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Gabriele Sorci - One of the best experts on this subject based on the ideXlab platform.
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Impact of host nutritional status on infection dynamics and Parasite Virulence in a bird-malaria system.
Journal of Animal Ecology, 2014Co-Authors: Stéphane Cornet, Coraline Bichet, Stephen Larcombe, Bruno Faivre, Gabriele SorciAbstract:Host resources can drive the optimal Parasite exploitation strategy by offering a good or a poor environment to pathogens. Hosts living in resource-rich habitats might offer a favourable environment to developing Parasites because they provide a wealth of resources. However, hosts living in resource-rich habitats might afford a higher investment into costly immune defences providing an effective barrier against infection. Understanding how Parasites can adapt to hosts living in habitats of different quality is a major challenge in the light of the current human-driven environmental changes. We studied the role of nutritional resources as a source of phenotypic variation in host exploitation by the avian malaria Parasite Plasmodium relictum. We investigated how the nutritional status of birds altered Parasite within-host dynamics and Virulence, and how the interaction between past and current environments experienced by the Parasite accounts for the variation in the infection dynamics. Experimentally infected canaries were allocated to control or supplemented diets. Plasmodium Parasites experiencing the two different environments were subsequently transmitted in a full-factorial design to new hosts reared under similar control or supplemented diets. Food supplementation was effective since supplemented hosts gained body mass during a 15-day period that preceded the infection. Host nutrition had strong effects on infection dynamics and Parasite Virulence. Overall, Parasites were more successful in control nonsupplemented birds, reaching larger population sizes and producing more sexual (transmissible) stages. However, supplemented hosts paid a higher cost of infection, and when keeping parasitaemia constant, they had lower haematocrit than control hosts. Parasites grown on control hosts were better able to exploit the subsequent hosts since they reached higher parasitaemia than Parasites originating from supplemented hosts. They were also more virulent since they induced higher mass and haematocrit loss. Our study highlights that Parasite Virulence can be shaped by the host nutritional status and that Parasite can adapt to the environment provided by their hosts, possibly through genetic selection.
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food availability and competition do not modulate the costs of plasmodium infection in dominant male canaries
Experimental Parasitology, 2013Co-Authors: Stephen Larcombe, Stéphane Cornet, Coraline Bichet, Bruno Faivre, Gabriele SorciAbstract:Understanding the different factors that may influence Parasite Virulence is of fundamental interest to ecologists and evolutionary biologists. It has recently been demonstrated that Parasite Virulence may occur partly through manipulation of host competitive ability. Differences in competitive ability associated with the social status (dominant or subordinate) of a host may determine the extent of this competition-mediated Parasite Virulence. We proposed that differences between subordinate and dominant birds in the physiological costs of infection may change depending on the level of competition in social groups. We observed flocks of domestic canaries to determine dominant or subordinate birds, and modified competition by providing restricted (high competition) or ad libitum food (low competition). Entire flocks were then infected with either the avian malaria Parasite, Plasmodium relictum or a control. Contrary to our predictions we found that the level of competition had no effect on the outcome of infection for dominant or subordinate birds. We found that dominant birds appeared to suffer greater infection mediated morbidity in both dietary treatments, with a higher and more sustained reduction in haematocrit, and higher parasitaemia, than subordinates. Our results show that dominance status in birds can certainly alter Parasite Virulence, though the links between food availability, competition, nutrition and Virulence are likely to be complex and multifaceted.
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Impact of host nutritional status on infection dynamics and Parasite Virulence in a bird‐malaria system
The Journal of animal ecology, 2013Co-Authors: Stéphane Cornet, Coraline Bichet, Stephen Larcombe, Bruno Faivre, Gabriele SorciAbstract:Host resources can drive the optimal Parasite exploitation strategy by offering a good or a poor environment to pathogens. Hosts living in resource-rich habitats might offer a favourable environment to developing Parasites because they provide a wealth of resources. However, hosts living in resource-rich habitats might afford a higher investment into costly immune defences providing an effective barrier against infection. Understanding how Parasites can adapt to hosts living in habitats of different quality is a major challenge in the light of the current human-driven environmental changes. We studied the role of nutritional resources as a source of phenotypic variation in host exploitation by the avian malaria Parasite Plasmodium relictum. We investigated how the nutritional status of birds altered Parasite within-host dynamics and Virulence, and how the interaction between past and current environments experienced by the Parasite accounts for the variation in the infection dynamics. Experimentally infected canaries were allocated to control or supplemented diets. Plasmodium Parasites experiencing the two different environments were subsequently transmitted in a full-factorial design to new hosts reared under similar control or supplemented diets. Food supplementation was effective since supplemented hosts gained body mass during a 15-day period that preceded the infection. Host nutrition had strong effects on infection dynamics and Parasite Virulence. Overall, Parasites were more successful in control nonsupplemented birds, reaching larger population sizes and producing more sexual (transmissible) stages. However, supplemented hosts paid a higher cost of infection, and when keeping parasitaemia constant, they had lower haematocrit than control hosts. Parasites grown on control hosts were better able to exploit the subsequent hosts since they reached higher parasitaemia than Parasites originating from supplemented hosts. They were also more virulent since they induced higher mass and haematocrit loss. Our study highlights that Parasite Virulence can be shaped by the host nutritional status and that Parasite can adapt to the environment provided by their hosts, possibly through genetic selection.
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Social interactions modulate the Virulence of avian malaria infection.
International journal for parasitology, 2013Co-Authors: Stephen Larcombe, Bruno Faivre, Stéphanie Bedhomme, Stéphane Garnier, Elise Cellier-holzem, Gabriele SorciAbstract:There is an increasing understanding of the context-dependent nature of Parasite Virulence. Variation in Parasite Virulence can occur when infected individuals compete with conspecifics that vary in infection status; Virulence may be higher when competing with uninfected competitors. In vertebrates with social hierarchies, we propose that these competition-mediated costs of infection may also vary with social status. Dominant individuals have greater competitive ability than competing subordinates, and consequently may pay a lower prevalence-mediated cost of infection. In this study we investigated whether costs of malarial infection were affected by the occurrence of the Parasite in competitors and social status in domestic canaries (Serinus canaria). We predicted that infected subordinates competing with non-infected dominants would pay higher costs than infected subordinates competing with infected dominants. We also predicted that these occurrence-mediated costs of infection would be ameliorated in infected dominant birds. We found that social status and the occurrence of Parasites in competitors significantly interacted to change haematocrit in infected birds. Namely, subordinate and dominant infected birds differed in haematocrit depending on the infection status of their competitors. However, in contrast to our prediction, dominants fared better with infected subordinates, whereas subordinates fared better with uninfected dominants. Moreover, we found additional effects of Parasite occurrence on mortality in canaries. Ultimately, we provide evidence for costs of parasitism mediated by social rank and the occurrence of Parasites in competitors in a vertebrate species. This has important implications for our understanding of the evolutionary processes that shape Parasite Virulence and group living.
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Parasite Virulence when the infection reduces the host immune response.
Proceedings of the Royal Society B: Biological Sciences, 2010Co-Authors: Stéphane Cornet, Gabriele SorciAbstract:Parasite infections often induce a reduction in host immune response either because of a direct manipulation of the immune system by the Parasite or because of energy depletion. Although infection-induced immunodepression can favour the establishment of the Parasite within the host, a too severe immunodepression may increase the risk of infection with opportunistic pathogens, stopping the period over which the Parasite can be transmitted to other hosts. Here, we explore how the risk of contracting opportunistic diseases affects the survival of the amphipod Gammarus pulex infected by the acanthocephalan Pomphorhynchus laevis. Previous work with this system has shown that upon infection, G. pulex has a substantially reduced immune response. Non-infected and P. laevis-infected hosts were maintained either in control or in micro-organism-enriched water, so as to vary the risk of encountering opportunistic pathogens. As predicted, we found that host mortality was exacerbated when infected gammarids were maintained in micro-organism-enriched water compared with clean, control water; whereas for non-infected gammarids, living in micro-organism-enriched water only moderately increased the risk of mortality. These results show that the Virulence of Parasites that reduce the host immune response is an environmentally sensitive trait that depends on the concomitant risk for the host of contracting opportunistic diseases. This extra source of host mortality probably represents a cost for P. laevis, and we tentatively predict that the optimal level of Parasite exploitation should depend on environmental conditions.
Andrew F Read - One of the best experts on this subject based on the ideXlab platform.
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Experimental manipulation of immune-mediated disease and its fitness costs for rodent malaria Parasites.
BMC evolutionary biology, 2008Co-Authors: Gráinne H. Long, Andrew F Read, Brian H. K. Chan, Judith E. Allen, Andrea L. GrahamAbstract:Background Explaining Parasite Virulence (harm to the host) represents a major challenge for evolutionary and biomedical scientists alike. Most theoretical models of Virulence evolution assume that Virulence arises as a direct consequence of host exploitation, the process whereby Parasites convert host resources into transmission opportunities. However, infection-induced disease can be immune-mediated (immunopathology). Little is known about how immunopathology affects Parasite fitness, or how it will affect the evolution of Parasite Virulence. Here we studied the effects of immunopathology on infection-induced host mortality rate and lifetime transmission potential – key components of Parasite fitness – using the rodent malaria model, Plasmodium chabaudi chabaudi.
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Evolution of Parasite Virulence when host responses cause disease
Proceedings. Biological sciences, 2007Co-Authors: Troy Day, Andrea L. Graham, Andrew F ReadAbstract:The trade-off hypothesis of Virulence evolution rests on the assumption that infection-induced mortality is a consequence of host exploitation by Parasites. This hypothesis lies at the heart of many empirical and theoretical studies of Virulence evolution, despite growing evidence that infection-induced mortality is very often a by-product of host immune responses. We extend the theoretical framework of the trade-off hypothesis to incorporate such immunopathology and explore how this detrimental aspect of host defence mechanisms affects the evolution of pathogen exploitation and hence infection-induced mortality. We argue that there are qualitatively different ways in which immunopathology can arise and suggest ways in which empirical studies can tease apart these effects. We show that immunopathology can cause infection-induced mortality to increase or decrease as a result of pathogen evolution, depending on how it covaries with pathogen exploitation strategies and with Parasite killing by hosts. Immunopathology is thus an important determinant of whether public and animal health programmes will drive evolution in a clinically beneficial or detrimental direction. Immunopathology complicates our understanding of disease evolution, but can nevertheless be readily accounted for within the framework of the trade-off hypothesis.
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Virulence and competitive ability in genetically diverse malaria infections
Proceedings of the National Academy of Sciences of the United States of America, 2005Co-Authors: Jacobus C De Roode, Brian H. K. Chan, Riccardo Pansini, Sandra Cheesman, Michelle E. H. Helinski, Silvie Huijben, Andrew R. Wargo, Andrew Stuart Bell, David Walliker, Andrew F ReadAbstract:Explaining Parasite Virulence is a great challenge for evolutionary biology. Intuitively, Parasites that depend on their hosts for their survival should be benign to their hosts, yet many Parasites cause harm. One explanation for this is that within-host competition favors Virulence, with more virulent strains having a competitive advantage in genetically diverse infections. This idea, which is well supported in theory, remains untested empirically. Here we provide evidence that within-host competition does indeed select for high Parasite Virulence. We examine the rodent malaria Plasmodium chabaudi in laboratory mice, a Parasite–host system in which Virulence can be easily monitored and competing strains quantified by using strain-specific real-time PCR. As predicted, we found a strong relationship between Parasite Virulence and competitive ability, so that more virulent strains have a competitive advantage in mixed-strain infections. In transmission experiments, we found that the strain composition of the Parasite populations in mosquitoes was directly correlated with the composition of the blood-stage Parasite population. Thus, the outcome of within-host competition determined relative transmission success. Our results imply that within-host competition is a major factor driving the evolution of Virulence and can explain why many Parasites harm their hosts.
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Genetic and environmental determinants of malaria Parasite Virulence in mosquitoes
Proceedings. Biological sciences, 2002Co-Authors: Heather M. Ferguson, Andrew F ReadAbstract:Models of malaria epidemiology and evolution are frequently based on the assumption that vector-parasitic associations are benign. Implicit in this assumption is the supposition that all Plasmodium Parasites have an equal and neutral effect on vector survival, and thus that there is no Parasite genetic variation for vector Virulence. While some data support the assumption of aVirulence, there has been no examination of the impact of Parasite genetic diversity. We conducted a laboratory study with the rodent malaria Parasite, Plasmodium chabaudi and the vector, Anopheles stephensi, to determine whether mosquito mortality varied with Parasite genotype (CR and ER clones), infection diversity (single versus mixed genotype) and nutrient availability. Vector mortality varied significantly between Parasite genotypes, but the rank order of Virulence depended on environmental conditions. In standard conditions, mixed genotype infections were the most virulent but when glucose water was limited, mortality was highest in mosquitoes infected with CR. These genotype-by-environment interactions were repeatable across two experiments and could not be explained by variation in anaemia, gametocytaemia, blood meal size, mosquito body size, infection rate or oocyst burden. Variation in the genetic and environmental determinants of Virulence may explain conflicting accounts of Plasmodium pathogenicity to mosquitoes in the malaria literature.
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genetic relationships between Parasite Virulence and transmission in the rodent malaria plasmodium chabaudi
Evolution, 1999Co-Authors: Margaret J Mackinnon, Andrew F ReadAbstract:Many Parasites evolve to become virulent rather than benign mutualists. One of the major theoretical models of Parasite Virulence postulates that this is because rapid within-host replication rates are necessary for successful transmission (Parasite fitness) and that Virulence (damage to the host) is an unavoidable consequence of this rapid replication. Two fundamental assumptions underlying this so-called evolutionary trade-off model have rarely been tested empirically: (1) that higher replication rates lead to higher levels of Virulence; and (2) that higher replication rates lead to higher transmission. Both of these relationships must have a genetic basis for this evolutionary hypothesis to be relevant. These assumptions were tested in the rodent malaria Parasite, Plasmodium chabaudi, by examining genetic relationships between Virulence and transmission traits across a population of eight Parasite clones isolated from the wild. Each clone was injected into groups of inbred mice in a controlled laboratory environment, and replication rate (measured by maximum asexual Parasitemia), Virulence (measured by live-weight loss and degree of anemia in the mouse), and transmission (measured by density of sexual forms, gametocytes, in the blood and proportion of mosquitoes infected after taking a blood-meal from the mouse) were assessed. It was found that clones differed widely in these traits and these clone differences were repeatable over successive blood passages. Virulence traits were strongly phenotypically and genetically (i.e., across clones) correlated to maximum Parasitemia thus supporting the first assumption that rapid replication causes higher Virulence. Transmission traits were also positively phenotyp- ically and genetically correlated to Parasitemia, which supports the second assumption that rapid replication leads to higher transmission. Thus, two assumptions of the Parasite-centered trade-off model of the evolution of Virulence were shown to be justified in malaria Parasites.
Jean Langhorne - One of the best experts on this subject based on the ideXlab platform.
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vector transmission regulates immune control of plasmodium Virulence
Nature, 2013Co-Authors: Philip J Spence, William Jarra, Prisca Levy, Adam J Reid, Lia Chappell, Thibaut Brugat, Mandy Sanders, Matthew Berriman, Jean LanghorneAbstract:Serial passage of the malaria Parasite through rodents, primates or human hosts increases Parasite Virulence, suggesting that vector transmission regulates Virulence, although direct evidence for this has been lacking; mosquito transmission is shown here to intrinsically modify asexual blood-stage Plasmodium chabaudi chabaudi, which elicits altered host immune responses that, in turn, modify disease severity. Serial passage of the malaria Parasite through rodents, primates or human hosts increases Parasite Virulence. The implication is that vector transmission modifies Virulence, but direct evidence for this has been lacking. Here Jean Langhorne and colleagues demonstrate that mosquito transmission intrinsically modifies asexual blood-stage Plasmodium chabaudi chabaudi, which in turn elicits altered host immune responses. The authors suggest that modification of Plasmodium in the mosquito vector may be the result of a combination of regulatory processes acting at multiple stages of the Parasite life cycle. This work highlights the importance of the interactions between the vector, Parasite and mammalian immune system in the pathogenesis of malaria. A thorough understanding of this triangular relationship may offer new options for vaccine design. Defining mechanisms by which Plasmodium Virulence is regulated is central to understanding the pathogenesis of human malaria. Serial blood passage of Plasmodium through rodents1,2,3, primates4 or humans5 increases Parasite Virulence, suggesting that vector transmission regulates Plasmodium Virulence within the mammalian host. In agreement, disease severity can be modified by vector transmission6,7,8, which is assumed to ‘reset’ Plasmodium to its original character3. However, direct evidence that vector transmission regulates Plasmodium Virulence is lacking. Here we use mosquito transmission of serially blood passaged (SBP) Plasmodium chabaudi chabaudi9 to interrogate regulation of Parasite Virulence. Analysis of SBP P. c. chabaudi before and after mosquito transmission demonstrates that vector transmission intrinsically modifies the asexual blood-stage Parasite, which in turn modifies the elicited mammalian immune response, which in turn attenuates Parasite growth and associated pathology. Attenuated Parasite Virulence associates with modified expression of the pir multi-gene family. Vector transmission of Plasmodium therefore regulates gene expression of probable variant antigens in the erythrocytic cycle, modifies the elicited mammalian immune response, and thus regulates Parasite Virulence. These results place the mosquito at the centre of our efforts to dissect mechanisms of protective immunity to malaria for the development of an effective vaccine.
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vector transmission regulates immune control of plasmodium Virulence
Nature, 2013Co-Authors: Philip J Spence, William Jarra, Prisca Levy, Adam J Reid, Lia Chappell, Thibaut Brugat, Mandy Sanders, Matthew Berriman, Jean LanghorneAbstract:Serial passage of the malaria Parasite through rodents, primates or human hosts increases Parasite Virulence, suggesting that vector transmission regulates Virulence, although direct evidence for this has been lacking; mosquito transmission is shown here to intrinsically modify asexual blood-stage Plasmodium chabaudi chabaudi, which elicits altered host immune responses that, in turn, modify disease severity.
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Mosquito transmission of the rodent malaria Parasite Plasmodium chabaudi
Malaria journal, 2012Co-Authors: Philip J Spence, William Jarra, Prisca Levy, Wiebke Nahrendorf, Jean LanghorneAbstract:Background Serial blood passage of Plasmodium increases Virulence, whilst mosquito transmission inherently regulates Parasite Virulence within the mammalian host. It is, therefore, imperative that all aspects of experimental malaria research are studied in the context of the complete Plasmodium life cycle.
Sébastien Lion - One of the best experts on this subject based on the ideXlab platform.
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Beyond Mortality: Sterility As a Neglected Component of Parasite Virulence
PLoS pathogens, 2015Co-Authors: Jessica L. Abbate, Sarah Kada, Sébastien LionAbstract:Virulence is generally defined as the reduction in host fitness following infection by a Parasite (see Box 1 for glossary) [1]. In general, Parasite exploitation of host resources may reduce host survival (mortality Virulence), decrease host fecundity (sterility Virulence), or even have sub-lethal effects that disturb the way individuals interact within a community (morbidity) [2,3]. In fact, the Virulence of many Parasites involves a combination of these various effects (Box 2). In practice, however, Virulence is most often defined as disease-induced mortality [1, 4-6]. This is especially true in the theoretical literature, where the evolution of sterility Virulence, morbidity, and mixed strategies of host exploitation have received relatively little attention. While the focus on mortality effects has allowed for easy comparison between models and, thus, rapid advancement of the field, we ask whether these theoretical simplifications have led us to inadvertently minimize the evolutionary importance of host sterilization and secondary Virulence effects. As explicit theoretical work on morbidity is currently lacking (but see [7]), our aim in this Opinion piece is to discuss what is understood about sterility Virulence evolution, its adaptive potential, and the implications for Parasites that utilize a combination of host survival and reproductive resources.
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Superinfection and the coevolution of Parasite Virulence and host recovery
Journal of Evolutionary Biology, 2015Co-Authors: Sarah Kada, Sébastien LionAbstract:Parasite strategies of host exploitation may be affected by host defence strategies and multiple infections. In particular, within-host competition between multiple Parasite strains has been shown to select for higher Virulence. However, little is known on how multiple infections could affect the coevolution between host recovery and Parasite Virulence. Here, we extend a coevolutionary model introduced by van Baalen (Proc. R. Soc. B, 265, 1998, 317) to account for superinfection. When the susceptibility to superinfection is low, we recover van Baalen's results and show that there are two potential evolutionary endpoints: one with avirulent Parasites and poorly defended hosts, and another one with high Virulence and high recovery. However, when the susceptibility to superinfection is above a threshold, the only possible evolutionary outcome is one with high Virulence and high investment into defence. We also show that within-host competition may select for lower host recovery, as a consequence of selection for more virulent strains. We discuss how different Parasite and host strategies (superinfection facilitation, competitive exclusion) as well as demographic and environmental parameters, such as host fecundity or various costs of defence, may affect the interplay between multiple infections and host-Parasite coevolution. Our model shows the interplay between coevolutionary dynamics and multiple infections may be affected by crucial mechanistic or ecological details.
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Spatial structure, host heterogeneity and Parasite Virulence: implications for vaccine‐driven evolution
Ecology Letters, 2015Co-Authors: Yazmín Hananí Zurita‐gutiérrez, Sébastien LionAbstract:Natural host-Parasite interactions exhibit considerable variation in host quality, with profound consequences for disease ecology and evolution. For instance, treatments (such as vaccination) may select for more transmissible or virulent strains. Previous theory has addressed the ecological and evolutionary impact of host heterogeneity under the assumption that hosts and Parasites disperse globally. Here, we investigate the joint effects of host heterogeneity and local dispersal on the evolution of Parasite life-history traits. We first formalise a general theoretical framework combining variation in host quality and spatial structure. We then apply this model to the specific problem of Parasite evolution following vaccination. We show that, depending on the type of vaccine, spatial structure may select for higher or lower Virulence compared to the predictions of non-spatial theory. We discuss the implications of our results for disease management, and their broader fundamental relevance for other causes of host heterogeneity in nature.
Stéphane Cornet - One of the best experts on this subject based on the ideXlab platform.
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Impact of host nutritional status on infection dynamics and Parasite Virulence in a bird-malaria system.
Journal of Animal Ecology, 2014Co-Authors: Stéphane Cornet, Coraline Bichet, Stephen Larcombe, Bruno Faivre, Gabriele SorciAbstract:Host resources can drive the optimal Parasite exploitation strategy by offering a good or a poor environment to pathogens. Hosts living in resource-rich habitats might offer a favourable environment to developing Parasites because they provide a wealth of resources. However, hosts living in resource-rich habitats might afford a higher investment into costly immune defences providing an effective barrier against infection. Understanding how Parasites can adapt to hosts living in habitats of different quality is a major challenge in the light of the current human-driven environmental changes. We studied the role of nutritional resources as a source of phenotypic variation in host exploitation by the avian malaria Parasite Plasmodium relictum. We investigated how the nutritional status of birds altered Parasite within-host dynamics and Virulence, and how the interaction between past and current environments experienced by the Parasite accounts for the variation in the infection dynamics. Experimentally infected canaries were allocated to control or supplemented diets. Plasmodium Parasites experiencing the two different environments were subsequently transmitted in a full-factorial design to new hosts reared under similar control or supplemented diets. Food supplementation was effective since supplemented hosts gained body mass during a 15-day period that preceded the infection. Host nutrition had strong effects on infection dynamics and Parasite Virulence. Overall, Parasites were more successful in control nonsupplemented birds, reaching larger population sizes and producing more sexual (transmissible) stages. However, supplemented hosts paid a higher cost of infection, and when keeping parasitaemia constant, they had lower haematocrit than control hosts. Parasites grown on control hosts were better able to exploit the subsequent hosts since they reached higher parasitaemia than Parasites originating from supplemented hosts. They were also more virulent since they induced higher mass and haematocrit loss. Our study highlights that Parasite Virulence can be shaped by the host nutritional status and that Parasite can adapt to the environment provided by their hosts, possibly through genetic selection.
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food availability and competition do not modulate the costs of plasmodium infection in dominant male canaries
Experimental Parasitology, 2013Co-Authors: Stephen Larcombe, Stéphane Cornet, Coraline Bichet, Bruno Faivre, Gabriele SorciAbstract:Understanding the different factors that may influence Parasite Virulence is of fundamental interest to ecologists and evolutionary biologists. It has recently been demonstrated that Parasite Virulence may occur partly through manipulation of host competitive ability. Differences in competitive ability associated with the social status (dominant or subordinate) of a host may determine the extent of this competition-mediated Parasite Virulence. We proposed that differences between subordinate and dominant birds in the physiological costs of infection may change depending on the level of competition in social groups. We observed flocks of domestic canaries to determine dominant or subordinate birds, and modified competition by providing restricted (high competition) or ad libitum food (low competition). Entire flocks were then infected with either the avian malaria Parasite, Plasmodium relictum or a control. Contrary to our predictions we found that the level of competition had no effect on the outcome of infection for dominant or subordinate birds. We found that dominant birds appeared to suffer greater infection mediated morbidity in both dietary treatments, with a higher and more sustained reduction in haematocrit, and higher parasitaemia, than subordinates. Our results show that dominance status in birds can certainly alter Parasite Virulence, though the links between food availability, competition, nutrition and Virulence are likely to be complex and multifaceted.
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Impact of host nutritional status on infection dynamics and Parasite Virulence in a bird‐malaria system
The Journal of animal ecology, 2013Co-Authors: Stéphane Cornet, Coraline Bichet, Stephen Larcombe, Bruno Faivre, Gabriele SorciAbstract:Host resources can drive the optimal Parasite exploitation strategy by offering a good or a poor environment to pathogens. Hosts living in resource-rich habitats might offer a favourable environment to developing Parasites because they provide a wealth of resources. However, hosts living in resource-rich habitats might afford a higher investment into costly immune defences providing an effective barrier against infection. Understanding how Parasites can adapt to hosts living in habitats of different quality is a major challenge in the light of the current human-driven environmental changes. We studied the role of nutritional resources as a source of phenotypic variation in host exploitation by the avian malaria Parasite Plasmodium relictum. We investigated how the nutritional status of birds altered Parasite within-host dynamics and Virulence, and how the interaction between past and current environments experienced by the Parasite accounts for the variation in the infection dynamics. Experimentally infected canaries were allocated to control or supplemented diets. Plasmodium Parasites experiencing the two different environments were subsequently transmitted in a full-factorial design to new hosts reared under similar control or supplemented diets. Food supplementation was effective since supplemented hosts gained body mass during a 15-day period that preceded the infection. Host nutrition had strong effects on infection dynamics and Parasite Virulence. Overall, Parasites were more successful in control nonsupplemented birds, reaching larger population sizes and producing more sexual (transmissible) stages. However, supplemented hosts paid a higher cost of infection, and when keeping parasitaemia constant, they had lower haematocrit than control hosts. Parasites grown on control hosts were better able to exploit the subsequent hosts since they reached higher parasitaemia than Parasites originating from supplemented hosts. They were also more virulent since they induced higher mass and haematocrit loss. Our study highlights that Parasite Virulence can be shaped by the host nutritional status and that Parasite can adapt to the environment provided by their hosts, possibly through genetic selection.
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Parasite Virulence when the infection reduces the host immune response.
Proceedings of the Royal Society B: Biological Sciences, 2010Co-Authors: Stéphane Cornet, Gabriele SorciAbstract:Parasite infections often induce a reduction in host immune response either because of a direct manipulation of the immune system by the Parasite or because of energy depletion. Although infection-induced immunodepression can favour the establishment of the Parasite within the host, a too severe immunodepression may increase the risk of infection with opportunistic pathogens, stopping the period over which the Parasite can be transmitted to other hosts. Here, we explore how the risk of contracting opportunistic diseases affects the survival of the amphipod Gammarus pulex infected by the acanthocephalan Pomphorhynchus laevis. Previous work with this system has shown that upon infection, G. pulex has a substantially reduced immune response. Non-infected and P. laevis-infected hosts were maintained either in control or in micro-organism-enriched water, so as to vary the risk of encountering opportunistic pathogens. As predicted, we found that host mortality was exacerbated when infected gammarids were maintained in micro-organism-enriched water compared with clean, control water; whereas for non-infected gammarids, living in micro-organism-enriched water only moderately increased the risk of mortality. These results show that the Virulence of Parasites that reduce the host immune response is an environmentally sensitive trait that depends on the concomitant risk for the host of contracting opportunistic diseases. This extra source of host mortality probably represents a cost for P. laevis, and we tentatively predict that the optimal level of Parasite exploitation should depend on environmental conditions.
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Variation and covariation in infectivity, Virulence and immunodepression in the host-Parasite association Gammarus pulex-Pomphorhynchus laevis.
Proceedings of the Royal Society B: Biological Sciences, 2009Co-Authors: Stéphane Cornet, Nathalie Franceschi, Loïc Bollache, Thierry Rigaud, Gabriele SorciAbstract:Parasites often manipulate host immunity for their own benefit, either by exacerbating or suppressing the immune response and this may directly affect the expression of Parasite Virulence. However, genetic variation in immunodepression, which is a prerequisite to its evolution, and the relationship between immunodepression and Virulence, have rarely been studied. Here, we investigated the variation among sibships of the acanthocephalan Parasite, Pomphorhynchus laevis, in infecting and in immunodepressing its amphipod host, Gammarus pulex. We also assessed the covariation between infectivity, Parasite-induced immune depression and host mortality (Parasite Virulence). We found that infectivity, the intensity of immunodepression and Virulence were variable among Parasite sibships. Infectivity and the level of immunodepression were not correlated across Parasite sibships. Whereas infectivity was unrelated to host mortality, we found that gammarids that were exposed to the Parasite sibships that immunodepressed their hosts the most survived better. This positive covariation between host survival and immunodepression suggests that gammarids exposed to the less immunodepressive Parasites could suffer from damage imposed by a higher activity of the phenoloxidase.
