Publication: Rosette formation by Plasmodium vivax
Issued Date
1995-01-01
Resource Type
ISSN
18783503
00359203
00359203
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2-s2.0-0029558866
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Mahidol University
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SCOPUS
Bibliographic Citation
Transactions of the Royal Society of Tropical Medicine and Hygiene. Vol.89, No.6 (1995), 635-637
Suggested Citation
Rachanee Udomsangpetch, Kesinee Thanikkul, Sasithon Pukrittayakamee, Nicholas J. White Rosette formation by Plasmodium vivax. Transactions of the Royal Society of Tropical Medicine and Hygiene. Vol.89, No.6 (1995), 635-637. doi:10.1016/0035-9203(95)90422-0 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/17326
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Title
Rosette formation by Plasmodium vivax
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Abstract
In contrast to Plasmodium falciparum, infections with P. vivax are seldom fatal. Red blood cells containing mature forms of P. falciparum sequester in the microvasculature of vital organs, and adhere to vascular endothelium (cytoadherence) and to uninfected red cells (rosetting). Rosetting of P. falciparum has been associated with the lethal syndrome of cerebral malaria. We have studied the rosetting properties of red blood cells infected with P. vivax obtained from adults with acute malaria in Thailand. Of 35 parasite isolates studied, 25 (71%) showed rosetting with a mean proportion of 41% of infected red cells (sd 34%, range 14–100%). Rosetting of P. vivax was related to maturation of the parasite; only cells containing parasites with visible malaria pigment rosetted. Rosetting and parasitaemia were not correlated. However, unlike P. falciparum, cells infected with P. vivax did not adhere to human umbilical vein endothelial cells, to C32 melanoma cells, to platelets, or to purified adhesion receptor molecule CD36. These findings suggest that thrombocytopenia in vivax malaria is not related to platelet-red cell attachment, and that rosetting alone is insufficient to cause the syndrome of cerebral malaria. © 1995 Oxford University Press.