Other important examples of antibiotic toxicity are optic neuropathy caused by ethambutol toxicity; ototoxicity and neuromuscular blockade from aminoglycoside and fluoroquinolone antibiotics; peripheral neuropathy, encephalopathy, and an Antabuse-like reaction to alcohol in patients taking metronidazole; a metronidazole-induced polyneuropathy, isoniazid (INH) neuropathy and optic neuropathy, and possibly a peripheral neuropathy caused by chloramphenicol.
Woodruff and colleagues, as well as others, reported a curious and reversible cerebellar syndrome caused by metronidazole with MRI signal changes in the dentate nuclei, or more widespread signal changes in other parts of the brainstem and cerebral white matter as noted by Kim and coworkers, who carried out a MRI study of 7 patients. Dysarthria, confusion, and gait ataxia seem to form the core of the clinical syndrome but imaging changes may be found coincidentally as well.
The most notorious toxic consequences with this group of drugs were seen with clioquinol, which was sold as Entero-Vioform and was used in many parts of the world to prevent traveler’s diarrhea and as a treatment for chronic gastroenteritis. In 1971, clinical observations began to appear in medical journals of a subacute myelo-opticoneuropathy (SMON). During the 1960s, more than 10,000 cases of this disease were collected in Japan by Tsubaki and colleagues. Usually the illness began with ascending numbness and weakness of the legs, paralysis of sphincters, and autonomic disorder. Later, vision was affected. The onset was acute in about two-thirds of the cases and subacute in the remainder. The occurrence of these neurologic complications was found to be related to the prolonged use of clioquinol. In Japan, the drug was withdrawn from the market, and the incidence of SMON immediately fell, supporting the theory that it was caused by the drug. Recovery was usually incomplete.
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