Fitness Costs Of Infection Research Articles

Laser-based killing of a macroparasite inside its live invertebrate host

Whether host phenotypic alterations induced by parasites are reversible or not is a core issue to understand underlying mechanisms as well as the fitness costs of infection and recovery to the host. Clearing infection is an essential step to address this issue, which turns out to be challenging with endoparasites of large size relative to that of their host. Here, we took advantage of the lethality, contactless and versatility of high-energy laser beam to design such tool, using thorny-headed worms and their amphipod intermediate host as a model system. We show that laser-based de-parasitization can be achieved using blue laser targeting carotenoid pigments in Polymorphus minutus but not in the larger and less pigmented Pomphorhynchus tereticollis. Using DNA degradation to establish parasite death, we found that 80% P. minutus died from within-host laser exposure. Survival rate of infected gammarids to laser treatment was higher than uninfected ones. The failure to kill P. tereticollis was also observed with nanosecond-green laser, an alternative laser source targeting lipid. We discuss the possible causes of amphipod death following parasite treatment and highlight the perspectives that this technology offers.

Reproductive consequences of transient pathogen exposure across host genotypes and generations.

To maximize fitness upon pathogenic infection, host organisms might reallocate energy and resources among life‐history traits, such as reproduction and defense. The fitness costs of infection can result from both immune upregulation and direct pathogen exploitation. The extent to which these costs, separately and together, vary by host genotype and across generations is unknown. We attempted to disentangle these costs by transiently exposing wild isolates and a lab‐domesticated strain of Caenorhabditis elegans nematodes to the pathogen Staphylococcus aureus, using exposure to heat‐killed pathogens to distinguish costs due to immune upregulation and pathogen exploitation. We found that host nematodes exhibit a short‐term delay in offspring production when exposed to live and heat‐killed pathogen, but their lifetime fecundity (total offspring produced) recovered to control levels. We also found genetic variation between host isolates for both cumulative offspring production and magnitude of fitness costs. We further investigated whether there were maternal pathogen exposure costs (or benefits) to offspring and revealed a positive correlation between the magnitude of the pathogen‐induced delay in the parent's first day of reproduction and the cost to offspring population growth. Our findings highlight the capacity for hosts to recover fecundity after transient exposure to a pathogen.

Disease Tolerance as an Inherent Component of Immunity.

Pathogenic organisms exert a negative impact on host health, revealed by the clinical signs of infectious diseases. Immunity limits the severity of infectious diseases through resistance mechanisms that sense and target pathogens for containment, killing, or expulsion. These resistance mechanisms are viewed as the prevailing function of immunity. Under pathophysiologic conditions, however, immunity arises in response to infections that carry health and fitness costs to the host. Therefore, additional defense mechanisms are required to limit these costs, before immunity becomes operational as well as thereafter to avoid immunopathology. These are tissue damage control mechanisms that adjust the metabolic output of host tissues to different forms of stress and damage associated with infection. Disease tolerance is the term used to define this defense strategy, which does not exert a direct impact on pathogens but is essential to limit the health and fitness costs of infection. Under this argument, we propose that disease tolerance is an inherent component of immunity.

Parasite insight: assessing fitness costs, infection risks and foraging benefits relating to gastrointestinal nematodes in wild mammalian herbivores.

Mammalian herbivores are typically infected by parasitic nematodes, which are acquired through direct, faecal-oral transmission. These parasites can cause significant production losses in domestic livestock, but much less is known about impacts on wild mammalian hosts. We review three elements of parasitism from the host's perspective: fitness costs of infection, risks of infection during foraging and benefits of nutritious pasture. The majority of wildlife studies have been observational, but experimental manipulation is increasing. Treatment with anthelmintics to manipulate parasite load has revealed varied impacts of parasites on fitness variables across host species, but has not produced consistent evidence for parasite-induced anorexia or impaired body condition. Some experimental studies of infection risk have manipulated faecal contamination and detected faecal avoidance by hosts. Only two field studies have explored the trade-off between infection risk and nutritional benefit generated by avoidance of contaminated patches. Overall, field studies of costs, risks and benefits of the host-parasite relationship are limited and few have examined more than one of these elements. Parasitism has much in common with predation, and future insights into anti-parasite responses by wild hosts could be gained from the conceptual and technical developments in research on anti-predator behaviour.This article is part of the Theo Murphy meeting issue 'Evolution of pathogen and parasite avoidance behaviours'.

Fitness costs of infection with Serratia symbiotica are associated with greater susceptibility to insecticides in the pea aphid Acyrthosiphon pisum.

Aphids are agricultural pests that damage crops by direct feeding and by vectoring important plant viruses. Bacterial symbionts can influence aphid biology, e.g. by providing essential nutrients or facilitating adaptations to biotic and abiotic stress. We investigated the pea aphid (Acyrthosiphon pisum Harris) and its commonly associated secondary bacterial symbiont Serratia symbiotica to study the effect of this symbiont on host fitness and susceptibility to the insecticides imidacloprid, chlorpyrifos methyl, methomyl, cyantraniliprole and spirotetramat. There is emerging evidence that members of the genus Serratia can degrade and/or detoxify diverse insecticides. Therefore, we hypothesized that S. symbiotica may promote resistance to these artificial stress agents in aphids. Our results showed that Serratia-infected aphids were more susceptible to most of the tested insecticides than non-infected aphids. This probably reflects the severe fitness costs associated with S. symbiotica, which negatively affects development, reproduction and body weight. Our study demonstrates that S. symbiotica plays an important role in the ability of aphid hosts to tolerate insecticides. These results provide insight into the potential changes in tolerance to insecticides in the field because there is a continuous and dynamic process of symbiont acquisition and loss that may directly affect host biology. © 2018 Society of Chemical Industry.

The within-host dynamics of infection in trans-generationally primed flour beetles.

Many taxa exhibit plastic immune responses initiated after primary microbial exposure that provide increased protection against disease-induced mortality and the fitness costs of infection. In several arthropod species, this protection can even be passed from parents to offspring through a phenomenon called trans-generational immune priming. Here, we first demonstrate that trans-generational priming is a repeatable phenomenon in flour beetles (Tribolium castaneum) primed and infected with Bacillus thuringiensis (Bt). We then quantify the within-host dynamics of microbes and host physiological responses in infected offspring from primed and unprimed mothers by monitoring bacterial density and using mRNA-seq to profile host gene expression, respectively, over the acute infection period. We find that priming increases inducible resistance against Bt around a critical temporal juncture where host septicaemic trajectories, and consequently survival, may be determined in unprimed individuals. Our results identify a highly differentially expressed biomarker of priming, containing an EIF4-e domain, in uninfected individuals, as well as several other candidate genes. Moreover, the induction and decay dynamics of gene expression over time suggest a metabolic shift in primed individuals. The identified bacterial and gene expression dynamics are likely to influence patterns of bacterial fitness and disease transmission in natural populations.

A computer simulation model of Wolbachia invasion for disease vector population modification.

BackgroundWolbachia invasion has been proved to be a promising alternative for controlling vector-borne diseases, particularly Dengue fever. Creating computer models that can provide insight into how vector population modification can be achieved under different conditions would be most valuable for assessing the efficacy of control strategies for this disease.MethodsIn this paper, we present a computer model that simulates the behavior of native mosquito populations after the introduction of mosquitoes infected with the Wolbachia bacteria. We studied how different factors such as fecundity, fitness cost of infection, migration rates, number of populations, population size, and number of introduced infected mosquitoes affect the spread of the Wolbachia bacteria among native mosquito populations.ResultsTwo main scenarios of the island model are presented in this paper, with infected mosquitoes introduced into the largest source population and peripheral populations. Overall, the results are promising; Wolbachia infection spreads among native populations and the computer model is capable of reproducing the results obtained by mathematical models and field experiments.ConclusionsComputer models can be very useful for gaining insight into how Wolbachia invasion works and are a promising alternative for complementing experimental and mathematical approaches for vector-borne disease control.

A long-term genetic survey of an ungulate population reveals balancing selection acting on MHC through spatial and temporal fluctuations in selection

We explored a 13-year genetic survey of the major histocompatibility complex (MHC) and neutral loci of the Soay sheep population of St Kilda to test the existence and causes of balancing selection at the MHC. The sheep population experiences demographic fluctuations, partly driven by the nematode Teladorsagia circumcincta. The spatial differentiation detected at the MHC was comparable to that at neutral loci between 1988 and 1996, but significantly lower between 1996 and 2000. The rate of temporal genetic differentiation was higher at the MHC, but within the Eastern heft only. These comparisons of spatial and temporal divergence at MHC and non-MHC loci provide strong evidence of balancing selection at the MHC, acting through spatial and temporal heterogeneity in selection pressure. This heterogeneity could be due to fluctuations in the selection imposed by parasites, either directly, because the prevalence in T. circumcincta varies in space and time, or indirectly, because the fitness costs of infection may vary with resource availability.