British Columbia

In April 2001, a 7-day-old standardbred foal was presented to the Abbotsford Animal Health Centre (AHC) for necropsy. The foal had experienced an acute onset of progressive respiratory disease at 4 d of age that had been unresponsive to treatment. Respiratory disease was not observed in other horses on the premises prior to, during, or following the illness.

At necropsy, the foal was in good body condition. Major gross abnormalities were restricted to the lower respiratory tract. The lungs failed to collapse, were edematous, and mottled red and tan in color. The parenchyma was rubbery in texture, with randomly scattered, small, firm nodules. The bronchial lymph nodes were enlarged and wet. There was moderate mediastinal edema. Serum immunoglobulin G levels measured 11.0 g/L. (reference range, 1.6 to 27.6 g/L)

Microscopically, there was marked multifocal necrosis and sloughing of terminal bronchiolar epithelium with necrotic debris in the lumina of many affected bronchioles. Parenchyma adjacent to affected bronchioles exhibited mild alveolar epithelial necrosis, with marked hemorrhage and mild fibrin exudation. In other areas, hemorrhage was insignificant, and alveolar intraluminal fibrin, intermixed with macrophages, predominated. A few alveoli demonstrated pneumocyte type 2 proliferation and hyaline membrane formation with a mild infiltrate of neutrophils and macrophages. Small numbers of multinucleated cells were observed in both alveolar and bronchiolar lumina.

The pattern of bronchiolar and alveolar epithelial necrosis strongly suggested a viral etiology (1). Routine bacterial culture of the lung was negative. Tests on lung tissue for equine herpesvirus 1, 2, and 4 (by polymerase chain reaction (PCR)), equine viral arteritis virus (by PCR), and adenovirus (by virus isolation) were negative. Influenza A virus was identified after inoculation of embryonated eggs with lung tissue. Amplification by PCR of a sequence from the highly conserved matrix gene of influenza A virus was used to detect the virus in both inoculated allantoic fluid and lung tissue from the foal (2). Immunohistochemical staining demonstrated influenza A viral antigens in the epithelium of a small number of terminal bronchioles (personal communication, Dr. K. West, Prairie Diagnostic Services, Saskatoon, Saskatchewan). On preliminary evaluation, the virus did not show hemagglutination inhibition with antisera for either equine influenza A type 1 or type 2.

The recovery of influenza A virus from the foal and the demonstration of influenza A viral antigens in bronchiolar lesions considered to be viral in nature suggested a causative relationship. Bronchointerstitial pneumonia has been reported as a cause of death in foals, with the suggestion that it probably had a viral etiology, despite negative virus isolation attempts (3). It has been reported that, by the time the lung lesions progress to regenerative epithelial hyperplasia, the virus is very difficult to identify; whereas, in the early stage of bronchiolar necrosis, intraepithelial influenza A viral antigens can be demonstrated readily by immunohistochemistry (4). Thus, it may be that removal of the virus along with sloughed necrotic epithelium renders attempts at viral identification futile in the later stages of the disease process, when death usually occurs. The active necrosis of bronchiolar epithelium in the present case likely facilitated viral isolation.

Bronchointerstitial pneumonia in foals < 1 wk of age is uncommon. Review of AHC case records from 1993 to 2001 revealed that only 2 of 7 foals diagnosed with bronchointerstitial pneumonia were < 1 wk of age. Similarly, in the report referred to above (3), only 2 of 19 affected foals were < 1 wk of age. The authors of this report concluded that the peak occurrence of bronchointerstitial pneumonia in 1.5- to 2.5-month-old foals coincided with declining maternally-derived immunoglobulins, implying that passive immunity is likely protective in young foals.

No predisposing factors were identified that would explain why the foal in this case contracted bronchointerstitial pneumonia. The foal experienced a normal birth, serum immunoglobulin levels at the time of death were adequate (5), and no concurrent disease process was identified. Since the dam did not become ill, presumably she was immune to the virus, and colostral protection of the foal would have been anticipated.

To our knowledge, this is the first report of a fatal case of bronchointerstitial pneumonia in a foal from which influenza A virus was isolated. The ability to isolate the virus was attributed to the relatively early stage of the pneumonia and the persistence of viral antigen in the bronchioles. It is unclear whether this case is etiologically representative of sporadic bronchointerstitial pneumonia in foals. Studies are underway to determine the identity of the influenza A virus. Further, as the virus did not identify with specific strain antisera of equine influenza A type 1 or type 2, serological studies are planned to determine whether or not the influenza A virus that was isolated plays a role in equine upper respiratory disease.