Two adult male fairy bluebirds (Irena puella) from two different zoological collections had histologic inflammatory lesions in the aorta, pulmonary trunk, and coronary arteries. Lesions in the aorta and pulmonary trunk were transmural, while coronary artery lesions were limited to the media and adventitia. The intima in vessels with transmural lesions was characterized by variably thick, subendothelial plaques consisting of collagen and/or spindloid cells and macrophages. Aggregates of epithelioid macrophages with abundant granular basophilic cytoplasm were present occasionally in the subintima and, more typically, in the media and adventitia. Medial epithelioid macrophage infiltrates were often arranged in rows, parallel to the medial collagen and elastin fibers, and there were occasional foci of medial mineralization. Inflammation was most marked in the adventitia of all vessels, which contained poorly organized infiltrates of lymphocytes, plasma cells, macrophages, epithelioid macrophages, and heterophils. Occasional multinucleated giant cells were also present. Ziehl-Neelsen stains identified large numbers of acid-fast bacilli in the cytoplasm of the epithelioid macrophages. Both birds had other lesions of mycobacteriosis. In one bird, these were limited to the presence of acid-fast organisms within histiocytic nodules adjacent to secondary and tertiary parabronchi in the lung. The other bird had a very small number of similar pulmonary nodules and disseminated granulomatous inflammation in the liver, both containing acid-fast organisms.
Granulomatous arteritis related to mycobacterial infection has not before, to our knowledge, been reported in animals. The distribution and nature of the lesions in these cases are similar to a syndrome in humans called Takayasu’s arteritis. Takayasu’s arteritis may involve the aorta, its branches, and the pulmonary arteries and is characterized by granulomatous inflammation of the media and adventitia. The etiology of the disease remains undetermined. Epidemiologic data, including an elevated incidence of active tuberculosis or positive skin reactivity to purified protein derivative (PPD) in affected patients compared to the general population, suggests a link with mycobacterial infection. Patients with Takayasu’s arteritis also have levels of serum antibodies to Mycobacterium tuberculosis extract, its 65 kDa heat shock protein, and a purified tuberculosis-specific 38 kDa protein, which are significantly higher than those in control sera and are comparable to, or higher than, sera from patients with pulmonary tuberculosis.1,2 It has been suggested that Takayasu’s arteritis may be an immune-mediated disorder triggered by mycobacterial antigens with immunologic similarity to native antigens in the arterial wall. The arteritis observed in the birds differs from the human syndrome in that macrophages with intracytoplasmic mycobacteria are present within the avian lesions but are not observed in Takayasu’s arteritis.
1. Aggarwal, A., M. Chag, N. Sinha, and S. Naik. 1996. Takayasu’s arteritis: role of Mycobacterium tuberculosis and its 65 kDa heat shock protein. Int. J. Cardiol. 55:49–55.
2. Hernandez-Pando, R., P. Reyes, C. Espitia, Y. Wang, G. Rook, and R. Mancilla. 1994. Raised agalactosyl IgG and antimycobacterial humoral immunity in Takayasu’s arteritis. J. Rheumatol. 21:1870–1876.