Diagnosing and managing canine eosinophilic bronchopneumopathy - Veterinary Medicine
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Diagnosing and managing canine eosinophilic bronchopneumopathy
A harsh, persistent cough with gagging and retching can signal this serious, but manageable disease. Here are the steps practitioners can to take to confirm a diagnosis and help improve a patient's clinical signs through corticosteroid therapy.


VETERINARY MEDICINE


Biopsy

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

THERAPY

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.


Table 1
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.


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.)
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 signs.

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.

PROGNOSIS

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.

CONCLUSION

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.

ACKNOWLEDGMENT

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

REFERENCES

1. Clercx C, Peeters D, Snaps F, et al. Eosinophilic bronchopneumopathy in dogs. J Vet Intern Med 2000;14(3):282-291.

2. Clercx C, Peeters D. Canine eosinophilic bronchopneumopathy. Vet Clin North Am Small Anim Pract 2007;37(5):917-935.

3. Corcoran BM, Thoday KL, Henfrey JW, et al. Pulmonary infiltration with eosinophils in 14 dogs. J Small Anim Pract 1991;32(10):494-502.

4. Peeters D, Day MJ, Clercx C. Distribution of leucocyte subsets in bronchial mucosa from dogs with eosinophilic bronchopneumopathy. J Comp Pathol 2005;133(2-3):128-135.

5. Clercx C, Peeters D, German AJ, et al. An immunologic investigation of canine eosinophilic bronchopneumopathy. J Vet Intern Med 2002;16(3):229-237.

6. Rajamäki MM, Järvinen AK, Sorsa T, et al. Clinical findings, bronchoalveolar lavage fluid cytology and matrix metalloproteinase-2 and -9 in canine pulmonary eosinophilia. Vet J 2002;163(2):168-181.

7. Moon M. Pulmonary infiltrates with eosinophilia. J Small Anim Pract 1992;33(1):19-23.

8. Cooper ES, Schober KE, Drost WT. Severe bronchoconstriction after bronchoalveolar lavage in a dog with eosinophilic airway disease. J Am Vet Med Assoc 2005;227(8):1257-1262.

9. Hawkins EC. Bronchoalveolar lavage. In: King LG, ed. Textbook of respiratory disease in dogs and cats. Philadelphia, Pa.: WB Saunders, 2004;118-128.

10. Peeters DE, McKiernan BC, Weisiger RM, et al. Quantitative bacterial cultures and cytological examination of bronchoalveolar lavage specimens in dogs. J Vet Intern Med 2000;14:534-541.

11. Cohn LA, DeClue AE, Reinero CR. Endocrine and immunologic effects of inhaled fluticasone propionate in healthy dogs. J Vet Intern Med 2008;22(1):37-43.

12. Bexfield NH, Foale RD, Davison LJ, et al. Management of 13 cases of canine respiratory disease using inhaled corticosteroids. J Small Anim Pract 2006;47(7):377-382.

13. Bauer T. Pulmonary hypersensitivity disorders. In: Kirk RW, ed. Current veterinary therapy X. Philadelphia, Pa.: WB Saunders, 1989;369-376.


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