Abstract Geographic differences in frequency and azole resistance among Candida glabrata may impact empiric antifungal therapy choice. We examined geographic variation in isolation and azole ...susceptibility of C. glabrata . We examined 23 305 clinical isolates of C. glabrata during ARTEMIS DISK global surveillance. Susceptibility testing to fluconazole and voriconazole was assessed by disk diffusion, and the results were grouped by geographic location: North America (NA) (2470 isolates), Latin America (LA) (2039), Europe (EU) (12 439), Africa and the Middle East (AME) (728), and Asia-Pacific (AP) (5629). Overall, C. glabrata accounted for 11.6% of 201 653 isolates of Candida and varied as a proportion of all Candida isolated from 7.4% in LA to 21.1% in NA. Decreased susceptibility (S) to fluconazole was observed in all geographic regions and ranged from 62.8% in AME to 76.7% in LA. Variation in fluconazole susceptibility was observed within each region: AP (range, 50–100% S), AME (48–86.9%), EU (44.8–88%), LA (43–92%), and NA (74.5–91.6%). Voriconazole was more active than fluconazole (range, 82.3–84.2% S) with similar regional variation. Among 22 sentinel sites participating in ARTEMIS from 2001 through 2007 (84 140 total isolates, 8163 C. glabrata ), the frequency of C. glabrata isolation increased in 14 sites and the frequency of fluconazole resistance (R) increased in 11 sites over the 7-year period of study. The sites with the highest cumulative rates of fluconazole R were in Poland (22% R), the Czech Republic (27% R), Venezuela (27% R), and Greece (33% R). C. glabrata was most often isolated from blood, normally sterile body fluids and urine. There is substantial geographic and institutional variation in both frequency of isolation and azole resistance among C. glabrata . Prompt species identification and fluconazole susceptibility testing are necessary to optimize therapy for invasive candidiasis.
The aim of this study was to test the antifungal susceptibility of 262 bloodstream yeast isolates (164 Candida albicans strain, 88 non-albicans Candida spp. and 10 non-Candida yeasts) recovered from ...169 surgical, neonatal, critically ill intensive care unit patients (ICU), and cancer patients (mixed patient population) to amphotericin B (AmB), fluconazole (FLU), 5-flucytosine (5-FC), itraconazole (ITRA), ketoconazole (KETO), miconazole (MICO), and nystatin (NYS), in order to correlate in-vitro resistance to fluconazole with the outcome of fungemia. The agar disk diffusion test was used to assess the susceptibility of the 262 bloodstream yeasts isolates. In addition, 78 strains isolated from cancer patients were also tested with the E-test. There were no differences in the susceptibility of the various C. albicans strains tested, except in 40 isolates from surgery patients, which showed a somewhat lower susceptibility to KETO and MICO to (3.7–5.5% resistance). There were no C. albicans strains resistant to AmB, NYS, or FLU. There were slight differences in the susceptibility patterns of the 88 non-albicans Candida spp. (NAC) isolates. Resistance to AmB and NYS appeared in 1 strain of C. guillermondii (minimum inhibitory concentration; MIC to AmB; 4μg/ml) and in 1 strain of C. parapsilosis (MIC to NYS, 8μg/ml and MIC to AmB, 2μg/ml). All other NACs were susceptible to both polyenes (AmB and NYS). Nine of the 11 strains of C. krusei were resistant to FLU (MIC ≥ 64μg/ml), the 2 exceptions showed, respectively, MICs for FLU of 6 and 32μg/ml ("dose-dependent" susceptibility). However, only 2 of 29 C. glabrata strains were fully FLU-resistant (MIC ≥ 64μg/ml), 27 being susceptible with MIC values of 0.5–8μg/ml. Apart from 9 C. krusei and 2 C. glabrata strains, 2 C. parapsilosis strains and 1 strain of C. tropicalis were also FLU-resistant. Among the 88 NACs, 17.04% were FLU-resistant and 3.7% were KETO- and ITRA-resistant. Resistance to 5-FC and AmB was minimal. We compared the outcomes of patients infected with FLU-resistant vs FLU-susceptible yeasts in 161 evaluable patients treated with FLU. Attributable mortality was significantly higher (19.0% vs 8.6%; P<0.01) in patients infected with the FLU-resistant yeasts.
The aim of this study was to retrospectively compare the incidence, risk factors, and outcome in patients seen over a 7-year period at the National Cancer Institute in the Slovak Republic, with ...vancomycin-sensitive or vancomycin-resistant enterococcal bacteremia. The total incidence of enterococcal bacteremia at the National Cancer Institute increased from 5.1% in 1991 to 11.1% in 1993 and then decreased to 4.3% in 1995. Analysis of the 77 episodes of enterococcal bacteremia from 66 patients showed that 69 episodes from 60 patients were due to vancomycin-sensitive Enterococcus faecalis (group 1) and 8 episodes from 8 patients were due to vancomycin-resistant Enterococcus faecium (group 2). The features most frequently associated with enterococcal bacteremia were the insertion of a central venous catheter, neutropenia lasting more than 10 days, previous therapy with cephalosporins or vancomycin, previous prophylaxis with quinolones, and the incidence of superinfections. There was no difference in the clinical course or outcome between the 2 study groups. Previous therapy with aminoglycosides, cephalosporins, vancomycin or imipenem, neutropenia less than 10 days in length, malignancies other than leukemia or solid tumors, and the incidence of breakthrough bacteremia significantly correlated with patients with vancomycin-resistant E. faecium rather than patients with vancomycin-sensitive E. faecalis. The overall mortality was similar in both groups and averaged 32.5% for all enterococcal bacteremic patients. In this study, the major risk factors associated with cancer patients for developing vancomycin-resistant enterococcal bacteremia were previous therapy with aminoglycosides, cephalosporins or vancomycin, superinfections with other organisms and the incidence of breakthrough bacteremia.
Objectives: The aims of this study were to evaluate risk factors, clinical presentation, outcome and antimicrobial susceptibility in patients with
Escherichia coli bacteremia occurring over seven ...years in a single cancer hospital.
Methods: Sixty five episodes of bacteremia from
E. coli appearing over seven years from 12,301 admissions in a single cancer institution were retrospectively analyzed.
Results: The proportion of bacteremia caused by
E. coli among Gram-negative bacteremia was 20.8% (the second most common organism after
Pseudomonas aeruginosa), and infection-associated mortality was 17%.The incidence in 1989–1995 varied from 14.3 to 24.7%. The most common risk factors were: solid tumors as the underlying disease (70.7%); central venous catheter insertion (32.3%); prior surgery (46.2%), and prior chemotherapy within 48 h (44.4%). Neutropenia and urinary catheters did not place patients at high risk in any of the subgroups. When we compared the two subgroups of 61 cases of bacteremia — monomicrobial and polymicrobial (when
E. coli was isolated from blood culture with another microorganism) — we found that acute leukemia and breakthrough (recurrence while receiving antibiotics) bacteremia were more frequently associated with polymicrobial
E. coli bacteremia. There was also a difference in infection-associated mortality: monomicrobial bacteremia due to
E. coli only had a significantly lower mortality in comparison with polymicrobial
E. coli bacteremia (8.9 vs 35.0%, respectively; P<0.03).
Conclusion: The susceptibility of 115
E. coli strains isolated from 65 episodes of bacteremia was stable. Only two episodes caused by quinolone-resistant strains occurred, both in 1995, after six years of using ofloxacin for prophylaxis in neutropenic patients in our hospital. We found that 85.2–91.3% of all strains were susceptible to aminoglycosides, 97.8% to quinolones, and 90–100% to third generation cephalosporins and imipenems.The patients most commonly infected had solid tumors and the mortality was only 17%.
Twelve cases of Trichosporon spp. fungemias occurring in a national cancer institution within 10 years are described. The trend of hematogenous trichosporonosis within the last 10 years is ...increasing. While no cases occurred in 1988-1991, after 1991, Trichosporon spp. was the most common species among non-Candida spp. fungemias in 1993-1997. The 12 cases of fungemia included 5 that started while the patients were receiving prophylaxis with oral itraconazole, and 2 appeared despite empiric therapy with amphotericin B. Five of the 12 fungemias were catheter associated. Risk factors for fungemia were: central venous catheter, broad-spectrum antibiotics (third-generation cephalosporins plus aminoglycoside); all but 1 had neutropenia and were receiving antineoplastic chemotherapy. All but 2 of the patients died of systemic fungal infection (83.3% mortality). Amphotericin B was administered to all but 1 patient, who was not treated because he died the day after his culture was found to be positive for T. beigelii, before antifungals were administered. All cases infected with T. pullulans were catheter related, and all these patients died. One of the remaining 9 fungemias was caused by T. capitatum (Blastoschizomyces capitatus), and 8 by T. beigelii. Only 2 patients were cured, 1 with a combination therapy with amphotericin B plus fluconazole, and 1 with amphotericin B monotherapy. Several risk factors (neutropenia, acute leukemia, prior therapy or prophylaxis with antifungals and catheter as source of fungemia, breakthrough fungemia) were significantly associated with Trichosporon spp. fungemia, in comparison to 63 C. albicans candidemia occurring in the same period at the same institution. Attributable mortality of hematogenous trichosporonosis was also significantly higher (83.3% vs. 15.8%, P<0.001) than that of hematogenous candidiasis.
Lymphadenitis with persisting fistulas in children is almost always conditioned by specific inflammation, tuberculosis, zoonoses, actinomycoses. Tuberculosis of the lymph nodes can either be primary ...or post-primary. In this case report we have dealt with a case of a rare primary lymph node tuberculosis that arose as a result of vaccination complications. Disturbance of cellular immunity was the reason for BCG lymphadenitis. In references, the reasons for BCG-itis as well as vaccination contra-indications have been described.
60 patients with 60 viridans streptococcal bacteraemic episodes (42 due to penicillin-sensitive and 18 due to penicillin-resistant viridans streptococci) were analysed in a population of 12,185 ...admissions and 1,380 bacteraemic episodes during a 7-year period in a National Cancer Institute. The incidence of viridans streptococci among bacteraemias decreased from 11.5% in 1989 to 2.5% in 1995 after penicillin was introduced for prophylaxis of febrile neutropenia in acute leukaemia in 1993. However, the proportion of penicillin-resistant viridans streptococcal bacteraemias increased from 0 in 1989 and 1990 before any prophylaxis was given, to 12.9-16.7% after quinolones were used for prophylaxis in 1991 and 1992, and to 44.4-81.8% in 1993-1995 after penicillin was added to the quinolones. Mortality rate was higher in the subgroup of penicillin-resistant viridans streptococcal bacteraemias (p < 0.05). Statistically significant risk factors in patients with penicillin-resistant (compared with penicillin-sensitive) viridans streptococcal bacteraemia were: acute leukaemia (p < 0.03), high doses of cytarabine (p < 0.05), mucocutaneous lesions (p < 0.004), breakthrough bacteraemia during prophylaxis with ofloxacine plus penicillin (p < 0.001). Multiple logistic regression analysis showed that only acute leukaemia (OR 2.05, CI 0.85-1.85, p < 0.0452) and penicillin-resistance (OR 0.71, CI 0.103-4.887, p < 0.0209) were significant independent predictors of inferior outcome. Breakthrough bacteraemia during empiric therapy with vancomycine occurred in 5 of 116 patients treated with vancomycine, and during therapy with ampicillin plus gentamicin in 6 patients of 18 treated.
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