Spatial heterogeneity lowers rather than increases host–parasite specialization

Abiotic environmental heterogeneity can promote the evolution of diverse resource specialists, which in turn may increase the degree of host–parasite specialization. We coevolved Pseudomonas fluorescens and lytic phage ?2 in spatially structured populations, each consisting of two interconnected subpopulations evolving in the same or different nutrient media (homogeneous and heterogeneous environments, respectively). Counter to the normal expectation, host–parasite specialization was significantly lower in heterogeneous compared with homogeneous environments. This result could not be explained by dispersal homogenizing populations, as this would have resulted in the heterogeneous treatments having levels of specialization equal to or greater than that of the homogeneous environments. We argue that selection for costly generalists is greatest when the coevolving species are exposed to diverse environmental conditions and that this can provide an explanation for our results. A simple coevolutionary model of this process suggests that this can be a general mechanism by which environmental heterogeneity can reduce rather than increase host–parasite specialization.     

How can immunopathology shape the evolution of parasite virulence?

Immunopathology (immune-mediated pathology) is a ubiquitous cause of disease during infection, but how will parasite exploitation strategies evolve in its presence? Immunopathology can act to increase parasite fitness if it increases transmission rate, but can equally act to decrease parasite fitness if it increases host mortality. The focus here is on understanding how immunopathology, mediated through different immune mechanisms, can influence parasite fitness and how experimental manipulations of the immune system can be carried out to examine this. A better understanding of how parasite fitness scales with, or responds to, immunopathology is crucial to understanding the nature of selection acting on parasite virulence traits and will allow more informed predictions to be made regarding the trajectory of parasite virulence evolution.     

The evolution of oscillatory behavior in age-structured species

A major challenge in ecology is to explain why so many species show oscillatory population dynamics and why the oscillations commonly occur with particular periods. The background environment, through noise or seasonality, is one possible driver of these oscillations, as are the components of the trophic web with which the species interacts. However, the oscillation may also be intrinsic, generated by density-dependent effects on the life history. Models of structured single-species systems indicate that a much broader range of oscillatory behavior than that seen in nature is theoretically possible. We test the hypothesis that it is selection that acts to constrain the range of periods. We analyze a nonlinear single-species matrix model with density dependence affecting reproduction and with trade-offs between reproduction and survival. We show that the evolutionarily stable state is oscillatory and has a period roughly twice the time to maturation, in line with observed patterns of periodicity. The robustness of this result to variations in trade-off function and density dependence is tested.     

THE EVOLUTIONARY IMPLICATIONS OF CONFLICT BETWEEN PARASITES WITH DIFFERENT TRANSMISSION MODES

Understanding the processes that shape the evolution of parasites is a key challenge for evolutionary biology. It is well understood that different parasites may often infect the same host and that this may have important implications to the evolutionary behavior. Here we examine the evolutionary implications of the conflict that arises when two parasite species, one vertically transmitted and the other horizontally transmitted, infect the same host. We show that the presence of a vertically transmitted parasite (VTP) often leads to the evolution of higher virulence in horizontally transmitted parasites (HTPs), particularly if the VTPs are feminizing. The high virulence in some HTPs may therefore result from coinfection with cryptic VTPs. The impact of an HTP on a VTP evolution depends crucially on the nature of the life‐history trade‐offs. Fast virulent HTPs select for intermediate feminization and virulence in VTPs. Coevolutionary models show similar insights, but emphasize the importance of host life span to the outcome, with higher virulence in both types of parasite in short‐lived hosts. Overall, our models emphasize the interplay of host and parasite characteristics in the evolutionary outcome and point the way for further empirical study.     

The effects of simulated rainfall on immature population dynamics of Aedes albopictus and female oviposition

Larvae of Aedes albopictus Skuse typically inhabit natural and artificial containers. Since these larval habitats are replenished by rainfall, Ae. albopictus may experience increased loss of immature stages in areas with high levels of rainfall. In this study, we investigated the effects of rainfall and container water level on population density, and oviposition activity of Ae. albopictus. In field and laboratory experiments, we found that rainfall resulted in the flushing of breeding habitats. Excess rain negatively impacted larval and pupal retention, especially in small habitats. When filled with water to overflowing, container habitats were significantly repellent to ovipositing females. Taken together, these data suggest that rainfall triggers population loss of Ae. albopictus and related species through a direct detrimental effect (flushing out) and an indirect effect (ovipositional repellency).     

The implications of immunopathology for parasite evolution

By definition, parasites harm their hosts, but in many infections much of the pathology is driven by the host immune response rather than through direct damage inflicted by parasites. While these immunopathological effects are often well studied and understood mechanistically in individual disease interactions, there remains relatively little understanding of their broader impact on the evolution of parasites and their hosts. Here, we theoretically investigate the implications of immunopathology, broadly defined as additional mortality associated with the host's immune response, on parasite evolution. In particular, we examine how immunopathology acting on different epidemiological traits (namely transmission, virulence and recovery) affects the evolution of disease severity. When immunopathology is costly to parasites, such that it reduces their fitness, for example by decreasing transmission, there is always selection for increased disease severity. However, we highlight a number of host-parasite interactions where the parasite may benefit from immunopathology, and highlight scenarios that may lead to the evolution of slower growing parasites and potentially reduced disease severity. Importantly, we find that conclusions on disease severity are highly dependent on how severity is measured. Finally, we discuss the effect of treatments used to combat disease symptoms caused by immunopathology.     

Local transmission processes and disease-driven host extinctions

Classic infectious disease theory assumes that transmission depends on either the global density of the parasite (for directly transmitted diseases) or its global frequency (for sexually transmitted diseases). One important implication of this dichotomy is that parasite-driven host extinction is only predicted under frequency-dependent transmission. However, transmission is fundamentally a local process between individuals that is determined by their and/or their vector’s behaviour. We examine the implications of local transmission processes to the likelihood of disease-driven host extinction. Local density-dependent transmission can lead to parasite-driven extinction, but extinction is more likely under local frequency-dependent transmission and much more likely when there is active local searching behaviour. Density-dependent directly transmitted diseases spread locally can therefore lead to deterministic host extinction, but locally frequency-dependent passive vector-borne diseases are more likely to cause extinctions. However, it is active searching behaviour either by a vector or between sexual partners that is most likely to cause the host to go extinct. Our work emphasises that local processes are essential in determining parasite-driven extinctions, and the role of parasites in the extinction of rare species may have been underplayed due to the classic assumption of global density-dependent transmission.     

Fight or learn to live with the consequences?

Individuals can fight their infectious diseases by reducing the growth of a pathogen (resistance), but they can also ameliorate the disease it causes (tolerance). A recent paper shows that there is variation between mouse strains in tolerance to a rodent malaria and that this was negatively correlated with resistance. This is important, because tolerance has major implications for the epidemiology and coevolution of host-parasite interactions, but has been neglected in the animal literature.