FACTORS DRIVING DISEASE EMERGENCE
Disease emergence is often associated with human activities (Daszak et al. 2001; McFarlane et al. 2013). The drivers of emergence are incompletely understood (most notably in the case of wildlife diseases), as are the actual mechanisms for causal effect (Plowright et al.
2008; Plowright et al. 2011). The relative importance and mechanisms of action of causal factors are likely to differ for each disease and may vary, even for a given pathogen, with geographical area and host species. Diseaseemergence may be a result of interaction between a multitude of factors, which may combine in a synergistic manner (e.g. environmental stress, exacerbated by inadequate nutrition and lack of genetic diversity may result in poor host immunity, leading to increased disease from infection). In most cases, intensive long-term study is required to understand the complexities of the disease in question, including the factors driving emergence (Daszak et al. 2000; Plowright et al. 2008; Tompkins et al. 2015). A key to understanding the importance, impacts and drivers of disease emergence is sufficient baseline knowledge of prior pathogen and disease prevalence, disease dynamics and ecology of the host, to determine if a change has occurred and if so what the drivers and outcomes might be. In many wildlife situations globally and within Australia, such knowledge is lacking or limited (Reiss et al. 2015; Tompkins et al. 2015).
Advances in epidemiological and diagnostic techniques are also likely significant factors in the increased identification of emerging wildlife pathogens (Morse 2001; Tompkins et al. 2015; Titcomb et al. 2019). However, the increasing proportion of EIDs originating from wildlife cannot be explained by an increase in detection alone and likely represents a true change in disease dynamics (Kruse et al. 2004; Cook and Karesh 2008; Jones et al.
2008; McFarlane et al. 2012).A range of factors have been identified as contributing to the emergence of infectious diseases.
Climate change and ecosystem alterations (often anthropogenic but sometimes natural in origin) may have flow-on effects on disease dynamics, including: reduced or altered availability of food or habitat leading to diet switching; reduced fitness or decreased immune competence in the host; a change in geographical range and seasonality for vectors; or increased persistence of pathogens in the environment because of changed rainfall and temperature patterns. Ongoing changes in climate and ecosystems will likely result in increased opportunities for disease spillover from existing to new hosts (Daszak et al. 2001; Black et al. 2008; Cook and Karesh 2008; Slen- ning 2010; Vitali and Jackson 2022).
Changes in exposure to pathogens or vectors may occur through movement of pathogens, vectors or their hosts. Increased global trade and air travel has allowed rapid dissemination of pathogens between continents (e.g. the global COVID-19 pandemic and the likely arrival of west Nile virus in North America by plane) (Kilpatrick 2011; Li et al. 2021). Both pathogens and vectors may move through natural agencies, such as the wind-borne arrival of bluetongue virus vectors into northern Europe (Carpenter et al. 2009). A previously naive population may be exposed to novel infectious agents from wildlife or feral populations, domestic animals or humans. Increased encroachment of humans and domestic animals on former ‘wilderness’ areas and arrival of wildlife in urbanised areas enhance opportunities for host mixing and spillover (Daszak et al. 2000).
Alterations in pathogens include changes in virulence or host range through recombination or mutation. Pathogens may adapt to a new host or vector after initial emergence or spillover, as occurred with West Nile virus after its arrival in America (Kilpatrick 2011). Development of antimicrobial resistance may further alter the potential impacts of pathogens (see Chapter 17).
Alterations in host factors include genetically depauperate populations, reduced host immunity and fitness, and variability in immune function and immune response. Environmental factors (such as exposure to toxins) may alter gene expression. Host populations may increase in density, because of habitat fragmentation or resource limitation, which may increase host stress and opportunities for pathogen transmission and persistence. The effects of environmental factors on genetic expression are largely unstudied and their impacts on emergence of new diseases in wildlife is not well understood (Williams et al. 2002).
In addition, it has been recognised that wildlife populations already facing threat from habitat loss, predation or climate change are under additional risk of population decline or extirpation from EID (Pedersen et al. 2007; Reiss et al. 2015; Preece et al. 2017).
Within the Australian context, some factors are likely to have a greater influence on the emergence of infectious disease, given the continent’s evolutionary isolation, unique mammalian fauna, recent European settlement and large-scale introduction of vertebrate pests and predators. These include:
• Naivety of indigenous wildlife to imported pathogens, because of long evolutionary periods of isolation, potentially leading to increased susceptibility to infectious agents (e.g. chlamydiosis (koalas), toxoplasmosis and sarcoptic mange). Studies have indicated the prevalence of emerging pathogens in marsupials and monotremes may be higher than expected, compared with other taxa (Tompkins et al. 2015).
• Rapid, wide-scale ecosystem alterations (largely anthropogenic in origin), including clearing of native vegetation, changes in patterns of landscape fire and introduction of exotic plants, domestic livestock, feral herbivores and exotic predators (and their respective pathogens) (Black et al. 2008; McFarlane et al. 2013).
• Increased interactions between wild, domestic and feral species (McFarlane et al. 2012).
• Changes in host ecology, fitness and genetics, such as clustering or isolation of populations of wildlife; change in immunological responses because of environmental challenges and toxins.
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