JANUARY 2023 VOLUME 32, NO.1

A PUBLICATION BY THE UNIVERSITY OF KENTUCKY DEPARTMENT OF VETERINARY SCIENCE, MAXWELL H. GLUCK EQUINE RESEARCH CENTER
FUNDED BY:

EQUUS / STANDARDBRED STATION, INC.
M&J INSURANCEIN T HIS IS S U E
INTERNATIONAL
Fourth Quarter 2022.......3
Botulism in Horses ......4,5
NATIONAL
Toxicologic causes ofabortion and stillbirthin horses inNorth America.............6,7
KENTUCKY
Cervical pole necrosis of
the equine placenta.....8,9

TH A N K YO U
SPON SO RS

C O MME N TARY
Investigating cases of toxicant exposure
and why there is no single ‘tox screen’
In cases of sudden death, abortion or neurologic
diseases, a toxicant is often included in the listof possible causes of disease. If toxicants are
suspected, a complete history and potential list of
possible toxicants will help guide testing. No true‘comprehensive’ toxicant screen exists in human orveterinary toxicology. Even in human toxicology
laboratories, “routine” or “comprehensive”
toxicology screens are generally limited toethanol (alcohol) and therapeutic and illicit
drugs and medications, which vary according toregional prevalence. Horses have a wider range ofpotential for exposure to toxicants, which varies
based on their environment and management
practices. When possible, a veterinary
toxicologist should be consulted prior to sample
submission to provide input on likely toxicants;
advise on sample collection and handling; andassist with selection of appropriate analyses.
Clinical signs, physical examination findings
and results of routine laboratory analyses (e.g.,CBC, serum chemistry, urinalysis) in toxicoses
are often nonspecific and indistinguishable from
non-toxicologic causes of disease. A thoroughand detailed history is therefore one of the mostimportant tools in identifying potential toxicant
exposures. For example, a history of multiple
sick or dead animals with similar signs over ashort period of time is one of the most common
indications of potential toxicant involvement.
Important details include recently opened bagsof feed or new bales of hay; new medications or
supplements; new water sources or interrupted
access to water; recent movement to a new barnor pasture;

recent weather changes or severe weather events;
recent nearby landscaping, tree trimming,or gardening; recent nearby application ofpesticides, fertilizers or other agriculturalchemicals; and any other changes on or near
the farm (e.g., construction, drilling or mining
activity). Once potential toxicants are identified,analytical confirmation can be considered.
Analytical techniques exist for some, but not all,toxicants. A veterinary toxicologist can direct
testing to ensure the correct sample is chosen forthe most appropriate test. In many cases, analysis
can confirm exposure but data on relevant bloodor tissue concentrations is lacking. Therefore, thecombination of clinical signs and confirmationof exposure will lead to a presumed diagnosis of
intoxication. Importantly, most analyses available
at veterinary diagnostic laboratories require an
idea of what class of toxicant is suspected. For
example, a request to test for “rodenticides” or“rat poison” alone is insufficient to determine
what analyses are appropriate. Several
laboratories have a method that can measure
warfarin, diphacinone, brodifacoum and otheranticoagulant rodenticides.
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Equine Disease Quarterly.
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JANUARY 2023 | 1

C O M ME N TARY
Analyses for other rodenticides, including theneurotoxicants bromethalin and strychnine,
the vitamin D analog cholecalciferol and themetallophosphide zinc phosphide, however,each require entirely different tissues, sample
preparation steps, reagents and instrument
settings or entire instruments. The history,
clinical signs and laboratory analyses can help
indicate which toxicants are likely and should betested for. Analytical methods are not available
for every potential toxicant and so confirmationof exposure is not possible in every case.
In addition to choosing relevant analyses, sample selection and handling is key to successful
toxicological testing. Some toxicants are distributed widely throughout the body and can be detected in multiple tissues. Others concentrate ina particular tissue and may be undetectable inothers. Additionally, other toxicants are present
in such small amounts in tissues that suspectedsource material (such as feed) is the best option
for testing. For some toxicants, container selection is extremely important. For example, a water sample collected in a used sports drink bottle that contained electrolytes is not suitable forsodium quantitation. However well the bottle isrinsed, the previous substance will contaminate
the collected water. Several resources are available to guide sample collection, handling, andshipping to facilitate accurate analytical results.

EQUINE DISEASEQUARTERLYEDITORS
Rebecca Ruby
Lutz Goehring
Allen Page
STAFF
Holly Wiemers
Anita Hatchet
Hendri Smeenk

One example you find here Representative
sampling is crucial to obtaining accurate results,
particularly in contaminated feeds. Many toxicants in feed are not uniformly present throughout a bag or batch, but in localized “hot spots.”
Multiple smaller samples should be collectedfrom different areas in the bag or bin, ideally witha grain probe. If a probe is not available, ½ to
1 cup samples should be obtained from various
depths and locations within a container. If hay
or alfalfa is implicated, bales or bags should be
opened and examined carefully for weeds, leaves,
flowers, berries, seeds or other unusual or unfamiliar plant material moldy, dusty or wet areas;
blister beetles and other insects or insect parts;
animal carcasses or fur; plastic,metal or other foreign material; and anything else unusual.
With square bales or bagged forage, it is not uncommon for a contaminant to be present in only a
few bales or bags, or even within a few flakes or
cubes, while the rest is normal. While large roundbales are more difficult to handle, they should still
be examined as closely as possible. Areas of obvious contamination can be submitted for testing,or core samples can be obtained if bales appear
normal.

2 | EQUINE DISEASE QUARTERLY

Providing the veterinary toxicologist with complete case information about a potential toxicosis, including the animal’s history, clinical signs,
physical examination findings, routine laboratory
results, and any other known information, especially prior to sample submission, can facilitate
accurate diagnosis and prevent frustration due toinappropriate sample collection or test requests.
In the U.S., suspected problems with animal
feeds, treats, medications or supplements should
be reported to the Food and Drug Administration’sCenter for Veterinary Medicine. FDA CVM regulates these products and investigates problems including adverse effects, lack of efficacy, suspected contamination and other issues. Because there
is no central mandatory reporting mechanism fortoxic exposures in veterinary species, FDA CVM
relies on voluntary reporting of problems. Anyone
associated with a case, including veterinarians,
technicians, owners, trainers and farm managers, can submit a report through an online portal
here or by phone to an FDA Consumer Complaint
Coordinator. A list of complaint coordinators bystate can be found here Additional information
on reporting problems, including what information to have, is here As part of a consumer complaint investigation, FDA CVM can help facilitate
testing of suspect products through its networkof accredited partner laboratories, the Veterinary
Laboratory Investigation and Response Network.

Dr. Megan Romano
University of Kentucky Veterinary
Diagnostic Laboratory
megan.romano@uky.edu

IN TERN AT ION A L
2022 Third & Fourth Quarters
International report on equine infectious diseases.
Urgent: A multiple-state botulism outbreakamong horses was reported in the United States ofAmerica with affected herds in Louisiana, Texas,
Colorado and New Mexico. The source of the toxin(see also article on equine botulism in this EDQ
issue) has been traced to alfalfa cubes produced by
Colorado-based Manzanola Feeds and labeled as‘Top of the Rockies’ Alfalfa Cubes. The productconsists of 1-inch cubes, packaged in 50 lb/22.7
kg bags and labeled with the following codes:
111222, 111322, 111422, 111522 and 111622.
The following report was composed withinformation provided by the University of
Kentucky Veterinary Diagnostic Laboratory
and Equine Diagnostic Solutions, Inc.—bothin Lexington, Kentucky; IDEXX Laboratories,
Germany; the International Thoroughbred
Breeders Federation; the International Collating
Centre in Newmarket, United Kingdom; and by
the American Association of Equine Practitioners’
Equine Disease Communication Center. This report
is retrospective and does not claim to be complete.
However, it provides an indication of heightened
activity of relevant contagious or environmentlinked diseases among equids. To further improve
this data, it is encouraged to report laboratoryconfirmed diseases of Equidae to the ICC.
Strangles is still the most consistently reported
disease from various regions across North America
and Europe, including the British Isles. Reporting
included laboratory confirmed farm outbreaks aswell as samples submitted to various laboratories.
Few outbreaks of equine influenza virus
were reported from regions of North America
and from various parts of Europe during thethird quarter. Outbreak numbers increased
significantly during the fourth quartercompared to third quarter for both areas.
Equine herpes virus (EHV) -4 or -1 respiratory
disease was reported infrequently in the USA
and more often from operations in the UK,
Ireland and continental Europe for both quarters.
During the third quarter, one EHV abortion wasreported from Japan and three from Argentina.
For the latter country, one would expect apregnancy in the third trimester, which is themost vulnerable period for EHV-1 associatedabortion. During the fourth quarter, threeabortions were reported in Kentucky (USA) and
one in continental Europe. Equid herpesvirusassociated myeloencephalopathy (EHM) follows
a seasonal pattern with the majority of outbreaks
associated with the cooler times of the year

(first, second and fourth quarters in the Northern
Hemisphere). Hence, only a few (four single case)outbreaks were reported from North America
and one from the UK during the third quarter.
In addition to seasonality, EHM outbreaks are
extremely rare in the Southern Hemisphere.
It is therefore noteworthy to report a single caseof EHM at the San Isidro racecourse in Buenos
Aires, Argentina. EHM outbreak frequencieschanged as expected for the fourth quarter with
10 EHM outbreaks reported in North America,
three outbreaks in continental Europe and one
outbreak in the UK. Within Kentucky, a single
case of EHM was detected in a barn at Churchill
Downs racecourse in Louisville. Several otherhorses from the same barn were found shedding
EHV-1; however, no further horse developed
EHM. Noteworthy, during the fourth quarter,
information of a (large scale) EHV-1 outbreakwith EHM and abortions involving multiple herds
was received from the Punjab region of India.
However, this information is awaiting official
reporting as diagnostic laboratory results have
not yet been shared. A little more than 20 equine
infectious anemia (EIA) virus positive animals(with rarely two animals simultaneously on afarm) were identified in North America. Cases
were evenly distributed over the third and fourth
quarters. There were also reports of EIA from
Italy (three reports) and Hungary (one report).
Increased vector activity during the third quarter
was likely the cause for the relatively high casenumbers of alphavirus encephalitis (exclusively
Eastern equine encephalitis) reported in the USA
and Mexico (one case). Flavivirus, mainly West
Nile virus (WNV), activity was increased for
distinct areas of Europe and Northern Africa.
Countries that border the Mediterranean basin
reported approximately 35 cases; Algeria, Greece
and Tunisia each reported a single case of WNV.
Most Mediterranean basin cases were reported
from Italy. Germany reported nine confirmed
cases from its central and nort heastern states.
Miscellaneous: Contagious equine metritis(CEM): Mostly single cases on 14 premises inGermany and France tested positive for Taylorellaequigenitalis, the causative agent of CEM.
Additionally, a single case of African horse
sickness was reported from Sub-Saharan Africa (Nigeria); a case of rabies was reported in the USA; and a case of Hendra virus infection was reported from Australia.

Material published in the
Quarterly is not subject
to copyright. Permissionis therefore granted toreproduce articles, althoughacknowledgment of the source
and author is requested.
Maxwell H. Gluck
Equine Research Center
Lexington, Kentucky USA,40546-0099
Telephone (859) 257-4757
Fax (859) 257-8542
gluck.ca.uky.edu

Lutz Goehring
University of Kentucky
Gluck Equine Research Centerl.goehring@uky.edu
JANUARY 2023 | 3

I N T E R N AT I ONAL
Botulism in Horses
Botulism is a neuromuscular disease characterized by flaccid paralysis that is causedby neurotoxins produced by the bacterium
Clostridium botulinum. Horses are oneof the most susceptible species, with bothindividual cases and group outbreaks reported.
C. botulinum is a Gram-positive, spore forming,
anaerobic bacterium. Spores are found in soil
and aquatic sediments throughout most of theworld, but the distribution of types vary based on
environmental factors. Eight types of C. botulinum
neurotoxin exist and are designated A, B, C1, C2,
D, E, F and G. While all cause similar disease,
there is variation in geographic distribution,
potency and antigenicity. In North America,
botulism in horses is most often caused by type
B toxin and less often by toxin types A and C1.
Three forms of equine botulism are recognized.
Intraintestinal toxicoinfectious botulism (shaker
foal syndrome), develops in rapidly growing foals
1-2 months of age. This form develops following
ingestion and overgrowth of C. botulinum in thegastrointestinal tract, typically caused by type B.
Young foals have a less developed gastrointestinal
microflora, which can permit spore activation,
vegetative growth and subsequent neurotoxin
production. Proliferation of C. botulinum type
B in gastric ulcers, foci of hepatic necrosis(diseased livers), navel or lung abscesses andskin and muscle wounds have also been reported.
Forage poisoning, the most common form of
intoxication in adult horses, follows ingestionof preformed neurotoxin in poorly preserved
hay, haylage, silage or other feedstuffs. Silage
and large, round, hay bales are most frequently
implicated in botulism caused by neurotoxins type
A and B. In horses, intoxication is most commonly
associated with forage and almost never withcommercial grain. Forage with a pH >4.5 is most
associated with the growth of C. botulinum andtoxin production. Type C botulism is associatedwith ingestion of feed or water contaminatedwith an infected rodent or small animal carcass.
Wound botulism, a less common form, results
following infection of the umbilicus or awound, such as a castration site. Regardless oftype, C. botulinum neurotoxin acts primarily
at the neuromuscular junction. The toxins
are internalized at the nerve ending andthrough a series of steps inhibit the release of
neurotransmitters needed for muscle contraction,
which results in flaccid paralysis. Once bound,toxin neutralization is not possible and normal
neurotransmitter release from the affected neurons

4 | EQUINE DISEASE QUARTERLY

will only return once new motor end plates havebeen generated, which may take 10-14 days.
Clinically, symmetrical flaccid paralysis is aconsistent finding with the onset and rate ofprogression dependent on the amount of toxinthat is absorbed. Initial clinical signs includedifficulty eating with apparent excess salivation,
weak eyelid tone, weak tail tone and exercise
intolerance. Affected animals also spend increased
amounts of time resting due to generalizedmuscle weakness, which is associated withtremors, carpal buckling and ataxia. Additionally,pharyngeal and tongue paralysis predisposes
the horse to aspiration pneumonia and quidding(dropping) their food. Paralysis of the diaphragmand intercostal muscles can also result in an
increased respiratory rate and decreased chest wall
expansion. Severely affected animals ultimately
die from respiratory paralysis and cardiac failure.
Botulism should be suspected in animals withflaccid paralysis displaying the aforementioned
clinical signs. Botulinum toxin does not affectthe spinal cord or brain but does affect the cranial
nerves; thus, symmetrical cranial nerve deficits
in an animal with normal mentation can help
differentiate botulism from other disorders. A
mouse bioassay can be used to obtain a definitive
diagnosis by inoculating serum or gastrointestinal
contents from an affected horse into a mouse.
However, horses are extremely sensitive to thetoxin and false negative test results are common;the mouse bioassay identifies botulism fromfecal samples in only about 30% of adult horses
with clinical disease. Detection of antibodies tobotulinum toxin in a recovering unvaccinated horsealso supports a diagnosis of botulism. However,antibody detection has limited treatment impact
due to the time required for antibodies to develop
Demonstration of spores in the intestine is notdiagnostic, as they can be ingested and detected
as contaminants. A quantitative real-time PCR(qPCR) for detection of the neurotoxin genesof C. botulinum types A, B and C, exists but is
not currently available for commercial use. The
combination of false negative tests and lack of
PCR testing means that a diagnosis of equinebotulism is typically based on clinical signs,
known exposure to a feed or wound source and/or
response to treatment. Immediate treatment witha polyvalent antitoxin prevents further binding of
the toxin to presynaptic membranes. However,antitoxin cannot reactivate neuromuscularjunctions that have already been affected. Thus,
antitoxin administration may have little effectin severely affected animals. Generally, only
one dose of antitoxin is needed and provides
passive protection for up to two months.

I N T E R N AT I ONAL

Antibiotics should be administered if
toxicoinfectious botulism is suspected or if
there are secondary lesions such as aspiration
pneumonia or decubital ulcers. Antibiotics thatcan cause neuromuscular blockade and possibly
exacerbate clinical signs, such as aminoglycosides,
should be avoided and neurostimulants, such as
neostigmine, should not be used. Supportive care,including the provision of a deep bed and a quiet
environment, is essential. Frequent turning ofrecumbent animals, nasogastric feeding and fluid
support for animals with pharyngeal and lingual
paralysis, frequent catheterization of the urinary
bladder, the application of ophthalmic ointments
and ventilatory support may be required.
A survival rate of 88% has been reported in foals
with toxicoinfectious botulism that received intensive nursing care (including mechanical ventilation and botulism antitoxin). However, this typeof treatment is not available in all areas and is quite
expensive. Without aggressive supportive care, themortality rate is high, with death usually occurring
one to three days after the onset of clinical signs.
The prognosis is variable in adult horses that haveingested preformed toxin (forage poisoning),
depending on the amount of toxin absorbed andthe severity of clinical signs. Mildly affectedanimals may recover with minimal treatment
while severely affected animals that become
recumbent have a poor prognosis. The mortality
rate has been reported to be as high as 90% inrecumbent adult horses, with death occurring
within hours of the appearance of signs.
In animals that survive, complete recovery

is most common, although development of fullmuscular strength can take weeks to months.
Persistent tongue weakness, not affecting theability to eat, has been reported following
recovery. A type B toxoid vaccine is available
and should be used in areas in which type B
botulism is common; vaccination is particularly
important in areas where neonatal botulism
occurs. Importantly, the type B vaccine only
provides protection against type B toxin.
There is no cross protection against type C toxin
and there is not a type C toxoid vaccine licensed
for use in North America. If botulism is suspected
to have been caused by ingestion of preformed
toxin in feed, an alternate feed source should
be provided while the origin of intoxication isinvestigated. Potentially contaminated feeds
should be either safely disposed of or sent for
confirmatory testing. Silage, haylage and otherfermented feeds should be fed with caution tohorses because of the risk of botulism. Regulations
requiring the reporting of botulism vary by stateand country (e.g., botulism is required to bereported to the Kentucky State Veterinarian). If
you suspect an animal has ingested botulism from acontaminated food source, the U.S. Food and Drug
Administration’s Center for Veterinary Medicine
or other regulatory body should be contacted.
Nathan M. Slovis DVM, Dipl. ACVIM,
CHTHagyard Equine Medical
InstituteLexington, KY 40511
nslovis@hagyard.com

JANUARY 2023 | 5

NATIONAL
Toxicologic causes of abortion andstillbirth in horses in North America
Abortion and stillbirth due to toxicant exposureis uncommon in horses in North America,
although incidence in other geographic regions
can vary. Toxicant-induced abortions can be due
to a compound’s effects on the placenta, on thefetus, on the mare or any combination thereof.
Any toxicant that produces significant clinicaldisease and stress in a pregnant mare could
potentially lead to abortion as a sequela. Veryfew toxicants cause primarily or exclusively
abortions with few or no signs observed in
the mare. In North America, two of the bestcharacterized toxicologic causes of abortion inhorses are ergopeptine alkaloids and swainsonine.
Ergopeptine alkaloids are most familiar to those in
the Southeastern United States in association withtall fescue grass. Certain strains of tall fescue (e.g.,
Kentucky-31) are infected with the ergopeptineproducing fungal endophyte Neotyphodium
coenophialum. Endophytes live within theplant, between its cells and are not visible to thenaked eye. N. coenophialum primarily produces
ergovaline and its epimer ergovalinine; otherergopeptine alkaloids are produced in muchsmaller quantities. N. coenophialum can also infectand produce similar ergopeptine alkaloid profiles
within perennial ryegrass (Lolium perenne).
Ergot fungus, Claviceps purpurea, infects
the seed heads of a wide variety of grasses
and small-grain forages. Most grasses can beaffected, as can oats, wheat, barley and manyother plants. “Ergotized” seed heads developsclerotia – clusters of dark brown or black
cylindrical fungal seeds or grains. Ergot fungus
produces several different ergopeptine alkaloids,
including ergocryptine, ergocornine, ergocristineand ergosine, often known collectively as ergot
alkaloids. Ergopeptine alkaloids can exert awide variety of effects in animals that ingest
them, depending on animal species, reproductive
status, dosage and time of year. Reproductive
effects can include increased rates of embryonic
death, prolonged luteal function and failureof normal udder development and lactation.
The most severe and dramatic effects occur in lateterm pregnant mares – abortion, premature placental
separation (“red bag”), overmature/dysmaturefoals and potentially catastrophic dystocia thatcan result in death of the mare as well as the foal.
Ergopeptine alkaloids act via several different
mechanisms, some of which affect the fetus,
some the mare and others the placenta. Endocrine
disruption occurs in both the mare and the fetus.

6 | EQUINE DISEASE QUARTERLY

In the mare, the alkaloids bind to dopamine
receptors, causing a decrease in circulating prolactin.
In the fetus, adrenocorticotropic hormone (ACTH)
secretion is inhibited. Placental insufficiency
and edema result from vasoconstrictive
effects of the alkaloids. Placental fibrosis andmucoid degeneration of arteries can also result.
Swainsonine is also produced by fungal
endophytes. In North America, several species of
Astragalus and Oxytropis, known as locoweeds,
are the most significant hosts of swainsonineproducing endophytes. Locoweeds are foundprimarily in rangelands in the Western UnitedStates. Slafractonia leguminicola (Rhizoctonia
leguminicola), the fungus that causes “black
patch” disease of red clover and other legumes,
also produces swainsonine. In other geographicalregions, plants containing swainsonine include
Swainsona canescens, a legume native toAustralia; Turbina cordata and several Ipomoea
species in South America and Australia; I. carnea,
found throughout the tropics worldwide; andSida carpinifolia in Brazil. Swainsonine affects
cellular metabolism by inhibiting mannosidases,
causing
accumulationofincompletely
metabolized oligosaccharides and glycoproteins,
cytoplasmic
vacuolation
andeventuallyvacuolar degeneration in multiple organs.
Most animal species are affected, although horses
appear to be the most sensitive. Classic signs ofswainsonine toxicosis in horses include aberrant
behavior and other neurologic abnormalities,
however, in pregnant mares swainsonine cancause embryonic or fetal death and abortion.
Any disease process causing anemia and/or
methemoglobinemia in pregnant mares canresult in fetal hypoxia and death; potential toxic
agents include anticoagulant rodenticides andcompounds that cause oxidative red blood cell
damage. Brodifacoum toxicosis was reported tohave caused abortion in a pregnant Arabian mare.
Although the mare survived with hospitalization
and aggressive treatment, she aborted the fetus.
Red maple (Acer rubrum) toxicosis was suspected
to have caused abortions in Percheron mares,
but confirmatory testing was not performed.
The mares were critically ill and ultimately
died, but necropsy was not performed todefinitively determine cause of death or abortion.
Any disease process causing anemia and/or
methemoglobinemia in pregnant mares can resultin fetal hypoxia and death; potential toxic agentsinclude anticoagulantrodenticides and compounds
that cause oxidative red blood cell damage.
Brodifacoum toxicosis was reported to have

NATIONAL

caused abortion in a pregnant Arabian mare.
Although the mare survived with hospitalization
and aggressive treatment, she aborted the fetus.
Red maple (Acer rubrum) toxicosis was suspected
to have caused abortions in Percheron mares, but
confirmatory testing was not performed. The mares
were critically ill and ultimately died, but necropsy
was not performed to definitively determine causeof death or abortion. Other toxicants that cancause methemoglobinemia and hemolytic anemia
include red maple hybrids, silver maple and sugar
maple; Pistacia species; Allium species (e.g.,garlic, chives, and others); propylene glycol; andphenothiazines. Several therapeutic medications
can cause abortions, including prostaglandin(often used for the purpose), oxytocin andglucocorticoids. Finally, any toxicant that causes
significant systemic disease and stress to apregnant mare has the potential to induce abortion.
Examples include ionophores, cantharidin,
antibiotic-associated colitis, and many others.

Diagnosis of toxicologic causes of abortion relies
on a history of exposure to significant quantities
of a toxicant and ruling out other, more common,
causes of abortion. Confirmatory testing is rarely
possible due to a lack of analytical methods and lackof established clinically significant concentrationsof a toxicant. In other cases, the time elapsed
between exposure and abortion may preclude
detection of a toxicant in blood or tissues. In
cases of suspected toxicologic causes of abortion,
a complete necropsy including microscopic
evaluation of fetal and placental tissues shouldbe performed, and a thorough history including
any possible exposures should be provided to thepathologist to direct potential ancillary testing,including consultation with a toxicologist.
Dr. Megan Romano
University of Kentucky Veterinary Diagnostic
Laboratory
megan.romano@uky.edu

JANUARY 2023 | 7

KENTUCKY
Cervical pole necrosis of
the equine placenta
Cervical pole necrosis (CPN), also known asplacental necrosis or placental infarction, is apoorly understood disease of the allantochorion
and an infrequent cause of non-infectious abortion
in horses. The pathogenesis of this unique lesion
is not definitively known, but the necrosis(dead tissue) has been theorized to occur either
secondarily to placental detachment at the cervicalstar or by ischemic insult (lack of blood flow)
related to hemodynamic abnormalities associatedwith long umbilical cords and vascular thrombosis.
The University of Kentucky Veterinary Diagnostic
Laboratory database was searched for cases of
CPN to better characterize this distinctive entity.
Fifty-seven cases of CPN were diagnosed at
the UKVDL from 2013 to 2022 (figure 1).
Thoroughbreds were overrepresented (52 cases),
but cases were also identified in Standardbreds(two cases), a Warmblood (one case) and inunidentified breeds (two cases). Clinical histories
associated with the mares ranged from no signsof impending abortion or no history (33 cases),treated for placentitis (10 cases), premature udder
development (nine cases), vaginal discharge(seven cases), placental separation identified
by ultrasonography (two cases), a fluid filled
fetal abdomen identified by ultrasonography(one case) and hydrops amnion (one case).
CPN resulted in abortion (44 cases), prematurebirth with subsequent neonatal death or
euthanasia (seven cases), birth of a viable term
foal (three cases) and premature birth of a
weak viable foal (one case). Two cases, which
included only the placental membranes for
examination, didn’t note the foal’s outcome.
Gross necropsy findings, in all cases, consisted of awell demarcated, paper-thin region of tan to green
placental necrosis associated with the cervicalpole in close proximity to the cervical star (figure2). Necrotic regions were bordered by a red andraised border that was distinctly evident on the

8 | EQUINE DISEASE QUARTERLY

allantoic surface. In addition to the cervicalpole lesion, rare cases also exhibited similar
regions of necrosis in the gravid and non-gravid
allantochorionic horns. Size was not always
noted, but when recorded, the necrotic regions
ranged in size from 16 to 800 cm2. Umbilical cord
lengths averaged 89.4 cm (case study range 37160 cm; normal range 32-90 cm), and placental
weights averaged 6.2 kg (range 1.8-12.7 kg).
Fetuses were estimated to range from 180 daysof gestation to term (average= 272), averaged
82 cm (range 47-109) from crown to rump andweighed 25.6 kg (range 5.5-69.1 kg) on average.
Additional diagnoses with CPN included fetal
septicemia without significant inflammation(seven cases), bacterial placentitis (five cases),various fetal malformations (three cases),bacterial placentitis with fetal septicemia (onecase), fetal bacterial pneumonia (one case), in
utero meconium passage with aspiration (onecase), premature placental separation (one case),umbilical cord torsion (one case) and one combinedcase of leptospirosis and hydrops amnion.
Based on UKVDL data, cervical pole necrosis is
an idiopathic, non-infectious, placental disease
that can result in abortion, premature birth,delivery of a weak foal or delivery of a viable
foal. CPN routinely results in less than 2% of
submitted abortions to the UKVDL. Cases in thisretrospective study indicate that CPN occurs inboth male and female fetuses, most commonlyin mid to late gestation and in fetuses with bothnormal length and long umbilical cords. Cases of
CPN were occasionally associated with secondary
bacterial infections, which likely developed due
to bacterial invasion through the devitalized
allantochorion. Future studies are needed to better
understand this unique cause of equine abortion.
Dr. Alan Loynachan
Veterinary Diagnostic Laboratory
University of Kentucky, Lexington, Kentucky
alan.loynachan@uky.edu

KENTUCKY

Figure 1. Cases of cervical pole necrosis
diagnosed by the UKVDL by year (20132022).

Figure 2. Allantoic surface of theallantochorion. A locally extensive and welldemarcated region of the allantochorion istannish-green and necrotic. A red, raised line
(black arrow) separates the dead region of
the placenta from the pink viable tissue.

JANUARY 2023 | 9