Plasmodium chabaudi: a rodent malaria model for in‐vivo and in‐vitro cytoadherence of malaria parasites in the absence of knobs

Abstract

The ability of Plasmodium chabaudi infected erythrocytes to bind to endothelial cells in vivo and to various murine cell lines in vitro is described. A procedure for the selective recovery of a sequestering subpopulation of schizont-infected erythrocytes from hepatic sinusoids of BALB/c mice, using a combination of body perfusion, trypsin treatment and Percoll density centrifugation was developed. The serial subinoculation of such a subpopulation was used to select for a clone of parasites (strain AJJ) with considerably better cytoadherent characteristics than the parent line (strain AJ). In contrast, it was demonstrated that another clone (PC7), showed no cytoadherence in vivo or in vitro. This study shows that parasite induced alterations occurred on the surface of erythrocytes infected with late developmental stages of P. chabaudi. The antigenicity of these molecules in the infected mouse was demonstrated using immune serum and affinity chromatography. Cytoadherence and surface antigenic changes in P. chabaudi schizont-infected erythrocytes were demonstrated in the absence of the submembranous 'knobs' associated with cytoadherence in P. falciparum.

Chronobiology ofPlasmodium chabaudi chabaudi :analysis of hourly recorded total and differential parasitaemia during a schizogonic cycle

“…2). Other authors (Hommel et al, 1982;Boyle et al, 1983: Cox et al, 1987Gilks et al, 1990) mentioned only part of these possibilities or used the curves for different purposes. The position of the para sitaemia drop at the end of each plateau phase per fectly coincides with the rising slope of the schizont peak.…”

“…Similar drops were observed with P. chabandi adami by Gautret (1993). This phenomenon has been explained by the disappearance of schizonts from the peripheral blood and their sequestration in the inner organs, mainly the liver and the spleen (Cox et al, 1987;Gilks et al, 1990). This peripheral withdrawal was estimated at 8-10 % of the preceeding plateau level.…”

Virulence in malaria: an evolutionary viewpoint

“…Cerebral malaria, a syndrome of P. falciparum in which parasites become lodged in the brain as a result of cytoadherence, and the form of disease responsible for most malaria-related deaths in Africa , is not an obvious feature of P. chabaudi. Lesions (Vuong et al 1999) and parasites (Mota et al 2000) have been found in the brain of P. chabaudi-infected mice, but most sequestration takes place in other vital organs such as the liver (Cox et al 1987;Mota et al 2000). Brain involvement similar to cerebral malaria does occur in related rodent species (P. berghei, Rest (1982) which also sequesters in other organs (Alger 1963), and in P. yoelii, Yoeli & Hargreaves 1974;Kaul et al 1994), but this appears to be only after adaptation to the novel host (mice) through serial passage.…”

Complex genetic control of susceptibility to malaria in mice

“…40,41 P. chabaudi AS undergoes sequestration, although in the spleen and liver and not in the brain, as does the human parasite. 42 Finally, infection of inbred mouse strains with this parasite results in non-lethal or lethal infections, dependent upon the genetic background of the host. 43,44 In this infection model, a rapid proliferation of the parasite during the first 6-8 days is followed by a curative phase, with inflammatory, immune and erythropoietic responses resulting in elimination of the parasites by days 21-28 in 'resistant' animals.…”