Cell proliferation in pathogenesis of esophagogastric lesions in pigs.

Abstract

Esophagogastric ulcer is an independent disease in swine that is characterized by ulcerous autodigestion of the cutaneous mucosa, which does not exhibit a tendency to recover, but, on the contrary, a tendency toward severe hemorrhaging, with a predominantly lethal outcome. Since it develops in the part of the stomach that is morphologically and functionally different from other glandular mucosa, it was questioned earlier whether it could be a peptic ulcer based on its nature. Spontaneous ulcers, usually of the stomach, commonly occur in many domestic animals. Some of these lesions are chronic and they may occur in either the glandular or squamous-lined regions of the stomach. As with the human disease, the pathogenesis in domestic animals is multifactorial, poorly understood, and variable between and within species. Environmental stress and dietary factors are very important in the ulcer disease in swine. It has been shown that the Helicobacter spp. is strongly associated with naturally occurring ulcer and preulcer lesions of the pars esophagea in swine, which raises the possibility that Helicobacter spp. is an important factor in the pathogenesis of these lesions. The dynamics of the development of esophagogastric ulcers imply hyperplastic lesions (parakeratosis and hyperkeratosis), keratolysis, erosions, peptic necrosis, and the development of ulcers with all the characteristics of peptic ulcerations in other localities. In addition, K6 is expressed in association with the mucosal changes. The pattern of the intermediate filaments of keratin suggests that epithelial proliferation, which leads to visible hyperkeratosis, constitutes the essence of gastric ulcers in swine.