Equine Disease Quarterly Newsletter

5

Equine Hepatotoxins, continued from page 4.

species, but the best way to prevent poisoning is
to monitor pastures and remove mushrooms.
Certain medications (e.g., phenylbutazone, flunixin, acetaminophen, salicylates, antifungals, andmany others) can cause liver damage, especially ifadministered in high doses, for prolonged periodsof time, or to animals with pre-existing conditions. Accurate dosing and careful consideration of
medication risks versus benefits can help minimize
chances of adverse effects.

Many other substances can cause liver damage
and may be more common in different geographic
areas. Consultation with a clinical veterinary
toxicologist should be considered when toxicosis
is suspected.
CONTACT:
Megan C. Romano, DVM, DABVT
megan.romano@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

Presorted Standard
US Postage Paid
Permit 51
Lexington KY

Department of Veterinary Science
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky 40546-0099
Address Service Requested

F U N D E D B Y U N D E R W R I T E R S AT L LOY D ' S , LO N D O N

JULY 2021
Volume 30, Number 3

Twenty Years’ Experience with West Nile Virus, 2001-2020

Until 1999, West Nile (WN) virus was unknown in the Western Hemisphere, muchless the USA. In August of that year, the virus
was identified in New York City and caused thedeaths of seven persons from viral encephalitis.
Coincidentally, the virus was also implicated in
the death of birds in New York’s Bronx Zoo andcrows in the precincts of the zoo.

513
102

Total = 765

Number of Cases

20

18
16

15

13

10

8

5

9
6 5

8

12
8

6

4
1

7
2 2

20
00
20
01
20
02
20
03
20
04
20
05
20
06
20
07
20
08
20
09
20
10
20
11
20
12
20
13
20
14
20
15
20
16
20
17
20
18
20
19
20
20

0

0

8

17

Year
Figure 1. Annual number of equine cases of WN virus infection in
Kentucky, 2000-2020.

Number of Cases

120

Total = 765

100
80
60
40
20
0

20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52
Week
Figure 2. Cumulative equine WN virus cases of infection by weekly
onset of illness in Kentucky, 2000-2020.

West Nile virus is a mosquito-transmitted arbovirus, member of the Japanese encephalitis virus
serocomplex, family Flaviviridae, known for many
years to be a highly adaptable virus, as evidenced
by its extensive distribution throughout the Old
World. As such, it was no surprise that WN virus
spread rapidly from its presumed point of introduction in New York. It initially extended southwards
along the eastern seaboard, while also migrating
westwards into the hinterland of the USA. With
the exception of Alaska and Hawaii, WN virus had
reached the remaining 48 states by 2004. The virus
was later confirmed in Alaska in 2018.
Kentucky reported its first cases of WN virus inbirds and horses in 2001 (Figure 1). Devastating
losses were recorded in crows and other membersof the corvid family, and eight cases were diagnosedin horses in counties in the north-central part of thestate. In 2002, the virus dramatically spread throughout much of Kentucky with the exception of theeastern part of the state. To date, 2002 was witness
to the greatest number of cases recorded in horses(513), humans (75), and birds in Kentucky. Case
numbers in horses (102) and humans (14) declined
significantly the following year. With the exceptionof minor surges in horse cases in 2006, 2012, 2013,2017, and 2018, the annual number of reported
cases of infection remained in single digits. With the
exception of 2006 and 2013, the same years also saw
corresponding minor surges in human cases (CDC,
ArboNET). Cases of WN virus infection have been
confirmed in horses every year since 2001 and, withthe exception of 2020, also in humans.
The seasonality of equine WN infections, basedon the weekly onset of illness, was consistent
with other arboviral encephalomyelitides (Figure2). Apropos of the 765 equine cases of infection
recorded in Kentucky since 2001, the onset ofvirus activity ranged from early June to mid-July,depending largely on the level of mosquito activ-

C O M M E N TA RY

ity in any particular year. The peak of infections
occurred approximately mid-September, and virus
activity ceased by mid-November.
A breakdown of the 20-year total of WN virus
infections in Kentucky revealed that the most common horse breeds/categories included American
Quarter horses (AQH), Tennessee Walking horses(TWH), Thoroughbreds, and pleasure horses, ofwhich AQH and TWH’s comprised almost 50%of the overall number. Females outnumbered males
57% to 43%. Ages of confirmed WN cases ranged
from three months to 39 years, with a median ofeight years. Of the 765 total cases, 541 (71%)
survived and 224 (29%) died or were euthanized.
The first equine vaccines against WN virusrelated disease received conditional licensure fromthe USDA in 2001. Even though vaccination iseffective in protecting against disease, the great
majority (86%) of WN cases recorded in Kentucky
had never been vaccinated or were only partially
vaccinated (10%). Only approximately 4% of cases
had current vaccination histories. While this is nottotally surprising, it is disappointing consideringthat WN virus is one of five core equine vaccinesstrongly recommended by the American Associa-

tion of Equine Practitioners. Of the 656 cases of
WN infection without prior vaccination history,
approximately 30% died or were euthanized.
Greater efforts are therefore needed to encourage
horse owners to take advantage of vaccination if
continued losses from WN virus infection are to
be reduced or even eliminated.
This review confirms that WN virus has become
endemic in Kentucky and will likely continue tocause horse and human disease. Its broad host andvector range, capability for transovarial transmission in mosquitoes, and horizontal transmission
in birds and a diversity of mammals has ensured
its perpetuation.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky
E.S. Rusty Ford
Rusty.ford@ky.gov(502) 782-5924
Equine Operations Consultant
Office State VeterinarianKY Department AgricultureFrankfort, KentuckyAs equine practitioners, we are charged with thehealth and welfare of our client’s horses, including dealing with infectious and non-infectious
Commentarycauses of neurologic disease. The veterinary industry
has rapidly changed in complexity, with a new
International
understanding of disease mechanisms, diagnostic
First Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 testing, and treatments. Many challenges remain
including how to make an accurate diagnosis, how
National
to establish neuroanatomic localization, and how
most effectively to treat affected horses. If a horse is
EquineHerpesvirus 1 .  .  .  .  .  .  .  . 3 suspected to have cervical vertebral stenotic myelopathy (wobbler syndrome), then cervical radiographs
Kentuckyare called for, often followed by a myelogram, CT
Common Equineor MRI scan to help pinpoint the site of compresHepatotoxins .  .  .  .  .  .  .  . 4sion.Horses with multifocal, asymmetric signs
West Nile Virus .  .  .  .  .  .  . 5 affecting brain, brainstem and cranial nerves alongwith weakness and ataxia are likely to have equine
protozoal myeloencephalitis (EPM). Accurate
diagnosis of this condition requires an evaluationof antibodies in blood and CSF. Although EPM
is most commonly caused by Sarcocystis neurona,clinical signs in some horses are a result of Neosporahughesi infection. The exposure rate for N. hughesi
appears much lower than for S. neurona. Risk factors for developing EPM include age (< 5 and >13
years), time of year (summer and spring), previous
cases on a farm, and presence of woodland andopossums on the farm. EPM prevalence is less onfarms where wildlife have little or no access to feed
and if a creek or river is on the premises. Stressful
College of Agriculture, events like concurrent disease, general anesthesia,
Food and Environmentor travel can increase the incidence of EPM. There
Department ofare three FDA approved drugs for the treatment of
Veterinary Sciencehorses suspected to have EPM.
Another important infectious cause of neurologic disease is equine herpesvirus 1 (EHV-1),
which is addressed in this issue of the Equine
Lloyd’s—An international
Disease Quarterly by Dr. Peter Timoney. EHV-1
insurance market foris problematic in that it can affect several body
bloodstock and othersystems (respiratory, reproductive, and central
specialist insurance.
IN THIS ISSUE

nervous system). The neurologic form of EHV-1
infection is termed equine herpesvirus myeloencephalopathy (EHM) and is caused by damage toblood vessels supplying the central nervous system.
These vascular insults result in stroke-like injuries.
Clinical signs often include ascending paralysis
with urine dribbling, loss of tail and anal tone andpelvic limb weakness.
A diagnosis of EHM is made easier whenseveral horses on the same premise present withfever, followed by ataxia, urine dribbling and insome cases abortion. Furthermore, diagnosis canbe established by recognition of clinical signs in
combination with a positive virus detection test
(PCR or virus isolation) on a nasal swab and unclotted blood sample. Following confirmation ofa diagnosis of EHM, affected animals or test positive animals should be isolated, and the premises
quarantined; movement of horses off an affectedfacility increases the risk of spread of infection.
Herpesvirus can affect horses of all ages but israrely seen in yearlings. The virus initially replicates in the mucosa of the upper respiratory tract,
spreads to the lymphoreticular system, followed bydevelopment of a viremia and infection of othersites in the body. Although currently available vaccines do not reliably prevent infection, the development of viremia, or the establishment of latency,
vaccination remains important in preventing and/or reducing the incidence of respiratory infections
and abortions and is considered the best recommendation for owners to keep their horses healthy.
Other infectious neurologic diseases that need tobe considered include West Nile virus infection,
rabies, and tetanus, all of which should be a partof the annual vaccination schedule for horses.
CONTACT:
Stephen M. Reed, DVM, Dip ACVIM(859) 233-0371
Rood and Riddle Equine Hospital
Lexington, Kentucky

2

3

Equine Disease Quarterly
Editors

Peter Timoney
Alan Loynachan
Rebecca Ruby

Staff

Diane Furry
Tawana Brown
Dennis Duross

Correspondence should be
addressed to the editors,
Department of Veterinary
Science, Maxwell H. Gluck
Equine Research Center,
University of Kentucky,
Lexington, Kentucky USA,40546-0099
Telephone (859) 257-4757
Fax (859) 257-8542
Internet address:
http://gluck.ca.uky.edu/
equine-disease-quarterly
Material published in the
Quarterly is not subject tocopyright. Permission istherefore granted toreproduce articles, althoughacknowledgment of thesource and author is requested.
The University of Kentucky
is an Equal Opportunity
Organization.

Printed on recycled paper

N AT I O N A L

First Quarter 2021

Equine Herpesvirus 1 Revisited:
Significance and Control Strategies

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
African horse sickness was reported as endemic
in the Republic of South Africa (RSA), except in
the controlled area in the Western Cape Province.
Sporadic cases (38 total) were recorded in six ofthe nine provinces.
France, Germany, the Netherlands, the UK, andthe USA confirmed outbreaks of equine influenza.
The number ranged from eight (France), five (Germany and the UK), and three in the Netherlands
to at least 13, in as many states, in the USA, where
the disease is endemic. Washington State reported
a case of co-infection with equine herpesvirus 1.
Many outbreaks involved only single cases.
Strangles is considered endemic in many countries with outbreaks recorded by Belgium (one),
Canada (two), France (13), the Netherlands (19),
Switzerland (five), and the USA (27). The majorityof outbreaks were comprised of a single case.
Equine herpesvirus 1 (EHV-1) respiratory
disease is endemic in most countries. Outbreaks
were diagnosed in Belgium (eight), France (20),Germany and Sweden (12 apiece), Qatar andSwitzerland (one each), Spain (two), the UK (five),and the USA (three). Belgium confirmed a case of
co-infection with equine herpesvirus 4 and 5.
Outbreaks of EHV-1 abortion were reported by
Belgium and Sweden (six), Canada (two), France
and the Netherlands (three), Germany (11), Ireland (seven), Japan (eight), the UK (eight), andthe USA (ten). With very few exceptions, all wererepresented by single cases of abortion. Outbreaksof EHV-1 neurologic disease were diagnosed
by Belgium (eight, one with four cases, anotherwith eight and a third with 24), Canada (sevenoutbreaks), France (five, one with four cases andanother with five cases), Germany (two), and Italy(four).
Equine herpesvirus 4 (EHV-4) respiratory outbreaks were reported by Belgium (six, one extensive), France (53, one extensive), the Netherlands
and the USA (two apiece), Belgium (five), France(two reported outbreaks of EHV-4 abortion, all
single cases), and Switzerland (one case). Germany

and the USA recorded cases of equine herpesvirus 2
and/or 5, some associated with clinical respiratory
disease.
Equine infectious anemia was confirmed in
Canada and Romania (two outbreaks in eachcountry, each comprising single cases), and theUSA (five outbreaks, all involving single cases).
The RSA regards equine piroplasmosis as endemic with a variable number of cases in eight of
the nine provinces, the majority were in Gauteng
Province.
Single cases of contagious equine metritis wereconfirmed on individual premises in Germany.
Coital exanthema (equine herpesvirus 3) was diagnosed on two premises (single cases) in France.
Four cases of leptospiral abortion were recorded in
Kentucky, USA, as were eight cases of nocardioform placentitis/abortion. Japan reported a case of
Salmonella Abortusequi in a non-Thoroughbred,
and Belgium diagnosed three cases of Streptococcus
zooepidemicus abortion on individual premises.
The USA reported salmonellosis (two cases
involving serogroup B) and clostridial enterocolitis (eight cases of Clostridium perfringens TypeA, beta-2 toxin; 99 cases of C. perfringens, toxin
untyped; 63 cases of Clostridiodes difficile), manyin Kentucky. Of four outbreaks of equine coronavirus confirmed by Switzerland, three were single
cases. Numerous outbreaks of neonatal diarrhea
were reported by Kentucky, some infected by anovel rotavirus. Kentucky also recorded two casesof Lawsonia enteropathy and four cases of Tyzzer’s
disease (Clostridium piliforme). Germany and the
RSA confirmed one and two cases of West Nilevirus infection, respectively.
A single case of Eastern equine encephalomyelitis was recorded in an unvaccinated horse in
Florida, USA. The USA also confirmed a case ofrabies in an unvaccinated mule in California.
The RSA reported that equine encephalosis wasendemic in the country, with a variable numberof cases diagnosed in eight of the nine provinces,mostly in Gauteng Province.
A case of “Pigeon fever,” (Corynebacterium
pseudotuberculosis) was diagnosed in Washington
State, USA.

E

quine herpesvirus 1 (EHV-1) is the most significant equine herpesvirus in terms of equine
health and economic impact to equine industries
worldwide. EHV-1 is believed to have co-evolved
with horses over millions of years. This co-evolutionary relationship resulted in the developmentof a life-long carrier state in a high percentage of
infected horses. This involves viral latency (silent
infection) of various sites (trigeminal ganglia inthe central nervous system, respiratory lymphoidtissues, and CD3+ T lymphocytes in the blood).
Latency ensures perpetuation of EHV-1 by serving
as a virus reservoir for infection and dissemination in susceptible populations. It is no wonderthat EHV-1 is ubiquitous in horse populations
worldwide.
A wide range of clinico-pathological syndromes
are attributed to EHV-1 infection. EHV-1 infections can result in respiratory disease in foals andtwo to three-year-old horses in training; contagious
abortion in mares; congenital disease and deathin foals infected in utero; and neurologic disease(myeloencephalopathy) in horses of variable ages,
especially older animals. Less frequently encountered EHV-1 diseases include: retinouveitis in
foals; fatal generalized peracute disease (pulmonary
viscerotropic infection) in young adult to older
adult horses; intestinal ganglionitis and impaction;and scrotal edema and loss of libido in stallions.
EHV-1 was implicated as the agent responsible
for annual occurrences of “abortion storms” in theThoroughbred breeding population in Kentucky
at least as far back as 1933 and is widely acknowledged as the most significant cause of equinecontagious abortion in many countries. Implementation of sound management practices andprophylactic vaccination of pregnant mares have,where practiced, greatly reduced the frequency
of EHV-1 abortion storms. Susceptible mares
exposed to EHV-1 late in pregnancy may carry toterm, but give birth to a diseased foal that invariably succumbs from fulminant viral pneumonitis.
Unless appropriate biosecurity measures are taken,
there is a high risk that affected foals can serve asa source of infection through direct or indirectmeans for healthy foals and pregnant mares.

The clinical syndrome that has attracted themost concern in recent years is equine herpesvirus
myeloencephalopathy (EHM). This syndrome has
been recorded with increasing frequency in North
America and Europe over the past 20 years (Figure1). In 2007, the USDA designated EHM caused
by a hypervirulent strain of EHV-1, a potentiallyemergent disease of the horse. EHM tends to beseasonal with increased case numbers in winterand spring.
A comprehensive biosecurity plan is critical toprevent and control outbreaks of EHM. Optimally,
its aim should be to prevent the introduction ofan equine pathogen viz. EHV-1 onto a premises,
be it a farm or event venue (equestrian, racetrack,
horse show), by whatever measures are consideredappropriate and necessary. This is especially important when dealing with an EHM outbreak. In
such a situation, the primary aim should restrict
the spread of infection at the index premises/
facility by quarantine of infected and exposed
horses. Furthermore, every effort should be madeto ensure that the outbreak is effectively containedand eliminate the possibility of virus spread toother premises/facilities. Restriction of movement of exposed horses off an affected premises
is crucially important, and failure to observe thisprecautionary measure carries a considerable riskof EHV-1 spread that can have very significant
consequences. This was exemplified at the NCHA
Western National Championship at Ogden, Utah
Number of EHV-1 Outbreaks

T

I N T E R N AT I O N A L

4

60

L

Matt Barton, Agricultural Communications

30
20

7

10
0

2011

22

19

15

12
4
2013

2

17

4
2015

2017

CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

Common Equine Hepatotoxins in Central Kentucky

41

40

Equine herpesvirus 1 remains a highly significant pathogen that has the potential to cause
a range of clinical syndromes in the horse andcan have considerable economic consequences forequine industries.

KENTUCKY

55

50

in May 2011, when exposed horses departed theevent and subsequently spread EHV-1 to 12 US
states and two Canadian provinces. An analogous
situation occurred at the CES Spring Tour in
Valencia, Spain in February 2021. During theextensive EHM outbreak at this event, a significant number of exposed horses were transported
back to their countries of origin. The outcome
was calamitous with multiple horses developing
neurologic disease, some of which died or wereeuthanized.

2019

Year
Figure 1. Recorded Outbreaks / Cases of Equine Herpesvirus 1
Myeloencephalopathy in the USA, 2011- May 10, 2021.

2021

iver disease in horses can occur due to manycauses, including infectious agents, neoplasia,
and toxicants. Clinical signs are often nonspecific,
and can include inappetence, depression, colic,weight loss, weakness, icterus (jaundice), yawning,head-pressing, abnormal behavior, and coagulation
abnormalities. Toxic agents can vary tremendously
depending on an animal’s environment and geographic location. This article describes some of thehepatotoxicants (liver toxins) that affect horses incentral Kentucky.
Pyrrolizidine alkaloids (PAs)—PAs are found ina variety of plant species and can cause chronic liverdisease and eventual liver failure with prolonged
ingestion. Due to the liver’s immense reserve andregenerative capacity, horses can appear normal until greater than 80% of the liver is affected. Severeclinical signs can then develop rapidly, giving theappearance of acute disease. PA-producing plants
found in Kentucky include ragwort, butterweed,
groundsel, and rattlebox (Senecio, Packera, andCrotalaria spp.). Most PA-producing plants areunpalatable when fresh, although horses may eat
them when other forage is lacking. The plants
become palatable when dried and can pose agreater threat in hay. Poisoning can be prevented
by providing high-quality forage and checking hay
for weeds.
Cocklebur (Xanthium strumarium)—Cockleburseedlings (2-leaf stage) contain large quantities of
the toxin carboxyatractyloside. Seedlings emerge
in early spring when other forage is limited and arereadily consumed by horses. High concentrationsof the toxin are present in the seeds, and horses
have been poisoned by cocklebur seed contamination of hay or grain. Cocklebur poisoning can beprevented by providing high-quality forage andinspecting hay and grain for cocklebur seeds.
Aflatoxin—A mycotoxin produced by speciesof Aspergillus molds under certain conditions.
Aflatoxin can contaminate corn, oats, or any
other high-energy feedstuff. Mold can contaminate
crops growing in fields, particularly if the plants
have been stressed by drought, frost, insects, orother harmful elements. Warm and damp storage
conditions and pests also facilitate mold growth.
Aflatoxin can be present in toxic concentrations
with or without visible mold. To avoid the risk ofmold and mycotoxins, feed should be purchasedfrom reputable sources; stored in a cool, dry location; and adequately protected from rodents andother pests.
Blue-green algae (cyanobacteria)—Underthe right environmental conditions, these microscopic organisms normally present in ponds,
lakes, streams, oceans, and other natural water
sources can undergo rapid growth (harmful algal
blooms, HABs). Certain species produce toxins,
including hepatotoxins (e.g., microcystins andnodularins). Horses can die rapidly after ingestion, and animals are often found dead in or nearwater sources. Excess nitrogen and phosphorus
from animal waste or fertilizer runoff can facilitate
HABs. Horses should be provided with fresh,clean water, and ponds or other natural water
sources should be fenced off to prevent blue-green
algae poisoning.
Amanitin—Toxin found in certain species ofmushrooms, including Amanita, Galerina, andLepiota spp. Mushrooms can appear suddenly inpastures and occasionally in stalls. Horses are lesslikely to ingest mushrooms than other animal
continued on page 5

23

Equine Disease Quarterly
Editors

Peter Timoney
Alan Loynachan
Rebecca Ruby

Staff

Diane Furry
Tawana Brown
Dennis Duross

Correspondence should be
addressed to the editors,
Department of Veterinary
Science, Maxwell H. Gluck
Equine Research Center,
University of Kentucky,
Lexington, Kentucky USA,40546-0099
Telephone (859) 257-4757
Fax (859) 257-8542
Internet address:
http://gluck.ca.uky.edu/
equine-disease-quarterly
Material published in the
Quarterly is not subject tocopyright. Permission istherefore granted toreproduce articles, althoughacknowledgment of thesource and author is requested.
The University of Kentucky
is an Equal Opportunity
Organization.

Printed on recycled paper

N AT I O N A L

First Quarter 2021

Equine Herpesvirus 1 Revisited:
Significance and Control Strategies

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
African horse sickness was reported as endemic
in the Republic of South Africa (RSA), except in
the controlled area in the Western Cape Province.
Sporadic cases (38 total) were recorded in six ofthe nine provinces.
France, Germany, the Netherlands, the UK, andthe USA confirmed outbreaks of equine influenza.
The number ranged from eight (France), five (Germany and the UK), and three in the Netherlands
to at least 13, in as many states, in the USA, where
the disease is endemic. Washington State reported
a case of co-infection with equine herpesvirus 1.
Many outbreaks involved only single cases.
Strangles is considered endemic in many countries with outbreaks recorded by Belgium (one),
Canada (two), France (13), the Netherlands (19),
Switzerland (five), and the USA (27). The majorityof outbreaks were comprised of a single case.
Equine herpesvirus 1 (EHV-1) respiratory
disease is endemic in most countries. Outbreaks
were diagnosed in Belgium (eight), France (20),Germany and Sweden (12 apiece), Qatar andSwitzerland (one each), Spain (two), the UK (five),and the USA (three). Belgium confirmed a case of
co-infection with equine herpesvirus 4 and 5.
Outbreaks of EHV-1 abortion were reported by
Belgium and Sweden (six), Canada (two), France
and the Netherlands (three), Germany (11), Ireland (seven), Japan (eight), the UK (eight), andthe USA (ten). With very few exceptions, all wererepresented by single cases of abortion. Outbreaksof EHV-1 neurologic disease were diagnosed
by Belgium (eight, one with four cases, anotherwith eight and a third with 24), Canada (sevenoutbreaks), France (five, one with four cases andanother with five cases), Germany (two), and Italy(four).
Equine herpesvirus 4 (EHV-4) respiratory outbreaks were reported by Belgium (six, one extensive), France (53, one extensive), the Netherlands
and the USA (two apiece), Belgium (five), France(two reported outbreaks of EHV-4 abortion, all
single cases), and Switzerland (one case). Germany

and the USA recorded cases of equine herpesvirus 2
and/or 5, some associated with clinical respiratory
disease.
Equine infectious anemia was confirmed in
Canada and Romania (two outbreaks in eachcountry, each comprising single cases), and theUSA (five outbreaks, all involving single cases).
The RSA regards equine piroplasmosis as endemic with a variable number of cases in eight of
the nine provinces, the majority were in Gauteng
Province.
Single cases of contagious equine metritis wereconfirmed on individual premises in Germany.
Coital exanthema (equine herpesvirus 3) was diagnosed on two premises (single cases) in France.
Four cases of leptospiral abortion were recorded in
Kentucky, USA, as were eight cases of nocardioform placentitis/abortion. Japan reported a case of
Salmonella Abortusequi in a non-Thoroughbred,
and Belgium diagnosed three cases of Streptococcus
zooepidemicus abortion on individual premises.
The USA reported salmonellosis (two cases
involving serogroup B) and clostridial enterocolitis (eight cases of Clostridium perfringens TypeA, beta-2 toxin; 99 cases of C. perfringens, toxin
untyped; 63 cases of Clostridiodes difficile), manyin Kentucky. Of four outbreaks of equine coronavirus confirmed by Switzerland, three were single
cases. Numerous outbreaks of neonatal diarrhea
were reported by Kentucky, some infected by anovel rotavirus. Kentucky also recorded two casesof Lawsonia enteropathy and four cases of Tyzzer’s
disease (Clostridium piliforme). Germany and the
RSA confirmed one and two cases of West Nilevirus infection, respectively.
A single case of Eastern equine encephalomyelitis was recorded in an unvaccinated horse in
Florida, USA. The USA also confirmed a case ofrabies in an unvaccinated mule in California.
The RSA reported that equine encephalosis wasendemic in the country, with a variable numberof cases diagnosed in eight of the nine provinces,mostly in Gauteng Province.
A case of “Pigeon fever,” (Corynebacterium
pseudotuberculosis) was diagnosed in Washington
State, USA.

E

quine herpesvirus 1 (EHV-1) is the most significant equine herpesvirus in terms of equine
health and economic impact to equine industries
worldwide. EHV-1 is believed to have co-evolved
with horses over millions of years. This co-evolutionary relationship resulted in the developmentof a life-long carrier state in a high percentage of
infected horses. This involves viral latency (silent
infection) of various sites (trigeminal ganglia inthe central nervous system, respiratory lymphoidtissues, and CD3+ T lymphocytes in the blood).
Latency ensures perpetuation of EHV-1 by serving
as a virus reservoir for infection and dissemination in susceptible populations. It is no wonderthat EHV-1 is ubiquitous in horse populations
worldwide.
A wide range of clinico-pathological syndromes
are attributed to EHV-1 infection. EHV-1 infections can result in respiratory disease in foals andtwo to three-year-old horses in training; contagious
abortion in mares; congenital disease and deathin foals infected in utero; and neurologic disease(myeloencephalopathy) in horses of variable ages,
especially older animals. Less frequently encountered EHV-1 diseases include: retinouveitis in
foals; fatal generalized peracute disease (pulmonary
viscerotropic infection) in young adult to older
adult horses; intestinal ganglionitis and impaction;and scrotal edema and loss of libido in stallions.
EHV-1 was implicated as the agent responsible
for annual occurrences of “abortion storms” in theThoroughbred breeding population in Kentucky
at least as far back as 1933 and is widely acknowledged as the most significant cause of equinecontagious abortion in many countries. Implementation of sound management practices andprophylactic vaccination of pregnant mares have,where practiced, greatly reduced the frequency
of EHV-1 abortion storms. Susceptible mares
exposed to EHV-1 late in pregnancy may carry toterm, but give birth to a diseased foal that invariably succumbs from fulminant viral pneumonitis.
Unless appropriate biosecurity measures are taken,
there is a high risk that affected foals can serve asa source of infection through direct or indirectmeans for healthy foals and pregnant mares.

The clinical syndrome that has attracted themost concern in recent years is equine herpesvirus
myeloencephalopathy (EHM). This syndrome has
been recorded with increasing frequency in North
America and Europe over the past 20 years (Figure1). In 2007, the USDA designated EHM caused
by a hypervirulent strain of EHV-1, a potentiallyemergent disease of the horse. EHM tends to beseasonal with increased case numbers in winterand spring.
A comprehensive biosecurity plan is critical toprevent and control outbreaks of EHM. Optimally,
its aim should be to prevent the introduction ofan equine pathogen viz. EHV-1 onto a premises,
be it a farm or event venue (equestrian, racetrack,
horse show), by whatever measures are consideredappropriate and necessary. This is especially important when dealing with an EHM outbreak. In
such a situation, the primary aim should restrict
the spread of infection at the index premises/
facility by quarantine of infected and exposed
horses. Furthermore, every effort should be madeto ensure that the outbreak is effectively containedand eliminate the possibility of virus spread toother premises/facilities. Restriction of movement of exposed horses off an affected premises
is crucially important, and failure to observe thisprecautionary measure carries a considerable riskof EHV-1 spread that can have very significant
consequences. This was exemplified at the NCHA
Western National Championship at Ogden, Utah
Number of EHV-1 Outbreaks

T

I N T E R N AT I O N A L

4

60

L

Matt Barton, Agricultural Communications

30
20

7

10
0

2011

22

19

15

12
4
2013

2

17

4
2015

2017

CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

Common Equine Hepatotoxins in Central Kentucky

41

40

Equine herpesvirus 1 remains a highly significant pathogen that has the potential to cause
a range of clinical syndromes in the horse andcan have considerable economic consequences forequine industries.

KENTUCKY

55

50

in May 2011, when exposed horses departed theevent and subsequently spread EHV-1 to 12 US
states and two Canadian provinces. An analogous
situation occurred at the CES Spring Tour in
Valencia, Spain in February 2021. During theextensive EHM outbreak at this event, a significant number of exposed horses were transported
back to their countries of origin. The outcome
was calamitous with multiple horses developing
neurologic disease, some of which died or wereeuthanized.

2019

Year
Figure 1. Recorded Outbreaks / Cases of Equine Herpesvirus 1
Myeloencephalopathy in the USA, 2011- May 10, 2021.

2021

iver disease in horses can occur due to manycauses, including infectious agents, neoplasia,
and toxicants. Clinical signs are often nonspecific,
and can include inappetence, depression, colic,weight loss, weakness, icterus (jaundice), yawning,head-pressing, abnormal behavior, and coagulation
abnormalities. Toxic agents can vary tremendously
depending on an animal’s environment and geographic location. This article describes some of thehepatotoxicants (liver toxins) that affect horses incentral Kentucky.
Pyrrolizidine alkaloids (PAs)—PAs are found ina variety of plant species and can cause chronic liverdisease and eventual liver failure with prolonged
ingestion. Due to the liver’s immense reserve andregenerative capacity, horses can appear normal until greater than 80% of the liver is affected. Severeclinical signs can then develop rapidly, giving theappearance of acute disease. PA-producing plants
found in Kentucky include ragwort, butterweed,
groundsel, and rattlebox (Senecio, Packera, andCrotalaria spp.). Most PA-producing plants areunpalatable when fresh, although horses may eat
them when other forage is lacking. The plants
become palatable when dried and can pose agreater threat in hay. Poisoning can be prevented
by providing high-quality forage and checking hay
for weeds.
Cocklebur (Xanthium strumarium)—Cockleburseedlings (2-leaf stage) contain large quantities of
the toxin carboxyatractyloside. Seedlings emerge
in early spring when other forage is limited and arereadily consumed by horses. High concentrationsof the toxin are present in the seeds, and horses
have been poisoned by cocklebur seed contamination of hay or grain. Cocklebur poisoning can beprevented by providing high-quality forage andinspecting hay and grain for cocklebur seeds.
Aflatoxin—A mycotoxin produced by speciesof Aspergillus molds under certain conditions.
Aflatoxin can contaminate corn, oats, or any
other high-energy feedstuff. Mold can contaminate
crops growing in fields, particularly if the plants
have been stressed by drought, frost, insects, orother harmful elements. Warm and damp storage
conditions and pests also facilitate mold growth.
Aflatoxin can be present in toxic concentrations
with or without visible mold. To avoid the risk ofmold and mycotoxins, feed should be purchasedfrom reputable sources; stored in a cool, dry location; and adequately protected from rodents andother pests.
Blue-green algae (cyanobacteria)—Underthe right environmental conditions, these microscopic organisms normally present in ponds,
lakes, streams, oceans, and other natural water
sources can undergo rapid growth (harmful algal
blooms, HABs). Certain species produce toxins,
including hepatotoxins (e.g., microcystins andnodularins). Horses can die rapidly after ingestion, and animals are often found dead in or nearwater sources. Excess nitrogen and phosphorus
from animal waste or fertilizer runoff can facilitate
HABs. Horses should be provided with fresh,clean water, and ponds or other natural water
sources should be fenced off to prevent blue-green
algae poisoning.
Amanitin—Toxin found in certain species ofmushrooms, including Amanita, Galerina, andLepiota spp. Mushrooms can appear suddenly inpastures and occasionally in stalls. Horses are lesslikely to ingest mushrooms than other animal
continued on page 5

23

Equine Disease Quarterly
Editors

Peter Timoney
Alan Loynachan
Rebecca Ruby

Staff

Diane Furry
Tawana Brown
Dennis Duross

Correspondence should be
addressed to the editors,
Department of Veterinary
Science, Maxwell H. Gluck
Equine Research Center,
University of Kentucky,
Lexington, Kentucky USA,40546-0099
Telephone (859) 257-4757
Fax (859) 257-8542
Internet address:
http://gluck.ca.uky.edu/
equine-disease-quarterly
Material published in the
Quarterly is not subject tocopyright. Permission istherefore granted toreproduce articles, althoughacknowledgment of thesource and author is requested.
The University of Kentucky
is an Equal Opportunity
Organization.

Printed on recycled paper

N AT I O N A L

First Quarter 2021

Equine Herpesvirus 1 Revisited:
Significance and Control Strategies

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
African horse sickness was reported as endemic
in the Republic of South Africa (RSA), except in
the controlled area in the Western Cape Province.
Sporadic cases (38 total) were recorded in six ofthe nine provinces.
France, Germany, the Netherlands, the UK, andthe USA confirmed outbreaks of equine influenza.
The number ranged from eight (France), five (Germany and the UK), and three in the Netherlands
to at least 13, in as many states, in the USA, where
the disease is endemic. Washington State reported
a case of co-infection with equine herpesvirus 1.
Many outbreaks involved only single cases.
Strangles is considered endemic in many countries with outbreaks recorded by Belgium (one),
Canada (two), France (13), the Netherlands (19),
Switzerland (five), and the USA (27). The majorityof outbreaks were comprised of a single case.
Equine herpesvirus 1 (EHV-1) respiratory
disease is endemic in most countries. Outbreaks
were diagnosed in Belgium (eight), France (20),Germany and Sweden (12 apiece), Qatar andSwitzerland (one each), Spain (two), the UK (five),and the USA (three). Belgium confirmed a case of
co-infection with equine herpesvirus 4 and 5.
Outbreaks of EHV-1 abortion were reported by
Belgium and Sweden (six), Canada (two), France
and the Netherlands (three), Germany (11), Ireland (seven), Japan (eight), the UK (eight), andthe USA (ten). With very few exceptions, all wererepresented by single cases of abortion. Outbreaksof EHV-1 neurologic disease were diagnosed
by Belgium (eight, one with four cases, anotherwith eight and a third with 24), Canada (sevenoutbreaks), France (five, one with four cases andanother with five cases), Germany (two), and Italy(four).
Equine herpesvirus 4 (EHV-4) respiratory outbreaks were reported by Belgium (six, one extensive), France (53, one extensive), the Netherlands
and the USA (two apiece), Belgium (five), France(two reported outbreaks of EHV-4 abortion, all
single cases), and Switzerland (one case). Germany

and the USA recorded cases of equine herpesvirus 2
and/or 5, some associated with clinical respiratory
disease.
Equine infectious anemia was confirmed in
Canada and Romania (two outbreaks in eachcountry, each comprising single cases), and theUSA (five outbreaks, all involving single cases).
The RSA regards equine piroplasmosis as endemic with a variable number of cases in eight of
the nine provinces, the majority were in Gauteng
Province.
Single cases of contagious equine metritis wereconfirmed on individual premises in Germany.
Coital exanthema (equine herpesvirus 3) was diagnosed on two premises (single cases) in France.
Four cases of leptospiral abortion were recorded in
Kentucky, USA, as were eight cases of nocardioform placentitis/abortion. Japan reported a case of
Salmonella Abortusequi in a non-Thoroughbred,
and Belgium diagnosed three cases of Streptococcus
zooepidemicus abortion on individual premises.
The USA reported salmonellosis (two cases
involving serogroup B) and clostridial enterocolitis (eight cases of Clostridium perfringens TypeA, beta-2 toxin; 99 cases of C. perfringens, toxin
untyped; 63 cases of Clostridiodes difficile), manyin Kentucky. Of four outbreaks of equine coronavirus confirmed by Switzerland, three were single
cases. Numerous outbreaks of neonatal diarrhea
were reported by Kentucky, some infected by anovel rotavirus. Kentucky also recorded two casesof Lawsonia enteropathy and four cases of Tyzzer’s
disease (Clostridium piliforme). Germany and the
RSA confirmed one and two cases of West Nilevirus infection, respectively.
A single case of Eastern equine encephalomyelitis was recorded in an unvaccinated horse in
Florida, USA. The USA also confirmed a case ofrabies in an unvaccinated mule in California.
The RSA reported that equine encephalosis wasendemic in the country, with a variable numberof cases diagnosed in eight of the nine provinces,mostly in Gauteng Province.
A case of “Pigeon fever,” (Corynebacterium
pseudotuberculosis) was diagnosed in Washington
State, USA.

E

quine herpesvirus 1 (EHV-1) is the most significant equine herpesvirus in terms of equine
health and economic impact to equine industries
worldwide. EHV-1 is believed to have co-evolved
with horses over millions of years. This co-evolutionary relationship resulted in the developmentof a life-long carrier state in a high percentage of
infected horses. This involves viral latency (silent
infection) of various sites (trigeminal ganglia inthe central nervous system, respiratory lymphoidtissues, and CD3+ T lymphocytes in the blood).
Latency ensures perpetuation of EHV-1 by serving
as a virus reservoir for infection and dissemination in susceptible populations. It is no wonderthat EHV-1 is ubiquitous in horse populations
worldwide.
A wide range of clinico-pathological syndromes
are attributed to EHV-1 infection. EHV-1 infections can result in respiratory disease in foals andtwo to three-year-old horses in training; contagious
abortion in mares; congenital disease and deathin foals infected in utero; and neurologic disease(myeloencephalopathy) in horses of variable ages,
especially older animals. Less frequently encountered EHV-1 diseases include: retinouveitis in
foals; fatal generalized peracute disease (pulmonary
viscerotropic infection) in young adult to older
adult horses; intestinal ganglionitis and impaction;and scrotal edema and loss of libido in stallions.
EHV-1 was implicated as the agent responsible
for annual occurrences of “abortion storms” in theThoroughbred breeding population in Kentucky
at least as far back as 1933 and is widely acknowledged as the most significant cause of equinecontagious abortion in many countries. Implementation of sound management practices andprophylactic vaccination of pregnant mares have,where practiced, greatly reduced the frequency
of EHV-1 abortion storms. Susceptible mares
exposed to EHV-1 late in pregnancy may carry toterm, but give birth to a diseased foal that invariably succumbs from fulminant viral pneumonitis.
Unless appropriate biosecurity measures are taken,
there is a high risk that affected foals can serve asa source of infection through direct or indirectmeans for healthy foals and pregnant mares.

The clinical syndrome that has attracted themost concern in recent years is equine herpesvirus
myeloencephalopathy (EHM). This syndrome has
been recorded with increasing frequency in North
America and Europe over the past 20 years (Figure1). In 2007, the USDA designated EHM caused
by a hypervirulent strain of EHV-1, a potentiallyemergent disease of the horse. EHM tends to beseasonal with increased case numbers in winterand spring.
A comprehensive biosecurity plan is critical toprevent and control outbreaks of EHM. Optimally,
its aim should be to prevent the introduction ofan equine pathogen viz. EHV-1 onto a premises,
be it a farm or event venue (equestrian, racetrack,
horse show), by whatever measures are consideredappropriate and necessary. This is especially important when dealing with an EHM outbreak. In
such a situation, the primary aim should restrict
the spread of infection at the index premises/
facility by quarantine of infected and exposed
horses. Furthermore, every effort should be madeto ensure that the outbreak is effectively containedand eliminate the possibility of virus spread toother premises/facilities. Restriction of movement of exposed horses off an affected premises
is crucially important, and failure to observe thisprecautionary measure carries a considerable riskof EHV-1 spread that can have very significant
consequences. This was exemplified at the NCHA
Western National Championship at Ogden, Utah
Number of EHV-1 Outbreaks

T

I N T E R N AT I O N A L

4

60

L

Matt Barton, Agricultural Communications

30
20

7

10
0

2011

22

19

15

12
4
2013

2

17

4
2015

2017

CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

Common Equine Hepatotoxins in Central Kentucky

41

40

Equine herpesvirus 1 remains a highly significant pathogen that has the potential to cause
a range of clinical syndromes in the horse andcan have considerable economic consequences forequine industries.

KENTUCKY

55

50

in May 2011, when exposed horses departed theevent and subsequently spread EHV-1 to 12 US
states and two Canadian provinces. An analogous
situation occurred at the CES Spring Tour in
Valencia, Spain in February 2021. During theextensive EHM outbreak at this event, a significant number of exposed horses were transported
back to their countries of origin. The outcome
was calamitous with multiple horses developing
neurologic disease, some of which died or wereeuthanized.

2019

Year
Figure 1. Recorded Outbreaks / Cases of Equine Herpesvirus 1
Myeloencephalopathy in the USA, 2011- May 10, 2021.

2021

iver disease in horses can occur due to manycauses, including infectious agents, neoplasia,
and toxicants. Clinical signs are often nonspecific,
and can include inappetence, depression, colic,weight loss, weakness, icterus (jaundice), yawning,head-pressing, abnormal behavior, and coagulation
abnormalities. Toxic agents can vary tremendously
depending on an animal’s environment and geographic location. This article describes some of thehepatotoxicants (liver toxins) that affect horses incentral Kentucky.
Pyrrolizidine alkaloids (PAs)—PAs are found ina variety of plant species and can cause chronic liverdisease and eventual liver failure with prolonged
ingestion. Due to the liver’s immense reserve andregenerative capacity, horses can appear normal until greater than 80% of the liver is affected. Severeclinical signs can then develop rapidly, giving theappearance of acute disease. PA-producing plants
found in Kentucky include ragwort, butterweed,
groundsel, and rattlebox (Senecio, Packera, andCrotalaria spp.). Most PA-producing plants areunpalatable when fresh, although horses may eat
them when other forage is lacking. The plants
become palatable when dried and can pose agreater threat in hay. Poisoning can be prevented
by providing high-quality forage and checking hay
for weeds.
Cocklebur (Xanthium strumarium)—Cockleburseedlings (2-leaf stage) contain large quantities of
the toxin carboxyatractyloside. Seedlings emerge
in early spring when other forage is limited and arereadily consumed by horses. High concentrationsof the toxin are present in the seeds, and horses
have been poisoned by cocklebur seed contamination of hay or grain. Cocklebur poisoning can beprevented by providing high-quality forage andinspecting hay and grain for cocklebur seeds.
Aflatoxin—A mycotoxin produced by speciesof Aspergillus molds under certain conditions.
Aflatoxin can contaminate corn, oats, or any
other high-energy feedstuff. Mold can contaminate
crops growing in fields, particularly if the plants
have been stressed by drought, frost, insects, orother harmful elements. Warm and damp storage
conditions and pests also facilitate mold growth.
Aflatoxin can be present in toxic concentrations
with or without visible mold. To avoid the risk ofmold and mycotoxins, feed should be purchasedfrom reputable sources; stored in a cool, dry location; and adequately protected from rodents andother pests.
Blue-green algae (cyanobacteria)—Underthe right environmental conditions, these microscopic organisms normally present in ponds,
lakes, streams, oceans, and other natural water
sources can undergo rapid growth (harmful algal
blooms, HABs). Certain species produce toxins,
including hepatotoxins (e.g., microcystins andnodularins). Horses can die rapidly after ingestion, and animals are often found dead in or nearwater sources. Excess nitrogen and phosphorus
from animal waste or fertilizer runoff can facilitate
HABs. Horses should be provided with fresh,clean water, and ponds or other natural water
sources should be fenced off to prevent blue-green
algae poisoning.
Amanitin—Toxin found in certain species ofmushrooms, including Amanita, Galerina, andLepiota spp. Mushrooms can appear suddenly inpastures and occasionally in stalls. Horses are lesslikely to ingest mushrooms than other animal
continued on page 5

Equine Disease Quarterly Newsletter

5

Equine Hepatotoxins, continued from page 4.

species, but the best way to prevent poisoning is
to monitor pastures and remove mushrooms.
Certain medications (e.g., phenylbutazone, flunixin, acetaminophen, salicylates, antifungals, andmany others) can cause liver damage, especially ifadministered in high doses, for prolonged periodsof time, or to animals with pre-existing conditions. Accurate dosing and careful consideration of
medication risks versus benefits can help minimize
chances of adverse effects.

Many other substances can cause liver damage
and may be more common in different geographic
areas. Consultation with a clinical veterinary
toxicologist should be considered when toxicosis
is suspected.
CONTACT:
Megan C. Romano, DVM, DABVT
megan.romano@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

Presorted Standard
US Postage Paid
Permit 51
Lexington KY

Department of Veterinary Science
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky 40546-0099
Address Service Requested

F U N D E D B Y U N D E R W R I T E R S AT L LOY D ' S , LO N D O N

JULY 2021
Volume 30, Number 3

Twenty Years’ Experience with West Nile Virus, 2001-2020

Until 1999, West Nile (WN) virus was unknown in the Western Hemisphere, muchless the USA. In August of that year, the virus
was identified in New York City and caused thedeaths of seven persons from viral encephalitis.
Coincidentally, the virus was also implicated in
the death of birds in New York’s Bronx Zoo andcrows in the precincts of the zoo.

513
102

Total = 765

Number of Cases

20

18
16

15

13

10

8

5

9
6 5

8

12
8

6

4
1

7
2 2

20
00
20
01
20
02
20
03
20
04
20
05
20
06
20
07
20
08
20
09
20
10
20
11
20
12
20
13
20
14
20
15
20
16
20
17
20
18
20
19
20
20

0

0

8

17

Year
Figure 1. Annual number of equine cases of WN virus infection in
Kentucky, 2000-2020.

Number of Cases

120

Total = 765

100
80
60
40
20
0

20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52
Week
Figure 2. Cumulative equine WN virus cases of infection by weekly
onset of illness in Kentucky, 2000-2020.

West Nile virus is a mosquito-transmitted arbovirus, member of the Japanese encephalitis virus
serocomplex, family Flaviviridae, known for many
years to be a highly adaptable virus, as evidenced
by its extensive distribution throughout the Old
World. As such, it was no surprise that WN virus
spread rapidly from its presumed point of introduction in New York. It initially extended southwards
along the eastern seaboard, while also migrating
westwards into the hinterland of the USA. With
the exception of Alaska and Hawaii, WN virus had
reached the remaining 48 states by 2004. The virus
was later confirmed in Alaska in 2018.
Kentucky reported its first cases of WN virus inbirds and horses in 2001 (Figure 1). Devastating
losses were recorded in crows and other membersof the corvid family, and eight cases were diagnosedin horses in counties in the north-central part of thestate. In 2002, the virus dramatically spread throughout much of Kentucky with the exception of theeastern part of the state. To date, 2002 was witness
to the greatest number of cases recorded in horses(513), humans (75), and birds in Kentucky. Case
numbers in horses (102) and humans (14) declined
significantly the following year. With the exceptionof minor surges in horse cases in 2006, 2012, 2013,2017, and 2018, the annual number of reported
cases of infection remained in single digits. With the
exception of 2006 and 2013, the same years also saw
corresponding minor surges in human cases (CDC,
ArboNET). Cases of WN virus infection have been
confirmed in horses every year since 2001 and, withthe exception of 2020, also in humans.
The seasonality of equine WN infections, basedon the weekly onset of illness, was consistent
with other arboviral encephalomyelitides (Figure2). Apropos of the 765 equine cases of infection
recorded in Kentucky since 2001, the onset ofvirus activity ranged from early June to mid-July,depending largely on the level of mosquito activ-

C O M M E N TA RY

ity in any particular year. The peak of infections
occurred approximately mid-September, and virus
activity ceased by mid-November.
A breakdown of the 20-year total of WN virus
infections in Kentucky revealed that the most common horse breeds/categories included American
Quarter horses (AQH), Tennessee Walking horses(TWH), Thoroughbreds, and pleasure horses, ofwhich AQH and TWH’s comprised almost 50%of the overall number. Females outnumbered males
57% to 43%. Ages of confirmed WN cases ranged
from three months to 39 years, with a median ofeight years. Of the 765 total cases, 541 (71%)
survived and 224 (29%) died or were euthanized.
The first equine vaccines against WN virusrelated disease received conditional licensure fromthe USDA in 2001. Even though vaccination iseffective in protecting against disease, the great
majority (86%) of WN cases recorded in Kentucky
had never been vaccinated or were only partially
vaccinated (10%). Only approximately 4% of cases
had current vaccination histories. While this is nottotally surprising, it is disappointing consideringthat WN virus is one of five core equine vaccinesstrongly recommended by the American Associa-

tion of Equine Practitioners. Of the 656 cases of
WN infection without prior vaccination history,
approximately 30% died or were euthanized.
Greater efforts are therefore needed to encourage
horse owners to take advantage of vaccination if
continued losses from WN virus infection are to
be reduced or even eliminated.
This review confirms that WN virus has become
endemic in Kentucky and will likely continue tocause horse and human disease. Its broad host andvector range, capability for transovarial transmission in mosquitoes, and horizontal transmission
in birds and a diversity of mammals has ensured
its perpetuation.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky
E.S. Rusty Ford
Rusty.ford@ky.gov(502) 782-5924
Equine Operations Consultant
Office State VeterinarianKY Department AgricultureFrankfort, KentuckyAs equine practitioners, we are charged with thehealth and welfare of our client’s horses, including dealing with infectious and non-infectious
Commentarycauses of neurologic disease. The veterinary industry
has rapidly changed in complexity, with a new
International
understanding of disease mechanisms, diagnostic
First Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 testing, and treatments. Many challenges remain
including how to make an accurate diagnosis, how
National
to establish neuroanatomic localization, and how
most effectively to treat affected horses. If a horse is
EquineHerpesvirus 1 .  .  .  .  .  .  .  . 3 suspected to have cervical vertebral stenotic myelopathy (wobbler syndrome), then cervical radiographs
Kentuckyare called for, often followed by a myelogram, CT
Common Equineor MRI scan to help pinpoint the site of compresHepatotoxins .  .  .  .  .  .  .  . 4sion.Horses with multifocal, asymmetric signs
West Nile Virus .  .  .  .  .  .  . 5 affecting brain, brainstem and cranial nerves alongwith weakness and ataxia are likely to have equine
protozoal myeloencephalitis (EPM). Accurate
diagnosis of this condition requires an evaluationof antibodies in blood and CSF. Although EPM
is most commonly caused by Sarcocystis neurona,clinical signs in some horses are a result of Neosporahughesi infection. The exposure rate for N. hughesi
appears much lower than for S. neurona. Risk factors for developing EPM include age (< 5 and >13
years), time of year (summer and spring), previous
cases on a farm, and presence of woodland andopossums on the farm. EPM prevalence is less onfarms where wildlife have little or no access to feed
and if a creek or river is on the premises. Stressful
College of Agriculture, events like concurrent disease, general anesthesia,
Food and Environmentor travel can increase the incidence of EPM. There
Department ofare three FDA approved drugs for the treatment of
Veterinary Sciencehorses suspected to have EPM.
Another important infectious cause of neurologic disease is equine herpesvirus 1 (EHV-1),
which is addressed in this issue of the Equine
Lloyd’s—An international
Disease Quarterly by Dr. Peter Timoney. EHV-1
insurance market foris problematic in that it can affect several body
bloodstock and othersystems (respiratory, reproductive, and central
specialist insurance.
IN THIS ISSUE

nervous system). The neurologic form of EHV-1
infection is termed equine herpesvirus myeloencephalopathy (EHM) and is caused by damage toblood vessels supplying the central nervous system.
These vascular insults result in stroke-like injuries.
Clinical signs often include ascending paralysis
with urine dribbling, loss of tail and anal tone andpelvic limb weakness.
A diagnosis of EHM is made easier whenseveral horses on the same premise present withfever, followed by ataxia, urine dribbling and insome cases abortion. Furthermore, diagnosis canbe established by recognition of clinical signs in
combination with a positive virus detection test
(PCR or virus isolation) on a nasal swab and unclotted blood sample. Following confirmation ofa diagnosis of EHM, affected animals or test positive animals should be isolated, and the premises
quarantined; movement of horses off an affectedfacility increases the risk of spread of infection.
Herpesvirus can affect horses of all ages but israrely seen in yearlings. The virus initially replicates in the mucosa of the upper respiratory tract,
spreads to the lymphoreticular system, followed bydevelopment of a viremia and infection of othersites in the body. Although currently available vaccines do not reliably prevent infection, the development of viremia, or the establishment of latency,
vaccination remains important in preventing and/or reducing the incidence of respiratory infections
and abortions and is considered the best recommendation for owners to keep their horses healthy.
Other infectious neurologic diseases that need tobe considered include West Nile virus infection,
rabies, and tetanus, all of which should be a partof the annual vaccination schedule for horses.
CONTACT:
Stephen M. Reed, DVM, Dip ACVIM(859) 233-0371
Rood and Riddle Equine Hospital
Lexington, Kentucky

Equine Disease Quarterly Newsletter

5

Equine Hepatotoxins, continued from page 4.

species, but the best way to prevent poisoning is
to monitor pastures and remove mushrooms.
Certain medications (e.g., phenylbutazone, flunixin, acetaminophen, salicylates, antifungals, andmany others) can cause liver damage, especially ifadministered in high doses, for prolonged periodsof time, or to animals with pre-existing conditions. Accurate dosing and careful consideration of
medication risks versus benefits can help minimize
chances of adverse effects.

Many other substances can cause liver damage
and may be more common in different geographic
areas. Consultation with a clinical veterinary
toxicologist should be considered when toxicosis
is suspected.
CONTACT:
Megan C. Romano, DVM, DABVT
megan.romano@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

Department of Veterinary Science
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky 40546-0099
Address Service Requested

F U N D E D B Y U N D E R W R I T E R S AT L LOY D ' S , LO N D O N

JULY 2021
Volume 30, Number 3

Twenty Years’ Experience with West Nile Virus, 2001-2020

Until 1999, West Nile (WN) virus was unknown in the Western Hemisphere, muchless the USA. In August of that year, the virus
was identified in New York City and caused thedeaths of seven persons from viral encephalitis.
Coincidentally, the virus was also implicated in
the death of birds in New York’s Bronx Zoo andcrows in the precincts of the zoo.

513
102

Total = 765

Number of Cases

20

18
16

15

13

10

8

5

9
6 5

8

12
8

6

4
1

7
2 2

20
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Figure 1. Annual number of equine cases of WN virus infection in
Kentucky, 2000-2020.

Number of Cases

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Figure 2. Cumulative equine WN virus cases of infection by weekly
onset of illness in Kentucky, 2000-2020.

West Nile virus is a mosquito-transmitted arbovirus, member of the Japanese encephalitis virus
serocomplex, family Flaviviridae, known for many
years to be a highly adaptable virus, as evidenced
by its extensive distribution throughout the Old
World. As such, it was no surprise that WN virus
spread rapidly from its presumed point of introduction in New York. It initially extended southwards
along the eastern seaboard, while also migrating
westwards into the hinterland of the USA. With
the exception of Alaska and Hawaii, WN virus had
reached the remaining 48 states by 2004. The virus
was later confirmed in Alaska in 2018.
Kentucky reported its first cases of WN virus inbirds and horses in 2001 (Figure 1). Devastating
losses were recorded in crows and other membersof the corvid family, and eight cases were diagnosedin horses in counties in the north-central part of thestate. In 2002, the virus dramatically spread throughout much of Kentucky with the exception of theeastern part of the state. To date, 2002 was witness
to the greatest number of cases recorded in horses(513), humans (75), and birds in Kentucky. Case
numbers in horses (102) and humans (14) declined
significantly the following year. With the exceptionof minor surges in horse cases in 2006, 2012, 2013,2017, and 2018, the annual number of reported
cases of infection remained in single digits. With the
exception of 2006 and 2013, the same years also saw
corresponding minor surges in human cases (CDC,
ArboNET). Cases of WN virus infection have been
confirmed in horses every year since 2001 and, withthe exception of 2020, also in humans.
The seasonality of equine WN infections, basedon the weekly onset of illness, was consistent
with other arboviral encephalomyelitides (Figure2). Apropos of the 765 equine cases of infection
recorded in Kentucky since 2001, the onset ofvirus activity ranged from early June to mid-July,depending largely on the level of mosquito activ-

C O M M E N TA RY

ity in any particular year. The peak of infections
occurred approximately mid-September, and virus
activity ceased by mid-November.
A breakdown of the 20-year total of WN virus
infections in Kentucky revealed that the most common horse breeds/categories included American
Quarter horses (AQH), Tennessee Walking horses(TWH), Thoroughbreds, and pleasure horses, ofwhich AQH and TWH’s comprised almost 50%of the overall number. Females outnumbered males
57% to 43%. Ages of confirmed WN cases ranged
from three months to 39 years, with a median ofeight years. Of the 765 total cases, 541 (71%)
survived and 224 (29%) died or were euthanized.
The first equine vaccines against WN virusrelated disease received conditional licensure fromthe USDA in 2001. Even though vaccination iseffective in protecting against disease, the great
majority (86%) of WN cases recorded in Kentucky
had never been vaccinated or were only partially
vaccinated (10%). Only approximately 4% of cases
had current vaccination histories. While this is nottotally surprising, it is disappointing consideringthat WN virus is one of five core equine vaccinesstrongly recommended by the American Associa-

tion of Equine Practitioners. Of the 656 cases of
WN infection without prior vaccination history,
approximately 30% died or were euthanized.
Greater efforts are therefore needed to encourage
horse owners to take advantage of vaccination if
continued losses from WN virus infection are to
be reduced or even eliminated.
This review confirms that WN virus has become
endemic in Kentucky and will likely continue tocause horse and human disease. Its broad host andvector range, capability for transovarial transmission in mosquitoes, and horizontal transmission
in birds and a diversity of mammals has ensured
its perpetuation.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky
E.S. Rusty Ford
Rusty.ford@ky.gov(502) 782-5924
Equine Operations Consultant
Office State VeterinarianKY Department AgricultureFrankfort, KentuckyAs equine practitioners, we are charged with thehealth and welfare of our client’s horses, including dealing with infectious and non-infectious
Commentarycauses of neurologic disease. The veterinary industry
has rapidly changed in complexity, with a new
International
understanding of disease mechanisms, diagnostic
First Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 testing, and treatments. Many challenges remain
including how to make an accurate diagnosis, how
National
to establish neuroanatomic localization, and how
most effectively to treat affected horses. If a horse is
EquineHerpesvirus 1 .  .  .  .  .  .  .  . 3 suspected to have cervical vertebral stenotic myelopathy (wobbler syndrome), then cervical radiographs
Kentuckyare called for, often followed by a myelogram, CT
Common Equineor MRI scan to help pinpoint the site of compresHepatotoxins .  .  .  .  .  .  .  . 4sion.Horses with multifocal, asymmetric signs
West Nile Virus  .  .  .  .  .  . 5 affecting brain, brainstem and cranial nerves alongwith weakness and ataxia are likely to have equine
protozoal myeloencephalitis (EPM). Accurate
diagnosis of this condition requires an evaluationof antibodies in blood and CSF. Although EPM
is most commonly caused by Sarcocystis neurona,clinical signs in some horses are a result of Neosporahughesi infection. The exposure rate for N. hughesi
appears much lower than for S. neurona. Risk factors for developing EPM include age (< 5 and >13
years), time of year (summer and spring), previous
cases on a farm, and presence of woodland andopossums on the farm. EPM prevalence is less onfarms where wildlife have little or no access to feed
and if a creek or river is on the premises. Stressful
College of Agriculture, events like concurrent disease, general anesthesia,
Food and Environmentor travel can increase the incidence of EPM. There
Department ofare three FDA approved drugs for the treatment of
Veterinary Sciencehorses suspected to have EPM.
Another important infectious cause of neurologic disease is equine herpesvirus 1 (EHV-1),
which is addressed in this issue of the Equine
Lloyd’s—An international
Disease Quarterly by Dr. Peter Timoney. EHV-1
insurance market foris problematic in that it can affect several body
bloodstock and othersystems (respiratory, reproductive, and central
specialist insurance.
IN THIS ISSUE

nervous system). The neurologic form of EHV-1
infection is termed equine herpesvirus myeloencephalopathy (EHM) and is caused by damage toblood vessels supplying the central nervous system.
These vascular insults result in stroke-like injuries.
Clinical signs often include ascending paralysis
with urine dribbling, loss of tail and anal tone andpelvic limb weakness.
A diagnosis of EHM is made easier whenseveral horses on the same premise present withfever, followed by ataxia, urine dribbling and insome cases abortion. Furthermore, diagnosis canbe established by recognition of clinical signs in
combination with a positive virus detection test
(PCR or virus isolation) on a nasal swab and unclotted blood sample. Following confirmation ofa diagnosis of EHM, affected animals or test positive animals should be isolated, and the premises
quarantined; movement of horses off an affectedfacility increases the risk of spread of infection.
Herpesvirus can affect horses of all ages but israrely seen in yearlings. The virus initially replicates in the mucosa of the upper respiratory tract,
spreads to the lymphoreticular system, followed bydevelopment of a viremia and infection of othersites in the body. Although currently available vaccines do not reliably prevent infection, the development of viremia, or the establishment of latency,
vaccination remains important in preventing and/or reducing the incidence of respiratory infections
and abortions and is considered the best recommendation for owners to keep their horses healthy.
Other infectious neurologic diseases that need tobe considered include West Nile virus infection,
rabies, and tetanus, all of which should be a partof the annual vaccination schedule for horses.
CONTACT:
Stephen M. Reed, DVM, Dip ACVIM(859) 233-0371
Rood and Riddle Equine Hospital
Lexington, Kentucky