Trends in Parasitology
Vivax series:The paroxysm of Plasmodium vivax malaria
Section snippets
In vivo studies on the paroxysm of P. vivax malaria
As was first demonstrated by Golgi in 1889 [1], a malarial paroxysm is preceded by the synchronous rupture of schizont-infected red blood cells. This observation led to the idea that malarial fever is the product of fever-inducing toxins (pyrogens) released by the parasites during schizont rupture. In 1904, in Vera Cruz, Mexico, an observation was made which seemed to confirm this view. Five ml of serum from blood collected from a P. vivax malaria patient at the height of a paroxysm was passed
Ex vivo studies on P. vivax paroxysm
The following sections discuss the observations made upon blood plasma or whole blood cells collected from P. vivax patients at or around the time of a paroxysm.
Conclusions
The mediators and mechanisms of P. vivax paroxysm have been discussed here based on observation and experiment on P. vivax patients, and on material collected directly from them. The event of P. vivax paroxysm and the mediators and processes that we have identified in association with it all lack acute serious pathogenic features. In particular, the activity of one specific host mediator, IFN-γ, and of one class of parasite products, GPI, have not registered prominently in any of our analyses
Acknowledgements
We thank Dominic Kwiatkowski, George E. Grau, Giuseppe Del Giudice, Ian A. Clark, Louis H. Miller and Lakshmi Kumaratilate for discussions and/or collaboration in the development of these investigations. The work has been supported at various times by grants from the Rockefeller Foundation, the TDR/UNDP/World Bank/WHO, the European Union and the Wellcome Trust, to whom we express our gratitude. K.N.M. is formerly of the University of Colombo, Department of Parasitology, Faculty of Medicine,
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