Bronchial diseases are common causes of loud cough and dyspnea in dogs and cats.
Bronchial diseases are common causes of loud cough and dyspnea in dogs and cats. The most commonly encountered bronchial diseases in cats are chronic bronchitis and asthma, whereas chronic bronchitis and kennel cough are more common in dogs. Lungworms can have similar clinical presentation in both dogs and cats. Tracheal collapse and left main stem bronchial compression are also associated with loud cough and dyspnea in dogs.
Infectious tracheobronchitis is a contagious respiratory disease of dogs caused primarily by Bordetella bronchiseptica associated or not with other bacteria and viral agents. It is more common in young, debilitated animals housed in crowded conditions. Dogs with uncomplicated infections have a dry hacking cough in an otherwise normal dog. Presence of pneumonia, fever or anorexia is associated with complicated infections. Chest radiographs are usually unremarkable in the uncomplicated disease and are useful to rule-out other conditions causing loud cough. Radiographic evidences of pneumonia can be found in dogs with complicated disease. Transtracheal wash should be performed in dogs with complicated disease to obtain material for cytology, culture (including Mycoplasma cultures) and sensitivity.
Uncomplicated disease is usually resolved within 14 days without therapy. Patients should, however, be isolated to decrease spreading of the disease. Patients with systemic signs, evidence of pneumonia or that have been sick for longer than 14 days should receive antibiotics. Antibiotics should be selected based on culture and sensitivity and the ability to achieve therapeutic concentration in the bronchial tree. Good empirical choices are tetracyclines and quinolones. Support therapy with nebulization and airway humidification, rest, proper nutrition and hydration should also be introduced.
In dogs, the left main stem bronchus is dorsal to the left atrium, making it prone to be compressed during left-sided heart disease associated with increase in left atrial size. This is more common in small breed dogs with mitral endocardiosis, but may also occur in some dogs with dilated cardiomyopathy. Therapy is directed at decreasing left atrial size. In patients without heart failure, ACE inhibitors are used initially. If there is inadequate response, hydralazine (0.5 – 3.0 mg/kg q12h PO) can be added to the protocol.
Chronic bronchitis is a chronic inflammation of unknown origin of the bronchial tree that may involve lobar bronchi and the smaller airways. Regardless of cause, chronic bronchial inflammation results in increased tracheobronchial secretions, cough and architectural changes in the bronchial tree. Airway epithelium suffers hypertrophy, metaplasia, and ulceration. Goblet cells and submucosal glands undergo hypertrophy and increase production of mucus, whereas bronchial mucosa and submucosa may become edematous andinfiltrated with inflammatory cells.
Typically, chronic bronchitis affects adult dogs (8 years or older) of small breeds. There is no sex predilection. The hallmark of chronic bronchitis is chronic cough (at least two months in duration). The cough often terminates with a gag suggesting that it is productive, although it may be dry in some dogs. Cough may worse with exercise. Tachypnea, shortness of breath, and cyanosis may also be exacerbate or precipitated by exercise. In advanced cases, dogs may display a marked expiratory effort with a prolonged expiratory phase of breathing. Auscultatory findings are variable and non-specific. Wheezing due to mucus plugging and expiratory airway collapse and crackles are present in a large number of dogs with chronic bronchitis. The abnormal sounds are best heard after maneuvers that force the patient to take deep inspirations (e.g. occlusion of nostrils for a few seconds).
Thoracic radiographs are usually abnormal, but they may be normal in early cases. Bronchial thickening are the most common radiographic abnormalities. Pulmonary hyperinflation, bronchiectasis, tracheobronchial collapse, right middle lung lobe atelectasis, bronchopneumonia, and right heart enlargement due to cor pulmonale also can be found in radiographs of dogs with chronic bronchitis. Bronchopulmonary cytology may reveal increased mucus, hyperplastic epithelial cells, and a variable mixture of inflammatory cells. Neutrophils are usually the predominant inflammatory cell with smaller numbers of lymphocytes and eosinophils. Culture may be sterile or yield growth of a number of different bacteria. Airways of dogs with chronic bronchitis may look erythematous with a roughened or granular appearance during bronchoscopic examination. Accumulation of a thick mucus, mucus plugs, and tracheobronchial collapse also can be observed.
Treatment of chronic bronchitis is guided by the clinical signs, cytologic evaluation and culture, the extent of radiographic changes, and response to therapy. Therapy may alleviate clinical signs. Control rather than cure is achieved, because many structural changes in the airways are irreversible. Environmental stress (e.g.tobacco smoke) and factors that may exacerbate clinical signs (e.g. excitement) should be identified and minimized. Weight reduction is advised to obese patients because diaphragmatic function is impaired, small airways close earlier than normal and ventilation may be impeded in these patients. Inhalation of humidified air via a vaporizer or nebulizer may help liquefy secretions. Animals should be lightly exercised or be coupaged and encouraged to cough after these procedures. Infections should be treated as guided by the tracheobronchial cultures. Bronchodilators may help in relieving reversible airway obstruction. They also decrease mucosal edema and have anti-inflammatory effects by preventing mediator release from inflammatory cells. In addition, teophylline (10 – 20 mg/kg q12h) increases strength of respiratory muscles and decreases the work associated with breathing. Beta2-adrenoceptor agonists (e.g. terbutaline; small dogs: 0.625 – 1.25 mg q12h; medium-sized dogs: 1.25 – 2.5 mg q12h; large dogs: 2.5 – 5 mg q12h) are effective bronchodilators because they act as functional antagonists or airway constriction regardless of the cause. They also stimulate secretion of airway mucus resulting in a less viscous secretion and enhanced cilliary activity. Cough suppressants may be used in selected cases. Dogs with nonbacterial bronchitis that have a cough that is distressful to the owner or that is followed by exhaustion or collapse are potential candidates for antitussive therapy. One should bear in mind however, that suppression of the cough reflex will be detrimental for the clearance of airway secretion in chronic bronchitis. Antinflammatory therapy with steroids is most effective in dogs with nonbacterial bronchitis, particularly those with eosinophilic bronchitis. Steroids can be used systemically or by inhalation.
Chronic bronchitis and asthma are frequently encountered clinical conditions in cats. Several subclassification of feline bronchial disease have been attempted. Differences, many times subtle, in presentation and laboratory findings have allowed investigators to suggest specific etiologies for these cases. It is important to remember, however, that regardless of the cause, cats with bronchial disease have similar clinical signs, and that the treatments used are also similar. Cats that have periods of normalcy between crises likely have asthma.
Bronchial diseases are more common in middle aged (2-8 year old) female cats, but cats of all ages can be affected. The Siamese breed may be overrepresented. The most common clinical sign is cough. The coughing episodes may vary from mild to severe and be paroxysmal in nature. Cats also may have dyspnea, wheezing, occasional sneezing, and vomiting. Severely affected cats may show open mouth breathing, a respiratory effort disproportionate to the animal's level of exercise, and cyanosis. Some owners report seasonal exacerbation of the clinical signs. The peak seasonal incidence, however, is variable. Duration of clinical signs may vary from less than 24 hours to several years. Some cats may have cough and dyspnea for months or years with asymptomatic periods between crises. On physical examination, most affected cats have abnormal lung sounds including crackles and wheezes. Some cats may also manifest expiratory dyspnea and tachypnea. Mild hyperthermia is present in about 25% of the cases.
Chest radiographs are essential in evaluating cats with bronchial disease and usually show a bronchial pattern. A mild to moderate interstitial pattern may be seen concurrently. Lung lobe collapse, overinflation of the lungs, patchy alveolar infiltrates, and emphysematous changes may also be observed. Parasitic infection of the lungs (e.g. Aelurostrongylus abstrusus and Paragonimus kellicotti), and heartworm disease should be ruled-out as potential causes for the clinical signs in affected cats. Bronchial cytology typically shows increased mucus and inflammatory cells, usually eosinophils or neutrophils. Positive bacteria cultures are encountered in approximately 25 % of cats. Most bacteria found in cats with chronic bronchial disease can also be isolated from the respiratory tree of normal cats. The main exception is Mycoplasma sp. found more commonly in cats with chronic airway disease.
The goals of therapy are to control secretions, improve alveolar ventilation, and normalize excessive reflexes. Mild affected cats may be treated conservatively with weight reduction, avoidance of trigger events and external stimuli for secretion (e.g. dusts, tobacco smoke). Fenbendazole (50 mg/kg/5 days) should be used routinely to treat lungworms. Albuterol can be used as an inhaler (1-2 puffs as needed). Cats with mild signs that occur daily can be managed with inhalers: albuterol and fluticasone (110 mcg q12h) or oral bronchodilators (Theo-dur tablets or Slo-bid capsules: 25 mg/cat q24h at night; or terbutaline: 0.625 mg/cat q12h) and short-acting steroids. Cats with moderate signs that occur daily and are "never" normal require at least a short course of prednisone for 10 – 15 days in addition to the inhalers.
Cats presenting an acute exacerbation of a long-standing bronchial disease should be managed in an emergency basis. After a physical examination with as little restrain as possible to rule out other possible reasons for the clinical signs, the cat should be stabilized with supplemental oxygen and bronchodilators. All other diagnostic steps should be delayed until the patient is more stable. Bronchodilators (terbutaline and immediate-release aminophylline) can usually be given orally because they reach peak plasma concentration in approximately 1 hour. Severely affected cats may require terbutaline subcutaneously at approximately 0.01 mg/kg. If no improvement is noted, the dose should be repeated once. Alternatively, albuterol can be used as an inhaler every 30 minutes for up to 4 hours. Intravenous corticosteroids are often recommended. In acute situations, however, steroids are more likely to be effective due to a mild bronchodilatory effect. Significant suppression of inflammation by the steroids takes time to occur.