Expansion of Ash Dieback towards the scattered Fraxinus excelsior range of the Italian peninsula

Hymenoscyphus fraxineus, causal agent of Ash Dieback, has posed a threat to Fraxinus excelsior (common ash) in Europe since the 1990s. In south-western Europe, optimal climatic conditions for H. fraxineus become scattered and host density decreases, reducing disease spread rates. To date, the Ash Dieback agent has not been reported from southern and most of central Italy, where native F. excelsior is present as small fragmented populations. This study examines the expansion of Ash Dieback into central Italy, and it considers the consequences of further local spread with regards to the loss of F. excelsior genetic resource. Symptomatic F. excelsior were sampled from sixteen sites in northern and central Italy during 2020. Specimens were analyzed with a culturomics and a quantitative PCR approach. A bibliographic search of F. excelsior floristic reports was conducted for the creation of a detailed range map. The combined use of both techniques confirmed the presence of H. fraxineus in all the sites of central Italy where host plants were symptomatic. These new records represent the southern limit of the current known distribution of this pathogen in Italy, and together with Montenegro, in Europe. The characterization of the F. excelsior scattered range suggests that further spread of Ash Dieback across southern Italy is a realistic scenario. This presents a threat not just to the southern European proveniences of F. excelsior, but to the species as a whole, should Ash Dieback lead to the loss of warm climate adapted genetic material, which may become increasingly valuable under climate change.

Impact of a nonnative parasitoid species on intraspecific interference and offspring sex ratio

In an assemblage of multiple predators sharing a single prey species, the combined effects of the component species may scale unpredictably because of emergent interspecific interactions. Prior studies suggest that chaotic but persistent community dynamics are induced by intra-/interspecific interactions between native and nonnative parasitoids competing over a shared host. Here, we test the impact of the nonnative parasitoid Heterospilus prosopidis (Hymenoptera: Braconidae) on the intraspecific interference and offspring sex ratio of the native parasitoid Anisopteromalus calandrae (Hymenoptera: Pteromalidae). We found that the nonnative parasitoid reduced intraspecific interference among native parasitoids and decreased the proportion of female offspring produced by the native parasitoid (predicted under conditions of reduced host availability). At higher host densities, the nonnative parasitoid contributed less to the total proportion of hosts parasitized, as its innate saturating Type II response changed to a dome-shaped Type IV response with increasing density of the native parasitoid, while the native parasitoid retained its increasing Type I response. This inverse host-density-dependent response between the two parasitoids and associated competitive superiority can explain the observed changes in parasitism; at high host densities, the searching efficiency of the native parasitoid increases via host feeding while the nonnative parasitoid experiences egg limitation. These results highlight the importance of the complementary top-down effects of multiple consumers on a single resource.

A microbial mutualist within host individuals increases parasite transmission between host individuals: Evidence from a field mesocosm experiment

The interactions among host-associated microbes and parasites can have clear consequences for disease susceptibility and progression within host individuals. Yet, empirical evidence for how these interactions impact parasite transmission between host individuals remains scarce. We address this scarcity by using a field mesocosm experiment to investigate the interaction between a systemic fungal endophyte, Epichloe coenophiala, and a fungal parasite, Rhizoctonia solani, in leaves of a grass host, tall fescue. Specifically, we investigated how this interaction impacted parasite transmission under field conditions in replicated experimental host populations. Epichloe-inoculated populations tended to have greater disease prevalence over time, though this difference had weak statistical support. More clearly, Epichloe-inoculated populations experienced higher peak parasite prevalences than Epichloe-free populations. Epichloe conferred a benefit in growth; Epichloe-inoculated populations had greater aboveground biomass than Epichloe-free populations. Using biomass as a proxy, host density was correlated with peak parasite prevalence, but Epichloe still increased peak parasite prevalence after controlling for the effect of biomass. Together, these results suggest that within-host microbial interactions can impact disease at the population level. Further, while Epichloe is clearly a mutualist of tall fescue, it may not be a defensive mutualist in relation to R. solani.

Diversity, multifaceted evolution, and facultative saprotrophism in the European Batrachochytrium salamandrivorans epidemic

While emerging fungi threaten global biodiversity, the paucity of fungal genome assemblies impedes thoroughly characterizing epidemics and developing effective mitigation strategies. Here, we generate de novo genomic assemblies for six outbreaks of the emerging pathogen Batrachochytrium salamandrivorans (Bsal). We reveal the European epidemic currently damaging amphibian populations to comprise multiple, highly divergent lineages demonstrating isolate-specific adaptations and metabolic capacities. In particular, we show extensive gene family expansions and acquisitions, through a variety of evolutionary mechanisms, and an isolate-specific saprotrophic lifecycle. This finding both explains the chytrid’s ability to divorce transmission from host density, producing Bsal’s enigmatic host population declines, and is a key consideration in developing successful mitigation measures.

Coral Disease and the Environment in the Pacific Ocean

<p>Coral diseases are a major threat to coral reef health and functioning worldwide. Little is known about how coral disease prevalence relates to multiple interacting changes in host densities, abiotic stressors, and levels of human impact. In particular, almost nothing is known about coral disease dynamics under changing abiotic conditions in the absence of direct anthropogenic stressors. Understanding how disease dynamics change relative to shifts in environmental conditions is crucial for the successful management and future survival of coral reefs. With the use of existing and novel field data and statistical modeling I examined the associations (abiotic and biotic) of multiple coral disease states across a variety of spatial scales encompassing a wide range of environmental conditions. Biomedical techniques were then used to relate these environmental associations to potential disease etiology. Study sites included areas with high levels of anthropogenic impact (e.g. Oahu, main Hawaiian Islands); to extremely remote quasi-pristine reefs removed from direct human influence (e.g. Palmyra Atoll National Wildlife Refuge). Over small spatial scales (100s m) at a marine reserve in the main Hawaiian Islands I modelled the spatial patterns of four coral diseases (Porites growth anomalies, Porites tissue loss, Porites trematodiasis and Montipora white syndrome). While Porites tissue loss and Montipora white syndrome were positively associated with poor environmental conditions (poor water quality, low coral cover), Porites growth anomalies and Porites trematodiasis were more prevalent in areas considered to be of superior quality (clearer water, increased host abundance, higher numbers of fish). At Palmyra Atoll, fatal tissue loss diseases were largely absent and although coral growth anomalies were present their prevalence was extremely low. Patterns of growth anomaly prevalence at Palmyra were positively associated with host abundance across four coral genera (Acropora, Astreopora, Montipora and Porites) and generally negatively associated with algal cover. Growth anomalies, although progressive and detrimental to the hosts, were most prevalent in the "healthiest" regions (the highest coral cover regions) of Palmyra. I hypothesised that differences seen in the types and prevalence of coral diseases between heavily populated parts of Hawaii and remote uninhabited locations such as Palmyra Atoll, could be a result of differing levels of either direct (e.g. pollution) or indirect (e.g. pollution leading to loss of key hosts) human stressors, in addition to natural changes in the environment. To begin disentangling the confounding effects of natural variability and human stressors on coral disease prevalence patterns I modelled two diseases (Acropora and Porites growth anomalies) across hundreds of sites throughout the Indo-Pacific Ocean (1000s km). Predictors included host densities, human population numbers, frequency of sea surface temperature anomalies, and input of ultra-violet radiation. Porites growth anomaly prevalence was positively associated with human population density (and to a lesser extent host density), while the prevalence of Acropora growth anomalies was strongly host density dependent. The positive association between the prevalence of Porites growth anomalies and human density suggests the presence and prevalence of the disease are related, directly or indirectly, to some environmental co-factor associated with increased human density at regional spatial scales. Although this association has been widely posited, this is one of the first wide scale studies unambiguously linking a coral disease with human population size. In summary, the types of coral diseases observed, their prevalence, and spatial patterns of distribution within reef systems are the result of multiple abiotic and biotic factors and stressors interacting, in some cases synergistically. Statistical modelling, in conjunction with biomedical techniques and field observations, proved essential to the understanding of coral disease ecology within single reefs and atolls to patterns across entire oceans.</p>

Dynamics model analysis of bacteriophage infection of bacteria

A bacteriophage (in short, phage) is a virus that can infect and replicate within bacteria. Assuming that uninfected and infected bacteria are capable of reproducing with logistic law, we investigate a model of bacteriophage infection that resembles simple SI-models widely used in epidemiology. The dynamics of host-parasite co-extinctions may exhibit four scenarios: hosts and parasites go extinct, parasites go extinct, hosts go extinct, and hosts and parasites coexist. By using the Jacobian matrix and Bendixson–Dulac theory, local and global stability analysis of uninfected and infected steady states is provided; the basic reproduction number of the model is given; general results are supported by numerical simulations. We show that bacteriophages can reduce a host density. This provides a theoretical framework for studying the problem of whether phages can effectively prevent, control, and treat infectious diseases.

Phage strategies facilitate bacterial coexistence under environmental variability

Bacterial communities are often exposed to temporal variations in resource availability, which exceed bacterial generation times and thereby affect bacterial coexistence. Bacterial population dynamics are also shaped by bacteriophages, which are a main cause of bacterial mortality. Several strategies are proposed in the literature to describe infections by phages, such as “Killing the Winner”, “Piggyback the loser” (PtL) or “Piggyback the Winner” (PtW). The two temperate phage strategies PtL and PtW are defined by a change from lytic to lysogenic infection when the host density changes, from high to low or from low to high, respectively. To date, the occurrence of different phage strategies and their response to environmental variability is poorly understood. In our study, we developed a microbial trophic network model using ordinary differential equations (ODEs) and performed ‘in silico’ experiments. To model the switch from the lysogenic to the lytic cycle, we modified the lysis rate of infected bacteria and their growth was turned on or off using a density-dependent switching point. We addressed whether and how the different phage strategies facilitate bacteria coexistence competing for limiting resources. We also studied the impact of a fluctuating resource inflow to evaluate the response of the different phage strategies to environmental variability. Our results show that the viral shunt (i.e. nutrient release after bacterial lysis) leads to an enrichment of the system. This enrichment enables bacterial coexistence at lower resource concentrations. We were able to show that an established, purely lytic model leads to stable bacterial coexistence despite fluctuating resources. Both temperate phage models differ in their coexistence patterns. The model of PtW yields stable bacterial coexistence at a limited range of resource supply and is most sensitive to resource fluctuations. Interestingly, the purely lytic phage strategy and PtW both result in stable bacteria coexistence at oligotrophic conditions. The PtL model facilitates stable bacterial coexistence over a large range of stable and fluctuating resource inflow. An increase in bacterial growth rate results in a higher resilience to resource variability for the PtL and the lytic infection model. We propose that both temperate phage strategies represent different mechanisms of phages coping with environmental variability. Our study demonstrates how phage strategies can maintain bacterial coexistence in constant and fluctuating environments.

A decade of stability for wMel Wolbachia in natural Aedes aegypti populations

Mosquitoes carrying Wolbachia endosymbionts are being released in many countries for arbovirus control. The wMel strain of Wolbachia blocks Aedes-borne virus transmission and can spread throughout mosquito populations by inducing cytoplasmic incompatibility. Aedes aegypti mosquitoes carrying wMel were first released into the field in Cairns, Australia, over a decade ago, and with wider releases have resulted in the near elimination of local dengue transmission. The long-term stability of Wolbachia effects is critical for ongoing disease suppression, requiring tracking of phenotypic and genomic changes in Wolbachia infections following releases. We used a combination of field surveys, phenotypic assessments, and Wolbachia genome sequencing to show that wMel has remained stable in its effects for up to a decade in Australian Ae. aegypti populations. Phenotypic comparisons of wMel-infected and uninfected mosquitoes from near-field and long-term laboratory populations suggest limited changes in the effects of wMel on mosquito fitness. Treating mosquitoes with antibiotics used to cure the wMel infection had limited effects on fitness in the next generation, supporting the use of tetracycline for generating uninfected mosquitoes without off-target effects. wMel has a temporally stable within-host density and continues to induce complete cytoplasmic incompatibility. A comparison of wMel genomes from pre-release (2010) and nine years post-release (2020) populations show few genomic differences and little divergence between release locations, consistent with the lack of phenotypic changes. These results indicate that releases of Wolbachia-infected mosquitoes for population replacement are likely to be effective for many years, but ongoing monitoring remains important to track potential evolutionary changes.

Functional and numerical responses of the predator Amblyseius swirskii to its prey Tetranychus turkestani in the laboratory

The tetranychid Tetranychus turkestani Ugarov and Nikolskii is a serious pest of many important crops around the world. Management of T. turkestani by augmentative biological control using predators such as the phytoseiid Amblyseius swirskii (Athias-Henriot) is envisioned as an environmentally safe alternative to acaricides. Foundational knowledge on T. turkestani – A. swirskii interactions in the laboratory are necessary to predict the outcome of A. swirskii augmentative releases in the field. In this study, the functional and numerical responses of adult A. swirskii females feeding on immature stages of T. turkestani were determined in the laboratory. Prey densities were 2, 4, 8, 16, 32, 64, or 128 individuals per Petri dish arena. The functional response of A. swirskii to prey showed a Holling's type II response. The attack rate and handling time estimates from the random predator equation were 0.1148/h and 0.3146 h, respectively, indicating that A. swirskii consumed 76.28 individuals per day at the maximum level. The number of eggs laid by the predator, i.e., the numerical response, increased as host density increased up to a maximum of 33.10 eggs per female; then oviposition rate leveled-off. This study suggests that A. swirskii is a suitable candidate for augmentative biological control of T. turkestani but follow-up experiments in greenhouses or open fields are necessary.

Defining an epidemiological landscape by connecting host movement to pathogen transmission

Environment drives the host movements that shape pathogen transmission through three mediating processes: host density, host mobility, and contact. These processes combine with pathogen life-history to give rise to an “epidemiological landscape” that determines spatial patterns of pathogen transmission. Yet despite its central role in transmission, strategies for predicting the epidemiological landscape from real-world data remain limited. Here, we develop the epidemiological landscape as an interface between movement ecology and spatial epidemiology. We propose a movement-pathogen pace-of-life heuristic for prioritizing the landscape’s central processes by positing that spatial dynamics for fast pace-of-life pathogens are best-approximated by the spatial ecology of host contacts; spatial dynamics for slower pace-of-life pathogens are best approximated by host densities; and spatial dynamics for pathogens with environmental reservoirs reflect a convolution of those densities with the spatial configuration of environmental reservoir sites. We then identify mechanisms that underpin the epidemiological landscape and match each mechanism to emerging tools from movement ecology. Finally, we outline workflows for describing the epidemiological landscape and using it to predict subsequent patterns of pathogen transmission. Our framework links transmission to environmental context, providing a scaffold for mechanistically understanding how environmental context can generate and shift existing patterns in spatial epidemiology.