Congenital anomalies of the respiratory tract are rare but do occur. Examples include cysts in the sinuses and turbinates, tracheal hypoplasia, and accessory lungs. A common cause of upper respiratory tract malfunction is rhinitis (which results in exudation of neutrophils, macrophages, and fluids), or erosion and ulceration (or both) of the nasal mucosa. It may be caused by viral, bacterial, fungal, or parasitic agents, as well as by hypersensitivity reactions, such as localized allergies and anaphylaxis (see
the immune system, see The Biology of the Immune System et seq). Atrophy of the turbinates (eg, in atrophic rhinitis of pigs) removes a major filtration function and exposes the lungs to much heavier loads of dust and microorganisms. The nasal cavity may be obstructed by tumors, granulomas, abscesses, or foreign bodies. Sinusitis can be a complication of upper respiratory infections, tooth root infection, or dehorning.
Laryngitis, tracheitis, and bronchitis result in coughing and possibly inspiratory or expiratory dyspnea. Coughing may be nonproductive if the irritation is caused by mucosal erosion, or productive if due to copious exudate in the major airways. Severe pulmonary edema and emphysema cause extreme respiratory insufficiency.
The most common respiratory disease is pneumonia, which is defined as inflammation of the lungs. There are many systems for classifying the various types of pneumonia. One useful method is to classify according to the distribution of lesions in the lungs. Focal pneumonia has one or more discrete foci in a random pattern, eg, abscessation due to emboli from other sites, tuberculosis, or actinomycosis. Lobular pneumonia accentuates the anatomic pattern of lobules, as in bronchopneumonia caused by Pasteurella multocida. Lobar pneumonia covers large areas of lobes and is often severe (eg, fibrinous pneumonic pasteurellosis of cattle). Diffuse or interstitial pneumonia often involves the entire lung, as in maedi of sheep or in hypersensitivity reactions. The appearance or etiology of a particular pneumonia can be described further, eg, gangrenous, parasitic (verminous), aspiration, etc.
Infection may develop as a result of one or a combination of factors: 1) defense mechanisms are overwhelmed, 2) the infectious agent is highly virulent, 3) the size of the inoculum is large, and/or 4) the animal's defense mechanisms are compromised. The initial problem in many pneumonias is thought to be a sudden alteration in the normal nasal bacterial flora, which results in a sudden dramatic increase in one or more species of bacteria. Bacterial proliferation is usually caused by a breakdown of the host defenses as a result of stress (eg, transportation, concurrent illness) or cellular insult (eg, viral infection, toxicity). These bacteria are breathed into the lung in large numbers and may overwhelm the normal defense mechanisms, localize, multiply, and initiate inflammation. In addition, stress is often a precursor of viral respiratory infections, particularly in groups of animals that have recently been congregated and stressed by travel, handling, and mixing. Some respiratory viral infections can cause temporary dysfunction of phagocytic mechanisms of the alveolar macrophages. This usually occurs several days after viral exposure. Inhaled bacteria proliferate and pneumonia ensues, often with an overwhelming infection and massive exudation into the alveoli.
Pneumonia also can be caused by direct infection with viruses, bacteria, and fungi, as well as by toxins arriving hematogenously, by inhalation, or by aspiration of food or gastric contents.
Through natural processes, possibly aided by appropriate therapy, the exudate may be removed from the lungs, and the mucosal lesions of the air passages may heal. However, serious sequelae can persist. Bronchiectasis is a chronic lesion of the bronchi and parenchyma characterized by irreversible cylindrical or saccular dilatation, secondary infection, and atelectasis. Ulceration of bronchioles caused by viral agents may lead to organized plugs of connective tissue in small bronchioles, a lesion called bronchiolitis obliterans, which may cause permanent obstruction, atelectasis, and severe respiratory insufficiency. Constriction of bronchi and bronchioles in chronic allergic bronchitis and bronchiolitis results in similar clinical signs. However, administration of bronchodilators results in rapid relief of airway obstruction in cases of allergic bronchitis (eg, heaves in horses). Some chronic pneumonias (eg, maedi in sheep) are characterized by firm diffuse lesions due to hyperplasia of lymphoid follicles, hyperplasia of smooth muscle around bronchioles, diffuse fibrosis, and diffuse lymphocytic infiltration. Aspiration pneumonia often leads to gangrene with severe toxemia accompanying the acute inflammatory reaction.
Most infectious pneumonias occur in the anteroventral portions of the lungs. However, infectious agents, as well as neoplasms, can invade the lungs via the blood, which may extensively impair pulmonary function, as can pulmonary edema from chronic heart failure. Pleuritis, empyema, hydrothorax, chylothorax, atelectasis, diaphragmatic hernia, or pneumothorax can also seriously impair respiratory function. Pulmonary thrombosis leads to acute, often fulminant, respiratory failure as a result of a lack of pulmonary arterial blood flow to ventilated regions of the lung. Infarction of the lung can reduce respiratory function but is rare because of the dual blood supply of the organ. Toxic injury, such as in 3-methylindole toxicity in cattle, causes edema, emphysema, and necrosis of alveolar epithelium followed by compensatory hyperplasia of these cells; the effects on gas exchange result in severe hypoxia and dyspnea.
Although pneumonia is most important, several other conditions that occur in the thorax can cause respiratory dysfunction. Pulmonary edema, the abnormal accumulation of fluid in the interstitial tissue, airways, or alveoli of the lungs, may occur in conjunction with circulatory disorders, particularly left ventricular failure or increased capillary permeability, occasionally in anaphylactic and allergic reactions, and in some infectious diseases. Head trauma can cause pulmonary edema in dogs. Dyspnea and open-mouth breathing may occur. Animals stand in preference to lying down, lie only in sternal recumbency, or may assume a sitting position. Auscultation of the chest may reveal wheezing and fluid sounds.
Pleuritis (pleurisy) may be caused by any pathogen that gains entrance to the pleural cavity, but it is often an extension of pneumonia. Rapid shallow breathing, fever, and thoracic pain are suggestive of pleuritis. Auscultation of the chest may reveal friction sounds.
Empyema (purulent exudate in the pleural cavity) is caused by pyogenic bacteria or fungi reaching the thoracic cavity via the blood or by extension of a pneumonia, traumatic reticulitis, or penetrating wound of the chest. Cough, fever, pain, and dyspnea may be present.
Hemothorax (the accumulation of blood in the pleural cavity) is usually caused by trauma to the thorax, systemic coagulopathy, or thoracic neoplasia. Hydrothorax (the accumulation of transudate in the pleural cavity) is usually due to interference with venous blood flow or lymph drainage. Chylothorax (the accumulation of chyle in the pleural cavity) is relatively rare and is seen most often in cats. It may be caused by rupture of the thoracic duct but often is idiopathic. The signs of all 3 conditions include respiratory embarrassment (eg, rapid shallow breathing with inspiratory dyspnea) and weakness.
Pneumothorax (air in the pleural cavity, see Evaluation and Initial Treatment of the Emergency Patient: Treatment) may be of traumatic or spontaneous origin. Air can enter the pleural cavity through penetrating wounds of the thoracic wall or by extension from pulmonary emphysema or ruptured bullae. The lung collapses if a large volume of air enters the pleural cavity. Bilateral pneumothorax may develop if the mediastinum is weak or incomplete. Inspiratory dyspnea or rapid, shallow breathing is evident.
Last full review/revision March 2012 by Ned F. Kuehn, DVM, MS, DACVIM