Chloroquine is currently the first-line treatment for P. vivax, but resistance has been rapidly increasing since it was first described in two cases of treatment failures in Papua New Guinea [4] . The clinical case reported here originated in Manaus, Brazil, where P. vivax chloroquine resistance and severe disease are now being reported [25, 26] . Interestingly, after the appearance of chloroquine resistance in P. vivax, reports of clinical severity exclusively associated with this human malaria parasite started to appear [2] . Moreover, multidrug resistance has been recently suggested to be associated, albeit not directly linked, with severe disease in P. vivax [14] . Remarkably, higher expression levels of pvmdr1 and pvcrt-o, in particular, were found in parasites from the patient with severe clinical symptoms compared to three patients with mild symptoms. The levels were increased by up to 2.9 fold in the case of pvmdr1 (when including all samples) and up to 21.9 fold in the case of pvcrt-o. Confounding effects due to sample concentrations or contamination with P. falciparum or human material were excluded by using P. vivaxspecific primers and β-tubulin as an internal control and calibrator. This data thus indicates that severe vivax disease could be associated to molecular markers.