We have previously reported that the Neisseria gonorrhoeae isolates from clinical failure cases treated with cefdinir and aztreonam, -lactams exhibited high MICs. These resistant isolates were clearly separated from the isolates exhibiting a low level of resistance to -lactams as shown by the MIC distribution of cefozopran. Restriction fragment length polymorphism DNA typing revealed that the outbreak of cefozopran-resistant isolates in Kitakyushu, Japan, occurred as a result of clonal spread.As a result of the absence of strains of Neisseria gonorrhoeae resistant to the expanded spectrum of cephems, the National Committee for Clinical Laboratory Standards (NCCLS) (8) has not defined the breakpoint MICs of expanded-spectrum cephems such as cefixime (CFM), cefpodoxime (CPD), cefepime (FEP), etc. A previous study reported the incidence of clinical failures in gonococcal urethritis treated with cefdinir (CDR) or aztreonam (ATM) (1). For the N. gonorrhoeae isolates from such clinical failure cases, high-level MICs of CDR, ATM, and other -lactams were observed. In order to investigate the prevalence of these resistant isolates in Kitakyushu, Japan, we examined 54 N. gonorrhoeae isolates from different cases occurring during 1999 for susceptibility to a variety of antimicrobial agents. Forty of 54 strains were isolated from male patients with gonococcal urethritis, while the remaining isolates were from female patients with gonococcal cervicitis. Identification of N. gonorrhoeae and testing for production of -lactamase were performed by ID-test-HN-20 Rapid (Nissui Pharmaceutical Co., Ltd., Tokyo, Japan) using colonies cultured on Thayer-Martin Agar Base, Modified (Nissui Pharmaceutical Co.). The MICs of various antimicrobials were determined by the twofold serial agar dilution method on BBL GC Agar Base (Becton Dickinson and Co., Cockeysville, Md) with 1% BBL IsoVitalX enrichment (Becton Dickinson Europe, Meylan, France) according to the guidelines of the NCCLS (8). The antimicrobial agents used in this study were purchased from or provided by the corresponding companies.The MIC distribution of cefozopran (CZO) for N. gonorrhoeae isolates was divided into two groups. The MICs for the high-level resistance group (8 to 16 g/ml) were more than 16 times greater than the MICs for the susceptible and low-level resistance groups (Ͻ0.5 g/ml). The MICs of CZO were correlated with those of CDR, CPD, cefpirome (CPI), FEP, ATM, cefuroxime, cefotiam, ceftizoxime (ZOX), CFM, and cefcapene (CPN). The MICs of CZO correlated poorly with those of penicillin (PEN), cefmetazole, flomoxef, and cefodizime (CDZ) despite the fact that all 17 CZO-resistant isolates for these four agents belonged to the high-level MIC group. CFM, CDZ and ceftriaxone (CRO) exhibited lower MICs but the resistant isolates belonged to the group with reduced susceptibility to these three agents. These new resistant strains were clearly divided into two groups by the MIC distribution of CZO, with all of the CZO-resistant isolates exhibiting either resistance or ...
We found ampicillin-and imipenem-resistant isolates of vanA-possessing Enterococcus faecalis with MICs of 8 to 16 g/ml and 4 to 32 g/ml, respectively. There have been few reports about penicillin-and imipenemresistant E. faecalis. Two mechanisms of beta-lactam resistance in E. faecalis, the production of beta-lactamase and the overproduction of penicillin-binding proteins (PBPs), have been reported. The resistant isolates in the current study did not produce any beta-lactamases and analysis of the PBPs showed no overproduction. However, the affinities of PBP4 for beta-lactams in the resistant strains were lower than those of susceptible strains but the affinities of other PBPs for beta-lactams did not change. Accordingly, whole pbp4 fragments from these resistant isolates were sequenced. Two amino acid substitutions at positions 520 and 605 were observed in the highly resistant strains compared to the susceptible ones, Pro520Ser and Tyr605His, and a single Tyr605His amino acid substitution was found in the low-resistance strains. These two point mutations exist in the region between the active-site-defining motifs SDN and KTG of the penicillin-binding domain, the main target of beta-lactams. A strong correlation was seen between these substitutions and decreasing affinities of PBP4 to beta-lactams. In E. faecalis, resistance due to mutations in PBPs has not been reported, though it has in Enterococcus faecium. Our results suggest that development of high-level resistance to penicillins and imipenem depends on point mutations of PBP4 at positions 520 and 605.
This study was conducted by the Japanese Society of Chemotherapy and is the first nationwide study on bacterial pathogens isolated from patients with urinary tract infections at 28 hospitals throughout Japan between January 2008 and June 2008. A total of 688 bacterial strains were isolated from adult patients with urinary tract infections. The strains investigated in this study are as follows: Enterococcus faecalis (n = 140), Escherichia coli (n = 255), Klebsiella pneumoniae (n = 93), Proteus mirabilis (n = 42), Serratia marcescens (n = 44), and Pseudomonas aeruginosa (n = 114). The minimum inhibitory concentrations of 39 antibacterial agents used for these strains were determined according to the Clinical and Laboratory Standards Institute (CLSI) manual. All Enterococcus faecalis strains were susceptible to ampicillin and vancomycin. Although a majority of the E. faecalis strains were susceptible to linezolid, 11 strains (7.8%) were found to be intermediately resistant. The proportions of fluoroquinolone-resistant Enterococcus faecalis, Escherichia coli, Proteus mirabilis, and S. marcescens strains were 35.7%, 29.3%, 18.3%, and 15.2%, respectively. The proportions of E. coli, P. mirabilis, K. pneumoniae, and S. marcescens strains producing extended-spectrum β-lactamase were 5.1%, 11.9%, 0%, and 0%, respectively. The proportions of Pseudomonas aeruginosa strains resistant to carbapenems, aminoglycosides, and fluoroquinolones were 9.2%, 4.4%, and 34.8%, respectively, and among them, 2 strains (1.8%) were found to be multidrug resistant. These data present important information for the proper treatment of urinary tract infections and will serve as a useful reference for periodic surveillance studies in the future.
A prospective, randomized trial in which 236 patients received oral levofloxacin, either at 600 mg/day for 1 day (n = 124) or 300 mg/day for 3 days (n = 112). Urinalysis, plasma white blood cell count (WBC) (per mm3), and C reactive protein (CRP) (mg/dl) levels were checked before prostate biopsy (PBX), on the day after PBX, and on the seventh day after PBX. Two patients (1.61%) who received 600 mg for 1 day and 2 patients (1.79%) who received 300 mg for 3 days had febrile infectious complications. There was no statistically significant difference between levofloxacin at 600 mg for 1 day and levofloxacin at 300 mg for 3 days regarding the elevation of WBC and CRP. We can perform PBX safely with levofloxacin at 600 mg for 1 day as prophylaxis and recommend this method from the point of view of the decrease of antibiotic-resistant strains.
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