Methicillin-resistant Staphylococcus epidermidis is an important cause of cerebrospinal fluid shunt infections and prosthetic valve endocarditis. Agar dilution miniimum inhibitory concentrations were determined for 100 strains of methicillin-resistant S. epidermidis which were isolated from clinical specimens. Vancomycin inhibited all 100 strains at s3.12 pug/ml, whereas clindamycin inhibited only 46 strains at <12.5 pg/mL. Methicillin-resistant S. epidermidis strains were resistant to achievable levels of erythromycin, with 90 strains having a minimum inhibitory concentration of 23.12 pg/ml. Of the five cephalosporins and one cephamycin tested, cefamandole was the most active in vitro, inhibiting 97 strains at S25 pug/ml. Antibiotic synergism was examined by a quantitative bacterial time-kill method. Synergism (.102 kill by the combination over the most effective single antibiotic at 24 h) was demonstrated with vancomycin (1.56 pLg/ml) plus cefamandole (6.25 pLg/ml) in 14 of 14 strains, vancomycin plus cephalothin (6.25 pLg/ml) in 14 of 14 strains, vancomycin plus rifampin (0.008 to 0.012 pg/ml) in 6 of 12 strains, rifampin plus cefamandole in 9 of 12 strains, and rifampin plus cephalothin in 10 of 12 strains. The emergence of populations of bacteria resistant to 0.2 pug of rifampin per ml developed in three offive methicillinresistant S. epidermidis strains tested. The addition of either vancomycin, cephalothin, or cefamandole to the rifampin prevented the emergence of resistance in these three strains. Clinical trials of synergistic antibiotic combination therapy for serious methicillin-resistant S. epidermidis infections are indicated.Staphylococcus epidermidis has been well established as a pathogen in the urinary tract (8), wounds (18), and, most importantly, infections involving indwelling artificial devices. S. epidermidis is the most common cause of prosthetic hip infections (10), cerebrospinal fluid shunt infections (1, 12), and prosthetic valve endocarditis (14, 15).The incidence of methicillin resistance in clinical isolates of S. epidermidis has ranged from 10% (11)
SummaryGram negative colonisation and infection of the urinary tract is a well recognised compli cation of the neuropathic bladder caused by sp inal cord injury (S CI). K. pneumoniae accounts for one third of all urinary tract infections in hospitalised SCI patients. Plasmid analysis has been shown to reliably fingerprint bacterial strains, particularly K. pneumoniae, so that growth from two separate locations in or on the body can be accu rately analysed as to migration from a reservoir to a target location.Eighty seven hospitalised SCI patients on intermittent catheterisation for a total of 5 86 patient-weeks were studied. Twice weekly catheterised urine sp ecimens and once weekly rectal swab cultures were taken from each patient. Thirty seven patients experienced at least one clinically significant (colony count> 10 OOOlmL) urinary tract colonisation caused by K. pneumoniae, representing 66 total colonisations. Further analysis of 31 of these 37 patients revealed: K. pneumoniae in all of their stool cultures (p < 0'05) and the identical strain of K. pneumoniae in the urine as well as the stool in 72% of the 66 colonisations (p < 0'05). Analysis of 14 patients without K. pneumoniae urinary col onisations showed absence of faecal K. pneumoniae in 3, and predominant growth in only 4. In 22 of the 37 patients, multiple K. pneumoniae urinary colonisations were noted, representing 27 pairs of colonisation. Fifteen of the pairs were found to be relaps ing (caused by two identical bacterial strains), and 12 were recurrent (caused by two dif ferent bacterial strains). Thirteen of the 1 5 relapsing pairs also had identical urine and stool K. pneumoniae strains (p < 0'05). All colonisations were treated with appropri ate antibiotics based on culture and sensitivity reports. Fourteen of the 15 relapsing colon isation pairs have identical antibiograms (p < 0'05), while all 12 of the recurrent colon isation pairs had different antibiograms (p < 0'05). The differences noted on sensitivity patterns (antibiograms) correlated with differences among strains of K. pneumoniae based up on plasmid analysis. Treatment of bacteriuria did not affect the nature of re peated colonisations regardless of the antibiotic chosen, the route of administration or the duration of treatment.
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