Necropsy of 4 neonatal calves with a peracute syndrome of abdominal distention, diarrhea, dehydration, shock, and death revealed abomasal tympany, marked edema, hemorrhage, and emphysema of ruminal and abomasal walls and histopathologic lesions characteristic of forestomach acidosis. The presence of acid damage and the production of substantial quantities of gas strongly suggested that the pathogenesis of the syndrome involved exuberant fermentation of intragastric substrate. This supposition led to attempts to experimentally induce the syndrome by dosing neonatal calves with an alimentary tract flora, followed by milk replacer supplemented with excessive fermentable carbohydrate (D-glucose and cornstarch). Two of the 5 calves thus treated developed a syndrome very similar to that observed in naturally affected calves. Literature suggests involvement of several Clostridial species, Sarcina spp., and possibly other microbes or a combination thereof to be involved in very similar syndromes. Therefore it is suggested that this complex of lesions and clinical signs is not dependent on a single etiologic agent. Rather, it is proposed that the natural occurrence of disease requires a quantity of highly fermentable substrate (starch, glucose, lactose, etc.) and a bacterial flora that is capable of rapidly fermenting that particular substrate with a resultant production of gas and acid.