Ruminant Diseases Of Respiratory System. Cypres.docx

Jasmin Joyce E. 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 The most common aerobic organisms are Streptococcus equi zooepidemicus Escherichia coli Actinobacillus spp Klebsiella spp Enterobacter spp Staphylococcus aureus Pasteurella spp. Anaerobic bacteria : Bacteroides spp Clostridium spp Peptostreptococcusspp Fusobacterium spp PATHOGENESIS •

•

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 • •

Fever, depression, lethargy, and inappetence. Clinical signs specific to pleuropneumonia include pleural pain evident as short strides, guarding, and flinching on percussion of the chest; shallow respiration; and endotoxemia. • Horses with pleural pain have an anxious facial expression; stand with their elbows abducted; and are reluctant to move, cough, or lie down. • Gait may be stiff or stilted, and some horses grunt in response to thoracic pressure, auscultation, or percussion. • Nasal discharge is a variable sign. Putrid breath or fetid nasal discharge indicates anaerobic bacterial infection and necrotic pulmonary tissue. • The respiratory pattern is characterized by rapid, shallow respiration due to pleural pain and restricted pulmonary expansion from pleural effusion. DIAGNOSIS 

Thoracic ultrasonography is ideal for investigation of pleural effusion Thoracocentesis is performed for diagnostic and therapeutic purposes in horses with pleuropneumonia.

TREATMENT  Medical therapy includes broad-spectrum antibiotics (eg, penicillin, gentamicin, metronidazole), NSAIDs, analgesics, and supportive care. bacteria should be instituted pending results of culture and sensitivity.  Thoracostomy allows manual removal of organized fibrinous material and necrotic lung

Rhodococcus equi Pneumonia in Foals Rhodococcus equi is the most serious cause of pneumonia in foals 1–4 mo old. ETIOLOGY Rhodococcus equi is a gram-positive, facultative intracellular pathogen that is nearly ubiquitous in soil. PATHOGENESIS Inhalation of dust particles laden with virulent R equi is the major route of pneumonic infection. Development of clinical disease is related to immunocompetency of individual foals; foals that produce little to no detectable γ interferon (IFN-γ) are at risk of developing pneumonia. Manure from pneumonic foals is a major source of virulent bacteria contaminating the environment. Foals with pulmonary infections swallow sputum laden with R equi, which readily replicates in their intestinal tract. CLINICAL SIGNS  Foals are lethargic, febrile, and tachypneic.  Diarrhea is seen in one-third of foals with R equi pneumonia and may be caused by colonic microabscessation.  Cough is a variable clinical sign; purulent nasal discharge is less common.  Thoracic auscultation reveals crackles and wheezes with asymmetric/regional distribution.  Pulmonary regions with marked consolidation lack breath sounds and exhibit dull resonance on thoracic percussion.  Panophthalmitis, guttural pouch empyema, sinusitis, pericarditis, nephritis, nonseptic uveitis, and hepatic and renal abscessation with R equi have been reported. DIAGNOSIS  CBC. Neutrophilic leukocytosis and hyperfibrinogenemia are common  Thoracic radiographic evaluation may reveal a pattern of perihilar alveolization, consolidation, and abscessation. The presence of nodular lung lesions and mediastinal lymphadenopathy in foals 1–4 mo old is highly suggestive of R equi.  Bacterial culture TREATMENT The combination of erythromycin (25 mg/kg, PO, qid; esters or salts) and rifampin (5–10 mg/kg, PO, bid) has historically been the treatment of choice for R equi infection in foals. Clarithromycin is the macrolide of choice for foals with severe disease

Equine Viral Arteritis (Epizootic cellulitis-pinkeye, Equine typhoid) EVA is an acute, contagious, viral disease of equids caused by equine arteritis virus (EAV). Typical cases are characterized by fever, depression, anorexia, leukopenia, dependent edema, conjunctivitis, supra- or periorbital edema, nasal discharge, respiratory distress, skin rash, temporary subfertility in affected stallions, abortion, and infrequently, illness and death in young foals 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.

PREVENTION AND CONTROL 



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.

Hendra Virus Infection ETIOLOGY Hendra virus is a large, pleomorphic enveloped RNA virus. Hendra virus is genetically and antigenically closely related to Nipah virus. Both viruses have been classified in a new genus, Henipavirus, in the subfamily Paramyxovirinae. PATHOGENESIS  The virus becomes more widely distributed in various tissues throughout the body as infection progresses, presumably as a result of a leukocyte-associated viremia. Virus has been demonstrated in the vascular endothelium of subarachnoid and cerebral vessels and in the vasculature of the renal glomerulus and pelvis, lamina propria of the stomach, spleen, various lymph nodes, and myocardium. When respiratory disease is present, there is progressive destruction of alveolar walls, with the appearance of alveolar and intravascular macrophages.

TRANSMISSION  The frothy nasal discharge could plausibly provide a source of virus for aerosol transmission. Hendra virus has been found in the urine, blood, and nasal and oral secretions of naturally infected horses and cats. CLINICAL SIGNS  fever and rapid deterioration.  Respiratory signs can include pulmonary edema and congestion, respiratory distress and terminal nasal discharge, which may be clear initially and progress to stable white or blood-stained froth.  Other clinical signs may include depression, highly increased heart rate, facial edema, muscle trembling, anorexia, congestion of oral mucous membranes, colic-like symptoms (generally quiet abdominal sounds on auscultation of the abdomen in preterminal cases), and stranguria in both males and females. Proximity to fruit bat roosts or feeding sites should increase the index of suspicion. DIAGNOSIS  Confirmation of the diagnosis is based on laboratory examination of appropriate specimens to detect virus, viral antigen, viral nucleic acid, or specific antibodies. TREATMENT AND PREVENTION  There is no specific antiviral treatment for Hendra virus infection.  A vaccine, containing a noninfectious protein component (G protein) of the virus, has been developedHealthy horses can be vaccinated from 4 mo of age with two doses at a 21-day interval, followed by boosters every 6 mo. Studies are being conducted to determine whether the period of booster vaccination can be extended to 1 yr. CONTROL  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.

Recurrent Airway Obstruction in Horses (Heaves, Chronic obstructive pulmonary disease) RAO is an episodic disease triggered by exposure to poorly-cured, moldy, or dusty feeds; confinement to a stable environment; inadequate stable ventilation; dust; or, in some cases, pollen. The precise cause of the disease is not known, but research suggests that the characteristic inflammation of the small airways results from an allergic response to dust, mold, or other trigger factors. CLINICAL SIGNS  chronic coughing which may produce mucous  labored breathing and elevated respiratory rate  increased abdominal movement during breathing  flared nostrils while resting  nasal discharge  exercise intolerance  depression  Characteristic auscultatory findings include a prolonged expiratory phase of respiration, wheezes, tracheal rattle, and overexpanded lung fields. 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.