Raltegravir resistance in the cerebrospinal fluid.

We report the first published case of integrase inhibitor resistance in the central nervous system compartment in the absence of evidence of integrase inhibitor resistance in the plasma of a patient without human immunodeficiency virus (HIV)-encephalitis in the context of other HIV-associated central nervous system infections.

[Implication of ermX genes in macrolide- and telithromycin-resistance in Corynebacterium jeikeium and Corynebacterium amycolatum]. / Implicacion de los genes ermX en la resistencia a los macrolidos y la telitromicina de Corynebacterium jeikeium y Corynebacterium amycolatum.

The activity of seven macrolides, clindamycin and telithromycin against clinical isolates of Corynebacterium spp. was studied. Of these, 36 isolates were identified as C. jeikeium and 57 as C. amycolatum. The frequency of resistance to erythromycin and other macrolides as well as clindamycin was high, with CMI(90) >256 microg/ml. Telithromycin showed the best activity, with 52.3% of C. amycolatum and 70% of C. jeikeium erythromycin-resistant strains susceptible to this ketolide. All strains had the MLSb constitutive phenotype. The ermX gene was present in all erythromycin-resistant strains, and in C. amycolatum was 100% homologous with that of C. striatum and C. diphtheriae.

In vitro activity of newer antibiotics against Corynebacterium jeikeium, Corynebacterium amycolatum and Corynebacterium urealyticum.

The in vitro activity of ciprofloxacin, erythromycin, telithromycin, teicoplanin, linezolid and quinupristin-dalfopristin was tested against human derived pathogenic corynebacteria. The MICs of these antibiotics were measured using the agar dilution method against 31 strains of Corynebacterium jeikeium, 58 Corynebacterium amycolatum (including 33 multidrug-resistant strains) and 64 Corynebacterium urealyticum clinical strains. A high resistance rate to ciprofloxacin and erythromycin was found in the three species. Telithromycin was much more active than erythromycin (MIC(90) of erythromycin >or=128 mg/l for all three species; MIC(90) of telithromycin: 4 mg/l for C. jeikeium, 64 mg/l for C. amycolatum and 1 mg/l for C. urealyticum). There were no teicoplanin-resistant (MIC(90) 1, 0.5 and 1 mg/l, respectively) or linezolid-resistant strains (MIC(90) 1, 0.2 and 0.5 mg/l, respectively). Quinupristin-dalfopristin was active against most strains with an activity similar to linezolid, but three C. jeikeium and one C. amycolatum showed MICs >or=4 mg/l. Telithromycin showed much better activity against corynebacteria than older macrolides. Synercid and linezolid were active against most isolates tested, including multidrug resistant strains.

[Activity of new quinolones against clinical isolates of Corynebacterium species]. / Actividad de nuevas quinolonasfrente a aislamientos clínicosde Corynebacterium spp.

The activity of six quinolones (ciprofloxacin, levofloxacin, trovafloxacin, moxifloxacin, clinafloxacin and grepafloxacin) against 86 clinical isolates of Corynebacterium spp. obtained from different clinical sources was studied. Of these, 30 isolates were identified as C. jeikeium, 30 as C. urealyticum and 26 as C. amycolatum. C. amycolatum was the most resistant species, with 85.5% of the strains analyzed resistant to all the quinolones studied. Clinafloxacin showed the best activity against these species with a concentration range between <0.01 and 8 mg/l, and MIC50 and MIC90 64 and 32 times lower, respectively, than the MICs of ciprofloxacin. The majority of the isolates (90%) of C. jeikeium and C. urealyticum were susceptible to all the quinolones studied. Only 9.9% of the C. jeikeium strains and 13.2% of the C. urealyticum strains were resistant to ciprofloxacin, which showed the lowest activity of the antimicrobial agents evaluated. Clinafloxacin, grepafloxacin and moxifloxacin were the most active quinolones against these two multiresistant species.

[Hemorrhagic cystitis caused by BK and JC polyomavirus in patients treated with bone marrow transplantation: clinical features and urologic management]. / Cistitis hemorrágica por poliomavirus BK y JC en pacientes sometidos a transplante de médula ósea: aspectos clínicos y manejo urológico.

INTRODUCTION: Differential diagnosis of hematuria after bone marrow transplantation (B.M.T.) may include polyomavirus (BK and JC)-associated haemorrhagic cystitis. Many reports have implied BK virus as the major pathogen in the development of hemorrhagic cystitis after BMT. BK viruria is also associated with ureteric stenosis in renal allografts recipients. Viral urinary tract infections are uncommon in healthy individuals, but we can find them frequently in patients under immunosuppressive conditions. MATERIAL AND METHODS: Retrospective study of 123 consecutive B.M.T. recipients in the period from 1995 to 2000, evaluating those with polyomavirus-associated hemorrhagic cystitis. We present patient's characteristics, primary disease, clinical features, diagnosis aspects and treatment of these "hidden hosts of urinary tract". RESULTS: 7 patients (5.7% of B.M.T.) developed BK or JC virus-associated hemorrhagic cystitis; 3 men and 4 women; median patient age was 29 years (range 14 to 45 years). Bacterial, mycobacterial and parasitic urine cultivates had negative results in all of them. The clinical course was characterized by a late onset of haemorrhagic cystitis (days +30 to +132 after BMT). All 7 patients developed macroscopic haematuria (duration 3 to 30 days). In 6 cases Graft Versus Host Disease (G.V.H.D.) criteria were found. Ultrasonographic studies revealed diffuse thickening of bladder wall in 5 patients. Hematuria was managed by hyperhydratation, blood transfusions, transurethral catheter and evacuation of blood clots, continuous bladder irrigation, urine alkalinization and antiviral therapy. No other more aggressive measures were required to stop the bleeding. Only 1 case of transient elevated creatinine. CONCLUSIONS: Polyomavirus-associated haemorrhagic cystitis must be considered in differential diagnosis of hematuria in bone marrow transplantation recipients. Urological management, according with the severity and duration of hematuria, is frequently required.

Molecular diversity of quinolone resistance in genetically related clinical isolates of Staphylococcus aureus and susceptibility to newer quinolones.

The genes encoding topoisomerases (gyrA and grlA) and the norA promoter of 100 fluoroquinolone-susceptible and -resistant Staphylococcus aureus clinical isolates obtained in two geographically distant hospitals were analysed. The relationship between mutations found and the susceptibility to newer quinolones was determined. Thirty-nine strains were grouped in seven clones by pulsed-field gel electrophoresis (PFGE). The remaining 61 strains were classified as unrelated strains. In three clones, all strains showed the same grlA-gyrA-norA mutation profiles. Strains in the rest of the groups showed different mutation profiles, even though PFGE indicated that they possessed genetically similar populations. One cluster showed a high level of diversity; five different mutation profiles were detected in the six isolates belonging to this pattern. Two isolates had a Glu84 to Lys mutation in grlA and another isolate had this mutation combined with a Ser84 to Leu mutation in gyrA. Combination of a Ser80 to Phe mutation in grlA and a Ser84 to Leu in gyrA was found in the two other isolates. One of these also had a thymine to a guanine transversion at a position 89 nucleotides upstream of the norA start codon in the norA promoter. These results show that fluoroquinolone resistance in clinical S. aureus strains does not necessarily result from the spread of resistant clones. Fluoroquinolone resistance may develop independently in strains belonging to the same PFGE pattern by accumulation of different mutations over a quinolone-susceptible ancestor wild type or single grlA mutant.