Hosts strongly influence parasite fitness. However, it is challenging to disentangle host effects on genetic vs plasticity-driven traits of parasites, since parasites can evolve quickly. It remains especially difficult to determine the causes and magnitude of parasite plasticity. In successive generations, parasites may respond plastically to better infect their current type of host, or hosts may produce generally ‘good’ or ‘bad’ quality parasites. Here, we characterized parasite plasticity by taking advantage of a system in which the parasite (the yeast Metschnikowia bicuspidata, which infects Daphnia) has no detectable heritable variation, preventing rapid evolution. In experimental infection assays, we found an effect of rearing host genotype on parasite infectivity, where host genotypes produced overall high or low quality parasite spores. Additionally, these plastically induced differences were gained or lost in just a single host generation. Together, these results demonstrate phenotypic plasticity in infectivity driven by the within-host rearing environment. Such plasticity is rarely investigated in parasites, but could shape epidemiologically important traits.

We formulate an immuno-epidemiological model of coupled “within-host” model of ODEs and“between-host” model of ODE and PDE, using the Human Immunodeficiency Virus (HIV) forillustration. Existence and uniqueness of solution to the “between-host” model isestablished, and an explicit expression for the basic reproduction number of the“between-host” model derived. Stability of disease-free and endemic equilibria isinvestigated. An optimal control problem with drug-treatment control on the within-hostsystem is formulated and analyzed; these results are novel for optimal control of ODEslinked with such first order PDEs. Numerical simulations based on the forward-backwardsweep method are obtained.

Infectious agents have considerable potential to regulate or constrain the population growth of vertebrate hosts in natural habitats. A broad theoretical framework provides many insights into how the biology of the parasite and the demography of the host interact to determine this impact. It may manifest itself as a steady influence over time via stable endemic infection or in a recurrent epidemic fashion, sometimes with unpredictable intervals between epidemics depending on the generation time of the pathogen (time from infection to recovery or host death), its ability to induce lasting immunity and the population growth rate of the host species. Building on these notions, the paper focuses on recent work on the population dynamics of genetically variable pathogen populations and examines the factors that determine the evolution of virulence and the maintenance of genetic diversity in both host and pathogen. Recent research extends conventional theoretical templates to include population genetic elements and the within-host dynamics of the parasite and its interaction with the vertebrate immune system.

Most mathematical models of malaria infection represent parasites as replicating continuously at a constant rate whereas in reality, malaria parasites replicate at a fixed age. The behaviour of continuous-time models when gametocytogenesis is included, in comparison to a more realistic discrete-time model that incorporates a fixed replication age was evaluated. Both the infection dynamics under gametocytogenesis and implications for predicting the amount parasites should invest into gametocytes (level of investment favoured by natural selection) are considered. It is shown that the many malaria models with constant replication rates can be represented by just 3 basic types. For these 3 types, it is then shown that under gametocytogenesis (i) in 2 cases, parasite multiplication and gametocyte production is mostly much too low, (ii) in the third, parasite multiplication and gametocyte production is mostly much too high, (iii) the effect of gametocyte investment on parasite multiplication is mostly too high, (iv) the effect of gametocyte investment on gametocyte production is nearly always too low and (v) with a simple approximation of fitness, the predicted level of gametocyte investment is mostly much too low. However, a continuous model with 48 age-compartments compares well to the discrete model. These findings are a further argument for modelling malaria infections in discrete time.

The success of a pathogen depends not only on its transmission to new hosts, but also on its ability to colonize and persist within its current host. Studies of within-host dynamics have focused on only a few diseases of humans, whereas little is known about the factors that influence pathogen populations as they develop inside non-human hosts. Here, we investigate pathogen dynamics occurring within bumble bees (Bombus impatiens) infected by the gut trypanosome Crithidia bombi. Infection by C. bombi showed several features characteristic of vertebrate diseases, including a rapid initial increase in infection intensity, marked oscillations in parasitaemia, and the stimulation of a systemic immune response in infected bees. Within-host dynamics generated substantial variation in the infectiousness and flower-visiting behaviour of bumble bees. Changes in bee foraging that arise from infection may influence the probability of C. bombi transmission between bees at flowers.

The fresh-water crustacean Daphnia magna may acquire an infection with the microsporidium Octosporea bayeri either by ingesting spores from the water (horizontally), or directly from its mother (vertically). Due to differences in the time and mechanisms of transmission, horizontal and vertical infections may lead to differences in the growth of the parasite within the host. This may influence parasite virulence, transmission to new hosts, and, consequently, epidemiology and evolution. Here we describe the within-host dynamics of 3 spore-types of O.bayeri from infections that were acquired either horizontally or vertically. In all treatments the number of spores increased exponentially until spore density reached a plateau, suggesting density-dependent within-host growth. The spore types seen differ in their growth dynamics, suggesting different roles in the parasite life-cycle. Horizontally-infected hosts harboured significantly fewer spores than vertically-infected hosts. Further, host survival was affected by infection route, with mortality being higher in horizontal infections than in vertical infections. Our results suggest that different routes of infection have an immediate effect on within-host parasite growth and thus on parasite fitness and epidemiology.