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).