respiratory diseases of equine
DESCRIPTION
TRANSCRIPT
Infectious Respiratory DiseasesD
isea
se
Oth
er
nam
e
Description Epidemiology Pathogenesis Clinical Signs Lesions Diagnosis Diff. diagnosis
Treatment Prevention and Control
Viral Infection
Equi
ne H
erpe
sviru
s In
fecti
on
-Equ
ine
vira
l rhi
nopn
eum
oniti
s-E
quin
e ab
ortio
n vi
rus Equine
herpesvirus 1 (EHV-1) and equine herpesvirus 4 (EHV-4)
Ubiquitous in horse populations worldwide
Transmission:Direct contactIndirect contact
The incubation period of EHV is 2–10 days.
1.fever of 102–107°F (38.9–41.7°C)
2.malaise3.pharyngitis4.cough5.Inappetence6.serous nasal
discharge7.neutropenia 8.lymphopenia9.submandibular or
retropharyngeal lymphadenopathy
Gross lesions 1.hyperemia 2.ulceration of
the respiratory epithelium
3.multiple, tiny, plum-colored foci in the lungs
Histologic lesions1.inflammation,
necrosis, and intranuclear inclusions of the respiratory epithelium and germinal centers of the associated lymph nodes
2. serofibrinous exudate in the alveoli
PCRVirus 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.Antipyretics
3.Antibiotic therapy
1.Isolation of new horses
2.Stress Management
3.Disinfection 4.Strict
sanitation5.Vaccination 6.Modified live
vaccines
Equi
ne In
fluen
za Most economically important contagious respiratory disease of horses. Highly contagious and spreads rapidly by direct contact
Orthomyxovirus A/Equi-1Orthomyxovirus 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.Depression6.anorexia 7.weakness
1.Nasal discharge2.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 isolation2.Serologic tests 3.Pulmonary
imaging4.Thoracic
radiographs
Equine Herpesvirus Infectionequine viral arteritis
1.Supportive treatment
2.NSAID3.Antibiotics 4.Rest
1.Hygienic management
2.Vaccination
Equi
ne V
iral A
rter
itis
Epiz
ootic
cel
luliti
s Pi
nk e
yeEq
uine
typh
oid
Rotla
ufse
uche
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 secretionsFomite contamination with respiratory secretionsVenereal transmissionCongenital 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 bronchopulmonary 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
Respiratory signs:1.serous nasal
discharge2.Cough3.Conjunctivitis4.Lacrimation5.palpebral and
periorbital edema
Gross lesions: (respiratory)Pulmonary edemaemphysemainterstitial pneumoniaexcess peritoneal, pleural, and pericardial fluidMicroscopic 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 isolation5.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 adenoviruses
5.Purpura hemorrhagica
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 groups5.identification
of carrier stallions
6.annual immunization of noncarrier breeding stallion populations
7.Vaccination
Hen
dra
Viru
s In
fecti
on
Equi
ne M
orbi
llivi
rus 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 horsesHendra 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 2009Fruit 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 waterFomites
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)depressiontachycardiatachypnea sweatingpoor capillary refillabnormal lung sounds (caused by pulmonary edema)
Neurologic deficits:ataxiahead pressingrecumbency
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.hemorrhage3.thrombosis of
capillaries4.necrosis of
alveolar walls5.alveolar
macrophages are evident in the lungs.
1.RT-PCR2.detection of
viral RNA3.immunoperoxi
dase staining/ seroconversion
4.Virus Neutralization assay
5.ELISA Samples: blood sample nasal or oral swab
1.African Horse Fever
2.anthrax3.botulism4.certain
bacterial infections
5.plant or chemical poisoning
NONE minimizing contact with bat body fluids .Control
1.Euthanasia2.deep burial of
cases 3.monitoring4.Isolation5.movement
restriction of in-contact animals
6.disinfection of potentially contaminated surfaces.
Afric
an H
orse
Sic
knes
s Zebras are considered to be the natural vertebrate host and reservoir of the AHSVCulicoides 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 stanceextended necknostril flaringcoughingFrothy 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 OrIdentificationPCR or by ELISA
EVAPurpura Hemorrhagica Equine Infectious AnemiaBabesiosis (Early Stages)
No specific treatmentSupportive and symptomatic treatment
Vector control Restricting import of infected animalsSlaughter of viremic animalsVaccination
Bacterial InfectionRh
odoc
occu
s eq
ui P
neum
onia 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.
AnorexiaLethargyFebrile stateTachypneaAcute respiratory distressFeverCough DiarrheaCrackles 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 pyogranulomatous bronchopneumonia with abscessation and associated suppurative lymphadenitis.
1. Bacterial culture Definitive diagnosis of R. equi pneumonia.
2. Thoracic radiography3. Thoracic ultrasound4. PCRSerologic testingagar 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.Bronchodilator therapy
4.Prophylactic antiulcer
1.decrease exposure to the organism
2.elimination of environmental conditions that favor dissemination of the organism
3.early detection of clinical cases
4.Surveillance programs
5.passive immunity for neonatal foals
Stra
ngle
s
Dis
tem
per 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 contactIndirect 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 suprapharyngeal 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 infection3.mucoid to
mucopurulent nasal discharge
4.depression5.difficulty swallowing6.inspiratory
respiratory noise7.extended head and
neck.
1.submandibular lymphadenopathy
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 signs2.Bacterial
culture 3.polymerase
chain reaction (PCR)
4.endoscopic examination of the upper respiratory tract
5.ultrasonography
6.radiographic examination
1.Warm compresses
2.applied to sites of lymphadenopathy to facilitate maturation of abscesses
3.povidone-iodine solution (3–5% diluted)
4.NSAID5.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
Pleu
ropn
eum
onia
Pleu
ritis
Pleu
risy infection of the
lungs and pleural spaceDevelops 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.Fever2.Depression3.Lethargy4.Inappetence5.Respiratory distress6.Cough7.Nasal discharge8.Exercise intolerance9.Reduced breath
sounds)10. Presence of pleural fluid 11. Pneumonia
Hematologic lesions:
1.Leukocytosis w/ mature neutrophilia
2.Hyperfibrinogenemia
3.Hypoalbuminemia
4.Hyperglobulinemia
5.Pleural fluid:6.Leukocytosis7.Hyperproteine
mia8.Presence of
intra- and extracellular bacteria
1.Thoracic ultrasonography
2.Thoracocentesis
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.Diaphragmatic hernia
5.Congestive heart failure
6.Hemangiosarcoma
7.African horse sickness
8.Pulmonary hydatidosis
9.Pulmonary infarction and pneumonia
1.Antibiotic therapy
2.Thoracostomy
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
Fung
al In
fecti
ons
Fung
al R
hini
tis Pythium
insidiosum Occurs predominantly in the united states, occasionally in Australia, and rarely in other warm climatic regions.
Respiratory stridorExercise intoleranceChronic unilateral,purulent nasal discharge which may contain blood
Numerous small granulating ulcers or fissures in the rostral part of the nasal cavity
endoscopy Surgical excisionTopical Amphotericin B
Cryptococcus neoformans
Mucopurulent and sanguinus and have a foul odor
Granuloma formation Invasive rhinitis and sinusitisDraining tracts through the facial bones
Biopsy Cytologyculture
Aspergillus spp. Non-invasive Mild yellowish mucoid nasal dischargeInvasiveScanty, 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
Fung
al P
neum
onia Blastomyces
dermatidis Coccidoides immitis Cryptococcus neoformans Histoplasma capulatum
inhalation of sporesInhalation of windborne arthrospores
Chronic coughNasal dischargeExercise intoleranceAnorexia Weight lossPleural effusion
- Commonly seen in coccidiomycosis
Radiography Ultrasonography Tracheobronchial asporates Serological detection
Antifungal drugs ( 10-12 weeks)For primary infectionShould ideally be based on sensitivity testing
Para
sitic
Infe
ction
Para
scar
is
equo
rum Found in foals less
than 4-6 mos. OldProductive coughHyperpnea Loss of weightOvert pneumonia
Endoscopic examinationFecalysis
Dic
tyoc
aulu
s ar
nfiel
di Rarely affects
horsesPersistent, non-progressive coughing
Tracheal aspirationEdoscopy Fecalysis
Echi
noco
ccus
gra
nulo
sus generally well-
tolerated in horses, and cysts in the liver and lung maybe an incidental finding at post-mortem examination
intermittent fever, depression, rapid shallow respiration,pectoral edema,
large pulmonaryor 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 debridement of the pleura and cyst on the surfaceof the diaphragm
DIS
EASE OTHER
NAMEDESCRIPTION ETIOLOGY/
EPIDEMIOLOGYPATHOGENESIS CLINICAL SIGNS LESIONS DIAGNOSIS DIFFERENTIAL
DIAGNOSISTREATMENT CONTROL
AND PREVENTION
MU
LTIN
OD
ULA
R PU
LMO
NAR
Y FI
BRO
SIS Interstitial
pneumonia/ Pulmonary 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 feverweight loss.
diffuse, severe, nodular interstitial pattern.
Histopathologic evaluation of biopsy
anti-inflammatory medications; antibiotics; corticosteroids;acyclovir
INFL
AMM
ATO
RY A
IRW
AY D
ISEA
SE Lower respiratory tract inflammation/Small airway inflammatory 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 (beclomethasone or fluticasone)
Use low-dust bedding; Enhance ventilation; Avoid feeding dusty hay
EXER
CISE
-IND
UCE
D P
ULM
ON
ARY
HEM
ORR
HAG
E IN
HO
RSES
(EIP
H) Epistaxis
Bleederoccurs 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 bronchoalveolar fluid from affected horses running on a treadmill by 33%
LARY
NG
EAL
HEM
IPLE
GIA
IN H
ORS
ES Roaring/ Left laryngeal hemiplegia
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
Prosteticlaryngoplasty,Laryngeal ;ventriculectomy performed via laryngotomy, or ventriculocordectomy performed via transendoscopic laser, improves airflow and reduces the “roaring” sound during exercise
Prosthetic laryngoplasty is commonly done in racing horses and is the only technique that satisfactorily reduces the impedance to inspiratory flow
PHAR
YNG
EAL
LYM
PHO
ID
HYP
ERPL
ASIA pharyngiti
scommon 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 painReduced 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.
DO
RSAL
DIS
PLAC
EMEN
T O
F TH
E SO
FT P
ALAT
E 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 ; nasopharyngeal endoscopy; lateral x-rays of the head.
Rest and anti-inflammatory therapy;Sternothyrohyoideusmyectomy;Soft palate resection (staphylectomy
EPIG
LOTT
IC E
NTR
APM
ENT 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
SUBE
PIG
LOTT
IC C
YST 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
FOU
RTH
BR
ANCH
IAL
ARCH
D
EFEC
T 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
Gutt
ural
Pou
ch E
MPY
EMA 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;
GU
TTU
RAL
POU
CH
TYM
PAN
Y 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
bronchopneumonia;Guttural pouch empyema
Medical management with NSAID and antimicrobial therapy
GU
TURA
L PO
UCH
M
YCO
SIS M
ycot
ic p
laqu
es
in th
e gu
ttura
l pou
ch a
re
typi
cally
loca
ted
on th
e 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
RUPT
URE
OF
THE
LON
GU
S CA
PITI
S M
USC
LE 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