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.
Since intermittent shedding of parasite ova may result in negative fecal examination results, a course of empirical anthelmintic
therapy with fenbendazole (50 mg/kg orally once daily for 14 days) should also be prescribed.2 Give clients an anti-inflammatory dose of prednisone to administer in case their dogs have an acute progression of clinical
signs, which may result from a profound inflammatory response to rapid parasite death.
After the treatments for infectious agents are completed, prednisone or prednisolone (1 mg/kg orally every 12 hours for 21
to 28 days) is recommended for initial anti-inflammatory therapy.1,6 Instruct clients that poluria, polydipsia, and polyphagia are expected side effects of corticosteroid therapy. The therapeutic
regimen is tailored by reducing the corticosteroid dose by 25% to 50% two weeks after clinical improvement is first noted
and every two to three weeks thereafter if clinical improvement persists.1,6 Inhaled corticosteroids are associated with a reduced incidence of adverse systemic effects and have been shown to be effective
in managing EBP.11,12 Inhalant corticosteroids such as fluticasone propionate may be substituted for oral corticosteroids or used in combination
with a reduced dose of oral corticosteroids (Table 1). Inhaled corticosteroids are administered via a metered dose inhaler attached to a spacer device connected to a facemask
(Figure 4). Corticosteroids can be discontinued in a minority of dogs, but most patients require lifelong therapy to control clinical
Figure 4. An inhalant corticosteroid is administered to a dog with eosinophilic bronchopneumopathy by using a spacer and a
facemask. (Photo courtesy of Dr. Corinne Goldman, South Carolina Veterinary Specialists.)
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
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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