02559309$$DView record in HAL
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Snippet Increasing antimalarial drug resistance once again threatens effective antimalarial drug treatment, malaria control, and elimination. Artemisinin combination...
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SubjectTerms Antigens, Bacterial
Antigens, Bacterial - genetics
Antigens, Surface
Antigens, Surface - genetics
Antimalarials
Antimalarials - pharmacology
Artemisinins
Artemisinins - pharmacology
Drug Resistance
Drug Resistance - genetics
Drug Therapy, Combination
Human health and pathology
Humans
Infectious diseases
Life Sciences
Malaria, Falciparum
Malaria, Falciparum - drug therapy
Malaria, Vivax
Malaria, Vivax - drug therapy
Plasmodium
Plasmodium - drug effects
Plasmodium - genetics
Title Antimalarial Drug Resistance: A Threat to Malaria Elimination
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https://hal.science/hal-02559309
https://pubmed.ncbi.nlm.nih.gov/PMC5495053
Volume 7
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