The Neurotoxicity of Antibacterial Agents

Abstract

Commonly used antibacterial agents may be associated with various neurotoxic reactions. Central nervous system toxicities include seizure disorders, encephalopathy, bulging fontanelles, and neuropsychiatric symptoms. These abnormalities have been associated with the use of the penicillins, cephalosporins, sulfonamides, tetracyclines, chloramphenicol, colistin, aminoglycosides, metronidazole, isoniazid, rifampin, ethionamide, cycloserine, and dapsone. Cranial nerve toxicities, such as myopia, optic neuritis, deafness, vertigo, and tinnitus, have been associated with the use of erythromycin, sulfonamides, tetracyclines, chloramphenicol, colistin, aminoglycosides, vancomycin, isoniazid, and ethambutol. Peripheral nerve symptoms consisting of paresthesias, motor weakness, or sensory impairment have been associated with the use of the penicillins, sulfonamides, chloramphenicol, colistin, metronidazole, isoniazid, ethionamide, and dapsone. Neuromuscular blockade has been associated with the use of the tetracyclines, polymyxins, lincomycin, clindamycin, and aminoglycosides. Management generally consists of supportive therapy and immediate discontinuation of therapy with the offending drug.

A Guide to the Management of Tuberculosis in Patients with Chronic Liver Disease

“…However, in patients with alcoholic hepatitis, an interaction between alcohol and cycloserine can lead to an increased risk of seizures. 49 Quinolones (levofloxacin, moxifloxacin, ofloxacin and gatifloxacin) are currently considered fairly safe, and their pharmacokinetics does not seem to be altered in patients who have advanced liver disease. [50][51][52] Hepatotoxic effects associated with quinolones are usually mild and reversible.…”

MR Imaging of Metronidazole-Induced Encephalopathy: Lesion Distribution and Diffusion-Weighted Imaging Findings

“…2,3 The incidence of MIE is unknown, though several previous studies have addressed brain change caused by metronidazole neurotoxicity. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] To our knowledge, several reports on 13 patients with MIE have documented MR brain imaging of abnormalities, [7][8][9][10][11][12][13][14][15][16] and diffusion-weighted imaging (DWI) data have been presented for 3 patients with MIE. 11,12,14 Previous case reports have focused on cerebellar lesions, and little radiologic investigation of MR imaging findings with respect to brain stem pathology and topographic lesion distribution has been performed in patients with MIE.…”

A synthetic mammalian gene circuit reveals antituberculosis compounds

“…EthR-mediated repression of ethA transcription requires rather high clinical doses of ethionamide [up to 1g/day (6, 18)], which is associated with severe side effects including neurotoxicity (19) and fatal hepatotoxicity (6), yet is often still insufficient to reach minimum inhibitory levels in the bloodstream (20). Therefore, 2-phenylethyl-butyrate-triggered dissociation of EthR from the ethA promoter resulting in derepression of ethA, which was confirmed by quantitative RT-PCR of ethA transcripts (2.93 Ϯ 0.04-and 9.7 Ϯ 1.7-fold increase in the presence of 0.5 and 2 mM 2-phenylethyl-butyrate, respectively), may increase the sensitivity of Mycobacterium to ethionamide-based therapy.…”