Spatio-temporal environmental correlation and population variability in simple metacommunities

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Spatial disease dynamics of free-living pathogens under pathogen predation

The epidemiological dynamics of potentially free-living pathogens are often studied with respect to a specific pathogen species (e.g., cholera) and most studies concentrate only on host-pathogen interactions. Here we show that metacommunity-level interactions can alter conventional spatial disease dynamics. We introduce a pathogen eating consumer species and investigate a deterministic epidemiological model of two habitat patches, where both patches can be occupied by hosts, pathogens, and consumers of free-living pathogens. An isolated habitat patch shows periodic disease outbreaks in the host population, arising from cyclic consumer-pathogen dynamics. On the other hand, consumer dispersal between the patches generate asymmetric disease prevalence, such that the host population in one patch stays disease-free, while disease outbreaks occur in the other patch. Such asymmetry can also arise with host dispersal, where infected hosts carry pathogens to the other patch. This indirect movement of pathogens causes also a counter-intuitive effect: decreasing morbidity in a focal patch under increasing pathogen immigration. Our results underline that community-level interactions influence disease dynamics and consistent spatial asymmetry can arise also in spatially homogeneous systems.Peer reviewe

Colonization, covariance and colour: environmental and ecological drivers of diversity-stability relationships

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Landscape structure and ecology influence the spread of a bat fungal disease

White-nose syndrome (WNS), affecting multiple North American bat species during the hibernation period, is a highly pathogenic disease caused by the psychrophilic fungus Pseudogymnoascus destructans (Pd). Because the fungal pathogen persists in the hibernation site environment independently of the hosts, previous theory on spatial disease dynamics cannot predict WNS epidemics. However, the ability to understand factors contributing to the spread of white-nose syndrome (WNS) in North America is crucial to the management of infected and susceptible bat populations as well as the conservation of threatened and endangered bat species. Utilizing recent theory on environmental opportunistic pathogens, we modelled the effect of (a) landscape clustering, (b) environmental conditions in hibernacula and (c) microbial competition on the spread of WNS. We used available, already published data to construct and parameterize our model, which takes into account the spatial distribution of hibernation sites, temperature conditions in both the outside ambient and hibernation site environment, bat population dynamics, dispersal and infection by the pathogen, which also has its host-independent dynamics with the environment. We also consider the effect of outside-host competition between the pathogen and other micro-organisms on spatial disease dynamics. Our model suggests that pathogen loads accumulate in poorly connected hibernacula at short host dispersal, which can help found the epidemic. In contrast, invasion of the landscape is most successful at long host dispersal distances, with homogenous hibernation site distribution and heterogeneous between-hibernation site temperatures. Also, increasing the mean temperature across hibernacula increases fungal growth rate, leading to higher disease prevalence and faster invasion rate. Increasing spatial heterogeneity in hibernaculum temperatures results in the formation of disease hotspots in warmer hibernacula, facilitating more effective spread of the disease in the landscape. Cold-adapted competing microbes can prevent invasion, and therefore, overwintering in cold hibernacula increases probability of host survival. Sites that were suboptimal for overwintering prior to WNS may have importance in preventing local extirpations. Although the model is tailored for WNS, due to pressing need for results that can assist in planning conservation measures, these novel results can be broadly applied to other environmentally transmitted diseases. A is available for this article.Peer reviewe

Confounding environmental colour and distribution shape leads to underestimation of population extinction risk

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Environmental weakening of trophic interactions drives stability in stochastic food webs

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Environmental variation generates environmental opportunist pathogen outbreaks

Many socio-economically important pathogens persist and grow in the outside host environment and opportunistically invade host individuals. The environmental growth and opportunistic nature of these pathogens has received only little attention in epidemiology. Environmental reservoirs are, however, an important source of novel diseases. Thus, attempts to control these diseases require different approaches than in traditional epidemiology focusing on obligatory parasites. Conditions in the outsidehost environment are prone to fluctuate over time. This variation is a potentially important driver of epidemiological dynamics and affect the evolution of novel diseases. Using a modelling approach combining the traditional SIRS models to environmental opportunist pathogens and environmental variability, we show that epidemiological dynamics of opportunist diseases are profoundly driven by the quality of environmental variability, such as the long-term predictability and magnitude of fluctuations. When comparing periodic and stochastic environmental factors, for a given variance, stochastic variation is more likely to cause outbreaks than periodic variation. This is due to the extreme values being further away from the mean. Moreover, the effects of variability depend on the underlying biology of the epidemiological system, and which part of the system is being affected. Variation in host susceptibility leads to more severe pathogen outbreaks than variation in pathogen growth rate in the environment. Positive correlation in variation on both targets can cancel the effect of variation altogether. Moreover, the severity of outbreaks is significantly reduced by increase in the duration of immunity. Uncovering these issues helps in understanding and controlling diseases caused by environmental pathogens.Peer reviewe

Effects of phenotypic variation on consumer coexistence and prey community structure

A popular idea in ecology is that trait variation among individuals from the same species may promote the coexistence of competing species. However, theoretical and empirical tests of this idea have yielded inconsistent findings. We manipulated intraspecific trait diversity in a ciliate competing with a nematode for bacterial prey in experimental microcosms. We found that intraspecific trait variation inverted the original competitive hierarchy to favour the consumer with variable traits, ultimately resulting in competitive exclusion. This competitive outcome was driven by foraging traits (size, speed and directionality) that increased the ciliate's fitness ratio and niche overlap with the nematode. The interplay between consumer trait variation and competition resulted in non-additive cascading effects-mediated through prey defence traits-on prey community assembly. Our results suggest that predicting consumer competitive population dynamics and the assembly of prey communities will require understanding the complexities of trait variation within consumer species.Peer reviewe

Ecology determines how low antibiotic concentration impacts community composition and horizontal transfer of resistance genes

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Holistic view on health : two protective layers of biodiversity

The western world has witnessed a rising epidemic of chronic inflammatory disorders, such as allergies and asthma. This epidemic is expected to spread also to the rest of the world, where allergies have to date been practically absent, along with adoption of western lifestyle. In parallel, biological diversity is globally declining. This inspired Ilkka Hanski, together with medical doctors, to formulate the biodiversity hypothesis of allergic disease. This hypothesis proposes that reduced contact with natural environments, including natural microbial diversity, is associated with unhealthy human microbiota, less able to educate the immune system. Contact with beneficial bacteria, particularly early in life, seems to be instrumental to the normal development of immune responses. Changes in lifestyle and diet, destruction of natural environments, and urbanisation threaten our natural exposure to these beneficial bacteria and thus also reduce their impact on our physiology. To ensure a healthy life, we need to preserve biodiversity in the environment and make sure it finds a favourable home in us. In this review, we will focus on the role of commensal microbiota in human health and wellbeing, as well as the interaction between our microbiota and environmental microbiota, highlighting the contribution of Ilkka Hanski.Peer reviewe