Reduced erythrocyte survival following clearance of malarial parasitaemia in Thai patients

Abstract

Erythrocyte survival times were measured in healthy Thai controls and in patients following clearance of asexual P. falciparum or P. vivax parasitaemia. In five controls the mean cell life (MCL) of compatible donor erythrocytes was 89.6 d (mean range 73-101 d) compared with a mean MCL of 56.8 d (range 30-66 d) for autologous erythrocytes in 12 falciparum patients. In one of these patients the survival curve was biphasic with a rapid loss of some labelled cells. The survival of compatible donor erythrocytes was also studied in 10 patients and two types of survival curve could be distinguished. In five patients the cells had a mean MCL of 64.4 d (range 42-90 d). In the others survival curves were curvilinear, suggesting a complex mechanism of cell clearance or the presence of more than one cell population. There was initially a more rapid rate of destruction. In P. vivax malaria the MCL of autologous erythrocytes in seven patients was a mean of 67.2 d (range 34-74 d) and that of compatible donor cells in six patients was 66.8 d (range 54-76 d). In all except one of these patients both autologous and donor cell survival curves could be fitted to straight lines. No increase in cell-bound IgG or C3 was evident in 12 patients tested. The differences between the mean MCL in all the groups of patients and the controls were statistically significant at the 5% level. This indicates an increased rate of erythrocyte destruction following clearance of P. falciparum or P. vivax parasites which is not antibody or complement mediated. The mechanism is unknown, but appears to be extrinsic to the erythrocytes themselves and may result from nonspecific activation of the reticuloendothelial function associated with the parasitic infection.

Red blood cell deformability as a predictor of anemia in severe falciparum malaria.

“…Full supportive care was given as described previously. 3 A control group of 22 healthy age-and sexmatched Thai volunteers provided a blood sample for measurement of RBC deformability.…”

“…It is thought to result from a combination of parasitized erythrocyte destruction at schizont rupture, accelerated removal of both parasitized and unparasitized red blood cells, and ineffective erythropoiesis. [3][4][5][6] Of these factors, removal of unparasitized red blood cells is the most important, accounting for approximately 90% of the reduction in hematocrit in acute malaria (Price R and others, unpublished data). We have shown previously that the threshold for splenic removal of heat-damaged or antibody-coated erythrocytes in acute malaria is lowered, suggesting enhancement of both mechanical filtrative function and Fc receptor-mediated clearance.…”

Cytometric analysis of blood cells from malaria‐infected patients and in vitro infected blood

“…Rheological changes are likely to contribute to splenic sequestration of parasitized red cells. Looareesuwan et al (9) have suggested that P. falciparum and P. uivax infections may lead to increased destruction of unparasitized red cells. Red cell changes, in theory, may result from the direct and indirect effects of the parasite on the red cell as well as the pathophysiological response of the patient.…”

Plasmodium falciparum rhoptry protein RSP2 triggers destruction of the erythroid lineage

“…Anemia is caused partly by the loss of red blood cells, both infected erythrocytes (IEs) and uninfected erythrocytes (UEs), which are destroyed by hemolysis or phagocytosis. 3 Rigidification of the membranes of IEs and UEs during infection may be an important factor in the destruction of these cells during passage through the spleen. 4,5 There seem to be many causes of anemia, and the underlying mechanisms remain elusive.…”