Genomic Characterization of Recrudescent Plasmodium malariae after Treatment with Artemether/Lumefantrine
Gavin G. Rutledge1
, Ian Marr1
, G. Khai Lin Huang, Sarah Auburn, Jutta Marfurt, Mandy Sanders, Nicholas J. White, Matthew Berriman, Chris I. Newbold, Nicholas M. Anstey, Thomas D. Otto
, and Ric N. Price
Author affiliations: Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom (G.G. Rutledge, M. Sanders, M. Berriman, C.I. Newbold, T.D. Otto); Royal Darwin Hospital, Casuarina, Northern Territory, Australia (I. Marr, G.K.L. Huang, N.M. Anstey, R.N. Price); Menzies School of Health Research and Charles Darwin University, Darwin, Northern Territory, Australia (S. Auburn, J. Marfurt, N.M. Anstey, R.N. Price); Mahidol University Faculty of Tropical Medicine, Mahidol-Oxford Tropical Medicine Research Unit, Bangkok, Thailand (N.J. White); University of Oxford Centre for Tropical Medicine and Global Health, Oxford, United Kingdom (N.J. White, R.N. Price); University of Oxford Weatherall Institute of Molecular Medicine, Oxford (C.I. Newbold)
Figure 1. Timeline of the clinical case of a patient with Plasmodium malariae infection diagnosed and treated at Royal Darwin Hospital, Darwin, Northern Territory, Australia, March–April 2015, showing the timing (A), treatment (B), parasite’s genotype as inferred from whole-genome sequencing (C), clinical presentation (D), and location (E). The rounded arrow indicates the recrudescence of the minor haplotype 2 in the initial infection to dominate monoclonally in the second infection. AL, artemether/lumefantrine; H1, haplotype 1; H2; haplotype 2; MP Ag, pan-malarial antigen; R1, reference haplotype.
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