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

APRIL 2017
Volume 26, Number 2

C O M M E N TA RY

The Future of Parasite Control?
IN THIS ISSUE
Commentary
International
Fourth Quarter2016  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2National
Causes of Mortality .  . 3Parasite Control  .  .  .  .  . 3Kentucky
Nocardioform
Placentitis .  .  .  .  .  .  .  .  .  .  . 4Equine Cardiac
Disease .  .  .  .  .  .  .  .  .  .  .  .  .  . 5

College of Agriculture,
Food and Environment
Department of
Veterinary ScienceIn this issue, Dr. Gene Lyons provides a brief
review of the history and current status of anthelmintic treatment of important equine gastrointestinal parasites. No new anthelmintics with newer
modes of action have been introduced since theearly 1980s, and levels of anthelmintic resistanceare ever increasing in cyathostomin and Parascaris
spp. parasites. While resistance is slow to develop,
work by Dr. Lyons has clearly illustrated that once
it appears in a given parasite, it is there to stay.
Today, we can expect resistance to at least one
drug class to be present in every equine operation
across the world, and an overwhelming majority
will feature multi-drug resistance. With only threeclasses to choose between, we are running out oftreatment options. A pertinent question to ask
is how to tackle this emerging crisis and what toexpect in the future.
The first step is to acknowledge the extent of
the problem. Despite recommendations given
during the past couple of decades, a majority of
individuals in the industry continue to use oldfashioned parasite control programs based on
frequent treatments given year-round without
any consideration of treatment efficacy, parasites
present, and climatic conditions. If no diagnostic
testing is done, resistance will not be identified.
For the long term, we need new anthelmintic
drug classes with new modes of action. It is important to learn from the past however, and realize that no drug class is going to remain effective
indefinitely, and that reverting back to treatment
regimens of the past would be a complete mistake.
The pharmaceutical industry is not anticipating
developing any equine products in the foreseeable
future. Recent pharmaceutical trends are aimed at
combination deworming products, i.e. formulations where two or more dewormers targetingthe same parasites are combined into the same
product. Research in the sheep industry has also

highlighted the importance of reducing treatment
intensity to avoid development of multi-drugresistance. A recent project by the author highlighted the importance of high starting efficacyof the given combination. If combination treatment efficacy is markedly less than the desired 95
percent or above, resistance may develop quickly.
The author’s laboratory is also testing a bacterial
dewormer. Strains of naturally occurring Bacillus
thuringiensis produce crystal proteins capable ofkilling worm parasites. If successful, this could
become an anthelmintic product in the future.
Perhaps the most important element in future
parasite control programs is utilization of good
diagnostic tools. Fecal egg counts will remain acornerstone of control programs, but they have
limitations in not providing information about
larval stages and specific types (species) of parasites
present. Recent collaborations have led to several
new diagnostics, including species- and stage-specific serum ELISAs for important strongyle parasites,
and an ultrasonographic technique for determining
ascarid burdens in foals. One current project is making use of DNA-sequencing technologies to identify
all parasite species present in a horse. Most recently,
we have developed an automated smartphone-based
fecal egg-counting system, which allows easier,quicker, and more precise fecal egg counts to be
determined. Taking these diagnostic approaches
collectively, the goal is to enable veterinarians andtheir equine clients to make more informed decisions about parasite control. The road to effective
and sustainable parasite control is evidence-based,with veterinarians playing a central role.
Contact:
Martin K. Nielsen, DVM, PhD, DipEVPC
martin.nielsen@uky.edu(859) 218-1103
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, KY

2

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

Fourth Quarter 2016

T

Equine Disease Quarterly
Editors

Peter Timoney
Alan Loynachan
Cynthia Gaskill

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

he International Collating Centre, Newmarket, United Kingdom, and other sources
reported the following disease outbreaks.
Isolated cases of African horse sickness wererecorded in South Africa, initially in Gauteng
Province (October) and subsequently in the NorthWest Province (December), both recognized as
endemic areas for the disease.
Equine influenza was reported by the UK and
the USA. The UK confirmed three outbreaks ofthe disease, two involving isolated cases in fivemonth-old foals and the third in a group of several
unvaccinated horses. Outbreaks of influenza wererecorded in four states in the USA, where thedisease is considered endemic.
France, Germany, Ireland, Switzerland, andthe USA reported multiple outbreaks of strangles
during the period under review. The number ofconfirmed outbreaks included 12 in France, fivein Germany, an estimated seven in Ireland, two in
Switzerland, and 37 in the USA, where the diseaseis endemic. Many of the outbreaks involved single
cases.
Equine herpesvirus 1 (EHV-1) related diseases
were reported by France, Germany, Japan, the UK,
and the USA. Respiratory disease was confirmed
in France (four outbreaks), the UK (six cases ona premises on which several cases of neurologic
disease also occurred), and the USA (widespreadin various states).
Cases of EHV-1 abortion were diagnosed in
France (single cases on two premises), Germany(one case), Japan (single cases on several premises,
involving Thoroughbred or non-Thoroughbred
mares), and the UK (single cases on two premises).
EHV-1 related neurologic disease (myeloencephalopathy) was recorded in France (two outbreaks,
one of which involved nine cases out of a groupof 60 horses), Switzerland (a single case), the UK(two outbreaks, one involving an initial case andsubsequently several additional cases), and theUSA (two outbreaks, with one involving two cases
on a high desert ranch and the other, six cases at
an equestrian center).

Equine herpesvirus 4 respiratory disease wasrecorded in France (15 outbreaks, the majority
represented by single cases of infection) and Switzerland (one outbreak involving four horses). The
USA reported activity with equine herpesvirus 2
and/or 5 in a number of states, some associatedwith evidence of respiratory disease.
Equine infectious anemia was confirmed in
Canada (single case in Saskatchewan), and theUSA (single case in Utah). France and Switzerland reported cases of equine piroplasmosis.
Piroplasmosis was considered endemic in France;
Switzerland recorded only an isolated case of thedisease.
A single case of equine coital exanthema (equine
herpesvirus 3) was diagnosed in Kentucky, USA.
Several cases of nocardioform placentitis wererecorded in Kentucky, USA.
The USA reported outbreaks/individual casesof salmonellosis in a number of states, all of which
related to infection with serogroup C1 Salmonellae.
A limited number of outbreaks of clostridial
enteritis due to Clostridium perfringens Type A/β-2
toxin genotype, were confirmed in Kentucky, USA.
Several cases of proliferative enteropathy (Lawsonia
intracellularis) were recorded in Kentucky andMichigan, USA.
The fourth quarter of 2016 saw an additional
15 cases of Eastern equine encephalomyelitis confirmed in five states in the USA, nine of which werein Wisconsin. West Nile encephalitis was reportedby Spain (nine cases) and the USA (20 cases involving six states of which 11 were in Oklahoma). The
majority of cases in the USA were in unvaccinatedhorses.
The USA continues to record outbreaks ofrhodococcal disease in numerous states; a limited
number were reported in the period under review.
The fourth quarter of 2016 also saw recorded
cases/outbreaks of several other diseases: ehrlichiosis in Switzerland (one outbreak), Getah
virus infection in Japan (single case), and equine
encephalosis (single case in the Western Cape
Province of South Africa).

3

N AT I O N A L

Causes of Mortality in Aged Horses in Kentucky

Contact:
Ashton B. Miller, Graduate Research Assistant,in collaboration with Alan Loynachan, DVM, PhD andAmanda Adams, PhD
ashton.miller@uky.edu(859) 257-4757
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, KY

Parasite Control: An UpdateInternal parasites of horses have been recognized
for centuries. Until the early 1900s, methods
for the control of equine endoparasites lacked ascientific basis. For example, in the 1600s one

recommendation was to incise the horse’s palate
with the intent that the ingested blood would kill
any internal parasites. Beginning in the 1940s andextending to the 1980s, new classes of antiparasitic

Figure 1. Nocardioform placentitis cases seen at UKVDL from1991 to Feb 21, 2017, by foaling season.
400
350

328

300
250
200
144

23

6

17 10 15 16

44

2017

40

2015

50
12

2013

4

31

2007

30

2003

2001

1999

16

41

2011

87
48

27

1997

2

11 25

1995

0

11

32

1993

50

29

2009

94

100

2005

150

1991

poorly-managed parasitic infections can contributeto the formation of adhesions, leading to intestinal
obstruction, and tapeworm infection can leadto colic due to cecal impaction. Once an ownernotices signs of colic and digestive distress, timely
veterinary intervention can sometimes improve
the outcome for a horse, particularly if corrective
surgery is warranted by a specific diagnosis.
Death due to disease or dysfunction of the cardiovascular system may be somewhat unexpected.
However, after delving more deeply into necropsy
records, a not-so-surprising story emerged. Uterine
artery rupture was responsible for approximately
half of the cases where the main cause of death
was attributed to the cardiovascular system. This
statistic appears to be associated with the presenceof numerous breeding farms in Central Kentucky.
Increased risk of uterine artery rupture is an important issue for owners and veterinarians worldwide
to consider when breeding mares over fifteen yearsof age. Additionally, the potential high risk foruterine artery rupture in older mares may highlightthe option of embryo transfers to surrogate mares
to obtain offspring from highly valued aged mares.
As with any medical procedure however, embryotransfer and surrogacy are not without risk andmay be restricted by certain breed registries.
While the main causes of death identified in thispreliminary review for horses over the age of fifteenin Kentucky certainly highlight potential problem
areas for the medical management of older horses,
a more extensive review of past cases is needed to
fully establish significant trends from this study.

Cases

ver the last century, the place of the horse insociety has shifted from that of an absolutenecessity, primarily used for transportation and labor, to more of a pleasure animal. Today, horses aremost commonly companion animals, lesson horses,
breeding stock, and sporting competitors, with more
limited use for farm and ranch work. This change
in usage has resulted in an increasing geriatric horse
population, and accordingly, the need to better understand the complexities of geriatric horse health.
The University of Kentucky Veterinary Diagnostic Laboratory (UKVDL) plays an importantrole in its support of Kentucky’s horse industry.
Between June 1, 2010, and June 30, 2012, onehundred and thirteen horses aged fifteen years andolder were submitted for necropsy to UKVDL.
Review of these necropsy cases revealed that themain organ system contributing to the death of thisgroup of aged horses was the digestive system, followed rather closely by the cardiovascular system.
Specific diagnoses of the digestive system thatwere noted in this group of geriatric horses included but were not limited to: strangulating lipoma;small intestinal entrapment, devitalization, and/or
rupture; gastric rupture; large colon displacement,
torsion, impaction and/or rupture; and necrotizing
colitis of bacterial or unknown etiology.
Although prevention of these disorders is not
generally possible, certain steps can be taken by owners to improve the digestive health of their horses. A
consistent diet with sufficient roughage promotes ahealthy digestive system for horses of all ages. However, as horses age, their teeth can wear unevenly andcrack or break, preventing proper mastication andhindering the digestion of food. Therefore, proper
dental care is crucial for older horses, along withappropriate nutritional substitutions for horses thatcan no longer chew forage adequately.
Maintaining an appropriate deworming regimen for horses of all ages can also go a long way
to preventing digestive dysfunction. For example,

Foaling Season

Figure 2. Nocardioform placentitis cases seen at UKVDL by monthfor 2011 and 2017 foaling seasons.
120

108

2011
2017

100
76

80
Cases

O

57

60

39

40
14

20
0

1

2

Oct

Nov

23

Dec

13

10

10
Jan

Feb

1
Mar

Foaling Season

Apr

May

Jun

3

4

Figure 1. Nocardioform placentitis cases seen at UKVDL from1991 to Feb 21, 2017, by foaling season.
400
350

328

300

200
144

23

6

17 10 15 16

44

2017

40

2015

50
12

2013

4

31

2007

30

2003

2001

16

41

2011

87
48

27

1997

1995

2

11 25

1993

0

11

32

1991

50

29

2009

94

100

2005

150

1999

Cases

250

Foaling Season

Figure 2. Nocardioform placentitis cases seen at UKVDL by monthfor 2011 and 2017 foaling seasons.
120

108

2011
2017

100
76

Cases

80
57

60

39

40
14

20
0

1

2

Oct

Nov

23

Dec

13

10

10
Jan

Feb

1
Mar

Foaling Season

Apr

May

Jun

4

Figure 1. Nocardioform placentitis cases seen at UKVDL from1991 to Feb 21, 2017, by foaling season.
400
350

328

300

200
144

23

6

17 10 15 16

44

2017

40

2015

50
12

2013

4

31

2007

30

2003

2001

16

41

2011

87
48

27

1997

1995

2

11 25

1993

0

11

32

1991

50

29

2009

94

100

2005

150

1999

Cases

250

Foaling Season

Figure 2. Nocardioform placentitis cases seen at UKVDL by monthfor 2011 and 2017 foaling seasons.
120

108

2011
2017

100
76

Cases

80

six to eight weeks. This frequent deworming wasthought 1) not to provide time needed for Strongylus spp. to mature, 2) to help decrease potential
cyathostome egg deposition on pastures, and 3)
not to allow time for ascarids to mature.
High strongyle fecal egg counts indicate contamination of pastures and increased potential
for ingestion of infective larvae by grazing horses.
Thus, profiling the number of eggs per gram (EPG)
of feces has been used in updating deworming
schedules. Since Strongylus spp. are now rarely
encountered, a deworming schedule can be more
flexible. Unfortunately, there is no direct relationship between EPG values and cyathostome
numbers.
A suggested deworming program is as follows:• Establish a strongyle EPG profile for individual
horses rather than deworming all horses; a studyof 1,114 Thoroughbred mares showed that
one fecal sampling per horse was sufficient forestablishing a strongyle EPG profile.
• For strongyles, use ivermectin or moxidectinalone or in combination with praziquantel
twice a year—consider treating in the spring
and fall. While benzimidazoles and pyrantel
may be ineffective on cyathostomes, they may
be efficacious in treating other parasite species.
• Treat foals every eight weeks of age for ascarid
infection until they become yearlings; oxibendazole is currently considered the drug of choice
followed by fenbendazole.
• Control Strongyloides with ivermectin or oxibendazole and tapeworms with praziquantel orpyrantel pamoate/tartrate.
Contact:
E.T. Lyons, PhD
elyons1@uky.edu(859) 218-1115
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, KY

57

60

39

40
14

20
0

compounds were developed approximately every
10 years. Currently in the USA, only benzimidazoles (fenbendazole and oxibendazole), tetrahydropyrimidines (pyrantel pamoate and pyrantel
tartrate), and macrocyclic lactones (ivermectin andmoxidectin alone or combined with praziquantel)
are commercially available for parasite control inhorses.
The major endoparasites of horses include bots,large strongyles, small strongyles or cyathostomes,
ascarids, and tapeworms. Large strongyles (Strongylus spp.) are one of the most significant equineparasites. The larval stages can cause disease due tomigration in blood vessels and abdominal organs.
Drug resistance is not evident in the case of largestrongyles. Cyathostome larvae do not migrateparenterally like Strongylus spp., but encyst in themucosa and submucosa of the large intestine of
the horse. Intestinal disease can be induced bycyathostomes when large numbers of larvae excyst
from the lining of the large intestine, a condition
called “larval cyathostomiasis.” Resistance to fenbendazole, oxibendazole and pyrantel pamoate is
now common among cyathostomes. Also, both
ivermectin and moxidectin have become less effective against immature (L4) cyathostomes in thelumen of the large intestine; thus the life cycle isshortened. Heavy infections with adult ascarids(Parascaris spp.) can cause intestinal blockage
and rupture because of their bulk. These too havebecome resistant to ivermectin, moxidectin, andpyrantel pamoate. The final group of equine endoparasites, tapeworms (Anoplocephala spp.), canalso result in intestinal hypertrophy, blockage,intussusception, and rupture; they do not exhibit
drug resistance.
Parasite treatment schedules have been basedon the life cycle of the parasites since the early
1900s. In the mid-1960s, it was suggested thathorses should be dewormed for strongyles every

1

2

Oct

Nov

KENTUCKY

23

Dec

Jan

Feb

Nocardioform Placentitis from an Epidemiological View

13

10

10

1
Mar

Foaling Season

Apr

May

Jun

T

he outbreak of nocardioform placentitis in
Kentucky’s 2011 foal crop was concerning to
the equine industry. While not on as large a scale
as seen in 2011, we are seeing more cases of thedisease in the 2017 foal crop in Kentucky than in
the last several years (Figure 1).
Nocardioform placentitis was first identified
and characterized in the mid-1980s. Sequencing of
the causative agents led to the term “nocardioform”

due to the phylogenic relatedness of this large family of bacteria. The most common organisms havebeen identified as various Amycolatopsis and Streptomyces spp. and Crossiella equi. Outcomes fromnocardioform placentitis can range from abortion,delivery of weak but viable foals, or delivery ofnormal foals; all outcomes are dependent upon
the severity of the placentitis. In some cases, foals
are not viable and are euthanized. In 2011, due to5subsidies paid for placental submissions and examination, the response from the local equine industry
was exceptional and the UKVDL witnessed thelargest number of nocardioform placentitis cases
submitted on record. The good news was that 70
percent of the 2011 cases resulted in viable foals.
Concerns of increased incidence of nocardioform placentitis in the 2017 foal crop surfaced in
December 2016 with a local veterinarian indicating he was seeing an increase in cases. UKVDL
pathologists and epidemiologists noticed an increase in cases submitted to the lab in January 2017and alerted local practitioners and farm managers
through listserv and social media.
Typically, nocardioform cases are first noted
as early as October and run through May of any
given year. The majority of cases are diagnosed
from December through April, usually peaking in
mid-March (Figure 2). Through the third week ofFebruary 2017, UKVDL has confirmed 44 casesof nocardioform placentitis. Of these 44 cases, 31
have resulted in abortion, 12 in viable foals, andin one case a live but non-viable foal.
The means of transmission is not yet identified.
Nocardioform lesions are not similar to those ofother types of bacterial placentitis or septicemic
bacterial placentitis. Environmental factors arebeing investigated thoroughly and early analysis
indicates an increase in nocardioform placentitis
cases after a summer of hot, dry weather. Nocar-

dioform placentitis cases are almost always lower inyears associated with a high incidence of leptospiralabortions, which is correlated with weather that iswetter than normal. Analysis of farms affected withnocardioform placentitis indicates larger farms withmore pregnant mares and higher stocking densities
are at greater risk. Preliminary data indicate thatmares that spend more time in the barn are at riskof developing the disease; increased grazing times
appear protective. There is a statistical indicationthat pre-breeding treatments with NSAIDs or progesterone could be protective, but this needs further
study. Mares that are given post-breeding humanchorionic gonadotropin (hCG) are at significantly
lower risk, but this also requires further study.
Based on cases of nocardioform placentitis received by UKVDL from January 1, 2010, throughFebruary 21, 2017, there is little evidence that thedisease recurs in particular mares. One exception
is a mare that had a placenta submitted in 2011that was positive for nocardioform and a fetus
submitted in 2016 that also was diagnosed withthe disease. The likelihood of recurrence of thedisease in previously affected mares would appear
extremely low.
Contact:
Jackie Smith, PhD, MSc, Dipl AVES
jsmit8@uky.edu(859) 257-7559
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, KY

Equine Cardiac DiseaseEquine cardiac disease is an uncommon but potentially serious condition. Clinical signs range
from poor performance to sudden death. Causesof cardiac disease in horses include congenital
malformation, chronic valvular degeneration, cardiomyopathy, inflammatory or infectious disease,ruptured chordae tendineae, and cardiotoxins.
This article describes common cardiotoxins thathave been implicated in affecting horses in Central
Kentucky.
Ionophores (e.g. monensin and lasalocid) arecommon feed additives and supplements intended
for cattle, pigs, or chickens. Exposure occurs whenhorses have access to concentrated mineral premixes containing ionophores formulated for cattleor through a feed-mixing error. Acute ionophore
intoxication causes anorexia, muscle tremors, rapid
heart rate, and respiratory distress due to heart failure. Chronic exposure results in unthriftiness, poor
performance, exercise intolerance, rapid breathing,and sudden death from cardiac damage.

Blister beetles can be found in alfalfa hay, andare toxic to horses because they contain a highly
irritating substance called cantharidin. Small
amounts of cantharidin cause irritation to the gastrointestinal and urinary tracts. Moderate amounts
cause cardiac muscle damage, low calcium, andsynchronous diaphragmatic flutter (“thumps”).
Large amounts cause shock and death within
hours.
Taxus is a common cause of poisoning of horses
in Central Kentucky. Taxus, or yew, is a popular
evergreen ornamental shrub. Almost all parts ofthe plant, including the seeds, contain highly
toxic compounds called taxines. In the winter, theconcentration of taxines is at its highest within
the plant. Even a small amount of plant material
can cause rapid heart failure. Because taxines act
so quickly, horses ingesting yew are often founddead without signs. When present, signs include
weakness, incoordination, slow heart rate, anddifficulty breathing.

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

White snakeroot is a perennial woodlands plantcommon throughout the Eastern United States.
White snakeroot contains a mixture of compounds
called “tremetol.” Intoxication is sporadic because
the concentration of tremetol in the plant varies
depending on location and prevailing growing
conditions. Tremetol causes congestive heart failureand cardiac degeneration in horses. Tremetol canpass into the milk, poisoning nursing foals.
Rhododendrons, azaleas, laurels, mountainpieris, and fetterbush all contain grayanotoxins.
Grayanotoxins cause either slow or rapid heartrate, abnormal rhythm, weak pulse, and cardiac
arrest. These plants are particularly attractive in
winter because their leaves remain green.
Milkweeds, or butterfly weeds, are wildflowers
as well as cultivated ornamentals. Some milkweeds
contain cardiotoxins called “cardenolides.” Signs
can begin within hours of plant ingestion andinclude slow or rapid heart rate, low blood pressure, and arrhythmias. Fresh cardiotoxic plants
are generally unpalatable. They are more edible asclippings or baled with hay, but are no less toxic
than fresh material.

Venomous snakes native to North America
include the pit vipers—rattlesnakes, water moccasins, and copperheads. In Central Kentucky,
timber rattlesnakes and copperheads are themost common. Most pit-viper venoms comprise
dozens of different components, some of them as
yet unidentified. Snakebites in horses most often
occur on or near the muzzle and can result insevere swelling and edema. If the nasal passages
become so swollen that labored breathing ensues,a tracheostomy may be necessary. Bleeding, tissue
necrosis, and secondary bacterial infection aroundthe bite wound are common sequelae. Some venoms contain cardiotoxins that damage the heart.
Antivenins are available but must be administeredin a timely manner, as they cannot reverse tissue
damage that has already occurred.
Many other substances can be cardiotoxic, including a number of additional plants, medications(e.g. xylazine and theophylline), and illicit drugs(e.g. amphetamines and cocaine).
Contact:
Megan Romano, DVM
Veterinary toxicology resident
Megan.romano@uky.edu(859) 257-6777
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, KY