Pleuropneumonia is defined as infection of the lungs and pleural space. In most instances, pleural infection develops secondary to bacterial pneumonia or penetrating thoracic wounds. Spontaneous pleuritis (without accompanying pneumonia) is uncommon in horses. In the USA, ~70% of horses with pleural effusion have pleuropneumonia. The primary differential diagnoses for pleural effusion are neoplastic effusions, heart failure, and hydatidosis.
Etiology and Pathogenesis:
Viral respiratory infection, long-distance transportation, general anesthesia, and strenuous exercise are common predisposing factors that impair pulmonary defense mechanisms, allowing secondary bacterial invasion. 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. Exercise-induced pulmonary hemorrhage may contribute to development of respiratory infection by providing a favorable environment for bacterial replication. Acute pulmonary infarction can be the inciting event for equine pleuropneumonia.
Polymicrobial and mixed anaerobic-aerobic infections are common in horses with pleuropneumonia, with more than one organism isolated from transtracheal aspirates. The most common aerobic organisms are Streptococcus equi zooepidemicus, Escherichia coli, Actinobacillus spp, Klebsiella spp, Enterobacter spp, Staphylococcus aureus, and Pasteurella spp. Anaerobic bacteria are isolated from 40%–70% of horses with pleuropneumonia; Bacteroides spp, Clostridium spp, Peptostreptococcus spp, and Fusobacterium spp are the most common. The etiology of pleural infection in horses is usually bacterial, although Mycoplasma felis and nocardial agents have been isolated from pleural effusions.
Clinical Findings and Lesions:
Horses with pleuropneumonia present with fever, depression, lethargy, and inappetence. Clinical signs specific to pleuropneumonia include pleural pain (pleurodynia) 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. A plaque of sternal edema is seen in horses with a large volume of pleural effusion. Horses with toxemia have injected mucous membranes, delayed capillary refill time (>2 sec), and tachycardia. Auscultation reveals a lack of breath sounds in the ventral lung fields and abnormal lung sounds (often crackles) in dorsal lung fields. Cardiac sounds may be muffled or absent or may radiate over a wider area. Although uncommon, pleural friction rubs are most prominent at end-inspiration and early expiration and are detected after thoracic drainage.
In horses with peracute pleuropneumonia, laboratory findings reflect bacterial sepsis or toxemia and include abnormalities such as leukopenia, neutropenia, left shift, hemoconcentration, and azotemia. Horses with more stable disease have leukocytosis, mature neutrophilia, hyperfibrinogenemia, hyperglobulinemia (chronic antigenic stimulation), hypoalbuminemia (loss in pleural space), and anemia of chronic disease.
Thoracic ultrasonography is ideal for investigation of pleural effusion and is indicated in horses with regions of poor to absent breath sounds, thoracic pain, and/or dull thoracic percussion. Transudative pleural fluid (neoplastic effusion) appears anechoic, whereas more cellular exudate appears echogenic. Gas echoes represent small air bubbles within pleural fluid, which may indicate an anaerobic pleural infection, a bronchopleural fistula, or iatrogenic introduction of air. Pulmonary atelectasis, consolidation, and abscessation can be identified if the lesions are located in peripheral lung fields. Ultrasonographic evidence of a large area of pulmonary consolidation, in conjunction with serosanguineous suppurative pleural effusion, is consistent with pulmonary infarction and necrotizing pneumonia. Adhesions of the visceral to parietal pleura can be visualized using thoracic ultrasonography, and these regions should be avoided during thoracocentesis.
Ultrasonography should be performed before pleurocentesis to determine the best site for maximal drainage and to avoid cardiac or diaphragmatic puncture. Thoracocentesis is performed for diagnostic and therapeutic purposes in horses with pleuropneumonia. Pleural fluid should be drained relatively slowly to avoid hypotension. The hemithorax that appears to contain the most fluid is drained first. Bilateral thoracocentesis is usually necessary. The chest tube may be removed immediately after drainage of the thoracic cavity or may be secured in place to allow continual drainage. Thoracic radiography is indicated after pleurocentesis to evaluate pulmonary parenchymal lesions, mediastinal structures, and the presence/severity of pneumothorax.
Gross examination of pleural fluid includes evaluation of color, odor, volume, and turbidity. Malodorous pleural fluid is associated with necrotic tissue and anaerobic infection and indicates a guarded prognosis. Cytologic evaluation of septic pleural fluid reveals purulent exudate (>90% neutrophils) with increased cellularity (25,000–200,000 cells/μL) and increased total protein (>3 g/dL). Intracellular and extracellular bacteria may be seen, and Gram stain examination is used to direct initial antimicrobial therapy. Bacterial culture and sensitivity should also be performed on transtracheal aspirate samples, which yield positive bacterial cultures more frequently than pleural fluid samples.
Management of horses with pleuropneumonia includes daily ultrasound examination to monitor fluid production, evaluate effective drainage, identify isolated fluid pockets, and assess peripheral pulmonary disease. The volume and character of pleural fluid will determine whether single, intermittent, or continual drainage is indicated. Continual drainage is preferable in cases with fibrinous, cellular, malodorous, and/or large volume of effusion. A one-way (Heimlich) valve allows constant drainage of pleural fluid with minimal risk of development of pneumothorax. An indwelling chest tube should remain in place as long as drainage is productive. Medical therapy includes broad-spectrum antibiotics, NSAIDs, analgesics, and supportive care. Broad-spectrum antimicrobial therapy targeting common aerobic and anaerobic bacteria (eg, penicillin, gentamicin, metronidazole) should be instituted pending results of culture and sensitivity. Intrathoracic fibrinolytic therapy has been reported to reduce fibrin deposition and pleural fluid accumulation. In some horses, the pleural infection does not resolve despite weeks to months of antimicrobial therapy and drainage via indwelling chest tubes. Thoracostomy allows manual removal of organized fibrinous material and necrotic lung; however, this technique should be limited to horses with chronic, stable, unilateral disease with resolving infection in the contralateral hemithorax.
Complications associated with pleuropneumonia include thrombophlebitis, laminitis, bronchopleural fistula, pulmonary abscess, and cranial thoracic mass.
The prognosis for horses with pleuropneumonia has greatly improved throughout the past 20 yr because of early recognition, advancements in diagnostic testing, and aggressive therapy. The survival rate is reported to be as high as 90% by some investigators, with a 60% chance of return to athletic performance. The duration of hospitalization is not indicative of outcome; however, a delay in initiation of appropriate therapy by >48 hr promotes development of anaerobic infection and, ultimately, poor response to treatment. Placement of an indwelling chest tube does not limit the prognosis for return to athletic function. Horses with hemorrhagic necrotizing pneumonia respond poorly to conventional therapy and have a low survival rate.