A 77-year-old man developed progressive difficulty in swallowing, garbled speech, and diplopia in the presence of a chronically ulcerated scar on his face. Toxigenic Corynebacterium diphtheriae (biotype intermedius) was cultured from the lesion, and he was treated with diphtheria antitoxin and antibiotics. Over several days he developed progressive respiratory muscle weakness, as evidenced by decreasing serial measurements of vital capacity (VC) and maximum inspiratory force (MIF), and required mechanical ventilation. Progressive peripheral muscle weakness followed, and VC and MIF further declined, eventually to as low as 150 ml and 5 cm H2O, respectively. Nerve conduction studies were consistent with the demyelinating neuropathy seen following diphtheria. Beginning at about Day 60, these abnormalities began to resolve, and despite recurrent atelectasis, nosocomial pneumonia, depression, and tracheal stenosis, the patient survived. He required mechanical ventilation for 72 days and was hospitalized 142 days, eventually regaining normal neuromusclar function. Occurring during an epidemic of diphtheria in Seattle, this case has features typical of cutaneous diphtheria and severe postdiphtheritic neuropathy. Clinicians should be aware of this possible etiology for unexplained acute respiratory muscle weakness. (Respir Care 1986;31:1102-1106.)