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.

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Little is know about the clinical significance of isolating Citrobacter in the clinical laboratory. During a one-year period, 116 Citrobacter isolates were obtained from 77 patients with 83 suspected infectious episodes. The majority of the suspected infectious episodes involved the urinary tract (45%) or respiratory tract (41%). Citrobacter diversus was associated with 42% of the episodes, Citrobacter freundii with 29%, and Citrobacter species with 29%. In 42% of the suspected infectious episodes, the presence of Citrobacter was considered clinically significant; in the others, the significance of the Citrobacter isolates was indeterminate or considered to be commensal. Two thirds of the significant infections were hospital-acquired. Most patients (73%) from whom Citrobacter was cultured had underlying diseases or factors predisposing to infection. These data suggest that Citrobacter is a cause of significant opportunistic nosocomial infection in the hospital.

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A man was hospitalized with bacteremic Achromobacter xylosoxidans type IIIa pneumonia. The authors are aware of no previously reported similar infections caused by this bacterium. A clinical cure was achieved with a combination of carbenicillin and kanamycin therapy. Microtiter susceptibility testing revealed that carbenicillin was the antibiotic to which A. xylosoxidans IIIa was most sensitive (minimal inhibitory concentration, 1.6 microgram/ml) and that synergy between carbenicillin and kanamycin existed. During the patient's hospitalization, deficiency of IgM (21 mg/dl) was found. Specific serum activity against A. xylosoxidans IIIa was detected by the agglutination method. Specific anti-A. xylosoxidans IIIa IgG, but not IgM, was detected by indirect immunofluorescence. It appears that a defect in immunologic recognition of A. xylosoxidans IIIa as an invasive bacterium, a defect in synthesis of specific IgM, or both, contributed to this patient's infection.

The plasma and urine concentrations of cefaclor were measured after oral administration of single and multiple doses to volunteers. Cefaclor was rapidly absorbed, rapidly excreted in the urine, well tolerated without toxicity, and failed to accumulate in the plasma with chronic dosing.

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