Variable prey development time suppresses predator–prey cycles and enhances stability

Although theoretical models have demonstrated that predator–prey population dynamics can depend critically on age (stage) structure and the duration and variability in development times of different life stages, experimental support for this theory is non‐existent. We conducted an experiment with a host–parasitoid system to test the prediction that increased variability in the development time of the vulnerable host stage can promote interaction stability. Host–parasitoid microcosms were subjected to two treatments: Normal and High variance in the duration of the vulnerable host stage. In control and Normal‐variance microcosms, hosts and parasitoids exhibited distinct population cycles. In contrast, insect abundances were 18–24% less variable in High‐ than Normal‐variance microcosms. More significantly, periodicity in host–parasitoid population dynamics disappeared in the High‐variance microcosms. Simulation models confirmed that stability in High‐variance microcosms was sufficient to prevent extinction. We conclude that developmental variability is critical to predator–prey population dynamics and could be exploited in pest‐management programs.     

Impact of life stage specific immune priming on invertebrate disease dynamics

The immune response of a host can have important impacts on host‐pathogen interactions, but investment in immunity often changes dynamically across the life history of a host. One form of investment involves the induction of a primed immune response against previously encountered pathogens that protects the host from re‐infection. In addition to providing immediate protective effects, immune priming can also provide two types of ‘delayed’ protection against pathogens: priming across life stages (ontogenic priming) and priming across generations (trans‐generational priming). Consequently both types of immune priming have the potential to mediate life history variability in host–pathogen interactions, which could have important consequences for disease prevalence and dynamics as well as for the demographic structure of the host population. Here we develop a stage‐structured SIRS model for an invertebrate host to explore the relative and combined impact of ontogenic priming and trans‐generational priming on infection prevalence, host population size, and population age structure. Our model predicts that both types of immune priming can dramatically reduce disease prevalence at equilibrium, but their individual and combined effects on population size and age structure depend on the magnitude of tradeoffs between immune protection and reproduction as well as on the symmetry of infection parameters between life stages. This model underscores the potential importance of life‐history based immune investment patterns for disease dynamics and highlights the need for wide‐spread empirical estimation of parameters that represent the maintenance of immune priming in insects.     

Host genetics and population structure effects on parasitic disease

Host genetic factors exert significant influences on differential susceptibility to many infectious diseases. In addition, population structure of both host and parasite may influence disease distribution patterns. In this study, we assess the effects of population structure on infectious disease in two populations in which host genetic factors influencing susceptibility to parasitic disease have been extensively studied. The first population is the Jirel population of eastern Nepal that has been the subject of research on the determinants of differential susceptibility to soil-transmitted helminth infections. The second group is a Brazilian population residing in an area endemic for Trypanosoma cruzi infection that has been assessed for genetic influences on differential disease progression in Chagas disease. For measures of Ascaris worm burden, within-population host genetic effects are generally more important than host population structure factors in determining patterns of infectious disease. No significant influences of population structure on measures associated with progression of cardiac disease in individuals who were seropositive for T. cruzi infection were found.     

Simultaneous determination of fluctuating age structure and mortality from field data

The use of a Leslie matrix for analysis of a population normally implies that the age structure of the population is known. However, this restriction can be overcome if the population can be partitioned into recognisably different stages, and some information on stage duration and fecundity is available, in which case the age structure may be determined by the analysis itself. As an example of this approach we consider the estimation of the mortality rate applying to a population from a sequence of observed stage frequency vectors. The technique does not require that the population has attained a stable age structure nor that distinct cohorts can be recognised.     

Temperature Alters Host Genotype-Specific Susceptibility to Chytrid Infection

The cost of parasitism often depends on environmental conditions and host identity. Therefore, variation in the biotic and abiotic environment can have repercussions on both, species-level host-parasite interaction patterns but also on host genotype-specific susceptibility to disease. We exposed seven genetically different but concurrent strains of the diatom Asterionella formosa to one genotype of its naturally co-occurring chytrid parasite Zygorhizidium planktonicum across five environmentally relevant temperatures. We found that the thermal tolerance range of the tested parasite genotype was narrower than that of its host, providing the host with a “cold” and “hot” thermal refuge of very low or no infection. Susceptibility to disease was host genotype-specific and varied with temperature level so that no genotype was most or least resistant across all temperatures. This suggests a role of thermal variation in the maintenance of diversity in disease related traits in this phytoplankton host. The duration and intensity of chytrid parasite pressure on host populations is likely to be affected by the projected changes in temperature patterns due to climate warming both through altering temperature dependent disease susceptibility of the host and, potentially, through en- or disabling thermal host refugia. This, in turn may affect the selective strength of the parasite on the genetic architecture of the host population.     

Dynamics of a feline retrovirus (FeLV) in host populations with variable spatial structure.

The predictions of epidemic models are remarkably affected by the underlying assumptions concerning host population dynamics and the relation between host density and disease transmission. Furthermore, hypotheses underlying distinct models are rarely tested. Domestic cats (Felis catus) can be used to compare models and test their predictions, because cat populations show variable spatial structure that probably results in variability in the relation between density and disease transmission. Cat populations also exhibit various dynamics. We compare four epidemiological models of Feline Leukaemia Virus (FeLV). We use two different incidence terms, i.e. proportionate mixing and pseudo-mass action. Population dynamics are modelled as logistic or exponential growth. Compared with proportionate mixing, mass action incidence with logistic growth results in a threshold population size under which the virus cannot persist in the population. Exponential growth of host populations results in systems where FeLV persistence at a steady prevalence and depression of host population growth are biologically unlikely to occur. Predictions of our models account for presently available data on FeLV dynamics in various populations of cats. Thus, host population dynamics and spatial structure can be determinant parameters in parasite transmission, host population depression, and disease control.     

Glacial refugia in pathogens: European genetic structure of anther smut pathogens on Silene latifolia and Silene dioica

Climate warming is predicted to increase the frequency of invasions by pathogens and to cause the large-scale redistribution of native host species, with dramatic consequences on the health of domesticated and wild populations of plants and animals. The study of historic range shifts in response to climate change, such as during interglacial cycles, can help in the prediction of the routes and dynamics of infectious diseases during the impending ecosystem changes. Here we studied the population structure in Europe of two Microbotryum species causing anther smut disease on the plants Silene latifolia and Silene dioica. Clustering analyses revealed the existence of genetically distinct groups for the pathogen on S. latifolia, providing a clear-cut example of European phylogeography reflecting recolonization from southern refugia after glaciation. The pathogen genetic structure was congruent with the genetic structure of its host species S. latifolia, suggesting dependence of the migration pathway of the anther smut fungus on its host. The fungus, however, appeared to have persisted in more numerous and smaller refugia than its host and to have experienced fewer events of large-scale dispersal. The anther smut pathogen on S. dioica also showed a strong phylogeographic structure that might be related to more northern glacial refugia. Differences in host ecology probably played a role in these differences in the pathogen population structure. Very high selfing rates were inferred in both fungal species, explaining the low levels of admixture between the genetic clusters. The systems studied here indicate that migration patterns caused by climate change can be expected to include pathogen invasions that follow the redistribution of their host species at continental scales, but also that the recolonization by pathogens is not simply a mirror of their hosts, even for obligate biotrophs, and that the ecology of hosts and pathogen mating systems likely affects recolonization patterns.     

Genetic assessment of environmental features that influence deer dispersal: implications for prion-infected populations

The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F _ST, assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersal-mediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission.     

Parasite communities and a fish spawn

High values of dominance index, low values of evenness and Shannon index are characteristic of component parasite communities of prespawning (Prosopium cylindraceum) and spawn migratory fishes (Coregonus autumnalis, Oncorhynchus nerka). Autogenic specialists are dominant in the component parasite communities of C. autumnalis. The component parasite communities of P. cylindraceum and O. nerka are dominant in a content of generalist species. The O. nerka parasite communities are communities "sentenced to death". Low values of dominance index, high values of evenness abd Shannon index are peculiar to component parasite communities of prespawning and spawning cyprinid fishes (Phoxinus phoxinus, Oreoleuciscus humilis). Autogenic specialists are dominant. Increase of dominance index and decrease of two other indexes characterize the postspawning period. The same tendency characterises infracommunities. Thus, the component parasite communities respond differently to the fish spawn of the cyprinid and coregonid/salmonid fishes. Similarity is in the dominance of autogenic specialists in one case only (C. autumnalis). These differences are defined by the mode of fish stock formation for spawn. The cyprinids congregate for spawning and move apart for foraging and vice versa is observed in the coregonids and salmonids. Autogenic specialists dominance seems to be the important adaptation to reduce a negative effect to host during spawning. Bush and Kennedy in 1994 established that "parasites live in patches (host individuals) and fragments (host populations)". They consider the host fragmentation as "hedging your bets against extinction" due to frequency and magnitude anthropogenic factors, which increase fragmenting of host populations. This conclusion was made for a species level. From the other hand the fragmentation is a natural feature for a single host population too. Such fragmentation is a host population structure. The role of fragmentation is obvious from the data on component parasite communities during fish spawn. The fragmentation decreases in the cyprinids and increases in the salmonids that leads to the growing of the cyprinid component parasite communities diversity and to declining the salmonid component parasite communities diversity. Nevertheless the role of host population structure in a component parsite community structure is not obvious, because parasites are able or not able to "recognise" different host subpopulation groups. It is well known from data on parasite species population biology. Such recognizable subpopulation groups or groups can be a "real fragment" for the parasite community. The question is what parameters could be used for this purpose on a component community level. Host population age structure can be used as an example, because the age groups are one of the invariable population characters. Value of Shannon index for component parasite communities of spawn migratory O. nerka (5+) is similar to that of fishes of 1+ age. Difference is statistically insignificant. It is insignificant between the parasite communities of 2+ and 3+ age groups too. Fishes of these two groups could be defined as a real united fragment. It spite of similarity between the fishes of 5+ age group and fish of 1+ age group they are not united fragment. The parasite community of 1+ age fishes is not stabilized yet and one of 5+ age is a community "sentenced to death". Thus the structuring of O. nerka freshwater parasite communities are defined by 3 real host age fragments: 1+ age group, 2 and 3+ age group, 4+ age group. It looks as that Shannon index is suitable parameter to study a parasite communities structure.     

Endemic disease in host populations with fully specified demography

This study explores the epidemiology of an aerogenically transmitted infectious disease following an S.I.R. pattern in a host population with completely specified age-specified maternity and mortality schedules. A fully age-structured demographic-epidemiologic model is developed, and its demographic and epidemiologic behaviour is explored in numerical studies. The impact of variations in host population demographic structure upon the effect of immunization programs is also studied.     

The importance of environmental spatial heterogeneity and host social structure in disease transmission

[First paragraph]The spatial structure of a host population determines the spatial probability distribution of interaction between individuals, and therefore influences the spatio-temporal dynamics of disease transmission within the host population (Keeling, 1999; Gudelj and White, 2004). Nigel Barlow recognised this and included non-linear transmission in his later models (Barlow, 1991), simulating the result of spatial heterogeneity of risk in susceptible hosts. These models produced behaviour that could not be found in models with homogeneously mixed host populations: more rapid disease dynamics and a greater robustness of disease to control measures. However, in this model there was no causal mechanism driving the initial spatial heterogeneity of risk in host individuals. Environmental heterogeneity is likely to be a key factor in determining the spatial distribution of host individuals (Cronin and Reeve, 2005). We attempted to explore how environmental heterogeneity may affect disease dynamics via its influence on the spatial distribution of host individuals. We developed a spatially explicit stochastic model that incorporated spatially variable host density distributions, primarily driven by environmental heterogeneity.     

Coevolutionary fine-tuning: evidence for genetic tracking between a specialist wasp parasitoid and its aphid host in a dual metapopulation interaction

In the interaction between two ecologically-associated species, the population structure of one species may affect the population structure of the other. Here, we examine the population structures of the aphid Metopeurum fuscoviride, a specialist on tansy Tanacetum vulgare, and its specialist primary hymenopterous parasitoid Lysiphlebus hirticornis, both of which are characterized by multivoltine life histories and a classic metapopulation structure. Samples of the aphid host and the parasitoid were collected from eight sites in and around Jena, Germany, where both insect species co-occur, and then were genotyped using suites of polymorphic microsatellite markers. The host aphid was greatly differentiated in terms of its spatial population genetic patterning, while the parasitoid was, in comparison, only moderately differentiated. There was a positive Mantel test correlation between pairwise shared allele distance (DAS) of the host and parasitoid, i.e. if host subpopulation samples were more similar between two particular sites, so were the parasitoid subpopulation samples. We argue that while the differences in the levels of genetic differentiation are due to the differences in the biology of the species, the correlations between host and parasitoid are indicative of dependence of the parasitoid population structure on that of its aphid host. The parasitoid is genetically tracking behind the aphid host, as can be expected in a classic metapopulation structure where host persistence depends on a delay between host and parasitoid colonization of the patch. The results may also have relevance to the Red Queen hypothesis, whereupon in the 'arms race' between parasitoid and its host, the latter 'attempts' to evolve away from the former.     

Fatal disease and demographic Allee effect: population persistence and extinction

If a healthy stable host population at the disease-free equilibrium is subject to the Allee effect, can a small number of infected individuals with a fatal disease cause the host population to go extinct? That is, does the Allee effect matter at high densities? To answer this question, we use a susceptible-infected epidemic model to obtain model parameters that lead to host population persistence (with or without infected individuals) and to host extinction. We prove that the presence of an Allee effect in host demographics matters even at large population densities. We show that a small perturbation to the disease-free equilibrium can eventually lead to host population extinction. In addition, we prove that additional deaths due to a fatal infectious disease effectively increase the Allee threshold of the host population demographics.     

Parasitic infection reduces dispersal of ciliate host

Parasitic infection can modify host mobility and consequently their dispersal capacity. We experimentally investigated this idea using the ciliate Paramecium caudatum and its bacterial parasite Holospora undulata. We compared the short-distance dispersal of infected and uninfected populations in interconnected microcosms. Infection reduced the proportion of hosts dispersing, with levels differing among host clones. Host populations with higher densities showed lower dispersal, possibly owing to social aggregation behaviour. Parasite isolates that depleted host populations most had the lowest impact on host dispersal. Parasite-induced modification of dispersal may have consequences for the spatial distribution of disease, host and parasite genetic population structure, and coevolution.     

Fatal disease and demographic Allee effect: population persistence and extinction

If a healthy stable host population at the disease-free equilibrium is subject to the Allee effect, can a small number of infected individuals with a fatal disease cause the host population to go extinct? That is, does the Allee effect matter at high densities? To answer this question, we use a susceptible–infected epidemic model to obtain model parameters that lead to host population persistence (with or without infected individuals) and to host extinction. We prove that the presence of an Allee effect in host demographics matters even at large population densities. We show that a small perturbation to the disease-free equilibrium can eventually lead to host population extinction. In addition, we prove that additional deaths due to a fatal infectious disease effectively increase the Allee threshold of the host population demographics.     

Duelling timescales of host movement and disease recovery determine invasion of disease in structured populations

The epidemic potential of a disease is traditionally assessed using the basic reproductive number, R ₀. However, in populations with social or spatial structure a chronic disease is more likely to invade than an acute disease with the same R ₀, because it persists longer within each group and allows for more host movement between groups. Acute diseases 'perceive' a more structured host population, and it is more important to consider host population structure in analyses of these diseases. The probability of a pandemic does not arise independently from characteristics of either the host or disease, but rather from the interaction of host movement and disease recovery timescales. The R _* statistic, a group-level equivalent of R ₀, is a better indicator of disease invasion in structured populations than the individual-level R ₀.     

Disease, frequency-dependent selection, and genetic polymorphisms: experiments with stripe rust and wheat

Abstract.— Pathogens have the potential to maintain genetic polymorphisms by creating frequency-dependent selection on their host. This can occur when a rare host genotype is less likely to be attacked by a pathogen (frequency-dependent disease attack) and has higher fitness at low frequency (negative frequency-dependent selection). In this study, we used wheat genotypes that were susceptible to different races of the pathogen Puccinia striiformis to test whether disease created frequency-selection on its host and whether such selection could maintain polymorphisms for resistance genes in the wheat populations. Four different two-way mixtures of wheat genotypes were planted at different frequencies in both the presence and absence of disease. Disease created frequency-dependent selection on its host in some populations. Unknown factors other than disease also created frequency-dependent selection in this system because, in some instances, rare genotype advantage was observed in the absence of disease. Although the pathogen created frequency-dependent selection on its host, this selection was not sufficient to maintain genetic polymorphism in the host populations. In all cases where frequency-dependent selection occurred only in the diseased plots, one of the two genotypes was predicted to dominate in the population and the same genotype was predicted to dominate in both the presence and absence of disease. Only in cases where frequency-dependent selection was not caused by disease was there evidence that genetic polymorphisms would be maintained in the population. The frequency-dependent selection described in this study is a consequence of epidemiological effects of disease and differs from the time-lagged frequency-dependent selection resulting from coevolution between hosts and parasites. The impact of this direct frequency-dependent selection on the maintenance of genetic polymorphisms in the host population is discussed.     

Similar yet different: co-analysis of the genetic diversity and structure of an invasive nematode parasite and its invasive mammalian host

Animal parasitic nematodes can cause serious diseases and their emergence in new areas can be an issue of major concern for biodiversity conservation and human health. Their ability to adapt to new environments and hosts is likely to be affected by their degree of genetic diversity, with gene flow between distinct populations counteracting genetic drift and increasing effective population size. The raccoon roundworm (Baylisascaris procyonis), a gastrointestinal parasite of the raccoon (Procyon lotor), has increased its global geographic range after being translocated with its host. The raccoon has been introduced multiple times to Germany, but not all its populations are infected with the parasite. While fewer introduced individuals may have led to reduced diversity in the parasite, admixture between different founder populations may have counteracted genetic drift and bottlenecks. Here, we analyse the population genetic structure of the roundworm and its raccoon host at the intersection of distinct raccoon populations infected with B. procyonis. We found evidence for two parasite clusters resulting from independent introductions. Both clusters exhibited an extremely low genetic diversity, suggesting small founding populations subjected to inbreeding and genetic drift with no, or very limited, genetic influx from population admixture. Comparison of the population genetic structures of both host and parasite suggested that the parasite spread to an uninfected raccoon founder population. On the other hand, an almost perfect match between cluster boundaries also suggested that the population genetic structure of B. procyonis has remained stable since its introduction, mirroring that of its raccoon host.     

Pathogen frequency in an age-structured population of<Emphasis Type="Italic"> Plantago lanceolata</Emphasis>

Life-history traits can play important roles in determining the course of ecological species interactions. We explored the consequences of host age on a host-pathogen interaction by quantifying pathogen frequency in an age-structured host population. Our project was motivated by an interest in whether the demographic structure of a host population has consequences for species interactions. In 2 successive years, we planted large cohorts of the perennial herb Plantago lanceolata in its natural environment and observed infection by Fusarium moniliforme, a non-lethal floral fungal pathogen, over 3 years. We documented substantial variation of pathogen frequency across years and between cohorts. Logistic regression revealed that pathogen frequency increased with the number of inflorescences produced and with evidence of prior pathogen presence, whereas it decreased with increasing plant longevity. In addition, interannual variation and an age-year interaction contributed to the observed pathogen frequencies. There was a significant positive effect of age on pathogen frequency overall, but this was not consistent over all ages. Pathogen frequency was higher in 2-year-old plants than in 1-year-olds, suggesting that age-structure can influence the host-pathogen interaction. This pattern did not continue into 3-year-old plants. A possible explanation for this is that selective mortality allows only generally robust plants, and consequently the most resistant plants, to survive to the oldest ages.     

Parasite transmission in social interacting hosts: monogenean epidemics in guppies

Background

Infection incidence increases with the average number of contacts between susceptible and infected individuals. Contact rates are normally assumed to increase linearly with host density. However, social species seek out each other at low density and saturate their contact rates at high densities. Although predicting epidemic behaviour requires knowing how contact rates scale with host density, few empirical studies have investigated the effect of host density. Also, most theory assumes each host has an equal probability of transmitting parasites, even though individual parasite load and infection duration can vary. To our knowledge, the relative importance of characteristics of the primary infected host vs. the susceptible population has never been tested experimentally.

Methodology/Principal Findings

Here, we examine epidemics using a common ectoparasite, Gyrodactylus turnbulli infecting its guppy host (Poecilia reticulata). Hosts were maintained at different densities (3, 6, 12 and 24 fish in 40 L aquaria), and we monitored gyrodactylids both at a population and individual host level. Although parasite population size increased with host density, the probability of an epidemic did not. Epidemics were more likely when the primary infected fish had a high mean intensity and duration of infection. Epidemics only occurred if the primary infected host experienced more than 23 worm days. Female guppies contracted infections sooner than males, probably because females have a higher propensity for shoaling.

Conclusions/Significance

These findings suggest that in social hosts like guppies, the frequency of social contact largely governs disease epidemics independent of host density.