Acute bronchointerstitial pneumonia is a sporadic, rapidly progressive disease of foals characterized by acute respiratory distress and high mortality.
The etiology of acute bronchointerstitial pneumonia in foals is not clear. It may result from different insults rather than a single factor, initiate a cascade of events, and result in a final common response of severe pulmonary damage and acute respiratory distress. Warm weather (>85°F [29.4°C]) is a common epidemiologic factor. Many foals have a history of antimicrobial therapy when clinical signs developed. No virus is consistently isolated, and no bacterial agent has been consistently identified. Enteric gram-negative organisms, Rhodococcus equi, Pseudomonas aeruginosa, and Pneumocystis jiroveci have been cultured from the lungs of affected foals.
The age of affected foals ranges from 1 wk to 8 mo. Acute bronchointerstitial pneumonia has an acute or peracute onset and is accompanied by high fever. The disease is rapidly progressive and may result in sudden death due to fulminant respiratory failure. Foals are unable or reluctant to move and are usually cyanotic. Severe respiratory distress is the most striking clinical sign. Clinicopathologic evaluation of foals with acute respiratory distress should include arterial blood gas, CBC, serum chemistry analysis, and thoracic radiographs. Hypoxemia, hypercapnea, and respiratory acidosis are consistent findings. These arterial blood gas findings quantify the severity of respiratory impairment and are used to monitor response to therapy. The hypoxemia of bronchointerstitial pneumonia is relatively resistant to supplemental oxygen therapy. Bronchointerstitial pneumonia is similar to bacterial pneumonia in that hyperfibrinogenemia and neutrophilic leukocytosis are seen in most foals.
Physical examination and clinicopathologic findings may appear similar to those of foals with severe R equi pneumonia (see Rhodococcus equi Pneumonia in Foals), and thoracic radiographic examination may be the most valuable diagnostic test to differentiate R equi pneumonia from bronchointerstitial pneumonia. Interstitial pneumonia appears as diffuse to caudodorsally distributed interstitial and bronchointerstitial pulmonary opacities. With advanced disease, the radiographic pattern progresses to include patches of a coalescing alveolar nodular pattern with air bronchograms. Transtracheal aspiration may be prohibitively dangerous to perform on a dyspneic foal but should be done when the foal becomes more stable to obtain samples for bacterial culture/sensitivity, cytologic evaluation, and virus isolation. Cytologic evaluation of tracheal aspirates reveals acute neutrophilic inflammation with or without evidence of sepsis. Bacterial organisms are often recovered from transtracheal aspiration samples or necropsy of foals with bronchointerstitial pneumonia; however, no single organism is consistently recovered.
Necropsy examination reveals diffusely enlarged lungs that fail to deflate upon opening of the thoracic cavity with rib impressions on the visceral pleural surface. The cut surface of lung is mottled, with dark red lung interspersed with more normal-appearing lung tissue and edematous separation of lobules. The most prominent histopathologic findings are severe, diffuse, necrotizing bronchiolitis, alveolar septal necrosis, and neutrophilic alveolitis. Surviving foals develop a proliferative epithelial and interstitial response, including bronchiolar and alveolar epithelial hyperplasia, type II cell hyperplasia, and hyaline membrane formation.
Because the cause of bronchointerstitial pneumonia is unknown, therapy is symptomatic. Treatment includes anti-inflammatory therapy, broad-spectrum antibiotics, thermoregulatory control, bronchodilation, supplemental oxygen, and supportive care. Anti-inflammatory therapy with corticosteroids (eg, dexamethasone 0.1 mg/kg/day, IV) appears to improve survival. An alcohol bath, an air-conditioned stall, and/or a fan are used in conjunction with NSAIDs to maintain rectal temperature <103.5°F (39.7°C). The suitability of an antibiotic regimen appears to have little bearing on the outcome of bronchointerstitial pneumonia. Nonetheless, broad-spectrum antibiotic therapy should be instituted to treat existing or impending secondary bacterial infections. Additional supportive therapy includes provision of a clean, comfortable environment; highly palatable, dust-free feeds; and ulcer prophylaxis.