Deforestation alters wildlife communities and modifies human-wildlife interactions, often increasing zoonotic spillover potential. When deforested land reverts to forest, species composition differences between primary and regenerating (secondary) forest could alter spillover risk trajectory. We develop a mathematical model of land-use change, where habitats differ in their relative spillover risk, to understand how land reversion influences spillover risk. We apply this framework to scenarios where spillover risk is higher in deforested land than mature forest, reflecting higher relative abundance of highly competent species and/or increased human-wildlife encounters, and where regenerating forest has either very low or high spillover risk. We find the forest regeneration rate, the spillover risk of regenerating forest relative to deforested land, and how rapidly regenerating forest regains attributes of mature forest determine landscape-level spillover risk. When regenerating forest has a much lower spillover risk than deforested land, reversion lowers cumulative spillover risk, but instaneous spillover risk peaks earlier. However, when spillover risk is high in regenerating and cleared habitats, landscape-level spillover risk remains high, especially when cleared land is rapidly abandoned then slowly regenerates to mature forest. These results suggest that proactive wildlife management and awareness of human exposure risk in regenerating forests could be important tools for spillover mitigation.

Guinea worm (Dracunculus medinensis) has exerted a high human health burden in parts of Africa. Complete eradication of Guinea worm disease (dracunculiasis) may be delayed by the circulation of the parasite in domestic dogs. As with humans, dogs acquire the parasite by directly ingesting infected copepods, and recent evidence suggests that consuming frogs that ingested infected copepods as tadpoles may be a viable transmission route (paratenic route). To understand the relative contributions of direct and paratenic transmission routes, we developed a mathematical model that describes transmission of Guinea worm between dogs, copepods and frogs. We explored how the parasite basic reproductive number (R0) depends on parameters amenable to actionable interventions under three scenarios: frogs/tadpoles do not consume copepods; tadpoles consume copepods but frogs do not contribute to transmission; and frogs are paratenic hosts. We found a non-monotonic relationship between the number of dogs and R0. Generally, frogs can contribute to disease control by removing infected copepods from the waterbody even when paratenic transmission can occur. However, paratenic transmission could play an important role in maintaining the parasite when direct transmission is reduced by interventions focused on reducing copepod ingestion by dogs. Together, these suggest that the most effective intervention strategies may be those which focus on the reduction of copepods, as this reduces outbreak potential irrespective of the importance of the paratenic route.

While vector-borne parasite transmission often operates via generalist-feeding vectors facilitating cross-species transmission in host communities, theory describing the relationship between host species diversity and parasite invasion in these systems is underdeveloped. Host community composition and abundance vary across space and time, generating opportunities for parasite invasion. To explore how host community variation can modify parasite invasion potential, we develop a model for vector-borne parasite transmission dynamics that includes a host community of arbitrary richness and species' abundance. To compare invasion potential across communities, we calculate the community basic reproductive ratio of the parasite. We compare communities comprising a set of host species to their subsets, which allows for flexible scenario building including the introduction of novel host species and species loss. We allow vector abundance to scale with, or be independent of, community size, capturing regulation by feeding opportunities and non-host effects such as limited oviposition sites. Motivated by equivocal data relating host species competency to abundance, we characterize plausible host communities via phenomenological relationships between host species abundance and competency. We identify an underappreciated mechanism whereby changes to communities simultaneously alter average competency and the vector to host ratio and demonstrate that the interaction can profoundly influence invasion potential.

Global species counts are a key measure of biodiversity and associated metrics of conservation. It is both scientifically and practically important to know how many species exist, how many undescribed species remain, and where they are found. We modify a model for the number of undescribed species using species description data and incorporating taxonomic information. We assume a Poisson distribution for the number of species described in an interval and use maximum likelihood to estimate parameter values of an unknown intensity function. To test the model's performance, we performed a simulation study comparing our method to a previous model under conditions qualitatively similar to those related to mammal species description over the last two centuries. Because our model more accurately estimates the total number of species, we predict that 5% of mammals remain undescribed. We applied our model to determine the biogeographic realms which hold these undescribed species.

Recent evidence suggests that sexual contact may give rise to transmission of Ebola virus long after infection has been cleared from blood. We develop a simple mathematical model that incorporates contact transmission and sexual transmission parametrized from data relating to the 2013–2015 West African Ebola epidemic. The model explores scenarios where contact transmission is reduced following infection events, capturing behaviour change, and quantifies how these actions reducing transmission may be compromised by sexual transmission in terms of increasing likelihood, size and duration of outbreaks. We characterize the extent to which sexual transmission operates in terms of the probability of initial infection resolving to sexual infectiousness and the sexual transmission rate, and relate these parameters to the overall case burden. We find that sexual transmission can have large effects on epidemic dynamics (increasing attack ratios from 25% in scenarios without sexual transmission but with contact-transmission-reducing behaviour, up to 80% in equivalent scenarios with sexual transmission).

The frequency of opportunities for transmission is key to the severity of directly transmitted disease outbreaks in multihost communities. Transmission opportunities for generalist microparasites often arise from competitive and trophic interactions. Additionally, contact heterogeneities within and between species either hinder or promote transmission. General theory incorporating competition and contact heterogeneities for disease-diversity relationships is underdeveloped. Here, we present a formal framework to explore disease-diversity relationships for directly transmitted parasites that infect multiple host species, including influenza viruses, rabies virus, distemper viruses, and hantaviruses. We explicitly include host regulation via intra- and interspecific competition, where the latter can be dependent on or independent of interspecific contact rates (covering resource utilization overlap, habitat selection preferences, and temporal niche partitioning). We examine how these factors interact with frequency- and density-dependent transmission along with traits of the hosts in the assemblage, culminating in the derivation of a relationship describing the propensity for parasite fitness to decrease in species assemblages relative to that in single-host species. This relationship reveals that increases in biodiversity do not necessarily suppress frequency-dependent parasite transmission and that regulation of hosts via interspecific competition does not always lead to a reduction in parasite fitness. Our approach explicitly shows that species identity and ecological interactions between hosts together determine microparasite transmission outcomes in multispecies communities.