Urbanization and the ecology of wildlife diseases

Abstract

Urbanization is intensifying worldwide, with two-thirds of the human population expected to reside in cities within 30 years. The role of cities in human infectious disease is well established, but less is known about how urban landscapes influence wildlife-pathogen interactions. Here, we draw on recent advances in wildlife epidemiology to consider how environmental changes linked with urbanization can alter the biology of hosts, pathogens and vectors. Although urbanization reduces the abundance of many wildlife parasites, transmission can, in some cases, increase among urban-adapted hosts, with effects on rarer wildlife or those living beyond city limits. Continued rapid urbanization, together with risks posed by multi-host pathogens for humans and vulnerable wildlife populations, emphasize the need for future research on wildlife diseases in urban landscapes.

Does urbanization explain differences in interactions between an insect herbivore and its natural enemies and mutualists?

“…Urbanization is arguably the greatest anthropogenic transformation that ecological systems experience, and while most studies of urban ecology focus on changes to the diversity and abundance of species inhabiting towns and cities, attention has only started to focus on how assemblages of interacting species are formed in urban areas, and how this is affected by the intensity of urbanization (Bennett and Gratton 2012;Quispe and Fenoglio 2015;Pereira-Peixoto et al 2016;Turrini et al 2016). Fragmentation reduces populations of native plants (Benitez-Malvido 1998;Jules 1998;Williams et al 2005), leads to decreased connectivity between vegetation patches and existing patches tend to be smaller (Medley et al 1995;McKinney 2002) and therefore of reduced quality as habitat for many animal species (Bradley and Altizer 2007;Faeth et al 2011;Turrini et al 2016). There are also some dramatic physical changes from increased densities of roads, buildings and other sealed structures and microclimatic changes such as the urban heat island effect (Bradley and Altizer 2007;Faeth et al 2011).…”

“…Fragmentation reduces populations of native plants (Benitez-Malvido 1998;Jules 1998;Williams et al 2005), leads to decreased connectivity between vegetation patches and existing patches tend to be smaller (Medley et al 1995;McKinney 2002) and therefore of reduced quality as habitat for many animal species (Bradley and Altizer 2007;Faeth et al 2011;Turrini et al 2016). There are also some dramatic physical changes from increased densities of roads, buildings and other sealed structures and microclimatic changes such as the urban heat island effect (Bradley and Altizer 2007;Faeth et al 2011). Together, these changes affect the likelihood of encountering species at higher trophic levels (Faeth et al 2005;Egerer et al 2017).…”

Poor health is associated with use of anthropogenic resources in an urban carnivore

“…rabies virus [21]), more reliant on easily accessible food [7,22] and less able to tolerate cold temperatures [23], all of which could promote interactions with humans. Rates of disease in urban-adapted species are sometimes higher than in rural areas because of higher densities of animals supported by anthropogenic resources [24], altered community structure that can increase contact between parasites and hosts [25], or from chronic stressors that increase disease susceptibility [26].…”

Do not feed the wildlife: associations between garbage use, aggression, and disease in banded mongooses (Mungos mungo)

“…Urbanization and other forms of anthropogenic landscape alteration are increasing worldwide, generating a need to understand the direct and indirect influence of human‐modified environments on disease emergence and dynamics in humans and wildlife (Bradley and Altizer 2007; Gottdenker et al. 2014).…”

“…In some cases, it is simply a “numbers game”: urbanization and other forms of human modification to the landscape can alter the number of species potentially involved in pathogen dilution or transmission (Keesing et al. 2010) or the population sizes or densities of competent hosts or vectors, which leads to a concomitant change in contact rates and pathogen transmission potential (Bradley and Altizer 2007; Acosta‐Jamett et al. 2011; Shapiro et al.…”