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INFECTIOUSNESS OF MALARIA-ENDEMIC HUMAN POPULATIONS TO VECTORS

Despite its key role in determining the stability and intensity of malaria transmission, the infectiousness of human populations to mosquitoes has rarely been estimated. Field-based analyses of malaria transmission have frequently relied on the prevalence of asexual parasites or gametocytes as proxies for infectiousness. We now summarize empirical data on human infectiousness from Africa and Papua New Guinea. Over a wide range of transmission intensities there is little relationship between the infectiousness of human populations to vector mosquitoes and mosquito-to-human transmission intensity. We compare these data with the predictions of a stochastic simulation model of Plasmodium falciparum epidemiology. This model predicted little variation in the infectiousness of the human population for entomologic inoculation rates (EIRs) greater than approximately 10 infectious bites per year, demonstrating that the lack of relationship between the EIR and the infectious reservoir can be explained without invoking any effects of acquired transmission-blocking immunity. The near absence of field data from areas with an EIR < 10 per year precluded validation of the model predictions for low EIR values. These results suggest that interventions reducing mosquito-to-human transmission will have little or no effect on human infectiousness at the levels of transmission found in most rural areas of sub-Saharan Africa. Unless very large reductions in transmission can be achieved, measures to prevent mosquito-to-human transmission need to be complemented with interventions that reduce the density or infectiousness of blood stage parasites.

Received September 18, 2005. Accepted for publication November 6, 2005.

Acknowledgments: We thank the members of the Technical Advisory Group (Michael Alpers, Paul Coleman, David Evans, Brian Greenwood, Carol Levin, Kevin Marsh, F. Ellis McKenzie, Mark Miller, and Brian Sharp), the Project Management Team at the Program for Appropriate Technology in Health (PATH) Malaria Vaccine Initiative, and GlaxoSmithKline Biologicals S.A. for their assistance.

Financial support: The mathematical modeling study was supported by the PATH Malaria Vaccine Initiative and GlaxoSmithKline Biologicals S.A.

Disclaimer: Publication of this report and the contents hereof do not necessarily reflect the endorsement, opinion, or viewpoints of the PATH Malaria Vaccine Initiative or GlaxoSmithKline Biologicals S.A.

^* Address correspondence to Thomas Smith, Swiss Tropical Institute, PO Box, CH-4002, Basel, Switzerland. E-mail: Thomas-A.Smith{at}unibas.ch

Authors’ addresses: Gerry F. Killeen, Ifakara Health Research and Development Center, Ifakara, Kilombero District, Tanzania, Telephone: 255-748-477-118, Fax: 255-23-262-5312, E-mail: gkilleen{at}ihrdc.or.tz. Amanda Ross and Thomas Smith, Swiss Tropical Institute, PO Box, CH-4002, Basel, Switzerland, Telephone: 41-61-284-8273, Fax: 41-61-284-8105, E-mails: amanda.ross{at}unibas.ch and Thomas-A.Smith{at}unibas.ch.

Reprint requests: Thomas Smith, Swiss Tropical Institute, PO Box, CH-4002, Basel, Switzerland.

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