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Apnea, attributed to sodium colistimethate therapy, occurred in a 50-year-old Negro male. Sufficient evidence now exists to confirm that colistimethate may be neurotoxic in humans. Awareness of potential colistimethate toxicity may dictate added caution in treating infections in patients with chronic debilitating diseases, chronic renal disease, hypoxic states, or those receiving muscle relaxants, adrenocorticosteroids, sedatives, narcotics, or anesthetic agents.

More than 300 recently isolated Shigella strains were tested for susceptibility, to sodium sulfadiazine by tube and plate dilution techniques. With a low inoculum (100 organisms), 59% of Shigella flexneri and 87% of S sonnei were sulfadiazine resistant. All strains were resistant by high inoculum testing (2 × 10 6 organisms). Antibiotic susceptibility testing by the plate dilution method using high inocula demonstrated by the following percentages of resistance: potassium penicillin G, 93%; streptomycin, 17%; tetracycline hydrochloride, 12%; chloramphenicol, 11%; ampicillin, 6%; sodium colistimethate, 2%; kanamycin sulfate, 1%; and neomycin sulfate, 1%. These studies indicate that sulfadiazine is no longer an appropriate drug for initiating treatment of shigellosis. Ampicillin and three orally administered non-absorbable antibiotics (colistimethate, kanamycin and neomycin) are the most effective drugs against shigellae in vitro.

Sodium colistimethate (Coly-Mycin Injectable) was administered intravenously to eight patients with Pseudomonas infections in doses of 2 to 2.5 mg/kg every 12 hours. Bacteriologic cure was achieved in five patients. The resulting serum concentrations of sodium colistimethate were approximately twice those obtained following intramuscular administration. Probenecid (Benemid) did not augment serum levels of the antibiotic. In the presence of moderately impaired renal function the intravenous dose should be decreased to 1 mg/kg every 12 hours. In severe renal failure, a dose of 2 mg/kg every two to three days should not be exceeded.

A previously well 4-year-old child died following administration of ten times the recommended dosage of colistimethate sodium. The clinical course was marked by acute renal failure and neuromyal paralysis and at autopsy acute tubular necrosis was the major finding.

To the Editor:— In the article by Drs. Hinman and Wolinsky, "Nephrotoxicity Associated With the Use of Cephaloridine" (200:724, 1967), the following was reported:Klebsiellawas isolated from the sputum of a patient with pneumonia; and was found to be susceptible to tetracycline, chloramphenicol, streptomycin, sulfisoxazole, kanamycin, polymyxin B and cephalothin; but was resistant to ampicillin by the disk method. By the tube dilution method, the minimum inhibitory concentration for cephaloridine was 25μg/ml. We consider this level to indicate relative resistance, and accordingly would not use cephaloridine in such a case. The patient had been previously treated with penicillin, chloramphenicol, and streptomycin, and then cephaloridine, up to 12 gm intravenously in 24 hours, was used. We do not recommend more than 4 gm daily intravenously. Sodium colistimethate was also administered. Prior to cephaloridine therapy, blood urea nitrogen levels were 13 and 23 mg/100 ml, but with this drug the

Infections caused by bacteria of the tribe Mimeae were reviewed.Mima polymorphaorHerellea vaginicolawas isolated by culture from 56 living patients and 9 autopsy cases, with pure cultures of these organisms from 11 living patients. Mimeae were found to be opportunistic pathogens with a highly variable degree of virulence. In three febrile patients, blood cultures yielded a pure growth ofH vaginicola, establishing the apparent pathogenicity of these organisms. Many of the infections were associated with an iatrogenic portal of entry, such as an intravascular catheter, with over half of the 18 wound infections occurring in head- and neck-surgery cases. Sodium colistimethate, kanamycin sulfate, methenamine mandelate, and polymyxin B sulfate were found to be the most effective therapeutic agents.