Reproductive Interference Alters Species Coexistence in Nematodes due to Asymmetric Sperm-Induced Harm.

Species coexistence is shaped by a range of biotic and abiotic factors. Beyond predation, parasitism and competition, one species may interfere with another's reproduction to induce sexual exclusion from a habitat. Here, we test for reproductive interference from inter-species mating between sympatric nematodes Caenorhabditis macrosperma and C.

Developmental synchrony and extraordinary multiplication rates in pathogenic organisms.

The multiplication rates of pathogenic organisms influence disease progression, efficacy of immunity and therapeutics, and potential for within-host evolution. Thus, accurate estimates of multiplication rates are essential for biological understanding. We recently showed that common methods for inferring multiplication rates from malaria infection data substantially overestimate true values (i.

Proliferation in malaria parasites: How resource limitation can prevent evolution of greater virulence.

For parasites, robust proliferation within hosts is crucial for establishing the infection and creating opportunities for onward transmission. While faster proliferation enhances transmission rates, it is often assumed to curtail transmission duration by killing the host (virulence), a trade-off constraining parasite evolution. Yet in many diseases, including malaria, the preponderance of infections with mild or absent symptoms suggests that host mortality is not a sufficient constraint, raising the question of what restrains evolution toward faster proliferation.

Extraordinary parasite multiplication rates in human malaria infections.

For pathogenic organisms, faster rates of multiplication promote transmission success, the potential to harm hosts, and the evolution of drug resistance. Parasite multiplication rates (PMRs) are often quantified in malaria infections, given the relative ease of sampling. Using modern and historical human infection data, we show that established methods return extraordinarily - and implausibly - large PMRs.

Mistimed malaria parasites re-synchronize with host feeding-fasting rhythms by shortening the duration of intra-erythrocytic development.

Aims: Malaria parasites exhibit daily rhythms in the intra-erythrocytic development cycle (IDC) that underpins asexual replication in the blood. The IDC schedule is aligned with the timing of host feeding-fasting rhythms. When the IDC schedule is perturbed to become mismatched to host rhythms, it readily reschedules but it is not known how.

Linking functional and molecular mechanisms of host resilience to malaria infection.

It remains challenging to understand why some hosts suffer severe illnesses, while others are unscathed by the same infection. We fitted a mathematical model to longitudinal measurements of parasite and red blood cell density in murine hosts from diverse genetic backgrounds to identify aspects of within-host interactions that explain variation in host resilience and survival during acute malaria infection. Among eight mouse strains that collectively span 90% of the common genetic diversity of laboratory mice, we found that high host mortality was associated with either weak parasite clearance, or a strong, yet imprecise response that inadvertently removes uninfected cells in excess.

Challenges in forming inferences from limited data: a case study of malaria parasite maturation.

Inferring biological processes from population dynamics is a common challenge in ecology, particularly when faced with incomplete data. This challenge extends to inferring parasite traits from within-host infection dynamics. We focus on rodent malaria infections (), a system for which previous work inferred an immune-mediated extension in the length of the parasite development cycle within red blood cells.

Uncovering drivers of dose-dependence and individual variation in malaria infection outcomes.

To understand why some hosts get sicker than others from the same type of infection, it is essential to explain how key processes, such as host responses to infection and parasite growth, are influenced by various biotic and abiotic factors. In many disease systems, the initial infection dose impacts host morbidity and mortality. To explore drivers of dose-dependence and individual variation in infection outcomes, we devised a mathematical model of malaria infection that allowed host and parasite traits to be linear functions (reaction norms) of the initial dose.

Evolutionary consequences of feedbacks between within-host competition and disease control.

Lay Summary: Competition often occurs among diverse parasites within a single host, but control efforts could change its strength. We examined how the interplay between competition and control could shape the evolution of parasite traits like drug resistance and disease severity.

Temperature-dependent variation in the extrinsic incubation period elevates the risk of vector-borne disease emergence.

Identifying ecological drivers of disease transmission is central to understanding disease risks. For vector-borne diseases, temperature is a major determinant of transmission because vital parameters determining the fitness of parasites and vectors are highly temperature-sensitive, including the extrinsic incubation period required for parasites to develop within the vector. Temperature also underlies dramatic differences in the individual-level variation in the extrinsic incubation period, yet the influence of this variation in disease transmission is largely unexplored.

Partitioning the influence of ecology across scales on parasite evolution.

Vector-borne parasites must succeed at three scales to persist: they must proliferate within a host, establish in vectors, and transmit back to hosts. Ecology outside the host undergoes dramatic seasonal and human-induced changes, but predicting parasite evolutionary responses requires integrating their success across scales. We develop a novel, data-driven model to titrate the evolutionary impact of ecology at multiple scales on human malaria parasites.

Anthropogenic nest sites provide warmer incubation environments than natural nest sites in a population of oviparous reptiles near their northern range limit.

Oviposition site choice affects a host of offspring phenotypes and directly impacts maternal fitness. Recent evidence suggests that oviparous reptiles often select nest sites where the landscape has been altered by anthropogenic activity, whereas natural nest sites are less often used. We leverage a long-term study of snapping turtle (Chelydra serpentina) to identify natural nest sites and anthropogenic nest sites and to compare habitat variables among nest site types.

The Challenge of Quantifying Synchrony in Malaria Parasites.

Malaria infection is often accompanied by periodic fevers, triggered by synchronous cycles of parasite replication within the host. The degree of synchrony in parasite development influences the efficacy of drugs and immune defenses and is therefore relevant to host health and infectiousness. Synchrony is thought to vary over the course of infection and across different host-parasite genotype or species combinations, but the evolutionary significance - if any - of this diversity remains elusive.

Adaptive plasticity in the gametocyte conversion rate of malaria parasites.

Sexually reproducing parasites, such as malaria parasites, experience a trade-off between the allocation of resources to asexual replication and the production of sexual forms. Allocation by malaria parasites to sexual forms (the conversion rate) is variable but the evolutionary drivers of this plasticity are poorly understood. We use evolutionary theory for life histories to combine a mathematical model and experiments to reveal that parasites adjust conversion rate according to the dynamics of asexual densities in the blood of the host.

Altered life history strategies protect malaria parasites against drugs.

Drug resistance has been reported against all antimalarial drugs, and while parasites can evolve classical resistance mechanisms (e.g., efflux pumps), it is also possible that changes in life history traits could help parasites evade the effects of treatment.

Epidemiological consequences of immune sensitisation by pre-exposure to vector saliva.

Blood-feeding arthropods-like mosquitoes, sand flies, and ticks-transmit many diseases that impose serious public health and economic burdens. When a blood-feeding arthropod bites a mammal, it injects saliva containing immunogenic compounds that facilitate feeding. Evidence from Leishmania, Plasmodium and arboviral infections suggests that the immune responses elicited by pre-exposure to arthropod saliva can alter disease progression if the host later becomes infected.

Predicting optimal transmission investment in malaria parasites.

In vertebrate hosts, malaria parasites face a tradeoff between replicating and the production of transmission stages that can be passed onto mosquitoes. This tradeoff is analogous to growth-reproduction tradeoffs in multicellular organisms. We use a mathematical model tailored to the life cycle and dynamics of malaria parasites to identify allocation strategies that maximize cumulative transmission potential to mosquitoes.

Quantifying Transmission Investment in Malaria Parasites.

Many microparasites infect new hosts with specialized life stages, requiring a subset of the parasite population to forgo proliferation and develop into transmission forms. Transmission stage production influences infectivity, host exploitation, and the impact of medical interventions like drug treatment. Predicting how parasites will respond to public health efforts on both epidemiological and evolutionary timescales requires understanding transmission strategies.

The role of models in translating within-host dynamics to parasite evolution.

Mathematical modelling provides an effective way to challenge conventional wisdom about parasite evolution and investigate why parasites 'do what they do' within the host. Models can reveal when intuition cannot explain observed patterns, when more complicated biology must be considered, and when experimental and statistical methods are likely to mislead. We describe how models of within-host infection dynamics can refine experimental design, and focus on the case study of malaria to highlight how integration between models and data can guide understanding of parasite fitness in three areas: (1) the adaptive significance of chronic infections; (2) the potential for tradeoffs between virulence and transmission; and (3) the implications of within-vector dynamics.

Synchrony in malaria infections: how intensifying within-host competition can be adaptive.

Malaria parasites exhibit great diversity in the coordination of their asexual life cycle within the host, ranging from asynchronous growth to tightly synchronized cycles of invasion and emergence from red blood cells. Synchronized reproduction should come at a high cost--intensifying competition among offspring--so why would some Plasmodium species engage in such behavior and others not? We use a delayed differential equation model to show that synchronized infections can be favored when (1) there is limited interference among parasites competing for red blood cells, (2) transmission success is an accelerating function of sexual parasite abundance, (3) the target of saturating immunity is short-lived, and (4) coinfections with asynchronous parasites are rare. As a consequence, synchrony may be beneficial or costly, in line with the diverse patterns of synchronization observed in natural and lab infections.

Coprinus cinereus rad50 mutants reveal an essential structural role for Rad50 in axial element and synaptonemal complex formation, homolog pairing and meiotic recombination.

The Mre11/Rad50/Nbs1 (MRN) complex is required for eukaryotic DNA double-strand break (DSB) repair and meiotic recombination. We cloned the Coprinus cinereus rad50 gene and showed that it corresponds to the complementation group previously named rad12, identified mutations in 15 rad50 alleles, and mapped two of the mutations onto molecular models of Rad50 structure. We found that C.

A synthesis of experimental work on parasite local adaptation.

The study of parasite local adaptation, whereby parasites perform better on sympatric hosts than on allopatric hosts and/or better on their own host population than do other parasites, is of great importance to both basic and applied biology. Theoretical examination of host-parasite coevolution predicts that parasite migration rate, generation time and virulence all contribute to the pattern of parasite local adaptation, such that parasites with greater dispersal ability, more frequent reproduction and/or high virulence ought to exhibit increased infectivity on local hosts. Here, we present a meta-analysis of experimental work from 57 host-parasite systems across 54 local adaptation studies to directly test theoretical predictions concerning the effect of each attribute on parasite adaptation.