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Am. J. Trop. Med. Hyg., 81(6), 2009, pp. 987-993
doi:10.4269/ajtmh.2009.09-0406;
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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High Levels of Plasmodium falciparum Rosetting in All Clinical Forms of Severe Malaria in African Children

Ogobara K. Doumbo, Mahamadou A. Thera, Abdoulaye K. Koné, Ahmed Raza, Louisa J. Tempest, Kirsten E. Lyke, Christopher V. Plowe, AND J. Alexandra Rowe*
Malaria Research and Training Center, Faculty of Medicine, Pharmacy and Dentistry, University of Bamako, Mali; Centre for Immunity, Infection and Evolution, Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, UK; Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, UK; Center for Vaccine Development and Howard Hughes Medical Institute, University of Maryland School of Medicine, Baltimore, Maryland

Plasmodium falciparum rosetting (the spontaneous binding of infected erythrocytes to uninfected erythrocytes) is a well-recognized parasite virulence factor. However, it is currently unclear whether rosetting is associated with all clinical forms of severe malaria, or only with specific syndromes such as cerebral malaria. We investigated the relationship between rosetting and clinical malaria in 209 Malian children enrolled in a case-control study of severe malaria. Rosetting was significantly higher in parasite isolates from severe malaria cases compared with non-severe hyperparasitemia and uncomplicated malaria controls (F2,117 = 8.15, P < 0.001). Analysis of sub-categories of severe malaria (unrousable coma, severe anemia, non-comatose neurological impairment, repeated seizures or a small heterogeneous group with signs of renal failure or jaundice) showed high levels of rosetting in all sub-categories, and no statistically significant differences in rosetting between sub-categories (F4,67 = 1.28, P = 0.28). Thus rosetting may contribute to the pathogenesis of all severe malaria syndromes in African children, and interventions to disrupt rosetting could be potential adjunctive therapies for all forms of severe malaria in Africa.

Received July 17, 2009. Accepted for publication August 26, 2009.

Acknowledgments: The authors are grateful to the Bandiagara Malaria Project team for their assistance and to the patients and their parents or guardians for participation in the study.

Financial support: This work was supported by the Wellcome Trust (Senior Research Fellowship to JAR, grant number 084226) and the U.S. National Institutes of Health (contract no. N01AI85346 and grant no. D43TW001589). KEL and CVP are supported by awards from the Doris Duke Charitable Foundation.

Disclaimer: None of the authors have commercial or other associations that might pose a conflict of interest.

* Address correspondence to J. Alexandra Rowe, Centre for Immunity, Infection and Evolution, Institute of Immunology and Infection Research, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK. E-mail: Alex.Rowe{at}ed.ac.uk

Authors’ addresses: Ogobara K. Doumbo, Mahamadou A. Thera, and Abdoulaye K. Koné, Malaria Research and Training Center, Département d’Epidémiologie des Affections Parasitaires, Faculté de Médecine, de Pharmacie et d’Odonto-Stomatologie, Bamako, Mali, E-mails: okd{at}MRTCBKO.org, mthera{at}MRTCBKO.org, and fankone{at}icermali.org. Ahmed Raza and J. Alexandra Rowe, Centre for Immunity, Infection and Evolution, Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK, E-mails: Ahmed.Raza{at}ed.ac.uk and Alex.Rowe{at}ed.ac.uk. Louisa J. Tempest, Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, UK, E-mail: Louisa.Tempest{at}ed.ac.uk. Kirsten E. Lyke and Christopher V. Plowe, Malaria Section, Center for Vaccine Development/Howard Hughes Medical Institute, University of Maryland School of Medicine, Baltimore, MD, E-mails: klyke{at}medicine.umaryland.edu and cplowe{at}medicine.umaryland.edu.




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