Managing pneumonia and pleuropneumonia in horses (Proceedings)

Pleuropneumonia is a devastating disease, which can result in permanent respiratory impairment if not treated promptly and properly.  Pleuropneumonia is frequently referred to as shipping fever: although it is most commonly seen as a consequence of long-distance shipping, it is important to remember that there are other important risk factors for pleuropneumonia, including recent viral infection, exercise-induced pulmonary hemorrhage, any cause of high particulate exposure, and recent high-speed exercise.

How do these risk factors contribute to the development of pneumonia and pleuropneumonia? Respiratory viruses result in necrosis of respiratory epithelium, resulting in removal of barriers to bacterial movement, as well as dysfunction of the mucociliary escalator, both of which potentiate bacterial infection. 

High-speed exercise can act in multiple ways: intense exercise or overtraining can result in an impaired immune system, and post-race, large amounts of inhaled particulates can be found in the horse's respiratory system – and the losers are exposed to greater amounts of particulates than the winner, by virtue of being in the dust trail of the winning horse.  Exercise-induced pulmonary hemorrhage accompanies these other effects of high-speed exercise, and provides an ideal  medium for bacterial infection.  The most important risk factor for pneumonia/pleuropneumonia, long-distance travel, has multiple implications.  First, horses are exposed to extremely high particulate levels during transport (Love, et al). 

This type of particulate exposure has clearly been shown to be associated with higher prevalence of bacterial infection in people and laboratory animals.  Transport also results in a depressed immune response, including decreased oxidative burst in neutrophils.  Finally, horses depend on dependent head carriage to properly drain their respiratory systems.  The common habit of tying up horses heads – while exposing them to a high particulate level by having a hay net at head level – greatly potentiates the risk factor of long-distance travel. 

The combination of these risk factors may lead to aspiration of pharyngeal secretions, or may simply reflect colonization and eventual infection with bacteria originating from the pharynx.  The most common aerobic bacteria include Streptococcus equi subspp zooepidemicus, E. coli, and various pasteurella and actinobacillus species.  In addition, the anaerobic species found include various bacteroides and clostridial species. 

Pleuropneumonia begins as pneumonia.  The inflammation associated with pneumonia results in increased capillary permeability, thus even uncomplicated pneumonia is commonly accompanied by at least small amounts of increased fluid in the pleural space.  Left untreated, or treated inappropriately, it progresses to an uncomplicated pleural inflammation, then to a parapneumonic effusion, and finally, to a well-developed pleural infection in addition to pneumonia.  At this stage, there is an outpouring of fibrin which, with time, develops into a fibrous response, and permanently limits expansion of the lung.  At this stage, a pleural peel is commonly seen, which is a thick, inelastic fibrous membrane encompassing the pleura and destroying the distinction between visceral and parietal pleura. 

The clinical signs of pneumonia/pleuropneumonia often begin with a fever, cough,  inappetance, and dullness.  The horse often responds to initial treatment, but if antibiotic coverage is inadequate, will relapse and worsen.  As pleural disease increases, horses may show signs of pleural pain, such as standing with abducted elbows, and may have short, shallow, rapid breaths.  Horses may have sufficient pain to present as suspected colic or even rhabdomyolysis cases.  In the case of anaerobic infection, a fetid smell may be detected at the nose.  A red-brown nasal discharge may reflect the presence of necrotic lung tissue. 

Auscultation may reveal harsh lung sounds cranially and, if there is a sufficient pleural effusion, the lack of auscultable lung sounds ventrally may allow the listener to establish the presence of a fluid line.  However, ultrasound is by far the most sensitive diagnostic modality in determining presence of pleural disease, as fluid is easily detected, and the presence of abscesses and loculations of fluid may be seen as differences in echogenicity.  Gas shadowing may indicate the presence of aerobic infection.  A sector scanner, using a 2.5- 5 Hz probe will give the best view of the chest, however, a linear, rectal probe is sufficient to reveal the presence of pleural fluid in a typical case of pleuropneumonia. 

Before the development of pleural fluid, inflammation of the pleura can often be deduced when ‘comet tails' or bright, irregular areas along the pleura are seen.  In more chronic cases, fibrin can be seen as fronds within the pleural fluid, although care must be taken not to mistake the ligament between the diaphragm and the heart as fibrin.  Consolidated lung can be detected as lucent areas (normal lung is not sonolucent) although it is difficult to determine the difference between atelectatic lung and consolidated lung. 

Fluid with a high cell count appears more echogenic and ‘cellular' than fluid that is primarily a transudate.  Ultrasound is invaluable in guiding treatment, as well, as pockets of fluid can be identified, and the most ventral, safest spot for thoracentesis can be chosen.  Radiography is seldom of great use in pleuropneumonia, as even after drainage, the outlines of the lung are largely obscured.  However, once the pleural effusion has been well-cleared, it can be of great use in following resolution of pneumonic disease.

Thoracentesis is essential in determining the character of the pleural effusion, and, with large amounts of effusion, is essential in easing the restrictive nature of the disease, and in improving ventilation.  Although the preferred site for thoracentesis is technically the 6th or 7th costochondral junction just dorsal to the costochondral junction, the author prefers to use ultrasound guidance to choose the most ventral, safest spot – i.e. far enough away from the heart! 

Samples of pleural fluid should be submitted for cytology and for aerobic and anaerobic culture and sensitivity.  Pleural fluid in the normal horse has in the range of 5000 cells/ul, and a total protein less than 2.0 g/dl.  Horses with pleuropneumonia often have cell counts ranging above 100,000/ul.  If there is a considerable amount of fluid (often many liters in each side) drains should be installed for a period of one to three or more days. 

The author uses a chest tube, with either Heimlich valves or one-way valves constructed of condoms wrapped around the bottom of the tube.  (This thin material allows drainage,  but is easily stuck together by the pleural fluid to prevent aspiration of air).  Although the horse's mediastinum is fenestrated, inflammation and infection usually rapidly cause it to be effectively non-fenestrated, and bilateral pneumothorax is rarely a concern.  However, the possibility should always be kept in mind, and there may be the need for possible negative pressure evacuation of air from the chest cavity.  Some authors advocate pleural lavage to remove fibrin and other debris, but there is no clear evidence to support  this practice. 

It is absolutely essential to do a tracheal aspirate in horses with pleuropneumonia.  The pleural effusion, even when high in white cells, often yields disappointing results on culture.  Remembering that the initial infection came from the pulmonary parenchyma, it makes sense that a tracheal aspirate is more reliable in yielding information about the type of bacteria present and the sensitivities of those bacteria. 

Initial treatment of pleuropneumonia involves very broad-spectrum antibiotic treatment, as it should be assumed, until proved otherwise, that a mixed aerobic gram negative and gram positive, as well as anaerobic infection is present.  An effective combination is a penicillin-type drug accompanied by an aminoglycoside and metronidazole (as the Bacteroides spp are resistant to penicillins). 

Other antibiotics with a broad spectrum that can be used include enrofloxacin, trimethoprim-sulfa (which has excellent penetration however many bacteria are resistant), and chloramphenicol (with due attention paid to human toxicities).  It is important for owners to know at the beginning of treatment that they are committing to long-term parenteral antibiotic treatment (often 3-6 weeks) with possible weeks of oral antibiotics thereafter.

Owners also need to be made aware that, as a systemic inflammatory disease, pleuropneumonia poses an increased risk of laminitis and thrombophlebitis.  During the acute stages of disease, the author commonly treats with polymixin B to counteract endotoxemia, ices the feet to reduce the delivery of inflammatory mediators, and treats with Banamine both for its anti-endotoxic effect as well as to treat pain and inflammation. 

As the dehydration that may accompany the acute stages of pleuropneumonia as well as treatment with non-steroidal anti-inflammatory drugs and aminoglycosides may predispose toward renal compromise, it is also important to monitor renal function closely.  Finally, owners must also be made aware that horses with pleuropneumonia will not be enjoying a rapid return to exercise – the author routinely recommends at least 3 months of rest after clinical recovery.