Effects of mammal host diversity and density on the infection level of Trypanosoma cruzi in sylvatic kissing bugs

Several reports have described host species diversity and identity as the most important factors influencing disease risk, producing either dilution or amplification of the pathogen in a host community. Triatomine vectors, mammals and the protozoan Trypanosoma cruzi (Trypanosomatida: Trypanosomatidae) Chagas are involved in the wild cycle of Chagas disease, in which infection of mammals occurs by contamination of mucous membranes or skin abrasions with insect‐infected faeces. We examined the extent to which host diversity and identity determine the infection level observed in vector populations (i.e. disease risk in humans). We recorded infection in triatomine colonies and on the coexisting host mammalian species in semi‐arid Chile. Host diversity, and total and infected host species densities are used as predictor variables for disease risk. Disease risk did not correlate with host diversity changes. However, the densities of each infected rodent species were positively associated with disease risk. We suggest that the infected host density surrounding the vector colonies is a relevant variable for disease risk and should be considered to understand disease dynamics. It is crucial to pay attention on the spatial scale of analysis, considering the pattern of vector dispersal, when the relationship between host diversity and disease risk is studied.     

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 used 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 suggest that the continued deployment of resistant host lines over wide regions of the United States has generated selection for increased host genotype range.     

LOCAL MALADAPTATION IN THE ANTHER-SMUT FUNGUS MICROBOTRYUM VIOLACEUM TO ITS HOST PLANT SILENE LATIFOLIA: EVIDENCE FROM A CROSS-INOCULATION EXPERIMENT

Conventional wisdom holds that parasites evolve more rapidly than their hosts and are therefore locally adapted, that is, better at exploiting sympatric than allopatric hosts. We studied local adaptation in the insect-transmitted fungal pathogen Microbotryum violaceum and its host plant Silene latifolia. Infection success was tested in sympatric (local) and allopatric (foreign) combinations of pathogen and host from 14 natural populations from a metapopulation. Seedlings from up to 10 seed families from each population were exposed to sporidial suspensions from each of four fungal strains derived from the same population, from a near-by population (< 10 km distance), and from two populations at an intermediate (< 30 km) and remote (< 170 km) distance, respectively. We obtained significant pathogen X plant interactions in infection success (proportion of diseased plants) at both fungal population and strain level. There was an overall pattern of local maladaptation of this pathogen: average fungal infection success was significantly lower on sympatric hosts (mean proportion of diseased plants = 0.32 ± 0.03 SE) than on allopatric hosts (0.40 ± 0.02). Five of the 14 fungal populations showed no strong reduction in infection success on sympatric hosts, and three even tended to perform better on sympatric hosts. This pattern is consistent with models of time-lagged cycles predicting patterns of local adaptation in host-parasite systems to emerge only on average. Several factors may restrict the evolutionary potential of this pathogen relative to that of its host. First, a predominantly selfing breeding system may limit its ability to generate new virulence types by sexual recombination, whereas the obligately outcrossing host 5. latifolia may profit from rearrangement of resistance alleles by random mating. Second, populations often harbor only a few infected individuals, so virulence variation may be further reduced by drift. Third, migration rates among host plant populations are much higher than among pathogen populations, possibly because pollinators prefer healthy over diseased plants. Migration among partly isolated populations may therefore introduce novel host plant resistance variants more often than novel parasite virulence variants. That migration contributes to the coevolutionary dynamics in this system is supported by the geographic pattern of infectivity. Infection success increased over the first 10–km range of host-pathogen population distances, which is likely the natural range of gene exchange.     

Comparing single- vs. mixed-genotype infections of Mycosphaerella graminicola on wheat: effects on pathogen virulence and host tolerance

Mixed-genotype infections (infections of a host by more than one pathogen genotype) are common in plant-pathogen systems. However their impact on the course of the infection and especially on pathogen virulence and host response to infection is poorly understood. We investigated the effects of mixed-genotype infections on several parameters: host resistance and tolerance, as well as pathogen aggressiveness and virulence. For these purposes, we inoculated three wheat lines with three Mycosphaerella graminicola genotypes, alone or in mixtures, in a greenhouse experiment. For some of the mixtures, disease severity and virulence were lower than expected from infection by the same genotypes alone, suggesting that competition between genotypes was reducing their aggressiveness and virulence. One host line was fully resistant, but there were differences in resistance in the other lines. The two host lines that became infected differed slightly in tolerance, but mixed-genotype infections had no effect on host tolerance.     

The Anaplasma phagocytophilum effector AmpA hijacks host cell SUMOylation

SUMOylation, the covalent attachment of a member of the small ubiquitin‐like modifier (SUMO) family of proteins to lysines in target substrates, is an essential post‐translational modification in eukaryotes. Microbial manipulation of SUMOylation recently emerged as a key virulence strategy for viruses and facultative intracellular bacteria, the latter of which have only been shown to deploy effectors that negatively regulate SUMOylation. Here, we demonstrate that the obligate intracellular bacterium, Anaplasma phagocytophilum, utilizes an effector, AmpA (A. phagocytophilum post‐translationally modified protein A) that becomes SUMOylated in host cells and this is important for the pathogen's survival. We previously discovered that AmpA (formerly APH1387) localizes to the A. phagocytophilum‐occupied vacuolar membrane (AVM). Algorithmic prediction analyses denoted AmpA as a candidate for SUMOylation. We verified this phenomenon using a SUMO affinity matrix to precipitate both native AmpA and ectopically expressed green fluorescent protein (GFP)‐tagged AmpA. SUMOylation of AmpA was lysine dependent, as SUMO affinity beads failed to precipitate a GFP‐AmpA protein when its lysine residues were substituted with arginine. Ectopically expressed and endogenous AmpA were poly‐SUMOylated, which was consistent with the observation that AmpA colocalizes with SUMO2/3 at the AVM. Only late during the infection cycle did AmpA colocalize with SUMO1, which terminally caps poly‐SUMO2/3 chains. AmpA was also detected in the cytosol of infected host cells, further supporting its secretion and likely participation in interactions that aid pathogen survival. Indeed, whereas siRNA‐mediated knockdown of Ubc9 – a necessary enzyme for SUMOylation – slightly bolstered A. phagocytophilum infection, pharmacologically inhibiting SUMOylation in infected cells significantly reduced the bacterial load. Ectopically expressed GFP‐AmpA served as a competitive agonist against native AmpA in infected cells, while lysine‐deficient GFP‐AmpA was less effective, implying that modification of AmpA lysines is important for infection. Collectively, these data show that AmpA becomes directly SUMOylated during infection, representing a novel tactic for A. phagocytophilum survival.     

Interactions between host sex and age of exposure modify the virulence–transmission trade‐off

The patterns of immunity conferred by host sex or age represent two sources of host heterogeneity that can potentially shape the evolutionary trajectory of disease. With each host sex or age encountered, a pathogen's optimal exploitative strategy may change, leading to considerable variation in expression of pathogen transmission and virulence. To date, these host characteristics have been studied in the context of host fitness alone, overlooking the effects of host sex and age on the fundamental virulence–transmission trade‐off faced by pathogens. Here, we explicitly address the interaction of these characteristics and find that host sex and age at exposure to a pathogen affect age‐specific patterns of mortality and the balance between pathogen transmission and virulence. When infecting age‐structured male and female Daphnia magna with different genotypes of Pasteuria ramosa, we found that infection increased mortality rates across all age classes for females, whereas mortality only increased in the earliest age class for males. Female hosts allowed a variety of trade‐offs between transmission and virulence to arise with each age and pathogen genotype. In contrast, this variation was dampened in males, with pathogens exhibiting declines in both virulence and transmission with increasing host age. Our results suggest that differences in exploitation potential of males and females to a pathogen can interact with host age to allow different virulence strategies to coexist, and illustrate the potential for these widespread sources of host heterogeneity to direct the evolution of disease in natural populations.     

Local adaptation and effect of host genotype on the rate of pathogen evolution: an experimental test in a plant pathosystem

Abstract Virulence is thought to be a driving force in host–pathogen coevolution. Theoretical models suggest that virulence is an unavoidable consequence of pathogens evolving towards a high rate of intrahost reproduction. These models predict a positive correlation between the reproductive fitness of a pathogen and its level of virulence. Theoretical models also suggest that the demography and genetic structure of a host population can influence the evolution of virulence. If evolution occurs faster in pathogen populations than in host populations, the predicted result is local adaptation of the pathogen population. In our studies, we used a combination of molecular and physiological markers to test these hypotheses in an agricultural system. We isolated five strains of the fungal pathogen Mycosphaerella graminicola from each of two wheat cultivars that differed in their level of resistance to this pathogen. Each of the 10 fungal strains had distinct genotypes as indicated by different DNA fingerprints. These fungal strains were re‐inoculated onto the same two host cultivars in a field experiment and their genotype frequencies were monitored over several generations of asexual reproduction. We also measured the virulence of these 10 fungal strains and correlated it to the reproductive fitness of each fungal strain. We found that host genotypes had a strong impact on the dynamics of the pathogen populations. The pathogen population collected from the moderately resistant cultivar Madsen showed greater stability, higher genotype diversity, and smaller selection coefficients than the pathogen populations collected from the susceptible cultivar Stephens or a mixture of the two host cultivars. The pathogen collection from the mixed host population was midway between the two pure lines for most parameters measured. Our results also revealed that the measures of reproductive fitness and virulence of a pathogen strain were not always correlated. The pathogen strains varied in their patterns of local adaptation, ranging from locally adapted to locally maladapted.     

Effects of endophytic fungi on the phenotypic plasticity of Lolium perenne (Poaceae)

The effects of high vs. low levels of endophytic fungi on the phenotypic plasticity of cloned genotypes were examined in perennial ryegrass (Lolium perenne L.). The objectives were to determine whether endophytic fungi influence plastic responses of host genotypes to variable soil nutrients and whether or not endophyte infection and host genotype interact to determine the extent of this plasticity. Twelve infected genotypes were cloned into ramets: half the ramets were treated with the systemic fungicide Benomyl to reduce or eliminate the endophyte, while the other half were untreated. Ramets of each genotype were subjected to high, medium, or low levels of nutrients in the greenhouse for 11 wk. Tiller number, leaf area, and leaf mass were determined after 11 and 25 wk. The fungicide significantly reduced the level of endophyte infection. Responses to nutrient conditions in relation to fungicide treatment were genotype specific: for some genotypes, high levels of endophytic fungi appeared to reduce plasticity, while for other genotypes the endophyte had no effect. The potential for microscopic symbionts to affect phenotypic plasticity in genetically variable populations has not often been recognized. However, the clandestine effects of symbionts on the plasticity of host genotypes could impact microevolutionary processes occurring within plant populations that occupy heterogeneous environments.     

Gut microbiota instead of host genotype drive the specificity in the interaction of a natural host-parasite system

Specific interactions between parasite genotypes and host genotypes (G_p × G_h) are commonly found in invertebrate systems, but are largely lacking a mechanistic explanation. The genotype of invertebrate hosts can be complemented by the genomes of microorganisms living on or within the host (‘microbiota’). We investigated whether the bacterial gut microbiota of bumble bees (Bombus terrestris) can account for the specificity of interactions between individuals from different colonies (previously taken as host genotype proxy) and genotypes of the parasite Crithidia bombi. For this, we transplanted the microbiota between individuals of six colonies. Both the general infection load and the specific success of different C. bombi genotypes were mostly driven by the microbiota, rather than by worker genotype. Variation in gut microbiota can therefore be responsible for specific immune phenotypes and the evolution of gut parasites may be driven by interactions with ‘microbiota types’ as well as with host genotypes.     

Abundance,composition and spatial variation in the egg bank of a tropical zooplankton community

The semi‐aquatic grasshopper Cornops aquaticum (Bruner, 1906) is native to South America, with a distribution from the Argentinian pampas to the Gulf of Mexico, and is currently being proposed as a biological control agent for the invasive water hyacinth (Eichhornia crassipes) in South Africa. This study reports results of a neutral molecular marker (microsatellites) study on C. aquaticum within its native range. The data were analysed for levels of diversity and structure within/between South American populations, and correlations between host plant, geography and environmental/climatic variables were investigated. We found no evidence to support associations between host plant use and microsatellite genotypes (hypothesis 1). High levels of gene flow and weak genetic clustering of populations indicate a lack of differentiation, therefore an interaction between climate and local genotype (hypothesis 2) seems unlikely. Our results suggest that C. aquaticum may not have “tightly” coevolved with its host Eichhornia spp. (Pontederiaceae) as originally thought, and that instar variation might be due to the effect of local climate on phenotype (hypothesis 3) or possibly a locally adaptive trait.     

Growth and hare, Lepus timidus, resistance of white birch, Betula pendula, clones grown in different soil types

Many plant species have the ability to expand laterally through space by clonal growth. Plant pathogens can affect clonal growth characteristics thereby altering the success of host plants within populations and of clonal species within communities. We conducted a greenhouse experiment to determine the effects of the systemic fungal pathogen, Epichloë glyceriae , on clonal growth patterns of its host grass, Glyceria striata . We found that infected and uninfected plants produced similar total biomass and numbers of tillers plus primary stolons per mother ramet. However, biomass allocation to tillering (vegetative growth) vs stolon production (clonal growth) was significantly affected by pathogen infection. Infected plants produced more stolons and clonal growth biomass than uninfected plants while mother ramets of uninfected plants produced more tillers and biomass than infected plants. Stolon architecture of infected and uninfected plants also differed. In two of three populations, infected plants produced stolons with greater biomass and shorter spacer lengths, even though mean stolon lengths were similar for infected and uninfected plants. These results contrast strongly with most other clonal plant-pathogen systems where infected plants are less vigorous and have reduced clonal growth compared to uninfected plants. Greater clonal growth may be an effective mechanism for host genotypes to persist and spread when seed production is prevented, as is the case with castrating pathogens like Epichloë glyceriae .     

POTENTIAL FOR THE LOSS OF SELF-INCOMPATIBILITY IN POLLEN-LIMITED POPULATIONS OF MAYAPPLE (PODOPHYLLUM PELTATUM)

Self-compatibility (SC) appears to be a derived trait in many unrelated taxa. A major selective force that could lead to the evolution of SC from self-incompatibility (SI) is inadequate pollination. Here we show that seed set is strongly pollenlimited in populations of mayapple, Podophyllum peltatum (Berberidaceae). Hand-pollination led to a 26-fold increase in seed set as compared to natural levels in 1989, and to a fivefold increase in 1990. The species is SI, but in a survey of 49 colonies in Ohio we found three that had more than 50% fruit set from self pollen (as compared to about 90% fruit set from hand-outcrossed flowers). However, when hand-selfing yielded fruits, the number of seeds per fruit was only about 10% of the seed set from hand-outcrossing. We discuss the relative fecundity of putative SC and SI genotypes in terms of conditions needed for the spread of SC in mayapple populations (little or no morphological change would be needed to ensure within-flower selfing). Seed set from putative SC genotypes appeared to be low enough to prevent them from replacing SI genotypes, even in the face of infrequent pollinator visits.     

Evolution of antigenic diversity in the tick‐transmitted bacterium Borrelia afzelii: a role for host specialization?

Antigenic diversity in pathogenic microbes can be a result of at least three different processes: diversifying selection by acquired immunity, host–pathogen coevolution and/or host specialization. Here, we investigate whether host specialization drives diversity at ospC (which encodes an immunodominant surface protein) in the tick‐transmitted bacterium Borrelia afzelii. We determined prevalence and infection intensity of ospC strains in naturally infected wild mammals (rodents and shrews) by 454 amplicon sequencing in combination with qPCR. Neither prevalence nor infection intensity of specific ospC strains varied in a species‐specific manner (i.e. there were no significant ospC × host species interactions). Rankings of ospC prevalences were strongly positively correlated across host species. Rankings of ospC infection intensities were correlated more weakly, but only in one case significantly < 1. ospC prevalences in the studied mammals were similar to those in ticks sampled at the study site, indicating that we did not miss any mammal species that are important hosts for specific ospC strains. Based on this, we conclude that there is at best limited host specialization in B. afzelii and that other processes are likely the main drivers of ospC diversity.     

Protection against a fungal pathogen conferred by the aphid facultative endosymbionts Rickettsia and Spiroplasma is expressed in multiple host genotypes and species and is not influenced by co‐infection with another symbiont

Many insects harbour facultative endosymbiotic bacteria, often more than one type at a time. These symbionts can have major effects on their hosts' biology, which may be modulated by the presence of other symbiont species and by the host's genetic background. We investigated these effects by transferring two sets of facultative endosymbionts (one Hamiltonella and Rickettsia, the other Hamiltonella and Spiroplasma) from naturally double‐infected pea aphid hosts into five novel host genotypes of two aphid species. The symbionts were transferred either together or separately. We then measured aphid fecundity and susceptibility to an entomopathogenic fungus. The pathogen‐protective phenotype conferred by the symbionts Rickettsia and Spiroplasma varied among host genotypes, but was not influenced by co‐infection with Hamiltonella. Fecundity varied across single and double infections and between symbiont types, aphid genotypes and species. Some host genotypes benefit from harbouring more than one symbiont type.     

A look into the genetic diversity of Lecanosticta acicola in northern Europe

For northern Europe Lecanosticta acicola is an emerging pine needle pathogen. This study gives a first look into the population genetics of the pathogen in Estonia, the first population documented in that region. The main aim of this study was to investigate the genetic diversity and population structure of the pathogen in this new region for the fungus. For this purpose, 104 isolates from 2010 to 2017 were analysed with 11 microsatellite and mating type markers. The stand where the pathogen's jump from an exotic host to the native Scots pine was recorded was also involved in this analysis. The analysis revealed low genetic diversity and a high number of clones that indicated L. acicola is an invasive species in northern Europe. Results suggest that several separate introductions have taken place and anthropogenic activity has apparently affected the spread of the pathogen. Clonal reproduction is dominating and although sexual reproduction is possible, it probably takes place infrequently.     

Isolation of anti-fungal phenolic compounds from petioles of two Hevea brasiliensis (rubber) genotypes and their effect on Phytophthora meadii

Phenolic compounds were present in greater amounts in non‐infected petioles of genotypes of Hevea brasiliensis that are resistant to Phytophthora leaf disease than in genotypes that are susceptible. Phenolic compounds extracted from petioles of either susceptible (PB86) or resistant (RRIC100) genotypes, before or after infection with Phytophthora meadii, had anti‐fungal properties. Artificially infected petioles of PB86 had phenolic acids, triterpenoids or flavonoids, whereas healthy petioles contained only triterpenoids or flavonoids. However, healthy or infected petioles of RRIC100 contained only trace amounts of the above compounds and of vanillin (3‐methoxy‐4‐hydroxybenzaldehyde). Vanillin and umbelliferone (7‐hydroxycoumarin) were shown to suppress zoospore germination of P. meadii on glass slides and to inhibit its growth in pea broth and V‐8 juice agar. Vanillin was slightly more active than umbelliferone. Resistance of RRIC100 to Phytophthora was suspected as being related to the polymerisation of phenolic compounds to form lignin, which may suppress further spread of the pathogen's mycelium into healthy tissues. Formation of lignin from phenolic aldehydes as a barrier to disease spread may be a critical factor in resistance.     

Genetic diversity of Typha latifolia (Typhaceae) and the impact of pollutants examined with tandem-repetitive DNA probes

Genetic diversity at variable-number-tandem-repeat (VNTR) loci was examined in the common cattail, Typha latifolia (Typhaceae), using three synthetic DNA probes composed of tandemly repeated “core” sequences (GACA, GATA, and GCAC). The principal objectives of this investigation were to determine whether: (1) the previously reported almost complete lack of polymorphism at allozyme loci in this species was indicative of a reduced amount of genetic diversity at VNTR loci as well; (2) VNTR markers were informative about possible clonal propagation; and (3) significant differences in genetic structure of sampling sites were associated with differences in environmental levels of pollutants at those sites. Previously, widespread sampling across the eastern United States, surveying across ten allozyme loci, has detected only two genotypes, involving a difference at a single locus, among 104 populations. In this study, the amount of genetic diversity detected at VNTR loci: (1) among ramets (N = 40; 40 genotypes detected) collected at ∼8-km intervals along a 320-km transect; (2) among ramets (N = 220; 117 genotypes detected) from five study sites separated by 50–3000 m; and (3) even among ramets within each study site [N = 44 per site; from 13 to 34 genotypes detected per site (270 m²)] exceeds that previously found in those more geographically widespread allozyme surveys. Among the 260 ramets analyzed here, the mean number of bands scored per individual was 48.61 (SD = 2.80). Mean genetic similarity among ramets collected along the 320-km transect was 0.91, which was within the range of mean genetic similarity within the five study sites (range: 0.89–0.95). Among the five study sites, 61% of the samples analyzed appeared to be clonal ramets, with up to 12 clones detected for 44 ramets sampled within a site. Clones grew intermingled and ranged up to 39 m in extent. Permutation tests of genetic similarity revealed significant genetic differentiation between each of the five study sites. Consistent with the previous allozyme studies, T. latifolia was characterized by extremely low genetic variation relative to levels of polymorphism detected at VNTR loci in other plant species. Estimated heterozygosity among ramets along the 320-km transect ranged from 0.11 to 0.13, while that within the five study sites ranged from 0.05 to 0.12. Estimates of F_st (0.32–0.41) also indicated considerable genetic subdivision among these stands. Significantly higher genetic diversity was detected at the two study sites that chemistry and toxicity data indicate to be the most severely impacted by pollutants. Although this correlation does not establish cause and effect, the results of this study indicate that the analysis of genetic diversity at VNTR loci may be a useful tool for monitoring anthropogenic-induced changes in the genetic structure of natural populations of plants.     

Influence of fungal infection on plant tissues: FTIR detects compositional changes to plant cell walls

Compositional change in plant cell walls as a result of infection by non-host (putative) endophytes and a host pathogen were studied by quantifying plant cell wall degrading enzymes (CWDEs) produced by these fungi, and by detecting cell wall changes via Fourier Transform Infrared spectroscopy (FTIR) and relative lignin/carbohydrate intensity ratios. Oil palm ramets were first inoculated with homogenized fungal suspension. The treated fungal suspensions were assayed for CWDEs whereas the ramets were powderized for FTIR analysis. Results revealed that putative endophytes and host pathogen expressed all CWDEs, suggesting their probable roles in infection and colonization. Following inoculation, plant cell wall composition showed missing dips in spectra depicting changes to carbohydrate, xylan and lignin constituents. The indistinguishable FTIR spectra for putative endophyte-inoculated and pathogen-inoculated ramets suggest that both endophytes and pathogen have elicited similar responses to plant cell walls. Relative lignin/carbohydrate ratios further demonstrated that the putative endophytes did not breakdown lignin and carbohydrate, further exemplifying the non-pathogenic and asymptomatic infection by the endophytes. This study presents the influence of putative endophytes on plant tissues of oil palm, and how this compared to pathogenic infection.     

High parasite infection level in non‐native invasive species: it is just a matter of time

The enemy release hypothesis is often used to explain the success of non‐native species invasions. Growing evidence indicates that parasite or pathogen species richness increases over time in invasive non‐native species; however, this increase should not directly translate into release from enemy pressure as infection intensity of parasites (number of parasites per host) has a more profound impact on host fitness. The changes in intensity of parasitic infections in invasive non‐native species have not yet been thoroughly analysed in newly colonized areas. The goal of this study was to determine whether gastrointestinal parasite (nematode and trematode) infection intensity has increased with time since the populations of American mink Neovison vison were established and how host demographic parameters affect infection intensity. We tested the enemy release hypothesis by substituting space for time, evaluating parasite abundance in American mink at six sites along a chronosequence of mink invasion history. Nematode and trematode abundance increased with time since mink introduction, from a few parasites on average per mink after 16 yr, to 200–250 parasites per mink after 34 yr. The rate of increase in parasite abundance varied among demographic groups of mink (sex and age). Both nematodes and trematodes were more abundant in males than in females, and in subadults than in adults. Higher nematode abundance negatively affected body condition of mink. Our results provide evidence that non‐native species are released from enemy pressure only in the first phase of invasion, and that infection is modulated by host demographics and season. These results contribute to the evaluation of the long‐term patterns of parasite accumulation in invasive non‐native species after their colonization of new territories.     

Dynamics of multiple infection and within-host competition by the anther-smut pathogen

Infection of one host by multiple pathogen genotypes represents an important area of pathogen ecology and evolution that lacks a broad empirical foundation. Multiple infection of Silene latifolia by Microbotryum violaceum was studied under field and greenhouse conditions using the natural polymorphism for mating-type bias as a marker. Field transmission resulted in frequent multiple infection, and each stem of the host was infected independently. Within-host diversity of infections equaled that of nearby inoculum sources by the end of the growing season. The number of diseased stems per plant was positively correlated with multiple infection and with overwintering mortality. As a result, multiply infected plants were largely purged from the population, and there was lower within-host pathogen diversity in the second season. However, among plants with a given number of diseased stems, multiply infected plants had a lower risk of overwintering mortality. Following simultaneous and sequential inoculation, strong competitive exclusion was demonstrated, and the first infection had a significant advantage. Dynamics of multiple infection initially included components of coinfection models for virulence evolution and then components of superinfection models after systemic colonization. Furthermore, there was evidence for an advantage of genotypes with mating-type bias, which may contribute to maintenance of this polymorphism in natural populations.