Explore the vast range of titles available.

The replication-transmission relativity theory, currently used to inform the development of multiscale models of infectious disease dynamics, needs a revision and extension to accommodate new basic science and clinical information about infectious disease dynamics. In this article, we revise and extend the replication-transmission relativity theory into a new scientific theory of infectious disease dynamics called the universal theory for the multiscale modelling of infectious disease dynamics. This new theory states that, for every host–pathogen interaction that results in an infectious disease system, there is no privileged or absolute scale of a disease system form that would determine the dynamics of the infectious disease system, only interactions between the scales of a level of organisation of the pathogen-centred disease system form and the scales of the corresponding levels of organisation of the host-centred disease system form. We further explain the utility of this theory, which is reflected in its flexibility and ability to incorporate new information and explain previous information that could not be accounted for by the replication-transmission relativity theory of infectious disease dynamics.

Disease outbreaks and pathogen introductions can have significant effects on host populations, and the ability of pathogens to persist in the environment can exacerbate disease impacts by fueling sustained transmission, seasonal epidemics, and repeated spillover events. While theory suggests that the presence of an environmental reservoir increases the risk of host declines and threat of extinction, the influence of reservoir dynamics on transmission and population impacts remains poorly described. Here we show that the extent of the environmental reservoir explains broad patterns of host infection and the severity of disease impacts of a virulent pathogen. We examined reservoir and host infection dynamics and the resulting impacts of Pseudogymnoascus destructans, the fungal pathogen that causes white-nose syndrome, in 39 species of bats at 101 sites across the globe. Lower levels of pathogen in the environment consistently corresponded to delayed infection of hosts, fewer and less severe infections, and reduced population impacts. In contrast, an extensive and persistent environmental reservoir led to early and widespread infections and severe population declines. These results suggest that continental differences in the persistence or decay of P. destructans in the environment altered infection patterns in bats and influencedwhether host populations were stable or experienced severe declines from this disease. Quantifying the impact of the environmental reservoir on disease dynamics can provide specific targets for reducing pathogen levels in the environment to prevent or control future epidemics.

The most frequent infectious diseases in humans—and those with the highest potential for rapid pandemic spread—are usually transmitted via droplets during close proximity interactions (CPIs). Despite the importance of this transmission route, very little is known about the dynamic patterns of CPIs. Using wireless sensor network technology, we obtained high-resolution data of CPIs during a typical day at an American high school, permitting the reconstruction of the social network relevant for infectious disease transmission. At 94% coverage, we collected 762,868 CPIs at a maximal distance of 3 m among 788 individuals. The data revealed a high-density network with typical small-world properties and a relatively homogeneous distribution of both interaction time and interaction partners among subjects. Computer simulations of the spread of an influenza-like disease on the weighted contact graph are in good agreement with absentee data during the most recent influenza season. Analysis of targeted immunization strategies suggested that contact network data are required to design strategies that are significantly more effective than random immunization. Immunization strategies based on contact network data were most effective at high vaccination coverage.

Strategies for containing an emerging infectious disease outbreak must be nonpharmaceutical when drugs or vaccines for the pathogen do not yet exist or are unavailable. The success of these nonpharmaceutical strategies will depend on not only the effectiveness of isolation measures but also the epidemiological characteristics of the infection. However, there is currently no systematic framework to assess the relationship between different containment strategies and the natural history and epidemiological dynamics of the pathogen. Here, we compare the effectiveness of quarantine and symptom monitoring, implemented via contact tracing, in controlling epidemics using an agent-based branching model. We examine the relationship between epidemic containment and the disease dynamics of symptoms and infectiousness for seven case-study diseases with diverse natural histories, including Ebola, influenza A, and severe acute respiratory syndrome (SARS). We show that the comparative effectiveness of symptom monitoring and quarantine depends critically on the natural history of the infectious disease, its inherent transmissibility, and the intervention feasibility in the particular healthcare setting. The benefit of quarantine over symptom monitoring is generally maximized for fast-course diseases, but we show the conditions under which symptom monitoring alone can control certain outbreaks. This quantitative framework can guide policymakers on how best to use nonpharmaceutical interventions and prioritize research during an outbreak of an emerging pathogen.

1. The disease costs of sociality have largely been understood through the link between group size and transmission. However, infectious disease spread is driven primarily by the social organization of interactions in a group and not its size. 2. We used statistical models to review the social network organization of 47 species, including mammals, birds, reptiles, fish and insects by categorizing each species into one of three social systems, relatively solitary, gregarious and socially hierarchical. Additionally, using computational experiments of infection spread, we determined the disease costs of each social system. 3. We find that relatively solitary species have large variation in number of social partners, that socially hierarchical species are the least clustered in their interactions, and that social networks of gregarious species tend to be the most fragmented. However, these structural differences are primarily driven by weak connections, which suggest that different social systems have evolved unique strategies to organize weak ties. 4. Our synthetic disease experiments reveal that social network organization can mitigate the disease costs of group living for socially hierarchical species when the pathogen is highly transmissible. In contrast, highly transmissible pathogens cause frequent and prolonged epidemic outbreaks in gregarious species. 5. We evaluate the implications of network organization across social systems despite methodological challenges, and our findings offer new perspective on the debate about the disease costs of group living. Additionally, our study demonstrates the potential of meta-analytic methods in social network analysis to test ecological and evolutionary hypotheses on cooperation, group living, communication and resilience to extrinsic pressures.

Social distancing as one of the main non-pharmaceutical interventions can help slow down the spread of diseases, like in the COVID-19 pandemic. Effective social distancing, unless enforced as drastic lockdowns and mandatory cordon sanitaire, requires consistent strict collective adherence. However, it remains unknown what the determinants for the resultant compliance of social distancing and their impact on disease mitigation are. Here, we incorporate into the epidemiological process with an evolutionary game theory model that governs the evolution of social distancing behaviour. In our model, we assume an individual acts in their best interest and their decisions are driven by adaptive social learning of the real-time risk of infection in comparison with the cost of social distancing. We find interesting oscillatory dynamics of social distancing accompanied with waves of infection. Moreover, the oscillatory dynamics are dampened with a non-trivial dependence on model parameters governing decision-makings and gradually cease when the cumulative infections exceed the herd immunity. Compared to the scenario without social distancing, we quantify the degree to which social distancing mitigates the epidemic and its dependence on individuals’ responsiveness and rationality in their behaviour changes. Our work offers new insights into leveraging human behaviour in support of pandemic response.

1. Long-term individual-based datasets on host-pathogen systems are a rare and valuable resource for understanding the infectious disease dynamics in wildlife. A study of European badgers (Meles meles) naturally infected with bovine tuberculosis (bTB) at Woodchester Park in Gloucestershire (UK) has produced a unique dataset, facilitating investigation of a diverse range of epidemiological and ecological questions with implications for disease management. 2. Since the 1970s, this badger population has been monitored with a systematic mark-recapture regime yielding a dataset of > 15,000 captures of >3,000 individuals, providing detailed individual life-history, morphometric, genetic, reproductive and disease data. 3. The annual prevalence of bTB in the Woodchester Park badger population exhibits no straightforward relationship with population density, and both the incidence and prevalence of Mycobacterium bovis show marked variation in space. The study has revealed phenotypic traits that are critical for understanding the social structure of badger populations along with mechanisms vital for understanding disease spread at different spatial resolutions. 4. Woodchester-based studies have provided key insights into how host ecology can influence infection at different spatial and temporal scales. Specifically, it has revealed heterogeneity in epidemiological parameters; intrinsic and extrinsic factors affecting population dynamics; provided insights into senescence and individual life histories; and revealed consistent individual variation in foraging patterns, refuge use and social interactions. 5. An improved understanding of ecological and epidemiological processes is imperative for effective disease management. Woodchester Park research has provided information of direct relevance to bTB management, and a better appreciation of the role of individual heterogeneity in disease transmission can contribute further in this regard. 6. The Woodchester Park study system now offers a rare opportunity to seek a dynamic understanding of how individual-, group- and population-level processes interact The wealth of existing data makes it possible to take a more integrative approach to examining how the consequences of individual heterogeneity scale to determine population-level pathogen dynamics and help advance our understanding of the ecological drivers of host-pathogen systems.

Significance The second plague pandemic in medieval Europe started with the Black Death epidemic of 1347–1353 and killed millions of people over a time span of four centuries. It is commonly thought that after its initial introduction from Asia, the disease persisted in Europe in rodent reservoirs until it eventually disappeared. Here, we show that climate-driven outbreaks of Yersinia pestis in Asian rodent plague reservoirs are significantly associated with new waves of plague arriving into Europe through its maritime trade network with Asia. This association strongly suggests that the bacterium was continuously reimported into Europe during the second plague pandemic, and offers an alternative explanation to putative European rodent reservoirs for how the disease could have persisted in Europe for so long. The Black Death, originating in Asia, arrived in the Mediterranean harbors of Europe in 1347 CE, via the land and sea trade routes of the ancient Silk Road system. This epidemic marked the start of the second plague pandemic, which lasted in Europe until the early 19th century. This pandemic is generally understood as the consequence of a singular introduction of Yersinia pestis , after which the disease established itself in European rodents over four centuries. To locate these putative plague reservoirs, we studied the climate fluctuations that preceded regional plague epidemics, based on a dataset of 7,711 georeferenced historical plague outbreaks and 15 annually resolved tree-ring records from Europe and Asia. We provide evidence for repeated climate-driven reintroductions of the bacterium into European harbors from reservoirs in Asia, with a delay of 15 ± 1 y. Our analysis finds no support for the existence of permanent plague reservoirs in medieval Europe.

Social interactions are required for the direct transmission of infectious diseases. Consequently, the social network structure of populations plays a key role in shaping infectious disease dynamics. A huge research effort has examined how specific social network structures make populations more (or less) vulnerable to damaging epidemics. However, it can be just as important to understand how social networks can contribute to endemic disease dynamics, in which pathogens are maintained at stable levels for prolonged periods of time. Hosts that can maintain endemic disease may serve as keystone hosts for multi-host pathogens within an ecological community, and also have greater potential to act as key wildlife reservoirs of agricultural and zoonotic diseases. Here, we examine combinations of social and demographic processes that can foster endemic disease in hosts. We synthesise theoretical and empirical work to demonstrate the importance of both social structure and social dynamics in maintaining endemic disease. We also highlight the importance of distinguishing between the local and global persistence of infection and reveal how different social processes drive variation in the scale at which infectious diseases appear endemic. Our synthesis provides a framework by which to understand how sociality contributes to the longterm maintenance of infectious disease in wildlife hosts and provides a set of tools to unpick the social and demographic mechanisms involved in any given host–pathogen system.

As biodiversity declines with anthropogenic land-use change, it is increasingly important to understand how changing biodiversity affects infectious disease risk. The dilution effect hypothesis, which points to decreases in biodiversity as critical to an increase in infection risk, has received considerable attention due to the allure of a win–win scenario for conservation and human well-being. Yet some empirical data suggest that the dilution effect is not a generalizable phenomenon. We explore the response of pathogen transmission dynamics to changes in biodiversity that are driven by habitat loss using an allometrically scaled multi-host model. With this model, we show that declining habitat, and thus declining biodiversity, can lead to either increasing or decreasing infectious-disease risk, measured as endemic prevalence. Whether larger habitats, and thus greater biodiversity, lead to a decrease (dilution effect) or increase (amplification effect) in infection prevalence depends upon the pathogen transmission mode and how host competence scales with body size. Dilution effects were detected for most frequency-transmitted pathogens and amplification effects were detected for density-dependent pathogens. Amplification effects were also observed over a particular range of habitat loss in frequency-dependent pathogens when we assumed that host competence was greatest in large-bodied species. By contrast, only amplification effects were observed for density-dependent pathogens; host competency only affected the magnitude of the effect. These models can be used to guide future empirical studies of biodiversity–disease relationships across gradients of habitat loss. The type of transmission, the relationship between host competence and community assembly, the identity of hosts contributing to transmission, and how transmission scales with area are essential factors to consider when elucidating the mechanisms driving disease risk in shrinking habitat. This article is part of the themed issue ‘Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.