Clinical efficacy of a synergistic combination of cefotaxime and amikacin against multiresistant Pseudomonas and Serratia infections.

The synergistic activity of cefotaxime and amikacin against 21 highly resistant Pseudomonas aeruginosa and Serratia marcescens isolates was evaluated in-vitro by the checkerboard tube dilution method and in-vivo in five patients with serious infections caused by these organisms. All isolates were resistant to gentamicin, tobramycin, amikacin, and cefotaxime. Synergy was observed in 90% of isolates and occurred when the MIC of amikacin was less than 256 mg/l and of cefotaxime less than 1024 mg/l. A clinical response occurred in 100% and bacteriological cure in 80% of patients. Our results demonstrate a high degree of synergism between amikacin and cefotaxime in-vitro and clinical efficacy in the treatment of infections due to multiply-resistant Pseudomonas and Serratia species.

Amikacin-resistant gram-negative bacilli: correlation of occurrence with amikacin use.

The incidence of amikacin resistance among gram-negative bacilli isolated at the New York V.A. Medical Center increased from 2.0% to greater than 7% during an 18-month period from January 1980 to July 1981. This increase coincided with a threefold increase in amikacin use at this institution. The amikacin-resistant (AKR) isolates most frequently recovered in 1981 were species of Klebsiella, Serratia, and Pseudomonas. These organisms were recovered from multiple sites, including urine, sputum, wounds, blood, peritoneal fluid, and pleural fluid. The amikacin-modifying enzyme 6'-N-acetyltransferase was detected in 27 (67.5%) of 40 randomly selected AKR isolates. These data indicate that resistance to amikacin in this hospital is enzymatically mediated in most strains of AKR Klebsiella and Serratia and in about one-third of AKR strains of P. aeruginosa. This finding supports the conclusion that amikacin resistance is enhanced by the pressure of increased amikacin use.

Myocardial abscess due to Klebsiella pneumoniae complicating acute infarction.

A case is described in which Klebsiella pneumoniae urosepsis associated with acute myocardial infarction resulted in myocardial abscess and papillary muscle rupture. The diagnosis was made during surgery for mitral valve replacement. The patient improved after therapy with cefotaxime; however, cardiac rupture occurred on the sixth postoperative day. The pathogenesis of myocardial abscess and the use of non-invasive techniques for diagnosis are discussed.

Ceftazidime therapy of infections caused by Enterobacteriaceae and Pseudomonas aeruginosa.

Sixteen patients with serious Gram-negative bacillary infections were treated with intravenous ceftazidime, 2 g every 8 h. The majority of patients had bacteraemia or pneumonitis or both. Ten patients were cured and six improved. Seven of ten patients infected with Pseudomonas aeruginosa were cured, and three improved. No adverse reactions occurred. Four strains of Ps. aeruginosa became resistant to ceftazidime in patients who were cured or improved clinically. Ceftazidime is effective as single drug therapy for serious Gram-negative infections, including those due to Ps. aeruginosa.

Efficacy of a twelve-hourly ceftriaxone regimen in the treatment of serious bacterial infections.

Eighteen patients with 21 serious infections were treated with ceftriaxone, 1 g intravenously every 12 h, for a mean duration of 8 days. Eighteen gram-negative and two gram-positive organisms were isolated. Sites of infection included blood (three patients), urinary tract (six patients), respiratory tract (seven patients), biliary tract (three patients), ascitic fluid (one patient), and skin (one patient). Serum, bile, and ascitic fluid concentrations of ceftriaxone were in excess of the minimal bactericidal concentration required for the infecting organism in all cases. A bacteriological response was demonstrated in 94% of the infections. A clinical response occurred in four infections from which no pathogens were recovered. In one patient, ceftriaxone failed to eradicate a peritoneal infection due to Bacteroides fragilis. In two patients, superinfection with enterococci developed both during and after therapy. Systemic tolerance to ceftriaxone was excellent.