Equine Disease Quarterly Newsletter

5

Polyuria and Polydipsia, continued from page 4.

acute or chronic kidney injury. Aminoglycosides(gentamicin, amikacin), oxytetracycline, nonsteroidal anti-inflammatories (phenylbutazone,
flunixin meglumine), polymyxin B, amphotericin
B, imidocarb dipropionate, and bisphosphonates
are all potentially toxic to the kidneys and havedocumented and/or anecdotal reports of renal
disease following their use. Additional diseases
associated with PU include but are not limited toliver failure, neoplasia, toxicities, inflammatory
conditions, and parasitism.

Diagnosis: Testing to determine the cause of PU/

PD should start with a chemistry profile and urine
analysis for the presence of elevations in kidney
enzymes, changes in electrolyte levels, high blood
glucose levels, and measurement of urine specificgravity to determine the concentration of theurine. Additional bloodwork may be necessary,and urinalysis and additional urine testing may
be useful for identifying early kidney disease. Occasionally, advanced testing is needed to diagnosis
the underlying cause of PU.

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

Presorted Standard
US Postage Paid
Permit 51
Lexington KY

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

OCTOBER 2021
Volume 30, Number 4

CONTACT:
Emily A. Barrell, DVM, MSc, DACVIM
ebarrell@umn.edu
Department of Veterinary Population Medicine
University of Minnesota College of Veterinary Medicine
Saint Paul, Minnesota

C O M M E N TA RY
IN THIS ISSUEKENTUCKY

Equine Rotavirus B and Neonatal Foal Diarrhea

Group A and B rotaviruses are significant enteric pathogens that cause diarrhea of variable
severity in humans and domestic animals. Despite
no difference in clinical signs or symptoms, it has
been well documented that there is no antibodymediated cross-protection between groups A and
B. The horse is a unique species in which only
group A rotaviruses typically cause foal diarrhea
outbreaks.
During the 2021 foaling season (February andMarch) in central Kentucky, increased frequencies
of diarrhea were noted in neonatal foals between
1 and 4 days of age. Mares had been previously
vaccinated with an inactivated monovalent equine
rotavirus A vaccine during their pregnancy. Foals
developed diarrhea at approximately 24 h of age
and diarrheic episodes typically lasted 3-4 days.
Some farms experienced up to 100% morbidity.
Newly born foals on affected farms quickly developed diarrhea, suggesting a highly contagious
disease. Clinical signs included inappetence, weakness, dehydration, severe electrolyte imbalance,
and watery yellow and foul-smelling diarrhea.
Hemorrhagic watery diarrhea was noticed in somecases. None of the foal’s dams developed diarrhea.
Diagnostic investigation of fecal samples from
diseased foals, which included PCR and microbial culture, failed to detect diarrhea-causing

pathogens, including equine rotavirus A. Interestingly, metagenomic sequencing data identified anabundant amount of novel rotavirus B genome infecal specimens from affected foals and absenceof other known enteric pathogens, suggesting an
etiological role of this rotavirus B in neonatal foal
diarrhea. Further evidence linking rotavirus B tothis outbreak of highly contagious foal diarrhea is
supported by the poor responses of the affectedfoals to antibiotic treatment as well as seemingly
ineffective equine rotavirus A-specific passive
maternal antibodies in affected foals against thisnew virus. Subsequent analysis of 33 foal diarrheic
samples by RT-qPCR identified 23 rotavirus Bpositive cases (69.69%). Despite a small sample
size, the prevalence of equine rotavirus B in diseased foals was similar to that reported in equine
rotavirus A-associated foal diarrhea outbreaks.
Bioinformatic analysis of the viral genome data
showed that the protein sequence of all 11 viralsegments had greater than 96% homology (relatedness) with group B rotaviruses previously foundin ruminants. Furthermore, evolutionary studies
demonstrated clustering of the equine virus withgroup B rotaviruses of caprine and bovine strainsthat circulated in the USA. These results indicate
the possibility that the equine rotavirus B was ofruminant origin.

In summary, evidence suggests that a novel,
ruminant-origin, group B rotavirus has emergedin horses and was associated with outbreaks ofneonatal foal diarrhea in the 2021 foaling season
in Kentucky. Emergence of the ruminant-like
group B rotavirus in foals clearly warrants further
investigation due to the significant impact of thedisease in neonatal foals and its economic impact
on the equine industry.
CONTACT:
Emma Adam, DVM, PhD, DACVIM, DACVS
emma.adam@uky.edu(859) 562-2186
Feng Li, DVM, PhD
feng.li@uky.edu(859) 218-1106
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

All photos: Matt Barton, Agricultural Communications

S

ince its inception in 1992, the Equine Disease
Quarterly has been distributed worldwide in a
Commentary
printed format. The funding to make this possible
was provided through the generosity of Lloyd’s ofInternational
London, Underwriters and Brokers and their KenSecond Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 tucky Agents, and in later years, by Underwriters at
Lloyd’s, London. Circulation of the Quarterly went
Exhaustion in
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 3 from several hundred copies in October 1992, toapproximately 17,000 copies in 2021, and reachedreaders in over 87 countries.
National
In late 2020, Lloyd’s Underwriters confirmed
Polyuria and
Polydipsia inthat because of changing circumstances, it could
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 4 no longer sustain support of the Equine Disease
Quarterly beyond 2021. Thankfully, a new sponsor,
KentuckyEquus Standardbred Station, Inc., recently came
Equine Rotavirus B
forward and generously agreed to help the continand Neonatal
Foal Diarrhea .  .  .  .  .  .  .  . 5 ued distribution of this worthwhile publication.
This recent development provides a long overdue
opportunity to bring about a change in how the
Quarterly can best be made available to its readership. Considered opinion is to transition from mailing print copies to an electronic format, where eachissue is available on the internet. This will have theimportant advantage that once each issue is posted,
it will be immediately available to the readershipwith a link to a pdf for downloading or printing.
In time, this will likely give rise to an increase incirculation of the Equine Disease Quarterly among
veterinarians and equine stakeholders, especiallyCollege of Agriculture, since the publication is available at no charge andFood and Environment material published is not subject to copyright.
Department of
While the distribution of future issues of theVeterinary Science
Quarterly will change to an electronic format, thepurpose of the publication will remain the sameas was stated in the Commentary of the first issue,
October 1992. It is to provide information on theincidence of particular diseases/syndromes and the
Lloyd’s—An international
insurance market for
emergence or re-emergence of previously unreported
bloodstock and otherdiseases. This will apply to outbreaks occurring inspecialist insurance.

Kentucky, the USA, and other parts of the world. It
will also serve as a reference source of the latest information on disease prevention and control strategies.
In preparation for the upcoming changes in
how the Quarterly will transition into an electronic
format, those currently receiving printed versions of
the publication are strongly encouraged to review
the information provided as follows and return their
responses by no later than November 15, 2021.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

To continue receiving the Equine
Disease Quarterly, please scan the
QR code or go to the following
link:
https://tinyurl.com/EDQemail
In a brief survey, you’ll be asked to provide youre-mail address, as well as your name and mailingaddress as printed on the Quarterly.
Please reply by November 15, 2021, to continue
receiving your issue without interruption.
Thank you for your ongoing interest in receiving
the Equine Disease Quarterly.

2

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

Second Quarter 2021

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 outbreaks.
African horse sickness was recorded throughout
the endemic area in the Republic of South Africa(RSA). Cases were confirmed in all nine provinces
including the controlled Protection Zone in theWestern Cape Province, where the disease was
identified on four premises.
Nepal reported an outbreak of glanders in 26
of 87 horses working at brick kilns and as “tangapullers.” Of these, 16 horses died.
France, Germany, Tunisia, the UK, and the
USA confirmed outbreaks of equine influenza. The
number of outbreaks included two each in France
and Tunisia, three in Germany, five in the UK,
and ten in the USA, where the disease is endemic.
With the exception of Tunisia, where 158 out of
861 horses were affected, the majority involved
one case.
Outbreaks of strangles were recorded by Belgium (14), Germany (one), the Netherlands (19),
Switzerland (seven), and the USA (35), where thedisease is endemic. The majority involved one case.
Equine herpesvirus 1 (EHV-1) infection is endemic in most countries. Outbreaks of respiratory
disease were reported by Belgium (three), France(10), Germany (one), Italy (11), the Netherlands,
the UK and the USA (four each), and Sweden(11), one of which was a case of co-infection with
Streptococcus zooepidemicus.
Outbreaks of EHV-1 abortion were confirmed
by Belgium, Ireland, Japan and the UK (threeapiece), Canada (one), France (four), Germany
and the Netherlands (two apiece), Sweden (five),and the USA (eight). The majority involved one
case.
Outbreaks of EHV-1 neurologic disease werediagnosed by Belgium, France and the UK (oneeach), Canada (two), Italy (10), and the USA(seven). Most outbreaks involved one case.
Equine herpesvirus 4 (EHV-4) respiratory
outbreaks were reported by Belgium (two), France(21), Italy (two), the Netherlands and Switzerland(one apiece), and the USA (reported in multiple
states).

Single cases of EHV-4 abortion were recorded
by Belgium and Ireland. Italy diagnosed a case of
EHV-4 neurologic disease.
The USA reported cases of equine herpesvirus 2
and/or 5, some associated with respiratory disease.
A case of equine adenovirus was diagnosed by
the USA. France confirmed two cases of equine
arteritis virus infection in stallions.
The USA reported 17 cases of Rhodococcus equi
infection.
Equine infectious anemia was confirmed by
Canada (single cases on four premises), Italy (nineoutbreaks, each involving one or two cases), andthe USA (seven outbreaks, four involving two toseven cases).
The RSA, Switzerland, and the USA reported
cases of equine piroplasmosis. The disease is endemic in RSA, with outbreaks recorded in eightof nine provinces, the majority in Gauteng. Switzerland confirmed two outbreaks, each involving asingle case, and the USA one outbreak, involving
two Quarter Horses.
Contagious equine metritis was diagnosed byGermany (10 outbreaks, all Icelandic horses) andthe UK (one case in an imported stallion). Belgium
reported one case of S. zooepidemicus abortion.
A range of enteric pathogens were recorded byvarious countries. The USA diagnosed outbreaksof salmonellosis, two involving serogroup B, one
serogroup C1 and one untyped Salmonella. Outbreaks of rotavirus infection were confirmed by
France (eight), Switzerland (one), and the USA(five involving rotavirus Type A and one TypeB). One outbreak of clostridial enterocolitis wasreported by Switzerland. The USA confirmed 129
PCR positive samples for Clostridium perfringens
and 107 for Clostridiodes difficile, the majority in
Kentucky. Outbreaks of equine coronavirus werediagnosed by Germany (two), Switzerland (one),and the USA (three cases). Single cases of Lawsonia
enteropathy and Potomac Horse fever were also
recorded by the USA.
Several neurological diseases were recorded
during the second quarter. Two cases of the dumb
form of rabies were confirmed in the USA, one in
Colorado and the other in Florida. The USA also
reported five outbreaks of Eastern equine encepha-lomyelitis and two of West Nile encephalitis. The
RSA recorded equine encephalosis as endemic in
the country, occurring in eight of nine provinces,with the majority of cases in Gauteng (33) and theNorthern Cape (31). Single cases of anaplasmosis

were diagnosed by Canada and Switzerland. Switzerland also reported a case involving co-infection
with anaplasmosis and ehrlichiosis. Outbreaks of
leptospirosis were confirmed by Germany (one)and Switzerland (two).

3

4

Exhaustion in HorsesExhausted horse syndrome refers to a range of
metabolic and physiologic conditions that
may occur when horses become fatigued. Affectedhorses may display a decrease in energy, appetite,or appear stiff and weak. In serious cases, cardiac
arrhythmias, shock, muscle damage, colic, anddiarrhea may develop. Horses that are underconditioned, performing in endurance events,
or exercised in hot or humid environments areat higher risk for exhaustion. If exercise is not
immediately halted and treatment initiated, thenlife-threatening complications may occur.
Exhaustion may develop with any prolonged
period of exercise such as endurance rides, threeday events, and extended trail rides. Many factors
contribute to the potential for exhaustion. Different breeds are better suited to prolonged exercise
while others excel at shorter, more high intensity
work. The animal’s training and fitness ideallyshould be suited for the event they are participating in, although even highly prepared animals
may develop exhaustion. Any underlying disease,including lameness, anemia, and respiratory disease will increase the risk of fatigue.
Exhaustion is a multifactorial condition. Heat,electrolyte imbalance and energy stores may
contribute. A large amount of heat is produced
while exercising. Heat needs to be appropriately
regulated and removed from an exercising animal
via sweat and air movement. If heat is not removed,
then the core body temperature steadily increases.
Approximately 65% of heat is lost via sweat, 25%
via respiratory evaporation, and the remaining
10% via other mechanisms. This is made moredifficult when the conditions include high heat andhumidity or when the animal is dehydrated. Sweat
contains important electrolytes such as sodium,
potassium, calcium and chloride which are lost as
the horse sweats. If electrolyte imbalances are notcorrected, then serious derangements occur leading to shifts in blood pH and cellular stability. The
primary energy source for muscles is stored glycogen, which is a finite resource. Glycogen stores canbe increased with training and exercise, but once
depleted the muscle lacks a primary energy sourceand exercise will slow or stop.

Horses with exhaustion will have an increased
heart rate, temperature, and respiratory rate. They
may appear depressed, unwilling to eat and drink,
and, in some cases, develop colic, shock, or laminitis. Horses that move with a stiff gait may havesignificant muscle damage and/or laminitis. These
animals should not be forced to move if treatment
can be provided on site. Affected horses are typically dehydrated and blood work shows evidence ofstress and electrolyte imbalances. Muscle enzyme
values will be increased and often continue to increase as muscle damage continues. Kidney values,
which reflect both dehydration and renal damage,
may be elevated and urine may be significantly
decreased in volume and dark brown/red in color.
Genetic testing, muscle biopsy or other diagnostic
testing may be needed to determine an underlying
cause in cases of repeated myopathy or suspectedexhaustion.
Treatment includes immediately stopping exercise and initiating assisted cooling. This can bedone with electric fans and running large volumesof cold water over the entire body. Intravenous
fluids can be given to restore hydration andelectrolyte status. Once there is evidence that theintestinal tract is functioning, then oral fluids may
be added to aid hydration; however, these should
not be administered until the horse has good gut
sounds and no signs of colic. Horses should not
be transported following exhaustion until clearedby their medical team.
Exhaustion is best prevented by acclimatization,
proper training, nutrition, and supplementation ofelectrolytes. Electrolyte products require adequate
water intake to be effective. Horses given concentrated electrolytes without appropriate water
consumption will actually increase dehydration.
Acclimatization to a climate with excessive heat,
altitude, or humidity may take up to two weeks.
Conditioning will create larger muscle glycogenstores, improve efficiency of heat elimination, andtrain horses to eat and drink during prolonged
work. It is also important to allow horses enoughtime to recover and rehydrate from transport prior
to beginning competition.

Event organizers will assess the safety associatedwith heat and humidity, and events may need
to be cancelled if environmental conditions are
considered dangerous. A rider may be the first torecognize that their horse is displaying abnormal
behavior or unwillingness to work, which is often
an early sign of exhaustion. Vet checks throughout
endurance events are designed to identify horses

showing early signs of fatigue. These checks may
require horses be rested or removed from competition before serious complications occur.
CONTACT:
Rebecca Ruby, MS, BVSc, Diplomate ACVP, ACVIM-LAIM
Rebecca.ruby@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

N AT I O N A L

Polyuria and Polydipsia in Horses

P

Matt Barton, Agricultural Communications

To continue
receiving theEquine Disease
Quarterly,
please scan
the QR codeor go to the following link:
https://tinyurl.com/EDQemail
Please reply by November
15, 2021.

olyuria (PU), defined as an increased volumeof urine, is a rare, but significant, indicator ofa variety of diseases. Polydipsia (PD), excessive
thirst and fluid intake, is the natural companion to
PU as these two clinical signs nearly always occur
together. A healthy, average-sized horse weighing
1,100 lb (500 kg) will typically drink ~13 gallons(50 L) of water each day, although this can vary
based on environmental factors, exercise, pregnancy status, illness, and more. Urine productionin healthy, adult horses is ~2.5-4 gallons (10-15 L)
per day for an average horse. An adult horse with
PD will have a daily fluid intake that is double
or more than normal, and horses with PU willoften have urine production in excess of 2-3 times
normal. Once it has been determined that a horse
is PU or PD, a veterinarian should be called toinvestigate the cause.
Psychogenic Polydipsia: Primary or psychogenic

PD (PPD) occurs when a horse drinks excessively
in the absence of a physiologic reason and is oneof the most common causes of PD and subsequent
PU. Diet, management, and housing have been
implicated as factors contributing to PPD. Thiscondition, sometimes considered a vice, can beseen in horses housed in stalls and can occur withother behavioral abnormalities such as chewing on
doors or eating bedding. Stressors such as changes
in housing, management, and environment havealso been reported to incite PPD. Dietary factors
such as high dry matter intake or compulsive salt
consumption may lead to excessive water consumption. Horses with PPD will produce copious
volumes of urine, more than those with Cushing’s
disease or chronic renal failure. Owners often
report that stalls or paddocks are soaking wet andthe horse drinks more than other horses. Urine will
be dilute, but these animals have normal kidney

function and are usually in good body condition.
Cushing’s Disease (Pituitary Pars Intermedia Dysfunction—PPID): The incidence of PU in horses

with PPID is highly variable, but has been estimated to be around 33%.

Chronic Renal Failure (CRF): The most common

causes of chronic renal failure (CRF) and endstage kidney disease in horses are drugs, toxins,
myopathy, and developmental abnormalities.
Although PU is a relatively common sign of CRF,
it sometimes goes unnoticed by owners, because
it is mild to moderate. This is especially true if ananimal is housed with other horses or is on pasture, making it hard to know how much urine anindividual horse is producing. Additional clinicalsigns are dependent on the stage of CRF, but can
include weight loss, ventral edema, rough or dullhair coat, decreased appetite, dental tartar and oral
ulcers, blood in the feces, and poor performance.
Diabetes: Two types of diabetes exist and can cause

PU/PD in horses, but both types are rare. Diabetes
insipidus occurs due to either decreased or absent
production of vasopressin, a hormone responsible
for absorption of water by the kidneys or insensitivity of the kidneys to vasopressin. Clinical signs
include enormous volumes of dilute urine. In
contrast, diabetes mellitus (DM) occurs due to insulin deficiency (type 1) or insulin resistance (type2). PU, PD, and weight loss are common signs inhorses with type 2 DM. Differentiation between
the two types of diabetes and their respective
subtypes is necessary for treatment and prognosis.
Other Causes of Polyuria: Drugs such as diuretics,

sedatives, and corticosteroids can cause PU inhorses, and other drugs can induce PU by inciting
continued on page 5

2

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

Second Quarter 2021

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 outbreaks.
African horse sickness was recorded throughout
the endemic area in the Republic of South Africa(RSA). Cases were confirmed in all nine provinces
including the controlled Protection Zone in theWestern Cape Province, where the disease was
identified on four premises.
Nepal reported an outbreak of glanders in 26
of 87 horses working at brick kilns and as “tangapullers.” Of these, 16 horses died.
France, Germany, Tunisia, the UK, and the
USA confirmed outbreaks of equine influenza. The
number of outbreaks included two each in France
and Tunisia, three in Germany, five in the UK,
and ten in the USA, where the disease is endemic.
With the exception of Tunisia, where 158 out of
861 horses were affected, the majority involved
one case.
Outbreaks of strangles were recorded by Belgium (14), Germany (one), the Netherlands (19),
Switzerland (seven), and the USA (35), where thedisease is endemic. The majority involved one case.
Equine herpesvirus 1 (EHV-1) infection is endemic in most countries. Outbreaks of respiratory
disease were reported by Belgium (three), France(10), Germany (one), Italy (11), the Netherlands,
the UK and the USA (four each), and Sweden(11), one of which was a case of co-infection with
Streptococcus zooepidemicus.
Outbreaks of EHV-1 abortion were confirmed
by Belgium, Ireland, Japan and the UK (threeapiece), Canada (one), France (four), Germany
and the Netherlands (two apiece), Sweden (five),and the USA (eight). The majority involved one
case.
Outbreaks of EHV-1 neurologic disease werediagnosed by Belgium, France and the UK (oneeach), Canada (two), Italy (10), and the USA(seven). Most outbreaks involved one case.
Equine herpesvirus 4 (EHV-4) respiratory
outbreaks were reported by Belgium (two), France(21), Italy (two), the Netherlands and Switzerland(one apiece), and the USA (reported in multiple
states).

Single cases of EHV-4 abortion were recorded
by Belgium and Ireland. Italy diagnosed a case of
EHV-4 neurologic disease.
The USA reported cases of equine herpesvirus 2
and/or 5, some associated with respiratory disease.
A case of equine adenovirus was diagnosed by
the USA. France confirmed two cases of equine
arteritis virus infection in stallions.
The USA reported 17 cases of Rhodococcus equi
infection.
Equine infectious anemia was confirmed by
Canada (single cases on four premises), Italy (nineoutbreaks, each involving one or two cases), andthe USA (seven outbreaks, four involving two toseven cases).
The RSA, Switzerland, and the USA reported
cases of equine piroplasmosis. The disease is endemic in RSA, with outbreaks recorded in eightof nine provinces, the majority in Gauteng. Switzerland confirmed two outbreaks, each involving asingle case, and the USA one outbreak, involving
two Quarter Horses.
Contagious equine metritis was diagnosed byGermany (10 outbreaks, all Icelandic horses) andthe UK (one case in an imported stallion). Belgium
reported one case of S. zooepidemicus abortion.
A range of enteric pathogens were recorded byvarious countries. The USA diagnosed outbreaksof salmonellosis, two involving serogroup B, one
serogroup C1 and one untyped Salmonella. Outbreaks of rotavirus infection were confirmed by
France (eight), Switzerland (one), and the USA(five involving rotavirus Type A and one TypeB). One outbreak of clostridial enterocolitis wasreported by Switzerland. The USA confirmed 129
PCR positive samples for Clostridium perfringens
and 107 for Clostridiodes difficile, the majority in
Kentucky. Outbreaks of equine coronavirus werediagnosed by Germany (two), Switzerland (one),and the USA (three cases). Single cases of Lawsonia
enteropathy and Potomac Horse fever were also
recorded by the USA.
Several neurological diseases were recorded
during the second quarter. Two cases of the dumb
form of rabies were confirmed in the USA, one in
Colorado and the other in Florida. The USA also
reported five outbreaks of Eastern equine encepha-lomyelitis and two of West Nile encephalitis. The
RSA recorded equine encephalosis as endemic in
the country, occurring in eight of nine provinces,with the majority of cases in Gauteng (33) and theNorthern Cape (31). Single cases of anaplasmosis

were diagnosed by Canada and Switzerland. Switzerland also reported a case involving co-infection
with anaplasmosis and ehrlichiosis. Outbreaks of
leptospirosis were confirmed by Germany (one)and Switzerland (two).

3

4

Exhaustion in HorsesExhausted horse syndrome refers to a range of
metabolic and physiologic conditions that
may occur when horses become fatigued. Affectedhorses may display a decrease in energy, appetite,or appear stiff and weak. In serious cases, cardiac
arrhythmias, shock, muscle damage, colic, anddiarrhea may develop. Horses that are underconditioned, performing in endurance events,
or exercised in hot or humid environments areat higher risk for exhaustion. If exercise is not
immediately halted and treatment initiated, thenlife-threatening complications may occur.
Exhaustion may develop with any prolonged
period of exercise such as endurance rides, threeday events, and extended trail rides. Many factors
contribute to the potential for exhaustion. Different breeds are better suited to prolonged exercise
while others excel at shorter, more high intensity
work. The animal’s training and fitness ideallyshould be suited for the event they are participating in, although even highly prepared animals
may develop exhaustion. Any underlying disease,including lameness, anemia, and respiratory disease will increase the risk of fatigue.
Exhaustion is a multifactorial condition. Heat,electrolyte imbalance and energy stores may
contribute. A large amount of heat is produced
while exercising. Heat needs to be appropriately
regulated and removed from an exercising animal
via sweat and air movement. If heat is not removed,
then the core body temperature steadily increases.
Approximately 65% of heat is lost via sweat, 25%
via respiratory evaporation, and the remaining
10% via other mechanisms. This is made moredifficult when the conditions include high heat andhumidity or when the animal is dehydrated. Sweat
contains important electrolytes such as sodium,
potassium, calcium and chloride which are lost as
the horse sweats. If electrolyte imbalances are notcorrected, then serious derangements occur leading to shifts in blood pH and cellular stability. The
primary energy source for muscles is stored glycogen, which is a finite resource. Glycogen stores canbe increased with training and exercise, but once
depleted the muscle lacks a primary energy sourceand exercise will slow or stop.

Horses with exhaustion will have an increased
heart rate, temperature, and respiratory rate. They
may appear depressed, unwilling to eat and drink,
and, in some cases, develop colic, shock, or laminitis. Horses that move with a stiff gait may havesignificant muscle damage and/or laminitis. These
animals should not be forced to move if treatment
can be provided on site. Affected horses are typically dehydrated and blood work shows evidence ofstress and electrolyte imbalances. Muscle enzyme
values will be increased and often continue to increase as muscle damage continues. Kidney values,
which reflect both dehydration and renal damage,
may be elevated and urine may be significantly
decreased in volume and dark brown/red in color.
Genetic testing, muscle biopsy or other diagnostic
testing may be needed to determine an underlying
cause in cases of repeated myopathy or suspectedexhaustion.
Treatment includes immediately stopping exercise and initiating assisted cooling. This can bedone with electric fans and running large volumesof cold water over the entire body. Intravenous
fluids can be given to restore hydration andelectrolyte status. Once there is evidence that theintestinal tract is functioning, then oral fluids may
be added to aid hydration; however, these should
not be administered until the horse has good gut
sounds and no signs of colic. Horses should not
be transported following exhaustion until clearedby their medical team.
Exhaustion is best prevented by acclimatization,
proper training, nutrition, and supplementation ofelectrolytes. Electrolyte products require adequate
water intake to be effective. Horses given concentrated electrolytes without appropriate water
consumption will actually increase dehydration.
Acclimatization to a climate with excessive heat,
altitude, or humidity may take up to two weeks.
Conditioning will create larger muscle glycogenstores, improve efficiency of heat elimination, andtrain horses to eat and drink during prolonged
work. It is also important to allow horses enoughtime to recover and rehydrate from transport prior
to beginning competition.

Event organizers will assess the safety associatedwith heat and humidity, and events may need
to be cancelled if environmental conditions are
considered dangerous. A rider may be the first torecognize that their horse is displaying abnormal
behavior or unwillingness to work, which is often
an early sign of exhaustion. Vet checks throughout
endurance events are designed to identify horses

showing early signs of fatigue. These checks may
require horses be rested or removed from competition before serious complications occur.
CONTACT:
Rebecca Ruby, MS, BVSc, Diplomate ACVP, ACVIM-LAIM
Rebecca.ruby@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

N AT I O N A L

Polyuria and Polydipsia in Horses

P

Matt Barton, Agricultural Communications

To continue
receiving theEquine Disease
Quarterly,
please scan
the QR codeor go to the following link:
https://tinyurl.com/EDQemail
Please reply by November
15, 2021.

olyuria (PU), defined as an increased volumeof urine, is a rare, but significant, indicator ofa variety of diseases. Polydipsia (PD), excessive
thirst and fluid intake, is the natural companion to
PU as these two clinical signs nearly always occur
together. A healthy, average-sized horse weighing
1,100 lb (500 kg) will typically drink ~13 gallons(50 L) of water each day, although this can vary
based on environmental factors, exercise, pregnancy status, illness, and more. Urine productionin healthy, adult horses is ~2.5-4 gallons (10-15 L)
per day for an average horse. An adult horse with
PD will have a daily fluid intake that is double
or more than normal, and horses with PU willoften have urine production in excess of 2-3 times
normal. Once it has been determined that a horse
is PU or PD, a veterinarian should be called toinvestigate the cause.
Psychogenic Polydipsia: Primary or psychogenic

PD (PPD) occurs when a horse drinks excessively
in the absence of a physiologic reason and is oneof the most common causes of PD and subsequent
PU. Diet, management, and housing have been
implicated as factors contributing to PPD. Thiscondition, sometimes considered a vice, can beseen in horses housed in stalls and can occur withother behavioral abnormalities such as chewing on
doors or eating bedding. Stressors such as changes
in housing, management, and environment havealso been reported to incite PPD. Dietary factors
such as high dry matter intake or compulsive salt
consumption may lead to excessive water consumption. Horses with PPD will produce copious
volumes of urine, more than those with Cushing’s
disease or chronic renal failure. Owners often
report that stalls or paddocks are soaking wet andthe horse drinks more than other horses. Urine will
be dilute, but these animals have normal kidney

function and are usually in good body condition.
Cushing’s Disease (Pituitary Pars Intermedia Dysfunction—PPID): The incidence of PU in horses

with PPID is highly variable, but has been estimated to be around 33%.

Chronic Renal Failure (CRF): The most common

causes of chronic renal failure (CRF) and endstage kidney disease in horses are drugs, toxins,
myopathy, and developmental abnormalities.
Although PU is a relatively common sign of CRF,
it sometimes goes unnoticed by owners, because
it is mild to moderate. This is especially true if ananimal is housed with other horses or is on pasture, making it hard to know how much urine anindividual horse is producing. Additional clinicalsigns are dependent on the stage of CRF, but can
include weight loss, ventral edema, rough or dullhair coat, decreased appetite, dental tartar and oral
ulcers, blood in the feces, and poor performance.
Diabetes: Two types of diabetes exist and can cause

PU/PD in horses, but both types are rare. Diabetes
insipidus occurs due to either decreased or absent
production of vasopressin, a hormone responsible
for absorption of water by the kidneys or insensitivity of the kidneys to vasopressin. Clinical signs
include enormous volumes of dilute urine. In
contrast, diabetes mellitus (DM) occurs due to insulin deficiency (type 1) or insulin resistance (type2). PU, PD, and weight loss are common signs inhorses with type 2 DM. Differentiation between
the two types of diabetes and their respective
subtypes is necessary for treatment and prognosis.
Other Causes of Polyuria: Drugs such as diuretics,

sedatives, and corticosteroids can cause PU inhorses, and other drugs can induce PU by inciting
continued on page 5

2

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

Second Quarter 2021

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 outbreaks.
African horse sickness was recorded throughout
the endemic area in the Republic of South Africa(RSA). Cases were confirmed in all nine provinces
including the controlled Protection Zone in theWestern Cape Province, where the disease was
identified on four premises.
Nepal reported an outbreak of glanders in 26
of 87 horses working at brick kilns and as “tangapullers.” Of these, 16 horses died.
France, Germany, Tunisia, the UK, and the
USA confirmed outbreaks of equine influenza. The
number of outbreaks included two each in France
and Tunisia, three in Germany, five in the UK,
and ten in the USA, where the disease is endemic.
With the exception of Tunisia, where 158 out of
861 horses were affected, the majority involved
one case.
Outbreaks of strangles were recorded by Belgium (14), Germany (one), the Netherlands (19),
Switzerland (seven), and the USA (35), where thedisease is endemic. The majority involved one case.
Equine herpesvirus 1 (EHV-1) infection is endemic in most countries. Outbreaks of respiratory
disease were reported by Belgium (three), France(10), Germany (one), Italy (11), the Netherlands,
the UK and the USA (four each), and Sweden(11), one of which was a case of co-infection with
Streptococcus zooepidemicus.
Outbreaks of EHV-1 abortion were confirmed
by Belgium, Ireland, Japan and the UK (threeapiece), Canada (one), France (four), Germany
and the Netherlands (two apiece), Sweden (five),and the USA (eight). The majority involved one
case.
Outbreaks of EHV-1 neurologic disease werediagnosed by Belgium, France and the UK (oneeach), Canada (two), Italy (10), and the USA(seven). Most outbreaks involved one case.
Equine herpesvirus 4 (EHV-4) respiratory
outbreaks were reported by Belgium (two), France(21), Italy (two), the Netherlands and Switzerland(one apiece), and the USA (reported in multiple
states).

Single cases of EHV-4 abortion were recorded
by Belgium and Ireland. Italy diagnosed a case of
EHV-4 neurologic disease.
The USA reported cases of equine herpesvirus 2
and/or 5, some associated with respiratory disease.
A case of equine adenovirus was diagnosed by
the USA. France confirmed two cases of equine
arteritis virus infection in stallions.
The USA reported 17 cases of Rhodococcus equi
infection.
Equine infectious anemia was confirmed by
Canada (single cases on four premises), Italy (nineoutbreaks, each involving one or two cases), andthe USA (seven outbreaks, four involving two toseven cases).
The RSA, Switzerland, and the USA reported
cases of equine piroplasmosis. The disease is endemic in RSA, with outbreaks recorded in eightof nine provinces, the majority in Gauteng. Switzerland confirmed two outbreaks, each involving asingle case, and the USA one outbreak, involving
two Quarter Horses.
Contagious equine metritis was diagnosed byGermany (10 outbreaks, all Icelandic horses) andthe UK (one case in an imported stallion). Belgium
reported one case of S. zooepidemicus abortion.
A range of enteric pathogens were recorded byvarious countries. The USA diagnosed outbreaksof salmonellosis, two involving serogroup B, one
serogroup C1 and one untyped Salmonella. Outbreaks of rotavirus infection were confirmed by
France (eight), Switzerland (one), and the USA(five involving rotavirus Type A and one TypeB). One outbreak of clostridial enterocolitis wasreported by Switzerland. The USA confirmed 129
PCR positive samples for Clostridium perfringens
and 107 for Clostridiodes difficile, the majority in
Kentucky. Outbreaks of equine coronavirus werediagnosed by Germany (two), Switzerland (one),and the USA (three cases). Single cases of Lawsonia
enteropathy and Potomac Horse fever were also
recorded by the USA.
Several neurological diseases were recorded
during the second quarter. Two cases of the dumb
form of rabies were confirmed in the USA, one in
Colorado and the other in Florida. The USA also
reported five outbreaks of Eastern equine encepha-lomyelitis and two of West Nile encephalitis. The
RSA recorded equine encephalosis as endemic in
the country, occurring in eight of nine provinces,with the majority of cases in Gauteng (33) and theNorthern Cape (31). Single cases of anaplasmosis

were diagnosed by Canada and Switzerland. Switzerland also reported a case involving co-infection
with anaplasmosis and ehrlichiosis. Outbreaks of
leptospirosis were confirmed by Germany (one)and Switzerland (two).

3

4

Exhaustion in HorsesExhausted horse syndrome refers to a range of
metabolic and physiologic conditions that
may occur when horses become fatigued. Affectedhorses may display a decrease in energy, appetite,or appear stiff and weak. In serious cases, cardiac
arrhythmias, shock, muscle damage, colic, anddiarrhea may develop. Horses that are underconditioned, performing in endurance events,
or exercised in hot or humid environments areat higher risk for exhaustion. If exercise is not
immediately halted and treatment initiated, thenlife-threatening complications may occur.
Exhaustion may develop with any prolonged
period of exercise such as endurance rides, threeday events, and extended trail rides. Many factors
contribute to the potential for exhaustion. Different breeds are better suited to prolonged exercise
while others excel at shorter, more high intensity
work. The animal’s training and fitness ideallyshould be suited for the event they are participating in, although even highly prepared animals
may develop exhaustion. Any underlying disease,including lameness, anemia, and respiratory disease will increase the risk of fatigue.
Exhaustion is a multifactorial condition. Heat,electrolyte imbalance and energy stores may
contribute. A large amount of heat is produced
while exercising. Heat needs to be appropriately
regulated and removed from an exercising animal
via sweat and air movement. If heat is not removed,
then the core body temperature steadily increases.
Approximately 65% of heat is lost via sweat, 25%
via respiratory evaporation, and the remaining
10% via other mechanisms. This is made moredifficult when the conditions include high heat andhumidity or when the animal is dehydrated. Sweat
contains important electrolytes such as sodium,
potassium, calcium and chloride which are lost as
the horse sweats. If electrolyte imbalances are notcorrected, then serious derangements occur leading to shifts in blood pH and cellular stability. The
primary energy source for muscles is stored glycogen, which is a finite resource. Glycogen stores canbe increased with training and exercise, but once
depleted the muscle lacks a primary energy sourceand exercise will slow or stop.

Horses with exhaustion will have an increased
heart rate, temperature, and respiratory rate. They
may appear depressed, unwilling to eat and drink,
and, in some cases, develop colic, shock, or laminitis. Horses that move with a stiff gait may havesignificant muscle damage and/or laminitis. These
animals should not be forced to move if treatment
can be provided on site. Affected horses are typically dehydrated and blood work shows evidence ofstress and electrolyte imbalances. Muscle enzyme
values will be increased and often continue to increase as muscle damage continues. Kidney values,
which reflect both dehydration and renal damage,
may be elevated and urine may be significantly
decreased in volume and dark brown/red in color.
Genetic testing, muscle biopsy or other diagnostic
testing may be needed to determine an underlying
cause in cases of repeated myopathy or suspectedexhaustion.
Treatment includes immediately stopping exercise and initiating assisted cooling. This can bedone with electric fans and running large volumesof cold water over the entire body. Intravenous
fluids can be given to restore hydration andelectrolyte status. Once there is evidence that theintestinal tract is functioning, then oral fluids may
be added to aid hydration; however, these should
not be administered until the horse has good gut
sounds and no signs of colic. Horses should not
be transported following exhaustion until clearedby their medical team.
Exhaustion is best prevented by acclimatization,
proper training, nutrition, and supplementation ofelectrolytes. Electrolyte products require adequate
water intake to be effective. Horses given concentrated electrolytes without appropriate water
consumption will actually increase dehydration.
Acclimatization to a climate with excessive heat,
altitude, or humidity may take up to two weeks.
Conditioning will create larger muscle glycogenstores, improve efficiency of heat elimination, andtrain horses to eat and drink during prolonged
work. It is also important to allow horses enoughtime to recover and rehydrate from transport prior
to beginning competition.

Event organizers will assess the safety associatedwith heat and humidity, and events may need
to be cancelled if environmental conditions are
considered dangerous. A rider may be the first torecognize that their horse is displaying abnormal
behavior or unwillingness to work, which is often
an early sign of exhaustion. Vet checks throughout
endurance events are designed to identify horses

showing early signs of fatigue. These checks may
require horses be rested or removed from competition before serious complications occur.
CONTACT:
Rebecca Ruby, MS, BVSc, Diplomate ACVP, ACVIM-LAIM
Rebecca.ruby@uky.edu(859) 257-8283
University of Kentucky Veterinary Diagnostic Laboratory
Lexington, Kentucky

N AT I O N A L

Polyuria and Polydipsia in Horses

P

Matt Barton, Agricultural Communications

To continue
receiving theEquine Disease
Quarterly,
please scan
the QR codeor go to the following link:
https://tinyurl.com/EDQemail
Please reply by November
15, 2021.

olyuria (PU), defined as an increased volumeof urine, is a rare, but significant, indicator ofa variety of diseases. Polydipsia (PD), excessive
thirst and fluid intake, is the natural companion to
PU as these two clinical signs nearly always occur
together. A healthy, average-sized horse weighing
1,100 lb (500 kg) will typically drink ~13 gallons(50 L) of water each day, although this can vary
based on environmental factors, exercise, pregnancy status, illness, and more. Urine productionin healthy, adult horses is ~2.5-4 gallons (10-15 L)
per day for an average horse. An adult horse with
PD will have a daily fluid intake that is double
or more than normal, and horses with PU willoften have urine production in excess of 2-3 times
normal. Once it has been determined that a horse
is PU or PD, a veterinarian should be called toinvestigate the cause.
Psychogenic Polydipsia: Primary or psychogenic

PD (PPD) occurs when a horse drinks excessively
in the absence of a physiologic reason and is oneof the most common causes of PD and subsequent
PU. Diet, management, and housing have been
implicated as factors contributing to PPD. Thiscondition, sometimes considered a vice, can beseen in horses housed in stalls and can occur withother behavioral abnormalities such as chewing on
doors or eating bedding. Stressors such as changes
in housing, management, and environment havealso been reported to incite PPD. Dietary factors
such as high dry matter intake or compulsive salt
consumption may lead to excessive water consumption. Horses with PPD will produce copious
volumes of urine, more than those with Cushing’s
disease or chronic renal failure. Owners often
report that stalls or paddocks are soaking wet andthe horse drinks more than other horses. Urine will
be dilute, but these animals have normal kidney

function and are usually in good body condition.
Cushing’s Disease (Pituitary Pars Intermedia Dysfunction—PPID): The incidence of PU in horses

with PPID is highly variable, but has been estimated to be around 33%.

Chronic Renal Failure (CRF): The most common

causes of chronic renal failure (CRF) and endstage kidney disease in horses are drugs, toxins,
myopathy, and developmental abnormalities.
Although PU is a relatively common sign of CRF,
it sometimes goes unnoticed by owners, because
it is mild to moderate. This is especially true if ananimal is housed with other horses or is on pasture, making it hard to know how much urine anindividual horse is producing. Additional clinicalsigns are dependent on the stage of CRF, but can
include weight loss, ventral edema, rough or dullhair coat, decreased appetite, dental tartar and oral
ulcers, blood in the feces, and poor performance.
Diabetes: Two types of diabetes exist and can cause

PU/PD in horses, but both types are rare. Diabetes
insipidus occurs due to either decreased or absent
production of vasopressin, a hormone responsible
for absorption of water by the kidneys or insensitivity of the kidneys to vasopressin. Clinical signs
include enormous volumes of dilute urine. In
contrast, diabetes mellitus (DM) occurs due to insulin deficiency (type 1) or insulin resistance (type2). PU, PD, and weight loss are common signs inhorses with type 2 DM. Differentiation between
the two types of diabetes and their respective
subtypes is necessary for treatment and prognosis.
Other Causes of Polyuria: Drugs such as diuretics,

sedatives, and corticosteroids can cause PU inhorses, and other drugs can induce PU by inciting
continued on page 5

Equine Disease Quarterly Newsletter

5

Polyuria and Polydipsia, continued from page 4.

acute or chronic kidney injury. Aminoglycosides(gentamicin, amikacin), oxytetracycline, nonsteroidal anti-inflammatories (phenylbutazone,
flunixin meglumine), polymyxin B, amphotericin
B, imidocarb dipropionate, and bisphosphonates
are all potentially toxic to the kidneys and havedocumented and/or anecdotal reports of renal
disease following their use. Additional diseases
associated with PU include but are not limited toliver failure, neoplasia, toxicities, inflammatory
conditions, and parasitism.

Diagnosis: Testing to determine the cause of PU/

PD should start with a chemistry profile and urine
analysis for the presence of elevations in kidney
enzymes, changes in electrolyte levels, high blood
glucose levels, and measurement of urine specificgravity to determine the concentration of theurine. Additional bloodwork may be necessary,and urinalysis and additional urine testing may
be useful for identifying early kidney disease. Occasionally, advanced testing is needed to diagnosis
the underlying cause of PU.

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

Presorted Standard
US Postage Paid
Permit 51
Lexington KY

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

OCTOBER 2021
Volume 30, Number 4

CONTACT:
Emily A. Barrell, DVM, MSc, DACVIM
ebarrell@umn.edu
Department of Veterinary Population Medicine
University of Minnesota College of Veterinary Medicine
Saint Paul, Minnesota

C O M M E N TA RY
IN THIS ISSUEKENTUCKY

Equine Rotavirus B and Neonatal Foal Diarrhea

Group A and B rotaviruses are significant enteric pathogens that cause diarrhea of variable
severity in humans and domestic animals. Despite
no difference in clinical signs or symptoms, it has
been well documented that there is no antibodymediated cross-protection between groups A and
B. The horse is a unique species in which only
group A rotaviruses typically cause foal diarrhea
outbreaks.
During the 2021 foaling season (February andMarch) in central Kentucky, increased frequencies
of diarrhea were noted in neonatal foals between
1 and 4 days of age. Mares had been previously
vaccinated with an inactivated monovalent equine
rotavirus A vaccine during their pregnancy. Foals
developed diarrhea at approximately 24 h of age
and diarrheic episodes typically lasted 3-4 days.
Some farms experienced up to 100% morbidity.
Newly born foals on affected farms quickly developed diarrhea, suggesting a highly contagious
disease. Clinical signs included inappetence, weakness, dehydration, severe electrolyte imbalance,
and watery yellow and foul-smelling diarrhea.
Hemorrhagic watery diarrhea was noticed in somecases. None of the foal’s dams developed diarrhea.
Diagnostic investigation of fecal samples from
diseased foals, which included PCR and microbial culture, failed to detect diarrhea-causing

pathogens, including equine rotavirus A. Interestingly, metagenomic sequencing data identified anabundant amount of novel rotavirus B genome infecal specimens from affected foals and absenceof other known enteric pathogens, suggesting an
etiological role of this rotavirus B in neonatal foal
diarrhea. Further evidence linking rotavirus B tothis outbreak of highly contagious foal diarrhea is
supported by the poor responses of the affectedfoals to antibiotic treatment as well as seemingly
ineffective equine rotavirus A-specific passive
maternal antibodies in affected foals against thisnew virus. Subsequent analysis of 33 foal diarrheic
samples by RT-qPCR identified 23 rotavirus Bpositive cases (69.69%). Despite a small sample
size, the prevalence of equine rotavirus B in diseased foals was similar to that reported in equine
rotavirus A-associated foal diarrhea outbreaks.
Bioinformatic analysis of the viral genome data
showed that the protein sequence of all 11 viralsegments had greater than 96% homology (relatedness) with group B rotaviruses previously foundin ruminants. Furthermore, evolutionary studies
demonstrated clustering of the equine virus withgroup B rotaviruses of caprine and bovine strainsthat circulated in the USA. These results indicate
the possibility that the equine rotavirus B was ofruminant origin.

In summary, evidence suggests that a novel,
ruminant-origin, group B rotavirus has emergedin horses and was associated with outbreaks ofneonatal foal diarrhea in the 2021 foaling season
in Kentucky. Emergence of the ruminant-like
group B rotavirus in foals clearly warrants further
investigation due to the significant impact of thedisease in neonatal foals and its economic impact
on the equine industry.
CONTACT:
Emma Adam, DVM, PhD, DACVIM, DACVS
emma.adam@uky.edu(859) 562-2186
Feng Li, DVM, PhD
feng.li@uky.edu(859) 218-1106
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

All photos: Matt Barton, Agricultural Communications

S

ince its inception in 1992, the Equine Disease
Quarterly has been distributed worldwide in a
Commentary
printed format. The funding to make this possible
was provided through the generosity of Lloyd’s ofInternational
London, Underwriters and Brokers and their KenSecond Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 tucky Agents, and in later years, by Underwriters at
Lloyd’s, London. Circulation of the Quarterly went
Exhaustion in
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 3 from several hundred copies in October 1992, toapproximately 17,000 copies in 2021, and reachedreaders in over 87 countries.
National
In late 2020, Lloyd’s Underwriters confirmed
Polyuria and
Polydipsia inthat because of changing circumstances, it could
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 4 no longer sustain support of the Equine Disease
Quarterly beyond 2021. Thankfully, a new sponsor,
KentuckyEquus Standardbred Station, Inc., recently came
Equine Rotavirus B
forward and generously agreed to help the continand Neonatal
Foal Diarrhea .  .  .  .  .  .  .  . 5 ued distribution of this worthwhile publication.
This recent development provides a long overdue
opportunity to bring about a change in how the
Quarterly can best be made available to its readership. Considered opinion is to transition from mailing print copies to an electronic format, where eachissue is available on the internet. This will have theimportant advantage that once each issue is posted,
it will be immediately available to the readershipwith a link to a pdf for downloading or printing.
In time, this will likely give rise to an increase incirculation of the Equine Disease Quarterly among
veterinarians and equine stakeholders, especiallyCollege of Agriculture, since the publication is available at no charge andFood and Environment material published is not subject to copyright.
Department of
While the distribution of future issues of theVeterinary Science
Quarterly will change to an electronic format, thepurpose of the publication will remain the sameas was stated in the Commentary of the first issue,
October 1992. It is to provide information on theincidence of particular diseases/syndromes and the
Lloyd’s—An international
insurance market for
emergence or re-emergence of previously unreported
bloodstock and otherdiseases. This will apply to outbreaks occurring inspecialist insurance.

Kentucky, the USA, and other parts of the world. It
will also serve as a reference source of the latest information on disease prevention and control strategies.
In preparation for the upcoming changes in
how the Quarterly will transition into an electronic
format, those currently receiving printed versions of
the publication are strongly encouraged to review
the information provided as follows and return their
responses by no later than November 15, 2021.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

To continue receiving the Equine
Disease Quarterly, please scan the
QR code or go to the following
link:
https://tinyurl.com/EDQemail
In a brief survey, you’ll be asked to provide youre-mail address, as well as your name and mailingaddress as printed on the Quarterly.
Please reply by November 15, 2021, to continue
receiving your issue without interruption.
Thank you for your ongoing interest in receiving
the Equine Disease Quarterly.

Equine Disease Quarterly Newsletter

5

Polyuria and Polydipsia, continued from page 4.

acute or chronic kidney injury. Aminoglycosides(gentamicin, amikacin), oxytetracycline, nonsteroidal anti-inflammatories (phenylbutazone,
flunixin meglumine), polymyxin B, amphotericin
B, imidocarb dipropionate, and bisphosphonates
are all potentially toxic to the kidneys and havedocumented and/or anecdotal reports of renal
disease following their use. Additional diseases
associated with PU include but are not limited toliver failure, neoplasia, toxicities, inflammatory
conditions, and parasitism.

Diagnosis: Testing to determine the cause of PU/

PD should start with a chemistry profile and urine
analysis for the presence of elevations in kidney
enzymes, changes in electrolyte levels, high blood
glucose levels, and measurement of urine specificgravity to determine the concentration of theurine. Additional bloodwork may be necessary,and urinalysis and additional urine testing may
be useful for identifying early kidney disease. Occasionally, advanced testing is needed to diagnosis
the underlying cause of PU.

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

OCTOBER 2021
Volume 30, Number 4

CONTACT:
Emily A. Barrell, DVM, MSc, DACVIM
ebarrell@umn.edu
Department of Veterinary Population Medicine
University of Minnesota College of Veterinary Medicine
Saint Paul, Minnesota

C O M M E N TA RY
IN THIS ISSUEKENTUCKY

Equine Rotavirus B and Neonatal Foal Diarrhea

Group A and B rotaviruses are significant enteric pathogens that cause diarrhea of variable
severity in humans and domestic animals. Despite
no difference in clinical signs or symptoms, it has
been well documented that there is no antibodymediated cross-protection between groups A and
B. The horse is a unique species in which only
group A rotaviruses typically cause foal diarrhea
outbreaks.
During the 2021 foaling season (February andMarch) in central Kentucky, increased frequencies
of diarrhea were noted in neonatal foals between
1 and 4 days of age. Mares had been previously
vaccinated with an inactivated monovalent equine
rotavirus A vaccine during their pregnancy. Foals
developed diarrhea at approximately 24 h of age
and diarrheic episodes typically lasted 3-4 days.
Some farms experienced up to 100% morbidity.
Newly born foals on affected farms quickly developed diarrhea, suggesting a highly contagious
disease. Clinical signs included inappetence, weakness, dehydration, severe electrolyte imbalance,
and watery yellow and foul-smelling diarrhea.
Hemorrhagic watery diarrhea was noticed in somecases. None of the foal’s dams developed diarrhea.
Diagnostic investigation of fecal samples from
diseased foals, which included PCR and microbial culture, failed to detect diarrhea-causing

pathogens, including equine rotavirus A. Interestingly, metagenomic sequencing data identified anabundant amount of novel rotavirus B genome infecal specimens from affected foals and absenceof other known enteric pathogens, suggesting an
etiological role of this rotavirus B in neonatal foal
diarrhea. Further evidence linking rotavirus B tothis outbreak of highly contagious foal diarrhea is
supported by the poor responses of the affectedfoals to antibiotic treatment as well as seemingly
ineffective equine rotavirus A-specific passive
maternal antibodies in affected foals against thisnew virus. Subsequent analysis of 33 foal diarrheic
samples by RT-qPCR identified 23 rotavirus Bpositive cases (69.69%). Despite a small sample
size, the prevalence of equine rotavirus B in diseased foals was similar to that reported in equine
rotavirus A-associated foal diarrhea outbreaks.
Bioinformatic analysis of the viral genome data
showed that the protein sequence of all 11 viralsegments had greater than 96% homology (relatedness) with group B rotaviruses previously foundin ruminants. Furthermore, evolutionary studies
demonstrated clustering of the equine virus withgroup B rotaviruses of caprine and bovine strainsthat circulated in the USA. These results indicate
the possibility that the equine rotavirus B was ofruminant origin.

In summary, evidence suggests that a novel,
ruminant-origin, group B rotavirus has emergedin horses and was associated with outbreaks ofneonatal foal diarrhea in the 2021 foaling season
in Kentucky. Emergence of the ruminant-like
group B rotavirus in foals clearly warrants further
investigation due to the significant impact of thedisease in neonatal foals and its economic impact
on the equine industry.
CONTACT:
Emma Adam, DVM, PhD, DACVIM, DACVS
emma.adam@uky.edu(859) 562-2186
Feng Li, DVM, PhD
feng.li@uky.edu(859) 218-1106
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

All photos: Matt Barton, Agricultural Communications

S

ince its inception in 1992, the Equine Disease
Quarterly has been distributed worldwide in a
Commentary
printed format. The funding to make this possible
was provided through the generosity of Lloyd’s ofInternational
London, Underwriters and Brokers and their KenSecond Quarter
2021  .  .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 2 tucky Agents, and in later years, by Underwriters at
Lloyd’s, London. Circulation of the Quarterly went
Exhaustion in
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 3 from several hundred copies in October 1992, toapproximately 17,000 copies in 2021, and reachedreaders in over 87 countries.
National
In late 2020, Lloyd’s Underwriters confirmed
Polyuria and
Polydipsia inthat because of changing circumstances, it could
Horses .  .  .  .  .  .  .  .  .  .  .  .  .  .  . 4 no longer sustain support of the Equine Disease
Quarterly beyond 2021. Thankfully, a new sponsor,
KentuckyEquus Standardbred Station, Inc., recently came
Equine Rotavirus B
forward and generously agreed to help the continand Neonatal
Foal Diarrhea .  .  .  .  .  .  .  . 5 ued distribution of this worthwhile publication.
This recent development provides a long overdue
opportunity to bring about a change in how the
Quarterly can best be made available to its readership. Considered opinion is to transition from mailing print copies to an electronic format, where eachissue is available on the internet. This will have theimportant advantage that once each issue is posted,
it will be immediately available to the readershipwith a link to a pdf for downloading or printing.
In time, this will likely give rise to an increase incirculation of the Equine Disease Quarterly among
veterinarians and equine stakeholders, especiallyCollege of Agriculture, since the publication is available at no charge andFood and Environment material published is not subject to copyright.
Department of
While the distribution of future issues of theVeterinary Science
Quarterly will change to an electronic format, thepurpose of the publication will remain the sameas was stated in the Commentary of the first issue,
October 1992. It is to provide information on theincidence of particular diseases/syndromes and the
Lloyd’s—An international
insurance market for
emergence or re-emergence of previously unreported
bloodstock and otherdiseases. This will apply to outbreaks occurring inspecialist insurance.

Kentucky, the USA, and other parts of the world. It
will also serve as a reference source of the latest information on disease prevention and control strategies.
In preparation for the upcoming changes in
how the Quarterly will transition into an electronic
format, those currently receiving printed versions of
the publication are strongly encouraged to review
the information provided as follows and return their
responses by no later than November 15, 2021.
CONTACT:
Peter J. Timoney, MVB, MS, PhD, FRCVS
ptimoney@uky.edu(859) 218-1094
Maxwell H. Gluck Equine Research Center
University of Kentucky
Lexington, Kentucky

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Thank you for your ongoing interest in receiving
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