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Ruminant Diseases of Respiratory System. Cypres
Ruminant Diseases of Respiratory System. Cypres
Cypres DVM3
Ruminant Medicine
SY 2018-2019
RESPIRATORY DISEASES OF HORSES
Pleuropneumonia in Horses
(Pleuritis, Pleurisy)
Pleuropneumonia is defined as infection of the lungs and pleural space.
ETIOLOGY
• Head restraint results in bacterial contamination and multiplication within the lower respiratory tract
within 12–24 hr and may be the single most important predisposing factor for development of
pneumonia associated with long-distance transport. Race and sport horses are particularly at risk. Most
horses with pleuropneumonia are athletic horses <5 yr old
• Acute pulmonary infarction can be the inciting event for equine pleuropneumonia.
CLINICAL FINDINGS
TREATMENT
ETIOLOGY
EAV is a small, enveloped SS RNA virus and the prototype virus of the genus Arterivirus, family
Arteriviridae, order Nidovirales. It has 10 open reading frames (ORFs), of which ORFs 2a, 2b, 3, 4, 5,
5a, 6, and 7 encode the viral structural proteins. EAV is one of the three most important equine viral
respiratory pathogens
PATHOGENESIS
After respiratory exposure, EAV invades the upper and lower respiratory tract and multiplies in
nasopharyngeal epithelium and tonsillar tissue and in bronchial and alveolar macrophages
TRANSMISSION
Transmission of EAV can occur by respiratory, venereal, and congenital routes or by indirect means.
Spread by the respiratory route is the principal mode of dissemination of the virus during the acute
phase of infection
CLINICAL SIGNS
Any combination of the following may be seen: fever lasting 2–9 days, leukopenia, depression,
anorexia, limb edema (lower hindlimbs), and edema of the scrotum and prepuce. Less frequently
encountered signs include conjunctivitis, lacrimation and photophobia, periorbital or supraorbital
edema, rhinitis and nasal discharge, edema of the ventral body wall (including the mammary glands
of mares), an urticarial-type skin reaction (often localized to the sides of the face, neck, or over the
pectoral region, although it can be generalized), stiffness of gait, dyspnea, petechiation of mucous
membranes, diarrhea, icterus, and ataxia.
DIAGNOSIS
This can be based on virus isolation, detection of viral nucleic acid, visualization of viral antigen by
immunohistochemical examination.
The most appropriate samples for virus isolation and/or detection of viral nucleic acid by reverse
transcriptase-PCR (RT-PCR) are nasopharyngeal swabs or washings and unclotted (citrated or EDTA)
blood samples.
TREATMENT
There is no specific antiviral treatment currently available for EVA. Symptomatic treatment (eg,
antipyretic, anti-inflammatory, and diuretic drugs) is indicated only in severe cases, especially in
stallions.
EVA is a manageable and preventable disease that can be controlled by observance of sound
management practices together with a targeted vaccination program. Only one commercial vaccine,
a modified-live virus product, is currently available.
The primary focus of current control programs is to restrict the spread of EAV in breeding
populations and to reduce the risk of outbreaks of virus-related abortion, death in young foals, and
establishment of the carrier state in stallions and postpubertal colts.
Control is based on euthanasia and deep burial of cases; monitoring, isolating, and restricting
movement of in-contact animals; and disinfection of potentially contaminated surfaces.
DIAGNOSIS
The diagnosis of RAO is determined in most horses on the basis of history and characteristic physical
examination findings
Radiographic findings in horses with RAO are peribronchial infiltration and overexpanded pulmonary
fields
TREATMENT
The single most important treatment is environmental management to reduce allergen exposure
Medical treatment consists of a combination of bronchodilating agents and corticosteroid preparations
Severely affected horses are ideally controlled with aerosolized bronchodilators
(eg, albuterol, ipratropium) and systemic corticosteroids (eg, dexamethasone 0.1 mg/kg/day, IV).
Laryngeal Hemiplegia in Horses
(Roaring, Left laryngeal hemiplegia)
ETIOLOGY
Progressive loss of the large myelinated fibers in the distal portion of the recurrent laryngeal nerves
results in neurogenic atrophy of the intrinsic laryngeal musculature, the most crucial of which is the
cricoarytenoideus dorsalis muscle.
Less common causes include direct trauma to the recurrent laryngeal nerve, accidental perivascular
injection of irritating substances, and plant and chemical intoxications. Lead toxicity should be
suspected in horses with bilateral laryngeal paralysis. The peroneal nerve may be affected with toxic
insults, and axonal dystrophy of the peroneal nerve may manifest as stringhalt. Although all breeds are
affected, prevalence is higher in males and long-necked/larger breeds.
Loss of neuromuscular control of the abductor muscle results in collapse of the arytenoid cartilage and
vocal fold, which reduces the glottal cross-sectional area. The resistance to airflow necessitates greater
respiratory effort.
CLINICAL SIGNS
The principal clinical signs are inspiratory noise during exercise and exercise intolerance
DIAGNOSIS
Confirmed by endoscopic observation of reduced or absent mobility of the arytenoid cartilage and vocal
fold. With laryngeal hemiplegia, the arytenoid cartilage and vocal fold are located in a median position
within the laryngeal lumen and are immobile.
TREATMENT
Prosthetic laryngoplasty is commonly done in racing horses and is the only technique that satisfactorily
reduces the impedance to inspiratory flow.
Laryngeal ventriculectomy performed via laryngotomy, or ventriculocordectomy performed via
transendoscopic laser, improves airflow and reduces the “roaring” sound during exercise.