The effect of dietary antioxidant supplementation in a vertebrate host on the infection dynamics and transmission of avian malaria to the vector.

Host susceptibility to parasites is likely to be influenced by intrinsic factors, such as host oxidative status determined by the balance between pro-oxidant production and antioxidant defences. As a result, host oxidative status acts as an environmental factor for parasites and may constrain parasite development. We evaluated the role of host oxidative status on infection dynamics of an avian malarial parasite by providing canaries (Serinus canaria) with an antioxidant supplementation composed of vitamin E (a lipophilic antioxidant) and olive oil, a source of monounsaturated fatty acids. Another group received a standard, non-supplemented food. Half of the birds in each group where then infected with the haemosporidian parasite, Plasmodium relictum. We monitored the parasitaemia, haematocrit level, and red cell membrane resistance, as well as the transmission success of the parasite to its mosquito vector, Culex pipiens. During the acute phase, the negative effect of the infection was more severe in the supplemented group, as shown by a lower haematocrit level. Parasitaemia was lower in the supplemented group during the chronic phase only. Mosquitoes fed on supplemented hosts were more often infected than mosquitoes fed on the control group. These results suggest that dietary antioxidant supplementation conferred protection against Plasmodium in the long term, at the expense of a short-term negative effect. Malaria parasites may take advantage of antioxidants, as shown by the increased transmission rate in the supplemented group. Overall, our results suggest an important role of oxidative status in infection outcome and parasite transmission

Data from: Testing local adaptation in a natural great tit-malaria system: an experimental approach

Finding out whether Plasmodium spp. are coevolving with their vertebrate hosts is of both theoretical and applied interest and can influence our understanding of the effects and dynamics of malaria infection. In this study, we tested for local adaptation as a signature of coevolution between malaria blood parasites, Plasmodium spp. and its host, the great tit, Parus major. We conducted a reciprocal transplant experiment of birds in the field, where we exposed birds from two populations to Plasmodium parasites. This experimental set-up also provided a unique opportunity to study the natural history of malaria infection in the wild and to assess the effects of primary malaria infection on juvenile birds. We present three main findings: i) there was no support for local adaptation; ii) there was a male-biased infection rate; iii) infection occurred towards the end of the summer and differed between sites. There were also site-specific effects of malaria infection on the hosts. Taken together, we present one of the few experimental studies of parasite-host local adaptation in a natural malaria system, and our results shed light on the effects of avian malaria infection in the wild

Data from: Avian malaria and bird humoral immune response

Background: Plasmodium parasites are known to impose fitness costs on their vertebrate hosts. Some of these costs are due to the activation of the immune response, which may divert resources away from self-maintenance. Plasmodium parasites may also immuno-deplete their hosts. Thus, infected individuals may be less able to mount an immune response to a new pathogen than uninfected ones. However, this has been poorly investigated. Methods: The effect of Plasmodium infection on bird humoral immune response when encountering a novel antigen was tested. A laboratory experiment was conducted on canaries (Serinus canaria) experimentally infected with Plasmodium relictum (lineage SGS1) under controlled conditions. Birds were immune challenged with an intra-pectoral injection of a novel non-pathogenic antigen (keyhole limpet haemocyanin, KLH). One week later they were challenged again. The immune responses to the primary and to the secondary contacts were quantified as anti-KLH antibody production via enzyme-linked immunosorbent assay (ELISA). Results: There was no significant difference in antibody production between uninfected and Plasmodium infected birds at both primary and secondary contact. However, Plasmodium parasite intensity in the blood increased after the primary contact with the antigen. Conclusions: There was no effect of Plasmodium infection on the magnitude of the humoral immune response. However, there was a cost of mounting an immune response in infected individuals as parasitaemia increased after the immune challenge, suggesting a trade-off between current control of chronic Plasmodium infection and investment against a new immune challenge

The factors that affect the likelihood of infection by the end of the experimental period.

<p><b>a)</b> The standard weight of parameters in the 95% confidence interval model set and the number of candidate models that they occur in after model averaging. b) The analysis repeated on the original scale and predicted prevalence ± 1 se for males and females. c) Exploring the direction of the target effect, LA, by explicitly keeping the LA parameter in all models. Under a scenario of parasite adaptation, we expect parasites to be more infective on local hosts. Prevalence is plotted on the original scale. For further details of the method see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141391#pone.0141391.g001" target="_blank">Fig 1</a>.</p

Summary of sample sizes.

<p>The number of birds at each release site according to site of origin, sex, number of controls (<i>ie</i> treated with Malarone) and number infected by the end of the experiment.</p><p>Summary of sample sizes.</p

The factors that affect variables related to host pathology at the infection peak.

<p>a- b) SMI: standardised mass index; c- d) temperature; e- f) haematocrit; g- h) oxidative stress: membrane resistance (time taken to haemolyse half of red blood cells when faced with free radical attack). The left hand panels (a, c, e, g) show the standard weight of the predictor parameters affecting the host response variables and the number of candidate models in the 95% confidence interval model set that they occur in. Note that the interaction term indicative of host LA (Infection x Origin x Release site) is not always present. In the right hand panels (b, d, f, h) the LA effect (Infection x Origin x Release site) is explored and in these models, the LA term is explicitly retained. The predicted model averaged parameter estimates ± 1 se of each response variable is plotted on the original scale. Note that parameters that were included as covariates were set as “fixed”, <i>i</i>.<i>e</i>, the SW = 1, and they are therefore not shown in the plots. For full model formulae and results see tables in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141391#pone.0141391.s001" target="_blank">S1 File</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141391#pone.0141391.s003" target="_blank">S3 File</a>. For further details of the method see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141391#pone.0141391.g001" target="_blank">Fig 1</a>. The prediction, under a scenario of parasite adaptation, is that local birds will suffer more and have lower SMI, temperature, haematocrit and membrane resistance.</p

A step-by-step guide to the statistical modelling and the model selection and averaging procedure implemented (modified from [59]).

<p>A step-by-step guide to the statistical modelling and the model selection and averaging procedure implemented (modified from [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141391#pone.0141391.ref059" target="_blank">59</a>]).</p

The relationship between temperature and infection intensity.

<p><b>a)</b> The standard weight of variables affecting temperature measured at the end of the experiment and the number of candidate models in the 95% CI model set measured at the end of the experiment with parasite intensity (logr) fitted explicitly. b) Predicted model averaged estimates of temperature (degrees) in relation to parasite intensity (logr).</p

complete data set

complete data set from the laboratory experiment. the sheet entitled "measurements_bird level" contains all bird individual measurements. the sheet entitled "food consumption_cage level" contains all food consumption measurements at the cage level

Additional file 1: Figure S1. of Exposure of the mosquito vector Culex pipiens to the malaria parasite Plasmodium relictum: effect of infected blood intake on immune and antioxidant defences, fecundity and survival

Bird parasitaemia and haematocrit. a Parasitaemia (log-transformed, arbitrary unit) before the first feeding session, at the end of all the feeding sessions and mean value for canaries in the chronic group (1 to 4) and in the acute group (5 to 8). Mean values significantly differed between the two groups (Wilcoxon rank test: W = 0, P = 0.029). b Haematocrit (fraction of red blood cells in the total blood volume) before the first feeding session, at the end of all the feeding sessions and mean value for canaries in the chronic group (1 to 4), in the acute group (5 to 8) and in the uninfected group (9 to 12). Mean values did not significantly differ between the three groups (F (2,9) = 1.08, P = 0.381). (PDF 183 kb