We prospectively studied Enterobacter colonization in cardiac surgery patients receiving cefazolin prophylaxis. Fifty-eight (67%) of 87 patients became colonized, 28 by the time of admission to a Cardiac Surgery Intensive Care Unit. Enterobacter cloacae was four times more prevalent than Enterobacter aerogenes. We found increased Enterobacter colonization, after prophylaxis, in 45% of surgery patients. None of 25 control patients, who underwent coronary angioplasty and received no antibiotic prophylaxis, showed increased colonization (P = .001). Both groups had similar baseline rates of Enterobacter carriage. Typing showed 50 distinct strains of E. cloacae and 11 of E. aerogenes; 25% of patients carried greater than or equal to 2 strains simultaneously. In the nine cases of horizontal transmission, source patients were intubated for greater than or equal to 5 days and had heavy throat carriage of Enterobacter. No environmental sources of transmission were found. Clinical Enterobacter infection developed in 12 patients; at least nine of these were infected with a strain that had been isolated by surveillance culture. We conclude that Enterobacter, part of the patients' endogenous flora, becomes an important pathogen when amplified by prophylactic antibiotics and is less often transmitted horizontally.
The hypothesis that emergence of gentamicin-resistant strains of Staphylococcus aureus and Staphylococcus epidermidis in a neonatal special care nursery was the result of transfer of a single plasmid between these two species was examined. In experiments with mixtures of staphylococci, either in mixed cultures or on human skin, isolates of S. aureus and S. epidermidis transferred their gentamicin-resistance plasmids both intra- and interspecifically. By electron microscopy, the molecular masses of the plasmids from S. aureus and S. epidermidis were the same, 12.2 +/- 0.36 (standard deviation) and 12.3 +/- 0.56 megadaltons, respectively. Restriction endonuclease analysis of the plasmids from five isolates of S. aureus and two isolates of S. epidermidis, with use of the enzymes HaeIII, EcoRI, XbaI, and HindIII, showed no differences in the digestion patterns of the seven gentamicin-resistance plasmids. The results supported the hypothesis that plasmid transfer between S. aureus and S. epidermidis occurs in nature.
Seven definite and three probable cases of pyogenic sacroiliitis are presented and compared to 72 cases found in the English literature. Patients may present with a subacute localized or an acute systemic illness. Six of our patients were parenteral drug abusers. Symptoms often were vague, but sacroiliac tenderness was invariably found on examination. Sacroiliac uptake of gallium67 citrate and/or technetium99m pyrophosphate suggested the diagnosis which was confirmed by fluoroscopically controlled joint aspiration when blood cultures were sterile. Gram-negative organisms, group B streptococci and a Staphylococcus were isolated. Antibiotic treatment for four to six weeks was uniformly successful. Surgery should be reserved for abscess or sequestrum formation, neither of which were encountered in this series.
We previously described a neonatal nursery epidemic of infections caused by a single strain of Staphylococcus aureus bearing a gentamicin resistance plasmid (Vogel et al., Antimicrob. Agents Chemother. 13:466-472, 1978
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