Anticoagulant rodenticides are widely used in urban areas to control rodent pests and are responsible for secondary poisoning in many nontarget wildlife species. We tested the livers of five coyotes (Canis latrans) in the Denver Metropolitan Area, Colorado, US, for anticoagulant rodenticides. All five livers were positive for brodifacoum, with values ranging from 95 ppb to 320 ppb, and one liver was positive for bromadiolone, with a value of 885 ppb. Both of these rodenticides are second-generation anticoagulants, which are more potent and more likely to cause secondary poisoning than first-generation anticoagulants due to their accumulation and persistence in the liver. We concluded that exposure to these rodenticides may have caused the death of at least two of the five coyotes, and urban coyotes in our study area are commonly exposed to rodenticides

Breck, Stewart W.

Fox, Karen A.

Gese, Eric M.

Poessel, Sharon A.

English

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University of Nebraska - Lincoln
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USDA National Wildlife Research Center - Staff
Publications
U.S. Department of Agriculture: Animal and Plant
Health Inspection Service
2015
Anticoagulant Rodenticide Exposure and Toxicosis
in Coyotes (Canis latrans) in the Denver
Metropolitan Area
Sharon A. Poessel
Utah State University, sharpoes@gmail.com
Stewart W. Breck
USDA/APHIS/WS National Wildlife Research Center, stewart.w.breck@aphis.usda.gov
Karen A. Fox
Colorado Parks and Wildlife
Eric M. Gese
Utah State University, eric.gese@usu.edu
Follow this and additional works at: https://digitalcommons.unl.edu/icwdm_usdanwrc
Part of the Life Sciences Commons
This Article is brought to you for free and open access by the U.S. Department of Agriculture: Animal and Plant Health Inspection Service at
DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in USDA National Wildlife Research Center - Staff Publications
by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln.
Poessel, Sharon A.; Breck, Stewart W.; Fox, Karen A.; and Gese, Eric M., "Anticoagulant Rodenticide Exposure and Toxicosis in
Coyotes (Canis latrans) in the Denver Metropolitan Area" (2015). USDA National Wildlife Research Center - Staff Publications. 1621.
https://digitalcommons.unl.edu/icwdm_usdanwrc/1621
DOI: 10.7589/2014-04-116 Journal of Wildlife Diseases, 51(1), 2015, pp. 265–268
# Wildlife Disease Association 2015
Anticoagulant Rodenticide Exposure and Toxicosis in Coyotes (Canis
latrans) in the Denver Metropolitan Area
Sharon A. Poessel,1,5 Stewart W. Breck,2 Karen A. Fox,3 and Eric M. Gese4 1Department of Wildland
Resources, Utah State University, 5230 Old Main Hill, Logan, Utah 84322, USA; 2US Department of Agriculture,
Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, Colorado 80521, USA;
3Colorado Parks and Wildlife, Wildlife Health Research Center, 317 W Prospect Road, Fort Collins, Colorado
80525, USA; 4US Department of Agriculture, Wildlife Services, National Wildlife Research Center, Department of
Wildland Resources, Utah State University, 5230 Old Main Hill, Logan, Utah 84322, USA; 5Corresponding
author (email: sharpoes@gmail.com)
ABSTRACT: Anticoagulant rodenticides are
widely used in urban areas to control rodent
pests and are responsible for secondary poi-
soning in many nontarget wildlife species. We
tested the livers of five coyotes (Canis latrans)
in the Denver Metropolitan Area, Colorado,
US, for anticoagulant rodenticides. All five
livers were positive for brodifacoum, with
values ranging from 95 ppb to 320 ppb, and
one liver was positive for bromadiolone, with a
value of 885 ppb. Both of these rodenticides are
second-generation anticoagulants, which are
more potent and more likely to cause secondary
poisoning than first-generation anticoagulants
due to their accumulation and persistence in
the liver. We concluded that exposure to these
rodenticides may have caused the death of at
least two of the five coyotes, and urban coyotes
in our study area are commonly exposed to
rodenticides.
Key words: Brodifacoum, bromadiolone,
poison, second-generation, toxicant, urban.
Anticoagulant rodenticides are used
extensively throughout urban areas to
control rodent populations (Hosea 2000;
Watt et al. 2005). These compounds act by
interrupting the normal synthesis of clot-
ting factors in the liver once bleeding
commences, resulting in fatal hemorrhag-
ing (Eason and Spurr 1995; Eason et al.
2002). Second-generation anticoagulants
(e.g., brodifacoum and bromadiolone) are
more potent than first-generation antico-
agulants (e.g., warfarin and chlorophaci-
none) because they can effectively poison
a rodent after only a single dose (Eason
and Spurr 1995; Berny et al. 2006).
Second-generation compounds also have
slower elimination times from the liver
(Eason and Spurr 1995; Erickson and
Urban 2004). This persistence in the liver
can lead to secondary poisoning of non-
target wildlife (Stone et al. 1999; Hosea
2000; Elliott et al. 2014), including coyotes
(Canis latrans) in urban areas (Hosea
2000; Riley et al. 2003; Gehrt and Riley
2010). We report finding anticoagulant
rodenticides in urban coyotes residing in
the Denver Metropolitan Area (DMA) of
Colorado, US.
We captured 32 coyotes in the DMA
using padded leg-hold traps and snares
and fitted them with global positioning
system radio collars from April 2012 to
May 2013 as part of an ecological study of
urban coyotes. Research protocols were
approved by the National Wildlife Re-
search Center, Institutional Animal Care
and Use Committee (QA-1972). We mon-
itored study animals with radio telemetry
from April 2012 to June 2014. Collars
were equipped with mortality sensors that
alerted us when a coyote died. Thirteen
collared coyotes died during the study.
When cause of death was unknown, the
coyote was necropsied at the Colorado
Division of Parks and Wildlife, Wildlife
Health Laboratory (Fort Collins, Colora-
do, USA). Liver samples were submitted
to the Texas A&M Veterinary Medical
Diagnostic Laboratory (College Station,
Texas, USA) to be screened for anticoag-
ulant rodenticides using high-performance
liquid chromatography. Brodifacoum, bro-
madiolone, chlorophacinone, difenacoum,
difethialone, diphacinone, and warfarin
were included in the screening. We began
testing liver samples from deceased ani-
mals only after a coyote was found dead
with sarcoptic mange because of the
relationship between mange and rodenti-
265
cide poisoning discovered in bobcats (Lynx
rufus) and mountain lions (Puma concolor)
by Riley et al. (2007), Uzal et al. (2007), and
Serieys et al. (2013). Thereafter, all nec-
ropsied coyotes were tested except for two
coyotes that were too decomposed to
obtain a valid liver sample. Hence, we only
tested five coyote livers for rodenticide
toxicosis. All five were positive for brodifa-
coum, with values ranging from 95 ppb to
320 ppb (Table 1). One coyote (the animal
with the highest level of brodifacoum) also
was positive for bromadiolone, with a value
of 885 ppb (Table 1). No other compounds
were found in the five liver samples.
Based on necropsy results, we conclud-
ed anticoagulant rodenticides contributed
to the death of at least two of the five
coyotes tested. The first case was a
juvenile male (24M) found dead in open
space, with no obvious external injuries or
other signs of trauma. Upon necropsy, we
found free blood in the abdominal cavity.
A puncture wound was present on the left
side of the body overlying the spleen but
not penetrating the abdominal wall. The
spleen was fractured and surrounded by
clotted blood. We found no radiographic
evidence of gunshot and no evidence of
bite wounds. The interpretation for cause
of death was acute severe hemorrhage,
disproportionate to the amount of trauma
observed. This coyote’s liver was positive
for brodifacoum (176 ppb; Table 1).
The second case was a juvenile male
coyote (21M) found dead on a two-lane
road, with minor evidence of skin tearing
over the ventral neck and chest. Necropsy
findings indicated additional moderate
tearing of the muscle in the region
overlying the thoracic inlet, although
injuries did not penetrate the chest cavity.
The chest was filled with blood. The
interpretation for cause of death was
severe acute hemorrhage, disproportion-
ate to the mild to moderate trauma
received from being hit by a vehicle. We
suspected rodenticide toxicosis, and the
liver was positive for brodifacoum and
bromadiolone (Table 1).
In two additional cases, we found
hemorrhage into body cavities with severe
lesions to explain the hemorrhage, but also
evidence of rodenticide exposure. An
adult male coyote (01M) had severe
lesions of sarcoptic mange, a gunshot
through the chest from a pellet rifle, and
free blood in the chest cavity. The liver
was positive for brodifacoum (150 ppb;
Table 1). A juvenile male coyote (17M)
had severe crushing lesions to the head
and body from being run over by a vehicle
and free blood in the chest and abdomen.
The liver was positive for brodifacoum
(95 ppb; Table 1). One additional coyote
(uncollared male) that we captured for our
study was euthanized due to self-inflicted
trap-related injuries, but the liver also was
positive for brodifacoum (95 ppb; Ta-
ble 1). Causes of death for nine collared
coyotes that were not tested for rodenti-
cide toxicosis included vehicle collision
(five coyotes), gunshot (one coyote), con-
flict resolution (one coyote removed from
Denver International Airport), and unde-
termined (two coyotes).
Our findings suggest anticoagulant ro-
denticides likely contributed to at least
TABLE 1. Values of anticoagulant rodenticides in coyote livers in the Denver Metropolitan Area, Colorado,
USA, 2012–13.
Coyote ID Date Brodifacoum (ppb) Bromadiolone (ppb)a
01M January 2013 150 N/A
17M February 2013 95 N/A
24M March 2013 176 N/A
21M April 2013 320 885
Uncollared April 2013 95 N/A
a N/A indicates the compound was not found in the coyote liver.
266 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 1, JANUARY 2015
two of the five mortalities, triggered by
mild to moderate trauma resulting in fatal
internal hemorrhaging. The detection of
anticoagulant rodenticides in coyotes in
the DMA indicates exposure to these
poisons, either directly or secondarily.
Because coyotes are omnivores, they could
have ingested poisoned rodent bait (Hosea
2000). However, Elliot et al. (2014)
determined that targeted rodents are
more likely to provide the exposure
pathway of anticoagulant rodenticides to
secondary consumers. Small rodents are
generally an important food source and
the dominant animal prey for coyotes in
urban areas (Morey et al. 2007; Lukasik
and Alexander 2012), resulting in a high
probability that repeated consumption of
poisoned rodents leads to rodenticide
toxicosis in urban coyotes.
The residue values of brodifacoum in
our study coyotes were generally lower
than those found in other coyote studies.
The acute oral LD50 value of brodifacoum
in dogs ranges from 250 ppb to 1,000 ppb
(Stone et al. 1999). In a study conducted
near Boston, Massachusetts, US, Way et
al. (2006) found brodifacoum values of
733 ppb and 542 ppb in two coyotes that
were presumably directly poisoned. Hosea
(2000) identified values up to 500 ppb of
brodifacoum in coyotes in California.
Erickson and Urban (2004) described
coyotes with values of brodifacoum up to
930 ppb. In our study, the two coyotes for
which we interpreted exaggerated hemor-
rhage were also the two cases with the
highest values of brodifacoum in their
livers, although these values were still
lower than the highest values found in
other studies. The lower values are not
surprising, however, considering both
cases had readily observable mild to
moderate trauma to initiate excessive
bleeding. Nevertheless, our results indi-
cated that poisoning at a lower level may
be enough to contribute to fatal hemor-
rhaging in these carnivores.
Only one coyote was positive for bro-
madiolone. The acute oral LD50 value of
bromadiolone in dogs ranges from
11,000 ppb to 15,000 ppb (Stone et al.
1999); the value in our study animal was
885 ppb. Both Erickson and Urban (2004)
and Hosea (2000) reported values of
bromadiolone in coyotes up to only
460 ppb. Our study coyote also was
positive for brodifacoum, and other inves-
tigators also have identified coyotes with
both of these rodenticides in liver tissue
(Hosea 2000; Erickson and Urban 2004).
Overall, brodifacoum appears to be more
prevalent and of higher concern in the
DMA than other rodenticides, although
our results indicated that multiple toxi-
cants may be in use throughout our study
area.
In addition to the five coyotes in the
DMA, we also tested the liver of another
coyote carcass found in rural Colorado
(Huerfano County) showing signs of
hemorrhage. The most likely cause of
death was trauma, but a definitive inter-
pretation was limited by advanced decom-
position. We found no evidence of any
rodenticides in the liver, indicating that
rodenticide toxicosis may not always occur
in coyotes. To further understand the
effects of anticoagulant rodenticides on
coyotes, future studies should compare
the values of these poisons in coyote livers
across urban and rural systems.
Our findings are consistent with those
of other studies that have determined
anticoagulant rodenticides are contribut-
ing to mortality in urban wildlife (Hosea
2000; Riley et al. 2007). The exposure of
all five tested coyotes to rodenticides,
especially brodifacoum, indicates the
ubiquity of these toxicants in the urban
landscape and their ability to reach higher
levels in the food chain (Riley et al. 2007).
One coyote liver contained more than one
rodenticide (both brodifacoum and bro-
madiolone), and multiple compounds have
been found in wildlife species in other
studies (Stone et al. 1999; Hosea 2000;
Erickson and Urban 2004). The effects of
exposure to multiple anticoagulant roden-
ticides in urban wildlife species should be
SHORT COMMUNICATIONS 267
a focus of future research to increase our
understanding of these toxicants and their
population effects on urban carnivores.
We thank J. Brinker, J. Kougher, S.
Koyle, D. Lewis, and F. Quarterone for
assistance with trapping and handling
coyotes. We also thank Texas A&M
Veterinary Medical Diagnostic Laboratory
for testing liver samples. Funding was
provided by the US Department of
Agriculture, Wildlife Services, National
Wildlife Research Center, and Colorado
Parks and Wildlife.
LITERATURE CITED
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Submitted for publication 22 April 2014.
Accepted 3 July 2014.
268 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 1, JANUARY 2015


Anticoagulant Rodenticide Exposure and Toxicosis in Coyotes (\u3ci\u3eCanis
latrans\u3c/i\u3e) in the Denver Metropolitan Area

DigitalCommons@University of Nebraska

University of Nebraska - LincolnDigitalCommons@University of Nebraska - LincolnUSDA National Wildlife Research Center - StaffPublicationsU.S. Department of Agriculture: Animal and PlantHealth Inspection Service2015Anticoagulant Rodenticide Exposure and Toxicosisin Coyotes (Canis latrans) in the DenverMetropolitan AreaSharon A. PoesselUtah State University, sharpoes@gmail.comStewart W. BreckUSDA/APHIS/WS National Wildlife Research Center, stewart.w.breck@aphis.usda.govKaren A. FoxColorado Parks and WildlifeEric M. GeseUtah State University, eric.gese@usu.eduFollow this and additional works at: https://digitalcommons.unl.edu/icwdm_usdanwrcPart of the Life Sciences CommonsThis Article is brought to you for free and open access by the U.S. Department of Agriculture: Animal and Plant Health Inspection Service atDigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in USDA National Wildlife Research Center - Staff Publicationsby an authorized administrator of DigitalCommons@University of Nebraska - Lincoln.Poessel, Sharon A.; Breck, Stewart W.; Fox, Karen A.; and Gese, Eric M., "Anticoagulant Rodenticide Exposure and Toxicosis inCoyotes (Canis latrans) in the Denver Metropolitan Area" (2015). USDA National Wildlife Research Center - Staff Publications. 1621.https://digitalcommons.unl.edu/icwdm_usdanwrc/1621DOI: 10.7589/2014-04-116 Journal of Wildlife Diseases, 51(1), 2015, pp. 265–268# Wildlife Disease Association 2015Anticoagulant Rodenticide Exposure and Toxicosis in Coyotes (Canislatrans) in the Denver Metropolitan AreaSharon A. Poessel,1,5 Stewart W. Breck,2 Karen A. Fox,3 and Eric M. Gese4 1Department of WildlandResources, Utah State University, 5230 Old Main Hill, Logan, Utah 84322, USA; 2US Department of Agriculture,Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, Colorado 80521, USA;3Colorado Parks and Wildlife, Wildlife Health Research Center, 317 W Prospect Road, Fort Collins, Colorado80525, USA; 4US Department of Agriculture, Wildlife Services, National Wildlife Research Center, Department ofWildland Resources, Utah State University, 5230 Old Main Hill, Logan, Utah 84322, USA; 5Correspondingauthor (email: sharpoes@gmail.com)ABSTRACT: Anticoagulant rodenticides arewidely used in urban areas to control rodentpests and are responsible for secondary poi-soning in many nontarget wildlife species. Wetested the livers of five coyotes (Canis latrans)in the Denver Metropolitan Area, Colorado,US, for anticoagulant rodenticides. All fivelivers were positive for brodifacoum, withvalues ranging from 95 ppb to 320 ppb, andone liver was positive for bromadiolone, with avalue of 885 ppb. Both of these rodenticides aresecond-generation anticoagulants, which aremore potent and more likely to cause secondarypoisoning than first-generation anticoagulantsdue to their accumulation and persistence inthe liver. We concluded that exposure to theserodenticides may have caused the death of atleast two of the five coyotes, and urban coyotesin our study area are commonly exposed torodenticides.Key words: Brodifacoum, bromadiolone,poison, second-generation, toxicant, urban.Anticoagulant rodenticides are usedextensively throughout urban areas tocontrol rodent populations (Hosea 2000;Watt et al. 2005). These compounds act byinterrupting the normal synthesis of clot-ting factors in the liver once bleedingcommences, resulting in fatal hemorrhag-ing (Eason and Spurr 1995; Eason et al.2002). Second-generation anticoagulants(e.g., brodifacoum and bromadiolone) aremore potent than first-generation antico-agulants (e.g., warfarin and chlorophaci-none) because they can effectively poisona rodent after only a single dose (Easonand Spurr 1995; Berny et al. 2006).Second-generation compounds also haveslower elimination times from the liver(Eason and Spurr 1995; Erickson andUrban 2004). This persistence in the livercan lead to secondary poisoning of non-target wildlife (Stone et al. 1999; Hosea2000; Elliott et al. 2014), including coyotes(Canis latrans) in urban areas (Hosea2000; Riley et al. 2003; Gehrt and Riley2010). We report finding anticoagulantrodenticides in urban coyotes residing inthe Denver Metropolitan Area (DMA) ofColorado, US.We captured 32 coyotes in the DMAusing padded leg-hold traps and snaresand fitted them with global positioningsystem radio collars from April 2012 toMay 2013 as part of an ecological study ofurban coyotes. Research protocols wereapproved by the National Wildlife Re-search Center, Institutional Animal Careand Use Committee (QA-1972). We mon-itored study animals with radio telemetryfrom April 2012 to June 2014. Collarswere equipped with mortality sensors thatalerted us when a coyote died. Thirteencollared coyotes died during the study.When cause of death was unknown, thecoyote was necropsied at the ColoradoDivision of Parks and Wildlife, WildlifeHealth Laboratory (Fort Collins, Colora-do, USA). Liver samples were submittedto the Texas A&M Veterinary MedicalDiagnostic Laboratory (College Station,Texas, USA) to be screened for anticoag-ulant rodenticides using high-performanceliquid chromatography. Brodifacoum, bro-madiolone, chlorophacinone, difenacoum,difethialone, diphacinone, and warfarinwere included in the screening. We begantesting liver samples from deceased ani-mals only after a coyote was found deadwith sarcoptic mange because of therelationship between mange and rodenti-265cide poisoning discovered in bobcats (Lynxrufus) and mountain lions (Puma concolor)by Riley et al. (2007), Uzal et al. (2007), andSerieys et al. (2013). Thereafter, all nec-ropsied coyotes were tested except for twocoyotes that were too decomposed toobtain a valid liver sample. Hence, we onlytested five coyote livers for rodenticidetoxicosis. All five were positive for brodifa-coum, with values ranging from 95 ppb to320 ppb (Table 1). One coyote (the animalwith the highest level of brodifacoum) alsowas positive for bromadiolone, with a valueof 885 ppb (Table 1). No other compoundswere found in the five liver samples.Based on necropsy results, we conclud-ed anticoagulant rodenticides contributedto the death of at least two of the fivecoyotes tested. The first case was ajuvenile male (24M) found dead in openspace, with no obvious external injuries orother signs of trauma. Upon necropsy, wefound free blood in the abdominal cavity.A puncture wound was present on the leftside of the body overlying the spleen butnot penetrating the abdominal wall. Thespleen was fractured and surrounded byclotted blood. We found no radiographicevidence of gunshot and no evidence ofbite wounds. The interpretation for causeof death was acute severe hemorrhage,disproportionate to the amount of traumaobserved. This coyote’s liver was positivefor brodifacoum (176 ppb; Table 1).The second case was a juvenile malecoyote (21M) found dead on a two-laneroad, with minor evidence of skin tearingover the ventral neck and chest. Necropsyfindings indicated additional moderatetearing of the muscle in the regionoverlying the thoracic inlet, althoughinjuries did not penetrate the chest cavity.The chest was filled with blood. Theinterpretation for cause of death wassevere acute hemorrhage, disproportion-ate to the mild to moderate traumareceived from being hit by a vehicle. Wesuspected rodenticide toxicosis, and theliver was positive for brodifacoum andbromadiolone (Table 1).In two additional cases, we foundhemorrhage into body cavities with severelesions to explain the hemorrhage, but alsoevidence of rodenticide exposure. Anadult male coyote (01M) had severelesions of sarcoptic mange, a gunshotthrough the chest from a pellet rifle, andfree blood in the chest cavity. The liverwas positive for brodifacoum (150 ppb;Table 1). A juvenile male coyote (17M)had severe crushing lesions to the headand body from being run over by a vehicleand free blood in the chest and abdomen.The liver was positive for brodifacoum(95 ppb; Table 1). One additional coyote(uncollared male) that we captured for ourstudy was euthanized due to self-inflictedtrap-related injuries, but the liver also waspositive for brodifacoum (95 ppb; Ta-ble 1). Causes of death for nine collaredcoyotes that were not tested for rodenti-cide toxicosis included vehicle collision(five coyotes), gunshot (one coyote), con-flict resolution (one coyote removed fromDenver International Airport), and unde-termined (two coyotes).Our findings suggest anticoagulant ro-denticides likely contributed to at leastTABLE 1. Values of anticoagulant rodenticides in coyote livers in the Denver Metropolitan Area, Colorado,USA, 2012–13.Coyote ID Date Brodifacoum (ppb) Bromadiolone (ppb)a01M January 2013 150 N/A17M February 2013 95 N/A24M March 2013 176 N/A21M April 2013 320 885Uncollared April 2013 95 N/Aa N/A indicates the compound was not found in the coyote liver.266 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 1, JANUARY 2015two of the five mortalities, triggered bymild to moderate trauma resulting in fatalinternal hemorrhaging. The detection ofanticoagulant rodenticides in coyotes inthe DMA indicates exposure to thesepoisons, either directly or secondarily.Because coyotes are omnivores, they couldhave ingested poisoned rodent bait (Hosea2000). However, Elliot et al. (2014)determined that targeted rodents aremore likely to provide the exposurepathway of anticoagulant rodenticides tosecondary consumers. Small rodents aregenerally an important food source andthe dominant animal prey for coyotes inurban areas (Morey et al. 2007; Lukasikand Alexander 2012), resulting in a highprobability that repeated consumption ofpoisoned rodents leads to rodenticidetoxicosis in urban coyotes.The residue values of brodifacoum inour study coyotes were generally lowerthan those found in other coyote studies.The acute oral LD50 value of brodifacoumin dogs ranges from 250 ppb to 1,000 ppb(Stone et al. 1999). In a study conductednear Boston, Massachusetts, US, Way etal. (2006) found brodifacoum values of733 ppb and 542 ppb in two coyotes thatwere presumably directly poisoned. Hosea(2000) identified values up to 500 ppb ofbrodifacoum in coyotes in California.Erickson and Urban (2004) describedcoyotes with values of brodifacoum up to930 ppb. In our study, the two coyotes forwhich we interpreted exaggerated hemor-rhage were also the two cases with thehighest values of brodifacoum in theirlivers, although these values were stilllower than the highest values found inother studies. The lower values are notsurprising, however, considering bothcases had readily observable mild tomoderate trauma to initiate excessivebleeding. Nevertheless, our results indi-cated that poisoning at a lower level maybe enough to contribute to fatal hemor-rhaging in these carnivores.Only one coyote was positive for bro-madiolone. The acute oral LD50 value ofbromadiolone in dogs ranges from11,000 ppb to 15,000 ppb (Stone et al.1999); the value in our study animal was885 ppb. Both Erickson and Urban (2004)and Hosea (2000) reported values ofbromadiolone in coyotes up to only460 ppb. Our study coyote also waspositive for brodifacoum, and other inves-tigators also have identified coyotes withboth of these rodenticides in liver tissue(Hosea 2000; Erickson and Urban 2004).Overall, brodifacoum appears to be moreprevalent and of higher concern in theDMA than other rodenticides, althoughour results indicated that multiple toxi-cants may be in use throughout our studyarea.In addition to the five coyotes in theDMA, we also tested the liver of anothercoyote carcass found in rural Colorado(Huerfano County) showing signs ofhemorrhage. The most likely cause ofdeath was trauma, but a definitive inter-pretation was limited by advanced decom-position. We found no evidence of anyrodenticides in the liver, indicating thatrodenticide toxicosis may not always occurin coyotes. To further understand theeffects of anticoagulant rodenticides oncoyotes, future studies should comparethe values of these poisons in coyote liversacross urban and rural systems.Our findings are consistent with thoseof other studies that have determinedanticoagulant rodenticides are contribut-ing to mortality in urban wildlife (Hosea2000; Riley et al. 2007). The exposure ofall five tested coyotes to rodenticides,especially brodifacoum, indicates theubiquity of these toxicants in the urbanlandscape and their ability to reach higherlevels in the food chain (Riley et al. 2007).One coyote liver contained more than onerodenticide (both brodifacoum and bro-madiolone), and multiple compounds havebeen found in wildlife species in otherstudies (Stone et al. 1999; Hosea 2000;Erickson and Urban 2004). The effects ofexposure to multiple anticoagulant roden-ticides in urban wildlife species should beSHORT COMMUNICATIONS 267a focus of future research to increase ourunderstanding of these toxicants and theirpopulation effects on urban carnivores.We thank J. Brinker, J. Kougher, S.Koyle, D. Lewis, and F. Quarterone forassistance with trapping and handlingcoyotes. We also thank Texas A&MVeterinary Medical Diagnostic Laboratoryfor testing liver samples. Funding wasprovided by the US Department ofAgriculture, Wildlife Services, NationalWildlife Research Center, and ColoradoParks and Wildlife.LITERATURE CITEDBerny PJ, de Oliveira LA, Videmann B, Rossi S.2006. Assessment of ruminal degradation, oralbioavailability, and toxic effects of anticoagulantrodenticides in sheep. Am J Vet Res 67:363–371.Eason CT, Murphy EC, Wright GRG, Spurr EB.2002. Assessment of risks of brodifacoum to non-target birds and mammals in New Zealand.Ecotoxicol 11:35–48.Eason CT, Spurr EB. 1995. Review of the toxicityand impacts of brodifacoum on non-targetwildlife in New Zealand. NZ J Zool 22:371–379.Elliott JE, Hindmarch S, Albert CA, Emery J, MineauP, Maisonneuve F. 2014. Exposure pathways ofanticoagulant rodenticides to nontarget wildlife.Environ Monit Assess 186:895–906.Erickson W, Urban D. 2004. Potential risks of ninerodenticides to birds and nontarget mammals: Acomparative approach. Environmental Protec-tion Agency Office of Prevention, Pesticides andToxic Substances, Washington, DC, 225 pp.Gehrt SD, Riley SPD. 2010. Coyotes (Canis latrans).In: Urban carnivores: Ecology, conflict, andconservation, Gehrt SD, Riley SPD, Cypher B,editors. Johns Hopkins University Press, Balti-more, Maryland, pp. 78–95.Hosea RC. 2000. Exposure of non-target wildlifeto anticoagulant rodenticides in California. In:Proceedings of the Nineteenth Vertebrate PestConference, San Diego, California, 6–9 March;Salmon TP, Crabb AC, editors. University ofCalifornia, Davis, pp. 236–244.Lukasik VM, Alexander SM. 2012. Spatial andtemporal variation of coyote (Canis latrans) dietin Calgary, Alberta. Cities Environ 4:Article 8.Morey PS, Gese EM, Gehrt S. 2007. Spatial andtemporal variation in the diet of coyotes inthe Chicago metropolitan area. Am Midl Nat158:147–161.Riley SPD, Bromley C, Poppenga RH, Uzal FA,Whited L, Sauvajot RM. 2007. Anticoagulantexposure and notoedric mange in bobcats andmountain lions in urban southern California.J Wildl Manag 71:1874–1884.Riley SPD, Sauvajot RM, Fuller TK, York EC,Kamradt DA, Bromley C, Wayne RK. 2003.Effects of urbanization and habitat fragmenta-tion on bobcats and coyotes in southernCalifornia. Conserv Biol 17:566–576.Serieys LEK, Foley J, Owens S, Woods L, BoydstonEE, Lyren LM, Poppenga RH, Clifford DL,Stephenson N, Rudd J, Riley SPD. 2013. Serumchemistry, hematologic, and post-mortem find-ings in free-ranging bobcats (Lynx rufus) withnotoedric mange. J Parasitol 99:989–996.Stone WB, Okoniewski JC, Stedelin JR. 1999.Poisoning of wildlife with anticoagulant roden-ticides in New York. J Wildl Dis 35:187–193.Uzal FA, Houston RS, Riley SPD, Poppenga R,Odani J, Boyce W. 2007. Notoedric mange intwo free-ranging mountain lions (Puma conco-lor). J Wildl Dis 43:274–278.Watt BE, Proudfoot AT, Bradberry SM, Vale JA.2005. Anticoagulant rodenticides. Toxicol Rev24:259–269.Way JG, Cifuni SM, Eatough DL, Strauss EG. 2006.Rat poison kills a pack of eastern coyotes, Canislatrans, in an urban area. Can Field Nat120:478–480.Submitted for publication 22 April 2014.Accepted 3 July 2014.268 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 1, JANUARY 2015

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Anticoagulant Rodenticide Exposure and Toxicosis in Coyotes (\u3ci\u3eCanis latrans\u3c/i\u3e) in the Denver Metropolitan Area

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