The events leading to invasion of erythrocytes following the pre-erythrocytic phase of the life cycle have been studied in great detail. Nonspecific attachment to the erythrocyte is followed by apical reorientation of the merozoite prior to invasion. The specificity of the process is exemplified by P. vivax parasites, which can only invade erythrocytes of Duffy-positive Fy Fy phenotype (Miller et al., 1976). The paroxysms of fever and chills that characterise acute malaria are related to the rupture of erythrocytes and release of merozoites and parasite products into the circulation. It is likely that the systemic symptoms are mediated by elevated cytokine levels, as anti-TNF antibodies have been shown to reduce fever in acute malaria (Kwiatkowski et al., 1993).
P. falciparum has two distinguishing features, which contribute to its increased pathogenicity in comparison to the other species: it has the capacity for amplification to high parasitaemia (sometimes in excess of 30%) because red blood cells of any age can be invaded; and mature forms of the parasite alter the surface of infected erythrocytes, causing them to sequester in particular vascular beds.
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