1. Infectious Respiratory Diseases
Disease
Other
name
Description Epidemiology Pathogenesis Clinical Signs Lesions Diagnosis
Diff.
diagnosis
Treatment
Prevention
and Control
Viral Infection
EquineHerpesvirusInfection
-Equineviralrhinopneumonitis
-Equineabortionvirus
Equine
herpesvirus 1
(EHV-1) and
equine
herpesvirus 4
(EHV-4)
Ubiquitous in
horse populations
worldwide
Transmission:
Direct contact
Indirect contact
The incubation
period of EHV is
2–10 days.
1.fever of 102–
107°F (38.9–
41.7°C)
2.malaise
3.pharyngitis
4.cough
5.Inappetence
6.serous nasal
discharge
7.neutropenia
8.lymphopenia
9.submandibular or
retropharyngeal
lymphadenopathy
Gross lesions
1.hyperemia
2.ulceration of
the respiratory
epithelium
3.multiple, tiny,
plum-colored
foci in the
lungs
Histologic
lesions
1.inflammation,
necrosis, and
intranuclear
inclusions of
the respiratory
epithelium
and germinal
centers of the
associated
lymph nodes
2. serofibrinous
exudate in the
alveoli
PCR
Virus isolation
Samples
needed:
nasopharyngeal
swab
citrated blood
sample (buffy
coat)
equine
influenza
equine viral
arteritis
No specific
treatment for
EHV infection
Supportive
medication:
1.Rest and
nursing
care
2.Antipyreti
cs
3.Antibiotic
therapy
1.Isolation of
new horses
2.Stress
Management
3.Disinfection
4.Strict
sanitation
5.Vaccination
6.Modified live
vaccines

2. EquineInfluenza
Most
economically
important
contagious
respiratory
disease of
horses.
Highly
contagious and
spreads rapidly
by direct
contact
Orthomyxovirus
A/Equi-1
Orthomyxovirus
A/Equi-2
Distinct influenza
viruses have been
found in horse
populations
worldwide except
in Iceland and
New Zealand.
Influenza is rarely
fatal except in
donkeys, zebras,
and debilitated
horses.
Transmision:
inhalation of
respiratory
secretions
Incubation period:
∼1–3 days
Virus attaches to
epithelial cells via
hemagglutinin
spikes and enters
cells via
endocytosis.
Virus damages
epithelial cells in
the respiratory
tree
desquamation
and focal erosion
of the respiratory
epithelium,
Interruption of
the protective
mucociliary
blanket
impairment of
clearance
accumulation of
mucus and
bacteria in the
airways
exposure of the
lamina propria
and irritant
receptors
leading to
frequent
coughing.
1.high fever (up to
106°F [41.1°C])
2.serous nasal
discharge
3.submandibular
lymphadenopathy
4.dry, harsh, and
nonproductive
coughing
5.Depression
6.anorexia
7.weakness
1.Nasal discharge
2.although scant
and serous
initially but
may become
mucopurulent
due to
secondary
bacterial
infection
3.Anemia,
leukopenia and
lymphopenia
4.Increased
neutrophil :
lymphocyte
ratio
5.Monocytosis
1.Virus isolation
2.Serologic tests
3.Pulmonary
imaging
4.Thoracic
radiographs
Equine
Herpesvirus
Infection
equine viral
arteritis
1.Supportive
treatment
2.NSAID
3.Antibiotics
4.Rest
1.Hygienic
management
2.Vaccination

3. EquineViralArteritis
Epizooticcellulitis
Pinkeye
Equinetyphoid
Rotlaufseuche
an acute,
contagious, viral
disease of
equids
ETIOLOGIC
AGENT:
Equine Arteritis
Virus (EAV)
EAV is present in
equine
populations in
many countries
worldwide, with
the notable
exceptions of
Japan and Iceland.
It is frequently
highest in
Standardbreds
and Warmbloods.
Transmission:
Aerosolization of
respiratory
secretions
Fomite
contamination
with respiratory
secretions
Venereal
transmission
Congenital
transmission
Incubation period:
7–19 days
After intranasal
challenge
(aerosolization),
the virus invades
the respiratory
tract epithelium
and the alveolar
macrophages.
By 72 hours after
infection,
replicating viruses
are detectable in
the
bronchopulmonar
y lymph nodes,
endothelium, and
circulating
macrophages.
Dissemination of
the virus by
hematogenous
routes allows
infection of
mesenteric lymph
nodes; spleen;
liver; kidneys;
nasopharyngeal,
pleural, and
peritoneal fluid;
and urine.
By 6 to 8 days
after infection,
the virus has
localized within
the endothelium
and medial
myocytes of
blood vessels,
where it causes a
necrotizing
arteritis, a
panvasculitis.
The clinical
Respiratory signs:
1.serous nasal
discharge
2.Cough
3.Conjunctivitis
4.Lacrimation
5.palpebral and
periorbital edema
Gross lesions:
(respiratory)
Pulmonary
edema
emphysema
interstitial
pneumonia
excess
peritoneal,
pleural, and
pericardial fluid
Microscopic
lesions:
Vasculitis
(smaller
arterioles and
venules)
seen in the
placenta and the
brain, liver,
spleen, and
lungs of the
fetus
1.reverse
transcriptase-
PCR
2.Virus
Neutralization
Test
3.ELISA tests
4.Virus isolation
5.Immunohistoc
hemical
examination
1.Equine
influenza
2.Equine
herpesvirus
1 and 4–
related
diseases
3.Infection
with equine
rhinitis A
and B
viruses
4.Equine
adenovirus
es
5.Purpura
hemorrhagi
ca
6.Equine
infectious
anemia
7.Hoary
alyssum
toxicosis
8.African
horse
sickness
fever
9.Getah virus
infection
10.Dourine
No Specific
Antiviral
Treatment
Symptomatic
treatment
indicated only
in severe
cases.
1.Sound
management
practices
2.isolation of
new arrivals
3.maintenance
of pregnant
mares in small
i
4.solated groups
5.identification
of carrier
stallions
6.annual
immunization
of noncarrier
breeding
stallion
populations
7.Vaccination

4. HendraVirusInfection
EquineMorbillivirus
Hendra virus
(HeV) is the
prototype
species of a new
genus
Henipavirus
within the
subfamily
Paramyxovirinae
First recognized
in Hendra,
Australia in
1995 as a new
zoonotic disease
of horses
Hendra virus is
classified as a
biosafety Level 4
agent
defined as
posing a high
risk of life-
threatening
disease in
humans
Hendra virus
infection and
disease in horses
has only been
reported in
Australia.
with 13 events
recorded between
1994 and 2009
Fruit bats are the
reservoir of
infection, and
disease
transmission
requires very
close contact with
infected horses or
bat droppings.
Transmission:
undetermined
mechanism
hypothetical
route:
through contact
with food or
water
contaminated
with material
from infected bats
Australian
paralysis tick
Ixodes holocylus.
This tick is a blood
feeder that feeds
both on bats and
horses
Consumption of
contaminated
food or water
Fomites
Tissue tropism
In Vascular
tissues including
pulmonary
epithelium and
capillaries
Extensive
destruction of
pulmonary
capillary
endothelium
The virus
replicates within
the upper and
lower respiratory
tract epithelium
and causes an
interstitial
pneumonia.
Pulmonary distress:
fever (>104° F)
depression
tachycardia
tachypnea
sweating
poor capillary refill
abnormal lung
sounds (caused by
pulmonary edema)
Neurologic deficits:
ataxia
head pressing
recumbency
Incubation period: 8
to 16 days or 4 to 10
days
The time between
the onset of signs
until death is usually
between 1 and 3
days.
Respiratory
lesions:
Gross lesions
1.Severe edema
and congestion
of the lungs
2.Marked
dilatation of
the subpleural
lymphatics.
3.Airways are
filled with thick
froth, which is
often blood-
tinged.
Microscopic
lesions
1.serofibrinous
alveolar edema
2.hemorrhage
3.thrombosis of
capillaries
4.necrosis of
alveolar walls
5.alveolar
macrophages
are evident in
the lungs.
1.RT-PCR
2.detection of
viral RNA
3.immunoperoxi
dase staining/
seroconversion
4.Virus
Neutralization
assay
5.ELISA
Samples:
blood sample
nasal or oral
swab
1.African
Horse Fever
2.anthrax
3.botulism
4.certain
bacterial
infections
5.plant or
chemical
poisoning
NONE minimizing
contact with
bat body fluids
.
Control
1.Euthanasia
2.deep burial of
cases
3.monitoring
4.Isolation
5.movement
restriction of
in-contact
animals
6.disinfection
of potentially
contaminate
d surfaces.

5. AfricanHorseSickness
Zebras are
considered to be
the natural
vertebrate host
and reservoir of
the AHSV
Culicoides imicola
is considered to
be the most
important field
vector for AHSV.
The disease is
limited
geographically to
areas of Africa,
the Middle East,
and Southern
Europe.
Once the virus
gains entry into
the host, it
replicates in the
regional lymph
nodes before
being spread
hematogenously
to most organs
and tissues in the
body. In the
lungs, spleen,
lymphoid tissues,
and in certain
endothelial cells,
a secondary viral
replication phase
ensues.
Incubation period
from inoculation
to secondary
viremic phase is
approximately 9
days.
Acute form
(Pulmonary Form)
fever (up to 107° F)
severe respiratory
distress:
tachypnea
base-wide stance
extended neck
nostril flaring
coughing
Frothy white and,
occasionally,
blood-tinged fluid
may be evident at
the nostrils.
The course of the
disease is usually 4
to 5 days.
The mortality rate
for this form is 95%.
Lesions are not
pathognomonic
for AHS
Diagnostic
Confirmation:
Viral Isolation
Or
Identification
PCR or by ELISA
EVA
Purpura
Hemorrhagica
Equine
Infectious
Anemia
Babesiosis
(Early Stages)
No specific
treatment
Supportive
and
symptomatic
treatment
Vector control
Restricting
import of
infected
animals
Slaughter of
viremic
animals
Vaccination

6. Bacterial InfectionRhodococcusequiPneumonia
Rhodococcus equi
causes life-
threatening
pneumonia in
foals between 1
and 5 months of
age
The bacterium has
a worldwide
distribution.
Transmission:
Inhalation of dust
particles laden
with virulent R.
equi
Swallowing of
sputum laden
with R equi
=Inhalation of
dust particles
laden with
virulent R
= R. equi
phagocytosed
by
macrophages
= The
replication of R.
equi within
macrophages
ultimately
results in the
death of the
host cell.
= Large
numbers of
cells migrate to
the site in
response to
infection with R.
equi, ultimately
resulting in
granuloma
formation.
= inflammatory
mediators may
allow
proliferation of
organisms and
cause the loss
of pulmonary
function.
Anorexia
Lethargy
Febrile state
Tachypnea
Acute respiratory
distress
Fever
Cough
Diarrhea
Crackles and wheezes
(Thoracic
Auscultation)
Disease are difficult to
detect until
pulmonary infection
reaches a critical mass
The most
common
manifestation
of R. equi
infection in
foals is chronic
pyogranulomat
ous
bronchopneum
onia with
abscessation
and associated
suppurative
lymphadenitis.
1. Bacterial
culture
Definitive diagnosis
of R. equi
pneumonia.
2. Thoracic
radiography
3. Thoracic
ultrasound
4. PCR
Serologic
testing
agar gel
immunodiffusion
(AGID)
enzyme-linked
immunosorbent
assay (ELISA)
overdiagnosis of R.
equi infection
Supportive
therapy
1.Judicial IV
fluid
therapy and
2.Nasal
insufflation
with oxygen
3.Bronchodila
tor therapy
4.Prophylactic
antiulcer
1.decrease
exposure to
the
organism
2.elimination
of
environment
al conditions
that favor
disseminatio
n of the
organism
3.early
detection of
clinical cases
4.Surveillance
programs
5.passive
immunity
for neonatal
foals

7. Strangles
Distemper
an infectious,
contagious
disease of Equidae
characterized by
abscessation of
the lymphoid
tissue of the
upper respiratory
tract.
causative
organism:
Streptococcus
equi equi
a gram-positive,
capsulated β-
hemolytic
Lancefield group C
coccus, which is
an obligate
parasite and a
primary pathogen.
Worldwide in
distribution
Transmission:
Direct horse-to-
horse contact
Indirect
transmission
includes
S. equi enters
through the
mouth or nose
and attaches to
cells in the crypt
of the lingual
and palatine
tonsils, as well
as to the
follicular-
associated
epithelium of
the pharyngeal
and tubal
tonsils.
Translocation
occurs in a few
hours to the
mandibular and
suprapharyngea
l lymph nodes
that drain the
pharyngeal and
tonsil region.
Failure of
neutrophils to
phagocytose
and kill the
streptococci
culminates in
the
accumulation of
many
extracellular
streptococci in
the form of long
chains
surrounded by
large numbers
of degenerating
neutrophils.
1.fever (103–106°F
[39.4–41.1°C])
2.First sign of infection
3.mucoid to
mucopurulent nasal
discharge
4.depression
5.difficulty swallowing
6.inspiratory
respiratory noise
7.extended head and
neck.
1.submandibular
lymphadenopat
hy
2.compression of
the dorsal
pharyngeal wall
3.abscessation in
other lymph
nodes of the
body -
Metastatic
strangles
(“bastard
strangles”)
Abdomen and
thorax , and
brain
1.Clinical signs
2.Bacterial
culture
3.polymerase
chain reaction
(PCR)
4.endoscopic
examination
of the upper
respiratory
tract
5.ultrasonograp
hy
6.radiographic
examination
1.Warm
compresses
2.applied to
sites of
lymphadeno
pathy to
facilitate
maturation
of abscesses
3.povidone-
iodine
solution (3–
5% diluted)
4.NSAID
5.Antibacteria
l
6.Administrati
on of
penicillin
1.Vaccination
2.Isolation
3.Sanitation
and
disinfection
4.Should
wear
protective
clothing or
change
clothes
before
traveling to
the next
equine
facility
5.Quarantine
14–21 days

8. Pleuropneumonia
Pleuritis
Pleurisy
infection of the
lungs and pleural
space
Develops
secondary to
bacterial
pneumonia or
penetrating
thoracic wounds
Worldwide in
distribution
occurring in all
ages and both
sexes.
Predisposing
factors.
1. Viral
respiratory
infection
2. long-distance
transport
3. general
anesthesia
4. strenuous
exercise
Suppresion
impaired
pulmonary
defense
mechanisms
Invasion
Bacterial
colonization
and infection of
the lower
airway, alveoli,
and lung
parenchyma
Proliferation
Influx of
inflammatory
cells
(neutrophils)
Tissue
destruction
Accumulation
of cell debris in
the alveoli and
airways.
Accumulation
Extension of
inflammation
and infection.
1.Fever
2.Depression
3.Lethargy
4.Inappetence
5.Respiratory distress
6.Cough
7.Nasal discharge
8.Exercise intolerance
9.Reduced breath
sounds)
10. Presence of pleural
fluid
11. Pneumonia
Hematologic
lesions:
1.Leukocytosis
w/ mature
neutrophilia
2.Hyperfibrinog
enemia
3.Hypoalbumine
mia
4.Hyperglobulin
emia
5.Pleural fluid:
6.Leukocytosis
7.Hyperproteine
mia
8.Presence of
intra- and
extracellular
bacteria
1.Thoracic
ultrasonograp
hy
2.Thoracocente
sis
3.Thoracic
radiography
4.Examination
of pleural fluid
5.Cytologic
evaluation
6.Bacterial
culture and
sensitivity
1.Intrathoracic
neoplasia
2.Penetrating
chest wounds
3.Esophageal
perforation
4.Diaphragmati
c hernia
5.Congestive
heart failure
6.Hemangiosar
coma
7.African horse
sickness
8.Pulmonary
hydatidosis
9.Pulmonary
infarction and
pneumonia
1.Antibiotic
therapy
2.Thoracosto
my
3.Pleural
space
drainage
4.Supportive
care
5.intravenous
fluid
therapy,
6.nutritional
support,
7.NSAID
therapy.
Reduction of
risk factors
associate
with the
disease
FungalInfections
FungalRhinitis
Pythium
insidiosum
Occurs
predominantly in
the united states,
occasionally in
Australia, and
rarely in other
warm climatic
regions.
Respiratory stridor
Exercise intolerance
Chronic
unilateral,purulent
nasal discharge which
may contain blood
Numerous
small
granulating
ulcers or
fissures in the
rostral part of
the nasal cavity
endoscopy Surgical
excision
Topical
Amphotericin
B
Cryptococcus
neoformans
Mucopurulent and
sanguinus and have a
Granuloma
formation
Biopsy
Cytology

9. foul odor Invasive rhinitis
and sinusitis
Draining tracts
through the
facial bones
culture
Aspergillus spp. Non-invasive
Mild yellowish mucoid
nasal discharge
Invasive
Scanty, foul smelling,
unilateral, purulent
discharge possibly
containing blood
Extensive
destruction of
the mucosa of
the nasal
turbinates and
the maxillary or
frontal sinuses
Cell culture Topical
treatment of
eniconazole
FungalPneumonia
Blastomyces
dermatidis
Coccidoides
immitis
Cryptococcus
neoformans
Histoplasma
capulatum
inhalation of
spores
Inhalation of
windborne
arthrospores
Chronic cough
Nasal discharge
Exercise intolerance
Anorexia
Weight loss
Pleural effusion
- Commonly seen in
coccidiomycosis
Radiography
Ultrasonograph
y
Tracheobronch
ial asporates
Serological
detection
Antifungal
drugs ( 10-12
weeks)
For primary
infection
Should
ideally be
based on
sensitivity
testing
ParasiticInfection
Parascaris
equorum
Found in foals less
than 4-6 mos. Old
Productive cough
Hyperpnea
Loss of weight
Overt pneumonia
Endoscopic
examination
Fecalysis
Dictyocaulu
sarnfieldi
Rarely affects
horses
Persistent, non-
progressive coughing
Tracheal
aspiration
Edoscopy
Fecalysis

10. Echinococcusgranulosus
generally well-
tolerated in
horses, and cysts
in the liver and
lung may
be an incidental
finding at post-
mortem
examination
intermittent fever,
depression, rapid
shallow respiration,
pectoral edema,
large
pulmonary
or pleural cysts
rupture,
resulting in a
large volume of
pleural
effusion.
Ultrasound
examination
1.albendazole
(10 mg/kg,
PO, SID x
30d)
2.thoracic
drainage
3.surgical
debridemen
t of the
pleura and
cyst on the
surface
of the
diaphragm
DISEASE
OTHER
NAME
DESCRIPTION ETIOLOGY/
EPIDEMIOLOGY
PATHOGENESIS CLINICAL SIGNS LESIONS DIAGNOSIS DIFFERENTIAL
DIAGNOSIS
TREATMENT CONTROL
AND
PREVENTI
ON
MULTINODULAR
PULMONARY
FIBROSIS
Interstitial
pneumoni
a/
Pulmonar
y fibrosis
heterogenous
group of
pulmonary
disorders that
produce
pulmonary fibrosis
in middle-aged to
older horses
toxins and
idiosyncratic
reactions
Tachycardia;
tachypnea,
respiratory difficulty
at rest,
Lethargy fever
weight loss.
diffuse, severe,
nodular
interstitial
pattern.
Histopathologi
c evaluation of
biopsy
anti-
inflammatory
medications;
antibiotics;
corticosteroids
;
acyclovir
INFLAMMATORYAIRWAYDISEASE
Lower
respirator
y tract
inflammat
ion/
Small
airway
inflammat
ory
disease
heterogeneous
group of
inflammatory
conditions of the
lower respiratory
tract that appear
to be primarily
noninfectious
allergic airway
disease, recurrent
pulmonary stress,
deep inhalation of
dust, atmospheric
pollutants, and/or
persistent
respiratory viral
infections
develops after an
overt viral
respiratory
infection and may
result from
inability of the
immune system
to fully eliminate
viruses or
bacteria from
small airways
chronic cough and
mucoid to
mucopurulent nasal
discharge
Slight swelling
of myelin
sheaths and
Schwann cells
with dilation of
intraneural
capillaries to
heavy
leukocytic
infiltration of
the nerves and
necrosis
Based on poor
race
performance
and clinical
signs.
Systemic
corticosteroid
therapy,
, aerosol
administration
of nedocromil
sodium or an
inhaled
corticosteroid
preparation
(beclomethaso
ne or
fluticasone)
Use low-
dust
bedding;
Enhance
ventilation;
Avoid
feeding
dusty hay

11. EXERCISE-INDUCEDPULMONARY
HEMORRHAGEINHORSES(EIPH)
Epistaxis
Bleeder
occurs in most
racehorses and is
observed in many
other horses used in
equine sports that
require strenuous
exercise for short
periods of time
high pulmonary
vascular pressures
during maximal
exercise,
neovascularization
secondary to
pulmonary
inflammation, and
intrathoracic shear
forces generated
during exercise
Results from
thickening of
pulmonary vein
walls, resulting in
decreased luminal
diameter and
increased
intravascular
pressure at the
level of the
pulmonary
capillaries.
epistaxis Endoscopic
observation of
blood in the
airways 30–90
min after
exercise provides
definitive
evidence of EIPH.
cytologic
examination of
bronchoalveolar
lavage,
cytologic
examination of
bronchoalveolar
lavage fluid,
Thoracic
radiography
guttural pouch
and ethmoid
hematoma
Flurosemide,
Other
vasodilators
Application
of nasal
dilator
bands
reduces RBC
counts in
bronchoalve
olar fluid
from
affected
horses
running on
a treadmill
by 33%
LARYNGEALHEMIPLEGIAINHORSES
Roaring/
Left
laryngeal
hemiplegi
a
Most common
cause of abnormal
inspiratory noise
in the exercising
horse.
characterized by
paresis or paralysis
of the left arytenoid
cartilage and vocal
fold. It manifests
clinically as exercise
intolerance and
inspiratory
respiratory noise
(“roaring”) during
exercise
-decreased airway
sizes
inspiratory noise
during exercise
exercise
intolerance.
Clinical signs;
Endoscopic
observation of
reduced or
absent
mobility of the
arytenoid
cartilage and
vocal fold.
Arytenoid
chondritis
Prosteticlaryng
oplasty,
Laryngeal
;ventriculecto
my performed
via
laryngotomy,
or
ventriculocord
ectomy
performed via
transendoscopi
c laser,
improves
airflow and
reduces the
“roaring”
sound during
exercise
Prosthetic
laryngopla
sty is
commonly
done in
racing
horses and
is the only
technique
that
satisfactori
ly reduces
the
impedance
to
inspiratory
flow
PHARYNGEAL
LYMPHOID
HYPERPLASIA
pharyngiti
s
common condition
of the dorsal
pharyngeal wall
observed in young
horses (1–3 yr old)
Result of exposure
to novel antigens:
bacteria, viruses,
organic dusts, and
other allergens
Pharyngal pain
Reduced appetite
small foci or
follicles of
lymphoid tissue
spread diffusely
over the roof
and lateral
walls of the
pharynx
Endoscopic
examination
rest and NSAID
administration
are warranted
in horses
demonstrating
pharyngeal
pain.

12. DORSALDISPLACEMENTOFTHESOFTPALATE a performance-
limiting condition
of the upper
respiratory tract
and is a relatively
common cause of
upper respiratory
noise during
exercise
the caudal free
margin of the soft
palate moves dorsal
to the epiglottis,
creating a
functional
obstruction within
the airway. The
cross-sectional area
of the pharynx is
reduced, and
airflow resistance
and turbulence are
increased.
Inflammation of
the URT due to
infection may
cause neuropathy
of the pharyngeal
branch of the
vagus n. as it
traverses the
floor of the
medial
compartment of
the guttural
pouch, resulting
in neuromuscular
dysfunction of the
pharyngeal
muscles that
control the soft
palate. The
retropharyngeal
lymph nodes are
in direct gurgling
respiratory
noisecontact with
the pharyngeal
branch of the
vagus nerve, and
retropharyngeal
lymphadenopathy
may result in
compression and
irritation
gurgling respiratory
noise/ “choking
down”; difficulty of
breathing
Based on
clinical signs ;
nasopharynge
al endoscopy;
lateral x-rays
of the head.
Rest and anti-
inflammatory
therapy;
Sternothyrohy
oideusmyecto
my;Soft palate
resection
(staphylectomy

13. EPIGLOTTICENTRAPMENT a less common
cause of
respiratory noise
and exercise
intolerance
the aryepiglottic
fold completely
envelops the apex
and lateral margins
of the epiglottis
inspiratory and
expiratory
respiratory noise
during exercise and
poor exercise
performance.
Less common signs
include cough, nasal
discharge, and
headshaking.
Redundant
folds, swollen
and ulcerated
epiglottis
Endoscopic
examination
axial division of
the
aryepiglottic
fold to free the
epiglottis
SUBEPIGLOTTICCYST
an uncommon
cause of
respiratory noise
in young horses.
They are likely
present from
birth, but remain
undetected until
the horse begins
exercise training
Most commonly
reported in
thoroughbreds and
standardbreds
suspected to arise
from remnants of
the thyroglossal
duct.
respiratory noise;
exercise
;intolerance
Large cysts may
produce coughing,
dysphagia, and
aspiration in foals.
endoscopic
examination of
the upper
respiratory
tract
Dorsal
displacement of
the soft palate
complete
removal of the
secretory lining
of the cyst
FOURTH
BRANCHIAL
ARCH
DEFECT
Aplasia or
hypoplasia of the
extrinsic structure
of the larynx
respiratory noise,
although mild
dysphagia,
eructation, and
cough
absence of one
or both wings
of the thyroid
cartilage,
Radiography;
Endoscopic
examination
GutturalPouchEMPYEMA
the accumulation
of purulent, septic
exudate in the
guttural pouch
Caused by bacteria
primarily
Streptococcus spp.
intermittent
purulent nasal dis
charge, painful
swelling in the
parotid area, and in
severe cases, stiff
head carriage and
stertorous
breathing. Fever,
depression, and
anorexia
swelling in the
parotid area,
endoscopic
examination of
the guttural
pouch;
radiography of
the pharynx
Systemic
antimicrobial
therapy;
guttural pouch
lavage and
drainage;
penicillin;

14. GUTTURALPOUCH
TYMPANY
Condition in young
horses in which
excessive air is
trapped in the
pouch(es)
Foals are most
commonly
presented 2-4
months of age
The affected
guttural pouch is
distended with air
and forms a
characteristic
nonpainful
swelling in the
parotid region.
Tympanitic swelling
of the viborg region;
resp. noise;
cough;dysphagia
is based on
clinical signs
and
radiographic
examination of
the skull
bronchopneum
onia;
Guttural pouch
empyema
Medical
management
with NSAID
and
antimicrobial
therapy
GUTURALPOUCH
MYCOSISMycoticplaques
inthegutturalpouchare
typicallylocatedonthe
caudodorsalaspectofthe
medialgutturalpouch,
overtheinternalcarotid
artery
Mycotic plaques
in the guttural
pouch are
typically located
on the
caudodorsal
aspect of the
medial guttural
pouch, over the
internal carotid
artery
Etiology is fungi
primarily aspergillus
spp
Clinical signs
arise from
damage to the
cranial nerves
and the arteries
within the
mucosal lining
of the guttural
pouch.
epistaxis endoscopic
examination
of the
guttural
pouch
topical and
systemic
antifungal
therapy,
based on
sensitivity
testing
RUPTUREOFTHELONGUS
CAPITISMUSCLE
second most
common cause
(after mycosis) of
severe
hemorrhage from
the guttural pouch
The longus capitis
muscle inserts into
the basiphenoid
and occipital bones
Epistaxis;head tilt;
nystagmus; ataxia
swelling and
hemorrhage
can be seen in
the most rostral
and medial
aspects of the
guttural pouch;
pharyngeal
collapse
Guttural pouch
mycosis
involves stall
rest for 4–6
wk; broad-
spectrum
antibiotics are
given for 5–7
days for any
infection at the
site of muscle
rupture
REFERENCES:
 http://www.thehorse.com/articles/28846/managing-inflammatory-airway-disease-in-horses-aaep-2011 Erica Larson, News Editor. March 16. 2012
 Christa Lesté-Lasserre, 2013. www.horse.com
 Bianca Schwarz, PhD, DVM, Dipl. ECEIM, head of the Internal Medicine Service in the Equine Clinic of Altforweiler, Germany, and a former researcher at the Equine Clinic of the
University of Vienna in Austria. T