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Antimicrobial Agents and Chemotherapy, June 2007, p. 2112-2116, Vol. 51, No. 6
0066-4804/07/$08.00+0     doi:10.1128/AAC.01385-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Improved Assessment of Plasmodium vivax Response to Antimalarial Drugs by a Colorimetric Double-Site Plasmodium Lactate Dehydrogenase Antigen Capture Enzyme-Linked Immunosorbent Assay{triangledown}

Pierre Druilhe,1* Philippe Brasseur,2 Catherine Blanc,1 and Michael Makler3

Bio-Medical Parasitology Unit, Institut Pasteur, Paris, France,1 UR 077 Paludologie Afro-Tropicale, Institut de Recherche pour le Développement, Dakar, Sénégal,2 Flow Inc., Portland, Oregon3

Received 6 November 2006/ Returned for modification 30 December 2006/ Accepted 18 March 2007

The occurrence of Plasmodium vivax resistance to chloroquine has been reported in several countries of Asia and South America. However, the resistance of P. vivax is insufficiently documented for three reasons: it has received far less attention than P. falciparum; in vivo investigations are handicapped by the existence of hypnozoites, which make it difficult to distinguish between recrudescences due to drug failure and relapses due to dormant forms in the liver; and in vitro studies are greatly limited by the poor growth of P. vivax. We report on the adaptation to P. vivax of a colorimetric double-site Plasmodium lactate dehydrogenase antigen capture enzyme-linked immunosorbent assay previously developed for P. falciparum. The assay proved remarkably sensitive, as under optimal conditions it could detect P. vivax parasitemia levels as low as 10–8. The technique, which relies on the detection of protein synthesis by the parasite, yielded steep drug-response curves, leading to the precise determination of the 50% inhibitory concentrations for a high proportion of isolates. Chloroquine-resistant parasites were identified in an area where this phenomenon had been documented by in vivo methods. Thus, the results indicate that the in vitro susceptibility of P. vivax can now be monitored easily and efficiently. The data suggest that the threshold of resistance is similar to that of P. falciparum, i.e., in the range of 100 nM for chloroquine and 15 nM for pyronaridine. However, further studies are required to precisely define the cutoff for resistance and the sensitivity to each drug.

* Corresponding author. Mailing address: Bio-Medical Parasitology Unit, Institut Pasteur, 25 rue du Dr. Roux, Paris 75015, France. Phone: 33 1 45 68 85 78. Fax: 33 1 45 68 86 40. E-mail: druilhe{at}pasteur.fr

{triangledown} Published ahead of print on 26 March 2007.

Antimicrobial Agents and Chemotherapy, June 2007, p. 2112-2116, Vol. 51, No. 6
0066-4804/07/$08.00+0     doi:10.1128/AAC.01385-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Baird, J. K. (2009). Resistance to Therapies for Infection by Plasmodium vivax. Clin. Microbiol. Rev. 22: 508-534 [Abstract] [Full Text]  
  • Russell, B., Chalfein, F., Prasetyorini, B., Kenangalem, E., Piera, K., Suwanarusk, R., Brockman, A., Prayoga, P., Sugiarto, P., Cheng, Q., Tjitra, E., Anstey, N. M., Price, R. N. (2008). Determinants of In Vitro Drug Susceptibility Testing of Plasmodium vivax. Antimicrob. Agents Chemother. 52: 1040-1045 [Abstract] [Full Text]  


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