Canine Chronic Bronchitis

Chronic bronchitis (CB) is the most common chronic respiratory impairment in dogs. The condition is defined as a chronic cough occurring for two consecutive months during the preceding year that is not attributable to another cause (e.g., neoplasia, congestive heart failure). This definition is based loosely on the definition of chronic bronchitis in humans, which is characterized by a well-defined cascade of clinical and histologic changes. The early changes are typically triggered by an inciting irritant stimulus and include increases in airway mucus production, impairment of mucociliary clearance, and alterations in the local immune response. The cascade of events in dogs is similar to that seen in humans, and, if left untreated, results in a cycle of chronic inflammation, chronic cough, copious mucoid airway secretions, and decreased mucociliary clearance.

Signalment

The average age at the time of diagnosis of chronic bronchitis is eight years of age or older, and many clients will report a several year histories of intermittent cough. All breeds of dog can be affected. Higher incidence has been reported in West Highland White Terriers, Poodles, Cocker Spaniels, Pomeranians, and German Shorthair Pointers. Many dogs afflicted with CB are obese but are typically otherwise healthy.

Diagnostic(s)

Because chronic bronchitis is a diagnosis of exclusion, it is important to complete a full diagnostic evaluation for any dog presented with a chronic cough. Common differentials for chronic cough in dogs should include congestive heart failure, heartworm disease, pneumonia, neoplasia, infectious tracheobronchitis, and tracheal collapse. Less common conditions include foreign bodies, parasitic bronchitis, and primary ciliary dyskinesis. The initial laboratory evaluation of the chronic bronchitis dog is an important means of characterizing the overall health of the dog, and serves as a screen for other potential aggravating or inciting conditions. Evaluation for all animals should include complete blood count, serum biochemical profile, urinalysis, fecal flotation, Baermann analysis, and heartworm antigen test. Additional screening tests may include serologic testing for infectious diseases (fungal, viral, Rickettsial) and echocardiography, where indicated.

Diagnostic imaging

Thoracic radiographs typically show bronchial or peribronchial patterns, and can also reveal secondary conditions including pneumonia, bronchiectasis, and right-sided cardiac enlargement secondary to pulmonary hypertension.

Bronchoscopy

Bronchoscopic examination in cases of chronic bronchitis usually reveals non-specific mucosal erythema with a roughened, cobblestone, or granular appearance, and copious amounts of mucus. Large airways may appear relatively normal in dogs with significant small airway collapse and mucus trapping. The airways of severely affected dogs may have a pale appearance as a result of fibrosis. Bronchoscopy is also a valuable tool for evaluation of tracheal and bronchial collapse secondary to chondromalacia, mainstem bronchus collapse secondary to cardiomegaly, and other large airway abnormalities (e.g.bronchoesophageal fistula, foreign bodies, lumenal tumors).

Airway Sampling

Bronchopulmonary cytology is typically characterized by non-degenerate neutrophilic inflammation. A smaller yet significant population of dogs will have cytology characterized by eosinophilic inflammation. Eosinophilic airway inflammation has historically been associated with hypersensitivity reactions, and has been erroneously used to make the distinction between “allergic” bronchitis and idiopathic chronic bronchitis. While eosinophils can certainly be recruited in allergic reactions, eosinophils can also be associated with neoplastic disease (e.g. lymphosarcoma), fungal infections, and systemic parasitism. Additionally, studies in humans suggest that acute exacerbations of chronic bronchitis can be associated with a transient inflammatory shift from neutrophils to eosinophils.

Most dogs with chronic bronchitis do not have active infection at the time of diagnosis. However, culture and sensitivity should always be performed on airway samples in the newly diagnosed bronchitic, in acute exacerbations of previously stable disease, or with radiographic evidence of bronchiectasis. Airway samples should be cultured for general aerobic and Mycoplasma culture.

Anaerobic culture should also be considered in patients with bronchopneumonia.

Treatment

CB is a slowly progressive condition for which there is no definitive cure. In the absence of intervention, the cycle of cough-induced inflammation and inflammation-induced cough will self- perpetuate. The three goals of therapeutic intervention in chronic bronchitis are, 1) do no further harm; 2) slow the progression of the histologic changes, and; 3) control the clinical signs. Because the inciting cause in dogs is rarely identified, the primary treatment of CB is based on controlling airway inflammation. Therapeutic tools commonly used in the control of CB include modulators of the inflammatory cascade, bronchodilators, anti-tussives, antimicrobials, environmental manipulation, and weight management. Surgical intervention may be indicated in management of severe secondary changes or exacerbating conditions (e.g. tracheal collapse, bronchiectasis).

Control of airway inflammation is the single most effective means of ameliorating the clinical signs of CB in humans. Most of the clinical signs of CB in humans and dogs (coughing, expiratory dysfunction, mucus hypersecretion) can be primarily or secondarily attributed to airway inflammation. Oral corticosteroids are successful as a sole therapy in resolving the clinical signs in the majority of canine CB patients, and have historically been considered the mainstay of therapy in veterinary medicine. The short-acting oral corticosteroids (prednisone, prednisolone) should be started at anti-inflammatory doses (1-2mg/kg/day divided BID), and tapered to the lowest effective dose. The dose reductions should initially be every 1-2 weeks until physiologic doses (0.25- 0.5mg/kg/day) are attained, at which point the dose should be maintained for 2-4 weeks. In the event of a relapse during the steroid taper, the previous dose at which signs were controlled should be reinstituted, and the duration at that dose should be doubled prior to tapering.

Side effects of oral corticosteroids are many and known, and can be prohibitive in some cases. These include polydipsia, polyuria, inappropriate urination, lethargy, aggression, polyphagia, weight gain, and corticosteroid withdrawal syndrome (iatrogenic hypoadrenocorticism). In cases where control is achieved but adverse effects are intolerable, combination therapy with bronchodilators or anti-tussives (when appropriate) may provide control at lower steroid doses. Anecdotal use of inhaled corticosteroids in dogs has been associated with improvement in clinical signs and reduction in prohibitive side effects. Fluticasone proprionate (Flovent, GlaxoSmithKline) at 200, 225, or 250g dose can be administered to dogs using tidal breathing with a spacer device and facemask. At a dose of 2 puffs q12h, a single vial lasts approximately 30 days. Limitations to the usage of inhaled corticosteroids in veterinary medicine are many, and include a lack of controlled studies demonstrating efficacy, delivery, and reduced systemic absorption, drug delivery problems, patient compliance, and cost.

The role of bronchoconstriction in canine CB remains unclear. Studies supporting the use of bronchodilators in CB have demonstrated improvements in objective data (pulmonary function tests) and subjective assessments (reduction in coughing, improvement in thoracic auscultation findings, owner perception of exercise tolerance). In addition, bronchodilators appear to have a steroid-sparing effect in some cases. Bronchodilators commonly used in canine CB are the methylxanthines and inhaled beta agonists (usually combined with inhaled corticosteroids). The mechanism of methylxanthine bronchodilation was initially attributed to phosphodiesterase inhibition. It is now believed that both the mechanism of activity and mechanism of adverse effects of this class of drugs are mediated by adenosine inhibition. In addition, the methylxanthines possess additional effects, including anti-inflammatory effects (sPL-A2 inhibition) and stimulation of respiratory musculature (cAMP-mediated). Metabolism of the methylxanthines is variable, and, when combined with limited formulations, can make dosing quite difficult, particularly in small dogs. Because of patient-to-patient variability in therapeutic and toxic dosages, administration should start at the low end of recommended doses, and increase to effect. Theophylline should be administered in slow-release formulations, and should start at 5-10mg/kg PO BID. Frequency and duration can be increased to as high as 20mg/kg BID should clinical signs warrant and adverse effects allow. Because of an increased risk of methylxanthine toxicity, co-administration of theophylline with fluoroquinolones should be avoided when possible.

Most dogs do not have active airway infections at the time of diagnosis. For this reason, antimicrobial therapy is rarely indicated in cases of CB. If indicated, therapeutic decisions should be based on culture and sensitivity results whenever possible. Empirical therapy selections (while awaiting C/S) should have coverage of common airway pathogens (Mycoplasma, Staphylococcus, Streptococcus, Pasteurella, Bordetella), and may include azalides, tetracyclines, fluoroquinolones, and macrolides.

The cough reflex in cases of CB is usually a protective and therapeutic mechanism. Coughing aids in the clearance of excess viscid secretions and can minimize aspiration of irritants and organisms in the face of an impaired mucociliary transport system (secondary ciliary dyskinesis). For these reasons, most coughs associated with chronic bronchitis should not be directly suppressed but should be alleviated by suppression of the inflammatory cascade.

Some coughs may require direct suppression, and include dry, hacking paroxysmal coughs (which may also be associated with concurrent tracheal collapse), coughs associated with cough-induced syncope, and night coughing. The most effective anti-tussives for use in canine CB are the narcotic cough suppressants, including hydrocodone (0.25-1.0mg/kg PO q6-12h), codeine (1-2 mg/kg PO q6-12h), and butorphanol (0.25-1.0 mg/kg PO q6-12h). The most common side effect is sedation, which can be beneficial in some cases for alleviation of night coughing.

Obesity is a major complicating factor in the management of canine CB cases. Weight management alone can improve exercise tolerance and oxygenation. The most important factors in creating a successful weigh management plan are client education and reasonable goals from the start. A weight-loss plan should try to target 1-3% weight loss per week, with the expectation that this rate will decrease as the dog approaches goal weight.

Environmental modifications can also help to decrease irritant, antigenic, or traumatic stimulation of the airways. Use of harnesses instead of collars can also reduce direct stimulation of the large airways.

The overall prognosis for canine CB is poor. It is important to emphasize to clients that the goal of management of CB is reduction of clinical signs and slowing the progression of this condition. It is also important to emphasize to clients that no chronic cough is benign, and that earlier intervention can prevent or delay the onset of potentially life-threatening sequelae (e.g., syncope, hypoxemia, pulmonary hypertension) and irreversible structural changes (e.g. bronchiectasis, fibrosis).

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