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Emerging vector-borne diseases are an important issue in global health. Many vector-borne pathogens have appeared in new regions in the past two decades, while many endemic diseases have increased in incidence. Although introductions and emergence of endemic pathogens are often considered to be distinct processes, many endemic pathogens are actually spreading at a local scale coincident with habitat change. We draw attention to key differences between dynamics and disease burden that result from increased pathogen transmission after habitat change and after introduction into new regions. Local emergence is commonly driven by changes in human factors as much as by enhanced enzootic cycles, whereas pathogen invasion results from anthropogenic trade and travel where and when conditions (eg, hosts, vectors, and climate) are suitable for a pathogen. Once a pathogen is established, ecological factors related to vector characteristics can shape the evolutionary selective pressure and result in increased use of people as transmission hosts. We describe challenges inherent in the control of vector-borne zoonotic diseases and some emerging non-traditional strategies that could be effective in the long term.

The recent introduction of Pseudogymnoascus destructans (the fungal pathogen that causes white-nose syndrome in bats) from Eurasia to North America has resulted in the collapse of North American bat populations and restructured species communities. The long evolutionary history between P. destructans and bats in Eurasia makes understanding host life history essential to uncovering the ecology of P. destructans. In this Review, we combine information on pathogen and host biology to understand the patterns of P. destructans spread, seasonal transmission ecology, the pathogenesis of white-nose syndrome and the cross-scale impact from individual hosts to ecosystems. Collectively, this research highlights how early pathogen detection and quantification of host impacts has accelerated the understanding of this newly emerging infectious disease.The fungal pathogen Pseudogymnoascus destructans, which causes white-nose syndrome in bats, has devastated bat populations in North America since its introduction from Eurasia in the 2000s. In this Review, Hoyt and colleagues describe the ecology of P. destructans in bats and its impacts on bats and the ecosystem.

Many invasive species that have been spread through the globalization of trade and travel are pathogens. A paradigmatic case is the introduction of West Nile virus (WNV) into North America in 1999. A decade of research on the ecology and evolution of WNV includes three findings that provide insight into the outcome of future pathogen introductions. First, WNV transmission in North America is highest in urbanized and agricultural habitats, in part because the hosts and vectors of WNV are abundant in human-modified areas. Second, after its introduction, the virus quickly adapted to infect local mosquito vectors more efficiently than the originally introduced strain. Third, highly focused feeding patterns of the mosquito vectors of WNV result in unexpected host species being important for transmission. This research provides a framework for predicting and preventing the emergence of foreign vector-borne pathogens.

Simultaneously controlling COVID-19 epidemics and limiting economic and societal impacts presents a difficult challenge, especially with limited public health budgets. Testing, contact tracing, and isolating/quarantining is a key strategy that has been used to reduce transmission of SARS-CoV-2, the virus that causes COVID-19 and other pathogens. However, manual contact tracing is a time-consuming process and as case numbers increase a smaller fraction of cases’ contacts can be traced, leading to additional virus spread. Delays between symptom onset and being tested (and receiving results), and a low fraction of symptomatic cases being tested and traced can also reduce the impact of contact tracing on transmission. We examined the relationship between increasing cases and delays and the pathogen reproductive number R t , and the implications for infection dynamics using deterministic and stochastic compartmental models of SARS-CoV-2. We found that R t increased sigmoidally with the number of cases due to decreasing contact tracing efficacy. This relationship results in accelerating epidemics because R t initially increases, rather than declines, as infections increase. Shifting contact tracers from locations with high and low case burdens relative to capacity to locations with intermediate case burdens maximizes their impact in reducing R t (but minimizing total infections may be more complicated). Contact tracing efficacy decreased sharply with increasing delays between symptom onset and tracing and with lower fraction of symptomatic infections being tested. Finally, testing and tracing reductions in R t can sometimes greatly delay epidemics due to the highly heterogeneous transmission dynamics of SARS-CoV-2. These results demonstrate the importance of having an expandable or mobile team of contact tracers that can be used to control surges in cases. They also highlight the synergistic value of high capacity, easy access testing and rapid turn-around of testing results, and outreach efforts to encourage symptomatic cases to be tested immediately after symptom onset.

The Earth's ecosystems have been altered by anthropogenic processes, including land use, harvesting populations, species introductions and climate change. These anthropogenic processes greatly alter plant and animal communities, thereby changing transmission of the zoonotic pathogens they carry. Biodiversity conservation may be a potential win–win strategy for maintaining ecosystem health and protecting public health, yet the causal evidence to support this strategy is limited. Evaluating conservation as a viable public health intervention requires answering four questions: (i) Is there a general and causal relationship between biodiversity and pathogen transmission, and if so, which direction is it in? (ii) Does increased pathogen diversity with increased host biodiversity result in an increase in total disease burden? (iii) Do the net benefits of biodiversity conservation to human well-being outweigh the benefits that biodiversity-degrading activities, such as agriculture and resource utilization, provide? (iv) Are biodiversity conservation interventions cost-effective when compared to other options employed in standard public health approaches? Here, we summarize current knowledge on biodiversity–zoonotic disease relationships and outline a research plan to address the gaps in our understanding for each of these four questions. Developing practical and self-sustaining biodiversity conservation interventions will require significant investment in disease ecology research to determine when and where they will be effective. This article is part of the themed issue ‘Conservation, biodiversity and infectious disease: scientific evidence and policy implications’.

Lyme disease is the most common tick-borne disease in temperate regions of North America, Europe and Asia, and the number of reported cases has increased in many regions as landscapes have been altered. Although there has been extensive work on the ecology and epidemiology of this disease in both Europe and North America, substantial uncertainty exists about fundamental aspects that determine spatial and temporal variation in both disease risk and human incidence, which hamper effective and efficient prevention and control. Here we describe areas of consensus that can be built on, identify areas of uncertainty and outline research needed to fill these gaps to facilitate predictive models of disease risk and the development of novel disease control strategies. Key areas of uncertainty include: (i) the precise influence of deer abundance on tick abundance, (ii) how tick populations are regulated, (iii) assembly of host communities and tick-feeding patterns across different habitats, (iv) reservoir competence of host species, and (v) pathogenicity for humans of different genotypes of Borrelia burgdorferi. Filling these knowledge gaps will improve Lyme disease prevention and control and provide general insights into the drivers and dynamics of this emblematic multi-host–vector-borne zoonotic disease. This article is part of the themed issue ‘Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.

The introduction of West Nile virus to North America in 1999 had profound impacts on human and wildlife health. Here, we review studies of WNV impacts on bird populations and find that overall impacts have been less than initially anticipated, with few species showing sustained changes in population size or demographic rates across multiple regions. This raises four questions: 1) What is the evidence for WNV impact on bird populations and how can we strengthen future analyses? We argue that future studies of WNV impacts should explicitly incorporate temporal variation in WNV transmission intensity, integrate field data with laboratory experimental infection studies, and correct for multiple comparisons. 2) What mechanisms might explain the relatively modest impact of WNV on most bird populations? We suggest that spatial and temporal variation in WNV transmission moderates WNV impacts on species that occur in multiple habitats, some of which provide refugia from infection. 3) Have species recovered from the initial invasion of WNV? We find evidence that many species and populations have recovered from initial WNV impact, but a few have not. 4) Did WNV cause cascading effects on other species and ecosystems? Unfortunately, few studies have examined the cascading effects of WNV population declines, but evidence suggests that some species may have been released from predation or competition. We close by discussing potentially overlooked groups of birds that may have been affected by WNV, and one highlight species, the yellow-billed magpie (Pica nutalli Audubon, 1837 [Passeriformes: Corvidae]), that appears to have suffered the largest range-wide impact from WNV.

Lyme disease is the most prevalent vector-borne disease in North America, and both the annual incidence and geographic range are increasing. The emergence of Lyme disease has been attributed to a century-long recovery of deer, an important reproductive host for adult ticks. However, a growing body of evidence suggests that Lyme disease risk may now be more dynamically linked to fluctuations in the abundance of small-mammal hosts that are thought to infect the majority of ticks. The continuing and rapid increase in Lyme disease over the past two decades, long after the recolonization of deer, suggests that other factors, including changes in the ecology of small-mammal hosts may be responsible for the continuing emergence of Lyme disease. We present a theoretical model that illustrates how reductions in small-mammal predators can sharply increase Lyme disease risk. We then show that increases in Lyme disease in the northeastern and midwestern United States over the past three decades are frequently uncorrelated with deer abundance and instead coincide with a range-wide decline of a key small-mammal predator, the red fox, likely due to expansion of coyote populations. Further, across four states we find poor spatial correlation between deer abundance and Lyme disease incidence, but coyote abundance and fox rarity effectively predict the spatial distribution of Lyme disease in New York. These results suggest that changes in predator communities may have cascading impacts that facilitate the emergence of zoonotic diseases, the vast majority of which rely on hosts that occupy low trophic levels.

The introduction of West Nile virus (WNV) to North America in 1999 and its subsequent rapid spread across the Americas demonstrated the potential impact of arboviral introductions to new regions, and this was reinforced by the subsequent introductions of chikungunya and Zika viruses. Extensive studies of host–pathogen–vector–environment interactions over the past two decades have illuminated many aspects of the ecology and evolution of WNV and other arboviruses, including the potential for pathogen adaptation to hosts and vectors, the influence of climate, land use and host immunity on transmission ecology, and the difficulty in preventing the establishment of a zoonotic pathogen with abundant wildlife reservoirs. Here, we focus on outstanding questions concerning the introduction, spread, and establishment of WNV in the Americas, and what it can teach us about the future of arboviral introductions. Key gaps in our knowledge include the following: viral adaptation and coevolution of hosts, vectors and the virus; the mechanisms and species involved in the large-scale spatial spread of WNV; how weather modulates WNV transmission; the drivers of large-scale variation in enzootic transmission; the ecology of WNV transmission in Latin America; and the relative roles of each component of host–virus–vector interactions in spatial and temporal variation in WNV transmission. Integrative studies that examine multiple factors and mechanisms simultaneously are needed to advance our knowledge of mechanisms driving transmission.

Nipah virus is a highly virulent zoonotic pathogen. In this report from Bangladesh, which included 40% of the world’s known cases, the risk factors for human-to-human transmission were evaluated. No asymptomatic cases were identified. Increased respiratory symptoms in the patient and prolonged close contact from caregivers were associated with secondary transmission.