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Fig. 3.3 Morphology of P. vivax, P. ovale and P. malariae. (A) P. vivax, ring forms. (B) P. vivax, trophozoites. (C) P. ovale, ring and free merozoites. (D) P. malariae, ring form. Photo courtesy of Mr Joe Manitta capillaries and postcapillary venules in the brain, lung, heart, bone marrow, kidney, liver, pancreas, intestine and other organs, and in the intervillous spaces of the placenta (Luse and Miller, 1971; White and Ho, 1992). Within 24 hours of erythrocyte invasion by merozoites, mature trophozoite and schizont-infected cells disappear from the peripheral blood and adhere to vascular endothelium (Figure 3.4). The slower blood flow and low oxygen tension provides a favourable environment for further parasite development. Sequestration also allows mature parasites to avoid passage through the spleen and likely clearance. In addition to adhesion to vascular endothelium, infected erythrocytes can adhere to uninfected erythrocytes (Figure 3.5) (see 'Rosetting', below) and clumps or layers of erythrocytes are sometimes observed extending into the vessel lumen in cerebral malaria. Sequestration from the peripheral blood stream may contribute to diagnostic difficulties in patients with highly synchronous infections (i.e. parasites all mature at the same time), as they may be critically ill at a time when parasites are at very low levels or occasionally undetectable in the peripheral circulation. P. vivax, P. ovale and P. malariae do not sequester, do not cause microcirculatory obstruction and are rarely fatal.

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