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    ILAR Journal, 2015, Vol, 56, No. 3, 306-311 4st 1020928arslo8s Wildlife Pathology Studies and How They Can Inform Public Health Tracey S. McNamara ‘Tracey S, McNamara is Professor of Pathology in the College of Veterinary Medicine at Westem University of Health Sciences in Pomona, California Adress conespondence and reprint request fa Tracey 5 MeNamara VM, iplomate ACV, FNA, Westen Univesity f Heath Senet, 39 Second Abstract Emerging zoonoses have had a serious impact on human and animal health in recent decades, More often than not, these disease outbreaks have taken public health by surprise because we have failed to shift the epidemiological curve to the farleft and detect zoonoses in animal populations prior to spillover to people. Not only can animals serve as valuable sentinels for ‘emerging zoonoses but also much can be gained by the study ofthe animals themselves. Key words: animal studies; bat viruses; emerging infectious zoonoses; West Nile virus; wildlife pathology; wildlife surveillance Introduction Rudolf Virchow said, “Between human and animal medicine there is no dividing line—nor should there be" (klauder 1953) ‘This hae never been more valid than today. Emerging zoonoses have increased in recent years with serious consequences for public health. Severe acute respiratory syndrome (SARS), Nipah virus (NIV), Hendra virus (eV), West Nile virus (WNV), monkey- pox, and, most recently Bola virus and Middle Eastern respirato- 2y syndrome (MERS.CoV} are all animal-related diseases. These zoonoses have served as wake-up cals to the public health, wild- life, and veterinary communities and heralded the need fo clas- ercollaboration (Chomel et l. 2007) Historically, public health, veterinary, and wildlife agenciee have not had close working telationships. More often than not Wwe have net been able to shit the epidemiology curve to the far left and identify zoonotic diseases in animal populations before spillover into humans. instead public health has used taxpayers as sentinels, Such wae the caze with WIV when early warning ‘came in the fren of dead crows 2 months before any human in- fections tookplace. Veterinary pathology studies on wildlife were “ultimately the key tothe recognition and understanding of WNV. ‘Wildlife studies have been critical to the understanding of ther recent emerging zoonoses, and their importance cannot be underestimated, Revenge of the Rainforest—Emerging Infectious Diseases and Wildlife Most emerging infectious diseases (EDs) are zoonoses (60.2% of IDs), andthe majority ofthese (7187) have originated in wildlife (Yones et a. 2008). recent retrospective study of 35 emerging Infectious episodes aver a 64-yeat period (1940-2004) also em= phasized the role of wildlife as a source of emerging infections {Cutler etal, 2010) Rodents andl bats, n particu, have been as- sociated with many serious disease outbreaks such as hantavirus pulmonary syndrome, Laces fever, and NiV encephalitis (Morens anc Fauci 2032). SARS was linked to colonies of hoxseshoe bats {Rhinoiophus sp.) infected with acoranavirus im Malaysia that sub- sequently spread to Hong Kong and Toronto, Canada, NIV and eV have algo both been linked to bate (Artois et al. 2011). Inapite ofthe tole that wild animals have played in recent 200- notic disease outbreaks, esearch efforts have typically been focused {©The Atha 2016 Published by Oxford Univesity res on Beal of he insite for Laboratory Anime] Research, alright veered. 306 toward either humans or domestic animals (Cutler et 2010, and {few survelance programs are speciicaly aimed at wildlife (Chomel fetal. 2007), There ae few diseases of wildlife that must be reported to regulatory agencies (Daevak et sl 2000), and wildlife agencies tasked with doing surveillance ae critically underfunded both in the United States and overseas. Wider surveillance in wildife has been calle for, but few coordinated efforts have been implemented te preempt zoonotic disease emergence with wildlife surveillance (Morse etal 2012, Don’t Blame Wildlife—Human Activities and Emerging Zoonoses There has been a tendency te blame wildlife for emerging zeono- see, The public ean be quick to eal for eradication of wildlife when the fact ie human activities are the driving force for where and how zoonoses occur (Katesh etal. 2012. ‘The emergence ofthese pathogens a significant health issues fs associated with arange of causal factors, most of ther inked to Ihuman activity. Changing agricultural practices, mavementofdo- ‘esti animals, anda range of environmental factors result in the emergence of zoonoses (Bengis etal. 2004), There has, however, been litte emphasis on the roles of human-induced habitat de struction o wildlife population sess on EID spread oron theneg- ative impacts of diseaze on wildlife (btke et al, 2015, Kyasanur Foret disease in 1957 occunred in previously undis~ turbed forest where land was clearcut fora cashew tree plantation. ‘Workers whe clested the forest became ill. Inthe 19506, the ermer= gence of Argentine hemorrhagic fever was divectly linked to & switch to com production that supported an explosion ofthe i= rus's main reeeroi, the corm mouse (Calomys musculus), NiV in ‘Malaysia in 1998 and 1989 was the result of deforestation and ex- pansion of pig farmers into bat habitat in association with the pro- duction of frut-beaving trees that led to indivect exposure to bats ‘that aned the virus (Chote! t al. 207) twas the destruction of| bat habitac that triggered encroachment of bate into pig farming’ fruit tree growing areas (Wynne and Wang 2013) NIV infection caused 265 human cases of encephalitis with a36% mortality rate. [Nivalee continues bea serious problem in many tural areas ‘of Bangladesh and india but fora different reason, Bats and peo- ple share a predilection for consuming raw date palm sap collected from trees in hanging containers. Bats come to feaston the sap andin doing so urinateinte the collection pts. The sap is later consumed raw by humans (Cutler etal, 219, Something as simple as placing bariers onthe pots may decrease transmission Of NV to people Human activites have algo resulted in human infections with bola virus. The bush meat trade has been implicated in recent bola outbreaks. In the May to November 2007 outbreak of Ebola sn the Democratic Republic of Congo, researchers found that fruit bate were massively hunted and eaten by villagers during theiran- nual migration. Bats represent a major source of protein for the ‘human population (Leroy etal 200 but are also a source of infection. Tracking, capturing, and butchering of wildlife in the eld and transporting of bshmeat ll involve risks and have also resulted inhuman cases of Ebola vius, Particularly high tsks ate associ- ated with the hunting of nonhuman primates (Cuter et al. 2010). Human transmission hae resulted from the handling of gorilla, chimpanzee, or duiker carcaces (Leroy etal. 2004) (Of note, the wild anitnal outbreaks of Ebola occurred before ‘each of the five human outbreaks between 2001 and 7002, Meni- toring information was used t alert health authorities of an i= ‘minent risk of exposure weeks before human outbreak occurred fon two occasions (2almer 2014) AR Journal, 2015, Vol.56,No.2. | 307 “Bomb the Bats” ‘When HeV oa first discovered in Australia, there was a populist call for bat eradication. A politician was quoted as saying “Bomb the bats” (Degeling and Kemidge 2019). This is an example of an uninformed and reactive response to a wildife-related emerging Infectious disease. Infact, although tic tre that more than 15 virus families have been identified in 200 species of 12 bat fami- Ties and that they are morelikely tobe infected with more zoonot- ic viruses than rodents (0'Shea et al, 2074), studies have shown no evidence that a decrease in bat dencity would reduce viral prevalence (#lowright eta. 2015) Instead, they found that dis- rupting bat colonies and increasing bat stress may increase the amplitude of viral shedding. (Halpin etal. 2011) n one study, Pteropus bate from Australia and Malaysia were inoculated with INiV and HeV by natural routes of infection. In spite of intensive sampling, researchers found no NiV in Malaysian bate, and eV ‘was resolated from only one Australian bat. These results sug- gest opportunities for henipavirus transmission may be limited And thatthe probability of spillover is low (Hfalpin et al. 2017) ‘A more balanced and reasoned approach to bat-associated EIDs would be to restore bat feeding habitat to discourage wrban- ‘zation ofbat populations due tontuitional stres, Simple things 1ike vaccinating and fencing horses away from frut-bearing ees here bats may roost and feed could decrease exposute to HeV {Plowright etal 2015) changing agricultural practices by the cre- ation of buffer zones between fruiting trees and damestic ani- ‘mals would decrease the incidence of NIV and HeV (Smith and ‘Wang 2013). In Bangladesh, the installation of barters on the diate palms thst prevent the bats from accessing the collection vesseleisa simple stratepy currently being investigated to control transmission of NIV (Smith and Wang 2013), Not only is wanton aestruction of bat populations unfeasible, its also il advised Bats have remarkable immune systems, and we need to study them, °The bat immune aystem is astonishingly tolerant of ‘most pathogens—a trait that could pose risks to people, but that also offers clues to preventing human disease of aging. in- chiding cancer’ (Angier 2075; Baker 2014) Bate have evolved ‘mechanisms to control vital replication more effectively than _most ther mammals (O'Shea eta. 2014) ‘What sete bats apart from other mammals is thei ability to fly. Flight results in a15-fld to 16-flé increase in bat metabolic rate in comparison withthe sevanfold increase in rodents run- ning to exhaustion or the twofold increase in metabolic rate of ‘most fying birds (O'Shea etal. 2014), Bats se 20 times more en- ergy than other mammal of the same size duting an average day {slexak27012) Thebody temperature is consistently above normal Ina fever-lke state Thie persistent fever state keeps viral replica- tion ata low level, and the virus never averrins the bat immune system (Grant2014). Butall this energy production generates free radicals that damage DNA In spite of that bats, are extremely Jang lived, some living up to 40 years of age, They live 3 t0 10 times longer than other mammals of similar size (Grant 2014) and demonstrate Tow levels of eancer (Wynne and Wang 2013). Bats have evolved a strategy to avoid DNA damage (yn 2073; Slezak 2012), Scientists looked at the fruit bat Pterpus alecto and the insectvorous bat Myetis david and found a concentration of| genes in the DNA damage checkpoint (Zhang etal 2013). They also found bats were missing a gene segment known to trigger extreme and potentially fatal cytokine storms (yn 2013), leading scientists fo speculate that if we can manipulate the human ita- imine response tobe more like a bat immune response, we may have a better chance of surviving diseases that bat are immune te (Slezak 2012). Instead of characterizing bats a5 “pat 308 | McNamara {feries on wings" (Crant 2014), we need to study them. Weneed to develop bat cel culture assays and bat-specificreagents to exars- ine lymphocyte proliferation, antibody and cytokine synthesis, cell-mediated immune responses, and a host of other mmuno- Jogi functions in bats that make them important reservoirs of emerging viruses (Calisher etal, 2006), We don't need batricige. ‘We need intensified wildlife research Tissue Is the Issue Necropsies of wildlife proved to be quite valuable during the "bola virus outbreaks. Virus detection was 32.7% (1/55) fer car~ cages but only 0.2% (13/5308) fer live-captured animals. An ‘Animal Morality Monitoring Network (AMMN) was established uring the period 2001 to 2003 in northeast Gabon and in north- west Republic of Congo and collected data from hunters on ani- smal motbidity/mortaliy. Over 60% of the 21 carcasees reported by hunters and tested were infected with che Ebola virus (Bisson fetal, 2015) During outbreaks of WNV, raptors emerged as excel- lent sentinels forthe virus in one study, raptor admissions tore- habitation clinics took place fourteen weeks eave than othet surveillance methods (Nemeth etal. 2007). When dealing with «previously unknown ora re-emerging zoonotic threat, the per- formance of systematic necropsies with tissue sampling for virus isolation and sequencing is eritical (Olson etal. 2012) Using animals as sentinels for human disease isin and of it- self strong justification for wildlife studies, However, emerging Zzoanozes can have devastating impacts on wild populations, and the negative impact thie has on conservation is unfortunately often overlooked. Ape specie that were abundant a decade ago have been decimated by Ebola virus. {n 2006, 000 gorillas died ue to Enola (Bermejo etal 2006). Nonkurman primate numbers drastically declined in the Republic of Congo alone during the two-year Ebola outireak from 200% to 2003 (6% decline in gorillas and 89% decline in chimpanzees) (Leroy eta 2004; Bisson etal 2015). Itis not known ifthese populations wil recover. Despite the ongoing thteat of the next zoonotic disease out break and the demonstrated importance of such wildlife survei- Ince as an early warning system for disease emergence, no systematic wildlife surveillance program existsin most countries @isson et al. 2015), West Nile Virus—What the Animal Studies Told Us in 1999 The WNV outbreak of 1999 an excellent example ofthe power- {ul contributions animal studies ean make to public health ‘Animal studies provided information on the breadth of species ‘susceptible to WNV infection, which had an impact on survei- lance efforts, Pathology studies on captive and free-ranging wild- Jife ultimately changed the tissue submission protocel for iagnostic testing. Veterinary serum banks provided insigh Into when the virus first appeared in New York City. The ability te fellow infected captive willie over time provided the frstin- ication of possible viral persistence, Many features and con- cems about WNV pertinent to human health were identified by veterinary pathologists shortly after WNV's recognition In the immediate aftermath of the discovery of WNV in the United States, public health wanted to use birds as sentinels and launch dead bird eurveillance, But which species of birds should be tested? The public health focus was solely on crows. However, histopatholegi, virus isolation, and immunohisto- ‘chemical (FHC) studies on the birds that had died atthe Bronx Zoo in New York City indicated a broad species range of susceptibility tothe virus (Steele etal, 2000), Bird epecies a8 die verze ae bald eagles (Halineetus leucopus), nowy owle(Bubo scandiaeus), and Chilean flamingoes (Phoencopteras chiens all feuccumbed to the virus, The 200 was fall of sentinel species. ‘When New York City entered the second summer of WNY, the first warning came not from trapped mosquitoes nor from sen- tinel chickens but from an IiIC-positive Guanay cormorant (Phalacrocorax bougainuili) atthe Bronx Zoo, The list of known susceptible bird species is now quite lengthy (Komar 2002), and {epecies other than crows have been found to play an impartant zelein vansmission of WNY, illustrating the danger of too nanow ‘focus when dealing with a new disease ‘ms 1989, there was scant information on which matnmaian species were susceptible to WNV infection, Many captive exotic mammals, as well as birds, were algo neurelogie with WIV. Ase resurvey of the captive collections atthe 200 facilities revealed rising ters in species az diverse as rhinoceros (Rhinoceros unicor nis), snow leopards (Penthere unca), and babirousa (Babyrousa babyrussa), Abroad range of mammalian species are now Jknown te be susceptible to WNY, including alligaters (Aligator imissisipiensis (Nevarez eal, 008), polar bears (Ureus artis) {Dutton et al. 2008), reindeer (Rangifer tarandus) (Palmar et a. 200A), harbor seals Phacavituina) (Duncan etal, 2003), grey seale (Ulalichoerus grypus) (Duncan et al, 2003), iller whales (Orcinus orca) (St Leger etal 2011), Barbary macaques (Macaca sylvanus) {Olberg et a. 2008), and psittacines (Palmieri etal, 2023). Urban centinele ike fox squirrels (Scurus niger (Root et. 2006), Eastern chipmunks (Tamias situs (Patt et a. 2007), and Eastern cotton- tailrabbite(Sylvagus flordans) (Tiawsivisup otal. 2005) have been found te develop viremiae sufficient to infect mosquitoes and ‘thus may play a role inthe spread of WNV. Imadaition toits extensive captive sentinel collection, the 200 dhad another unique resource. It had frezers filled with banked serum samples from some animals going back many years. The availability of serum banks allowed the US Army Medical Re- earch Institute of Infectious Disease (USAMRUL) to establish the temporal sequence of WIV. By evaluating paired serum sars- ples ftom Bronx Zoo elephants, they were able to demonstrate {hat WNV appeared forthe fist time in the captive collection in August 1998, ‘Too litle emphasis ic placed on the value ofthese veterinary biomaterials. As WNV swept acess the United States, remen- ous effort and manpower went into collecting dead birds fer testing. Unfortunately, amples that tested negative fer WNV ‘were not banked for additional testing. After al ofthe effort and considerable expense that had been requited to collect and testbirds on a nationwide basis, only one diagnosis was pursued. Had tssues been banked, we could have tested those birds that were negative for WNV for other viruses euch as highly patho- {genic avian infkienza, which later emerged a2 a major concern ‘This farther underscores the need fora One Health approach to emerging zoonotic threat The launch of the dead bird surveillance program raised an impertant question a8 to which tissues should be collected for testing. Traditional literature suggested the primary target issue {for WNV was the brain, However, gross pathologic examina- tion, virus isolation, and IHC studies on the Byonx Zoo cazes and wild crows indicated that many tissues could be positive in a WINV-infected bird. Working with USAMRIID, IHC and virusiso- lation were done on all ofthe tissues that had been collected at necropsy on the captive collection bids and wild crows. Of all ofthe tissues, only kidney was positive 100% ofthe time (Steele ft al, 2000), A year later, after further studies, the New York State Department of Health amended its submission protocol and requested batched tiesues (rom each bird for testing, but -many positive cases were probably missed during eary surveil lance efforts due to too narow a case definition, Inthe fall of1999, the accepted dogma was that WNV was only transmitted through the bite of a mosquito, However, WNV-pos- itive birds had dramatic enterie pathology and demonstrated abundant viral antigen on IHC staining of intestine and kidney, Which suggests they were shedding large volumes of vinus into the environment. This raised the question of whether alternative odes of transmission could be involved in the epceriology of |WNV. Aerosol transmission had been known to occur with WNV sma laboratory setting if WNV-positive flatningoes were shed- {ing virus into their pond, ould other flamingoes be getting in- fected via ingestion of the virus via the fecal-ral oute or were they being exposed via aerosol? There was also abundant vital antigen in ovarian and testicular tissue, which euggested vertical transmission was aso a possibility. However, there was no fede- ralorstate funding available to do the necessary transmission studies. Ultimately, the Bronx Zoo, ina frst-of-its-kind public- private partnership, donated $25,000 to the National Wildlife Health Genter in Madison, Wisconsin, which had the necessary 41-3 level biosecurity co run the experimental studies. These studies confirmed that birds were acquiring WNV via aerosol as well as via the fecal-oral route orna et al 2002), which had éi- rect impact on how zoos handled suspect cases. This finding wl- ‘imately le to the creation af a rapid diagnostic test using oral and cloacal swabs that was adopted by many health departments (Kemar et al. 2002; Stone eta. 2004). By 2002, patients had ac- (quired WNV via transfusions and organ transplants (Charatan 2002; Cushing ta. 2009), babies had been born with WNV or be- ceame infected through breastfeeding (CDC 2007), and alternative modes of transmission were formally recognized in humane. ‘Another concer raised by the animal studies was the level of viremise in infected bids, WNV INC indicated birds were “not in Departmentof Defense terminology. There was concern the binds could presenta health riskto animal handlers. Vetevinavians and ‘wildlife rehabilitators treating and housing neurologic crows and raptors might be getting exposed to lage volumes of virus, Butit ‘was generally a¢sumed the viremiae with this new strain of WNV would be low, like those that occur with St, Louis encephai ‘When viremia studies were performed, the results were aston- sshing, and they prompted the Centers fer Disease Control and Prevention to announce its plans to do occupational hazard snidies on veterinarians and bird handlers, In Smithsonian ‘magazine, Dr. Thomas Monath, virologist extraordinaire, said, *couldn'thelieve the incredible viremias these birds cook up there's no precedent for it, There were from a trillion to ten t= lion viral particles per militr of blood, That's beyond no prece- Gent. That's almost beyond belie. No celf-respecting bird can ‘gin up a viremia higher than 100,000 particles with St Louis en- cephalitis (SLE) virus. So some birds are almost a billion-fold tore infectious with West Nile than with SLE" (all 2002). Basie histopathology and IMC offered ancther preview into Buman pathology. One ofthe zoos’ bird mortalities had demonstrated pathology and IiCstaining f the anteriorhorn cells of the spinal, cord consistent with poliomyelitis. The frst human patients had presented with profound muscle paralysis that had not ft with the initial diagnosis of SLE. Poliomyelitis in patients with WNV newroinvasive disease wae fist publiehed in 2002 (Glaze et a. 2002), at animal studies suggested te possibility im August 2999. Many ofthe neurologic issues that later emerged as concerns sn hurnan patients were fist seen in veterinary pathology stud- Jes. One ofthe more sabering and prescient histopathelogie find- ‘ngs in 00 animals was the presence of ngoinginvlammation of WAR Journal, 2015, Vol.56,No.2. | 309 the brain weeks to months after initial infection with WINV, In 1998, WINV was believed to cause a mld febrile self-limiting ll- ness in the majority of patients, with a small percentage develop- ‘ng neurcinvasive disease, Howaver, a 1983 Russian publication (Pogodina t al, 1983) on primates inoculated with a number of stains of WNY found all were capable of producing long-term neutologic sequelae and vital persistence regardess of neurclog- fe status ofthe animals, Was WNV-88 realy self-limiting? What dig the primate studies mean for us? With this in mind, patholo- gists at the Bronx Zoo intensively evaluated the brains ofall Jknowm seropositive animals regardless oftheir clinical signs at the time of infection. Evaluation of a snow leopard (Panthera unio) and a Greater indian rhinoceros (Rhinoceros unicorns) that died 3 and 8 months after infection showed éramatic Iympho- plasmacytie perivascular cuffing, An asymptomatic babitousa (Gobyrousa babyrussa) died 10 months after seroconversion and also had evidence of ongoing inflammation, which suggested ‘even subclinical infections might result in long-term central ner- vous system pathology and possible viral persistence. In 2004, ‘was ecognized that WNV infection could rarult in a protracted convalescent period with long-term problems with memory, Confusion, clinical depression, muscle weakness, tremors (Carson et al. 2006; Hall etal. 2008; Hughes et al, 2007; Klee ‘tal 2004; Sevar 2007), and Parkinsonian-lke disorders (Hughes ta. 2007} 18 months after infection. Sixty percent of encephalit- se patients in a Houston study reported symptoms 5 years after infection (Voelker 2002). Patients with milder forms of illness are just a likely to suffer long-term health probleme as enceph- alicis cases. Eighty-four percent of patients ina study on West Nile fever parted persistent fatigue, 587 had memory problems, and 49% had ongoing muscle weakness (Carson et a 2005). 1 ‘wasn’t until 2006 that WAV was found in the brain and ceebrospi- nal uid ofa human patient 4 months ater initial diagnosis (Penn (tal 2005) The hamster was established as @ madel for West Nile encephalitis in 2001 (Kao eta. 2001) twas mot until 2010 that a ‘murine model of viral persistence was established (Appler eta 2010) It showed that WNV persisted in the central nervous system and petipheral tissues for up to six months after infection in mice with subelinicl infections, What does this mean for the estimated 12 millon people with asymptomatic WNV infections inthe Unit- fed States and possible subclinical disease? Ironically, in 2005, 4 dhamstr study on WNV persistence found virus was shed inthe ‘wine upto 8months afterinfecion (Tess etal 2005), which shifted ‘the focus back othe impact af WIV an the kidney. Viral RNA was erected in the urine of an encepbalte patient @ days after symp- tem anset in 2005 (Fonte al. 2005) A 2012 long-term study of pa- tients in Houston found an association between neuroinvasive Infection and the development of chronic kidney disease (Nolan ct al. 2012). We may be seeing the tip ofan iceberg in terms of, long-term sequelae af WNV. Conclusion Imtoday's world itis impossible to separate public health, veter= nary, wilde, and ecosystem health studies along traditional lines. "The One Health concept recognizes thatthe health of hu- ‘mans is inextricably linked to the health of animals and the en- vironment (Morse et al, 2012). The Emerging Pandemic Threats (EP) program of United ‘States Agency for intermational Development, which wae launched 4m 2008, is an exciting example of recent synergy actoss human and animal health sectors, in the past, the sharp division be- ‘ween veterinary medicine and public health resulted in a failure te detect disease in sentinel animal populations in a timely 310 | MeNamara -manner. EPT draws upon expertise from all health sectors in the Ihope that we may beable to detect zoonotic health threats priar to spilloverinto the human population. The predict portion ofthe project includes the University of Califomis-Davie veterinary ‘school, the Smithsonian institution, and nongovernmental orga- nizations such as Ecohealth Alliance and the Wildlife Conserva- tion Society, which represent wildlife and ecosystem health, We need to contine to build these bridges and get back to what was recognized atthe turn of the century: "Between human and ani- ‘mal mecicine there is no dividing line—nor should there be’ (Klsuder 1958), References Angler N. 2015, No time for bats. New York Times. Available on= ine (hitp-/ www nytimes.com/2015/01/13/science/no-time- for-bats-to-rest-easy nim), accessed june 5, 2015, Apples KK, own AN, Stewart, Behr Mj, Demarest VL, Wong’), ‘Bernard KA, 2010 Persistence of West Nile vir in the central nervous system and periphery of mice. PLOS One 5110649, ‘Artois M, Blancou}, Dupeyroux0, Gilot-Fremont E2011. Sustain- able contol of zoonatic pathogens in wildlife How tobe fair tawild animale? 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