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63 results for “infection costs”
Reciprocal costs of infection and reproduction in D. melanogaster
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Experimental infection of bumble bees with honey bee associated viruses: no direct fitness costs but potential future threats to novel wild bee hosts
<p>Pathogen spill-over represents an important cause of biodiversity decline. For wild bee species such as bumble bees, many of which are in decline, correlational data point toward viral spill-over from naged honey bees as a potential cause. Yet impacts of honey bee viruses on wild bees are rarely evaluated. Here, in a series of highly controlled laboratory infection assays with well characterised viral inocula, we show that three viral types isolated from honey bees (<i>Deformed wing virus</i> genotype A, <i>Deformed wing virus</i> genotype B and <i>Black queen cell virus</i>) readily replicate within hosts of the bumble bee <i>Bombus terrestris</i>. Impacts of these honey bee-derived viruses – either injected or fed – on the mortality of <i>B. terrestris </i>workers were, however, negligible and likely dependent on host condition. Our results highlight the potential threat of viral spill-over from honey bees to novel wild bee species, though they also underscore the importance of additional studies on this and other non- bee species under field-realistic conditions to evaluate whether pathogen spill-over has a negative impact on wild bee individuals and population fitness.</p>
Data from: Social living simultaneously increases infection risk and decreases the cost of infection
Elevated parasite infection risk is considered to be a near universal cost of social living. However, living in groups may also provide benefits that reduce the negative impacts of infection. These potential 'tolerance' benefits of living socially are theoretically possible, but have rarely been described. In this study, we used an anthelmintic treatment experiment in wild Grant's gazelles (Nanger granti), who are commonly infected with gastrointestinal nematodes (GIN), to show that social living confers both costs and benefits related to GIN parasitism. We show that although larger group size increases GIN infection risk, a key cost of GIN infection – the suppression of food intake − is simultaneously moderated by living in larger groups. Our findings help illuminate the complex role parasites play in the evolution of host social behavior.
Data from: Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection
Individual variation in parasite defenses, such as resistance and tolerance, can underlie heterogeneity in fitness and could influence disease transmission dynamics. Glucocorticoid hormone concentrations often change in response to fluctuating environmental conditions and mediate changes in immune function, resource allocation, and tissue repair. Thus, changes in glucocorticoid hormone concentrations might mediate individual variation in investment in resistance versus tolerance. In this study, we experimentally increased glucocorticoid concentrations in red-winged blackbirds (Agelaius phoeniceus) that were naturally infected with haemosporidian parasites and assessed changes in resistance and tolerance of infection. Glucocorticoid treatment increased burdens of Plasmodium, the parasite causing avian malaria, but only in the absence of co-infection with another Haemosporidian, Haemoproteus. Thus, glucocorticoids might reduce resistance to infection, but co-infection can mitigate the negative consequences of increased hormone concentrations. Glucocorticoid treatment also decreased tolerance of infection. We found no evidence that the inflammatory immune response or rate of red blood cell production underlie the effects of glucocorticoids on resistance and tolerance. Our findings suggest that exogenous glucocorticoids can increase the costs of haemosporidian infections by both increasing parasite numbers and reducing an individual's ability to cope with infection. These effects could scale up to impact populations of both host and parasite.
Data from: Pharmaceutical pollution alters the cost of bacterial infection and its relationship to pathogen load
<p><span>The relationship between pathogen proliferation and the cost of infection experienced by a host drives the ecology and evolution of host-pathogen dynamics. While environmental factors can shape this relationship, there is currently limited knowledge on the consequences of emerging contaminants, such as pharmaceutical pollutants, for the commonly observed trade-off between a pathogen's growth within the host and the damage it causes, termed its virulence. Here, we investigated how exposure to fluoxetine (Prozac), a commonly detected psychoactive pollutant, could alter this key relationship using the water flea <em>Daphnia magna</em> and its bacterial pathogen <em>Pasteuria ramosa </em>as a model system. Across a variety of fluoxetine concentrations, we found that fluoxetine shaped the damage a pathogen caused, such as the reduction in fecundity or intrinsic growth experienced by infected individuals, but with minimal change in average pathogen spore loads. Instead, fluoxetine modified the relationship between the degree of pathogen proliferation and its virulence, with both the strength of this trade-off and the component of host fitness most affected varying by fluoxetine concentration and host genotype. Our study underscores the potential for pharmaceutical pollution to modify the virulence of an invading pathogen, as well as the fundamental trade-off between host and pathogen fitness, even at the trace amounts increasingly found in natural waterways. </span></p>
Data from: Differential host responses to parasitism shape divergent fitness costs of infection
Fitness costs of infection are fundamental to understanding the ecology and evolution of host-parasite interactions. However, these costs, and particularly their underlying mechanisms, are challenging to evaluate in wild populations. Here, we quantified total and species-specific costs of gastrointestinal worms on African buffalo, by combining the power of an anthelmintic treatment experiment that perturbed the entire worm community with a longitudinal study that tracked the two most dominant community members. Reducing all worms improved buffalo body condition, which was strongly associated with increases in survival and reproduction. Species-specific analyses revealed that condition-mediated fitness costs of infection differed between parasite species. Hosts that gained the blood-sucking worm Haemonchus, lost condition, and this loss may have been mediated by reductions in forage intake. Hosts that resisted Haemonchus by elevating IL-4 and eosinophil immune defences were able to reduce their parasite loads and gain back condition. Conversely, hosts that gained Cooperia, a less pathogenic worm, gained condition and had higher survival and reproductive success. Elevating immune defences had no effect on Cooperia abundance. Coupled with the positive relationship observed between Cooperia and host condition, our data suggest that hosts might benefit from tolerating Cooperia rather than incurring the costs of resistance. Overall, our study reveals that differential host responses to parasites play a key role in mediating the costs of infection.
Data from: Differential host responses to parasitism shape divergent fitness costs of infection
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Data from: Pharmaceutical pollution alters the cost of bacterial infection and its relationship to pathogen load
Open the record for dataset details and reuse information.
Data from: Social living simultaneously increases infection risk and decreases the cost of infection
Open the record for dataset details and reuse information.
Experimental infection of bumble bees with honey bee associated viruses: no direct fitness costs but potential future threats to novel wild bee hosts
Open the record for dataset details and reuse information.
Data from: Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection
Open the record for dataset details and reuse information.
Data from: Population-specific effect of Wolbachia on the cost of fungal infection in spider mites
<p>Many studies have revealed the ability of the endosymbiotic bacterium <i>Wolbachia </i>to protect its arthropod hosts against diverse pathogens. However, as <i>Wolbachia </i>may also increase the susceptibility of its host to infection, predicting the outcome of a particular <i>Wolbachia</i>-host-pathogen interaction remains elusive. Yet, understanding such interactions and their eco-evolutionary consequences is crucial for disease and pest control strategies. Moreover, how natural <i>Wolbachia </i>infections affectartificially introduced pathogens for biocontrol has never been studied. <i>Tetranychus urticae </i>spider mites are herbivorous crop pests, causing severe damage on numerous economically important crops. Due to the rapid evolution of pesticide resistance, biological control strategies using entomopathogenic fungi are being developed. However, although spider mites are infected with various <i>Wolbachia </i>strains worldwide, whether this endosymbiont protects them from fungi is as yet unknown. Here, we compared the survival of two populations, treated with antibiotics or naturally harbouring different <i>Wolbachia </i>strains, after exposure to the fungal biocontrol agents <i>Metarhizium brunneum </i>and <i>Beauveria bassiana</i>. To control for potential effects of the bacterial community of spider mites, we also compared the susceptibility of two populations naturally uninfected by <i>Wolbachia</i>, treated with antibiotics or not. In one population, <i>Wolbachia</i>-infected mites had a better survival than uninfected ones in absence of fungi but not in their presence, whereas in the other population <i>Wolbachia </i>increased the mortality induced by <i>B. bassiana</i>. In one naturally <i>Wolbachia</i>-uninfected populations, the antibiotic treatment increased the susceptibility of spider mites to <i>M. brunneum</i>, but it had no effect in the other treatments. These results suggest that natural <i>Wolbachia </i>infections may not hamper and may even improve the success of biological control using entomopathogenic fungi. However, they also draw caution on the generalization of such effects, given the complexity of within-host pathogens interaction and the potential eco-evolutionary consequences of the use of biocontrol agents for <i>Wolbachia</i>-host associations.</p>
Data from: Indirect effects of parasitism: costs of infection to other individuals can be greater than direct costs borne by the host
Parasitic infection has a direct physiological cost to hosts but may also alter how hosts interact with other individuals in their environment. Such indirect effects may alter both host fitness and the fitness of other individuals in the host's social network, yet the relative impact of direct and indirect effects of infection are rarely quantified. During reproduction, a host's social environment includes family members who may be in conflict over resource allocation. In such situations, infection may alter how resources are allocated, thereby redistributing the costs of parasitism between individuals. Here, we experimentally reduce parasite burdens of parent and/or nestling European shags (Phalacrocorax aristotelis) infected with Contracaecum nematodes in a factorial design, then simultaneously measure the impact of an individual's infection on all family members. We found no direct effect of infection on parent or offspring traits but indirect effects were detected in all group members, with both immediate effects (mass change and survival) and longer-term effects (timing of parents' subsequent breeding). Our results show that parasite infection can have a major impact on individuals other than the host, suggesting that the effect of parasites on population processes may be greater than previously thought.
Data from: The jack-of-all-trades is master of none: a pathogen's ability to infect a greater number of host genotypes comes at a cost of delayed reproduction.
A trade-off between a pathogen's ability to infect many hosts and its reproductive capacity on each host genotype is predicted to limit the evolution of an expanded host range, yet few empirical results provide evidence for the magnitude of such trade-offs. Here, we test the hypothesis for a trade-off between the number of host genotypes that a fungal pathogen can infect (host genotype range) and its reproductive capacity on susceptible plant hosts. We utilized strains of the oat crown rust fungus that carried widely varying numbers of virulence (avr) alleles known to determine host genotype range. We quantified total spore production and the expression of four pathogen life history stages: infection efficiency, time until reproduction, pustule size, and spore production per pustule. In support of the trade-off hypothesis, we found that virulence level, the number of avr alleles per pathogen strain, was correlated with significant delays in the onset of reproduction and with smaller pustule sizes. Modeling from our results, we conclude that trade-offs have the capacity to constrain the evolution of host genotype range in local populations. In contrast, long term trends in virulence level suggests that the continued deployment of resistant host lines over wide regions of the USA has generated selection for increased host genotype range.
Data from: Evolution of Drosophila resistance against different pathogens and infection routes entails no detectable maintenance costs
Pathogens exert a strong selective pressure on hosts, entailing host adaptation to infection. This adaptation often affects negatively other fitness-related traits. Such trade-offs may underlie the maintenance of genetic diversity for pathogen resistance. Trade-offs can be tested with experimental evolution of host populations adapting to parasites, using two approaches: (1) measuring changes in immunocompetence in relaxed-selection lines and (2) comparing life-history traits of evolved and control lines in pathogen-free environments. Here, we used both approaches to examine trade-offs in Drosophila melanogaster populations evolving for over 30 generations under infection with Drosophila C Virus or the bacterium Pseudomonas entomophila, the latter through different routes. We find that resistance is maintained after up to 30 generations of relaxed selection. Moreover, no differences in several classical life-history traits between control and evolved populations were found in pathogen-free environments, even under stresses such as desiccation, nutrient limitation, and high densities. Hence, we did not detect any maintenance costs associated with resistance to pathogens. We hypothesize that extremely high selection pressures commonly used lead to the disproportionate expression of costs relative to their actual occurrence in natural systems. Still, the maintenance of genetic variation for pathogen resistance calls for an explanation.
Data from: Evolutionary costs and benefits of infection with diverse strains of Spiroplasma in pea aphids
The heritable endosymbiont Spiroplasma infects many insects and has repeatedly evolved the ability to protect its hosts against different parasites. Defenses do not come for free to the host, and theory predicts that more costly symbionts need to provide stronger benefits to persist in host populations. We investigated the costs and benefits of Spiroplasma infections in pea aphids (Acyrthosiphon pisum), testing 12 bacterial strains from three different clades. Virtually all strains decreased aphid lifespan and reproduction, but only two had a (weak) protective effect against the parasitoid Aphidius ervi, an important natural enemy of pea aphids. Spiroplasma induced fitness costs were variable, with strains from the most slowly evolving clade reaching higher titers and curtailing aphid lifespan more strongly than other strains. Some Spiroplasma strains shared their host with a second endosymbiont, Regiella insecticola. Although the result of an unfortunate handling error, these co-infections proved instructive, because they showed that the cost of infection with Spiroplasma may be attenuated in the presence of Regiella. These results suggest that mechanisms other than protection against A. ervi maintain pea aphid infections with diverse strains of Spiroplasma, and that studying them in isolation will not provide a complete picture of their effects on host fitness.
Data from: The costs of parasite infection: effects of removing lungworms on performance, growth and survival of free-ranging cane toads
1.Most research on the effects of parasites on their hosts has focused on the parasites of mammals or birds (especially, domesticated taxa) rather than systems in which the hosts are ectothermic wildlife species. 2.We used experimental methods (antihelminthic drugs) to quantify the effects of lungworms (Rhabdias pseudosphaerocephala) on their anuran hosts, the invasive cane toad (Rhinella marina). 3.In captivity, eradicating lungworms enhanced toad activity (measures of boldness and level of spontaneous activity), performance (locomotor speed, climbing ability), and foraging success (feeding rate). 4.In free-ranging toads (n = 123) at a site in tropical Australia, eradicating lungworm infection increased rates of host survival by 8%, movement by 20%, growth by 28% and elaboration of male secondary sexual characteristics by 30%. The presence of the lungworm thus has a substantial negative effect on fitness-related traits of the host. 5.Given their long shared evolutionary history and the mild inflammatory and immune response elicited by the parasite in the host, the magnitude of the effects of parasite removal were surprising. Parasites may impose hidden costs, related to modification of host behaviour or metabolism. Experimental removal of parasites can be a useful means of quantifying costs of infection.
Bacterial supergroup specific 'Cost' of Wolbachia infections in Nasonia vitripennis
<p><i>Wolbachia </i>is known to alter host reproductive biology for its benefit. It also introduces both positive and negative fitness effects in the vast majority of its host population. Here we describe the effect of maintenance of <i>Wolbachia</i> infection in the parasitoid host <i>Nasonia</i> <i>vitripennis</i>. We have separated the two <i>Wolbachia</i> infections in <i>N. vitripennis</i> to get single lines of <i>Wolbachia </i>supergroup A and supergroup B. We compare the effect of <i>Wolbachia</i> infection on various life-history traits between uninfected, single A, single B, and double infection strains. Contrary to the previous reports, our results suggest that there is a "cost" associated with the maintenance of <i>Wolbachia</i> infection where traits like progeny family size, fecundity, and longevity in females, while the number of copulations performed by males is compromised in <i>Wolbachia</i> infected strains. The double infection of <i>Wolbachia</i> has more detrimental impacts on the host as compared to single infections. The findings of this study raise important questions on the mechanism of survival and maintenance of these reproductive parasites in arthropod hosts.</p>
Evaluation of Cost of Nosocomial Infection
ClinicalTrials.gov study NCT03253640. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
48 Hours After Surgery Shower Patient's Wound Infection Rate, Pain Score, Patient Satisfaction and Cost.
ClinicalTrials.gov study NCT01846598. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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