A Retrospective Examination of Sporozoite- and Trophozoite-Induced Infections with Plasmodium Falciparum: Development of Parasitologic and Clinical Immunity during Primary Infection

Abstract

Abstract. A retrospective analysis was made of the parasitologic and fever records of 318

Plasmodium vivax Blood-Stage Dynamics

“…Peak parasitemia was higher in trophozoite-than in sporozoite-induced infections but, in contrast to Boyd (1938), not earlier. Our results on the duration of trophozoiteversus sporozoite-induced infections differ from the results of Coatney et al (1971) with a larger sample of St. Elizabeth P. vivax infections, as cited previously, and from our results with P. falciparum (Collins and Jeffery, 1999).It is not clear whether the magnitudes of the fevers fit the observation by Kitchen (1949) that P. vivax fever "frequently exceeds 106 F." The timing of the peak fever was several days in advance of the range given by Kitchen (1949), however. In the sporozoite-induced infections, the mean 28.4-day duration of the febrile phase was longer (by 9 days) and the mean maximum fever of 105.8 F higher (by 1.6-3.3 F) than those cited by Coatney et al (1971) for mosquitoinduced infections.…”

“…Decades of experience with the common malariatherapy "strains" seemed to confirm the presence and persistence of characteristic differences between primary infections with each of them (Boyd, 1940a;Kaplan et al, 1946), e.g., between the El Limon, McLendon, and SanteeCooper strains of P. falciparum (Collins and Jeffery, 1999). Several citations in the first paragraph of this paper are generalizations from the authors' extensive experience, each predominantly with 1 strain of P. vivax: Chesson (Whorton et al, 1947), McCoy (Kitchen, 1949), or Madagascar (Shute, 1958 Chesson infections and so may not apply to the authors' experience with St. Elizabeth infections.…”

“…The paper gives no details about the "particular procedure" of mosquito and blood inoculations but claims that it led to infections with higher fevers, higher mortality (if untreated), and more consistent transmission to Anopheles, changes "evidenced not only by an increase in the number of asexual parasites but particularly by the earlier appearance and greater number of gametocytes." We are wary of the discrepancies between this account and reports on the same strain in the same facility during the same period that were published 5 yr earlier (James, 1931) and 15 yr later (Covell and Nicol, 1951), however.Decades of experience with the common malariatherapy "strains" seemed to confirm the presence and persistence of characteristic differences between primary infections with each of them (Boyd, 1940a;Kaplan et al, 1946), e.g., between the El Limon, McLendon, and SanteeCooper strains of P. falciparum (Collins and Jeffery, 1999). Several citations in the first paragraph of this paper are generalizations from the authors' extensive experience, each predominantly with 1 strain of P. vivax: Chesson (Whorton et al, 1947), McCoy (Kitchen, 1949), or Madagascar (Shute, 1958 Chesson infections and so may not apply to the authors' experience with St. Elizabeth infections.…”

“…He also wrote (Boyd, 1941) that "artificially induced infections in human subjects do not exhibit the chronicity which characterizes the naturally induced infections." Our previous work on uninterrupted P. falciparum infections indicated that, with all but a non-gametocyte-producing variant of 1 strain, the mean duration of detectable primary parasitemia was greater in the sporozoite-than in the trophozoite-induced infections (Collins and Jeffery, 1999). …”

Virulence in malaria: an evolutionary viewpoint

“…The maximum parasitaemia reached in P. falciparum typically does not exceed 5% or 10 8 parasites ml Ϫ1 (e.g. Field & Niven 1937;Collins & Jeffery 1999) and all-case fatality rates are ca. 0.1-1% (Molineaux & Gramiccia 1980;Greenwood et al 1987;Alles et al 1998;Snow et al 1999).…”