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Abstract

BackgroundThe development and propagation of malaria parasites in their vertebrate host is a complex process in which various host and parasite factors are involved. Sometimes the evolution of parasitaemia seems to be quelled by parasite load. In order to understand the typical dynamics of evolution of parasitaemia, various mathematical models have been developed. The basic premise ingrained in most models is that the availability of uninfected red blood cells (RBC) in which the parasite develops is a limiting factor in the propagation of the parasite population.Presentation of the hypothesisWe would like to propose that except in extreme cases of severe malaria, there is no limitation in the supply of uninfected RBC for the increase of parasite population.Testing the hypothesisIn this analysis we examine the biological attributes of the parasite-infected RBC such as cytoadherence and rosette formation, and the rheological properties of infected RBC, and evaluate their effects on blood flow and clogging of capillaries. We argue that there should be no restriction in the availability of uninfected RBC in patients.Implication of the hypothesisThere is no justification for the insertion of RBC supply as a factor in mathematical models that describe the evolution of parasitaemia in the infected host. Indeed, more recent models, that have not inserted this factor, successfully describe the evolution of parasitaemia in the infected host.

Apoptosis stalks Plasmodium falciparum maintained in continuous culture condition

“…The expected fragments of 45 and 28 kDa were observed in all the developmental stages (lanes 1-12), a pattern absent from uninfected erythrocyte preparation. A protein of approximately 28 kDa was present in uninfected erythrocytes (lane 13) and has been reported before in other negative controls [ 2 ].…”

“…In absence of specific anti- parasitic immune responses such as in vitro culture conditions, it is reasonable to assume that the parasite growth rate reflects a balance between cell proliferation and cell loss. This assumption is strengthened by the following observations: 1) in vitro, the parasitaemia of Plasmodium falciparum cultures increases by a factor of 3-8 within 48 hours whereas theoretically it should increase 16 fold [ 1 ], and 2) in vivo, the evolution of parasitaemia in fast growing strains seems to be quelled by parasite density even when the RBC supply is not limiting [ 2 ]. It is tempting to speculate that the disparity between expected and observed parasite density is a function of self-regulation.…”

Quinoline Binding Site on Malaria Pigment Crystal: A Rational Pathway for Antimalaria Drug Design

“…The toxic heme is rendered less harmful in the parasite by one electron oxidation to produce hematin (Fe 3+ -PPIX), which then precipitates forming nonreactive submicron to micron-sized crystals known as hemozoin, in an exclusive organellesthe acidic food vacuole. 3,5 Hemozoin, the malaria pigment, is a marker of malaria infection in RBC assays. This process of hemozoin formation is now being considered 4,6,7 as a type of biomineralization.…”

Magnetic isolation of Plasmodium falciparum schizonts iRBCs to generate a high parasitaemia and synchronized in vitro culture

“…Although some culture conditions have been improved, the technique is essentially the same as described by Trager and Jensen [ 4 ], and difficulties to obtain cultures with a parasitaemia higher than 10% still remain. Theoretically the parasitaemia of an in vitro P. falciparum culture could increase up to 16-fold per life cycle, however only an increase of three- to eight-fold is observed in 48 hours [ 6 , 7 ]. The inhibition of malaria parasite development has been associated with medium acidification due to the secretion of lactic acid [ 8 , 9 ].…”