VITEK 2 is a new automatic system for the identification and susceptibility testing of the most clinically important bacteria. In the present study 198 clinical isolates, including Pseudomonas aeruginosa (n ‫؍‬ 146), Acinetobacter baumannii (n ‫؍‬ 25), and Stenotrophomonas maltophilia (n ‫؍‬ 27) were evaluated. Reference susceptibility testing of cefepime, cefotaxime, ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem, piperacillin, tobramycin, levofloxacin (only for P. aeruginosa), co-trimoxazole (only for S. maltophilia), and ampicillin-sulbactam and tetracycline (only for A. baumannii) was performed by microdilution (NCCLS guidelines). The VITEK 2 system correctly identified 91.6, 100, and 76% of P. aeruginosa, S. maltophilia, and A. baumannii isolates, respectively, within 3 h. The respective percentages of essential agreement (to within 1 twofold dilution) for P. aeruginosa and A. baumannii were 89.0 and 88.0% (cefepime), 91.1 and 100% (cefotaxime), 95.2 and 96.0% (ceftazidime), 98.6 and 100% (ciprofloxacin), 88.4 and 100% (gentamicin), 87.0 and 92.0% (imipenem), 85.0 and 88.0% (meropenem), 84.2 and 96.0% (piperacillin), and 97.3 and 80% (tobramycin). The essential agreement for levofloxacin against P. aeruginosa was 86.3%. The percentages of essential agreement for ampicillin-sulbactam and tetracycline against A. baumannii were 88.0 and 100%, respectively. Very major errors for P. aeruginosa (resistant by the reference method, susceptible with the VITEK 2 system [resistant to susceptible]) were noted for cefepime (0.7%), cefotaxime (0.7%), gentamicin (0.7%), imipenem (1.4%), levofloxacin (2.7%), and piperacillin (2.7%) and, for one strain of A. baumannii, for imipenem. Major errors (susceptible to resistant) were noted only for P. aeruginosa and cefepime (2.0%), ceftazidime (0.7%), and piperacillin (3.4%). Minor errors ranged from 0.0% for piperacillin to 22.6% for cefotaxime against P. aeruginosa and from 0.0% for piperacillin and ciprofloxacin to 20.0% for cefepime against A. baumannii. The VITEK 2 system provided co-trimoxazole MICs only for S. maltophilia; no very major or major errors were obtained for co-trimoxazole against this species. It is concluded that the VITEK 2 system allows the rapid identification of S. maltophilia and most P. aeruginosa and A. baumannii isolates. The VITEK 2 system can perform reliable susceptibility testing of many of the antimicrobial agents used against P. aeruginosa and A. baumannii. It would be desirable if new versions of the VITEK 2 software were able to determine MICs and the corresponding clinical categories of agents active against S. maltophilia.Several automated systems are available for the identification and susceptibility testing of the clinically most important bacteria (21). The VITEK system (bioMérieux-Vitek, Hazelwood, Mo.) was originally designed as an onboard system for the detection and identification of urinary tract pathogens from astronauts in spacecraft. It was first introduced in clinical laboratories in 1979 and has since been evaluate...

The relationships between porin deficiency, active efflux of fluoroquinolones, and extended-spectrum ␤-lactamase (ESBL) production were determined for 53 clinical isolates of Klebsiella pneumoniae. Thirty-two ESBL-positive strains (including 22 strains expressing porins and 10 strains lacking porins) and 21 ESBLnegative strains were evaluated. Active efflux of norfloxacin was defined as a >50% increase in the accumulation of norfloxacin in the presence of carbonyl cyanide m-chlorophenylhydrazone (CCCP) in comparison with the corresponding basal value in the absence of CCCP. The quinolone resistance-determining regions of both gyrA and parC from 13 strains, representing all isolates with different porin profiles and with or without active efflux, were determined. Porin loss was significantly more common among ESBL-positive strains (10 of 32 [31.2%]) than among ESBL-negative strains (0 of 2 [0%]) (P < 0.01). Active efflux was observed in 7 of 10 (70%) strains lacking porins and in 4 of 43 (9.3%) strains producing porins (P < 0.001). The 11 strains showing active efflux corresponded to 3 of 21 (14.3%) ESBL-negative strains and 8 of 32 (25.5%) ESBL-positive strains (P > 0.05). Basal values of norfloxacin accumulation were higher in strains lacking active efflux than in those that had this mechanism (P < 0.05). In the absence of topoisomerase changes, the contribution of either porin loss or active efflux to fluoroquinolone resistance in K. pneumoniae was negligible. It is concluded that among K. pneumoniae strains of clinical origin, porin loss was observed only in those producing ESBL, and that a significant number of porin-deficient strains also expressed active efflux of norfloxacin. In terms of fluoroquinolone resistance, both mechanisms are significant only in the presence of topoisomerase modifications.

The in vitro adherence of ten strains of Enterococcus faecalis and ten strains of Enterococcus faecium to siliconized latex urinary catheters and to silicone elastomer was evaluated. Bacterial suspensions (2.5x10(5) cfu/ml) in tryptic soy broth containing 0.5 cm segments from each type of catheter were incubated at 37 degrees C. At specified intervals, the segments were washed to remove nonadherent bacteria and sonicated for 1 min, and colony-forming units were quantified. Bacterial adherence occurred rapidly, reaching maximal peaks after 24 h of incubation. Enterococcus faecium adherence to both biomaterials was significantly lower than that of Enterococcus faecalis. No differences were observed between the two elastomers. Bacterial adherence was not related to bacterial surface hydrophobicity, hemolysin or gelatinase production.

The in vitro activities of gemifloxacin, ciprofloxacin, ampicillin, doxycycline, gentamicin, and vancomycin were evaluated against 15 Listeria monocytogenes strains and 205 coryneform bacteria isolated from clinical samples. The percentages of strains inhibited by gemifloxacin at 0.5 g/ml were 100% (L. monocytogenes), 93.3% (Brevibacterium spp.), 90% (Corynebacterium minutissimum), 42.5% (Corynebacterium amycolatum), 20% (Corynebacterium striatum), 12.5% (Corynebacterium jeikeium), and 10% (Corynebacterium urealyticum). One hundred percent of the L. monocytogenes strains were inhibited by 0.25 g of gemifloxacin per ml, whereas 0% of the strains were inhibited by 0.25 g of ciprofloxacin per ml. Vancomycin at 2 g/ml inhibited all strains. Doxycycline and gentamicin at 4 g/ml inhibited 94 and 49% of the strains, respectively, while ampicillin at 0.5, 2, and 8 g/ml inhibited 24, 61, and 66% of the strains, respectively. It is concluded that gemifloxacin shows good in vitro activity against L. monocytogenes and coryneform bacteria except C. jeikeium and C. urealyticum.

The incidence of false positive RPR results in the HIV-infected population is significantly higher than that of the non-HIV-infected patients.