Cattle

In cattle the most common cause is erosion of pulmonary vessels adjacent to lesions of embolic pneumonia associated with vena caval thrombosis and hepatic abscessation. The onset of hemorrhage may be sudden and affected animals hemorrhage profusely and die after a short course of less than 1 hour. Marked epistaxis and hemoptysis, severe dyspnea, muscular weakness and pallor of the mucous membranes are characteristic. In other cases, episodes of epistaxis and hemoptysis may occur over a period of several days or a few weeks along with a history of dyspnea.

Etiology

EIPH occurs in horses during strenuous exercise.

Epidemiology

EIPH is primarily a disease of horses, although it has been reported in racing camels.¹ EIPH occurs in horses worldwide and there does not appear to be any geographical distribution. It is a disorder of horses that run at high speed, such as Thoroughbred or Standardbred racehorses. The disorder is uncommon in endurance horses or draft breeds, although it does occur in horses used for these activities. As a general rule, the more intense the exercise or the higher the speed attained, the greater the proportion of horses with EIPH.

The prevalence of EIPH varies with the method used to detect it and the frequency with which horses are examined, as discussed later in this section. Epistaxis associated with exercise is almost always attributable to pulmonary hemorrhage and occurs only in a small proportion of racehorses.^2-5 Epistaxis occurs in only 3% of horses that have blood detected in the trachea by endoscopic examination performed within 2 hours of racing.⁵ The prevalence of epistaxis in racehorses varies between 0.1 and 9.0%, with the frequency depending on the breed, age and sex of horses selected for study, the type of racing and the timing and frequency of observation of horses after racing. Epistaxis is more common in older horses.^2,3 There are conflicting reports of a sex predisposition, although epistaxis may be more common in female Thoroughbreds.^2,3 Epistaxis is more common after races of less than 1600 m than in longer races,² although not all sources agree on this point.^3,6 However, horses in steeplechase races, which are typically longer than 2000 m, are at greater risk of epistaxis than are horses in flat races.^2,6 Epistaxis is relatively uncommon and most horses with EIPH do not have epistaxis.

There are a variety of other methods of detecting EIPH, including endoscopic examination of the airways and microscopic examination of tracheal aspirates or bronchoalveolar lavage fluid.

Almost all Thoroughbred racehorses in active training have hemosiderophages in bronchoalveolar lavage fluid, indicating that all have some degree of EIPH.⁷ The prevalence of EIPH decreases when diagnosis is based on endoscopic examination of horses after exercise or racing.

Exercise-induced pulmonary hemorrhage is very common in Thoroughbred racehorses, with estimates of prevalence, based on a single endoscopic examination of the trachea and bronchi, of 43–75%.^6,8-10 The prevalence increases with the frequency of examination, with over 80% of horses having evidence of EIPH on at least one occasion after examination after each of three consecutive races.¹¹ The prevalence of EIPH in Standardbred racehorses is assumed to be lower, with 26–34% of horses reported to have blood in the trachea after racing.^12,13 However, these studies were based on a single examination and one¹² only reported as positive those horses with blood covering more than one half the tracheobronchial tree. When examined after each of three races, 87% of Standardbred racehorses have evidence of EIPH on at least one occasion,¹⁴ suggesting that EIPH is as common in Standardbred racehorses as it is in Thoroughbred racehorses.

Exercise-induced pulmonary hemorrhage occurs in approximately 62% of racing Quarter horses, and has been observed in Quarter horses used for barrel racing.¹⁵ The disorder occurs in racing Appaloosa horses.¹⁶ Approximately 11% of polo ponies are affected with EIPH.¹⁷ The disease occurs in draft horses but is not well documented.

Age is considered a risk factor for EIPH, with the prevalence of the disorder being higher in older horses.^8-10 There is no consistent association of sex with prevalence of EIPH.^8-1013 Among Thoroughbred racehorses the prevalence of EIPH increases with increasing speed,^10,18 being greater in Thoroughbreds after racing than after breezing (galloping). Lesions of EIPH are not detected in young Thoroughbred racehorses that have trained at speeds of less than 7 m/s.^10,18

Pathogenesis

The cause of EIPH is rupture of alveolar capillary membranes with subsequent extravasation of blood into interstitial and alveolar spaces.¹⁹ The source of blood in such instances is the pulmonary circulation. Bleeding from bronchial circulation during exercise has been suggested, based on histological evidence of bronchial angiogenesis in horses that have experienced previous episodes of EIPH,²⁰ but contribution of the bronchial circulation to EIPH has not been demonstrated. Regardless of the contribution of bronchial circulation to blood in the airways, the likely initial lesion is in capillaries associated with the pulmonary circulation. Hemorrhage into the interstitial space and alveoli, with subsequent rostral movement of blood in the airways, results in blood in the trachea and bronchi.

Rupture of alveolar capillaries occurs secondary to an exercise-induced increase in transmural pressure (pressure difference between the inside of the capillary and the alveolar lumen). If the transmural stress exceeds the tensile strength of the capillary wall, the capillary ruptures.¹⁹ The proximate cause of alveolar capillary rupture is the high transmural pressure generated by positive intracapillary pressures, which are largely attributable to capillary blood pressure, and the lower intra-alveolar pressure generated by the negative pleural pressures associated with inspiration.

During exercise, the absolute magnitudes of both pulmonary capillary pressure and alveolar pressure increase, with a consequent increase in transmural pressure. Strenuous exercise is associated with marked increases in pulmonary artery pressure in horses.^22-24 Values for mean pulmonary arterial pressure at rest of 20–25 mmHg increase to more than 90 mmHg during intense exercise because of the large cardiac output achieved by exercising horses. The increases in pulmonary artery pressure, combined with an increase in left atrial pressure during exercise, probably result in an increase in pulmonary capillary pressure. Combined with the increase in pulmonary capillary pressure is a marked decrease (more negative) in pleural, and therefore alveolar, pressure during exercise. The pleural pressure of normal horses during inspiration decreases from approximately –0.7 kPa (–5.3 mmHg) at rest to as low as –8.5 kPa (64 mmHg) during strenuous exercise.²⁵ Together, the increase in pulmonary capillary pressure and decrease (more negative) in intrapleural (alveolar) pressure contribute to a marked increase in stress in the alveolar wall. Although the alveolar wall and pulmonary capillaries of horses are stronger than those of other species, rupture may occur because the wall stress in the alveolus exceeds the mechanical strength of the capillary.²⁶

Other theories of the pathogenesis of EIPH include: small-airway disease, upper airway obstruction, hemostatic abnormalities, changes in blood viscosity and erythrocyte shape, intrathoracic sheer forces associated with gait, and bronchial artery angiogenesis.^20,27 It is likely that the pathogenesis of EIPH involves several processes, including pulmonary hypertension, lower alveolar pressure and changes in lung structure, that summate to induce stress failure of pulmonary capillaries.

Obstruction of either the upper or lower airways has been proposed as a cause of EIPH. Inspiratory airway obstruction results in more negative intrapleural, and therefore alveolar, pressures. This effect is exacerbated by exercise, with the result that alveolar transmural pressure is greater in horses with airway obstruction.^28,29 The higher transmural pressure in such horses may increase the severity of EIPH, although this has not been demonstrated. Moreover, while inspiratory airway obstruction may predispose to EIPH, the prevalence of this condition is much less than that of EIPH, indicating that it is not the sole factor inducing EIPH in most horses.

Horses with moderate to severe EIPH have histological evidence of inflammation of the small airways,^18,30 and there is a clear association between the presence of EIPH and inflammatory changes in bronchoalveolar or tracheal aspirate fluid.⁶ However, instillation of autologous blood into the airways induces a marked inflammatory response in normal horses,³¹ and it is therefore unclear whether inflammation alone induces or predisposes to EIPH or whether the inflammation is a result of EIPH. Theoretically, small-airway inflammation and bronchoconstriction have the potential to produce intrathoracic airway obstruction and, therefore, a more negative alveolar pressure. Given that small-airway disease is common in horses, there is the potential for an important effect of factors, such as viral infections, air pollution and allergic airway disease, to contribute to the initiation or propagation of EIPH.

The characteristic location of lesions of EIPH in the caudodorsal lung fields has led to the proposal that hemorrhage is a result of tissue damage occurring when waves of stress, generated by forelimb foot strike, are focused and amplified into the narrowing cross-sectional area of the caudal lung lobes.²⁷ According to the theory, the locomotor impact of the forelimbs results in transmission of forces through the scapula to the body wall, from where they pass into the lungs and caudally and dorsally. As the wave of pressure passes into the narrower caudodorsal regions of the lungs it generates progressively greater shearing forces that disrupt tissue and cause EIPH. However, studies of intrapleural pressures have not demonstrated the presence of a systemic pressure wave passing through the lung and do not provide support for this hypothesis.³²

Horses with EIPH have been suspected of having defects in either hemostasis or fibrinolysis. However, while exercise induces substantial changes in blood coagulation and fibrinolysis, these is no evidence that horses with EIPH have defective coagulation or increased fibrinolysis.^33,34

Regardless of the cause, rupture of pulmonary capillaries and subsequent hemorrhage into airways and interstitium causes inflammation of both airways and interstitium with subsequent development of fibrosis and alteration of tissue compliance. Heterogeneity of compliance within the lungs, and particularly at the junction of normal and diseased tissue, results in the development of abnormal shear stress with subsequent tissue damage. These changes are exacerbated by inflammation and obstruction of small airways, with resulting uneven inflation of the lungs.³⁵ The structural abnormalities, combined with pulmonary hypertension and the large intrathoracic forces associated with respiration during strenuous exercise, cause repetitive damage at the boundary of normal and diseased tissue with further hemorrhage and inflammation. The process, once started, is lifelong and continues for as long as the horse continues to perform strenuous exercise.²⁰

Clinical findings

Poor athletic performance or epistaxis are the most common presenting complaints for horses with EIPH. While poor performance may be attributable to any of a large number of causes, epistaxis associated with exercise is almost always secondary to EIPH.

Epistaxis due to EIPH occurs during or shortly after exercise and is usually first noticed at the end of a race, particularly when the horse is returned to the paddock or winner’s circle and is allowed to lower its head. It is usually bilateral and resolves within hours of the end of the race. Epistaxis may occur on more than one occasion, especially when horses are raced or exercised at high speed soon after an initial episode.

Clinical pathology

Examination of airway secretions or lavage fluid

The presence of red cells or macrophages containing either effete red cells or the breakdown products of hemoglobin (hemosiderophages) in tracheal or bronchoalveolar lavage fluid provides evidence of EIPH. Detection of red cells or hemosiderophages in tracheal aspirates or bronchoalveolar lavage fluid is believed to be both sensitive and specific in the diagnosis of EIPH.⁷ Examination of airway fluids indicates the presence of EIPH in a greater proportion of horses than does tracheobronchoscopic examination after strenuous exercise or racing. The greater sensitivity of examination of airway fluid is probably attributable to the ability of this examination to detect the presence of small amounts of blood or its residual products and the longevity of these products in the airways. While endoscopic examination may detect blood in occasional horses up to 7 days after an episode of EIPH, cellular evidence of pulmonary hemorrhage persists for weeks after a single episode.⁴² Red blood cells and macrophages containing red cells are present in bronchoalveolar lavage fluid or tracheal aspirates for at least 1 week after strenuous exercise or instillation of autologous blood into airways and hemosiderophages are present for at least 21 days and possibly longer.⁴²

Recent studies have reported on the use of red cell numbers in bronchoalveolar lavage fluid as a quantitative indicator of EIPH. However, this indicator of EIPH severity has not been validated nor demonstrated to be more reliable or repeatable than tracheobronchoscopic examination and visual scoring. Furthermore, considerable concern exists over the suitability of red cell counts in bronchoalveolar lavage fluid for assessment of severity of EIPH given that an unknown area, although presumably small, of the lung is examined by lavage and that there is a risk that this area of lung may not be representative of the lung as a whole, similar to the situation of examination of bronchoalveolar lavage fluid of horses with pneumonia. Bronchoalveolar lavage of sections of both lungs, achieved using an endoscope, may obviate some of these concerns.

Tracheal aspirates may be obtained any time after exercise by aspiration either during tracheobronchoscopic examination or through a percutaneous intratracheal needle. Aspirates obtained through an endoscope may not be sterile, depending on the collection technique. Bronchoalveolar lavage fluid can be obtained through either an endoscope wedged in the distal airway or a cuffed tube inserted blindly into a distal airway. Collection of fluid through an endoscope has the advantage of permitting examination of the distal airways and selection of the area of lung to be lavaged. However, it does require the use of an endoscope that is longer (2 m) than those readily available in most equine practices. Use of a commercial bronchoalveolar lavage catheter does not require use of an endoscope and this procedure can be readily performed in field situations.

DIFFERENTIAL DIAGNOSIS

Epistaxis and hemorrhage into airways can occur as a result of a number of diseases (Table 10.5).

Table 10.5 Causes of epistaxis in horses

Necropsy

Exercise-induced pulmonary hemorrhage is a rare cause of death of racehorses, but among race horses that die during racing for reasons other than musculoskeletal injuries, EIPH is common.³⁷ Necropsy examination of horses is usually incidental to examination for another cause of death. Pertinent abnormalities in horses with EIPH are restricted to the respiratory tract. Grossly, horses examined within hours of strenuous exercise, such as horses examined because of catastrophic musculoskeletal injuries incurred during racing, may have severe petechiation in the caudodorsal lung fields. Horses with chronic disease have blue/gray or blue/brown discoloration of the visceral pleural surfaces of the caudodorsal lung fields that is often sharply demarcated, especially on the diaphragmatic surface. The discoloration affects both lungs equally with 30–50% of the lung fields being discolored in severe cases. Affected areas do not collapse to the same extent as unaffected areas and, in the deflated lung, have a spleen-like consistency. On cut surface, the discolored areas of lung are predominantly contiguous with the dorsal pleural surface and extend ventrally into the lung parenchyma. Areas of affected lung may be separated by normal lung. There is proliferation of bronchial vessels, predominantly arteries and arterioles, in affected areas. Histologically, affected areas exhibit bronchiolitis, hemosiderophages in the alveolar lumen and interstitial spaces, and fibrosis of interlobular septa, pleural and around vessels and bronchioles.

Treatment

Therapy of EIPH is usually a combination of attempts to reduce the severity of subsequent hemorrhage and efforts to minimize the effect of recent hemorrhage. Treatment of EIPH is problematic for a number of reasons. Firstly, the pathogenesis of EIPH has not been determined although the available evidence supports a role for stress failure of pulmonary capillaries secondary to exercise-induced pulmonary hypertension. Secondly, there is a lack of information using large numbers of horses under field conditions that demonstrates an effect of any medication or management practice (with the exception of bedding) on EIPH. There are numerous studies of small numbers of horses (< 40) under experimental conditions but these studies often lacked the statistical power to detect treatment effects and, furthermore, the relevance of studies conducted on a treadmill to horses racing competitively is questionable. Treatments for EIPH are usually intended to address a specific aspect of the pathogenesis of the disease and will be discussed in that context.

Prevention and control

There are no documented preventive strategies. Rest is an obvious recommendation for horses with EIPH, but the hemorrhage is likely to recur when the horse is next strenuously exercised. The duration of rest and the optimal exercise program to return horses to racing after EIPH is unknown, although some jurisdictions require exercise no more intense than trotting for 2 months. Firm recommendations cannot be made on duration of rest because of a lack of objective information.

Although a role for lower airway disease (either infectious or allergic) in the genesis of EIPH has not been demonstrated, control of infectious diseases and minimization of noninfectious lower airway inflammation appears prudent.

Concern about the role of impact waves in the genesis of EIPH has led to discussion of ‘low-stress’ training protocols, but these have not been adequately evaluated.

Pulmonary defense mechanisms

Under normal conditions the major airways and the lung parenchyma prevent the entry of and neutralize or remove injurious agents, so that the lung contains very few, if any, organisms beyond the large airways. Many infections of the respiratory tract originate from aerosolized particles carrying infectious agents that arise external to or within the respiratory tract. In order to induce an infection by the aerosol route, an etiological agent must be aerosolized, survive in the aerosol, be deposited at a vulnerable site in the respiratory tract of a susceptible host, and then multiply. Thus the pathogenesis of these respiratory infections is related to the deposition of particles and infectious agents within the respiratory tract.

Under normal conditions a complex of biochemical, physiological and immunological defense mechanisms protects the respiratory tract from inhaled particles that could be injurious or infectious. The major defense mechanisms of the respiratory tract include:

Most of the research on defense mechanisms has been done in man and in laboratory animals.

Species susceptibility

The anatomical and physiological features of the respiratory system of cattle may predispose them to the development of pulmonary lesions much more than other farm animal species. Cattle have a small physiological gaseous exchange capacity and greater resultant basal ventilatory activity. The small gaseous exchange capacity may predispose cattle to low bronchiolar or alveolar oxygen levels during exposure to high altitudes and during periods of active physical or metabolic activity. During these times, low oxygen tension or hypoxia may slow mucociliary and alveolar macrophage activity and decrease pulmonary clearance rates. The basal ventilatory activity is comparatively greater than other mammals, which results in the inspired air becoming progressively more contaminated with infectious, allergenic or noxious substances.

The bovine lung also has a higher degree of compartmentalization than other species. This may predispose to airway hypoxia peripheral to airways that become occluded. This results in reduced phagocytic activity and the retention or multiplication of infectious agents. In addition, because of the low numbers of alveolar macrophages in the bovine lung the pulmonary clearance mechanism may not be as effective as in other species. There is also a low level or atypical bioactivity of lysozyme in bovine respiratory mucus, which may make cattle more susceptible to infection of the respiratory tract than other species.

Development of pneumonia

The process by which pneumonia develops varies with the causative agent and its virulence and with the portal by which it is introduced into the lung.

Bacteria are introduced largely by way of the respiratory passages and cause a primary bronchiolitis that spreads to involve surrounding pulmonary parenchyma. The reaction of the lung tissue may be in the form of an acute fibrinous process as in pasteurellosis and contagious bovine pleuropneumonia, a necrotizing lesion as in infection with F. necrophorum or as a more chronic caseous or granulomatous lesion in mycobacterial or mycotic infections. Spread of the lesion through the lung occurs by extension but also by passage of infective material along bronchioles and lymphatics. Spread along the air passages is facilitated by the normal movements of the bronchiolar epithelium and by coughing. Bronchiectasis and pulmonary abscesses are complications and common causes of failure to respond to therapy. Hematogenous infection by bacteria results in a varying number of septic foci, which may enlarge to form lung abscesses. Pneumonia occurs when these abscesses rupture into air passages and spread as a secondary bronchopneumonia.

Viral infections are also introduced chiefly by inhalation and cause a primary bronchiolitis, but there is an absence of the acute inflammatory reaction that occurs in bacterial pneumonia. Spread to the alveoli causes enlargement and proliferation of the alveolar epithelial cells and the development of alveolar edema. Consolidation of the affected tissue results but again there is an absence of acute inflammation and tissue necrosis so that toxemia is not a characteristic development. Histologically the reaction is manifested by enlargement and proliferation of the alveolar epithelium, alveolar edema, thickening of the interstitial tissue and lymphocytic aggregations around the alveoli, blood vessels and bronchioles. This interstitial type of reaction is characteristic of viral pneumonias.

The pathophysiology of all pneumonias, regardless of the way in which lesions develop, is based upon interference with gaseous exchange between the alveolar air and the blood. Anoxia and hypercapnia develop, which results in polypnea, dyspnea or tachypnea. Consolidation results in louder than normal breath sounds, especially over the anteroventral aspects of the lungs, unless a pleural effusion is present to muffle the sounds. In bacterial pneumonias there is the added effect of toxins produced by the bacteria and necrotic tissue; the accumulation of inflammatory exudate in the bronchi is manifested by abnormal lung sounds such as crackles and wheezes on auscultation. Interstitial pneumonia results in consolidation of pulmonary parenchyma without involvement of the bronchi, and on auscultation loud breath sounds predominate in the early stages.

Extension of the pneumonia to the visceral surface of the pleura results in pleuritis, pleuropneumonia, pleural effusion and thoracic pain. Fibrinous pleuritis is a common complication of pneumonic pasteurellosis in cattle. Pleuritis and pleural effusion secondary to pneumonia and pulmonary abscess are commonly recognized in adult horses with the pleuropneumonia complex associated with aerobic and anaerobic bacteria.¹⁰ Anaerobic bacterial pleuropneumonia in the horse is accompanied by a putrid odor of the breath, the sputum or the pleural fluid.⁸ It is suggested that most anaerobic bacterial pulmonary infections in the horse are the result of aspiration of oropharyngeal contents, and are most commonly located in the right lung because of the proximity of the right main stem bronchus. Some horses with pleuropneumonia may develop acute hemorrhagic pulmonary infarction and necrotizing pneumonia.³¹

Restriction of gaseous exchange occurs because of the obliteration of alveolar spaces and obstruction of air passages. In the stage before blood flow through the affected part ceases, the reduction in oxygenation of the blood is made more severe by failure of part of the circulating blood to come into contact with oxygen. Cyanosis is most likely to develop at this stage and to be less pronounced when hepatization is complete and blood flow through the part ceases. An additional factor in the production of anoxia is the shallow breathing that occurs. Pleuritic pain causes reduction in the respiratory excursion of the chest wall but when no pleurisy is present the explanation of the shallow breathing probably lies in the increased sensitivity of the Hering–Breuer reflex. Retention of carbon dioxide with resulting acidosis is most likely to occur in the early stages of pneumonia because of this shallow breathing.

Medical imaging

Thoracic radiography and ultrasonography are now commonly performed in veterinary teaching hospitals and specialty clinics. They can provide considerable diagnostic assistance in assessing the severity of the lesion and explaining certain clinical manifestations that may be difficult to interpret. Ultrasonography is a useful diagnostic aid in cattle and horses with anaerobic bacterial pleuropneumonia and pulmonary abscessation.^8,33,34 Gas echoes within pleural or abscess fluid were found to be a sensitive and specific indicator of anaerobic infection as was a putrid breath or pleural fluid.

In cattle with pleuropneumonia, ultrasonographic examination of both sides of the thorax may reveal accumulations of anechogenic and hypoechogenic fluid in the pleural space in the ventral aspect of the thorax.^33,35 In cattle, pleural effusion associated with pleuritis is usually unilateral because the pleural sacs do not communicate. Bilateral pleural effusion may indicate either bilateral pulmonary disease or a noninflammatory cause such as right-sided congestive heart failure or hypoproteinemia.

Respiratory secretions

The laboratory examination of the exudates and secretions of the respiratory tract is the most common diagnostic procedure performed when presented with cases of pneumonia. Nasal swabs, tracheobronchial aspirates and bronchoalveolar lavage samples can be submitted for isolation of viruses, bacteria and fungi, cytological examination and determination of antimicrobial sensitivity. Tracheobronchial aspirates are considered more reliable for the cytological examination of pulmonary secretions in horses with suspected pneumonia or pleuropneumonia.³⁶ Bronchoalveolar lavage samples may be normal in horses affected with pneumonia or pleuropneumonia. In suspected cases of pleuropneumonia the collection and culture of pleural fluid is a valuable aid to diagnosis¹⁰ and both anaerobic and aerobic bacteria must be considered.¹⁰

Thoracocentesis

When pleural effusion is suspected, thoracocentesis can be used to obtain pleural fluid for analysis.

Hematology

Hematological examination can indicate if the infection is bacterial or viral in nature and its severity. The hematocrit will be elevated in severely toxemic animals that are not drinking water. Severe bacterial bronchopneumonia and pleuritis is characterized by marked changes in the leukon. Serum fibrinogen concentrations are markedly elevated in horses with pleuropneumonia and pleuritis.³⁷ Some limited studies indicate that the measurement of acute-phase proteins in bovine respiratory disease may be a valuable diagnostic and prognostic aid.³⁸

Serology

When viral interstitial pneumonia is suspected, acute and convalescent sera are recommended for viral neutralization titer evaluation. For specific diseases such as porcine pleuropneumonia, serum can be taken from a percentage of the herd and submitted for serotyping to determine which serotype is most prevalent in the herd.

Fecal samples

When lungworm pneumonia is suspected, fecal samples can be submitted for detection of the larvae.

Necropsy

In outbreaks of respiratory disease wherein the diagnosis is uncertain, necropsy of selected early cases will often assist in making a diagnosis.

Antimicrobial therapy

In specific bacterial infections as listed above, isolation of affected animals and careful surveillance of the remainder of the group to detect cases in the early stages should accompany the administration of specific antimicrobials to affected animals. The choice of antimicrobial will depend on the tentative diagnosis, the experience with the drug in previous cases and the results of drug sensitivity tests. The common bacterial pneumonias of all species will usually recover quickly (24–72 h) if treated with an adequate dose of the drug of choice early in the course of the disease. Animals with severe pneumonia will require daily treatment for several days until recovery occurs. Those with bacterial pneumonia and toxemia must be treated early on an individual basis. Each case should be identified and carefully monitored for failure to recover, and an assessment made. Clinical field trials to evaluate different antimicrobials for the treatment of acute bovine respiratory disease occurring under natural conditions are becoming more common and more meaningful, particularly under commercial feedlot conditions.³⁹

Antimicrobial agents in a long-acting base may be used to provide therapy over a 4–6-day period instead of the daily administration of the shorter-acting preparations. However, the blood levels from the long-acting preparations are not as high as the shorter-acting preparations and treatment with these compounds are not as effective in severely affected animals.

Selection of antimicrobials is based on the principles detailed in Chapter 4. Briefly, antimicrobials for treatment of bacterial respiratory disease should be active against the causative agent, should be able to achieve therapeutic concentrations in diseased lung and should be convenient to administer. The antimicrobials should be affordable and, if used in animals intended as human food, must be approved for use in such animals.

Antimicrobials for treatment of lung disease are preferably those that achieve therapeutic concentrations in diseased lung tissue after administration of conventional doses. This has been convincingly demonstrated for the macrolide (azithromycin, erythromycin),⁴⁰ triamilide (tulathromycin)⁴¹ and fluoroquinolone (danofloxacin, enrofloxacin)^42,43 antimicrobials and fluorfenicol⁴⁴ in a variety of species. The beta-lactam antimicrobials (penicillin, ceftiofur) are effective in treatment of pneumonia in horses, pigs and ruminants despite having chemical properties that do not favor their accumulation in lung tissue.

Routes of administration include oral (either individually or in medicated feed or water), parenteral (subcutaneous, intramuscular, intravenous), or inhalational. Intratracheal administration of antimicrobials to animals with respiratory disease is not an effective means of achieving therapeutic drug concentrations in diseased tissue. Aerosolization and inhalation of antimicrobials has the theoretic advantage of targeting therapy to the lungs and minimizing systemic exposure to the drug. However, while administration by inhalation achieves good concentrations of drug in bronchial lining fluid, the drug does not penetrate unventilated regions of the lungs, in which case parenteral or oral administration of antimicrobials is indicated. Administration of gentamicin to horses and ceftiofur sodium to calves with pneumonia has been investigated. Aerosol administration of gentamicin to normal horses results in gentamicin concentrations in bronchial lavage fluid 12 times that achieved after intravenous administration.⁴⁵ Aerosolized ceftiofur sodium (1 mg/kg) is superior to intramuscular administration in treatment of calves with M. haemolytica.⁴⁶

Treatment of parasitic lung disease, such as that caused by migrating larvae or lung worms, is by administration of appropriate anthelmintics such as ivermectin, moxidectin or the benzimidazoles. Refer to the sections in this book that deal with these diseases for details of the specific treatments. Treatment of P. jiroveci pneumonia involves the administration of a sulfonamide–trimethoprim combination or dapsone (3 mg/kg orally every 24 h).⁴⁷

The antimicrobials and other drugs recommended for the treatment of each specific pneumonia listed under Etiology are presented with each specific disease elsewhere in the book. The common causes for failure to respond favorably to treatment for bacterial pneumonia include:

There is no specific treatment for the viral pneumonias and while many of the Mycoplasma spp. are sensitive to antimicrobials in vitro, the pneumonias associated with them do not respond favorably to treatment. This may be due to the intracellular location of the Mycoplasma making them inaccessible to the drugs. Because viral and mycoplasmal pneumonias are commonly complicated by secondary bacterial infections, it is common practice to treat acute viral and mycoplasmal pneumonias with antimicrobials until recovery is apparent.

Intensive and prolonged therapy may be required for the treatment of diseases such as equine pleuropneumonia. It may include daily care and treatment in a veterinary clinic consisting of daily lavage of the pleural cavity including thoracostomy to drain pulmonary abscesses, and intensive antimicrobial therapy and monitoring for several weeks.⁴⁸

Other drugs

Nonsteroidal anti-inflammatory drugs are useful in the treatment of infectious respiratory disease of cattle and horses, and likely other species. The drugs act by inhibiting the inflammatory response induced by the infecting organism and tissue necrosis. Meloxicam (0.5 mg/kg subcutaneously, once), when administered with tetracycline, improves weight gain and reduces the size of lesions in lungs of cattle with bovine respiratory disease complex over those of animals treated with tetracycline alone.⁴⁹ NSAIDs also improve the clinical signs of cattle with respiratory disease.⁵⁰ Use of these drugs is routine in horses with pneumonia or pleuritis.

Corticosteroids have been used for their anti-inflammatory effect in the treatment of acute pneumonia. However, there is no clinical evidence that they are beneficial.

Bronchodilators have been investigated in the treatment of pneumonia in food animals. The beta-2 adrenergic agonists are potent and effective bronchodilators that can be administered orally, intravenously or by inhalation. These drugs also enhance mucociliary clearance of material from the lungs. Most administration is orally or by inhalation. The use of beta-2 adrenergic agonist bronchodilator drugs in food animals is not permitted in most countries because of the risk of contamination of foodstuffs intended for consumption by people. This is particularly the case with clenbuterol, a drug approved in many countries for use in horses that is administered to cattle illicitly as a growth promoter. People can be poisoned by clenbuterol in tissues of treated cattle. Theophylline has been evaluated as a bronchodilator to relieve respiratory distress in cattle with pneumonia.⁵¹ When it was given orally at a dose of 28 mg/kg BW daily for 3 days, along with antimicrobial therapy, to calves with naturally acquired respiratory disease, the respiratory rate and rectal temperature decreased. However, some calves died, presumably from the accumulation of lethal concentrations of plasma theophylline. It is recommended that the drug should not be used unless plasma levels can be monitored.

Supportive therapy and housing

Affected animals should be housed in warm, well-ventilated, draft-free accommodation and provided with ample fresh water and light, nourishing food. During convalescence premature return to work or exposure to inclement weather should be avoided. If the animal does not eat, oral or parenteral force-feeding should be instituted. If fluids are given intravenously care should be exercised over the speed with which they are administered. Injection at too rapid a rate may cause overloading of the right ventricle and death due to acute heart failure.

Supportive treatment may include the provision of oxygen, if it is available, especially in the critical stages when hypoxia is severe. In foals the oxygen can be administered through an intranasal tube passed back to the nasopharynx and delivered at the rate of about 8 L/min for several hours. Oxygen therapy is detailed in the general section on treatment of respiratory disease above.

Lipid pneumonia

Lipid pneumonia usually results from aspiration of mineral oil (liquid paraffin) administered for gastrointestinal disease. Pneumonia is sometimes the result of inadvertent administration of the oil into the trachea through a misplaced stomach tube, or inhalation following oral administration of oil. However, aspiration of oil can occur even when it is delivered into the stomach through a nasogastric tube,³ presumably because of regurgitation of oil either around the tube or after the tube has been removed. Administration of oil to sedated or severely depressed animals may increase the risk of aspiration.

Clinical signs include cough, tachypnea, tachycardia, pyrexia, respiratory distress and abnormal lung sounds. Radiographs can reveal an alveolar and interstitial pattern. Examination of tracheal aspirates reveals a neutrophilic inflammation and the presence of lipid. Lipid can be readily identified by Sudan or oil red O staining of smears of the aspirate in acute cases. Necropsy examination reveals consolidated lungs. On cut section of these areas oil can be visible. Chronic cases have tissue necrosis and severe interstitial pneumonia. Lipid droplets can be identified in affected lung tissue after oil red O staining of sections.⁴ The presence and nature of the lipid can be demonstrated by thin-layer chromatography and gas chromatography.⁴ The prognosis for recovery is poor. Treatment is supportive and includes anti-inflammatory drugs, antimicrobials, and oxygen. There is no specific treatment. Prevention includes careful insertion of nasogastric tubes, verification of their placement in the stomach and not administering mineral oil to animals with a distended stomach or ones that are heavily sedated or severely depressed.

Esophageal obstruction

Esophageal obstruction is a common and important cause of pneumonia in horses.^2,5 Of 18 horses with esophageal obstruction that had thoracic radiographs performed, eight had evidence of aspiration pneumonia.⁵ Obstruction of the esophagus in horses, and in other species, leads to the accumulation of saliva and feed material in the esophagus oral to the obstruction. When the esophagus is full, this material accumulates in the pharynx with subsequent aspiration into the trachea resulting in contamination of the trachea and lower airways with feed material and oropharyngeal bacteria. Feed material is irritant and also causes obstruction of the smaller airways. Pulmonary defense mechanisms are weakened or overwhelmed by the contamination and infection and pneumonia result. The duration of esophageal obstruction is a good indicator of the risk of aspiration pneumonia, although the extent of contamination of the trachea with feed material is not.⁵ Affected horses are pyrexic, tachycardic, and toxemic. Lung sounds can include crackles and wheezes, but the only auscultatory abnormality can be decreased breath sounds in the ventral thorax. Radiography reveals a characteristic pattern of bronchopneumonia restricted, at least initially, to the cranioventral and caudoventral lung lobes in adult horses. Ultrasonography reveals comet tail lesions in the ventral lung fields and variable consolidation. Pleuritis is a not uncommon sequel to aspiration pneumonia. Examination of tracheal aspirates demonstrates neutrophilic inflammation with presence of degenerate neutrophils, bacteria that are both intracellular and extracellular, and plant material. Culture of tracheal aspirates yields one or more of a wide variety of bacteria including S. zooepidemicus, Pasteurella sp., Actinobacillus sp, E. coli, and anaerobes. Treatment involves prompt relief of the esophageal obstruction and administration of broad-spectrum antimicrobials such as a combination of penicillin, aminoglycoside, and metronidazole. The prognosis for recovery from aspiration pneumonia secondary to esophageal obstruction is guarded to fair, partly because the animal has to recover from two diseases – the pneumonia and the esophageal obstruction. Prevention of aspiration pneumonia in horses with esophageal obstruction includes prompt relief of the obstruction and administration of broad-spectrum antimicrobials.

Meconium aspiration syndrome

Aspiration of meconium during parturition is associated with severe lung disease in newborns. Passage of meconium in utero, and subsequent aspiration by the fetus, is a sign of fetal distress. It is suggested that fetal distress results in expulsion of meconium into the amniotic fluid. This is followed by aspiration of contaminated amniotic fluid. The passage of meconium-contaminated amniotic fluid into the lungs may occur prior to birth when the fetus gasps for air in an attempt to correct hypoxemia or when the calf takes its first breath and aspirates meconium from the oropharynx. Normally, fetal aspiration of amniotic fluid does not occur because the inspiratory forces are insufficient to allow amniotic fluid to reach the lungs, and the lung liquid, a locally produced viscous material present in the trachea and lungs, constantly flows up the major airways to the oropharynx. The result is that the fetus is doubly challenged in that it must deal with both the cause of the fetal distress and the pneumonia induced by aspiration of meconium. Although meconium is sterile, it induces a severe inflammatory response in the lungs.

The meconium aspiration syndrome is best described in newborn calves,⁶ although there are numerous reports of its experimental induction in piglets and lambs as a model of the human disease. In a series of calves under 2 weeks of age submitted to a diagnostic laboratory, 42.5% had evidence of meconium, squamous cells or keratin in the lung. Diffuse alveolitis with exudation of neutrophils, macrophages, multinucleated cells and obstruction of small airways with atelectasis were common.

Treatment of aspiration pneumonia in farm animals is not well described. Administration of antimicrobials is prudent. Anti-inflammatory drugs are indicated. Pentoxifylline is used in human neonates with meconium aspiration, but there are no reports of its use for this purpose in farm animals.

Dusty feed

Although farm animals fed on dusty feeds inhale many dust particles and bacteria, which can be readily isolated from the lung, this form of infection rarely results in the development of pneumonia. Much of the dust is filtered out in the bronchial tree and does not reach the alveoli. However, this may be of importance in the production of the primary bronchiolitis that so often precedes alveolar emphysema in horses. The inhalation of feed particles in pigs in a very poorly ventilated environment has been demonstrated to cause foreign body pneumonia. Also, a dry, dusty atmosphere can be created in a piggery by overfrequent changing of wood shavings used as bedding, and this can lead to the production of foreign body pneumonia. Liquids and droplets penetrate to the depths of the alveoli and run freely into the dependent portions, and aspiration pneumonia often results.

Primary diseases

Secondary diseases

Hydrothorax

Hemothorax

Other causes

Sporadic and nonspecific diseases may be accompanied by pleurisy. Examples include septicemias due to Pseudomonas aeruginosa; bacteremia with localization causing a primary septic pleural effusion. In horses, the infection is usually S. equi and the original disease is strangles. In goats, it is usually spread from a mycoplasmal pneumonia.

Perforation of the diaphragm occurs in traumatic reticuloperitonitis in cattle and goats. Spread into the pleural cavity can occur without actual penetration of the diaphragm, as it enters via the lymphatics. Abomasopleural fistula secondary to abomasal ulceration can cause pleuritis in cattle.⁷

Chronic pleuritis is an important cause of loss in commercial piggeries. The prevalence can be as low as 5.6% of pigs at slaughter in specific-pathogen-free piggeries and as high as 27% in conventional piggeries.⁸

Medical imaging

Radiographic examination may reveal the presence of a fluid line and fluid displacement of the mediastinum and heart to the unaffected side and collapse of the lung. However, in cattle, pleural effusion cannot be located precisely by radiography because only laterolateral radiographs of the thorax can be taken.⁹ Ultrasonography is superior for the visualization of small volumes of pleural fluid that cannot be detected by auscultation and acoustic percussion of the thorax.

Ultrasonography

Ultrasonography is more reliable for the detection of pleural fluid in horses and cattle than radiography.^10,11 Pleural fluid is easily detected as hypoechoic to anechoic fluid between the parietal pleural surface, diaphragm and lung (Fig. 10.2). Transudative pleural fluid appears homogeneously anechoic to hypoechoic. Exudative fluid is commonly present in horses and cattle with pleuropneumonia and often contains echogenic material.¹² Serosanguineous or hemorrhagic fluid is also more echogenic than transudates. Fibrin appears as filmy and filamentous strands floating in the effusion with loose attachments to the pleural surfaces. Pockets of fluid loculated by fibrin are commonly imaged in horses with fibrinous pleuropneumonia. Adhesions appear as echogenic attachments between the parietal and visceral pleural surfaces; the adhesions restrict independent motion of the surfaces. The presence of small, bright echoes (gas echoes) swirling in pleural or abscess fluid is associated with anaerobic infection of the pleural cavity. Gas echoes are usually most abundant in the dorsal aspects of the pleural cavity. Other lung and pleural abnormalities that may be visualized include compression atelectasis, consolidation, abscesses and displacement of the lung as pleural effusion accumulates.

Fig. 10.2 Ultrasonogram and schematic of the thorax in a cow with pleuropneumonia due to infection with Mannheimia haemolytica. There is an accumulation of anechoic pleural effusion, which compresses the lung. The ultrasonogram was obtained from the distal region of the sixth intercostal space of the left thoracic wall with a 5.0 MHz linear scanner. 1 = Thoracic wall; 2 = Anechoic fluid; 3 = Lung. Ds, Dorsal; Vt, Ventral.

(Reproduced with kind permission of U. Braun.)

Prognosis

The prognosis depends on the severity and extent of the pleuritis and the presence of pneumonia. The presence of dull areas over the ventral two-thirds of the thorax on both sides and more than about 6 L of pleural fluid in the pleural cavity of a mature horse suggests an unfavorable prognosis. If the disease is in an advanced stage when first recognized and there is extensive fibrinous inflammation, the response to treatment can be protracted and extensive long-term daily care will be necessary. Also, the common failure to culture the primary causative agent, particularly in horses, makes specific therapy difficult.

Thoracocentesis (pleurocentesis)

Thoracocentesis to obtain a sample of the fluid for laboratory examination is necessary for a definitive diagnosis. The fluid is examined for its odor, color and viscosity, protein concentration and presence of blood or tumor cells, and is cultured for bacteria. It is important to determine whether the fluid is an exudate or a transudate. Pleural fluid from horses affected with anaerobic bacterial pleuropneumonia may be foul-smelling. Examination of the pleural fluid usually reveals an increase in leukocytes up to 40 000–100 000/μL and protein concentrations of up to 50 g/L (5.0 g/dL). The fluid should be cultured for both aerobic and anaerobic bacteria and Mycoplasma spp.

Hematology

In peracute bacterial pleuropneumonia in horses and cattle, leukopenia and neutropenia with toxic neutrophils are common. In acute pleuritis with severe toxemia, hemoconcentration, neutropenia with a left shift and toxic neutrophils are common. In subacute and chronic stages normal to high leukocyte counts are often present. Hyperfibrinogenemia, decreased albumin–globulin ratio and anemia are common in chronic pleuropneumonia.

Antimicrobial therapy

The primary aim of treatment is to control the infection in the pleural cavities using the systemic administration of antimicrobials, which should be selected on the basis of culture and sensitivity of pathogens from the pleural fluid. Before the antimicrobial sensitivity results are available it is recommended that broad-spectrum antimicrobials be used. Long-term therapy daily for several weeks may be necessary.

Drainage and lavage of pleural cavity

Drainage of pleural fluid removes exudate from the pleural cavity and allows the lungs to re-expand. Criteria for drainage include:

Clinical experience suggests that drainage improves the outcome.

Pleural fluid can be drained using intermittent thoracocentesis or indwelling chest tubes.³ Intermittent drainage is satisfactory in an animal with a small amount of fluid. Small (12–20 French) chest tubes are temporarily inserted at 2–3-day intervals to remove the fluid. Aspiration may not be easy in some cases as the drainage tube may become blocked with fibrin and respiratory movements may result in laceration of the lung. Drainage may be difficult or almost impossible in cases in which adhesion of visceral and parietal pleura are extensive and fluid is loculated.

Indwelling chest tubes may be required unilaterally or bilaterally depending on the patency of mediastinal fenestration and the degree of fluid loculation. A large bore (24–32 French) chest tube is inserted and secured to prevent it from sliding out. Unidirectional drainage through the tube is facilitated by a Heimlich valve and monitored regularly. Pleural fluid is allowed to drain or drip passively, since suction often results in obstruction of the tube with fibrin or peripheral lung tissue. Loculation of fluid may interfere with proper drainage and necessitate replacement of tubes. Complications include subcutaneous cellulitis or pneumothorax.

Pleural lavage may assist in removal of fibrin, inflammatory debris, and necrotic tissue; it can prevent loculation, dilute thick pleural fluid and facilitate drainage. One chest tube is placed dorsally and one ventrally; 5–10 L of sterile, warm isotonic saline is infused into each hemithorax by gravity flow. After infusion, the chest tube is reconnected to a unidirectional valve and the lavage fluid is allowed to drain.

Thoracotomy has been used successfully for the treatment of pericarditis and pleuritis and lung abscesses in cattle.¹³ Claims are made for the use of dexamethasone at 0.1 mg/kg BW to reduce the degree of pleural effusion. In acute cases of pleurisy in the horse analgesics such as phenylbutazone are valuable to relieve pain and anxiety, allowing the horse to eat and drink more normally.

Fibrinolytic therapy

Pleural adhesions are unavoidable and may become thick and extensive with the formation of loculation which traps pleural fluid, all of which prevents full recovery. However, some animals will stabilize at a certain level of chronicity, will survive for long periods and may be useful for light work or as breeding animals. Fibrinolytic agents such as streptokinase have been used in human medicine to promote the thinning of pleural fluid, provide enzymatic debridement of the pleurae, lyse adhesions and promote drainage of loculi. However, these have not been evaluated in farm animals with pleuritis.

Risk factors

The risk of a horse developing pleuropneumonia is increased by a factor of:

Other suggested risk factors include general anesthesia, surgery, disorders of the upper airway, exercise-induced pulmonary hemorrhage, esophageal obstruction, and dysphagia.

Complications

Complications of pleuropneumonia include:

Development of intrathoracic abscesses is evident as chronic disease, weight loss, cough and fever, readily detected by a combination of ultrasonographic and radiographic examination.

Cranial thoracic masses are evident as an elevation in heart rate, prominent jugular pulse, spontaneous jugular thrombosis, and forelimb pointing. The signs are referable to a mass in the cranial thorax displacing the heart caudally and to the left and impairing venous return to the heart in the cranial vena cava.²³ Ultrasonographic and radiographic examination reveals the presence of the mass.

Bronchopleural fistulae develop when a section of pulmonary parenchyma sloughs, leaving an open bronchiole that communicates with the pleural space. Mild pneumothorax develops. The bronchopleural fistula can be diagnosed by infusion of fluorescein dye into the pleural space and detecting its presence at the nares, or by pleuroscopic examination.^24,26

Prognosis

The prognosis for life for horses able to be treated aggressively is very good (60–95%)^3,13 and the prognosis for return to previous function if the horse survives is reasonable (60%).¹³ The prognosis for return to previous function for horses that develop chronic disease and complications is poor (31%).¹³

Antimicrobial treatment

The prompt institution of systemic, broad-spectrum antimicrobial therapy is the single most important component of treatment of horses with pleuropneumonia. Antimicrobial therapy is almost always started before the results of bacterial culture of pleural fluid or tracheal aspirate are received and the antimicrobial sensitivity of isolated bacteria are determined. Use of antibiotics or combinations of antibiotics with a broad spectrum of antimicrobial activity is important because of the polymicrobial nature of most infections and because the wide range of Gram-positive and Gram-negative bacteria that may be associated with the disease makes prediction of the susceptibility of the causative organisms difficult. Furthermore, superinfection with bacteria, especially Enterobacteriaceae and obligate anaerobes, commonly occurs in horses with disease initially associated with a single bacterial species. Administration of drugs that are effective in the treatment of penicillin-resistant obligate anaerobes is also important.

Recommended doses for antimicrobials used in the treatment of pleuropneumonia are provided in Table 10.6. Antimicrobial therapy should be broad-spectrum to include coverage of the likely bacteria involved in the disease. It should therefore provide coverage against Streptococcus spp., Actinobacillus/Pasteurella spp., Enterobacteriaceae and anaerobes, including Bacteroides spp. A combination of penicillin G, an aminoglycoside and metronidazole provides broad-spectrum coverage and is a frequently used empirical therapy until the results of bacterial culture are known. Results of bacterial culture and subsequent antimicrobial susceptibility testing may aid selection of further antimicrobials. However, superinfection with Gram-negative and anaerobic bacteria is common and there is a sound rationale for continued use of a combination of antimicrobials providing broad-spectrum coverage throughout treatment of the disease.

Table 10.6 Antimicrobial agents and recommended doses for treatment of pleuropneumonia in horses

IV, intravenously; PO, orally; IM = intramuscularly; q, dose administered every ‘h’ hours.

Antimicrobial therapy will be prolonged in most cases, usually being required for at least 1 month and often several months. As the disease resolves it may be possible to change from parenteral antibiotics to orally administered antibiotics such as a combination of trimethoprim–sulfonamide, although the clinical response to this combination is sometimes disappointing, doxycycline or enrofloxacin.

The decision to discontinue antimicrobial therapy should be based on lack of fever, nasal discharge, respiratory distress or cough, lack of evidence of intrathoracic abscesses on ultrasonographic and radiographic examination of the thorax, and resolution of neutrophilia and hyperfibrinogenemia. There should be no appreciable pleural fluid on ultrasonographic examination.

Thoracic drainage

Chronic, effective drainage of the pleural cavity and intrathoracic abscesses is critical for successful treatment of horses with pleuropneumonia.³¹ Horses with sterile pleural fluid may require only a single drainage of pleural fluid. More severely affected horses may require intermittent drainage on each of several days, and most cases will require insertion of a tube into the pleural space to provide continuous drainage for several days to several weeks. Horses with chronic disease may benefit from a thoracotomy that provides continuous drainage and the ability to lavage the chest. Ultrasonographic examination of the chest is very useful in identifying the presence of pleural fluid, the optimal sites for drainage and the efficacy of drainage.

Intermittent thoracic drainage can be achieved by inserting a bovine teat cannula or similar blunt cannula into the pleural space. This should be done aseptically and under local anesthesia. If ultrasonographic examination is not available, the cannula should be placed in the sixth to eighth intercostal space on the right side or the seventh to ninth on the left side just above the level of the olecranon. Pleural fluid that does not contain large fibrin clots (which clog the cannula) can be drained and the cannula removed. However, the process is slow if large quantities of fluid must be removed. Intermittent drainage is indicated when the quantities of pleural fluid are small (< 5 L), relatively cell free or localized. This situation is most likely to occur in horses with acute disease.

Insertion of large plastic chest tubes (20–30 French, 6–10 mm outside diameter) facilitates rapid fluid removal, allows drainage of viscid fluid and provides continuous drainage. The chest tube should be inserted in an aseptic fashion under local anesthesia at sites indicated by ultrasonographic examination or as described above. A one-way valve should be attached to the external end of the tube to prevent aspiration of air and development of a pneumothorax. A balloon or condom with the end removed is an effective one-way valve. The chest tube is secured to the chest wall with a purse-string suture. The tube may be retained for several days to a week, but should be monitored frequently (every few hours) and cleared of fibrin clots as needed.

Complications of drainage of pleural fluid include: collapse of the animal if the fluid is removed too rapidly; pneumothorax; sudden death due to cardiac puncture or laceration of a coronary vessel; and perforation of abdominal viscera. Collapse can be prevented by administering fluids intravenously during pleural fluid drainage and by removing the fluid gradually (over a period of 30 min). Some horses develop a cellulitis around the chest tube that requires that the tube be removed.

Thoracotomy may be required in chronic cases to provide drainage of intrathoracic abscesses or chronic pleural effusion that is refractory to treatment with antimicrobials.³¹ Thoracotomy is an effective intervention in many horses with advanced pleuropneumonia and should not be considered an emergency or heroic procedure.

Pleural lavage

Infusion and subsequent removal of 5–10 L of warm saline or balance polyionic electrolyte solution into the affected pleural space may be beneficial in the treatment of cases with viscid fluid or fluid containing large amounts of fibrin and cell debris. The fluid can be infused through the chest tube that is used to drain the pleural space. Care should be taken not to introduce bacteria with the infusion.

Supportive therapy

Acutely or severely ill horses may be dehydrated, azotemic, and have acid–base disturbance. These horses should be treated with appropriate fluids administered intravenously.

Pleuropneumonia is a painful disease and every attempt should be made to relieve the horse’s chest pain. NSAIDs, including flunixin meglumine (1 mg/kg, orally, intramuscularly or intravenously, every 8 h) or phenylbutazone (2.2 mg/kg, orally or intravenously, every 12 h) often provide effective analgesia and presumably reduce inflammation in the pleural space.

Horses should be provided with good nursing care, including a comfortable stall, free access to palatable water, and a good diet. Affected horses will often not eat adequately and should be tempted with fresh and nutritious fodder.

Attention should be paid to the horse’s feet to detect early signs of laminitis and allow appropriate measures to be taken.