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Susceptibility to garenoxacin, levofloxacin, moxifloxacin, cefoxitin and faropenem +/- EPIs (CCCP, MC-207,110, reserpine and verapamil) was determined. Expression of bmeB efflux pumps was measured, topoisomerase genes were sequenced and beta-lactamase production was determined.
Reactivation of human polyomavirus BK (BKV) may cause polyomavirus-associated nephropathy or polyomavirus-associated hemorrhagic cystitis in renal- or bone marrow-transplant patients, respectively. Lack of treatment options has led to exploration of fluoroquinolones that inhibit topoisomerase II and IV in prokaryotes and possibly large T-antigen (LT-ag) helicase activity in polyomavirus. We characterized the effects of ofloxacin and levofloxacin on BKV replication in the natural host cells - primary human renal proximal tubular epithelial cells (RPTECs). Ofloxacin and levofloxacin inhibited BKV load in a dose-dependent manner yielding a ∼90% inhibition at 150 μg/ml. Ofloxacin at 150 μg/ml inhibited LT-ag mRNA and protein expression from 24h post infection (hpi). BKV genome replication was 77% reduced at 48 hpi and a similar reduction was found in VP1 and agnoprotein expression. At 72 hpi, the reduction in genome replication and protein expression was less pronounced. A dose-dependent cytostatic effect was noted. In infected cells, 150 μg/ml ofloxacin led to a 26% and 6% inhibition of cellular DNA replication and total metabolic activity, respectively while 150 μg/ml levofloxacin affected this slightly more, particularly in uninfected cells. Cell counting and xCELLigence results revealed that cell numbers were not reduced. In conclusion, ofloxacin and levofloxacin inhibit but do not eradicate BKV replication in RPTECs. At a concentration of ofloxacin giving ∼90% inhibition in BKV load, no significant cytotoxicity was observed. This concentration can be achieved in urine and possibly in the kidneys. Our results support a mechanism involving inhibition of LT-ag expression or functions but also suggest inhibition of cellular enzymes.
This study from 2005 to 2009 showed that the levofloxacin resistance rates of E. coli were high at over 25%. The risk factors that affected the levofloxacin resistance rates of E. coli were underlying neurogenic bladder, ciprofloxacin administration history, urolithiasis, levofloxacin administration history, and older age. Levofloxacin should be prescribed cautiously in patients with these risk factors until the pathogen is identified.
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M-MTT could be used as a simple, rapid, low-cost technology to test the susceptibility of MDR-TB strains to several second-line and alternative drugs, with the objective of orienting future treatment regimens.
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A prospective pharmacokinetic study was performed in Caucasian patients from an intensive care unit with respiratory support to evaluate the influence of this circumstance on the pharmacokinetic behaviour of levofloxacin.
The l-isomer of ofloxacin (levofloxacin) was twice as active as ofloxacin and the d-isomer was inactive against 654 Streptococcus pneumoniae isolates. For disc susceptibility tests of pneumococci, 5 micrograms levofloxacin discs can be used with interpretive criteria of < or = 12 mm for resistant (MIC > or = 8.0 mg/L) and > or = 16 mm for susceptible (MIC < or = 2.0 mg/L). For quality control of levofloxacin tests, S. pneumoniae ATCC 49619 should give zones 20-25 mm in diameter and MICs 0.5-2.0 mg/L.
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Antibiotic resistance in Streptococcus pneumoniae has become an important issue in the last years. Penicillin resistance rates vary among countries and among different regions in countries. It is important to know penicillin resistance rates among isolates, in planning empirical antimicrobial therapy in pneumococcal infections. In this study, the antibiotic resistance rates of S. pneumoniae strains isolated from sterile body sites were investigated with both E-test and disc diffusion methods for penicillin, erythromycin, levofloxacin, and with only disc diffusion method for chloramphenicol, ceftriaxone, vancomycin, rifampin, trimethoprim-sulfamethoxazole (TMP-SMX), clindamycin, and tetracycline. A total of 165 strains were included into the study of which 52 were isolated from blood, 46 from cerebrospinal fluids, 25 from pleural fluids, 24 from dacryocystitis materials, 13 from tympanocentesis materials, 3 from joint fluids and 2 from wound specimens. Intermediate resistance to penicilin was 18.8%, while the resistance rates to TMP-SMX, tetracycline, chloramphenicol, erythromycin and levofloxacin were detected as 21.2%, 10.9%, 9.7%, 5.4% and 0.6%, respectively. None of the isolates were highly resistant to penicillin, nor resistant to vancomycin, ceftriaxone and rifampin. In conclusion, penicillin is still the first line therapeutic agent for pneumococcal infections except for severe infections such as meningitis, in our region.
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Escherichia coli was the most commonly isolated pathogen in the Canadian Ward Surveillance Study 2007-2009 (3789 isolates). Susceptibility to cefazolin (34.1%), trimethoprim-sulfamethoxazole (73.8%), ciprofloxacin (78.4%), and levofloxacin (78.8%) was lowest. Susceptibility was above 90% for meropenem (100%), tigecycline (99.9%), piperacillin-tazobactam (97.6%), nitrofurantoin (96.9%), ceftazidime (95.6%), amoxicillin-clavulanate (94.9%), ceftriaxone (94.1%), cefoxitin (92.3%), and gentamicin (90.8%). Over the study period, there was a significant reduction in susceptibility to amoxicillin-clavulanate and trimethoprim-sulfamethoxazole for urinary tract isolates. Inpatient status was associated with greater resistance to nearly all antimicrobials including greater multidrug resistance (MDR). Increasing age was associated with resistance to fluoroquinolones, ceftriaxone, piperacillin-tazobactam, and MDR. Female gender was associated with susceptibility to fluoroquinolones and nitrofurantoin. In conclusion, greater antimicrobial resistance and MDR in E. coli were observed in inpatients, males, and with increasing age. The deterioration of susceptibility to trimethoprim-sulfamethoxazole continues with the greatest reduction in urinary isolates. Significant regional differences in resistance rates were apparent.
Patients initiated on etanercept should be counseled and receive appropriate screening before drug initiation. All febrile and newly occurring concomitant illnesses should be promptly evaluated. General practitioners should discontinue etanercept treatment and institute prompt and aggressive intervention if infection develops.
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The overall colonization rate was 49.2% and it was considerably higher among children in the day care center. Pneumococcal carriage was more common among day care attenders and cohabitants with young siblings. The most prevalent serotypes were 6B, 19F, 6A, 14, 15C and 23F, which accounted for 61.2% of the isolates. All isolates were susceptible to clindamycin, levofloxacin, rifampicin and vancomycin. The highest rate of non-susceptibility was observed for sulphamethoxazole-trimethoprim (51.2%). Penicillin non-susceptible pneumococci (PNSP) accounted for 27.3% of the isolates (MICs of 0.12-4 μg/ml). Penicillin non-susceptibility was strongly associated with serotypes 14 and 23F. Hospital attendance and the presence of respiratory or general symptoms were frequently associated with PNSP carriage. The two erythromycin-resistant isolates (MICs of 2 and 4 μg/ml) belonged to serotype 6A, presented the M phenotype and harbored the mef(A/E) gene.
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The eradication rate was 83.33% (60/72) in group A, 88.89% (64/72) in group B, and 80.56% (58/71) in group C. The ulcer cicatrisation rate was 86.44% (51/59) in group A, 90.16% (55/61) in group B, and 84.91% (45/53) in group C. The sequential therapy yielded a higher eradication rate and ulcer cicatrisation rate than the standard triple and bismuth pectin quadruple therapies. Statistically, the eradication rate of group B was significantly different from groups A and C (P < 0.05), but the difference of ulcer cicatrisation rate and side effects was not statistically significant among the three groups (P > 0.05). The three protocols were generally well tolerated.