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We identified 131 patients, with a median age of 41.2 years. Isolates were most frequently found in the intensive care unit (ICU). Candida albicans was the most prevalent species (66.4% of the isolates), followed by C. parapsilosis (14%). Fluconazole resistance was found in 3.2% and 17.6% of the isolates according to the 2008 and 2012 breakpoints, respectively. Fluconazole was used as empirical antifungal therapy in 68.8% of the cases, and amphotericin B in 22%. Hospital crude mortality rate was 35.9%. Mortality was associated with age and the presence of shock at the time of Candida detection. Fluconazole therapy was a protective factor for mortality.
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Candida parapsilosis was recently reclassified into 3 closely related species, C. parapsilosis sensu stricto, Candida orthopsilosis, and Candida metapsilosis. Variation in susceptibility characteristics and prevalence of the 3 genomic species could have therapeutic and epidemiologic implications. The aim of this study is to characterize the genetic and antifungal susceptibility profiles of 97 C. parapsilosis isolates from 71 patients. Among the 71 nonduplicate isolates, 85.9% (61/71) were identified as C. parapsilosis sensu stricto, 5.6% (4/71) as C. metapsilosis, and 8.5% (6/71) as C. orthopsilosis species based on sequences of the internal transcribed spacer (ITS) region. The delineation of these 3 species is concordant with that achieved by pulsed-field gel electrophoresis of BssHII restriction fragments at 75% similarity. Antifungal susceptibility tests showed that most isolates were susceptible to flucytosine, azoles, amphotericin B, and echinocandins, whereas 3 C. metapsilosis isolates from 1 patient showed resistance and susceptible-dose dependence to fluconazole. The C. metapsilosis isolates exhibited significantly higher MIC values to both fluconazole and voriconazole than those of C. parapsilosis sensu stricto and C. orthopsilosis. On the other hand, the C. metapsilosis isolates showed significantly lower MIC values on 24 h to caspofungin than those of C. parapsilosis sensu stricto and C. orthopsilosis. For micafungin, the isolates of C. parapsilosis sensu stricto had significantly higher MIC values on 24 h than those of C. orthopsilosis and C. metapsilosis. Compared to Candida albicans, mutations from proline to alanine were identified on the hot spot 1 of Fks1 in all these C. parapsilosis sensu lato isolates regardless of their MIC levels. Some of the C. orthopsilosis and C. metapsilosis isolates expressed the isoleucine to valine substitution on the hot spot 2 region. However, the amino acid variations in these isolates did not correlate to their MIC values of echinocandin.
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Forty-three pediatric patients with candidemia,
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Onychomycosis is an infection of the finger-and/or toenails by fungal microorganisms. If untreated, the process advances and destroys the nail plate. It may spread to involve the skin and does not heal spontaneously. There are different clinical presentations of onychomycosis which vary with the nature of the fungus and how it invades the nail unit. These different clinical forms require different therapeutic approaches. The successful treatment of onychomycosis requires special knowledge of the various clinical presentations, of the differential diagnosis and of recent advances in medical mycology. Therefore onychomycosis is best treated by dermatologists.
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The medical management of B. bassiana keratitis has previously been unsuccessful. The use of topical natamycin combined with oral fluconazole in the management of this case is discussed.
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Neurospora crassa was susceptible to azole drugs: ketoconazole (MIC 1 microgram/ml), fluconazole (MIC 5 micrograms/ml), and SCH39304 (MIC 5 micrograms/ml). Mutants of N. crassa resistant to ketoconazole were selected and genetically characterized. The seven characterized resistance mutations represented at least four genetic loci. Some mutants, but not all, were also resistant to fluconazole and to SCH39304.
The patient was a male infant born preterm at 30 weeks gestation. During his first week of life, he developed a systemic infection with an associated symptomatic hydrocephalus. Systemic candidaisis with neuromeningeal complication was diagnosed five weeks later. Despite treatment including cerebrospinal fluid (CSF) shunting and antimycotic medications (flucytosin and amphotericin B), the candidal infection did not resolve. Infectious and mechanical complications of the CSF drainage were treated by several surgical interventions during the following months. At 10 months of life, there was clinical and laboratory evidence of active persistent neuromeningeal candidaisis. Finally, candidal infection was eradicated with intravenous administration of fluconazole. After five year follow-up, the intellectual and psychological status of the patient was quite satisfactory, and no neurological deficits were found on clinical examination.
The incidence of Candida bloodstream infection (BSI) has been on the rise in several countries worldwide. Species distribution is changing; an increase in the percentage of non-albicans species, mainly fluconazole non-susceptible C. glabrata was reported. Existing microbiology diagnostic methods lack sensitivity, and new methods need to be developed or further evaluation for routine application is necessary. Although reliable, standardized methods for antifungal susceptibility testing are available, the determination of clinical breakpoints remains challenging. Correct species identification is important and provides information on the intrinsic susceptibility profile of the isolate. Currently, acquired resistance in clinical Candida isolates is rare, but reports indicate that it could be an issue in the future. The role of the clinical microbiology laboratory is to isolate and correctly identify the infective agent and provide relevant and reliable susceptibility data as soon as possible to guide antifungal therapy.
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Therapeutic treatment for systemic mycoses is severely hampered by the extremely limited number of antifungals. The difficulty of treatment of fungal infections in the central nervous system is further compounded by the poor central nervous system (CNS) penetration of most antifungals due to the blood-brain barrier. Only a few fungistatic azole drugs, such as fluconazole, show reasonable CNS penetration. Here we demonstrate that sertraline (Zoloft), the most frequently prescribed antidepressant, displays potent antifungal activity against Cryptococcus neoformans, the major causative agent of fungal meningitis. In in vitro assays, this neurotropic drug is fungicidal to all natural Cryptococcus isolates tested at clinically relevant concentrations. Furthermore, sertraline interacts synergistically or additively with fluconazole against Cryptococcus. Importantly, consistent with our in vitro observations, sertraline used alone reduces the brain fungal burden at an efficacy comparable to that of fluconazole in a murine model of systemic cryptococcosis. It works synergistically with fluconazole in reducing the fungal burden in brain, kidney, and spleen. In contrast to its potency against Cryptococcus, sertraline is less effective against strains of Candida species and its interactions with fluconazole against Candida strains are often antagonistic. Therefore, our data suggest the unique application of sertraline against cryptococcosis. To understand the antifungal mechanisms of sertraline, we screened a whole-genome deletion collection of Saccharomyces cerevisiae for altered sertraline susceptibility. Gene ontology analyses of selected mutations suggest that sertraline perturbs translation. In vitro translation assays using fungal cell extracts show that sertraline inhibits protein synthesis. Taken together, our findings indicate the potential of adopting this antidepressant in treating cryptococcal meningitis.
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Blood and urine samples were collected when signs of sepsis were present. Antifungal susceptibility of Candida strains was determined; in addition, all blood and 72% of urine C. albicans isolates were analyzed by using multi-locus sequence type (MLST). The mean incidences of candidemia and candiduria were 6.7 and 27.4/1000 admissions, respectively. Eight percent of candiduric patients developed candidemia with the same species. The mean interval between ICU admission and candidemia was 19.0 +/- 2.9 days, and 17.2 +/- 1.1 days for candiduria. C. albicans and C. glabrata were isolated in 54.2% and 17% of blood and 66.5% and 21.6% of urine Candida-positive cultures, respectively. Fluconazole was the most frequently prescribed agent. In all candidemic patients, the prescribed curative antifungal agent was active in vitro against the responsible identified strain. Crude ICU mortality was 61.8% for candidemic and 31.3% for candiduric patients. Seventy-five percent of the patients were infected with a unique C. albicans strain; cross-transmission between seven patients was suggested in one hospital.
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The following four groups were compared; Group 1: Control group with pure PMMA, Group 2: Antibacterial drug group with chlorhexidine gluconate in powder form + PMMA, Group 3: Antifungal drug group with fluconazole in powder form + PMMA, Group 4: Antimicrobial agent group with silver zinc zeolite in powder form + PMMA. After processing, the specimens were subjected for flexural strength testing using three-point bending test in a universal testing machine.
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Resistance to fluconazole is a possible event during prolonged suppressive drug therapy for cryptococ-cal meningitis, the most frequently encountered life-threatening manifestation of cryptococcosis. The knowledge of this resistance at the molecular level is important for management of cryptococcosis. In order to identify genes involved in azole resistance in Cryptococcus neoformans, a cDNA subtraction library technique was chosen as a strategy. First, a fluconazole-resistant mutant BPY22.17 was obtained from a susceptible clinical isolate BPY22 by in vitro exposure to the drug. Then, a subtractive hybridization procedure was used to compare gene expression between the obtained strains. We identified a cDNA overexpressed in the fluconazole-resistant strain BPY22.17 that was used as a probe to isolate the entire gene in a C. neoformans genomic library. Sequence analysis of this gene identified an ATP Binding Cassette (ABC) transporter-encoding gene called C. neoformans AntiFungal Resistance 1 (CnAFR1). Disruption of CnAFR1 gene in the resistant isolate (BPY22.17) resulted in an enhanced susceptibility of the knock-out mutant cnafr1 against fluconazole, whereas reintroduction of the gene in cnafr1 resulted in restoration of the resistance phenotype, thus confirming that CnAFR1 is involved in fluconazole resistance of C. neoformans. Our findings therefore reveal that an active drug efflux mechanism can be involved in the development of azole resistance in this important human pathogen.
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Because non-Candida albicans species are responsible for a significant number of chronic fungal vaginal infections and are more resistant to therapy with fluconazole, fungal cultures are a valuable aid in confirming the diagnosis and selecting appropriate therapy.
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Recent findings on the epidemiology and treatment of funguria are reviewed. Funguria, or candiduria, is a common nosocomial condition and may develop as early as the first two weeks of hospitalization. Risk factors include antibacterial therapy, an indwelling urinary catheter, urologic procedures, female sex, diabetes, and immunosuppressive therapy. Candida albicans is the species most commonly isolated from the urine of infected patients. Spontaneous resolution of funguria is relatively infrequent. Furthermore, although nonpharmacologic measures, such as removing unnecessary antibacterials and changing or removing indwelling urinary catheters, may be beneficial, they are often inadequate without additional, pharmacologic therapy. The most serious complication of untreated asymptomatic funguria is candidemia. Bladder irrigations with amphotericin B have been the standard of therapy for many years; recently, the optimal concentration and method of irrigation (continuous versus intermittent) have been debated. Studies indicate that intravesical amphotericin B and oral fluconazole therapy are each effective in clearing funguria. Intravesical amphotericin B appears to act more rapidly; however, the effect of systemic fluconazole therapy often persists longer than that of amphotericin B irrigation, and oral therapy is more convenient and less expensive. Oral fluconazole appears to have a more delayed but more lasting effect on funguria than amphotericin B bladder irrigation. Studies are needed to determine whether intravesical amphotericin B still has a role in the treatment of funguria and to refine strategies involving fluconazole.
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The cumulative incidence rate in these centers was higher than other reports from tertiary care hospitals from Latin America. Knowledge of local epidemiologic patterns permits the design of more specific strategies for prevention and preemptive therapy of CBSI.
We selected 69 clinical isolates of Candida, which demonstrated an MIC of >32 μg/ml for fluconazole, and subjected them to broth microdilution in presence and absence of Ibuprofen.
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tert -Butylhydroperoxide (t BOOH) tolerant Candida albicans mutants developed from clinical isolates were characterized with increased tolerance of the oxidative stress generating agents t BOOH and H2O2, continuous induction of the antioxidative defence system, reduced pseudohypha and hypha-forming capabilities, decreased phospholipase secretion and delayed growth in Sabouraud dextrose agar and broth media. Changes in antimycotic (fluconazole, voriconazole, amphotericin B, 5-fluorocytosine) tolerances as well as in total and cytochrome c-dependent respirations showed versatile patterns, meanwhile the intensified alternative oxidase-dependent respiration of the mutants indicated that this respiratory pathway was an important element of the antioxidative defence in general. Because the phenotypes of increased oxidative stress tolerance and reduced virulence attribute production always emerged concomitantly in t BOOH-tolerant mutants the natural selection of C. albicans strains more tolerant of oxidative stress is unlikely. Not surprisingly, a screening study failed to detect any C. albicans strains with increased oxidative stress tolerance among 46 randomly selected clinical isolates.
Silver nanoparticles (Ag-NPs) are known to have inhibitory and bactericidal effects. Resistance of fungal infections has emerged in recent years and is a major health problem. Here, we report the extracellular biosynthesis of Ag-NPs using a common fungus, Alternaria alternata. Also in this study, these nanoparticles were evaluated for their part in increasing the antifungal activity of fluconazole against Phoma glomerata, Phoma herbarum, Fusarium semitectum, Trichoderma sp., and Candida albicans. The antifungal activity of fluconazole was enhanced against the test fungi in the presence of Ag-NPs. Fluconazole in combination with Ag-NPs showed the maximum inhibition against C. albicans, which was confirmed from the increase in fold area of inhibition, followed by P. glomerata and Trichoderma sp., which showed less increase in the fold area, whereas no significant enhancement of activity was found against P. herbarum and F. semitectum.
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Candida glabrata causes significant medical problems in immunocompromised patients. Many strains of this yeast are intrinsically resistant to azole antifungal agents, and treatment is problematic, leading to high morbidity and mortality rates in immunosuppressed individuals. The primary goal of this study was to investigate the genes involved in the drug resistance of clinical isolates of C. glabrata.
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Antifungal triazole agents (fluconazole, voriconazole, itraconazole and posaconazole) are widely used for the management of invasive fungal infections (IFI). These drugs are indicated both for the prophylaxis and treatment of IFI, particularly in candidiasis and aspergillosis, major cause of mortality in immunocompromised patients. Due to a large interindividual pharmacokinetic variability leading to sub-therapeutic or toxic concentrations and to concentration-efficacy and/or -toxicity relationships, therapeutic drug monitoring (TDM) of antifungal triazole is fully justified. This review provides an overview of literature based data that confirm the usefulness of such TDM and its level of evidence as well as the practical guidelines for its implementation. In addition, we discuss the interest of new tools to improve the clinical management of IFI, such as genotyping tests optimizing initial voriconazole dosing regimen or the development of a new solid oral tablet of posaconazole improving its bioavailability and limiting absorption disorders.
During the past 50 years, the predominant etiologic agent of tinea capitis in the United States and in Western Europe has changed from Microsporum audouinii to Trichophyton tonsurans. This is thought to be due in part to the sensitivity of M audouinii to griseofulvin treatment and, in part, due to the importing of T tonsurans by people emigrating from geographic areas where that vector had been the prominent cause of tinea capitis. With these changes, prospects for newer therapies with the novel antimycotic agents itraconazole, fluconazole, and terbinafine are reviewed. (J Am Acad Dermatol 2000;42:1-20.)