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WARMER TEMPERATURES REDUCE THE VECTORIAL CAPACITY OF MALARIA MOSQUITOES

Sunday, 13th of May 2012 Print

‘These results highlight the need to understand the interactive effects of environmental temperature on multiple host-disease life-history traits and challenge the assumptions of many current disease models that ignore this complexity.’

  • WARMER TEMPERATURES REDUCE THE VECTORIAL CAPACITY OF MALARIA MOSQUITOES

Full text is at http://rsbl.royalsocietypublishing.org/content/8/3/465.full

 

Biol. Lett. 23 June 2012 vol. 8 no. 3 465-468

 

Warmer temperatures reduce the vectorial capacity of malaria mosquitoes

1.    Krijn P. Paaijmans1,2,*, Simon Blanford1,2,3, Brian H. K. Chan1,2,3 and

  Matthew B. Thomas1,2

+ Author Affiliations

1.    1Center for Infectious Disease Dynamics, Pennsylvania State University, University Park, PA 16802, USA

2.    2Department of Entomology, Pennsylvania State University, University Park, PA 16802, USA

3.    3Department of Biology, Pennsylvania State University, University Park, PA 16802, USA

1.    *Author for correspondence (krijn@paaijmans.nl).

Abstract

The development rate of parasites and pathogens within vectors typically increases with temperature. Accordingly, transmission intensity is generally assumed to be higher under warmer conditions. However, development is only one component of parasite/pathogen life history and there has been little research exploring the temperature sensitivity of other traits that contribute to transmission intensity. Here, using a rodent malaria, we show that vector competence (the maximum proportion of infectious mosquitoes, which implicitly includes parasite survival across the incubation period) tails off at higher temperatures, even though parasite development rate increases. We also show that the standard measure of the parasite incubation period (i.e. time until the first mosquitoes within a cohort become infectious following an infected blood-meal) is incomplete because parasite development follows a cumulative distribution, which itself varies with temperature. Including these effects in a simple model dramatically alters estimates of transmission intensity and reduces the optimum temperature for transmission. These results highlight the need to understand the interactive effects of environmental temperature on multiple host-disease life-history traits and challenge the assumptions of many current disease models that ignore this complexity.

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