Plasmodium Vivax Blood-Stage Dynamics

Abstract

We examine the dynamics of parasitemia and gametocytemia reflected in the preintervention charts of 221 malaria-naive U.S. neurosyphilis patients infected with the St. Elizabeth strain of Plasmodium vivax, for malariatherapy, focusing on the 109 charts for which 15 or more days of patency preceded intervention and daily records encompassed an average 98% of the duration of each infection. Our approximations of merogony cycles (via "local peaks" in parasitemia) seldom fit patterns that correspond to "textbook" tertian brood structures. Peak parasitemia was higher in trophozoite-induced infections than in sporozoite-induced ones. Relative densities of male and female gametocytes appeared to alternate, though without a discernably regular period. Successful transmission to mosquitoes did not depend on detectable gametocytemia or on absence of fever. When gametocytes were detected, transmission success depended on densities of only male gametocytes. Successful feeds occurred on average 4.7 days later in an infection than did failures. Parasitemia was lower in homologous reinfection, gametocytemia lower or absent.

Virulence in malaria: an evolutionary viewpoint

“…Figure 5a shows that asexual parasite density and gametocyte density among infected hosts are highly correlated across age groups and across seasons. Data from a separate study (Tchuinkam et al 1993) illustrate how transmission of P. falciparum to mosquitoes increases with the log of gametocyte density, this in a linear way (figure 5b), consistent with other field studies on this relationship (reviewed in Carter & Graves and McKenzie et al (2002) for data on P. ovale and P. vivax). Thus it is reasonable to assume that transmission to mosquitoes in the Garki Project was a log-linear function of the average gametocyte densities reported, further assuming that host age does not alter the infectivity per gametocyte, as supported by most studies where this has been examined (Rutledge & Gould 1969;Graves et al 1988;Tchuinkam et al 1993).…”

“…Between-strain variation in gametocyte production in vitro in P. falciparum has also been demonstrated (Graves et al 1984). There is also evidence of between-strain variation for some of these characteristics in P. vivax (reviewed in McKenzie et al 2002). However, there appear to be only two published studies, one in P. falciparum and one in P. vivax, that have examined the relationships among virulence, transmission, growth rate and infection length.…”

Malaria - the Master Masquerader

“…The increased antigenicity of RBCs caused by plasmodial infection [7], or plasmodial antigens per se may be responsible for the massive mast cell degranulation in the present case. Whether this was mediated by immunological or direct mechanisms is unknown.…”

“…Plasmodial sporozoites inoculated while taking a blood meal, multiply in the liver producing daughter merozoites, which after release into the bloodstream, attach themselves to specific receptors on erythrocytes. This attachment is known to make the erythrocytes antigenic by altering red cell membrane, exposing the hitherto hidden surface antigen and inserting new parasite derived proteins [7].…”

Factors that delay malaria diagnosis and treatment in the municipality of Riberalta in Bolivia

“…Los gametocitos de Plasmodium falciparum hacen su aparición en un tiempo aproximado de 7 a 15 días, después de la picadura del vector, principalmente en la microcirculación de los tejidos profundos (4,5), mientras que los gametocitos de Plasmodium vivax aparecen en sangre periférica entre 2 y 3 días después de la picadura del vector, y sobreviven tres días más (6)(7)(8).…”