Oral toxicity of botulinal toxin is manifested when the toxin is absorbed from one or more anatomic regions of the intestinal tract and reaches target neurons. Toxin is absorbed primarily in the small intestine, although in infants the large intestine may be a site of absorption. Nanogram amounts of toxin that escape proteolytic digestion in the intestine may be sufficient to produce neurologic symptoms. It is estimated that approximately 10(11) molecules of toxin reaching peripheral nerve endings is sufficient to cause clinical botulism in adults, although the amount required to cause infant botulism is probably less. Absorption of toxin from the intestine is achieved by means of an endocytic mechanism, as is the absorption of nutritional proteins. Specific toxin receptors may be involved in the movement of toxin from the gastro-intestinal epithelium to target neurons across cellular barriers.