Equine Disease Quarterly Newsletter

5vitamin E supplementation, please refer to a recent
issue of the UC Davis Horse Report: https://ceh.
vetmed.ucdavis.edu/sites/g/files/dgvnsk4536/files/
inline-files/Horse_Report_Fall_2018_web.pdf.
Baseline blood vitamin E concentrations should
always be assessed before initiating any vitamin
E supplementation. Owners should consult
with their veterinarians to determine if vitamin

E supplementation is required and identify thebest supplementation regimen for their particularhorse.
CONTACT:
Carrie Finno, DVM, PhD, DACVIM (Large Animal)
cjfinno@ucdavis.edu
530-752-2739
UC Davis School of Veterinary Medicine
Davis, California

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

Re-feeding the Starved HorseF

inding yourself in the position of providing
care to a starved horse can be an emotionalsituation for any horse enthusiast. The desire to
do everything possible to return the horse to full
health, including providing ample nutrition, canbe the initial impulse. Sadly, the desire to feed thehorse well can have catastrophic consequences resulting in a re-feeding syndrome that may result in
the need for euthanasia. While it may be tempting
to provide unlimited access to feed, when it comesto feeding starved horses, less truly should be therule of thumb.
Horses rely on body stores of inert carbohydrate
and fat to fuel the large number of metabolic
processes within the body. These stores are constantly replenished through the diet. In a horsethat is starved, these stores become depleted andso instead, protein is utilized for energy. All proteinin the body is actively contributing to importantfunctions and is not stored for the purpose ofproviding energy. In this scenario, the body is not
picky about what source of protein gets used forenergy. Therefore, as protein is burned as a fuelsource, skeletal muscle and vital organs become
negatively impacted.
When a starved horse is “re-fed” and provided
carbohydrates, in particular glucose, blood insulin increases. This helps move glucose from thecirculation into cells and with it electrolytes. Thiscan result in inadequate levels of key electrolytes
such as phosphorus, potassium and magnesiumin the circulation as well as leaving red blood cells
without adequate energy. These red blood cells arethen unable to adequately release oxygen to various
tissues resulting in heart, kidney and respiratoryorgan failure and ultimately death.
Research studies have shown that a greater
success rate is achieved when starved horses are
rehabilitated using forages containing low non-structural carbohydrate (NSC) as this limits theinsulin response. If using grass hays, they should betested for NSC content and ideally have an NSC
content of less than 10 percent. If only untested
grass hay is available, feeding alfalfa may be a better
choice as alfalfa has a low NSC content and also
tends to provide good amounts of magnesium andphosphorus.
Very small amounts of feed should be fed thatprovide no more than about 50 percent of thehorse’s calculated daily digestible energy (DE)requirement. Different research studies have useddifferent feeding protocols. One fed alfalfa at 50
percent of the calculated daily DE requirement for
the first 3 days of re-feeding and then increased
the amount to 75 percent for days 4 and 5 before
increasing to a full 100 percent on day 6. Anotherstudy fed frequent handfuls of grass hay for the firstday and then provided netted hay that was hungoutside the stalls so that the horses had to eat the
hay through the bars. These researchers introduced
0.5 pounds of complete feed and increased thisby the same amount every 3 days until they werebeing fed no more than 3 lbs at any feeding.
Re-feeding syndrome can develop as quickly
as the first day of re-feeding or may not become
apparent for 3 to 4 weeks. The keys to successful
rehabilitation lie in starting off with very small
meals that provide limited calories and utilizing
forages and feeds with an NSC content at or below
10 percent. Sticking to these guidelines despite
the natural desire to want to lavish the horse withfood will provide the greatest chance of success innursing the starved horse back to health.
CONTACT:
Clair Thunes, PhD
916-248-8987
clair@summit-equine.com
Summit Equine Nutrition LLC
Gilbert, Arizona

JANUARY 2021
Volume 30, Number 1

C O M M E N TA RY
IN THIS ISSUECOMMENTARY: continued from the front pageare not useful in assessing the status of many nutrients. For some, homeostatic mechanisms maintainrelatively consistent blood levels, even in the face ofsignificant dietary deficiencies. For nutrients suchas selenium, indicators of functional status may be
more useful than serum selenium concentrations
alone. Even for nutrients whose levels fluctuate in
the blood with dietary intake, a blood level is only
useful if it can be interpreted in relation to horse
health. Laboratories should have established orreferenced normal ranges to evaluate blood mineral or vitamin concentrations. Ideally, reference
ranges should be developed from normal healthy
horses of different physiological states, as age andphysiological function (gestating, exercising, growing) affect nutrient needs. Unfortunately specificreference ranges for blood constituents in equinesare very limited.

Horses are often described as fragile, but they
are also extremely resilient and adaptable. Horses
evolved to deal with times of food abundanceas well as food scarcity. Short periods of foodscarcity may result in nutritional deficiency; foodabundance allows for restoration of body reserves.
Clinical diseases only typically will develop asa result of chronic deficiencies. As both articles
in this issue point out, overzealous feeding andsupplementation can have negative consequences.
For this reason, dietary changes, even those aimed
at correction of nutritional deficiencies, should bemade gradually. Perhaps, optimal horse feeding ismore like the tortoise and less like the hare.
CONTACT:
Laurie Lawrence, PhD
llawrenc@email.uky.edu
859-257-7509
Department of Animal and Food Sciences
University of Kentucky
Lexington, KentuckyProper nutrition is key to producing and maintaining horses of all types, while poor nutrition
Commentary
or feeding management can increase the risk ofvarious health disorders. In this issue, Dr. ClairInternational
Thunes focuses on refeeding the starved horse, andThird Quarter2020  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 Dr. Carrie Finno addresses vitamin E deficiency.
Both articles highlight consequences of inadequate
Prepubic Tendon
Rupture .  .  .  .  .  .  .  .  .  .  .  .  . 3 or imbalanced nutrition.
Nutrient deficiencies may be primary or secondary. Primary deficiencies result when the diet
National
contains inadequate amounts of one or more nutriVitamin E
Deficiency .  .  .  .  .  .  .  .  .  .  . 4 ents. Starvation can occur when feed resources are
scarce, producing a deficiency in calories, protein,Re-feeding the
Starved Horse .  .  .  .  .  .  . 5 and nutrients. Primary deficiencies in specific nutrients, such as vitamin E, occur with improperly
balanced diets. Secondary deficiencies occur when
the diet is nutritionally adequate, but some otherfactor affects nutrient intake or absorption. For
example, starvation can occur if a horse is unable
to eat due to a mouth injury, even though feed isavailable. Secondary deficiencies may be causedby dietary substances or medications that interferewith the absorption of a specific nutrient. Excessive
concentrations of dietary zinc inhibit copper absorption and lead to copper deficiency in growing
horses despite adequate dietary copper.
From a nutritionist’s perspective, identificationof dietary deficiencies requires a diet evaluation.
This involves determining the amount and comCollege of Agriculture, position of the feeds provided. Commercial feed
Food and Environment laboratories offer affordable and rapid analysis
Department offor many important nutrients including protein,
Veterinary Sciencecalcium, phosphorus and several trace minerals.
In contrast, selenium, iodine, and most vitaminsrequire a specialized laboratory. It is important toremember that most nutritional deficiencies manifest after months to years of dietary inadequacy.
Lloyd’s—An international
insurance market for
Therefore analysis of the current diet may not
bloodstock and othernecessarily reflect a past diet.
specialist insurance.

MATT BARTON

Due to variation in nutrient pools within
the body and stability of various minerals andvitamins, laboratory submission of whole blood,
serum, or liver may be required. Prior to sample
collection, the laboratory should be consulted toconfirm the type of sample needed and the optimal
conditions for shipping samples to the laboratory.
Dr. Finno indicates that baseline concentrationsof circulating vitamin E may indicate the need forsupplementation. However, blood concentrations
continued on the back page2

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

Third Quarter 2020

T

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

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
Thailand and Malaysia recorded outbreaks of
African horse sickness (AHS). Thailand reported
outbreaks in August (one case in a horse) and
September (two cases in captive Chapman’s zebras). Malaysia confirmed its first ever incursionof AHS in August; five horses on a single premises.
Affected equids in the outbreaks in both countries
were euthanized.
Belgium, France, Germany, Italy, Sweden, andthe USA confirmed outbreaks of equine influenza.
These ranged from one (Belgium, France and
Italy), three (Sweden), four (Germany), to at leastnine in the USA, where the disease is endemic.
Strangles is considered endemic in many countries with outbreaks reported from Belgium (two),
Canada (one), France (nine), the Netherlands (12,one involving 15 cases), Switzerland (eight), andthe USA (41 outbreaks in 17 states, the majority
with multiple cases).
Equine herpesvirus 1 (EHV-1) related diseases
are endemic in most countries. Cases were confirmed in France, Japan, Republic of South Africa(RSA), Sweden, Switzerland, the UK, and theUSA. Single outbreaks of respiratory disease wererecorded in France, RSA, and the UK. One caseof EHV-1 abortion was confirmed in Japan in an
unvaccinated mare. EHV-1 neurologic disease
was reported by Sweden (single case), Switzerland(three outbreaks), and the USA (seven outbreaks
involving five states, with two outbreaks in California and Maine); the majority involved single cases.
Equine herpesvirus 4 (EHV-4) respiratory disease was recorded by France (20 outbreaks, mostly
single cases), Japan (one outbreak involving eightunvaccinated horses) and the Netherlands (fiveoutbreaks, one involving seven 4-5 month old
foals). Switzerland reported an outbreak of EHV-4
neurologic disease.
Belgium and the USA confirmed cases of equine
herpesvirus 2 and/or 5. Infection with EHV-2 wasdiagnosed in a 2-month-old foal in Belgium, andnumerous infections by either virus were diagnosed
in several states in the USA, some associated withrespiratory disease.

A case of adenovirus infection was reported ina foal in Ireland.
The USA confirmed four outbreaks of equine
infectious anemia, three in Texas, one involving
two cases, and one in Georgia. Three outbreaks
involved single cases.
Equine piroplasmosis was recorded in Finland(one case), RSA (disease is endemic) and Switzerland (one outbreak).
Denmark reported the isolation of Taylorellaequigenitalis, the cause of contagious equine metritis, from three stallions.
Equine coital exanthema (equine herpesvirus
3) was diagnosed in Argentina (two outbreaks
involving 29 Thoroughbreds) and the USA (onecase).
Belgium confirmed single cases of leptospiralabortion on two premises. A case of Leptospiraassociated recurrent uveitis was diagnosed in astallion by France.
Salmonellosis was reported by Switzerland (twooutbreaks) and the USA (10 cases, two involving
serogroup C1, five serogroup D1, and three weren’t
serogrouped).
France confirmed 19 outbreaks of rotavirus
diarrhea in foals, the majority were single cases. A
total of 17 cases were diagnosed by the USA, themajority in 60- to 90-day-old foals in Kentucky
involving G3 and/or G14 genotypes.
One case of proliferative enteropathy caused by
Lawsonia intracellularis was reported by the USA.
Canada (four outbreaks, all single cases) and theUSA (17 outbreaks in 10 states, one involving 10
cases) confirmed outbreaks of equine neorickettsiosis (Potomac Horse Fever).
Eastern equine encephalomyelitis was reported
by Canada (two outbreaks, each involving single
cases) and the USA (104 cases in 11 states), withhighest numbers in Michigan (33), Wisconsin(20), and Florida (13).
West Nile encephalitis was recorded by Canada(one case), France (three outbreaks, one case each),Germany (eight outbreaks), Hungary (one outbreak), Italy (nine outbreaks), Portugal (one case),
Spain (13 outbreaks, three were single cases), andthe USA (27 cases in seven states, four on one
premises).

A case of rabies was confirmed in a Warmblood
horse in Maryland, USA.
Switzerland confirmed two outbreaks of Borna
disease, and one outbreak of anaplasmosis.
Vesicular stomatitis continued to spread in the
USA in the third quarter of 2020, extending toArkansas, Missouri and Oklahoma, in addition
to five previously reported states. A total of 198
equine outbreaks were recorded, all associated with
the Indiana serotype.
Rhodococcus equi related diseases were confirmedby the USA.

3

N AT I O N A L

Consequences of Vitamin E Deficiency

Vitamin E is an essential nutrient for horses.
This antioxidant helps maintain normal neurological function by limiting the damage causedby oxidative stress and free radicals. The best sourceof vitamin E is fresh green grass. Horses that graze
on lush green pastures often have adequate access to vitamin E. However, many stabled horses
are not maintained on pasture. Vitamin E levels
decrease and eventually are lost as soon as grassis harvested, so even the highest-quality hay will
not meet vitamin E requirements. Some horses
maintained on diets deficient in vitamin E canexperience significant health consequences.
Vitamin E helps a horse’s muscles and nerves
function properly. A dietary deficiency can lead tothree specific diseases: (1) equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy(eNAD/EDM), (2) equine motor neuron disease(EMND) and (3) vitamin E deficient myopathy(VEM). These diseases are typically diagnosed
based on clinical signs, exclusion of other disorders,
and low concentrations of vitamin E in the blood.
Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy occurs in young
animals and has a genetic predisposition. Affectedhorses may stand with forelimbs too far apart (ortoo close together), have difficulty navigating curbs
or hills, or lack coordination while walking andmaking tight turns. Signs of the disease can vary,some horses show mild performance issues, whileothers are severely debilitated. Although the exact
cause of the degeneration is unknown, a specificinteraction between genetics and nutrition during
the first few years of life is required for this disease
to manifest.
Researchers in the Finno Laboratory are working to develop a genetic test for eNAD/EDM.
Until one is available, the recommendation is toprovide vitamin E supplementation to horses that
do not have regular access to pasture, especiallypregnant mares and newborn foals. This may noteliminate the disease, but it appears that less severe
neurological signs may develop if foals receive
supplementation during the early stages of life.

Prepubic Tendon RuptureT

he prepubic tendon extends from the brimof the pelvis and joins with the abdominal
muscles to support the abdomen and abdominal
viscera. Mares can rupture (tear) the prepubic
tendon, either partially or fully, and the associatedmuscles of the abdominal wall. Prepubic tendon
rupture is an uncommon but serious condition inlate pregnancy that may have a poor prognosis andcan result in death of the mare and fetus.
The exact cause of prepubic tendon rupture
is not known, however, the condition is morecommon in older mares that have had multiple
pregnancies, draft breeds, mares carrying twins,
and mares with placental abnormalities such ashydrops (hydroallantois or hydroamnion).
Mares with prepubic tendon ruptures exhibit
signs of colic-like pain, elevated heart and respiratory rates, and reluctance to move or lie down.
Changes in the shape of the ventral abdomen (underbelly) may be first noted, followed by a rapidly
progressive swelling (edema) that can extend fromthe udder towards the chest. The udder may beswollen and teats may point toward the mare’s headinstead of downwards, and blood may drip fromthe teats. Touching the ventral abdomen is often
resented. Some mares will adopt a ‘sawhorse’ stancewith a tilted pelvis and elevation of the tailhead.
Other mares may die after a short illness. Diagnosis
of prepubic tendon rupture is difficult to confirm
and is usually based on characteristic clinical signs.
The choice of therapy for mares with prepubic
tendon rupture varies. It will depend on the extent
of the rupture, ability to control the mare’s pain,
and stage of gestation. The relative value of themare and foal may also be considered. Complete
rupture of the prepubic tendon has a poor prognosis for the mare because the tendon cannot besurgically repaired.
Conservative therapy will usually involve restricting the mare to stall rest, carefully applying‘belly bandages’ to support the ventral abdomen,

4

and alleviation of pain using a variety of drugs.
Progestins may be given to keep the uterus in aquiet (not contracting) state. Close monitoringof the fetus to detect fetal stress is required withfrequent ultrasound examinations via the mare’s
abdomen to monitor fetal heart rate and activity.
Stage of gestation is an important factor whentherapy options are being considered. If the mareis close to term (330 days of gestation or later),induction of labor or a caesarean section may beconsidered. If the mare is induced, then foaling
must be assisted as she has limited or no ability tocontract abdominal muscles during active labor.
If the foal is successfully delivered, it is consideredat high risk of developing problems such as neonatal sepsis. Colostrum supplementation may beneeded, and the foal may not be able to suckle themare due to severe udder swelling.
For mares that rupture the prepubic tendon
before 330 days of gestation and in which pain canbe managed, a decision may be made to support
the mare so the fetus can reach 330 days of gestation or longer. The last part of pregnancy is very
important in determining viability of the foal, as
most of the fetal maturation that ensures the foal
is ready for life outside the uterus happens in thelast 10 days of gestation. For mares in which pain
cannot be well managed, euthanasia should beconsidered.
Mares with prepubic tendon rupture thatsurvive foaling or caesarean section should not
be bred again. Some mares that survive foaling
may subsequently need to be euthanized due tointractable pain.
CONTACT:
Erica Gee, BVSc, PhD, DipACT
e.k.gee@massey.ac.nz+6463505328
School of Veterinary Science
Massey University
Palmerston North, New Zealand

Equine motor neuron disease typically occurs
in older horses that have been vitamin E deficientfor more than 18 months. The disease affects lower
motor neurons, which are nerves that supply the
direct neurological input into all muscles. In theirabsence, the associated muscles atrophy, resulting
in the clinical signs of weakness and weight loss
characteristic of this disease. Affected horses may
carry their heads low and lie down for longer
periods. Research from Cornell University has
shown that approximately 40% of horses affectedby EMND improve with vitamin E supplementation, 40% stabilize but remain disfigured, and 20%
progress in disease severity.
Vitamin E deficient myopathy is typicallyfound in horses with a shorter duration of vitamin E deficiency. Affected horses exhibit muscle
weakness, low muscle vitamin E concentrations
and mitochondrial alterations (i.e. changes to the“power house” energy storage unit of the cell) inskeletal muscle but show no evidence of neurologic
impairment. With proper supplementation, affected animals are generally able to recover within
three months.
These diseases are currently the only conditions
definitively associated with vitamin E deficiency.
At this time, nothing is known about vitamin E
metabolism in horses, the appropriate dosage, or
its actual efficacy in preventing or treating otherneurological conditions. In humans, the same
enzymes that metabolize vitamin E also metabolize
approximately 50 percent of therapeutic drugs,
so supplementation with vitamin E could potentially alter the effects of other drugs if a horse ison multiple therapies. Therefore, while vitamin
E supplementation may not necessarily be harmful with respect to other neurologic diseases, it isunlikely to be beneficial.
Since there are no effective treatments for mostdiseases caused by vitamin E deficiency, prevention
is key. If horses are not able to access fresh pasturesto graze, vitamin E must be supplemented in theirdiets. However, not all vitamin E supplements
are created equally. For detailed information on

Abnormal stance of a horse with equine neuroaxonal dystrophy/equine
degenerative myeloencephalopathy (eNAD/EDM) from vitamin E
deficiency.
CARRIE FINNO

continued on page 5

2

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

Third Quarter 2020

T

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

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
Thailand and Malaysia recorded outbreaks of
African horse sickness (AHS). Thailand reported
outbreaks in August (one case in a horse) and
September (two cases in captive Chapman’s zebras). Malaysia confirmed its first ever incursionof AHS in August; five horses on a single premises.
Affected equids in the outbreaks in both countries
were euthanized.
Belgium, France, Germany, Italy, Sweden, andthe USA confirmed outbreaks of equine influenza.
These ranged from one (Belgium, France and
Italy), three (Sweden), four (Germany), to at leastnine in the USA, where the disease is endemic.
Strangles is considered endemic in many countries with outbreaks reported from Belgium (two),
Canada (one), France (nine), the Netherlands (12,one involving 15 cases), Switzerland (eight), andthe USA (41 outbreaks in 17 states, the majority
with multiple cases).
Equine herpesvirus 1 (EHV-1) related diseases
are endemic in most countries. Cases were confirmed in France, Japan, Republic of South Africa(RSA), Sweden, Switzerland, the UK, and theUSA. Single outbreaks of respiratory disease wererecorded in France, RSA, and the UK. One caseof EHV-1 abortion was confirmed in Japan in an
unvaccinated mare. EHV-1 neurologic disease
was reported by Sweden (single case), Switzerland(three outbreaks), and the USA (seven outbreaks
involving five states, with two outbreaks in California and Maine); the majority involved single cases.
Equine herpesvirus 4 (EHV-4) respiratory disease was recorded by France (20 outbreaks, mostly
single cases), Japan (one outbreak involving eightunvaccinated horses) and the Netherlands (fiveoutbreaks, one involving seven 4-5 month old
foals). Switzerland reported an outbreak of EHV-4
neurologic disease.
Belgium and the USA confirmed cases of equine
herpesvirus 2 and/or 5. Infection with EHV-2 wasdiagnosed in a 2-month-old foal in Belgium, andnumerous infections by either virus were diagnosed
in several states in the USA, some associated withrespiratory disease.

A case of adenovirus infection was reported ina foal in Ireland.
The USA confirmed four outbreaks of equine
infectious anemia, three in Texas, one involving
two cases, and one in Georgia. Three outbreaks
involved single cases.
Equine piroplasmosis was recorded in Finland(one case), RSA (disease is endemic) and Switzerland (one outbreak).
Denmark reported the isolation of Taylorellaequigenitalis, the cause of contagious equine metritis, from three stallions.
Equine coital exanthema (equine herpesvirus
3) was diagnosed in Argentina (two outbreaks
involving 29 Thoroughbreds) and the USA (onecase).
Belgium confirmed single cases of leptospiralabortion on two premises. A case of Leptospiraassociated recurrent uveitis was diagnosed in astallion by France.
Salmonellosis was reported by Switzerland (twooutbreaks) and the USA (10 cases, two involving
serogroup C1, five serogroup D1, and three weren’t
serogrouped).
France confirmed 19 outbreaks of rotavirus
diarrhea in foals, the majority were single cases. A
total of 17 cases were diagnosed by the USA, themajority in 60- to 90-day-old foals in Kentucky
involving G3 and/or G14 genotypes.
One case of proliferative enteropathy caused by
Lawsonia intracellularis was reported by the USA.
Canada (four outbreaks, all single cases) and theUSA (17 outbreaks in 10 states, one involving 10
cases) confirmed outbreaks of equine neorickettsiosis (Potomac Horse Fever).
Eastern equine encephalomyelitis was reported
by Canada (two outbreaks, each involving single
cases) and the USA (104 cases in 11 states), withhighest numbers in Michigan (33), Wisconsin(20), and Florida (13).
West Nile encephalitis was recorded by Canada(one case), France (three outbreaks, one case each),Germany (eight outbreaks), Hungary (one outbreak), Italy (nine outbreaks), Portugal (one case),
Spain (13 outbreaks, three were single cases), andthe USA (27 cases in seven states, four on one
premises).

A case of rabies was confirmed in a Warmblood
horse in Maryland, USA.
Switzerland confirmed two outbreaks of Borna
disease, and one outbreak of anaplasmosis.
Vesicular stomatitis continued to spread in the
USA in the third quarter of 2020, extending toArkansas, Missouri and Oklahoma, in addition
to five previously reported states. A total of 198
equine outbreaks were recorded, all associated with
the Indiana serotype.
Rhodococcus equi related diseases were confirmedby the USA.

3

N AT I O N A L

Consequences of Vitamin E Deficiency

Vitamin E is an essential nutrient for horses.
This antioxidant helps maintain normal neurological function by limiting the damage causedby oxidative stress and free radicals. The best sourceof vitamin E is fresh green grass. Horses that graze
on lush green pastures often have adequate access to vitamin E. However, many stabled horses
are not maintained on pasture. Vitamin E levels
decrease and eventually are lost as soon as grassis harvested, so even the highest-quality hay will
not meet vitamin E requirements. Some horses
maintained on diets deficient in vitamin E canexperience significant health consequences.
Vitamin E helps a horse’s muscles and nerves
function properly. A dietary deficiency can lead tothree specific diseases: (1) equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy(eNAD/EDM), (2) equine motor neuron disease(EMND) and (3) vitamin E deficient myopathy(VEM). These diseases are typically diagnosed
based on clinical signs, exclusion of other disorders,
and low concentrations of vitamin E in the blood.
Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy occurs in young
animals and has a genetic predisposition. Affectedhorses may stand with forelimbs too far apart (ortoo close together), have difficulty navigating curbs
or hills, or lack coordination while walking andmaking tight turns. Signs of the disease can vary,some horses show mild performance issues, whileothers are severely debilitated. Although the exact
cause of the degeneration is unknown, a specificinteraction between genetics and nutrition during
the first few years of life is required for this disease
to manifest.
Researchers in the Finno Laboratory are working to develop a genetic test for eNAD/EDM.
Until one is available, the recommendation is toprovide vitamin E supplementation to horses that
do not have regular access to pasture, especiallypregnant mares and newborn foals. This may noteliminate the disease, but it appears that less severe
neurological signs may develop if foals receive
supplementation during the early stages of life.

Prepubic Tendon RuptureT

he prepubic tendon extends from the brimof the pelvis and joins with the abdominal
muscles to support the abdomen and abdominal
viscera. Mares can rupture (tear) the prepubic
tendon, either partially or fully, and the associatedmuscles of the abdominal wall. Prepubic tendon
rupture is an uncommon but serious condition inlate pregnancy that may have a poor prognosis andcan result in death of the mare and fetus.
The exact cause of prepubic tendon rupture
is not known, however, the condition is morecommon in older mares that have had multiple
pregnancies, draft breeds, mares carrying twins,
and mares with placental abnormalities such ashydrops (hydroallantois or hydroamnion).
Mares with prepubic tendon ruptures exhibit
signs of colic-like pain, elevated heart and respiratory rates, and reluctance to move or lie down.
Changes in the shape of the ventral abdomen (underbelly) may be first noted, followed by a rapidly
progressive swelling (edema) that can extend fromthe udder towards the chest. The udder may beswollen and teats may point toward the mare’s headinstead of downwards, and blood may drip fromthe teats. Touching the ventral abdomen is often
resented. Some mares will adopt a ‘sawhorse’ stancewith a tilted pelvis and elevation of the tailhead.
Other mares may die after a short illness. Diagnosis
of prepubic tendon rupture is difficult to confirm
and is usually based on characteristic clinical signs.
The choice of therapy for mares with prepubic
tendon rupture varies. It will depend on the extent
of the rupture, ability to control the mare’s pain,
and stage of gestation. The relative value of themare and foal may also be considered. Complete
rupture of the prepubic tendon has a poor prognosis for the mare because the tendon cannot besurgically repaired.
Conservative therapy will usually involve restricting the mare to stall rest, carefully applying‘belly bandages’ to support the ventral abdomen,

4

and alleviation of pain using a variety of drugs.
Progestins may be given to keep the uterus in aquiet (not contracting) state. Close monitoringof the fetus to detect fetal stress is required withfrequent ultrasound examinations via the mare’s
abdomen to monitor fetal heart rate and activity.
Stage of gestation is an important factor whentherapy options are being considered. If the mareis close to term (330 days of gestation or later),induction of labor or a caesarean section may beconsidered. If the mare is induced, then foaling
must be assisted as she has limited or no ability tocontract abdominal muscles during active labor.
If the foal is successfully delivered, it is consideredat high risk of developing problems such as neonatal sepsis. Colostrum supplementation may beneeded, and the foal may not be able to suckle themare due to severe udder swelling.
For mares that rupture the prepubic tendon
before 330 days of gestation and in which pain canbe managed, a decision may be made to support
the mare so the fetus can reach 330 days of gestation or longer. The last part of pregnancy is very
important in determining viability of the foal, as
most of the fetal maturation that ensures the foal
is ready for life outside the uterus happens in thelast 10 days of gestation. For mares in which pain
cannot be well managed, euthanasia should beconsidered.
Mares with prepubic tendon rupture thatsurvive foaling or caesarean section should not
be bred again. Some mares that survive foaling
may subsequently need to be euthanized due tointractable pain.
CONTACT:
Erica Gee, BVSc, PhD, DipACT
e.k.gee@massey.ac.nz+6463505328
School of Veterinary Science
Massey University
Palmerston North, New Zealand

Equine motor neuron disease typically occurs
in older horses that have been vitamin E deficientfor more than 18 months. The disease affects lower
motor neurons, which are nerves that supply the
direct neurological input into all muscles. In theirabsence, the associated muscles atrophy, resulting
in the clinical signs of weakness and weight loss
characteristic of this disease. Affected horses may
carry their heads low and lie down for longer
periods. Research from Cornell University has
shown that approximately 40% of horses affectedby EMND improve with vitamin E supplementation, 40% stabilize but remain disfigured, and 20%
progress in disease severity.
Vitamin E deficient myopathy is typicallyfound in horses with a shorter duration of vitamin E deficiency. Affected horses exhibit muscle
weakness, low muscle vitamin E concentrations
and mitochondrial alterations (i.e. changes to the“power house” energy storage unit of the cell) inskeletal muscle but show no evidence of neurologic
impairment. With proper supplementation, affected animals are generally able to recover within
three months.
These diseases are currently the only conditions
definitively associated with vitamin E deficiency.
At this time, nothing is known about vitamin E
metabolism in horses, the appropriate dosage, or
its actual efficacy in preventing or treating otherneurological conditions. In humans, the same
enzymes that metabolize vitamin E also metabolize
approximately 50 percent of therapeutic drugs,
so supplementation with vitamin E could potentially alter the effects of other drugs if a horse ison multiple therapies. Therefore, while vitamin
E supplementation may not necessarily be harmful with respect to other neurologic diseases, it isunlikely to be beneficial.
Since there are no effective treatments for mostdiseases caused by vitamin E deficiency, prevention
is key. If horses are not able to access fresh pasturesto graze, vitamin E must be supplemented in theirdiets. However, not all vitamin E supplements
are created equally. For detailed information on

Abnormal stance of a horse with equine neuroaxonal dystrophy/equine
degenerative myeloencephalopathy (eNAD/EDM) from vitamin E
deficiency.
CARRIE FINNO

continued on page 5

2

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

Third Quarter 2020

T

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

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
Thailand and Malaysia recorded outbreaks of
African horse sickness (AHS). Thailand reported
outbreaks in August (one case in a horse) and
September (two cases in captive Chapman’s zebras). Malaysia confirmed its first ever incursionof AHS in August; five horses on a single premises.
Affected equids in the outbreaks in both countries
were euthanized.
Belgium, France, Germany, Italy, Sweden, andthe USA confirmed outbreaks of equine influenza.
These ranged from one (Belgium, France and
Italy), three (Sweden), four (Germany), to at leastnine in the USA, where the disease is endemic.
Strangles is considered endemic in many countries with outbreaks reported from Belgium (two),
Canada (one), France (nine), the Netherlands (12,one involving 15 cases), Switzerland (eight), andthe USA (41 outbreaks in 17 states, the majority
with multiple cases).
Equine herpesvirus 1 (EHV-1) related diseases
are endemic in most countries. Cases were confirmed in France, Japan, Republic of South Africa(RSA), Sweden, Switzerland, the UK, and theUSA. Single outbreaks of respiratory disease wererecorded in France, RSA, and the UK. One caseof EHV-1 abortion was confirmed in Japan in an
unvaccinated mare. EHV-1 neurologic disease
was reported by Sweden (single case), Switzerland(three outbreaks), and the USA (seven outbreaks
involving five states, with two outbreaks in California and Maine); the majority involved single cases.
Equine herpesvirus 4 (EHV-4) respiratory disease was recorded by France (20 outbreaks, mostly
single cases), Japan (one outbreak involving eightunvaccinated horses) and the Netherlands (fiveoutbreaks, one involving seven 4-5 month old
foals). Switzerland reported an outbreak of EHV-4
neurologic disease.
Belgium and the USA confirmed cases of equine
herpesvirus 2 and/or 5. Infection with EHV-2 wasdiagnosed in a 2-month-old foal in Belgium, andnumerous infections by either virus were diagnosed
in several states in the USA, some associated withrespiratory disease.

A case of adenovirus infection was reported ina foal in Ireland.
The USA confirmed four outbreaks of equine
infectious anemia, three in Texas, one involving
two cases, and one in Georgia. Three outbreaks
involved single cases.
Equine piroplasmosis was recorded in Finland(one case), RSA (disease is endemic) and Switzerland (one outbreak).
Denmark reported the isolation of Taylorellaequigenitalis, the cause of contagious equine metritis, from three stallions.
Equine coital exanthema (equine herpesvirus
3) was diagnosed in Argentina (two outbreaks
involving 29 Thoroughbreds) and the USA (onecase).
Belgium confirmed single cases of leptospiralabortion on two premises. A case of Leptospiraassociated recurrent uveitis was diagnosed in astallion by France.
Salmonellosis was reported by Switzerland (twooutbreaks) and the USA (10 cases, two involving
serogroup C1, five serogroup D1, and three weren’t
serogrouped).
France confirmed 19 outbreaks of rotavirus
diarrhea in foals, the majority were single cases. A
total of 17 cases were diagnosed by the USA, themajority in 60- to 90-day-old foals in Kentucky
involving G3 and/or G14 genotypes.
One case of proliferative enteropathy caused by
Lawsonia intracellularis was reported by the USA.
Canada (four outbreaks, all single cases) and theUSA (17 outbreaks in 10 states, one involving 10
cases) confirmed outbreaks of equine neorickettsiosis (Potomac Horse Fever).
Eastern equine encephalomyelitis was reported
by Canada (two outbreaks, each involving single
cases) and the USA (104 cases in 11 states), withhighest numbers in Michigan (33), Wisconsin(20), and Florida (13).
West Nile encephalitis was recorded by Canada(one case), France (three outbreaks, one case each),Germany (eight outbreaks), Hungary (one outbreak), Italy (nine outbreaks), Portugal (one case),
Spain (13 outbreaks, three were single cases), andthe USA (27 cases in seven states, four on one
premises).

A case of rabies was confirmed in a Warmblood
horse in Maryland, USA.
Switzerland confirmed two outbreaks of Borna
disease, and one outbreak of anaplasmosis.
Vesicular stomatitis continued to spread in the
USA in the third quarter of 2020, extending toArkansas, Missouri and Oklahoma, in addition
to five previously reported states. A total of 198
equine outbreaks were recorded, all associated with
the Indiana serotype.
Rhodococcus equi related diseases were confirmedby the USA.

3

N AT I O N A L

Consequences of Vitamin E Deficiency

Vitamin E is an essential nutrient for horses.
This antioxidant helps maintain normal neurological function by limiting the damage causedby oxidative stress and free radicals. The best sourceof vitamin E is fresh green grass. Horses that graze
on lush green pastures often have adequate access to vitamin E. However, many stabled horses
are not maintained on pasture. Vitamin E levels
decrease and eventually are lost as soon as grassis harvested, so even the highest-quality hay will
not meet vitamin E requirements. Some horses
maintained on diets deficient in vitamin E canexperience significant health consequences.
Vitamin E helps a horse’s muscles and nerves
function properly. A dietary deficiency can lead tothree specific diseases: (1) equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy(eNAD/EDM), (2) equine motor neuron disease(EMND) and (3) vitamin E deficient myopathy(VEM). These diseases are typically diagnosed
based on clinical signs, exclusion of other disorders,
and low concentrations of vitamin E in the blood.
Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy occurs in young
animals and has a genetic predisposition. Affectedhorses may stand with forelimbs too far apart (ortoo close together), have difficulty navigating curbs
or hills, or lack coordination while walking andmaking tight turns. Signs of the disease can vary,some horses show mild performance issues, whileothers are severely debilitated. Although the exact
cause of the degeneration is unknown, a specificinteraction between genetics and nutrition during
the first few years of life is required for this disease
to manifest.
Researchers in the Finno Laboratory are working to develop a genetic test for eNAD/EDM.
Until one is available, the recommendation is toprovide vitamin E supplementation to horses that
do not have regular access to pasture, especiallypregnant mares and newborn foals. This may noteliminate the disease, but it appears that less severe
neurological signs may develop if foals receive
supplementation during the early stages of life.

Prepubic Tendon RuptureT

he prepubic tendon extends from the brimof the pelvis and joins with the abdominal
muscles to support the abdomen and abdominal
viscera. Mares can rupture (tear) the prepubic
tendon, either partially or fully, and the associatedmuscles of the abdominal wall. Prepubic tendon
rupture is an uncommon but serious condition inlate pregnancy that may have a poor prognosis andcan result in death of the mare and fetus.
The exact cause of prepubic tendon rupture
is not known, however, the condition is morecommon in older mares that have had multiple
pregnancies, draft breeds, mares carrying twins,
and mares with placental abnormalities such ashydrops (hydroallantois or hydroamnion).
Mares with prepubic tendon ruptures exhibit
signs of colic-like pain, elevated heart and respiratory rates, and reluctance to move or lie down.
Changes in the shape of the ventral abdomen (underbelly) may be first noted, followed by a rapidly
progressive swelling (edema) that can extend fromthe udder towards the chest. The udder may beswollen and teats may point toward the mare’s headinstead of downwards, and blood may drip fromthe teats. Touching the ventral abdomen is often
resented. Some mares will adopt a ‘sawhorse’ stancewith a tilted pelvis and elevation of the tailhead.
Other mares may die after a short illness. Diagnosis
of prepubic tendon rupture is difficult to confirm
and is usually based on characteristic clinical signs.
The choice of therapy for mares with prepubic
tendon rupture varies. It will depend on the extent
of the rupture, ability to control the mare’s pain,
and stage of gestation. The relative value of themare and foal may also be considered. Complete
rupture of the prepubic tendon has a poor prognosis for the mare because the tendon cannot besurgically repaired.
Conservative therapy will usually involve restricting the mare to stall rest, carefully applying‘belly bandages’ to support the ventral abdomen,

4

and alleviation of pain using a variety of drugs.
Progestins may be given to keep the uterus in aquiet (not contracting) state. Close monitoringof the fetus to detect fetal stress is required withfrequent ultrasound examinations via the mare’s
abdomen to monitor fetal heart rate and activity.
Stage of gestation is an important factor whentherapy options are being considered. If the mareis close to term (330 days of gestation or later),induction of labor or a caesarean section may beconsidered. If the mare is induced, then foaling
must be assisted as she has limited or no ability tocontract abdominal muscles during active labor.
If the foal is successfully delivered, it is consideredat high risk of developing problems such as neonatal sepsis. Colostrum supplementation may beneeded, and the foal may not be able to suckle themare due to severe udder swelling.
For mares that rupture the prepubic tendon
before 330 days of gestation and in which pain canbe managed, a decision may be made to support
the mare so the fetus can reach 330 days of gestation or longer. The last part of pregnancy is very
important in determining viability of the foal, as
most of the fetal maturation that ensures the foal
is ready for life outside the uterus happens in thelast 10 days of gestation. For mares in which pain
cannot be well managed, euthanasia should beconsidered.
Mares with prepubic tendon rupture thatsurvive foaling or caesarean section should not
be bred again. Some mares that survive foaling
may subsequently need to be euthanized due tointractable pain.
CONTACT:
Erica Gee, BVSc, PhD, DipACT
e.k.gee@massey.ac.nz+6463505328
School of Veterinary Science
Massey University
Palmerston North, New Zealand

Equine motor neuron disease typically occurs
in older horses that have been vitamin E deficientfor more than 18 months. The disease affects lower
motor neurons, which are nerves that supply the
direct neurological input into all muscles. In theirabsence, the associated muscles atrophy, resulting
in the clinical signs of weakness and weight loss
characteristic of this disease. Affected horses may
carry their heads low and lie down for longer
periods. Research from Cornell University has
shown that approximately 40% of horses affectedby EMND improve with vitamin E supplementation, 40% stabilize but remain disfigured, and 20%
progress in disease severity.
Vitamin E deficient myopathy is typicallyfound in horses with a shorter duration of vitamin E deficiency. Affected horses exhibit muscle
weakness, low muscle vitamin E concentrations
and mitochondrial alterations (i.e. changes to the“power house” energy storage unit of the cell) inskeletal muscle but show no evidence of neurologic
impairment. With proper supplementation, affected animals are generally able to recover within
three months.
These diseases are currently the only conditions
definitively associated with vitamin E deficiency.
At this time, nothing is known about vitamin E
metabolism in horses, the appropriate dosage, or
its actual efficacy in preventing or treating otherneurological conditions. In humans, the same
enzymes that metabolize vitamin E also metabolize
approximately 50 percent of therapeutic drugs,
so supplementation with vitamin E could potentially alter the effects of other drugs if a horse ison multiple therapies. Therefore, while vitamin
E supplementation may not necessarily be harmful with respect to other neurologic diseases, it isunlikely to be beneficial.
Since there are no effective treatments for mostdiseases caused by vitamin E deficiency, prevention
is key. If horses are not able to access fresh pasturesto graze, vitamin E must be supplemented in theirdiets. However, not all vitamin E supplements
are created equally. For detailed information on

Abnormal stance of a horse with equine neuroaxonal dystrophy/equine
degenerative myeloencephalopathy (eNAD/EDM) from vitamin E
deficiency.
CARRIE FINNO

continued on page 5

Equine Disease Quarterly Newsletter

5vitamin E supplementation, please refer to a recent
issue of the UC Davis Horse Report: https://ceh.
vetmed.ucdavis.edu/sites/g/files/dgvnsk4536/files/
inline-files/Horse_Report_Fall_2018_web.pdf.
Baseline blood vitamin E concentrations should
always be assessed before initiating any vitamin
E supplementation. Owners should consult
with their veterinarians to determine if vitamin

E supplementation is required and identify thebest supplementation regimen for their particularhorse.
CONTACT:
Carrie Finno, DVM, PhD, DACVIM (Large Animal)
cjfinno@ucdavis.edu
530-752-2739
UC Davis School of Veterinary Medicine
Davis, California

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

Re-feeding the Starved HorseF

inding yourself in the position of providing
care to a starved horse can be an emotionalsituation for any horse enthusiast. The desire to
do everything possible to return the horse to full
health, including providing ample nutrition, canbe the initial impulse. Sadly, the desire to feed thehorse well can have catastrophic consequences resulting in a re-feeding syndrome that may result in
the need for euthanasia. While it may be tempting
to provide unlimited access to feed, when it comesto feeding starved horses, less truly should be therule of thumb.
Horses rely on body stores of inert carbohydrate
and fat to fuel the large number of metabolic
processes within the body. These stores are constantly replenished through the diet. In a horsethat is starved, these stores become depleted andso instead, protein is utilized for energy. All proteinin the body is actively contributing to importantfunctions and is not stored for the purpose ofproviding energy. In this scenario, the body is not
picky about what source of protein gets used forenergy. Therefore, as protein is burned as a fuelsource, skeletal muscle and vital organs become
negatively impacted.
When a starved horse is “re-fed” and provided
carbohydrates, in particular glucose, blood insulin increases. This helps move glucose from thecirculation into cells and with it electrolytes. Thiscan result in inadequate levels of key electrolytes
such as phosphorus, potassium and magnesiumin the circulation as well as leaving red blood cells
without adequate energy. These red blood cells arethen unable to adequately release oxygen to various
tissues resulting in heart, kidney and respiratoryorgan failure and ultimately death.
Research studies have shown that a greater
success rate is achieved when starved horses are
rehabilitated using forages containing low non-structural carbohydrate (NSC) as this limits theinsulin response. If using grass hays, they should betested for NSC content and ideally have an NSC
content of less than 10 percent. If only untested
grass hay is available, feeding alfalfa may be a better
choice as alfalfa has a low NSC content and also
tends to provide good amounts of magnesium andphosphorus.
Very small amounts of feed should be fed thatprovide no more than about 50 percent of thehorse’s calculated daily digestible energy (DE)requirement. Different research studies have useddifferent feeding protocols. One fed alfalfa at 50
percent of the calculated daily DE requirement for
the first 3 days of re-feeding and then increased
the amount to 75 percent for days 4 and 5 before
increasing to a full 100 percent on day 6. Anotherstudy fed frequent handfuls of grass hay for the firstday and then provided netted hay that was hungoutside the stalls so that the horses had to eat the
hay through the bars. These researchers introduced
0.5 pounds of complete feed and increased thisby the same amount every 3 days until they werebeing fed no more than 3 lbs at any feeding.
Re-feeding syndrome can develop as quickly
as the first day of re-feeding or may not become
apparent for 3 to 4 weeks. The keys to successful
rehabilitation lie in starting off with very small
meals that provide limited calories and utilizing
forages and feeds with an NSC content at or below
10 percent. Sticking to these guidelines despite
the natural desire to want to lavish the horse withfood will provide the greatest chance of success innursing the starved horse back to health.
CONTACT:
Clair Thunes, PhD
916-248-8987
clair@summit-equine.com
Summit Equine Nutrition LLC
Gilbert, Arizona

JANUARY 2021
Volume 30, Number 1

C O M M E N TA RY
IN THIS ISSUECOMMENTARY: continued from the front pageare not useful in assessing the status of many nutrients. For some, homeostatic mechanisms maintainrelatively consistent blood levels, even in the face ofsignificant dietary deficiencies. For nutrients suchas selenium, indicators of functional status may be
more useful than serum selenium concentrations
alone. Even for nutrients whose levels fluctuate in
the blood with dietary intake, a blood level is only
useful if it can be interpreted in relation to horse
health. Laboratories should have established orreferenced normal ranges to evaluate blood mineral or vitamin concentrations. Ideally, reference
ranges should be developed from normal healthy
horses of different physiological states, as age andphysiological function (gestating, exercising, growing) affect nutrient needs. Unfortunately specificreference ranges for blood constituents in equinesare very limited.

Horses are often described as fragile, but they
are also extremely resilient and adaptable. Horses
evolved to deal with times of food abundanceas well as food scarcity. Short periods of foodscarcity may result in nutritional deficiency; foodabundance allows for restoration of body reserves.
Clinical diseases only typically will develop asa result of chronic deficiencies. As both articles
in this issue point out, overzealous feeding andsupplementation can have negative consequences.
For this reason, dietary changes, even those aimed
at correction of nutritional deficiencies, should bemade gradually. Perhaps, optimal horse feeding ismore like the tortoise and less like the hare.
CONTACT:
Laurie Lawrence, PhD
llawrenc@email.uky.edu
859-257-7509
Department of Animal and Food Sciences
University of Kentucky
Lexington, KentuckyProper nutrition is key to producing and maintaining horses of all types, while poor nutrition
Commentary
or feeding management can increase the risk ofvarious health disorders. In this issue, Dr. ClairInternational
Thunes focuses on refeeding the starved horse, andThird Quarter2020  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 Dr. Carrie Finno addresses vitamin E deficiency.
Both articles highlight consequences of inadequate
Prepubic Tendon
Rupture .  .  .  .  .  .  .  .  .  .  .  .  . 3 or imbalanced nutrition.
Nutrient deficiencies may be primary or secondary. Primary deficiencies result when the diet
National
contains inadequate amounts of one or more nutriVitamin E
Deficiency .  .  .  .  .  .  .  .  .  .  . 4 ents. Starvation can occur when feed resources are
scarce, producing a deficiency in calories, protein,Re-feeding the
Starved Horse .  .  .  .  .  .  . 5 and nutrients. Primary deficiencies in specific nutrients, such as vitamin E, occur with improperly
balanced diets. Secondary deficiencies occur when
the diet is nutritionally adequate, but some otherfactor affects nutrient intake or absorption. For
example, starvation can occur if a horse is unable
to eat due to a mouth injury, even though feed isavailable. Secondary deficiencies may be causedby dietary substances or medications that interferewith the absorption of a specific nutrient. Excessive
concentrations of dietary zinc inhibit copper absorption and lead to copper deficiency in growing
horses despite adequate dietary copper.
From a nutritionist’s perspective, identificationof dietary deficiencies requires a diet evaluation.
This involves determining the amount and comCollege of Agriculture, position of the feeds provided. Commercial feed
Food and Environment laboratories offer affordable and rapid analysis
Department offor many important nutrients including protein,
Veterinary Sciencecalcium, phosphorus and several trace minerals.
In contrast, selenium, iodine, and most vitaminsrequire a specialized laboratory. It is important toremember that most nutritional deficiencies manifest after months to years of dietary inadequacy.
Lloyd’s—An international
insurance market for
Therefore analysis of the current diet may not
bloodstock and othernecessarily reflect a past diet.
specialist insurance.

MATT BARTON

Due to variation in nutrient pools within
the body and stability of various minerals andvitamins, laboratory submission of whole blood,
serum, or liver may be required. Prior to sample
collection, the laboratory should be consulted toconfirm the type of sample needed and the optimal
conditions for shipping samples to the laboratory.
Dr. Finno indicates that baseline concentrationsof circulating vitamin E may indicate the need forsupplementation. However, blood concentrations
continued on the back pageEquine Disease Quarterly Newsletter

5vitamin E supplementation, please refer to a recent
issue of the UC Davis Horse Report: https://ceh.
vetmed.ucdavis.edu/sites/g/files/dgvnsk4536/files/
inline-files/Horse_Report_Fall_2018_web.pdf.
Baseline blood vitamin E concentrations should
always be assessed before initiating any vitamin
E supplementation. Owners should consult
with their veterinarians to determine if vitamin

E supplementation is required and identify thebest supplementation regimen for their particularhorse.
CONTACT:
Carrie Finno, DVM, PhD, DACVIM (Large Animal)
cjfinno@ucdavis.edu
530-752-2739
UC Davis School of Veterinary Medicine
Davis, California

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

Re-feeding the Starved HorseF

inding yourself in the position of providing
care to a starved horse can be an emotionalsituation for any horse enthusiast. The desire to
do everything possible to return the horse to full
health, including providing ample nutrition, canbe the initial impulse. Sadly, the desire to feed thehorse well can have catastrophic consequences resulting in a re-feeding syndrome that may result in
the need for euthanasia. While it may be tempting
to provide unlimited access to feed, when it comesto feeding starved horses, less truly should be therule of thumb.
Horses rely on body stores of inert carbohydrate
and fat to fuel the large number of metabolic
processes within the body. These stores are constantly replenished through the diet. In a horsethat is starved, these stores become depleted andso instead, protein is utilized for energy. All proteinin the body is actively contributing to importantfunctions and is not stored for the purpose ofproviding energy. In this scenario, the body is not
picky about what source of protein gets used forenergy. Therefore, as protein is burned as a fuelsource, skeletal muscle and vital organs become
negatively impacted.
When a starved horse is “re-fed” and provided
carbohydrates, in particular glucose, blood insulin increases. This helps move glucose from thecirculation into cells and with it electrolytes. Thiscan result in inadequate levels of key electrolytes
such as phosphorus, potassium and magnesiumin the circulation as well as leaving red blood cells
without adequate energy. These red blood cells arethen unable to adequately release oxygen to various
tissues resulting in heart, kidney and respiratoryorgan failure and ultimately death.
Research studies have shown that a greater
success rate is achieved when starved horses are
rehabilitated using forages containing low non-structural carbohydrate (NSC) as this limits theinsulin response. If using grass hays, they should betested for NSC content and ideally have an NSC
content of less than 10 percent. If only untested
grass hay is available, feeding alfalfa may be a better
choice as alfalfa has a low NSC content and also
tends to provide good amounts of magnesium andphosphorus.
Very small amounts of feed should be fed thatprovide no more than about 50 percent of thehorse’s calculated daily digestible energy (DE)requirement. Different research studies have useddifferent feeding protocols. One fed alfalfa at 50
percent of the calculated daily DE requirement for
the first 3 days of re-feeding and then increased
the amount to 75 percent for days 4 and 5 before
increasing to a full 100 percent on day 6. Anotherstudy fed frequent handfuls of grass hay for the firstday and then provided netted hay that was hungoutside the stalls so that the horses had to eat the
hay through the bars. These researchers introduced
0.5 pounds of complete feed and increased thisby the same amount every 3 days until they werebeing fed no more than 3 lbs at any feeding.
Re-feeding syndrome can develop as quickly
as the first day of re-feeding or may not become
apparent for 3 to 4 weeks. The keys to successful
rehabilitation lie in starting off with very small
meals that provide limited calories and utilizing
forages and feeds with an NSC content at or below
10 percent. Sticking to these guidelines despite
the natural desire to want to lavish the horse withfood will provide the greatest chance of success innursing the starved horse back to health.
CONTACT:
Clair Thunes, PhD
916-248-8987
clair@summit-equine.com
Summit Equine Nutrition LLC
Gilbert, Arizona

JANUARY 2021
Volume 30, Number 1

C O M M E N TA RY
IN THIS ISSUECOMMENTARY: continued from the front pageare not useful in assessing the status of many nutrients. For some, homeostatic mechanisms maintainrelatively consistent blood levels, even in the face ofsignificant dietary deficiencies. For nutrients suchas selenium, indicators of functional status may be
more useful than serum selenium concentrations
alone. Even for nutrients whose levels fluctuate in
the blood with dietary intake, a blood level is only
useful if it can be interpreted in relation to horse
health. Laboratories should have established orreferenced normal ranges to evaluate blood mineral or vitamin concentrations. Ideally, reference
ranges should be developed from normal healthy
horses of different physiological states, as age andphysiological function (gestating, exercising, growing) affect nutrient needs. Unfortunately specificreference ranges for blood constituents in equinesare very limited.

Horses are often described as fragile, but they
are also extremely resilient and adaptable. Horses
evolved to deal with times of food abundanceas well as food scarcity. Short periods of foodscarcity may result in nutritional deficiency; foodabundance allows for restoration of body reserves.
Clinical diseases only typically will develop asa result of chronic deficiencies. As both articles
in this issue point out, overzealous feeding andsupplementation can have negative consequences.
For this reason, dietary changes, even those aimed
at correction of nutritional deficiencies, should bemade gradually. Perhaps, optimal horse feeding ismore like the tortoise and less like the hare.
CONTACT:
Laurie Lawrence, PhD
llawrenc@email.uky.edu
859-257-7509
Department of Animal and Food Sciences
University of Kentucky
Lexington, KentuckyProper nutrition is key to producing and maintaining horses of all types, while poor nutrition
Commentary
or feeding management can increase the risk ofvarious health disorders. In this issue, Dr. ClairInternational
Thunes focuses on refeeding the starved horse, andThird Quarter2020  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 Dr. Carrie Finno addresses vitamin E deficiency.
Both articles highlight consequences of inadequate
Prepubic Tendon
Rupture .  .  .  .  .  .  .  .  .  .  .  .  . 3 or imbalanced nutrition.
Nutrient deficiencies may be primary or secondary. Primary deficiencies result when the diet
National
contains inadequate amounts of one or more nutriVitamin E
Deficiency .  .  .  .  .  .  .  .  .  .  . 4 ents. Starvation can occur when feed resources are
scarce, producing a deficiency in calories, protein,Re-feeding the
Starved Horse .  .  .  .  .  .  . 5 and nutrients. Primary deficiencies in specific nutrients, such as vitamin E, occur with improperly
balanced diets. Secondary deficiencies occur when
the diet is nutritionally adequate, but some otherfactor affects nutrient intake or absorption. For
example, starvation can occur if a horse is unable
to eat due to a mouth injury, even though feed isavailable. Secondary deficiencies may be causedby dietary substances or medications that interferewith the absorption of a specific nutrient. Excessive
concentrations of dietary zinc inhibit copper absorption and lead to copper deficiency in growing
horses despite adequate dietary copper.
From a nutritionist’s perspective, identificationof dietary deficiencies requires a diet evaluation.
This involves determining the amount and comCollege of Agriculture, position of the feeds provided. Commercial feed
Food and Environment laboratories offer affordable and rapid analysis
Department offor many important nutrients including protein,
Veterinary Sciencecalcium, phosphorus and several trace minerals.
In contrast, selenium, iodine, and most vitaminsrequire a specialized laboratory. It is important toremember that most nutritional deficiencies manifest after months to years of dietary inadequacy.
Lloyd’s—An international
insurance market for
Therefore analysis of the current diet may not
bloodstock and othernecessarily reflect a past diet.
specialist insurance.

MATT BARTON

Due to variation in nutrient pools within
the body and stability of various minerals andvitamins, laboratory submission of whole blood,
serum, or liver may be required. Prior to sample
collection, the laboratory should be consulted toconfirm the type of sample needed and the optimal
conditions for shipping samples to the laboratory.
Dr. Finno indicates that baseline concentrationsof circulating vitamin E may indicate the need forsupplementation. However, blood concentrations
continued on the back page2

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

Third Quarter 2020

T

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

he International Thoroughbred Breeders
Federation, International Collating Centre,
Newmarket, United Kingdom, and other sources
reported the following equine disease events.
Thailand and Malaysia recorded outbreaks of
African horse sickness (AHS). Thailand reported
outbreaks in August (one case in a horse) and
September (two cases in captive Chapman’s zebras). Malaysia confirmed its first ever incursionof AHS in August; five horses on a single premises.
Affected equids in the outbreaks in both countries
were euthanized.
Belgium, France, Germany, Italy, Sweden, andthe USA confirmed outbreaks of equine influenza.
These ranged from one (Belgium, France and
Italy), three (Sweden), four (Germany), to at leastnine in the USA, where the disease is endemic.
Strangles is considered endemic in many countries with outbreaks reported from Belgium (two),
Canada (one), France (nine), the Netherlands (12,one involving 15 cases), Switzerland (eight), andthe USA (41 outbreaks in 17 states, the majority
with multiple cases).
Equine herpesvirus 1 (EHV-1) related diseases
are endemic in most countries. Cases were confirmed in France, Japan, Republic of South Africa(RSA), Sweden, Switzerland, the UK, and theUSA. Single outbreaks of respiratory disease wererecorded in France, RSA, and the UK. One caseof EHV-1 abortion was confirmed in Japan in an
unvaccinated mare. EHV-1 neurologic disease
was reported by Sweden (single case), Switzerland(three outbreaks), and the USA (seven outbreaks
involving five states, with two outbreaks in California and Maine); the majority involved single cases.
Equine herpesvirus 4 (EHV-4) respiratory disease was recorded by France (20 outbreaks, mostly
single cases), Japan (one outbreak involving eightunvaccinated horses) and the Netherlands (fiveoutbreaks, one involving seven 4-5 month old
foals). Switzerland reported an outbreak of EHV-4
neurologic disease.
Belgium and the USA confirmed cases of equine
herpesvirus 2 and/or 5. Infection with EHV-2 wasdiagnosed in a 2-month-old foal in Belgium, andnumerous infections by either virus were diagnosed
in several states in the USA, some associated withrespiratory disease.

A case of adenovirus infection was reported ina foal in Ireland.
The USA confirmed four outbreaks of equine
infectious anemia, three in Texas, one involving
two cases, and one in Georgia. Three outbreaks
involved single cases.
Equine piroplasmosis was recorded in Finland(one case), RSA (disease is endemic) and Switzerland (one outbreak).
Denmark reported the isolation of Taylorellaequigenitalis, the cause of contagious equine metritis, from three stallions.
Equine coital exanthema (equine herpesvirus
3) was diagnosed in Argentina (two outbreaks
involving 29 Thoroughbreds) and the USA (onecase).
Belgium confirmed single cases of leptospiralabortion on two premises. A case of Leptospiraassociated recurrent uveitis was diagnosed in astallion by France.
Salmonellosis was reported by Switzerland (twooutbreaks) and the USA (10 cases, two involving
serogroup C1, five serogroup D1, and three weren’t
serogrouped).
France confirmed 19 outbreaks of rotavirus
diarrhea in foals, the majority were single cases. A
total of 17 cases were diagnosed by the USA, themajority in 60- to 90-day-old foals in Kentucky
involving G3 and/or G14 genotypes.
One case of proliferative enteropathy caused by
Lawsonia intracellularis was reported by the USA.
Canada (four outbreaks, all single cases) and theUSA (17 outbreaks in 10 states, one involving 10
cases) confirmed outbreaks of equine neorickettsiosis (Potomac Horse Fever).
Eastern equine encephalomyelitis was reported
by Canada (two outbreaks, each involving single
cases) and the USA (104 cases in 11 states), withhighest numbers in Michigan (33), Wisconsin(20), and Florida (13).
West Nile encephalitis was recorded by Canada(one case), France (three outbreaks, one case each),Germany (eight outbreaks), Hungary (one outbreak), Italy (nine outbreaks), Portugal (one case),
Spain (13 outbreaks, three were single cases), andthe USA (27 cases in seven states, four on one
premises).

A case of rabies was confirmed in a Warmblood
horse in Maryland, USA.
Switzerland confirmed two outbreaks of Borna
disease, and one outbreak of anaplasmosis.
Vesicular stomatitis continued to spread in the
USA in the third quarter of 2020, extending toArkansas, Missouri and Oklahoma, in addition
to five previously reported states. A total of 198
equine outbreaks were recorded, all associated with
the Indiana serotype.
Rhodococcus equi related diseases were confirmedby the USA.

3

N AT I O N A L

Consequences of Vitamin E Deficiency

Vitamin E is an essential nutrient for horses.
This antioxidant helps maintain normal neurological function by limiting the damage causedby oxidative stress and free radicals. The best sourceof vitamin E is fresh green grass. Horses that graze
on lush green pastures often have adequate access to vitamin E. However, many stabled horses
are not maintained on pasture. Vitamin E levels
decrease and eventually are lost as soon as grassis harvested, so even the highest-quality hay will
not meet vitamin E requirements. Some horses
maintained on diets deficient in vitamin E canexperience significant health consequences.
Vitamin E helps a horse’s muscles and nerves
function properly. A dietary deficiency can lead tothree specific diseases: (1) equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy(eNAD/EDM), (2) equine motor neuron disease(EMND) and (3) vitamin E deficient myopathy(VEM). These diseases are typically diagnosed
based on clinical signs, exclusion of other disorders,
and low concentrations of vitamin E in the blood.
Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy occurs in young
animals and has a genetic predilection. Affectedhorses may stand with forelimbs too far apart (ortoo close together), have difficulty navigating curbs
or hills, or lack coordination while walking andmaking tight turns. Signs of the disease can vary,some horses show mild performance issues, whileothers are severely debilitated. Although the exact
cause of the degeneration is unknown, a specificinteraction between genetics and nutrition during
the first few years of life is required for this disease
to manifest.
Researchers in the Finno Laboratory are working to develop a genetic test for eNAD/EDM.
Until one is available, the recommendation is toprovide vitamin E supplementation to horses that
do not have regular access to pasture, especiallypregnant mares and newborn foals. This may noteliminate the disease, but it appears that less severe
neurological signs may develop if foals receive
supplementation during the early stages of life.

Prepubic Tendon RuptureT

he prepubic tendon extends from the brimof the pelvis and joins with the abdominal
muscles to support the abdomen and abdominal
viscera. Mares can rupture (tear) the prepubic
tendon, either partially or fully, and the associatedmuscles of the abdominal wall. Prepubic tendon
rupture is an uncommon but serious condition inlate pregnancy that may have a poor prognosis andcan result in death of the mare and fetus.
The exact cause of prepubic tendon rupture
is not known, however, the condition is morecommon in older mares that have had multiple
pregnancies, draft breeds, mares carrying twins,
and mares with placental abnormalities such ashydrops (hydroallantois or hydroamnion).
Mares with prepubic tendon ruptures exhibit
signs of colic-like pain, elevated heart and respiratory rates, and reluctance to move or lie down.
Changes in the shape of the ventral abdomen(underbelly) may be first noted, followed by a rapidly progressive swelling (edema) that can extend
from the udder towards to chest. The udder may
be swollen and teats may point toward the mare’shead instead of downwards, and blood may drip
from the teats. Touching the ventral abdomen isoften resented. Some mares will adopt a ‘sawhorse’
stance with a tilted pelvis and elevation of thetailhead. Other mares may die after a short illness.
Diagnosis of prepubic tendon rupture is difficult
to confirm and is usually based on characteristic
clinical signs.
The choice of therapy for mares with prepubic
tendon rupture varies. It will depend on the extent
of the rupture, ability to control the mare’s pain,
and stage of gestation. The relative value of themare and foal may also be considered. Complete
rupture of the prepubic tendon has a poor prognosis for the mare because the tendon cannot besurgically repaired.
Conservative therapy will usually involve restricting the mare to stall rest, carefully applying

4‘belly bandages’ to support the ventral abdomen,
and alleviation of pain using a variety of drugs.
Progestins may be given to keep the uterus in aquiet (not contracting) state. Close monitoringof the fetus to detect fetal stress is required withfrequent ultrasound examinations via the mare’s
abdomen to monitor fetal heart rate and activity.
Stage of gestation is an important factor whentherapy options are being considered. If the mareis close to term (330 days of gestation or later),induction of labor or a caesarean section may beconsidered. If the mare is induced, then foaling
must be assisted as she has limited or no ability tocontract abdominal muscles during active labor.
If the foal is successfully delivered, it is consideredat high risk of developing problems such as neonatal sepsis. Colostrum supplementation may beneeded, and the foal may not be able to suckle themare due to severe udder swelling.
For mares that rupture the prepubic tendon
before 330 days of gestation and in which pain canbe managed, a decision may be made to support
the mare so the fetus can reach 330 days of gestation or longer. The last part of pregnancy is very
important in determining viability of the foal, as
most of the fetal maturation that ensures the foal
is ready for life outside the uterus happens in thelast 10 days of gestation. For mares in which pain
cannot be well managed, euthanasia should beconsidered.
Mares with prepubic tendon rupture thatsurvive foaling or caesarean section should not
be bred again. Some mares that survive foaling
may subsequently need to be euthanized due tointractable pain.
CONTACT:
Erica Gee BVSc PhD DipACT
e.k.gee@massey.ac.nz+6463505328
School of Veterinary Science
Massey University
Palmerston North, New Zealand

Equine motor neuron disease typically occurs
in older horses that have been vitamin E deficientfor more than 18 months. The disease affects lower
motor neurons, which are nerves that supply the
direct neurological input into all muscles. In theirabsence, the associated muscles atrophy, resulting
in the clinical signs of weakness and weight loss
characteristic of this disease. Affected horses may
carry their heads low and lie down for longer
periods. Research from Cornell University has
shown that approximately 40% of horses affectedby EMND improve with vitamin E supplementation, 40% stabilize but remain disfigured, and 20%
progress in disease severity.
Vitamin E deficient myopathy is typicallyfound in horses with a shorter duration of vitamin E deficiency. Affected horses exhibit muscle
weakness, low muscle vitamin E concentrations
and mitochondrial alterations (i.e. changes to the“power house” energy storage unit of the cell) inskeletal muscle but show no evidence of neurologic
impairment. With proper supplementation, affected animals are generally able to recover within
three months.
These diseases are currently the only conditions
definitively associated with vitamin E deficiency.
At this time, nothing is known about vitamin E
metabolism in horses, the appropriate dosage, or
its actual efficacy in preventing or treating otherneurological conditions. In humans, the same
enzymes that metabolize vitamin E also metabolize
approximately 50 percent of therapeutic drugs,
so supplementation with vitamin E could potentially alter the effects of other drugs if a horse ison multiple therapies. Therefore, while vitamin
E supplementation may not necessarily be harmful with respect to other neurologic diseases, it isunlikely to be beneficial.
Since there are no effective treatments for mostdiseases caused by vitamin E deficiency, prevention
is key. If horses are not able to access fresh pasturesto graze, vitamin E must be supplemented in theirdiets. However, not all vitamin E supplements
are created equally. For detailed information on

Abnormal stance of a horse with equine neuroaxonal dystrophy/equine
degenerative myeloencephalopathy (eNAD/EDM) from vitamin E
deficiency.
CARRIE FINNO

continued on page 5