Can infectious diseases eradicate host species? The effect of infection-age structure.

It is a fundamental question in mathematical epidemiology whether deadly infectious diseases only lead to a mere decline of their host populations or whether they can cause their complete disappearance. Upper density-dependent incidences do not lead to host extinction in simple, deterministic SI or SIS (susceptible-infectious) epidemic models. Infection-age structure is introduced into SIS models because of the biological accuracy offered by considering arbitrarily distributed infectious periods. In an SIS model with infection-age structure, survival of the susceptible host population is established for incidences that depend on the infection-age density in a general way. This confirms previous host persistence results without infection-age for incidence functions that are not generalizations of frequency-dependent transmission. For certain power incidences, hosts persist if some infected individuals leave the infected class and become susceptible again and the return rate dominates the infection-age dependent infectivity in a sufficient way. The hosts may be driven into extinction by the infectious disease if there is no return into the susceptible class at all.

Discrete-time population dynamics of spatially distributed semelparous two-sex populations.

Spatially distributed populations with two sexes may face the problem that males and females concentrate in different parts of the habitat and mating and reproduction does not happen sufficiently often for the population to persist. For simplicity, to explore the impact of sex-dependent dispersal on population survival, we consider a discrete-time model for a semelparous population where individuals reproduce only once in their life-time, during a very short reproduction season. The dispersal of females and males is modeled by Feller kernels and the mating by a homogeneous pair formation function. The spectral radius of a homogeneous operator is established as basic reproduction number of the population, [Formula: see text]. If [Formula: see text], the extinction state is locally stable, and if [Formula: see text] the population shows various degrees of persistence that depend on the irreducibility properties of the dispersal kernels. Special cases exhibit how sex-biased dispersal affects the persistence of the population.

Discrete-time population dynamics on the state space of measures.

If the individual state space of a structured population is given by a metric space S, measures µ on the σ-algebra of Borel subsets T of S offer a modeling tool with a natural interpretation: µ(T) is the number of individuals with structural characteristics in the set T. A discrete-time population model is given by a population turnover map F on the cone of finite nonnegative Borel measures that maps the structural population distribution of a given year to the one of the next year. Under suitable assumptions, F has a first order approximation at the zero measure (the extinction fixed point), which is a positive linear operator on the ordered vector space of real measures and can be interpreted as a basic population turnover operator. For a semelparous population, it can be identified with the next generation operator. A spectral radius can be defined by the usual Gelfand formula.We investigate in how far it serves as a threshold parameter between population extinction and population persistence. The variation norm on the space of measures is too strong to give the basic turnover operator enough compactness that its spectral radius is an eigenvalue associated with a positive eigenmeasure. A suitable alternative is the flat norm (also known as (dual) bounded Lipschitz norm), which, as a trade-off, makes the basic turnover operator only continuous on the cone of nonnegative measures but not on the whole space of real measures.

How ticks keep ticking in the adversity of host immune reactions.

Ixodid ticks are acknowledged as one of the most important hematophagous arthropods because of their ability in transmitting a variety of tick-borne diseases. Mathematical models have been developed, based on emerging knowledge about tick ecology, pathogen epidemiology and their interface, to understand tick population dynamics and tick-borne diseases spread patterns. However, no serious effort has been made to model and assess the impact of host immunity triggered by tick feeding on the distribution of the tick population according to tick stages and on tick population extinction and persistence. Here, we construct a novel mathematical model taking into account the effect of host immunity status on tick population dynamics, and analyze the long-term behaviours of the model solutions. Two threshold values, [Formula: see text] and [Formula: see text], are introduced to measure the reproduction ratios for the tick-host interaction in the absence and presence of host immunity. We then show that these two thresholds (sometimes under additional conditions) can be used to predict whether the tick population goes extinct ([Formula: see text]) and the tick population grows without bound ([Formula: see text]). We also prove tick permanence (persistence and boundedness of the tick population) and the existence of a tick persistence equilibrium if [Formula: see text]. As the host species adjust their immunity to tick infestation levels, they form for the tick population an environment with a carrying capacity very much like that in logistic growth. Numerical results show that the host immune reactions decrease the size of the tick population at equilibrium and apparently reduce the tick-borne infection risk.

Times from Infection to Disease-Induced Death and their Influence on Final Population Sizes After Epidemic Outbreaks.

For epidemic models, it is shown that fatal infectious diseases cannot drive the host population into extinction if the incidence function is upper density-dependent. This finding holds even if a latency period is included and the time from infection to disease-induced death has an arbitrary length distribution. However, if the incidence function is also lower density-dependent, very infectious diseases can lead to a drastic decline of the host population. Further, the final population size after an epidemic outbreak can possibly be substantially affected by the infection-age distribution of the initial infectives if the life expectations of infected individuals are an unbounded function of infection age (time since infection). This is the case for lognormal distributions, which fit data from infection experiments involving tiger salamander larvae and ranavirus better than gamma distributions and Weibull distributions.

Do fatal infectious diseases eradicate host species?

In simple SI epidemic and endemic models, three classes of incidence functions are identified for their potential to be associated with host extinction: weakly upper density-dependent incidences are never associated with host extinction. Power incidences that depend on the number of susceptibles and infectives by powers strictly between 0 and 1 are associated with initial-constellation-dependent host extinction for all parameter values. Homogeneous incidences, of which frequency-dependent incidence is a very particular case, and power incidences are associated with global host extinction for certain parameter constellations and with host survival for others. Laboratory infection experiments with salamander larvae are equally well fitted by power incidences and certain upper density-dependent incidences such as the negative binomial incidence and do not rule out homogeneous incidences such as an asymmetric frequency-dependent incidence either.

From homogeneous eigenvalue problems to two-sex population dynamics.

Enclosure theorems are derived for homogeneous bounded order-preserving operators and illustrated for operators involving pair-formation functions introduced by Karl-Peter Hadeler in the late 1980s. They are applied to a basic discrete-time two-sex population model and to the relation between the basic turnover number and the basic reproduction number.

Persistence versus extinction for a class of discrete-time structured population models.

We provide sharp conditions distinguishing persistence and extinction for a class of discrete-time dynamical systems on the positive cone of an ordered Banach space generated by a map which is the sum of a positive linear contraction A and a nonlinear perturbation G that is compact and differentiable at zero in the direction of the cone. Such maps arise as year-to-year projections of population age, stage, or size-structure distributions in population biology where typically A has to do with survival and individual development and G captures the effects of reproduction. The threshold distinguishing persistence and extinction is the principal eigenvalue of (II−A)(−1)G'(0) provided by the Krein-Rutman Theorem, and persistence is described in terms of associated eigenfunctionals. Our results significantly extend earlier persistence results of the last two authors which required more restrictive conditions on G. They are illustrated by application of the results to a plant model with a seed bank.

Stability and persistence in ODE models for populations with many stages.

A model of ordinary differential equations is formulated for populations which are structured by many stages. The model is motivated by ticks which are vectors of infectious diseases, but is general enough to apply to many other species. Our analysis identifies a basic reproduction number that acts as a threshold between population extinction and persistence. We establish conditions for the existence and uniqueness of nonzero equilibria and show that their local stability cannot be expected in general. Boundedness of solutions remains an open problem though we give some sufficient conditions.

Delay differential systems for tick population dynamics.

Ticks play a critical role as vectors in the transmission and spread of Lyme disease, an emerging infectious disease which can cause severe illness in humans or animals. To understand the transmission dynamics of Lyme disease and other tick-borne diseases, it is necessary to investigate the population dynamics of ticks. Here, we formulate a system of delay differential equations which models the stage structure of the tick population. Temperature can alter the length of time delays in each developmental stage, and so the time delays can vary geographically (and seasonally which we do not consider). We define the basic reproduction number [Formula: see text] of stage structured tick populations. The tick population is uniformly persistent if [Formula: see text] and dies out if [Formula: see text]. We present sufficient conditions under which the unique positive equilibrium point is globally asymptotically stable. In general, the positive equilibrium can be unstable and the system show oscillatory behavior. These oscillations are primarily due to negative feedback within the tick system, but can be enhanced by the time delays of the different developmental stages.

Chemostats and epidemics: competition for nutrients/hosts.

In a chemostat, several species compete for the same nutrient, while in an epidemic, several strains of the same pathogen may compete for the same susceptible hosts. As winner, chemostat models predict the species with the lowest break-even concentration, while epidemic models predict the strain with the largest basic reproduction number. We show that these predictions amount to the same if the per capita functional responses of consumer species to the nutrient concentration or of infective individuals to the density of susceptibles are proportional to each other but that they are different if the functional responses are nonproportional. In the second case, the correct prediction is given by the break-even concentrations. In the case of nonproportional functional responses, we add a class for which the prediction does not only rely on local stability and instability of one-species (strain) equilibria but on the global outcome of the competition. We also review some results for nonautonomous models.

Persistence of bacteria and phages in a chemostat.

The model of bacteriophage predation on bacteria in a chemostat formulated by Levin et al. (Am Nat 111:3-24, 1977) is generalized to include a distributed latent period, distributed viral progeny release from infected bacteria, unproductive adsorption of phages to infected cells, and possible nutrient uptake by infected cells. Indeed, two formulations of the model are given: a system of delay differential equations with infinite delay, and a more general infection-age model that leads to a system of integro-differential equations. It is shown that the bacteria persist, and sharp conditions for persistence and extinction of phages are determined by the reproductive ratio for phage relative to the phage-free equilibrium. A novel feature of our analysis is the use of the Laplace transform.

Species decline and extinction: synergy of infectious disease and Allee effect?

Host-parasite models with density-dependent (mass action) incidence and a critical Allee effect in host growth can explain both species decline and disappearance (extinction). The behaviour of the model is consistent with both the novel pathogen hypothesis and the endemic pathogen hypothesis for chytridiomycosis. Mathematically, the transition from decline to disappearance is mediated by a Hopf bifurcation and is marked by the occurrence of a heteroclinic orbit. The Hopf bifurcation is supercritical if intra-specific host competition increases with host density at a large power and subcritical if the power is small. In the supercritical case, host-parasite coexistence can be at equilibrium or periodic; in the subcritical case it is only at equilibrium.

An epidemic model with post-contact prophylaxis of distributed length I. Thresholds for disease persistence and extinction.

A possible control strategy against the spread of an infectious disease is the treatment with antimicrobials that are given prophylactically to those who had a contact with an infective person. The treatment continues until recovery or until it becomes obvious that there was no infection in the first place. The model considers susceptible, treated uninfected exposed, treated infected, (untreated) infectious, and recovered individuals. Since treatment lengths have an arbitrary distribution, the model system consists of ordinary differential and integral equations. A sharp threshold condition is established in terms of a basic replacement ratio (disease reproduction number) that separates disease extinction from uniform disease persistence. We use results from dynamical systems persistence theory proving the existence of a global compact attractor along the way. Existence and multiplicity of endemic equilibria are also studied.

A sharp threshold for disease persistence in host metapopulations.

A sharp threshold is established that separates disease persistence from the extinction of small disease outbreaks in an S→E→I→R→S type metapopulation model. The travel rates between patches depend on disease prevalence. The threshold is formulated in terms of a basic replacement ratio (disease reproduction number), ℛ(0), and, equivalently, in terms of the spectral bound of a transmission and travel matrix. Since frequency-dependent (standard) incidence is assumed, the threshold results do not require knowledge of a disease-free equilibrium. As a trade-off, for ℛ(0)>1, only uniform weak disease persistence is shown in general, while uniform strong persistence is proved for the special case of constant recruitment of susceptibles into the patch populations. For ℛ(0)<1, Lyapunov's direct stability method shows that small disease outbreaks do not spread much and eventually die out.

An apparent paradox of horizontal and vertical disease transmission.

The question as to how the ratio of horizontal to vertical transmission depends on the coefficient of horizontal transmission is investigated in host-parasite models with one or two parasite strains. In an apparent paradox, this ratio decreases as the coefficient is increased provided that the ratio is taken at the equilibrium at which both host and parasite persist. Moreover, a completely vertically transmitted parasite strain that would go extinct on its own can coexist with a more harmful horizontally transmitted strain by protecting the host against it.

Kolmogorov's differential equations and positive semigroups on first moment sequence spaces.

Spatially implicit metapopulation models with discrete patch-size structure and host-macroparasite models which distinguish hosts by their parasite loads lead to infinite systems of ordinary differential equations. In several papers, a this-related theory will be developed in sufficient generality to cover these applications. In this paper the linear foundations are laid. They are of own interest as they apply to continuous-time population growth processes (Markov chains). Conditions are derived that the solutions of an infinite linear system of differential equations, known as Kolmogorov's differential equations, induce a C0-semigroup on an appropriate sequence space allowing for first moments. We derive estimates for the growth bound and the essential growth bound and study the asymptotic behavior. Our results will be illustrated for birth and death processes with immigration and catastrophes.

Progression age enhanced backward bifurcation in an epidemic model with super-infection.

We consider a model for a disease with a progressing and a quiescent exposed class and variable susceptibility to super-infection. The model exhibits backward bifurcations under certain conditions, which allow for both stable and unstable endemic states when the basic reproduction number is smaller than one.

Emergent Allee effects in top predators feeding on structured prey populations.

Top predators that forage in a purely exploitative manner on smaller stages of a size-structured prey population have been shown to exhibit an Allee effect. This Allee effect emerges from the changes that predators induce in the prey-population size distribution and represents a feedback of predator density on its own performance, in which the feedback operates through and is modified by the life history of the prey. We demonstrate that these emergent Allee effects will occur only if the prey, in the absence of predators, is regulated by density dependence in development through one of its juvenile stages, as opposed to regulation through adult fecundity. In particular, for an emergent Allee effect to occur, over-compensation is required in the maturation rate out of the regulating juvenile stage, such that a decrease in juvenile density will increase the total maturation rate to larger/older stages. If this condition is satisfied, predators with negative size selection, which forage on small prey, exhibit an emergent Allee effect, as do predators with positive size selection, which forage on large adult prey. By contrast, predators that forage on juveniles in the regulating stage never exhibit emergent Allee effects. We conclude that the basic life-history characteristics of many species make them prone to exhibiting emergent Allee effects, resulting in an increased likelihood that communities possess alternative stable states or exhibit catastrophic shifts in structure and dynamics.

An endemic model with variable re-infection rate and applications to influenza.

An epidemic model is considered, where immunity is not absolute, but individuals that have recovered from the disease can be re-infected at a rate which depends on the time that has passed since their recovery (recovery age). Such a model, e.g., can account for the genetic drift in the influenza virus. In the special case that the model has no vital dynamics, there is no obvious disease-free equilibrium and so the model lacks the usual interplay between the basic replacement ratio being >1 and the disease-free equilibrium being unstable. In fact, this relatively simple model which combines ordinary differential equations with a transport equation shares with general structured population models the feature that the appropriate state space of the solution semiflow is a space of measures, here on the compacted right real half line, with the weak* topology. The disease-free equilibrium, in terms of recovered individuals, is then represented as a Dirac measure concentrated at infinity. Still it is difficult to linearize about it. This makes the concept of persistence very important, for one can show the following: if the basic replacement ratio is >1, the disease is uniformly strongly persistent, i.e., the number of infectives is ultimately bounded away from 0 with the bound not depending on the initial data. We also derive various conditions for the local and global stability of the endemic equilibrium in terms of the re-infection rate. For instance, the endemic equilibrium is likely to be locally asymptotically stable if the re-infection rate is a highly sub-homogeneous function of recovery age. Conversely, if the re-infection rate is a step function which is zero at small recovery age, the endemic equilibrium can be unstable.