Urbanization and Disease Emergence: Dynamics at the Wildlife–Livestock–Human Interface
Authors: James M. Hassell, Michael Begon, Melissa J. Ward, Eric M. Fèvre
Journal: Trends in Ecology & Evolution (2016)

Urbanization can create diverse wildlife–livestock–human interfaces. Interfaces represent a critical point for cross-species transmission and emergence of pathogens. Interfaces should be studied as complex, multihost communities. Molecular epidemiology can add real-world complexity to the study of disease emergence. Urbanization is characterized by rapid intensification of agriculture, socioeconomic change, and ecological fragmentation, which can have profound impacts on the epidemiology of infectious disease. Here, we review current scientific evidence for the drivers and epidemiology of emerging wildlife-borne zoonoses in urban landscapes, where anthropogenic pressures can create diverse wildlife–livestock–human interfaces. We argue that these interfaces represent a critical point for cross-species transmission and emergence of pathogens into new host populations, and thus understanding their form and function is necessary to identify suitable interventions to mitigate the risk of disease emergence. To achieve this, interfaces must be studied as complex, multihost communities whose structure and form are dictated by both ecological and anthropological factors. Urbanization is characterized by rapid intensification of agriculture, socioeconomic change, and ecological fragmentation, which can have profound impacts on the epidemiology of infectious disease. Here, we review current scientific evidence for the drivers and epidemiology of emerging wildlife-borne zoonoses in urban landscapes, where anthropogenic pressures can create diverse wildlife–livestock–human interfaces. We argue that these interfaces represent a critical point for cross-species transmission and emergence of pathogens into new host populations, and thus understanding their form and function is necessary to identify suitable interventions to mitigate the risk of disease emergence. To achieve this, interfaces must be studied as complex, multihost communities whose structure and form are dictated by both ecological and anthropological factors. Emerging infectious diseases (EIDs) (see Glossary) are recognized as pathogens 'whose incidence in host populations has increased within the past two decades or threatens to increase in the near future' [1Smolinsky M.S. et al.Smolinski M.S. Microbial Threats to Health: Emergence, Detection, and Response. National Academies Press, 2003Google Scholar]. As well as describing the spread of newly evolved or previously undetected pathogens, pathogens that are increasing their geographic spread, increasing their impact, changing their clinical presentation or moving into human hosts for the first time, the term emergence can also be used to describe the reappearance (or re-emergence) of a known infection after a decline in incidence [1Smolinsky M.S. et al.Smolinski M.S. Microbial Threats to Health: Emergence, Detection, and Response. National Academies Press, 2003Google Scholar]. It is estimated that between 60 and 80% of newly emerging infections are zoonotic in origin and thus are (at least initially) dependent on an animal reservoir for survival [2Woolhouse M.E.J. Gowtage-Sequeria S. Host range and emerging and reemerging pathogens.Emerg. Infect. Dis. 2005; 11: 1842-1847Crossref PubMed Google Scholar, 3Jones K.E. et al.Global trends in emerging infectious diseases.Nature. 2008; 451: 990-993Crossref PubMed Scopus (2213) Google Scholar]. Of these emerging zoonoses, at least 70% have a wildlife origin, with cross-species spread and onward transmission representing a natural response to the evolutionary pressures of pathogen ecology [3Jones K.E. et al.Global trends in emerging infectious diseases.Nature. 2008; 451: 990-993Crossref PubMed Scopus (2213) Google Scholar, 4Karesh W.B. et al.Ecology of zoonoses: natural and unnatural histories.Lancet. 2012; 380: 1936-1945Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar]. Although both wildlife and domesticated animal reservoirs can be considered important sources of EIDs, it is the anthropogenic influence on ecological systems that dictates the level of risk that operates at the interface between humans and animals in zoonotic disease emergence. The impact of humans on the ecosystems within which they exist have occurred for as long as there have been humans. However, over the past 10 000 years, human–ecosystem interactions have become increasingly profound following a series of chronological transitions: (i) the establishment of local settlements, agriculture, and domestication of livestock; (ii) regional contact through trade; (iii) intercontinental exploration, imperialism, and industrialization; and (iv) globalization, urbanization, and climate change [5McMichael J. Environmental and social influences on emerging infectious diseases: past, present and future.Philos. Trans. R. Soc. Lond. B. Biol. Sci. 2004; 359: 1049-1058Crossref PubMed Scopus (143) Google Scholar]. Current levels of human–ecosystem interaction, driven by increased environmental encroachment and land-use change (exploitation of natural resources and agricultural practices), and environmental effects such as climate change, will result in habitat alteration and changes in species assemblage and contact rates that promote the emergence of zoonotic disease. Spread and persistence of newly emerged (or re-emerged) pathogens can then be perpetuated by a combination of factors including expanding global human populations and urbanization, international trade and travel, intensive livestock keeping systems, proliferation of reservoir populations, and antimicrobial drug use [4Karesh W.B. et al.Ecology of zoonoses: natural and unnatural histories.Lancet. 2012; 380: 1936-1945Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar, 6Daszak P. 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Human population density and growth are significant predictors of historical EID events, and thus urbanization is likely to have a profound effect on public health as rural pathogens adapt to urban conditions, and other pathogens emerge (or re-emerge) in urban areas [3Jones K.E. et al.Global trends in emerging infectious diseases.Nature. 2008; 451: 990-993Crossref PubMed Scopus (2213) Google Scholar]. Human factors such as population density, migration, trade, sanitation, and access to clean water can promote the transmission of pathogens and alter vector dynamics, while social factors that drive health inequality (socioeconomic status, housing, race, ethnicity, gender, and education) also influence the epidemiology of infectious disease in urban areas [13Bradley C.A. Altizer S. Urbanization and the ecology of wildlife diseases.Trends Ecol. 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Spatial overlap between hosts, and overlap in vector ranges are key requirements for the emergence of directly transmitted and vector-borne pathogens, respectively. As such, in order to investigate the conditions in which urbanization might lead to the emergence of zoonotic disease across species, and thus risk factors for transmission to humans, it is necessary to simplify the complexity of urban systems by considering them as a network of interfaces across which pathogens can be transmitted; the physical interfaces at which humans and animals interact and pathogens are exchanged exist within the context of societal and policy interfaces (as depicted in the schematic in Figure 1). These networks exist at different scales. At a local-scale, households form part of what can be considered urban communities; groups of similar physical interfaces that are characterized by a set of societal (e.g., demographic and socioeconomic) characteristics. These communities are linked by the movement of people, livestock and their products, and wildlife, and the environment (which can conveniently be defined as networks of connectivity) [15Alberti M. The effects of urban patterns on ecosystem function.Int. Reg. Sci. Rev. 2005; 28: 168-192Crossref Scopus (391) Google Scholar, 16Pickett S.T.A. et al.Urban ecological systems: scientific foundations and a decade of progress.J. Environ. Manage. 2011; 92: 331-362Crossref PubMed Scopus (355) Google Scholar]. As a result, key drivers that could promote interaction between humans and animals are: (i) livestock-keeping practices, production systems, and the movements of livestock and animal products in urban areas; and (ii) the direct effects of urbanization on the physical environment, ecosystems in which urban centers are developed, and animal communities that exist freely within these [8Jones B.A. et al.Zoonosis emergence linked to agricultural intensification and environmental change.Proc. 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With the emergence of high-profile pathogens that exhibit wide host plasticity (such as Ebola and avian influenza viruses), a community approach is being increasingly embraced for studying the multihost ecology of zoonotic pathogens. Studying the role of wildlife in multihost disease systems is complicated by ecological and behavioral attributes unique to these species, and the influence of natural and human systems; both of which complicate conceptual models of disease transmission [33Hayman D.T.S. et al.Ecology of zoonotic infectious diseases in bats: current knowledge and future directions.Zoonoses Public Health. 2013; 60: 2-21Crossref PubMed Scopus (57) Google Scholar]. Following the disease reservoirs framework recently revised by Viana et al. [34Viana M. et al.Assembling evidence for identifying reservoirs of infection.Trends Ecol. Evol. 2014; 29: 270-279Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar] and Caron et al. 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Contact is a key feature of both reservoir and disease emergence dynamics; R0 is closely linked to the rate of contact between susceptible and infectious individuals and the recovery or mortality rate of infected individuals, and the force of infection (and thus risk of human spillover) is determined by prevalence of infection in the maintenance population and/or bridge hosts, the rate of contact between humans and infected individuals, and the probability that infection occurs upon contact [36Begon M. et al.A clarification of transmission terms in host-microparasite models: numbers, densities and areas.Epidemiol. Infect. 2002; 129: 147-153Crossref PubMed Scopus (229) Google Scholar, 37Davis S. Calvet E. 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The pathogen pool hypothesis assumes exposure to novel diseases from a diverse pool of pathogens in wildlife to which humans or livestock, as naïve hosts, have not had prior exposure. In reality, it seems unlikely that these two hypotheses are mutually exclusive; evidence from empirical studies generally favors a dynamic model for disease emergence [41Lloyd-Smith J.O. et al.Nine challenges in modelling the emergence of novel pathogens.Epidemics. 2014; 10: 35-39Crossref PubMed Scopus (19) Google Scholar]. As such, the extent to which perturbation (changes in species richness, abundance, and contact rate) or the zoonotic pathogen pool dictate risk of emergence at urban interfaces, is probably dependent on the impact of urbanization on community ecology, and the degree of coevolution between sympatric wildlife, humans, and livestock at each interface. Associations between urbanization and the prevalence of pathogens in populations of free-ranging wildlife have been described for a wide taxonomic range of host species and pathogens (reviewed in [13Bradley C.A. Altizer S. Urbanization and the ecology of wildlife diseases.Trends Ecol. Evol. 2007; 22: 95-102Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar]). Evidence suggests that through altered habitat structure and changes to resource availability, urbanization results in significant changes to the structure of wildlife communities, which are subsequently characterized by low biodiversity with proportional increases in abundance of certain generalist species [42Faeth S.H. et al.Trophic dynamics in urban communities.Bioscience. 2005; 55: 399Crossref Google Scholar, 43Galbraith J.A. et al.Supplementary feeding restructures urban bird communities.Proc. Natl. Acad. Sci. U.S.A. 2015; 112: e2648-e2657Crossref PubMed Scopus (43) Google Scholar]. 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Increases in synanthropic species population density can elevate contact rates (through changes in host ranging patterns and densities), and thus increase the risk of pathogen transmission via direct contact and orofecal routes [37Davis S. Calvet E. Fluctuating rodent populations and risk to humans from rodent-borne zoonoses.Vector-Borne Zoonotic Dis. 2005; 5: 305-314Crossref PubMed Scopus (96) Google Scholar, 44Evans K.L. et al.Habitat influences on urban avian assemblages.Ibis. 2009; 151: 19-39Crossref Scopus (154) Google Scholar]. Fragmentation of these populations, in contrast, can result in genetic bottlenecks and subsequently reduced effective immune responses [48Sommer S. The importance of immune gene variability (MHC) in evolutionary ecology and conservation.Front. Zool. 2005; 2: 16-33Crossref PubMed Scopus (417) Google Scholar]. 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As described, the dynamics of infection at these interfaces are determined by changes in diversity, abundance and contact rates between reservoir and target hosts, thus influencing risk of cross-species pathogen transmission. Several systematic reviews have identified high-risk interfaces for zoonotic disease transmission on a global scale; specific interfaces for spillover from wildlife include human dwellings, agricultural fields, and occupational exposure, while broader descriptions include agricultural intensification and environmental change [8Jones B.A. et al.Zoonosis emergence linked to agricultural intensification and environmental change.Proc. Natl. Acad. Sci. U.S.A. 2013; 110: 8399-8404Crossref PubMed Scopus (150) Google Scholar, 52Kreuder Johnson C. et al.Spillover and pandemic properties of zoonotic viruses with high host plasticity.Sci. Rep. 2015; 5: 14830Crossref PubMed Google Scholar]. However, as argued by Jones et al. [8Jones B.A. et al.Zoonosis emergence linked to agricultural intensification and environmental change.Proc. Natl. Acad. Sci. U.S.A. 2013; 110: 8399-8404Crossref PubMed Scopus (150) Google Scholar], attempts to describe systems within which pathogens emerge or change in virulence have predominantly focused on global generalizations, which might not be appropriate to capture the heterogeneity of interfaces. Instead, interfaces and the driving factors that define them should be studied at appropriate, spatially explicit scales [53Wood J.L.N. et al.A framework for the study of zoonotic disease e