The most frequently observed clinical sign in dogs with EBP is cough, which is documented in 95% to 100% of cases.1,6 The cough is characterized as persistent and harsh and is typically followed by gagging or retching, likened to a "smoker's cough."1 Other common clinical signs include dyspnea, exercise intolerance, and nasal discharge that may be serous, mucoid, or mucopurulent.1,6 Lethargy and anorexia are usually not reported but may be noted if concomitant pneumonia is present.2 The clinical picture may vary from acute, life-threatening dyspnea to chronic, occasional cough.1,6,7
Physical examination and laboratory evaluation
Thoracic radiography is necessary to check for other conditions that may result in cough and dyspnea, including cardiac disease, chronic bronchitis, a foreign body, pulmonary or tracheobronchial neoplasia, fungal granulomas, and pneumonia. Yet, as with physical examination findings, radiographic findings associated with EBP are often variable and nonspecific.3 The most common radiographic abnormality is a diffuse, mixed bronchointerstitial pattern that is usually more severe than the pattern seen with chronic bronchitis.1 Other radiographic lesions that may be noted include alveolar infiltrates, peribronchial cuffing, bronchiectasis, pulmonary nodules, and bronchial wall thickening (Figures 1A & 1B).1,3,7 The severity of radiographic abnormalities appears to correlate with the severity of clinical signs.3,6
Since radiographic findings are not specific enough to confirm EBP, airway cytology is essential for diagnosis. Cytologic samples from the airways may be collected by transtracheal aspiration, endotracheal washing, bronchoalveolar lavage, or bronchial brushing. Samples should be centrifuged immediately after collection or kept on ice until sample preparation is possible. After centrifugation, the pelleted cells should be transferred to a slide, air-dried, and then stained with a modified Wright's stain (Diff-Quik—Dade Behring) for microscopic evaluation.
Bronchoalveolar lavage may be performed with or without the guidance of a flexible bronchoscope. Bronchoscopy carries the advantage of allowing the bronchial mucosa to be directly observed, providing additional data to support the diagnosis. Abnormalities observed during bronchoscopy of patients with EBP include irregular to polyploid bronchial mucosa, mucosal hyperemia, copious yellow-green exudates, and, rarely, dynamic collapse of the bronchi during expiration (Figures 2A & 2B).1,3,6
EBP is characterized by the predominance of eosinophils on cytologic examination of airway samples (Figure 3).1,3,6-8 In contrast, macrophages are the predominant cell type in samples from healthy dogs.9 Eosinophils compose 50% to 90% of the inflammatory cells in airway samples obtained from most dogs with EBP.1,6,8 Increased numbers of airway eosinophils may also be noted with other respiratory conditions such as neoplasia, parasitism, and fungal infection. Microscopic examination of airway samples may help detect these conditions if atypical cells, parasite larvae, or fungal organisms are observed. Concurrently, an increased percentage of neutrophils is often found in airway samples from dogs with EBP.1,3,6
Airway samples should always be submitted for quantitative bacterial cultures to detect concurrent bacterial infection. Impaired function of the mucociliary clearance apparatus secondary to inflammation can predispose patients to an accumulation of infectious organisms within the airways. It has been shown that bacterial growth of 1.7 x 103 CFU/ml of bronchoalveolar lavage fluid is necessary to distinguish true bacterial infection from colonization of the lower airways by commensal organisms.10 To further distinguish between commensal or contaminant organisms and true infection, culture results should be interpreted in the context of cytology results. Observation of etiologic agents within phagoyctic cells is supportive of true infection.
Airway cytology is sufficient to diagnose EBP in most cases, but bronchial pinch biopsies may be obtained with or without endoscopic guidance when cytologic examination results are equivocal. Typical histologic findings include eosinophilic infiltrates beneath or within the respiratory epithelium and varying degrees of mucosal thickening, infiltration by other inflammatory cell types, collagenolysis, and fibrosis.1,5
The primary goal of therapy for EBP is to decrease the severity of clinical signs. Clients should be informed that complete resolution of clinical disease rarely occurs even with appropriate treatment.1 The cornerstone of therapy is the reduction of lung and airway inflammation. However, anti-inflammatory corticosteroid therapy should be withheld until concurrent bacterial infection, if present, is eliminated.
Antimicrobial drugs should be selected based on bacterial culture and antimicrobial sensitivity results, and antimicrobials should be administered for two to four weeks or, ideally, until repeated bacterial cultures of the lower airways result in no growth. It is important to tell clients that clinical signs may not improve during the course of antimicrobial therapy. Mucolytic or expectorant agents are usually unnecessary, and cough suppressants should be avoided in order to allow for expectoration of mucus from the airways.
Because EBP is suspected to have an allergic etiology, potential allergenic triggers should be eliminated if possible. Aerosolized deodorizers and perfumes, particulate matter in bedding (cedar chips, straw, and sawdust), cigarette smoke, and dusty environments should be avoided.
Most patients with EBP respond well to appropriate therapy, with clinical signs improving within days of initiating treatment.1,3,6,7 Irregular therapy with repository parenteral corticosteroids and abrupt cessation of oral corticosteroid therapy are associated with the poorest clinical responses.13 After the start of treatment, peripheral eosinophilia resolves and radiographic improvement is seen in most patients.1,6 Relapse may be noted weeks to months after discontinuation of therapy in some cases.1,3 If relapse occurs, reinstitute therapy with the lowest corticosteroid dose that controlled clinical signs, and follow a slower dose-tapering regimen.
Canine eosinophilic bronchopneumopathy is proposed to result from a hypersensitivity condition that leads to eosinophilic infiltration of the lower airways and pulmonary parenchyma, manifesting clinically as a harsh, unrelenting cough. It can be differentiated from chronic bronchitis by its occurrence in young dogs most commonly, the predominance of eosinophils in airway samples, and the occasional finding of concomitant nasal discharge. Therapy consists of anti-inflammatory oral or inhaled corticosteroids or a combination of these drugs. Complete resolution of clinical signs is rare, and most patients require lifelong treatment.
The authors thank Dr. Stephan Carey for his assistance in reviewing this manuscript.
Christine M. Venema, DVM
Coretta C. Patterson, DVM, DACVIM
Department of Small Animal Clinical Sciences
College of Veterinary Medicine
Michigan State University
East Lansing, MI 48824
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