Abstract

As early as 1982, Dutch authors (2) pointed out that loss of contraction of the esophageal groove of initially healthy veal calves causes chronic indigestion (latent chronic ruminal acidosis), so-called "ruminal drinking syndrome." In subsequent years, the etiology of the disease has been studied intensively (6, 7). In advanced stages, the ruminal mucosa of such calves is substantially proliferated and hyperkeratotic.
 The forestomach disease described by the Munich team (4,5,3), on the other hand, is due to acute complications of primary ailments or is the result of feeding errors. Inborn and acquired "drinking weakness"/anorexia (both have a multitude of causes), as well as force-feeding by stomach tube may cause the esophageal groove to close incompletely or not at all. As a result of this, larger amounts of fluid flow into the rumen and reticulum often followed by an acute ruminal acidosis. The forestomachs of calves diseased in this manner were investigated pathomorphologically in a systematic study (details see 1) that also made note of clinical findings. The results of this investigation will be conveyed below.

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