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A series of novel coumarinazoles were designed, synthesized, and characterized by IR, NMR, MS and HRMS spectra. The bioactive assay for the newly prepared compounds against six bacteria and five fungi manifested that most new compounds exhibited good or even stronger antibacterial and antifungal activities in comparison with reference drugs Chloromycin, Norfloxacin and Fluconazole. Bis-azole alcohols 7a and 7d-e showed better anti-Candida utilis activity than mono-azole derivatives 4a and 4d-e at the tested concentrations, and they were more potent than the clinical Fluconazole. While triazole alcohol 7a gave comparable anti-Candida albicans and anti-Candida mycoderma activity to Fluconazole and better anti-MRSA activity than mono-triazole one 4a and clinical Norfloxacin. 1H-Benzoimidazol-2-ylthio coumarin derivatives 4e and 7e gave the strongest anti-Escherichia coli JM109 efficacy. Oxiran-2-ylmethoxy moiety was found to be a beneficial fragment to improve antibacterial and antifungal activity to some extent.
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CD is both more effective and less costly than OFX for the treatment of acute otitis media in patients with tympanostomy tubes.
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Infections due to the yeast Rhodotorula are rare in humans. R. mucilaginosa is responsible for the majority of human cases, and immunocompromised individuals with central venous catheters are at greatest risk. There are few reports of bloodstream infections due to R. mucilaginosa in immunocompetent patients. We present a case report of fungemia due to R. mucilaginosa in an immunocompetent, critically ill patient, with good evolution with catheter removal and fluconazole therapy. We briefly review the spectrum of infections due to R. mucilaginosa and the management of bloodstream infections due to this yeast.
Voriconazole, a recently licensed extended-spectrum azole, with demonstrated efficacy against aspergillus, is currently being tested as a potential prophylactic agent against aspergillus and other invasive fungal infections. Logistic issues--such as patient selection, choice of comparator, blinding of study drugs, duration of study drug administration, and how to handle empirical amphotericin B for possible invasive fungal infections--and analytic concerns, including choice and definition of the primary end point and the potential confounding effect of informative censoring (as a result of noninfectious events), were considered in the design of the clinical trial.
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In this study, a simple, rapid and sensitive ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) method is described for determination of fluconazole (FLA) in human plasma samples using phenacetin as the internal standard (IS). Sample preparation was accomplished through one-step protein precipitation by methanol, and chromatographic separation was performed on an Acquity BEH C18 column (2.1 mm×50 mm, 1.7 μm) with mobile phase consisted of acetonitrile and water containing 0.1% formic acid (40:60, v/v) at a flow of 0.45 mL/min. Mass spectrometric analysis was performed using a QTrap 5500 mass spectrometer coupled with an electro-spray ionization (ESI) source in the positive ion mode. The MRM transition of m/z 307.2→238.2 was used to quantify for FLA. The linearity of this method was found to be within the concentration range of 10-6 000 ng/mL for FLA in human plasma. Only 1.0 min was needed for an analytical run. The method herein described was superior to previous methods and was successfully applied to the pharmacokinetic study of FLA in healthy Chinese volunteers after oral administration.
ITC and PCZ were moderately effective against S. brasiliensis (MIC90 = 2 and 2 μg/mL, respectively) and S. schenckii (MIC90 = 4 and 2 μg/mL, respectively). PCZ also showed low MICs against the rare species S. mexicana. 5FC, CAS, and FLC showed no antifungal activity against any Sporothrix species. The minimum fungicidal concentration ranged from 2 to >16 μg/mL for AMB against S. brasiliensis and S. schenckii, while the MFC90 was >16 μg/mL for ITC, VRC, and PCZ.
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The drugs were effective in 83% of patients: poor effect was in 28%, moderate--in 21% and good--in 34% of cases. 5 (17%) patients did not respond. Mild, moderate and severe AD responded in 87, 36 and 60% of patients, respectively. The highest response was registered in patients without sensitization to yeast fungi (78%) or low sensitization (83%). In high sensitization the effect occurred in 57% of the cases.
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Cases were defined as culture-confirmed invasive C. gattii infections among residents of Oregon and Washington States during 2004-2011. Clinical data were abstracted from medical records through one year of follow-up. Recommended initial treatment for central nervous system (CNS), bloodstream, and severe pulmonary infections is amphotericin B and 5-flucytosine; for non-severe pulmonary infections, recommended initial treatment is fluconazole. Alternative initial treatment was defined as any other initial antifungal treatment.
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The incidence of fungal and yeast infections, especially Candida and Aspergillus, as well as other newer fungal infections has increased considerably in recent years. Treatment failures are due to microbiological or clinical resistance, the latter being related to the drug, host factors, the fungus and the therapeutic procedures. An overview of efforts to find correlations between microbiological and clinical resistance is presented. The NCCLS M27-A consensus document for in vitro susceptibility testing of Candida and Cryptococcus is a good attempt at this, as is the M38-P for some filamentous fungi. The data available thus far indicate that there is a relationship between in vitro resistance and clinical failure, but not between in vitro susceptibility and therapeutic success. Furthermore, the breakpoints (MIC) that can be applied to the susceptibility tests are established based more on the resistance limits than on susceptibility. MIC data are also essential to obtain distribution profiles of MIC values for fungal populations and for future correlations of MICs with clinical response.
We report on a 39-year-old AIDS patient who presented a generalized cryptococcal disease with involvement of the lungs and central nervous system. Although the initial symptoms were mild and uncharacteristic, the radiological finding of cavernous destructions of the lungs (cryptococcoma) was detectable. The patient recovered after an initial 3 week therapy with amphotericin B and fluconazole followed by secondary prevention with fluconacole. The cavernous destructions receded within 4 months. Though the respiratory tract is the presumed port of entry for Cryptococcus neoformans, a cavernous destruction of pulmonary tissue without a diffuse infiltration of the lungs is a rare manifestation of cryptococcosis even in HIV patients.
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To describe the epidemiological profile and antifungal susceptibility patterns of fungal isolates in our unit, and to identify key risk factors associated with the development of IFI.
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Many issues need to be addressed by the Intensive Care Unit physician in the decision-making process regarding antifungal therapy for Candida infection, most importantly pharmacokinetic concerns and/or organ failure limitations. In addition, the extensive use of antifungal agents can select for Candida spp. that exhibit decreased susceptibility to these agents. However, the risk appears low, even in the case of prophylactic or pre-emptive antifungal therapy, but this needs to be confirmed in large-scale studies.
Biofilms are microbial communities, embedded in a polymeric matrix, growing attached to a surface. Nearly all device-associated infections involve growth in the biofilm life style. Biofilm communities have characteristic architecture and distinct phenotypic properties. The most clinically important phenotype involves extraordinary resistance to antimicrobial therapy, making biofilm infections very difficulty to cure without device removal. The current studies examine drug resistance in Candida albicans biofilms. Similar to previous reports, we observed marked fluconazole and amphotericin B resistance in a C. albicans biofilm both in vitro and in vivo. We identified biofilm-associated cell wall architectural changes and increased beta-1,3 glucan content in C. albicans cell walls from a biofilm compared to planktonic organisms. Elevated beta-1,3 glucan levels were also found in the surrounding biofilm milieu and as part of the matrix both from in vitro and in vivo biofilm models. We thus investigated the possible contribution of beta-glucans to antimicrobial resistance in Candida albicans biofilms. Initial studies examined the ability of cell wall and cell supernatant from biofilm and planktonic C. albicans to bind fluconazole. The cell walls from both environmental conditions bound fluconazole; however, four- to fivefold more compound was bound to the biofilm cell walls. Culture supernatant from the biofilm, but not planktonic cells, bound a measurable amount of this antifungal agent. We next investigated the effect of enzymatic modification of beta-1,3 glucans on biofilm cell viability and the susceptibility of biofilm cells to fluconazole and amphotericin B. We observed a dose-dependent killing of in vitro biofilm cells in the presence of three different beta-glucanase preparations. These same concentrations had no impact on planktonic cell viability. beta-1,3 Glucanase markedly enhanced the activity of both fluconazole and amphotericin B. These observations were corroborated with an in vivo biofilm model. Exogenous biofilm matrix and commercial beta-1,3 glucan reduced the activity of fluconazole against planktonic C. albicans in vitro. In sum, the current investigation identified glucan changes associated with C. albicans biofilm cells, demonstrated preferential binding of these biofilm cell components to antifungals, and showed a positive impact of the modification of biofilm beta-1,3 glucans on drug susceptibility. These results provide indirect evidence suggesting a role for glucans in biofilm resistance and present a strong rationale for further molecular dissection of this resistance mechanism to identify new drug targets to treat biofilm infections.
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11 of 26 investigators reported a total of 33 patients with substantial alopecia related to fluconazole therapy. Underlying mycoses included blastomycosis, sporotrichosis, histoplasmosis, cryptococcosis, coccidioidomycosis, and mucosal candidiasis. In separate MSG studies, 17 of 136 (12.5%) and 8 of 40 (20%) patients had substantial reversible alopecia associated with fluconazole therapy. Eight patients who were not in the protocol had similar adverse effects. Twenty-nine of 33 patients (88%) received at least 400 mg of fluconazole daily for a mean of 7.1 months. Alopecia developed a median of 3 months after initiation of fluconazole therapy and involved the scalp in all patients. Other sites were involved in about one third of patients. Three patients required wigs because of extensive hair loss. Alopecia resolved within 6 months of discontinuation of fluconazole therapy or reduction of the daily dose by at least 50%.
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Among all 140 cases positive for filamentous fungi in sputum culture, only 22 cases could be diagnosed as IPFI. Two of 22 IPFI cases were confirmed by post-operative pathology, 1 case was confirmed by positive blood culture for filamentous fungi and the remaining 19 cases were diagnosed clinically according to the nature of hosts, characteristics of pulmonary infections and microbiological evidence (positive sputum culture for filamentous fungi, 2 - 5 times for each case). Most of etiological fungi in IPFI patients belonged to Aspergillus. And the identity of isolated fungal strain was mostly one strain for each patient. In IPFI group, patients who had been treated with broad-spectrum antibiotics (100%), steroids (13, 59.1%) or immunosuppressant (7, 31.8%) or who had pulmonary X-ray imaging changes (100%), primary diseases (21, 95.5%), hypoalbuminemia (18, 81.8%) or hemoptysis (10, 45.5%), were significantly more than those in non-IPFI group (66.9%, 34.7%, 18.6%, 79.7%, 72.0%, 45.8% and 4.2% respectively; P < 0.05 for each item). In IPFI group, itraconazole, amphotericin B and/or voriconazole were administrated, 8 patients (36.4%) were cured and 14 patients (63.6%) passed away. In non-IPFI group, the patients were treated with antibiotics, fluconazole, anti-tuberculosis, steroids or combined with immunosuppressant, chemotherapy or bronchoalveolar lavage; 96 cases (81.4%) were cured or showed improvement, and 22 cases (18.6%) died or gave up further treatment.
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Pulmonary cryptococcosis typically occurs in immunocompromised patients, but it can also occur in immunocompetent patients. Our objective was to describe the clinical manifestations, diagnosis, and management of primary pulmonary cryptococcosis in immunocompetent patients.
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The antimycotic activity of fluconazole against the filamentous form of Pityrosporum ovale was studied in vitro. P. ovale was grown on human stratum corneum in vitro with and without the addition of different concentrations of fluconazole. In control cultures hyphae were produced in 25% of the cells compared to only 4% after exposure to fluconazole 1 microgram/ml. In control cultures 16% of the fungal cells showed signs of necrosis, due to the normal turnover rate of the cells, compared to 65% of the fungal cells exposed to 1 microgram/ml of fluconazole. In the transmission electron microscope the typical thick-walled fungal cells with their characteristic budding were observed in control cultures. However, after exposure to 1 microgram/ml of fluconazole that P. ovale cells showed extensive signs of necrosis, with loss of internal organelles and disinterruption of the cell wall. The results obtained in this in vitro model mimic the in vivo situation in pityriasis versicolor. There is a parallel between the good results obtained in this system and the good clinical effect of fluconazole in Pityrosporum-related diseases.
Using conventional PCR, 27 (84.4%) of the isolates were identified as C. neoformans var. grubii mating-type alpha and serotype A. Using the AFLP fingerprinting, it was shown that 16 (50%) of the C. neoformans strains were genotype AFLP1, 13 (40.6%) were genotype AFLP1B, 2 (6.3%) were genotype AFLP2, and 1 (3.1%) was found to be a hybrid between both C. neoformans varieties (genotype AFLP3). The antifungal susceptibility profiles for amphotericin B, fluconazole and voriconazole showed that all the 32 C. neoformans are sensitive to these antifungal compounds.