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close this bookGuidelines for the Treatment of Malaria (WHO; 2006; 266 pages) View the PDF document
View the documentGlossary
View the documentAbbreviations
open this folder and view contents1. Introduction
View the document2. The clinical disease
open this folder and view contents3. Treatment objectives
open this folder and view contents4. Diagnosis of malaria
open this folder and view contents5. Resistance to antimalarial medicines9
open this folder and view contents6. Antimalarial treatment policy
open this folder and view contents7. Treatment of uncomplicated P. Falciparum malaria10
open this folder and view contents8. Treatment of severe falciparum malaria14
close this folder9. Treatment of malaria caused by P. vivax, P. ovale or P. malariae19
View the document9.1 Diagnosis
View the document9.2 Susceptibility of P. vivax, P. ovale and P. malariae to antimalarials
View the document9.3 Treatment of uncomplicated vivax malaria
View the document9.4 Treatment of severe vivax malaria
View the document9.5 Treatment of malaria caused by P. ovale and P. malariae
View the document9.6 Monitoring therapeutic efficacy for vivax malaria
View the document10. Mixed malaria infections
open this folder and view contents11. Complex emergencies and epidemics
open this folder and view contentsAnnexes
 

9.6 Monitoring therapeutic efficacy for vivax malaria

The antimalarial sensitivity of vivax malaria needs monitoring, to track and respond to emerging resistance to chloroquine. The 28-day in vivo test for P. vivax is similar to that for P. falciparum (see Annex 6), although the interpretation is slightly different. Genotyping may distinguish a reinfection from a recrudescence and from acquisition of a new infection, but it is not possible to distinguish reliably between a relapse and a recrudescence as they derive from the same infection. If parasitaemia recurs within 16 days of administering treatment then relapse is unlikely, but after that time, relapse cannot be distinguished from a recrudescence. Any P. vivax infection that recurs within 28 days, whatever its origin, must be resistant to chloroquine (or any other slowly eliminated antimalarial) provided adequate treatment has been given. In the case of chloroquine, adequate absorption can be confirmed by measurement of the whole blood concentration at the time of recurrence. Any P. vivax infection that has grown in vivo through a chloroquine blood concentration ≥100 ng/ml must be chloroquine resistant. Short-term in vitro culture allows assessment of in vitro susceptibility. There are no molecular markers yet identified for chloroquine resistance. Antifolate resistance can be monitored by molecular genotyping of the gene that encodes dihydrofolate reductase (Pvdhfr).

 

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