Pleuropneumonia represents a severe manifestation of bronchopneumonia and is defined as an infection of the lungs that extends to include the pleura and pleural space. Clinical signs of pleuropneumonia are often nonspecific early in the course of disease (fever, general malaise) but warrant further investigation in a horse with a history of recent long-distance transport. Pleurodynia, rapid and shallow respiratory pattern, and signs of a systemic inflammatory response suggest advanced disease. Diagnosis relies on thoracic imaging and identification of a septic process from tracheobronchial aspiration (TBA) or pleurocentesis. Culture and sensitivity of TBA or pleural fluid guide antimicrobial selection for treatment of pleuropneumonia.
Etiology and Pathogenesis of Pleuropneumonia in Horses
The most common risk factor associated with pleuropneumonia (“shipping fever”) is long-distance transport, especially with the horse’s head restrained in an elevated position. Under these conditions, bacterial colonization of the lower respiratory tract occurs within 12–24 hours. Clinical signs of pleuropneumonia are usually noted within 7 days of transport but can develop in as few as 24 hours. Other risk factors for pleuropneumonia include recent respiratory viral infections or stressful events including strenuous exercise or general anesthesia. Elevated head carriage in transport, viral infection (EHV and influenza), and stress impair important pulmonary defense mechanisms including mucociliary clearance and phagocytic and bactericidal activity of macrophages and neutrophils, allowing secondary bacterial invasion. Young (< 5 YO) race and sport horses are particularly at risk; however, horses of all ages and disciplines can be affected.
Polymicrobial and mixed anaerobic-aerobic infections are common in horses with pleuropneumonia. Bacterial organisms can sometimes be isolated from both the TBA and pleural fluid with differences in organisms isolated between these locations. Streptococcus equi zooepidemicus is most frequently isolated. Identification of anaerobic bacteria occurs in approximately 30% of horses with pleuropneumonia and has been associated with a poorer prognosis. Mycoplasma spp have also been isolated from pleural effusions and TBA samples; however, their importance as a pathogen in pleuropneumonia is unclear.
Common aerobic bacteria:
Streptococcus equi zooepidemicus
Escherichia coli
Actinobacillus spp
Klebsiella spp
Enterobacter spp
Staphylococcus aureus
Pasteurella spp
Common anaerobic bacteria:
Bacteroides spp
Clostridium spp
Peptostreptococcus spp
Fusobacterium spp
The development of bacterial pleuropneumonia arises when bacterial colonization and associated inflammation within the lower airways and parenchyma extends to the visceral pleura and pleural space. Inflammation of the pleura results in exudative production of pleural fluid, increased capillary permeability and fibrin generation.
Pleural effusion without accompanying bacterial bronchopneumonia is relatively uncommon in horses. Differentials for pleural effusion include fungal pneumonia, neoplasia, penetrating trauma to the chest wall, esophageal rupture, pericarditis, congestive heart failure, or severe hypoproteinemia.
Clinical Findings and Lesions of Pleuropneumonia in Horses
Identification of fever, general malaise, tachypnea, and tachycardia, especially in a horse with a recent history of long-distance transport should prompt further clinical evaluation for presence of pneumonia. Clinical findings in horses with pleuropneumonia will vary according to the stage and severity of disease. Early signs are nonspecific and include acute onset of fever, tachycardia, depression, lethargy, inappetence, and occasionally mild colic. Weight loss and respiratory distress are common as disease progresses. Persistent fever and tachycardia, injected mucous membranes, delayed capillary refill time (> 2 seconds), and laminitis indicate systemic inflammatory response syndrome (SIRS) secondary to endotoxemia.
The parietal pleura is well innervated and clinical signs more specific to pleuropneumonia can be attributed to pain (pleurodynia) associated with pleural inflammation. Signs of pleurodynia include reluctance to turn, bend the trunk or lie down, a short or stilted gait, braced stance with elbows abducted, pain or grunting when pressure is applied over the intercostal spaces (e.g. during auscultation or percussion), and an anxious facial expression. These signs can sometimes be mistaken for colic.
Cough, if present, is often soft, shallow, and nonproductive. Respiration is rapid and shallow due to pleural pain and restricted pulmonary expansion from pleural effusion. Bilateral, mucopurulent nasal discharge is a variable sign. Putrid breath or fetid nasal discharge indicates anaerobic bacterial infection or necrotizing pneumonia. A plaque of sternal edema is seen in horses with a large volume of pleural effusion.
Decreased or absent lung sounds in the ventral lung fields below the pleural effusion. Abnormal lung sounds (often crackles) can be present in dorsal lung fields. Thoracic percussion can be used to delineate the extent of pleural effusion. 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 during early stages of disease.
Diagnosis of Pleuropneumonia in Horses
Tracheobronchial aspirate and thoracocentesis: TBA and pleural fluid cytological analysis along with culture and sensitivity confirm diagnosis and guide treatment
Diagnostic imaging
Hematologic analysis
Tracheobronchial aspirate (TBA) is a valuable diagnostic method in horses with pleuropneumonia and can be obtained sterilely via percutaneous or endoscopic-guided aspiration. Evaluation of TBA and pleural fluid should include gross and cytologic examination, Gram stain, and bacterial culture and sensitivity. Septic fluid has increased cellularity and is predominantly comprised of degenerate neutrophils. Intra and extracellular bacteria may be seen and Gram stain examination is useful to direct initial antimicrobial treatment while awaiting results of culture and sensitivity. Total protein concentration is often increased (> 3 g/dL) in septic pleural fluid. Ideally, samples of pleural fluid and TBA fluid should be submitted concurrently for aerobic and anaerobic culture and sensitivity. While TBA samples produce positive bacterial cultures more frequently, differences in culture results can exist between the two sampling sites. Malodorous pleural fluid is associated with necrotic tissue and anaerobic infection and indicates a guarded prognosis.
Courtesy of Dr. Allison Stewart.
Thoracocentesis is performed for diagnostic and therapeutic purposes in horses with pleuropneumonia. Pleural drainage is indicated in horses with evidence of a septic effusion, with signs of respiratory distress attributable to excessive fluid accumulation, or when the pleural fluid has a fetid odor. The site for thoracocentesis should be sufficiently ventral to the fluid line to allow effective drainage and should avoid close proximity to the heart or diaphragm. 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.
Courtesy of Dr. Kara Lascola.
Thoracic ultrasonography is superior for investigation of the pleural surface and pleural effusion and is indicated in horses with regions of poor to absent breath sounds, thoracic pain, and/or dull thoracic percussion. Ultrasonography is also useful for determining the ideal site for thoracocentesis and pleural fluid drainage. The extent of fluid cellularity correlates with fluid echogenicity; cellular (septic) exudate appears echogenic. In horses with pleuropneumonia, ultrasound can also be useful to detect fibrin (appearing as floating echogenic strands), pleural adhesions, atelectatic or consolidated regions of lung, pulmonary abscesses, and pneumothorax. Gas echoes (small bright bubbles) within pleural fluid may indicate anaerobic bacterial infection, a bronchopleural fistula, necrotizing pneumonia, or iatrogenic introduction of air from thoracocentesis. A large area of pulmonary consolidation, in conjunction with serosanguineous suppurative pleural effusion, is consistent with necrotizing pneumonia.
Thoracic radiography is useful to detect deeper pulmonary parenchymal lesions, mediastinal structures, and the presence/severity of pneumothorax; however, it should only be performed after drainage of pleural fluid.
Laboratory abnormalities do not always correlate with the severity of clinical signs but can be useful for directing supportive treatment and monitoring response to treatment. In horses with peracute or acute pleuropneumonia, laboratory findings reflect bacterial sepsis and systemic inflammation and include abnormalities such as leukopenia, neutropenia with a toxic left shift, hemoconcentration, and azotemia. Horses with more stable disease have leukocytosis, mature neutrophilia, increased serum amyloid A, hyperfibrinogenemia, hyperglobulinemia (chronic antigenic stimulation), hypoalbuminemia (loss in pleural space), and anemia of chronic disease.
Treatment of Pleuropneumonia in Horses
Antimicrobials
Additional medical treatment and supportive care
Broad-spectrum antimicrobial treatment is the mainstay of treatment in horses with pleuropneumonia. Initial drug selection while awaiting results from culture and sensitivity should include intravenous antimicrobials with known activity against aerobic and anaerobic bacteria commonly isolated from horses with pleuropneumonia such as Streptococcus equi zooepidemicus (eg, penicillin, gentamicin, metronidazole). Aerosolized delivery of antimicrobials (gentamicin, ceftiofur) has been described as an adjunct treatment. Antimicrobial administration may last several months. Changes in antimicrobial selection should be based on results from culture and sensitivity, patient response, or the need to transition to oral antimicrobials.
Additional medical treatment includes NSAIDs, analgesics, supplemental oxygen, distal limb cryotherapy to prevent laminitis, pleural lavage, and intrapleural fibrinolytic treatment to decrease fibrin deposition and pleural fluid accumulation. Daily ultrasound examinations are useful to monitor fluid production, evaluate effective drainage, identify isolated fluid pockets, and assess peripheral pulmonary disease and formation of fibrinous adhesions. 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.
Thoracotomy may be a life-saving procedure in cases where prolonged medical treatment with antimicrobials and pleural drainage with lavage has failed to resolve the infection and when there is extensive accumulation of fibrin or debris within the pleural space. Ideally this technique should be limited to horses with chronic, stable, disease with a walled-off lesion or persistent unilateral disease (pockets of fibrin and thick debris, purulent material) and resolving infection in the contralateral hemithorax.
Supportive care is essential and includes provision of a dust-free and well-ventilated environment as well as nutritional and fluid support as needed.
Complications associated with pleuropneumonia include thrombophlebitis secondary to catheter placement, laminitis, coagulopathy or other complications of SIRS, diarrhea associated with antimicrobial treatment, cellulitis associated with indwelling chest tubes, pneumothorax secondary to bronchopleural fistula, and development of pulmonary abscesses.
The prognosis for horses with pleuropneumonia depends on severity of disease and response to treatment, but has greatly improved throughout the past 20 years because of early recognition, advancements in diagnostic testing, and aggressive treatment. Reported survival rates in horses with pleuropneumonia vary between approximately 40%–90% depending on the severity of disease and how long clinical signs were present prior to initiation of appropriate medical treatment. The involvement of anaerobic bacteria has been associated with reduced survival in some studies. Reported rates for return to athletic performance are approximately 60% and although this outcome was not impacted by duration of hospitalization or placement of an indwelling chest tube, those horses with pulmonary or cranial thoracic abscesses, or bronchopleural fistulas did have a poorer prognosis for return to athletic performance. Horses with hemorrhagic necrotizing pneumonia respond poorly to conventional treatment and have a low survival rate.
Key Points
Pleuropneumonia represents a severe manifestation of bacterial bronchopneumonia that can affect horses of all ages; a history of recent long distance transport is a common finding in horses with pleuropneumonia but is not the only risk factor.
Treatment of pleuropneumonia typically requires longterm administration of broad-spectrum antimicrobials and the placement of indwelling chest tubes for drainage of pleural fluid. Thoracotomy can be useful in long standing cases of pleuropneumonia that do not respond to standard treatment.
When diagnosed and treated early, uncomplicated pleuropneumonia has a good prognosis for recovery and return to performance.
Anaerobic infection is less common but has a poorer prognosis.
For More Information
Also see pet health content regarding pleuropneumonia in horses.
