3.2 Experiment 2: glyphosate and nutritional stress
Glyphosate exposure (0.05mg/L) and food treatments had no significant
effect on larval mortality (model 7: χ²1 = 2.76, p =
0.097, χ²1 = 0.01, p = 0.904, respectively). Variation
in larvae development time was explained by food treatment, glyphosate
exposure and mosquito sex (model 8: F= 366.08, p < 0.0001, F=
8.123, p = 0.004, F= 655.21, p < 0.0001, respectively). While
nutritional stress impacted negatively the development time
(Figure 1A ), larvae exposed to glyphosate developed faster than
unexposed larvae (Figure 1B ). As expected males had a shorter
development time than females (male: 9.9 ± 0.1 day, female: 13.4 ± 0.2).
Food treatments and sex, but not glyphosate exposure, impacted mosquito
size (model 9: F= 39.20, p < 0.0001, F= 384.85, p <
0.0001, F= 2.06, p = 0.153, respectively). Males were smaller than
females and adults from larvae reared under standard diet condition were
bigger than adults from larvae reared under nutritional stress (mean ±
s.e. optimal feeding condition = 0.30 ± 0.003, food limitation = 0.28 ±
0.003).
The amount of blood ingested by females as well as the number of laid
eggs did not vary between treatments (blood meal size: model 10:
glyphosate exposure = χ²1= 1.27, p = 0.259; food
treatments = χ²1= 1.29, p = 0.256; eggs number: model
11: glyphosate exposure χ²1= 0.01, p = 0.99; food
treatment = χ²1= 3.49, p = 0.066). A positive
relationship was observed between blood meal size and the number of laid
eggs (model 11: χ²1= 5.70, p = 0.017).
Significant interaction of glyphosate exposure and food treatments was
observed regarding the probability of females to be infected by malaria
parasites (model 12: χ²1 = 7.67, p = 0.006,Figure 2A ). In the absence of glyphosate, nutritional stress
tended to decrease the infection prevalence (infection prevalence =
nutritional stress: 0.80, standard diet: 0.95; contrast analysis:
χ²1 = 2.74, p = 0.097). However, in the presence of
glyphosate, the infection prevalence observed in females from larvae
reared with standard diet was roughly a third lower than that of females
from the nutritional stress treatment (infection prevalence =
nutritional stress: 0.95, standard diet condition: 0.66; contrast
analysis: χ²1 = 5.18, p = 0.022). It is also interesting
to note that when larvae are reared without nutritional stress, the
infection prevalence observed in mosquitoes exposed to glyphosate was
significantly lower than in unexposed mosquitoes (contrast analysis:
χ²1 = 5.37, p = 0.020, Figure 2A ). Infection
prevalence tended to but was not significantly impacted by blood meal
size (model 12: χ²1 = 3.13, p = 0.076).
The intensity of the infection was not impacted by glyphosate exposure,
food treatments or by the interaction between the two factors (model 13:
χ²1 = 0.56, p = 0.455, χ²1 = 0.98, p =
0.321, χ²1 = 0.08, p = 0.782, respectively,Figure 2B ), but a positive relationship was observed between
blood meal size and oocyst burden (model 13: χ²1= 13.97,
p = 0.0001).
Discussion
In this study we assessed the consequences of larval exposure to pure
glyphosate or glyphosate-based herbicide on Culex pipiensmosquito life history traits and susceptibility to avian malaria
parasite infection. While we did not observe significant effect of
glyphosate on mosquito life history traits, we found that this compound
reduced the prevalence of Plasmodium parasite infection under
standard diet. Interestingly this effect was lost when the larvae were
subjected to nutritional stress.