Ultrastructural pathology of 3-methylindole-induced pneumotoxicity in cattle. I. Glycogen accumulation in the alveolar type II cells and tubular myelin accumulation in the alveoli.

3-Methylindole (3MI) was orally administered as a single dose of 0.1-0.2 gm/kgm which then produced acute pulmonary edema in cattle. Electronmicroscopic examination of lung tissue collected after 72 hours revealed vesiculation and desquamation of alveolar type I cells as well as hyperplasia of the alveolar type II cells. Hyaline membrane formation, along with massive accumulation of tubular myelin in the alveolar spaces, was observed. Pulmonary capillaries were occluded with microthrombi and leukocytes infiltrated the interstitium as well as the alveoli. Accumulation of large aggregates of glycogen in the alveolar type II cells were the most unusual changes seen in the experimental animals. It is suggested that accumulation of tubular myelin is a structural manifestation of surfactant inactivation by the plasma proteins. Furthermore, the disease process may be complicated by a compositional or quantitative defect in the surfactant produced by the alveolar type II cells, which are pathologically loaded with glycogen.