Traumatogenic herpetic eye disease may be initiated via several pathophysiologic pathways. Trauma of the trigeminal ganglion or adequate systemic alterations are the most effective means of destabilizing ganglionic latency of the herpesvirus with consequent neuronal peripheral virus shedding. Peripheral stimuli seem to have far less effect on ganglionic latency--at least in man. The authors report on a rare case of proven herpetic primary disease. The trigger was probably a small intrastromal foreign body which caused an unusual alteration of the cornea with long-standing healing disorders.