Tracheobronchitis is an acute or chronic inflammation of the trachea and bronchial airways; it may be primary or secondary depending on the etiologic agent. Bronchitis may extend from the bronchioles to the lung parenchyma.
Canine infectious tracheobronchitis (kennel cough, see Infectious Tracheobronchitis of Dogs) is often secondary to viral infection of the respiratory system. Other causes of tracheobronchitis in dogs include parasites, eg, Aelurostrongylus abstrusus (also in cats), Capillaria aerophila, Crenosoma vulpis, and Oslerus osleri.
Tracheitis may be secondary either to diseases of the oropharynx or to chronic coughing related to heart disease or noncardiac pulmonary disease. Other causes include smoke aspiration and exposure to noxious chemical fumes. Exacerbation of a chronic bronchitis affecting middle-aged and older dogs may follow sudden changes in the weather or other environmental stresses. Feline bronchial asthma (allergic bronchitis) is a syndrome in cats with similarities to asthma in people. Young cats and Siamese and Himalayan breeds are most affected. Feline asthma is associated with airway hyperresponsiveness, airflow obstruction, airway remodeling, and eosinophilic airway inflammation. Asthma in cats is induced by an aberrant immune response with upregulation of cytokines, leading to IgE production. Foreign bodies in the airway and developmental abnormalities such as laryngeal deformities may predispose to bronchitis. Chronic bronchitis most often affects small breeds of dogs, although it is also seen in large breeds. It is characterized by persistent cough for at least 2 mo in the absence of specific pulmonary disease. Bronchiectasis may occur as the end stage of chronic bronchitis in dogs. Recognition of tracheobronchitis as an often secondary disease syndrome underlies the importance of diagnosis and control of an associated primary disease.
Spasms of coughing are the outstanding sign. These are most severe after rest or a change of environment or at the beginning of exercise. On auscultation, respiratory sounds may be essentially normal. In advanced cases, inspiratory crackles and expiratory wheezes are heard. Body temperature may be slightly increased. The acute stage of bronchitis passes in 2–3 days; the cough, however, may persist for 2–3 wk. Severe bronchitis and pneumonia are difficult to differentiate; the former often extends into the lung parenchyma and results in pneumonia. Feline bronchial asthma may result in cyanosis and dyspnea and may be accompanied by eosinophilia.
During the acute and subacute inflammatory stages, the air passages are filled with frothy, serous, or mucopurulent exudate. In chronic bronchitis, they contain excessive viscid mucus. The epithelial linings are roughened and opaque, a result of diffuse fibrosis, edema, and mononuclear cell infiltration. There is hypertrophy and hyperplasia of the tracheobronchial mucous glands and goblet cells. The act of coughing is an attempt to remove the accumulations of mucus and exudate from the respiratory passages.
The diagnosis is made from the history and clinical signs and by elimination of other causes of coughing. In chronic bronchitis, chest radiographs may show an increase in linear and peribronchial markings. Bronchoscopy reveals inflamed epithelium and often mucopurulent mucus in the bronchi. In addition, the procedure allows collection of biopsy and swab samples for in vitro assay. Bronchial washing is an additional diagnostic aid that may demonstrate causative agents or significant cellular responses (eg, eosinophils).
In mild or acute cases, supportive therapy may be effective, but treatment of concurrent disease is also indicated. Rest, warmth, and proper hygiene are important. Broad-spectrum antimicrobial chemotherapy is indicated for treatment of cough when infection is documented. Corticosteroids are the mainstay of therapy to reduce airway inflammation in dogs with chronic bronchitis. Persistent, nonproductive coughing is best controlled by antitussives that contain codeine. If conservative medical management is unsuccessful, laboratory tests and radiographs of the thorax and cervical trachea should be evaluated to eliminate other differential diagnoses. Bronchoalveolar lavage or transtracheal wash for cytology and culture sensitivity may be indicated to identify an etiologic agent and to determine appropriate antimicrobial chemotherapy. Pulmonary physiotherapy consisting of sodium chloride nebulization and gentle coupage may loosen secretions and stimulate expectoration. A bathroom environment with steam from a hot shower may be substituted for nebulization.
Oral (prednisolone, dexamethasone) or inhaled (fluticasone, budesonide) corticosteroids are indicated for treatment of feline asthma. Bronchodilators (albuterol, terbutaline) may be considered for adjunctive therapy in combination with glucocorticoids but not as sole therapy for feline asthma. Feline aerosol chambers and inhaler therapy are available for aerosol drug delivery in cats with feline asthma. Cyprohepatidine, an antiserotonergic drug, has been suggested; however, studies have failed to show significant reduction in eosinophilic airway inflammation. Experimental studies suggest that cyclosporine A therapy may hold promise to inhibit development of eosinophilic airway inflammation and airway remodeling through inhibition of T-cell activation and cytokine synthesis. Avoidance of environmental aeroallergens (eg, cigarette smoke, perfumes, pollens, molds, dust) must be considered in management of these cats.
Infectious Tracheobronchitis of Dogs
Infectious tracheobronchitis results from inflammation of the upper airways. It is a mild, self-limiting disease but may progress to fatal bronchopneumonia in puppies or to chronic bronchitis in debilitated adult or aged dogs. The illness spreads rapidly among susceptible dogs housed in close confinement (eg, veterinary hospitals or kennels).
Canine parainfluenza virus, canine adenovirus 2 (CAV-2), or canine distemper virus can be the primary or sole pathogen involved. Canine reoviruses (types 1, 2, and 3), canine herpesvirus, and canine adenovirus 1 (CAV-1) are of questionable significance in this syndrome. Bordetella bronchiseptica may act as a primary pathogen, especially in dogs <6 mo old; however, it and other bacteria (usually gram-negative organisms such as Pseudomonas sp, Escherichia coli, and Klebsiella pneumoniae) may cause secondary infections after viral injury to the respiratory tract. Concurrent infections with several of these agents are common. The role of Mycoplasma sp has not been clearly established. Stress and extremes of ventilation, temperature, and humidity apparently increase susceptibility to, and severity of, the disease.
The prominent clinical sign is paroxysms of harsh, dry coughing, which may be followed by retching and gagging. The cough is easily induced by gentle palpation of the larynx or trachea. Affected dogs demonstrate few if any additional clinical signs except for partial anorexia. Body temperature and WBC counts usually remain normal. Development of more severe signs, including fever, purulent nasal discharge, depression, anorexia, and a productive cough, especially in puppies, indicates a complicating systemic infection such as distemper or bronchopneumonia. Stress, particularly due to adverse environmental conditions and improper nutrition, may contribute to a relapse during convalescence.
Tracheobronchitis should be suspected whenever the characteristic cough suddenly develops 5–10 days after exposure to other susceptible or affected dogs. Severity usually diminishes during the first 5 days, but the disease persists for 10–20 days. Tracheal trauma secondary to intubation may produce a similar but generally less severe syndrome. Thoracic radiographs are essential to determine the severity of disease and to exclude other causes of cough.
Preferably, affected dogs should not be hospitalized because the disease is usually highly contagious (and also self-limiting). Appropriate management practices, including good nutrition, hygiene, and nursing care, as well as correction of predisposing environmental factors, hasten recovery. Cough suppressants containing codeine derivatives, such as hydrocodone (0.25 mg/kg, PO, bid-qid) or butorphanol (0.05–0.1 mg/kg, PO or SC, bid-qid), should be used only as needed to control persistent nonproductive coughing. Antibiotics are usually not needed except in severe chronic cases; cephalosporins, quinolones, chloramphenicol, and tetracycline are preferable because they reach effective concentrations in the tracheobronchial mucosa. When needed, the antibiotic should be selected by culture and sensitivity tests of specimens collected by transtracheal aspiration or bronchoscopy. Antibiotics given PO or IM may not significantly reduce the numbers of B bronchiseptica in the distal trachea or major bronchi. Thus, in severely affected dogs that are not responsive to parenteral antibiotics, kanamycin sulfate (250 mg) or gentamicin sulfate (50 mg) diluted in 3 mL of saline may be administered by aerosolization bid for 3 days. Aerosolization treatment should be preceded by administration of bronchodilators. Endotracheal injection of antibiotics (eg, gentamicin) is a possible alternative to aerosolization. Corticosteroids may help alleviate clinical signs but should be used concurrently with an antibacterial agent; they are contraindicated in severely ill, coughing dogs.
Dogs should be immunized with modified-live virus vaccines against distemper, parainfluenza, and CAV-2, which also provides protection against CAV-1. Commercial products frequently combine these agents and may include modified live parvovirus and leptospiral antigens. An initial vaccination should be given at 6–8 wk and repeated twice at 3- to 4-wk intervals until the dog is 14–16 wk old. Revaccination should be performed annually. When the risk of B bronchiseptica infection is significant, a live, avirulent, intranasal vaccine or parenteral products containing subunit bacterial extracts should be used. A combination of an avirulent B bronchiseptica and a modified-live parainfluenza vaccine is available for intranasal use. One inoculation is administered to puppies >3 wk old.
Last full review/revision November 2013 by Ned F. Kuehn, DVM, MS, DACVIM