Bronchointerstitial Pneumonia and Respiratory Distress in Young Horses: Clinical, Clinicopathologic, Radiographic, and Pathological Findings in 23 Cases (1984–1989)

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Abstract
Twenty‐three foals, between 1 and 7 months old, with signs of acute respiratory distress, were examined at the Veterinary Medical Teaching Hospital (VMTH), University of California, Davis, between 1984 and 1989. Characteristic features included sudden onset of severe respiratory distress and tachypnea, cyanosis unresponsive to nasal oxygen, pyrexia, hypoxemia, hypercapneic respiratory acidosis, poor response to treatment, and histopathologic lesions of bronchiolitis and bronchointerstitial pneumonia. Seven of the 23 foals were normal before the onset of respiratory distress, 3 foals were found dead, aqd 13 foals were being treated for respiratory tract infections at the time of presentation. Laboratory data obtained for 13 horses showed increased plasma fibrinogen concentration (630.7 ±193 mg/dL), leukocy‐tosis (18,607 ± 7,784/μL), and neutrophilia (13,737 ± 8,211/μL). Thoracic radiographs showed a diffuse increase in interstitial and bronchointerstitial pulmonary opacity and, in 5 foals, an alveolar pulmonary pattern of increased density was also seen. In 3 foals heavy interstitial infiltration proceeded to a coalescing nodular radiographic appearance. Microbiological culture of tracheobronchial aspirates (TBA) from 9 foals yielded bacterial growth, but no one bacterial species was consistently isolated. Microbiological culture of postmortem specimens of the lung from 6 foals yielded growth of bacteria that included Escherichia coli, Enterobacter spp., Proteus mirabilis, Klebsiella pneumonias, Rhodococcus equi, or β‐hemolytic Streptococcus spp. Tracheobronchial aspirates from 4 foals and lung samples collected from a further 4 foals at necropsy yielded no bacterial growth. Cultures were not taken from two foals premortem or postmortem. Virologic examination of TBA, lung tissue, or pooled organ tissue from 12 foals was negative. Viral culture of TBA from 1 foal showed cytopathic effects and positive immunoflu‐orescence for equine herpes virus type II (EHV‐II). In addition to the 3 foals that were found dead, 11 foals died or were euthanatized. Pathologic lesions were limited to the lungs in 50% of the foals; the remainder also had bowel lesions suggestive of hypoxic injury. The predominant histopathologic pulmonary lesions included bronchiolitis, bronchiolar and alveolar epithelial hyperplasia, and necrosis. Many bronchioles were filled with mucoid and fibrinocellular exudate. The peribronchiolar interstitium and adjacent alveolar spaces were also infiltrated with inflammatory cells and contained proteinaceous edema fluid. Type II cell hyperplasia and hyaline membrane formation were observed in the majority of foals and in 2 foals alveolar multinucleate giant cells were also present. Nine of 13 foals (69%) on which treatment was attempted at the VMTH survived after aggressive medical care that included external thermoregulatory control, oxygen by nasal insufflation, antimicrobial drugs, bronchodilating agents, nonsteroidal anti‐inflammatory drugs, and corticosteroids. Persistent radiographic evidence of increased interstitial density was noted up to 24 months after initial presentation, and one horse remained exercise intolerant for at least 15 months after discharge. The exact etiopathogenesis of this disorder and long‐term sequalae in the survivors have yet to be fully determined. However, it is likely that a number of different insults rather than a single agent may initiate the pulmonary damage that leads to severe interstitial pneumonia and subsequent acute respiratory distress or apparent sudden death in foals. (Journal of Veterinary Internal Medicine 1993; 7:277–288. Copyright © 1993 by the American College of Veterinary Internal Medicine.)