Neisseria gonorrhoeae infections have been empirically treated in Hong Kong with a single oral 400-mg dose of ceftibuten since 1997. Following anecdotal reports of the treatment failure of gonorrhea with oral extended-spectrum cephalosporins, the current study was undertaken to determine the antimicrobial susceptibility pattern and molecular characteristics of isolates of N. gonorrhoeae among patients with putative treatment failure in a sexually transmitted disease clinic setting. Between October 2006 and August 2007, 44 isolates of N. gonorrhoeae were studied from patients identified clinically to have treatment failure with empirical ceftibuten. The ceftibuten MICs for three strains were found to have been 8 mg/liter. These strains were determined by N. gonorrhoeae multiantigen sequence typing to belong to sequence type 835 (ST835) or the closely related ST2469. The testing of an additional eight archived ST835 strains revealed similarly elevated ceftibuten MICs. The penA gene sequences of these 11 isolates all had the mosaic pattern previously described as pattern X. Of note is that the ceftriaxone susceptibility results of these strains all fell within the susceptible range. It is concluded that ceftibuten resistance may contribute to the empirical treatment failure of gonorrhea caused by strains harboring the mosaic penA gene, which confers reduced susceptibility to oral extended-spectrum cephalosporins. Screening for such resistance in the routine clinical laboratory may be undertaken by the disk diffusion test. The continued monitoring of antimicrobial resistance and molecular characteristics of N. gonorrhoeae isolates is important to ensure that control and prevention strategies remain effective.
Our results are demonstrated in Table 1. E. coli, S. marcescens and Enterobacter spp. isolates were inhibited at MIC values of 1, 2 and 2 mg/L, respectively. For K. pneumoniae, MIC 50 and MIC 90 values of tigecycline were 0.25 and 2 mg/L, respectively. The Etest results were confirmed by the broth microdilution method. According to US Food and Drug Administration recommendation for tigecycline (susceptible 2 mg/L and resistant 8 mg/L), all isolates were susceptible and only one (1%) K. pneumoniae strain displayed an intermediate MIC of 4 mg/L. When the European Committee on Antimicrobial Susceptibility Testing breakpoint criteria (susceptible 1 mg/L and resistant .2 mg/L) were used, the percentage of tigecycline susceptibility decreased. Only 4 (31%) Enterobacter spp. and 78 (89%) K. pneumoniae isolates tested were susceptible. Furthermore, all S. marcescens were characterized as intermediate. 1,2 The isolates collected in this study were broadly resistant to b-lactams, fluoroquinolones and variably to aminoglycosides. Currently, multidrug-resistant Gram-negative bacteria remain the most problematic pathogens worldwide, especially in intensive care units. Carbapenem antibiotics were important agents for the management of those infections. Over the past few years, the progressive increase in carbapenem-resistant Gram-negative non-fermentative bacilli as well as the spread of genes encoding carbapenem-hydrolysing enzymes in enterobacterial species is of great concern, leaving limited choices for therapeutic regimens. 5 Tigecycline was active against MBL-producing members of the family Enterobacteriaceae, inhibiting 99% of them at a concentration of 2 mg/L. A recent study demonstrated that tigecycline was effective against multiresistant K. pneumoniae strains producing Klebsiella pneumoniae carbapenemase (KPC), an ESBL belonging to molecular class A enzymes with activity against carbapenems. 6 In addition, it was active against clinical isolates possessing bla VIM , but the number of MBL producers tested was small. 3 Our results confirm the in vitro activity of tigecycline against Enterobacteriaceae possessing carbapenemases. Its broad-spectrum activity combined with its stability against common resistance mechanisms and the lack of crossresistance with other classes of antibiotics 1,2 make tigecycline a therapeutic agent for the treatment of infection caused by multiresistant microorganisms. However, the in vitro results require support from clinical studies.
In an attempt to assess the level of quinolone resistance and its association with other antimicrobial resistance in faecal Escherichia coli isolated from routine outpatient specimens in Hong Kong, ciprofloxacin-supplemented MacConkey agar was used to screen for resistant isolates. Antimicrobial susceptibility testing of the isolates was done by VITEK 2 and previous amplification-based methods were employed to characterize the genetic determinants behind some of the resistance phenotypes. One hundred and seventy-six (43%) of 409 specimens had quinolone-resistant E. coli isolated (199 isolates). Quinolone resistance was found to be associated with resistances to penicillins (>80%) and co-trimoxazole (69%). Nonsusceptibility to combinations of penicillins and clavulanic acid was above 20% and up to 50% for the aminoglycosides gentamicin and tobramycin. CTX-M-type extended-spectrum β-lactamases were found responsible for most cephalosporin resistances but the transferable quinolone resistance determinant qnrA was not detected. Our data suggested that a high percentage of E. coli isolates as part of the alleged normal intestinal microflora in humans appeared to be resistant to quinolones. Co-resistance to various other frequently used antimicrobials was also observed. Transferable genetic determinants were found to be involved in some cases.
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