1. Equine Reproductive Disorders
(Compiled by Embing, ACSK et Pereira, AJ for VM 175)
Name
Other
name
Description Epidemiology Pathogenesis Clinical signs Lesions Diagnosis Diff.diagnosis Treatment
Control &
Prevention
Abortion
I). Non-
Infectious
cause
 Most abortions
related to twinning
occur at 8–9 months
of gestation and may
be preceded by
premature lactation
 Ectopic pregnancy –
it‘s rare but may
result in abortion at 7
– 10 months of
gestation
 Mare reproductive
loss syndrome -
Majority of early
abortion occur at 40-
80 days of gestation.
Most abortion
related to
twinning occurs
at 8 -9 months
of gestation and
may be
preceded by
premature
lactation.
Twinning - most
common cause of
abortion in horses.
Placental insufficiency
ultimately causes
abortion of twins.
Umbilical cord
abnormalities such as
torsion due to
abnormal length
(>100cm) have been
incriminated in
abortion.
Clinical signs of
Mare reproductive
syndrome:
 Colic
 Fever
 Purulent vulvar
discharge
 Majority remain
clinically normal
Fetal circulatory
disturbances,
such as
subcutaneous
edema, a
swollen, soft
liver, and
microscopic
mineralization of
placental
vessels, are also
signs of umbilical
cord obstruction.
Diagnosis of abortion
due to cord torsion
requires evidence of
localized swelling or
hemorrhage because
torsions occur in some
normal births
No chemotherapy
Pasture management
to control number of
eastern tent
caterpillar and other
management to
prevent exposure of
pregnant mare to
caterpillar.
II). Infectious causes
a)EquinoR
hinopneu
monitis
Equine
Herpesv
irus 1
Infection
This is the most
important viral cause of
abortion in horses.
Abortion is usually after
7 mo of gestation and is
not preceded by
maternal illness
Outbreaks of
respiratory
disease occur
annually among
foals in areas
with
concentrated
horse
populations.
The age,
seasonal, and
geographic
distributions
vary and are
determined by
immune status
and horse
population
Following infection,
the virus would
remain in the lymph
nodes and most
adult horses would
be exposed to
equine herpes virus
at some point in
their life
 Fever of 38.9–
41.7°C
 Neutropenia and
lymphopenia,
 Serous nasal
discharge,
 Malaise,
 Pharyngitis,
 Cough,
 Inappetence,
Submandibular or
retropharyngeal
lymphadenopathy.
Placenta may be
edematous or
normal.
Gross fetal
lesions include
subcutaneous
edema, jaundice,
increased
volume of
thoracic fluid,
and an enlarged
liver with yellow-
white lesions
 Fluorescent antibody
test
 PCR
 virus isolation from
fetal tissues
 No treatment
 Rest and
nursing care are
indicated to minimize
secondary bacterial
complications.
Antipyretics are
recommended for
horses with a fever
40°C.
 Antibiotic
therapy is instituted
upon suspicion of
secondary bacterial
infection.
Prevention is based
on vaccinating at 5, 7,
and 9 mo of gestation
as well as preventing
exposure of pregnant
mares to horses
attending shows or
other equine events

2. b) Equine
viral
arteritis
Epizooti
c
cellulitis
Pinkeye
Equine
typhoid
Equine viral arteritis
(EVA) is an acute,
contagious, viral
disease of equids
caused by equine
arteritis virus (EAV)
Natural and
experimental
host range of
EAV is
restricted
principally to
equids, there
are very limited
data to suggest
the virus may
also infect
alpacas and
llamas. There is
no evidence
that EAV is
transmissible to
people.
EAV invades the
upper and lower
respiratory tract and
multiplies in
nasopharyngeal
epithelium,tonsillar
tissue, bronchial and
alveolar
macrophages.
Infected cells of the
monocytic lineage
and CD3+ T
lymphocytes
transport the virus to
the regional lymph
nodes, where it
undergoes a further
cycle of replication
before being released
into the bloodstream.
The cell-associated
viremia that follows
ensures
dissemination of EAV
throughout the body.
 Fever
 Depression
 Anorexia
 Leucopenia
 Supra- or periorbital
edema,
 Nasal discharge,
Respiratory distress,
 Skin rash,
 Temporary
subfertility in
affected stallions,
 Abortion, and
infrequently, illness
and death in young
foals
 Strains of EAV can
cause abortion
throughout much of
pregnancy (3 mo to
more than 10 mo).
Abortion may occur
late in the acute
phase or early in the
convalescent phase
of the infection, with
or without prior
clinical signs of EVA
Edema,
Congestion, and
hemorrhages,
especially in the
subcutis of the
limbs and
abdomen;
excess
peritoneal,
pleural, and
pericardial fluid;
and edema and
hemorrhage of
the intra-
abdominal and
thoracic lymph
nodes and of the
small and large
intestine,
especially the
cecum and
colon.
Aborted fetuses
are often partly
autolyzed.
History of EVA shortly
before abortion,
virus isolation or PCR of
placenta and/or fetal
tissues, or by
seroconversion of the
dam
No specific antiviral
treatment available
Symptomatic treatment
(eg, antipyretic, anti-
inflammatory, and
diuretic drugs) is
indicated only in severe
cases, especially in
stallions.
Prevention of EVA is
by management to
minimize viral
transmission in
breeding populations
and to prevent
development of
carrier stallions.
Vaccinaiton of non-
pregnant mares
c). Bacterial abortion
Potomac
horse
fever
caused
by Ehrlichiaristicii may
be followed by
abortion in mid- to late
gestation
Potomac horse f
ever is found
throughout in
North America
and has been
reported in most
regions of the
United States
and Canada
One route of
exposure is believed
to be inadvertent
ingestion of hatched
aquatic insects that
carry N risticii in the
metacercarial stage
of a trematode. The
incubation period is
~10–18 days
Mild depression
Anorexia, followed by
a fever of 38.9°–
41.7°C
placentitis and
the placenta is
often retained
Histologically,
there is fetal
colitis
PCR oxytetracycline (6.6
mg/kg, IV, bid)
fluids
NSAIDs
There is a vaccine for
Potomac horse fever,
but its efficacy in
preventing abortion is
not known.
Leptospir
osis
Most fetuses are
aborted after 6 mo of
gestation and the
Leptospirosis is
responsible for
2–4% of all
There are no
gross lesions in
the fetus or
luorescent antibody
staining of placenta or
fetal kidney, liver, or lung
Antibiotics have not
been shown to
significantly reduce the
There are no
leptospiral vaccines
for horses.

3. mares are usually
healthy. Infection does
not appear to spread
horse-to-horse, and
often only a single
mare on a farm aborts
equine
abortions
annually,
although high
rainfall and
flooding may
result in
abortion
outbreaks.
placenta, but
microscopically
there is
suppurativeplace
ntitis
and by fetal serology. shedding period. In
acute disease, systemic
antibiotics are useful,
and antibiotics are also
used to prevent further
abortions in co-housed
or exposed pregnant
mares
Brucellos
is
It is commonly called
fistulous withers or poll
evil.
The disease is
prevalent in
most countries
of the world. It
primarily affects
cattle, buffalo,
bison, pigs,
sheep, goats,
dogs, elk, and
occasionally
horses. The
disease in
people,
sometimes
referred to as
undulant fever
WhenBrucellaabortus
is ingested, the
bacteria travel
through the oral
mucosa to the
regional lymph
nodes. Infection leads
to bacteraemia, which
is usually transient;
the organisms
ultimately settle in the
reproductive tissues
or musculoskeletal
system.
late abortions in
mares,
Generalized illness
marked by fever,
stiffness, and lethargy
may be seen.
Suppurative
bursitis, a pus-
filled
inflammation of
connective tissue
over the
shoulders or poll.
Affected bursae
have thickened
capsule and
clear fluid, unless
fistulated in
which case
exudates is
usually purulent.
Osteomyelitis of
dorsal spinous
process may
present
Isolation of Brucella spp.
Serological test.
Fistulous withers
may also result
from infection of
the supraspinous
bursa by other
agents, usually
secondary to
trauma or
penetration of a
foreign body
Other causes of
abortion and
fever.
Treatment is
unsuccessful because
of the intracellular
sequestration of the
organisms in lymph
nodes, the mammary
gland, and
reproductive organs.
NSAIDS to reduce fever
and inflammation
such as
flunixinmeglumine or
phenyl butazone
Horses should not be
housed or pastured
with seropositive
cattle.
Trauma is considered
to be a predisposing
factor for the
development of
fistulous withers,
properly-fitting
saddles and tack
should always be
used.
reduce the incidence
of Onchocercaspp.
Vaccination with
strain 19 vaccine
Cystic
ovary
disease
The presence of
persistent follicles,
anovulatory follicles or
cystic structures on the
ovary accompanied by
pathological condition.
When diagnosing, it
must be remembered
that normal follicle size
during estrus is 4–6
cm in diameter
it is most
common in
cattle,
particularly the
dairy breeds,
but it occurs
sporadically in
dogs, cats, pigs,
and perhaps
mares
Ovulation failure can
also be found in
mares that are having
irregular estrous
cycles during the
spring or fall
transition phases of
the reproductive cycle
Presence of
persistent
follicles
The granulosa
cell tumor
condition in
mares causes
marked
enlargement of
one ovary.
 The condition is
diagnosed mainly
through rectal
palpation where the
presence of cysts can
be felt on ovaries.
 Ultrasound
Difficult to treat
Surgical removal of
the cyst of the
affected ovary.
Equine
coital
Enxanthe
ma
Genital
horse
pox
Equine coital
exanthema (ECE) is
an infectious,
venereally transmitted
Occasionally
stallions are
more severely
affected than
Equine coital
exanthema (ECE) is
a predominantly
sexually-transmitted
Dull
Anorectic‘
Febrile
Vesicles appear
within 2-5 days
on the penis and
Based on clinical signs
Serology
Virus isolation
Demonstration of viral
Trauma
Early
squamous cell
carcinoma
When infection is
suspected or
diagnosed in a
stallion, mating

4. mucocutaneous
disease of mares and
stallions caused by a
herpesvirus. The
disease is
characterised by the
development of
superficial pock-like
eruptions and erosions
or ulcers on the
external genital
organs.
Incubation period: 2-
10 days
Transmission :
Venereal
mares.
The disease is
generally limited
to reproductive
tract.
The virus is
endemic in UK
and most horse
breeding
populations
internationally.
disease caused by
infection with
EquidHerpesvirus 3
(EHV-3), a highly
contagious but
otherwise non-
invasive and
relatively benign
virus.
later on the
prepuce
Mares develop
multifocal areas
of sharply
demarcated
vulvar erosions
that develop into
scabs which then
slough leaving
ulcerated areas
up to 1.5 cm in
diameter.
Lesions rarely
occur on the
nasal and oral
mucosa.
DNA in the skin lesion Frostbite
Habronemiasis
bacterial
infection.
should cease until
the stallion is
confirmed free of
disease
Sanitation
A commercial
vaccine against
ECE has not been
developed.
Mastitis Mastitis is
inflammation of the
mammary gland and is
almost always due to a
bacterial infection.
Streptococcus
zooepidemicus is the
most frequent
pathogen, but S
equi, S
equisimilis,Sagalactiae
, and S viridans are
also found.
Acute mastitis
occurs
occasionally in
lactating mares,
most commonly
in the drying-off
period, in one or
both glands.
Infectious organism
can colonize the
mammary gland
tissue by routes that
are; hematogenous,
percutaneous or
ascending.
Establishment of
infection and
production of disease
state depend on
virulence of
organism, ability of
local defense
mechanism,
Ascending infection
can occur via the teat
canal, or a breach in
the mammary gland
integument.
Warm, swollen and
painful udder
Edema on the
abdomen in front of
the udder
Other signs of illness
such as fever and
depression may
occur
Suppurous
lactation
secretion
An increased
degenerated and
non-degenerated
neutrophils and
necrotic debris.
Physical examination
Bacterial isolation and
sensitivity test.
Histopathology –
mammary gland biopsy
may be helpful
Cushing disease
Edema near the
mammary gland
may also be a
symptom of other
conditions, such
as a viral
infection, liver
disease, immune
disorders or
other problems.
Frequent hand milking
to remove inflammatory
cells, fluid and bacteria..
Chemotherapy:Trimeth
oprim-ulfonamide
combination of
penicillin (20,000 IU/kg,
IM, bid) and gentamicin
sulfate (2 mg/kg, IV, tid)
To help prevent
mastitis, check
udders often, and be
aware of each mare‘s
udder appearance—
and note abnormal
changes, especially
in lactating mares.
Avoid any
unnecessary handling
of the udder and
make sure your
hands are clean (or
wear sterile gloves).
Contagio
us equine
Metritis
Contagious equine
metritis (CEM) is an
acute, highly
contagious venereal
disease of horses.
CEM is caused by the
The disease
occurs primarily
in Europe, but
technical
challenges in
propagation of
CEM is transmitted
primarily at
mating, but infected
fomites (instruments
and equipment) also
play a role
Copious
mucopurulent
discharges in mares.
Chronically infected
mares show no signs.
Most mares don‘t
Edema and
hyperemia of
endometrium,
endocervix and
vaginal mucosa.
Microscopic
Isolation of causative
organism.
Serological tests.
o Chlorhexidine
o Nitrofurazone
o Surgical excision of
clitoral sinuses may
be required to rid
them of infection.
Control of CEM
depends on
identification of
infected carrier
animal and on their
treatment or

5. gram-negative,
microaerophiliccoccob
acillus Taylorellaequig
enitalis, also known as
the contagious equine
metritis organism
(CEMO).
the causative
organism
prevent
accurate
determination of
the precise
distribution of
the disease.
conceive at the time
of infected mating.
lesions include
invasion of
affected tissue
by neutrophils
during acute
stage and by
macrophages,
lymphocytes and
plasma cells later
in the course of
infection
elimination from
breeding program.
Strict import
regulation
CONGENITAL & INHERITED ANOMALIES OF REPRODUCTIVE SYSTEM
Cryptorch
idism
rig Failure of one or both
testicles to descend
into the scrotum and is
seen in all domestic
animals.
It is the most common
disorder of sexual
development in
horses.
Bilateral
cryptorchidism results
in sterility. Unilateral
cryptorchidism is more
common
Cryptorchids are
classified as
‗abdominal‘ or
‗inguinal‘, depending
on the location of the
retained
testicle.Inguinal
retention is by far the
more common of the
two.
It is common in
stallions and
boars and is the
most common
disorder of
sexual
development in
dogs.
All breeds of
horses may be
exhibit
cryptorchidism,
but there is a
higher
frequency in
Quarter Horses,
Saddlebreds,
Percherons,
and ponies.
As the foetus
develops, the
testicles start to
descend towards the
inguinal canal and
usually pass through
the canal and into the
scrotum during the
final weeks of
pregnancy. The
testicle can be
retained anywhere
along its descentThe
condition is likely the
result of a complex
combination of
genetic, hormonal,
and mechanical
factors.
Physical examination None The condition is
considered heritable,
so affected pets
should be castrated
to help prevent
continuation of this
congenital defect.
Retained
Fetal
Membran
e
Equine fetal
membranes are
normally expelled
within 3 hours after
parturition, but
Mares that have
retained their
fetal
membranes
appear to be at
The cause of
retention of fetal
membranes often is
not known, but the
condition is
Non-expulsion of the
fetal membrane after
3 hours.
It is common practice to
administer oxytocin (5
U, IM, every 2–3 hr)
beginning 3–4 hr after
parturition if the
In cases of prolonged
retention of fetal
membranes,
antimicrobials should
be administered

6. expulsion may be
delayed for 8–12 hours
or even longer without
signs of illness.
increased risk of
recurrence of
the condition,
and Friesian
mares may be
particularly
predisposed.
Retention of just
a portion of the
fetal
membranes
entirely within
the uterus
(usually at the
tip of the
previously
nongravid
uterine horn) is
less
conspicuous but
equally likely to
result in
complications.
For this reason,
the chorionic
surface of the
expelled
membranes
should be
examined to
ensure that they
have been
completely
expelled.
associated with
infection, abortion,
short or prolonged
gestation, uterine
atony, and dystocia.
Retention of fetal
membranes may
mediate development
of metritis or even
peritonitis. Laminitis
is a potential
sequela.
membranes have not
yet been expelled.
Manual removal of
retained membranes
carries the risk of
uterine damage or
prolapse and is not
recommended beyond
gentle tugging to
displace already
loosened membranes.
prophylactically,
along with NSAID
and other therapeutic
strategies aimed at
preventing laminitis
Uterine
Prolapse
and
Eversion
Prolapse of the uterus
invariably occurs
immediately after or
within several hours of
parturition, when the
cervix is open and the
uterus lacks tone.
It is rare in
mares
Invagination of the tip
of the uterus,
excessive traction to
relieve dystocia or
retained fetal
membranes,
uterine atony,
hypocalcemia, and
lack of exercise have
Replacement of the
prolapsed uterus in
mares is usually done
with the mare sedated
but standing, taking
care not to perforate the
uterus.
Treatment involves
Complications tend to
develop when
laceration, necrosis,
and infection occur,
or when treatment is
delayed. Shock,
hemorrhage, and
thromboembolism are
potential sequelae of

7. all been incriminated
as contributory
causes.
removing the placenta
(if still attached),
thoroughly cleaning the
endometrial surface,
and repairing any
lacerations. Rubbing
the surface of the
uterus with glycerol
helps reduce edema
and provides
lubrication. The uterus
is then returned to its
normal position. An
epidural anesthetic
should be administered
first. The cleansed
uterus should be
elevated to the level of
the vulva on a tray or
hammock supported by
assistants, and then
replaced by applying
steady pressure
beginning at the
cervical portion (or at
the level of the
invagination of the non-
prolapsed uterine horn)
and gradually working
toward the apex. Once
the uterus is replaced, a
hand should be inserted
to the tip of both uterine
horns to be sure that
there is no remaining
invagination that could
incite abdominal
straining and another
prolapse. Installation of
warm, sterile saline
solution is useful for
ensuring complete
replacement of the tip of
the uterine horn without
a prolonged prolapse.
In some instances,
the bladder and
intestines may
prolapse into the
everted uterus. These
require careful
replacement before
the uterus is
replaced. The bladder
may be drained with
a catheter or needle
passed through the
uterine wall. Elevation
of the hindquarters
and pressure on the
uterus aid in
replacement of
bladder and
intestines. It may be
necessary to incise
the uterus carefully
(in a longitudinal
direction) to replace
these organs.
Supportive treatment
and antibiotic therapy
are indicated.

8. trauma.
Vaginal
and
Cervical
Prolapse
Cervicovaginal
prolapse is
more common
in stabled than
in pastured
animals,
suggesting that
lack of exercise
may be a
contributing
factor.
Predisposing factors
include increased
intra-abdominal
pressure associated
with increased size of
the pregnant uterus,
intra-abdominal fat,
or rumen distention
superimposed upon
relaxation and
softening of the pelvic
girdle and associated
soft-tissue structures
in the pelvic canal
and perineum
mediated by
increased circulating
concentrations of
estrogens and relaxin
during late
pregnancy. Intra-
abdominal pressure
is increased in
recumbent animals.
The prolapse begins
as an
intussusception-like
folding of the vaginal
floor just cranial to
the vestibulovaginal
junction. Discomfort
caused by this
eversion, coupled
with irritation and
swelling of the
exposed mucosa,
results in straining
and more extensive
prolapse. Eventually
the entire vagina may
be prolapsed, with
the cervix
For replacement of the
prolapsed vagina, an
epidural anesthetic is
first administered. The
organ is washed and
rinsed, and the bladder
is emptied if necessary.
Usually, this can be
achieved by elevating
the prolapsus to allow
straightening of the
urethra; occasionally,
needle puncture
through the vaginal wall
may be necessary. The
vagina is well lubricated
(glycerol provides
lubrication and reduces
congestion and edema
by osmotic action) and
replaced and then held
in position until it feels
warm again.
Retention is achieved
by insertion of a Buhner
suture—a deeply
buried, circumferential
suture placed around
the vestibulum to
provide support at the
point at which the initial
eversion of the vaginal
wall occurs. The Buhner
suture has largely
superseded earlier
attempts to prevent
prolapse by various
patterns of sutures in
the vulvar lips (which do
not prevent the initial
eversion of the vagina
into the vestibulum) or
Permanent fixation
techniques
(cervicopexy or
vaginopexy) in which
the cervix or vaginal
wall is anchored to
other pelvic
structures have been
described. They may
be useful in individual
cases of chronic or
recurrent prolapse,
but most cases are
resolved by a well-
placed Buhner
suture.

9. conspicuous at the
most caudal part of
the prolapsus. The
bladder or loops of
intestine may be
contained within the
prolapsed vagina. As
the bladder moves
into the prolapsed
vagina, the urethra
may be occluded.
The bladder then fills
and enlarges, which
hinders replacement
of the prolapsed
vagina unless the
bladder is first
drained. The bladder
may even rupture
with potentially fatal
consequences.
by methods that relied
on placement of a
retention device within
the vagina (which tend
to cause discomfort and
further straining).
Buhner sutures should
generally be removed
before parturition to
prevent extensive
laceration. Although the
cervical os may be
edematous and
inflamed, cervicovaginal
prolapse seldom
interrupts pregnancy
and does not
specifically predispose
to dystocia or
postpartum uterine
prolapse, which has a
different etiology.
Vulvitis
and
Vaginitis
Contusion and
hematoma of the
vagina are noted
infrequently after
parturition in all
species but particularly
in mares and sows.
Necrotic vaginitis,
vestibulitis, and vulvitis
may follow dystocia in
all species.
Possible
consequences of
necrotic vaginitis
include permanent
stricture of the vagina,
transvaginal
adhesions, or
perivaginalabscessatio
n.
Onset of signs,
consisting of arched
back, elevated tail,
anorexia, dysuria,
straining, vulvar and
perivulvar swelling,
and possibly a fetid,
serous discharge,
begins within 1–4
days of parturition
and may persist for
2–4 wk.
. In most cases, only
gentle and conservative
treatment is needed.
Prophylactic antibiotic
treatment is wise
because clostridial or
other organisms may
proliferate in the
damaged tissue and
cause tetanus,
blackleg, or other
forms of clostridial
myositis.

10. Mammary
Tumors
The cause of
mammary tumors is
unknown
Mammary
tumors are rare
in mares
Hormones play an
important role in the
hyperplasia and
neoplasia of
mammary tissue, but
the exact mechanism
is unknown. Estrogen
or progesterone
receptors (or both)
have been reported
on mammary tumor
cells in animals;
these may influence
the pathogenesis of
hormone-induced
mammary neoplasia
as well as the
response to hormone
therapy.
A mammary tumor is
usually suspected on
detection of a mass
during physical
examination. The length
of time the mass has
been present is usually
unknown, but the rate of
growth may be helpful in
determining prognosis.
Palpation of the regional
lymph nodes can help
determine the extent of
spread. Thoracic
radiographs, preferably 3
views (a ventral-dorsal
and 2 laterals), should be
taken to detect
pulmonary metastases.
Fine-needle aspirates
may differentiate
between inflammatory
and neoplastic lesions
but may lead to
erroneous conclusions
and delay of surgery.
The diagnosis is
determined by
histopathology and
is important in defining
treatment and prognosis.
From a practical view,
all mammary tumors
should be regarded as
potentially malignant
regardless of the size or
number of glands
involved.
Mammary tumors are
treated surgically,
although there is no
consensus as to the
best procedure.
Removal of the tumor
alone (lumpectomy),
simple mastectomy
(removal of the affected
gland only), modified
radical mastectomy
(removal of the affected
gland and those that
share lymphatic
drainage and
associated lymph
nodes), and radical
mastectomy (removal of
the entire mammary
chain and associated
lymph nodes) all have
their proponents.
In theory, the use of
anticancer drugs to
combat micrometastatic
disease (adjuvant
chemotherapy) is a
reasonable
consideration. Neither
radiation therapy nor
antiestrogenic
compounds have been
effective.
Dourine Dourine is an often
chronic venereal
disease of horses that
is transmitted during
The disease is
recognized on
the
Mediterranean
Signs may develop
over weeks or
months. Early signs
include
Characteristic
plaques 2–10 cm
in diameter
appear on the
Demonstration of
trypanosomes from
urethral or vaginal
discharges, skin plaques,
Quinapyramine sulfate
(curative),
Quinapyraminedimethyl
sulfate(prophylactic),
When eradication is
required, strict control
of breeding and
elimination of stray

11. coitus and caused
byTequiperdum.
coast of Africa
and in the
Middle East,
southern Africa,
and South
America;
distribution is
probably wider.
Mortality in
untreated cases
is 50–70%.
mucopurulentdischar
ge from the urethra in
stallions and from the
vagina in mares,
followed by gross
edema of the
genitalia.
skin, and the
horse becomes
progressively
emaciated.
or peripheral blood is
difficult unless the
material is centrifuged.
Infected horses can be
detected with the
complement fixation test
but only in areas where T
evansi or T brucei are
not found because they
have common antigens.
An ELISA test may
become available for
diagnosis.
horses has been
successful.
Alternatively, infected
horses may be
identified using the
complement fixation
test; euthanasia is
mandatory.
References:
Buckelew, Thomas P. Parasitology Images: An Auto-tutorial with Additional Instructional Aids. California University of Pennsylvania. Retrieved from: ―http://workforce.calu.edu/Buckelew/trypanosoma_equiperdum
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Buergelt, C.D., & Del Piero, Fabio.2014.Color atlas of equine pathology.USA: Jhon Wiley and sons, inc.
Carleton, C.L. Equine theriogenology. Blackwell‘s five minute veterinary consult clinical companion
Eilts, Bruce. (2009).Equine Pregnancy.School of Veterinary Medicine.Louisiana State University. Baton Rouge, LA. Retrieved From: ―http://www.vetmed.lsu.edu/eiltslotus/
theriogenology-5361/equine%20pregnancy_2.htm‖. Retrieved on : 29 December 2013.
Eilts, Bruce. (2007).Non-infectious Infertility.School of Veterinary Medicine.Louisiana State University. Baton Rouge, LA. Retrieved From: ―http://www.vetmed.lsu.edu/eiltslotus/
theriogenology-5361/cannine%20noninfection%20_2.htm‖. Retrieved on : 29 December 2013.
Gilbert, Robert O. (2012). Overview of Mammary Tumors.The Merck Veterinary Manual. Retrieved from: ―http://www.merckmanuals.com/vet/reproductive_system/
mammary_tumors/overview_of_mammary_tumors.html‖. Retrieved on: 04 December 2013.
Gilbert, Robert O. (2012). Overview of Uterine Prolapse and Eversion. The Merck Veterinary Manual. Retrieved From: ―http://www.merckmanuals.com/vet/
reproductive_system/uterine_prolapse_and_eversion/overview_of_uterine_prolapse_and_eversion.html‖. Retrieved on: 04 December 2013.
Gilbert, Robert O. (2012). Overview of Vaginal and Cervical Prolapse.The Merck Veterinary Manual. Retrieved from: ―http://www.merckmanuals.com/vet/reproductive_system/
vaginal_and_cervical_prolapse/overview_of_vaginal_and_cervical_prolapse.html‖. Retrieved on: 04 December 2013.

12. Gilbert, Robert O. (2012). Overview of Vulvitis and Vaginitis in Large Animals.The Merck Veterinary Manual. Retrieved from:―http://www.merckmanuals.com/vet/reproductive
_system/vulvitis_and_vaginitis_in_large_animals/overview_of_vulvitis_and_vaginitis_in_large_animals.html‖. Retrieved on: 04 December 2013.
Gilbert, Robert O. (2012). Retained Fetal Membranes in Mares.The Merck Veterinary Manual. Retrieved from: ―http://www.merckmanuals.com/vet/reproductive_system/retained_fetal_membranes_in_large_animals/
retained_fetal_membranes_in_mares.html?qt=retained%20fetal%20membrane&alt=sh‖. Retrieved on: 04 December 2013.
Holmes, Peter H. (2011). Trypanosomiasis.The Merck Veterinary Manual. Retrieved from:―http://www.merckmanuals.com/vet/circulatory_system/blood_parasites/trypanosomiasis.html?qt=dourine&alt=sh‖. Retrieved on: 04
December 2013.
Kahn, C.M. 2010. The Merck veterinary manual.10th Ed. USA: Merk and Co., Inc.
Knottenbelt, DC; Pascoe, PR. (2003).Color Atlas of Diseases and Disorders of the Horse. Saunders. Philadelphia, USA. pp.386-7.
Mair, T.S., &Diver,T.J. Brucellosis in the horse. Bell Equine Veterinary Clinic, Mereworth, Maidstone, Kent ME18 5GS, UK; and †Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New
York 14853, USA. Retrived on December 09. 2013 @http://www.bellequine.co.uk/downloads/275-280_eve_man_08-027_mair.pdf
Abortion.School of veterinary medicine.Louisiana state university.
McCue, P.M. Mastitis in mares. Equine reproduction laboratory.Colarado State University.Retrived December 09,2013 @ http://csu-cvmbs.colostate.edu/Documents/Learnmares46-reprodprob-mastitis-apr09.pdf
Munroe, Graham A.; Weese, J. Scott. (2011). Equine Clinical Medicine, Surgery and Reproduction.Manson Publishing. London, UK. p.290.
Opperdoes, Fred. (1997). Trypanosomes Infecting Man and Animals. De Duve Institute. Retrieved from: ―http://www.icp.ucl.ac.be/~opperd/parasites/tryps2.htm‖.Retrieved on: 29 December 2013.
Orsini, James A; Divers, Thomas J. (2014). Equine Emergencies: Treatment and Procedures , 4th Ed. Elsevier. St. Louis, MO. p.440.
Pozor, Malgorzata. (2013). Equine placenta – marvelous organ and a lethal weapon.Retrieved from: ―http://extension.vetmed.ufl.edu/files/2013/01/Equine-placenta-marvelous-organ-and-a-lethal-weapon-updated-on-Jan-29-
2.pdf‖.Retrieved on: 24 December 2013.
Radostits, O.M.,et al. 2007.Veterinary medicine: a textbook of diseases of cattle, sheeps, goats, pigs and horses. 10th Ed. Saunders Ltd.
Sorden, Steve; Andreasen, Claire. (2013). Disease Images: Dourine. The Center for Food Security and Public Health. Retrieved from: ―http://www.cfsph.iastate.edu/
DiseaseInfo/disease-images.php?name=dourine‖. Retrieved on : 29 December 2013.
Spadari, A.; Valentini, S.; Sarli, G.; Spinella, G.; Millanta, F. (2008). Mammary Adenoma in a Mare: Clinical, Histopahtological and Immunohistochemical Findings. Equine Veterinary Education, 20: 4–7.
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