Allergic pneumonitis is an acute or chronic hypersensitivity reaction of the lungs and small airways.
An underlying cause is rarely determined in pulmonary hypersensitivity reactions in dogs and cats. Type I or immediate hypersensitivity is probably the most common mechanism, although Type III and IV mechanisms may also be involved (see The Biology of the Immune System et seq). The cellular infiltrate is typically eosinophilic; however, mixed inflammatory infiltrates consisting of mononuclear cells, eosinophils, and neutrophils, or predominantly lymphocytic infiltrates can be seen.
Eosinophilic bronchopneumopathy (formerly pulmonary infiltration with eosinophilia [PIE], see Localized Allergic Reactions) is a group of diseases associated with both pulmonary-associated and peripheral eosinophilia. Not all types of allergic pneumonitis, however, are associated with eosinophilic bronchopneumopathy. Causes of eosinophilic bronchopneumopathy include migrating parasites, reaction to microfilariae of heartworms, lungworms, chronic bacterial or fungal infections (eg, histoplasmosis, aspergillosis), viruses, external antigens, and unknown precipitating factors. Canine heartworm (see Heartworm Disease) pneumonitis occurs when dogs become sensitized to microfilariae. A similar reaction may be seen in cats with heartworms. Migrating intestinal parasites and primary lung parasites may induce either subclinical or mild signs of allergic pneumonitis.
Pulmonary nodular eosinophilic granulomatous syndrome is a rare, severe eosinophilic bronchopneumopathy–like syndrome that occurs in dogs and is most often associated with heartworm infection or possibly an uncontrollable progressive form of eosinophilic bronchopneumopathy. In this condition, a severe granulomatous hypersensitivity reaction to microfilariae (or other antigen) results in mixed alveolar and interstitial pulmonary infiltrates plus variably sized, multiple pulmonary nodules scattered throughout the lung fields. Associated pathology may include eosinophilic granulomatous lymphadenitis, tracheitis, tonsillitis, splenitis, enteritis, gastritis, and pericholangitis. Pulmonary hypersensitivity also may be caused by drugs and reactions to inhaled allergens; however, this is poorly documented in small animals.
Chronic cough is the most common sign. It may be mild or severe, productive or nonproductive, and progressive or nonprogressive. Weight loss, tachypnea, dyspnea, wheezing, exercise intolerance, and occasionally hemoptysis may be seen. Severely affected animals may exhibit moderate to severe dyspnea and cyanosis at rest. Auscultation varies from unremarkable to increased breath sounds, crackles, or wheezes. Fever is usually absent. The degree of dyspnea and coughing is related to the severity of inflammation within the airways and alveoli.
This is based largely on history and on radiographic and clinicopathologic findings. Thoracic radiographs frequently show irregular patchy alveolar infiltrates and increased bronchial and interstitial markings. Radiographic evidence of heartworm disease or parasitic pulmonary disease may suggest an underlying cause. Typical hematologic changes are mild leukocytosis, variable peripheral eosinophilia (4%–50%), and occasionally basophilia. Fecal analysis and an occult heartworm test are indicated when lung parasitism or heartworm disease is suspected. Bronchoalveolar lavage for cytologic analysis, culture, and detection of larval forms is often helpful. In allergic pneumonitis, bronchoalveolar lavage cytology generally reveals a predominance of eosinophils. Bacterial cultures of aseptically collected lavage specimens are commonly negative.
When an underlying cause can be found, elimination of the offending agent and a short-term course of glucocorticoids resolves the problem. Prednisolone beginning at 1–2 mg/kg, PO, tapered over 10–14 days is often sufficient. When eosinophilic bronchopneumopathy is secondary to heartworm disease or pulmonary parasites, treatment with prednisolone before or during treatment for the parasite controls the pulmonary signs. When an underlying cause cannot be determined, prolonged therapy with prednisolone for 3–12 wk is often required. When severe bronchoconstriction is suspected, bronchodilators or β2-agonists may be helpful. Severely dyspneic animals may require short-term oxygen therapy.