Editing IPCC:AR6/WGII/Chapter-2 (section)

==== 2.4.2.7 Observed Impacts of Climate Change on Diseases of Wildlife and Associated Impacts on Humans ====

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Assessment of changes in diseases of terrestrial and freshwater wild organisms was scarce in WGII AR4, AR5, IPCC SR1.5 and IPCC SRCCL. Further, most emerging infectious diseases (EIDs) are zoonoses, that is, they are transmissible between humans and animals, and are climate sensitive ( [[#Woolhouse--2001|Woolhouse et al., 2001]] ; [[#Woolhouse--2005|Woolhouse and Gowtage-Sequeria, 2005]] ; [[#McIntyre--2017|McIntyre et al., 2017]] ; [[#Salyer--2017|Salyer et al., 2017]] ). AR4 found weak-to-moderate evidence that disease vectors and their diseases had changed their distributions in concert with climate change, but attribution studies were lacking ( [[#Smith--2014|Smith et al., 2014]] ). In AR5, WGII AR5 Chapter 11 , geographic expansion of a few VBDs to higher latitudes and elevations were detected and associated with regional climate trends, but the non-climatic drivers were not well assessed, leading to a ''medium confidence'' in attribution ( [[#Smith--2014|Smith et al., 2014]] )). Here, we build on previous assessments by focussing on changes in the population dynamics and geographic distribution of diseases in wild animals as well as diseases in humans and domestic animals that are harboured, amplified and transmitted by wild animal reservoir hosts and vectors.

Increased disease incidence is correlated with regional climatic changes, as expected from a basic understanding of underlying biology and relationships between temperature, precipitation, and disease ecology ( ''robust evidence'' , ''high agreement'' ) ( [[#Norwegian%20Polar%20Institute--2009|Norwegian Polar Institute, 2009]] ; [[#Tersago--2009|Tersago et al., 2009]] ; [[#Tabachnick--2010|Tabachnick, 2010]] ; [[#Paz--2015|Paz, 2015]] ; [[#Dewage--2019|Dewage et al., 2019]] ; [[#Deksne--2020|Deksne et al., 2020]] ; [[#Shocket--2020|Shocket et al., 2020]] ; [[#Couper--2021|Couper et al., 2021]] ). Whether increases in diseases in wild and domestic animals correspond to an increased risk of disease in nearby human populations is complicated by the potential buffering effects of the local medical system, access to health care and the socioeconomic status, education, behaviours and general health of the human population (see also [[IPCC:Wg2:Chapter:Chapter-7|Chapter 7]] and Cross-Chapter Box ILLNESS in this chapter).

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<span id="direct-effects-of-climate-and-climate-change-on-reproduction-seasonality-the-length-of-the-growing-season-and-the-transmission-of-pathogens-vectors-and-hosts"></span>
===== 2.4.2.7.1 Direct effects of climate and climate change on reproduction, seasonality, the length of the growing season and the transmission of pathogens, vectors and hosts =====

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VBDs require arthropod vector hosts (e.g., insects or ticks), while other infectious diseases (e.g., fungi, bacteria and helminths) have free-living life stages and/or complex life cycles that require intermediate hosts (e.g., snails), all of which have temperature-driven rates of development and replication/reproduction ( ''robust evidence'' , ''high agreement'' ) ( [[#Mordecai--2013|Mordecai et al., 2013]] ; [[#Liu-Helmersson--2014|Liu-Helmersson et al., 2014]] ; [[#Moran--2014|Moran and Alexander, 2014]] ; [[#Bernstein--2015|Bernstein, 2015]] ; [[#Marcogliese--2016|Marcogliese, 2016]] ; [[#Ogden--2016|Ogden and Lindsay, 2016]] ; [[#Mordecai--2017|Mordecai et al., 2017]] ; [[#Short--2017|Short et al., 2017]] ; [[#Caminade--2019|Caminade et al., 2019]] ; [[#Cavicchioli--2019|Cavicchioli et al., 2019]] ; [[#Mordecai--2019|Mordecai et al., 2019]] ; [[#Liu--2020|Liu et al., 2020]] ; [[#Rocklöv--2020|Rocklöv and Dubrow, 2020]] ). Additionally, microbes such as bacteria thermally adapt to temperature changes through multiple mechanisms, indicating that warming will not reduce antibiotic resistance ( [[#MacFadden--2018|MacFadden et al., 2018]] ; [[#Pärnänen--2019|Pärnänen et al., 2019]] ; [[#Shukla--2019|Shukla, 2019]] ; [[#McGough--2020|McGough et al., 2020]] ; [[#Rodriguez-Verdugo--2020|Rodriguez-Verdugo et al., 2020]] ).

There is increasing evidence of the role of extreme events in disease outbreaks ''(very high confidence)'' ( [[#Tjaden--2018|Tjaden et al., 2018]] ; [[#Bryson--2020|Bryson et al., 2020]] ). Heat waves have been associated with outbreaks of helminth pathogens, especially in sub-Arctic and Arctic areas. For example, a severe outbreak of microfilaremia, a VBD spread by mosquitoes and flies, plagued reindeer in northern Europe following extreme high temperatures ( [[#Laaksonen--2010|Laaksonen et al., 2010]] ). More frequent and severe extreme events such as floods, droughts, heat waves and storms can either increase or decrease outbreaks, depending upon the region and disease ( ''robust evidence'' , ''high agreement'' ) ( [[#Anyamba--2001|Anyamba et al., 2001]] ; [[#Marcheggiani--2010|Marcheggiani et al., 2010]] ; [[#Brown--2013|Brown and Murray, 2013]] ; [[#Paz--2015|Paz, 2015]] ; [[#Boyce--2016|Boyce et al., 2016]] ; [[#Wu--2016b|Wu et al., 2016b]] ; [[#Wilcox--2019|Wilcox et al., 2019]] ; [[#Nosrat--2021|Nosrat et al., 2021]] ). Heavy precipitation events have been shown to increase some infectious diseases with aquatic life-cycle components such as mosquito-borne, helminth, and rodent-borne diseases ( ''robust evidence'' , ''high agreement'' ) ( [[#Anyamba--2001|Anyamba et al., 2001]] ; [[#Zhou--2005|Zhou et al., 2005]] ; [[#Wu--2008|Wu et al., 2008]] ; [[#Brown--2013|Brown and Murray, 2013]] ; [[#Anyamba--2014|Anyamba et al., 2014]] ; [[#Boyce--2016|Boyce et al., 2016]] ). Conversely, flooding also increases flow rate and decreases parasite load and diversity in other aquatic wildlife ( [[#Hallett--2008|Hallett and Bartholomew, 2008]] ; [[#Bjork--2009|Bjork and Bartholomew, 2009]] ; [[#Marcogliese--2016|Marcogliese, 2016]] ; [[#Marcogliese--2016|Marcogliese et al., 2016]] ) and can reduce mosquito abundance by flushing them out of the system ( [[#Paaijmans--2007|Paaijmans et al., 2007]] ; [[#Paz--2015|Paz, 2015]] ).

Droughts reduce the aquatic habitat of some mosquito species while simultaneously increasing the availability of stagnant standing pools of water that are ideal breeding habitats for other species, such as dengue-vector ''Aedes'' mosquitoes ( ''medium evidence'' , ''medium agreement'' ) ( [[#Chareonviriyaphap--2003|Chareonviriyaphap et al., 2003]] ; [[#Chretien--2007|Chretien et al., 2007]] ; [[#Padmanabha--2010|Padmanabha et al., 2010]] ; [[#Trewin--2013|Trewin et al., 2013]] ; [[#Paz--2015|Paz, 2015]] ). Extreme drought has been associated with an increase in bluetongue virus haemorrhagic disease in wildlife in eastern North America, although the mechanisms involved were not identified ( [[#Christensen--2020|Christensen et al., 2020]] ). Heat waves in some regions, especially coastal regions, have increased parasitism and decreased host richness and abundance, leading to population crashes ( [[#Larsen--2014|Larsen and Mouritsen, 2014]] ; [[#Mouritsen--2018|Mouritsen et al., 2018]] ). Changes in temperature and precipitation, especially extreme events, can alter community structure ( [[#Larsen--2011|Larsen et al., 2011]] ) by increasing or decreasing parasites and their host organisms, and even altering host behaviour in ways that are advantageous to parasites ( [[#Macnab--2012|Macnab and Barber, 2012]] ).

Climate change not only affects the occurrence of pathogens and their hosts in terms of geographic space but also impacts the temporal patterns of disease transmission. Warmer winters allow greater over-winter survival of arthropod vectors, which, coupled with lengthened transmission seasons, drive increases in vector population sizes, pathogen prevalence, and thus the proportion of vectors infected ( ''robust evidence'' , ''high agreement'' ) ( [[#Laaksonen--2009|Laaksonen et al., 2009]] ; [[#Molnár--2013|Molnár et al., 2013]] ; [[#Waits--2018|Waits et al., 2018]] ). For example, a parasitic nematode lung worm ( ''Umingmakstrongylus pallikuukensis'' ) has shortened its larval development time by half (from two years to one year), which has increased infection rates in North American musk oxen ( [[#Norwegian%20Polar%20Institute--2009|Norwegian Polar Institute, 2009]] ).

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===== Case Study 1: Climate change impacts on pathogenic helminths in Europe =====

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Parasitic helminths can reduce growth and yield, kill livestock and infect humans and wildlife, leading to health, agricultural and economic losses ( [[#Fairweather--2011|Fairweather, 2011]] ; [[#Charlier--2016|Charlier et al., 2016]] ; [[#Charlier--2020|Charlier, 2020]] ). Attribution of increased incidence and risk of helminth disease to climate change is stronger than for other human diseases, thanks to long-term records and careful analysis of other anthropogenic drivers (e.g., LUC, agricultural/livestock intensification, and anti-helminthic intervention and resistance) ( [[#van%20Dijk--2008|van Dijk et al., 2008]] ; [[#van%20Dijk--2010|van Dijk et al., 2010]] ; [[#Fox--2011b|Fox et al., 2011b]] ; [[#Martínez-Valladares--2013|Martínez-Valladares et al., 2013]] ; [[#Charlier--2016|Charlier et al., 2016]] ; [[#Innocent--2017|Innocent et al., 2017]] ; [[#Mehmood--2017|Mehmood et al., 2017]] ).

In Europe, evidence from laboratory studies, long-term surveillance, statistical analyses and modelling shows that multiple helminth pathogens and their host snails have extended their transmission windows and increased their survival, fecundity, growth and abundances ( ''robust evidence'' , ''high agreement'' ). Furthermore, they have expanded or shifted their ranges poleward due to increases in temperature, precipitation and humidity ( ''robust evidence'' , ''high agreement'' ) ( [[#Lee--1995|Lee et al., 1995]] ; [[#Pritchard--2005|Pritchard et al., 2005]] ; [[#Poulin--2006|Poulin, 2006]] ; [[#van%20Dijk--2008|van Dijk et al., 2008]] ; [[#van%20Dijk--2010|van Dijk et al., 2010]] ; [[#Fairweather--2011|Fairweather, 2011]] ; [[#Fox--2011b|Fox et al., 2011b]] ; [[#Martínez-Valladares--2013|Martínez-Valladares et al., 2013]] ; [[#Bosco--2015|Bosco et al., 2015]] ; [[#Caminade--2015|Caminade et al., 2015]] ; [[#Caminade--2019|Caminade et al., 2019]] ). These documented changes in climate, hosts and pathogens have been linked to a higher incidence and more frequent outbreaks of disease in livestock across Europe ( ''very high confidence'' ).

<span id="case-study-2-chytrid-fungus-and-climate-change"></span>
===== Case Study 2: Chytrid fungus and climate change =====

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Infection by the chytrid fungus, Bd ''(Batrachochytrium dendrobatidis),'' can cause chytridiomycosis in amphibians. Bd is widely distributed globally and has caused catastrophic disease in amphibians, associated with the decline of 501 species and extinction of a further 90 species, primarily in tropical regions of the Americas and Australia ( [[#Scheele--2019|Scheele et al., 2019]] ; [[#Fisher--2020|Fisher and Garner, 2020]] ). Bd successfully travelled with high-elevation Andean frog species as they expanded their elevational ranges upward, driven by regional warming, to &gt; 5200 m ( [[#Seimon--2017|Seimon et al., 2017]] ).

New findings since AR5 from controlled laboratory experiments (manipulating temperature, humidity and water availability), intensive analyses of observed patterns of infection and disease in nature, and modelling studies have led to an emerging consensus that interactions between chytrids and amphibians are climate-sensitive, and that the interaction of climate change and Bd has driven many of the globally observed declines and extinctions of ~90 amphibian species ( ''robust evidence'' , ''high agreement'' ) ( [[#Rohr--2010|Rohr and Raffel, 2010]] ; [[#Puschendorf--2011|Puschendorf et al., 2011]] ; [[#Rowley--2013|Rowley and Alford, 2013]] ; [[#Raffel--2015|Raffel et al., 2015]] ; [[#Sauer--2018|Sauer et al., 2018]] ; [[#Cohen--2019a|Cohen et al., 2019a]] ; [[#Sauer--2020|Sauer et al., 2020]] ; [[#Turner--2021|Turner et al., 2021]] ).

The ‘thermal mismatch hypothesis’ posits that vulnerability to disease should be higher at warm temperatures in cool-adapted species and higher at cool temperatures in warmth-adapted species and is generally supported ( [[#Pounds--2006|Pounds et al., 2006]] ). However, the most recent studies reveal more complex mechanisms underlying amphibian disease–climate change dynamics, including variation in thermal preferences among individuals in a single amphibian population ( ''robust evidence'' , ''high agreement'' ) ( [[#Zumbado-Ulate--2014|Zumbado-Ulate et al., 2014]] ; [[#Sauer--2018|Sauer et al., 2018]] ; [[#Cohen--2019b|Cohen et al., 2019b]] ; [[#Neely--2020|Neely et al., 2020]] ; [[#Sauer--2020|Sauer et al., 2020]] ).

Bd is not universally harmful; it has been recorded as endemic in frog populations that do not suffer disease, where it may be commensal rather than parasitic ( [[#Puschendorf--2006|Puschendorf et al., 2006]] ; [[#Puschendorf--2011|Puschendorf et al., 2011]] ; [[#Rowley--2013|Rowley and Alford, 2013]] ). Projections of future impacts are difficult, as the virulence is variable across Bd populations and dependent upon the evolutionary and ecological history and evolutionary potential of both a local amphibian population and the endemic or invading Bd ( ''robust evidence'' , ''high agreement'' ) ( [[#Retallick--2004|Retallick et al., 2004]] ; [[#Daskin--2011|Daskin et al., 2011]] ; [[#Puschendorf--2011|Puschendorf et al., 2011]] ; [[#Phillips--2013|Phillips and Puschendorf, 2013]] ; [[#Rowley--2013|Rowley and Alford, 2013]] ; [[#Zumbado-Ulate--2014|Zumbado-Ulate et al., 2014]] ; [[#Sapsford--2015|Sapsford et al., 2015]] ; [[#Voyles--2018|Voyles et al., 2018]] ; [[#Bradley--2019|Bradley et al., 2019]] ; [[#Fisher--2020|Fisher and Garner, 2020]] ; [[#McMillan--2020|McMillan et al., 2020]] ). Further, specific local habitats might serve as regional climate refugia from chytrid infection (e.g., hot and dry) ( ''medium evidence'' , ''high agreement'' ) ( [[#Zumbado-Ulate--2014|Zumbado-Ulate et al., 2014]] ; [[#Cohen--2019b|Cohen et al., 2019b]] ; [[#Neely--2020|Neely et al., 2020]] ; [[#Turner--2021|Turner et al., 2021]] ).

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<span id="changes-in-geographic-distribution-and-connectivity-patterns-of-pathogens"></span>
===== 2.4.2.7.2 Changes in geographic distribution and connectivity patterns of pathogens =====

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As species’ geographic ranges and migration patterns are modified by climate change ( [[#2.4.2.1|Section 2.4.2.1]] , Table 2.2), pathogens accompany them. Diverse vectors and associated parasites, pests and pathogens of plants and animals are being recorded at higher latitudes and elevations in conjunction with regional temperature increases and precipitation changes ( ''robust evidence'' , ''high agreement'' ), although analysis of realised disease incidence often lacks the inclusion of non-climatic versus climate drivers, compromising attribution ( [[#Ollerenshaw--1959|Ollerenshaw and Rowlands, 1959]] ; [[#Purse--2005|Purse et al., 2005]] ; [[#Laaksonen--2010|Laaksonen et al., 2010]] ; [[#van%20Dijk--2010|van Dijk et al., 2010]] ; [[#Alonso--2011|Alonso et al., 2011]] ; [[#Genchi--2011|Genchi et al., 2011]] ; [[#Pinault--2011|Pinault and Hunter, 2011]] ; [[#Jaenson--2012|Jaenson et al., 2012]] ; [[#Loiseau--2012|Loiseau et al., 2012]] ; [[#Kweka--2013|Kweka et al., 2013]] ; [[#Medlock--2013|Medlock et al., 2013]] ; [[#Dhimal--2014a|Dhimal et al., 2014a]] ; [[#Dhimal--2014b|Dhimal et al., 2014b]] seasonal; [[#Siraj--2014|Siraj et al., 2014]] ; [[#Khatchikian--2015|Khatchikian et al., 2015]] ; [[#Hotez--2016a|Hotez, 2016a]] ; [[#Hotez--2016b|Hotez, 2016b]] ; [[#Bett--2017|Bett et al., 2017]] ; [[#Mallory--2017|Mallory and Boyce, 2017]] ; [[#Strutz--2017|Strutz, 2017]] ; [[#Booth--2018|Booth, 2018]] ; [[#Dumic--2018|Dumic and Severnini, 2018]] ; [[#Carignan--2019|Carignan et al., 2019]] ; [[#Gorris--2019|Gorris et al., 2019]] ; [[#Le--2019|Le et al., 2019]] ; [[#Stensgaard--2019b|Stensgaard et al., 2019b]] snails and; [[#Brugueras--2020|Brugueras et al., 2020]] ; [[#Gilbert--2021|Gilbert, 2021]] ).

At least six major VBDs affected by climate drivers have recently emerged in Nepal and are now considered endemic, with climate change implicated as a primary driver as LULCC has been assessed to have a minimal influence on these diseases ( ''high confidence'' ) (Table SM2.1). There is ''increasing evidence'' that climate warming has extended the elevational distribution of ''Anopheles'' , ''Culex'' and ''Aedes'' mosquito vectors above 2000 m in Nepal ( ''limited evidence'' , ''high agreement'' ) ( [[#Dahal--2008|Dahal, 2008]] ; [[#Dhimal--2014a|Dhimal et al., 2014a]] ; [[#Dhimal--2014b|Dhimal et al., 2014b]] ; [[#Dhimal--2015|Dhimal et al., 2015]] ), with similar trends being recorded in neighbouring Himalayan regions ( ''medium evidence'' , ''high agreement'' ) ( [[#Phuyal--2020|Phuyal et al., 2020]] ; [[#Dhimal--2021|Dhimal et al., 2021]] ). Host animals in novel areas may be immunologically naive, and therefore more vulnerable to severe illness ( [[#Bradley--2005|Bradley et al., 2005]] ; [[#Hall--2016|Hall et al., 2016]] ).

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<span id="case-study-3-arctic-and-sub-arctic-disease-expansion-and-intensification"></span>
===== Case Study 3: Arctic and sub-Arctic disease expansion and intensification =====

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High Arctic regions have warmed by more than double the global average, &gt;2°C in most areas (Sections 2.3.1.1.2, Figure 2.11, and Atlas 11.2.1.2 in ( [[#IPCC--2021a|IPCC, 2021a]] )). Experimental field ecology studies and computational models of Arctic and sub-Arctic regions indicate that milder winters have reduced the mortality of vectors and reservoir hosts and increased their habitat as forested taiga expands into previously treeless tundra (Table SM2.1) ( [[#Parkinson--2014|Parkinson et al., 2014]] ). Warmer temperatures and longer seasonal windows have allowed faster reproduction/replication, accelerated development and increased the number of generations per year of pathogens, vectors and some host animals, which, in turn, increases the populations of disease organisms and disease transmission (Sections 2.4.2.4, 2.4.4.3.3). Higher numbers of ticks, mosquitoes, ''Culicoides'' biting midges, deer flies, horseflies and Simuliidae black flies, that transmit a variety of pathogens, are being documented in high-latitude regions and where they have been historically absent ( ''robust evidence'' , ''high agreement'' ) ( [[#Waits--2018|Waits et al., 2018]] ; [[#Caminade--2019|Caminade et al., 2019]] ; [[#Gilbert--2021|Gilbert, 2021]] ). In concert with these poleward shifts of hosts and vectors, pathogens, particularly tick-borne pathogens and helminth infections, have increased dramatically in incidence and severity from once-rare occurrences and have appeared in new regions ( ''very high confidence'' ) ( [[#Caminade--2019|Caminade et al., 2019]] ; [[#Gilbert--2021|Gilbert, 2021]] ).

Zoonoses and VBDs that have been historically rare or never documented in the Arctic and sub-Arctic regions of Europe, Asia, and North America, such as anthrax, cryptosporidiosis, elaphostrongylosis, filariasis ( [[#Huber--2020|Huber et al., 2020]] ), tick-borne encephalitis and tularemia ( [[#Evander--2009|Evander and Ahlm, 2009]] ; [[#Parkinson--2014|Parkinson et al., 2014]] ; [[#Pauchard--2016|Pauchard et al., 2016]] ), are spreading poleward and increasing in incidence, associated with warming temperatures ( ''robust evidence'' , ''high agreement'' , ''very high confidence'' ) (Table SM2.1) ( [[#Omazic--2019|Omazic et al., 2019]] ). Recent anthrax outbreaks and mass mortality events of humans and reindeer, respectively, have been linked to abnormally hot summer temperatures that caused the permafrost to melt and exposed diseased animal carcasses, releasing thawed, highly infectious ''Bacillus anthracis'' spores ( ''medium evidence'' , ''medium agreement'' ) (Ezhova et al., 2019; [[#Hueffer--2020|Hueffer et al., 2020]] ; [[#Ezhova--2021|Ezhova et al., 2021]] ). Multiple contributing factors conspired over different timescales to compound a 2016 anthrax outbreak occurring on the Yamal peninsula: (i) rapid permafrost thawing for 5 years preceding the outbreak, (ii) thick snow cover the year before the outbreak insulated the warmed permafrost and kept it from re-freezing, and (iii) anthrax vaccination rates had decreased or ceased in the region (Ezhova et al., 2019; [[#Ezhova--2021|Ezhova et al., 2021]] ). These precursors converged with an unusually dry and hot summer that: (i) melted permafrost, creating an anthrax exposure hazard; (ii) increased the vector insect population; and (iii) weakened the immune systems of reindeer, thereby increasing their susceptibility ( [[#Waits--2018|Waits et al., 2018]] ; [[#Hueffer--2020|Hueffer et al., 2020]] ).

Warmer temperatures have increased blood-feeding insect harassment of reindeer with compounding consequences: (1) increased insect-bite rates lead to higher parasite loads, (2) time spent by reindeer in trying to escape biting flies reduces foraging while simultaneously increasing their energy expenditure, (3) the combination of (1) and (2) leads to poor body condition which subsequently leads to (4) reduced winter survival and fecundity ( [[#Mallory--2017|Mallory and Boyce, 2017]] ). As temperatures warm and connectivity increases between the Arctic and the rest of the world, tourism, resource extraction and increased commercial transport will create additional risks of biological invasion by infectious agents and their hosts ( [[#Pauchard--2016|Pauchard et al., 2016]] ). These increases in introduction risk compounded with climate change have already begun to harm Indigenous Peoples dependent on hunting and herding livestock (horses and reindeer) that are suffering increased pathogen infection ''(high confidence)'' ( [[#Deksne--2020|Deksne et al., 2020]] ; [[#Stammler--2020|Stammler and Ivanova, 2020]] ).

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===== 2.4.2.7.3 Biodiversity–disease links =====

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Anthropogenic impacts, such as disturbances caused by climate change, can reduce biodiversity via multiple mechanisms and increase the risk of human diseases ( ''limited evidence'' , ''low agreement'' ), but more research is needed to understand the underlying mechanisms ( [[#Civitello--2015|Civitello et al., 2015]] ; [[#Young--2017b|Young et al., 2017b]] ; [[#Halliday--2020|Halliday et al., 2020]] ; [[#Rohr--2020|Rohr et al., 2020]] ; [[#Glidden--2021|Glidden et al., 2021]] ). Known wildlife hosts of human-shared pathogens and parasites overall comprise a greater proportion of local species richness (18–72% higher) and abundance (21–144% higher) at sites under substantial human use (agricultural and urban land) compared with nearby undisturbed habitats ( [[#Gibb--2020|Gibb et al., 2020]] ).

Exploitation of wildlife and degradation of natural habitats have increased opportunities for a ‘spill over’ of pathogens from wildlife to human populations and also the emergence of zoonotic disease epidemics and pandemics ( ''robust evidence'' , ''high agreement'' ); animal and human migrations driven by climate change have added to this increased risk ( ''medium evidence'' , ''medium agreement'' ) (see [[#2.4.2.1|Section 2.4.2.1]] , Chapter 8, Cross-Chapter Box MOVING PLATE in Chapter 5) ( [[#Patz--2004|Patz et al., 2004]] ; [[#Cleaveland--2007|Cleaveland et al., 2007]] ; [[#Karesh--2012|Karesh et al., 2012]] ; [[#Altizer--2013|Altizer et al., 2013]] ; [[#Allen--2017|Allen et al., 2017]] ; [[#Plowright--2017|Plowright et al., 2017]] ; [[#Faust--2018|Faust et al., 2018]] ; [[#Carlson--2020|Carlson et al., 2020]] ; [[#Gibb--2020|Gibb et al., 2020]] ; [[#Hockings--2020|Hockings et al., 2020]] ; [[#IPBES--2020|IPBES, 2020]] ; [[#Volpato--2020|Volpato et al., 2020]] ; [[#Glidden--2021|Glidden et al., 2021]] ). Agricultural losses and subsequent food scarcity, increasing due to climate change, can also lead to an increase in the use of bushmeat, and thus increase the risk of diseases jumping from wild animals to humans ( ''medium evidence'' , ''high agreement'' ) ( [[#Brashares--2004|Brashares et al., 2004]] ; [[#Leroy--2004|Leroy et al., 2004]] ; [[#Wolfe--2004|Wolfe et al., 2004]] ; [[#Rosen--2010|Rosen and Smith, 2010]] ; [[#Kurpiers--2016|Kurpiers et al., 2016]] ).

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<span id="implications-of-changes-in-diseases-in-wild-animals-for-humans"></span>
===== 2.4.2.7.4 Implications of changes in diseases in wild animals for humans =====

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Changes in temperature, precipitation, humidity and extreme events have been associated with more frequent disease outbreaks, increases in disease incidence and severity, novel diseases and the emergence of vectors in new areas for wild animals, with a mechanistic understanding of the roles of these drivers from experimental studies providing ''high confidence'' for the role of climate change. However, attributing how this has impacted human infectious diseases remains difficult, and definitive attribution studies are lacking. The specific role of recent climate change is difficult to examine in isolation in most regions where human disease incidence has also been affected by LUC (particularly agricultural and urban expansion), changes in public health access and measures, socioeconomic changes, increased global movement of people and changes in vector and rodent control programs, supporting ''medium confidence'' in the role of climate change driving the observed changes in vector-borne and infectious human diseases globally. Exceptions are in areas noted above (the Arctic, sub-Arctic, and high-elevation regions), in which climate change fingerprints are strong and concurrent changes in non-climatic drivers are less pronounced than in other regions ( ''high confidence'' for climate change attribution) (see Table SM2.1, Sections 5.5.1.3, 7.2.2.1, Cross-Chapter Box ILLNESS this Chapter) ( [[#Harvell--2002|Harvell et al., 2002]] ; [[#Norwegian%20Polar%20Institute--2009|Norwegian Polar Institute, 2009]] ; [[#Tersago--2009|Tersago et al., 2009]] ; [[#Tabachnick--2010|Tabachnick, 2010]] ; [[#Altizer--2013|Altizer et al., 2013]] ; [[#Garrett--2013|Garrett et al., 2013]] ; [[#Paz--2015|Paz, 2015]] ; [[#Wu--2016b|Wu et al., 2016b]] ; [[#Caminade--2019|Caminade et al., 2019]] ; [[#Dewage--2019|Dewage et al., 2019]] ; [[#Coates--2020|Coates and Norton, 2020]] ; [[#Deksne--2020|Deksne et al., 2020]] ; [[#Shocket--2020|Shocket et al., 2020]] ; [[#Couper--2021|Couper et al., 2021]] ; [[#Gilbert--2021|Gilbert, 2021]] ).

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