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