No abstract

The pathogenesis of dysphagia in achalasia and diffuse esophageal spasm (DES) is not understood completely, and the primary site of damage in these two entities is not known. This project was undertaken to study the ultrastructural changes present in the muscular wall of the esophagus in eight patients with achalasia and nine patients with DES, compared with seven controls. The ultrastructural alterations in the smooth muscle of all patients were neither pronounced nor consistent. However, nonspecific changes, including filament disarray, mottling of the fiber density in myocytes, thick and long cytoplasmic dense bodies, long dense plaques, and few nexus junctions were seen in both achalasia and DES. In addition, the smooth muscle cells in achalasia exhibited nuclear and cytoplasmic inclusions. Statistical analysis of the number of muscle cells per unit area suggested that the gross thickening of the muscular wall of the esophagus in cases of DES is because of hyperplasia and not hypertrophy of muscle cells. A striking change seen in achalasia esophagi and a few cases of DES, as compared to the controls, was the marked loss of small nerve fibers and the paucity of granules in the remaining fibers. This study points to a neurogenic pathogenesis for dysphagia in achalasia with secondary nonspecific changes in the smooth muscle in these two diseases. No nerve abnormalities were noticed in DES.

Sarcocysts are highly prevalent in the musculature of horses (Equus caballus) in various regions; however, the systematics of Sarcocystis species in equids is confusing. 3 There are 4 reported species of Sarcocystis in equids: S. asinus, S. bertrami, S. equicanis, and S. fayeri. All utilize canids as definitive hosts; however, transplacental infection can occur. 2,4 The interrelationships and validity of the above species are unclear. Pathogenicity of infection is variable, ranging from mild to severe chronic illness in naturally and experimentally infected horses. 5-7 We describe the histologic and ultrastructural appearance of intense Sarcocystis fayeri infection in a malnourished horse. A 3-4-year-old mare was euthanized for humane reasons, having been in deteriorating condition for 2-3 months. At

The ultrastructure of the esophageal wall in progressive systemic sclerosis (scleroderma) was studied in 7 patients and compared with other esophageal diseases. In scleroderma, fibrosis and capillary basement membrane changes were the most characteristic abnormalities. Muscle fibers of patients with scleroderma showed thickened dense bodies and plaques and increased cell organelles in comparison with other disease groups, while neural structures were normal. Our data supported a primary vascular cause, rather than a neurogenic or myopathic process, for esophageal dysfunction in scleroderma.The esophagus is the most frequently involved internal organ in progressive systemic sclerosis (scleroderma). Although many patients remain asymptomatic, others have significant reflux and/or dysphagia, which can become extremely debilitating because of ulceration and stricture formation. Manometric studies characteristically reveal the upper esophagus to be normal but the lower two-thirds to have dimin-