Abstract

Exposure to stress during an insect’s larval development can have carry-over effects on adult life history traits and susceptibility to pathogens. We investigated the effects of larval nutritional stress for the first time using field mosquito vectors and malaria parasites. In contrast to previous studies, we show that larval nutritional stress may affect human to mosquito transmission antagonistically: nutritionally deprived larvae showed lower parasite prevalence for only one gametocyte carrier; they also had lower fecundity. However, they had greater survival rates that were even higher when infected. When combining these opposing effects into epidemiological models, we show that larval nutritional stress induced a decrease in malaria transmission at low mosquito densities and an increase in transmission at high mosquito densities, whereas transmission by mosquitoes from well-fed larvae was stable. Our work underscores the importance of including environmental stressors towards understanding host–parasite dynamics to improve disease transmission models and control.

Highlights

  • Out of the 2,600 larvae used for each treatment, a total of 2,106 (81 ± 0.02%) larvae exposed to low food conditions and 1,994 (77 ± 0.02%) exposed to high food conditions survived to the adult stage (X21 = 1.7, P = 0.2; Fig. S1a)

  • The environment experienced by an individual during its development can greatly influence its adult phenotype through carry-over effects. Nutrition is one such environmental factor that can impact host-pathogen interactions by affecting both partners. This is of great importance in vector-borne diseases as any alterations in individual life history traits could have crucial implications for transmission through changes in key parameters of vectorial capacity[12,14,15,21,22,23,31,32]

  • Using a sympatric An. coluzzii-P. falciparum species combination, we have shown that larval food stress greatly impacted several mosquito life history traits and may affect malaria transmission

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Summary

Introduction

There was a significant interaction between infection status and larval diet (X22 = 7.9, P = 0.02; Fig. 2): the increase in longevity for infected individuals compared to unexposed and exposed-uninfected individuals was greater for low food than for high food mosquitoes. The gametocyte carrier and the gametocyte carrier by larval diet interaction significantly affected parasite prevalence (X23 = 54.7, P < 0.0001 and X23 = 8.02, P = 0.046, respectively; Fig. 3), with low food females being significantly less likely to be infected than high food females only for gametocyte carrier B (X21 = 7.3, P = 0.007, all other comparisons being non significant).

Results
Conclusion
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