Immunity to non-cerebral severe malaria is acquired after one or two infections

@article{Gupta1999ImmunityTN,
  title={Immunity to non-cerebral severe malaria is acquired after one or two infections},
  author={Sunetra Gupta and Robert W. Snow and Christl Ann Donnelly and Kevin Marsh and Chris I Newbold},
  journal={Nature Medicine},
  year={1999},
  volume={5},
  pages={340-343}
}
In areas of stable transmission, clinical immunity to mild malaria is acquired slowly, so it is not usually effective until early adolescence. Life-threatening disease is, however, restricted to a much younger age group, indicating that resistance to the severe clinical consequences of infection is acquired more quickly. Understanding how rapidly immunity develops to severe malaria is essential, as severe malaria should be the primary target of intervention strategies, and predicting the result… 

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Correction: Age Interactions in the Development of Naturally Acquired Immunity to Plasmodium falciparum and Its Clinical Presentation

Reducing exposure to P. falciparum antigens through chemoprophylaxis early in life can delay immunity acquisition, and provides insight on the interplay between immunity and exposure-reduction interventions.
...

References

SHOWING 1-10 OF 15 REFERENCES

Acquired immunity and postnatal clinical protection in childhood cerebral malaria

It is clear that although the delayed peak in incidence of cerebral malaria (with age) can be generated by assuming that subsequent exposures carry a higher risk of disease, such an explanation is not compatible with the observation that severe disease rates are low among infants and young children in areas of high transmissibility.

Risk of severe malaria among African infants: direct evidence of clinical protection during early infancy.

Examination of hospital admissions in four geographically and demographically well-defined areas with differing intensities of P. falciparum transmission provides direct evidence for the very early acquisition of clinical immunity and for the existence of a period of clinical protection, which together may explain why the cumulative risk of malarial disease throughout childhood appears to decline with increasing transmission intensity.

Epidemiological significance of repeated infections with homologous and heterologous strains and species of Plasmodium.

  • G. Jeffery
  • Medicine, Biology
    Bulletin of the World Health Organization
  • 1966
The use of immunofluorescent methods may provide a clearer understanding of the mechanism of partial immunity as it affects reinfection and the relationship of this partial immunity to the epidemiology and chemotherapy of the disease in endemic areas is of importance.

Malaria infection in infancy in rural Malawi.

Intervention strategies to reduce the risk of early infant infection need to be targeted toward mothers of infants at high risk in a rural area of Malawi with intense malaria transmission.

Parasite antigens on the infected red cell surface are targets for naturally acquired immunity to malaria

It is shown that the PfEMPI variants expressed during episodes of clinical malaria were less likely to be recognized by the corresponding child's own preexisting antibody response than by that of children of the same age from the same community.

Plasmodium falciparum malaria in the first year of life in an area of intense and perennial transmission

There were marked increases in P. falciparum prevalence, parasite densities, overall fever incidence and the incidence of malaria fevers with age for the first 6 months of life, and there was no initial period of protection against infection in neonates.

High incidence of asymptomatic malara infections in a birth cohort of children less than one year of age in Ghana, detected by multicopy gene polymerase chain reaction.

The level of malaria-specific IgG at birth was positively correlated with risk of infection in children 6-12 months of age, indicating that maternally derived anti-malarial IgG is correlated with exposure to malaria infection.

Infant parasite rates and immunoglobulin M seroprevalence as a measure of exposure to Plasmodium falciparum during a randomized controlled trial of insecticide-treated bed nets on the Kenyan coast.

It was demonstrated that parasite prevalence, IgM seropositivity, and the force of transmission were all significantly reduced by 50%.