Clinical and Parasitological Observations on Induced Malaria

James, Stephen P.; Nicol, W. D.; Shute, P. G.

doi:10.1177/003591573602900802

Cited by 33 publications

(34 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many laboratory studies in malaria have shown that high or low virulence phenotypes accrued through serial passage can be maintained upon transmission through mosquitoes (James et al 1936; Coatney et al 1961; Alger et al 1971; Walliker et al 1976; Knowles and Walliker 1980; Walliker 1981; Barnwell et al 1983), although occasional major losses (or gains) of virulence do occur (Alger et al 1971; Walliker et al 1976; Knowles and Walliker 1980; Gilks et al 1990). Mosquito transmission could play a significant role in virulence evolution that is driven by inhost selective processes (as distinct from the between-host selective processes underlying the vaccination hypothesis in Gandon et al [2001]).…”

Section: Resultsmentioning

confidence: 99%

Immunity Promotes Virulence Evolution in a Malaria Model

2004

View full text Add to dashboard Cite

Evolutionary models predict that host immunity will shape the evolution of parasite virulence. While some assumptions of these models have been tested, the actual evolutionary outcome of immune selection on virulence has not. Using the mouse malaria model, Plasmodium chabaudi, we experimentally tested whether immune pressure promotes the evolution of more virulent pathogens by evolving parasite lines in immunized and nonimmunized (“naïve”) mice using serial passage. We found that parasite lines evolved in immunized mice became more virulent to both naïve and immune mice than lines evolved in naïve mice. When these evolved lines were transmitted through mosquitoes, there was a general reduction in virulence across all lines. However, the immune-selected lines remained more virulent to naïve mice than the naïve-selected lines, though not to immunized mice. Thus, immune selection accelerated the rate of virulence evolution, rendering parasites more dangerous to naïve hosts. These results argue for further consideration of the evolutionary consequences for pathogen virulence of vaccination.

show abstract

Section: Resultsmentioning

confidence: 99%

Immunity Promotes Virulence Evolution in a Malaria Model

2004

View full text Add to dashboard Cite

show abstract

“…In southern Europe there was often a bimodal pattern with a late summer peak of falciparum malaria [19]. The epidemiological studies of malaria epidemics in Sind (now Pakistan) and Ceylon (Sri Lanka) followed a similar pattern [19,25,39]. This suggested that long-latency P. vivax was also responsible for the peak of vivax malaria cases which occurred the year after the falciparum malaria epidemics in these two tropical areas (although other interpretations are also possible).…”

Section: Introductionmentioning

confidence: 99%

Determinants of relapse periodicity in Plasmodium vivax malaria

White

2011

Malar J

564

670

View full text Add to dashboard Cite

Plasmodium vivax is a major cause of febrile illness in endemic areas of Asia, Central and South America, and the horn of Africa. Plasmodium vivax infections are characterized by relapses of malaria arising from persistent liver stages of the parasite (hypnozoites) which can be prevented only by 8-aminoquinoline anti-malarials. Tropical P. vivax relapses at three week intervals if rapidly eliminated anti-malarials are given for treatment, whereas in temperate regions and parts of the sub-tropics P. vivax infections are characterized either by a long incubation or a long-latency period between illness and relapse - in both cases approximating 8-10 months. The epidemiology of the different relapse phenotypes has not been defined adequately despite obvious relevance to malaria control and elimination. The number of sporozoites inoculated by the anopheline mosquito is an important determinant of both the timing and the number of relapses. The intervals between relapses display a remarkable periodicity which has not been explained. Evidence is presented that the proportion of patients who have successive relapses is relatively constant and that the factor which activates hypnozoites and leads to regular interval relapse in vivax malaria is the systemic febrile illness itself. It is proposed that in endemic areas a large proportion of the population harbours latent hypnozoites which can be activated by a systemic illness such as vivax or falciparum malaria. This explains the high rates of vivax following falciparum malaria, the high proportion of heterologous genotypes in relapses, the higher rates of relapse in people living in endemic areas compared with artificial infection studies, and, by facilitating recombination between different genotypes, contributes to P. vivax genetic diversity particularly in low transmission settings. Long-latency P. vivax phenotypes may be more widespread and more prevalent than currently thought. These observations have important implications for the assessment of radical treatment efficacy and for malaria control and elimination.

show abstract

“…He subsequently suggested that the explosive nature of the Ceylon epidemic must have been due to a sudden increase in the infectivity of the adult population, and that, therefore, the beginning of the epidemic was characterised by relapses in the adult population that then generated the necessary human transmission population [11,12]. This was countered at the time by malariologists who believed, based on fever charts and the absence of gametocytes, that the initial wave of morbidity was due to novel infections [13]. However, to date there has been no satisfactory explanation to account for the age-structured nature of the morbidity rise, other than relapses (of both Plasmodium vivax and Plasmodium falciparum ) in the adult population.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Rácz

Diallo

Brey

2004

Malar J

View full text Add to dashboard Cite

The regional malaria epidemics of the early 1900s provided the basis for much of our current understanding of malaria epidemiology. Colonel Gill, an eminent malariologist of that time, suggested that the explosive nature of the regional epidemics was due to a sudden increased infectiousness of the adult population. His pertinent observations underlying this suggestion have, however, gone unheeded. Here, the literature on Plasmodium seasonal behaviour is reviewed and three historical data sets, concerning seasonal transmission of Plasmodium falciparum, are examined. It is proposed that the dramatic seasonal increase in the density of uninfected mosquito bites results in an increased infectiousness of the human reservoir of infection and, therefore, plays a key role in "kick-starting" malaria parasite transmission.

show abstract

Clinical and Parasitological Observations on Induced Malaria

Cited by 33 publications

References 0 publications

Immunity Promotes Virulence Evolution in a Malaria Model

Immunity Promotes Virulence Evolution in a Malaria Model

Determinants of relapse periodicity in Plasmodium vivax malaria

Untitled

Contact Info

Product

Resources

About