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Preparation resistance grow and continue to evolve, despite the introduction of new antifungal agents, it complicates the treatment of patients. The susceptibility testing in vitro, in many cases, and are used to select the tool and ability to handle a specific infection, but in order to detect the resistance, i.e., perhaps the most important applications, the agent does not work It is a thing to identify. In antimicrobial susceptibility testing in Europe and clinical, standardized methods for reliability in antifungal susceptibility tested in vitro is now available European Commission Institute for Standards Institute and the United States (CLSI) in (EUCAST) on directly below. (In combination with other forms of data) for calculating epidemiology omit values and clinical breakpoints (ECVs) data collected by a standardized test, these are useful. Pathogens (WT) is to be selected to optimize the detection of wild-type strains, they should be species-specific, clinical cut-off value is not broken distribution WT important target species. ECVs are the most sensitive means to identify strains resistant mechanism acquired. Various mechanisms are can lead to acquired resistance of Candida species to obtain a mutation in the gene encoding the (ERG11) target enzyme and azole drugs that induce efflux pump encoded by CDR genes or MDR most often some. Were usually acquired resistance of Candida species to echinocandin mediated by acquisition of point mutations in the gene encoding the major subunit of the target enzyme of the FCC. Preparation resistance is associated with breakthrough infection and poor clinical outcome elevated minimum inhibitory concentrations between prevention and anti-fungal treatment. More and more, and are more resistant to echinocandin antifungal agents and azole isolates of C glabrata Candida due to Candida grab Lata. This situation should be taken further. Aspergillus fumigatus azole resistance rate is low, but the isolates including multidrug-resistant azole part of Europe, reports of emergence of resistance.
In spite of antifungal therapy have been improved in the past 30 years, the phenomenon of anti-fungal resistance is a major problem in clinical practice yet. Molecular mechanisms over the past 10 years, is associated with a phenomenon such as these are widely understood. In this paper, after a brief overview of the antifungal agents currently available, it will be described in detail molecular mechanisms of antifungal resistance. This is the main thing mechanism of resistance is something essential by deregulation of anti-fungal resistance effector gene was found. This deregulation is due to point mutations found in the transcriptional regulator of effector genes. I can resistor is monitored directly, point mutations in the gene encoding the antifungal target is generated. In addition, further, we describe a new strategy is performed to detect an alternative target for antifungal treatment and current. Identification of novel antifungal agents is accomplished by screening a collection of synthetic chemical compounds or natural. The discovery of antifungal estimation novel targets is performed by a whole genome approach to better understanding of pathogenic fungi in human biology.
Until recently, techniques for antifungal susceptibility testing has not been standardized. Laboratory Standards Institute Clinical and announced the reference method for susceptibility testing of yeast and fungi. These guidelines, we created a standard for comparison with clinical data. The European Commission for the study of sensitivity to antibiotics, has announced the guidelines for separation of Aspergillus and Candida test. However, doctors are faced with the challenge of how to interpret the results of the in vitro antifungal susceptibility test yet. MIC values are not associated with the response to direct treatment at all times. To predict treatment failure in vitro resistance HIV-infected patients, esophageal candidiasis or oral pharynx, but such a relationship has not been replicated in other settings. 90% of the cases is shown by the "rules of 60-90" says infections caused by susceptible strains, and corresponds to the appropriate treatment in, mismatch of in vitro data between in vivo and is resistant bacteria infections is an example% while the reaction at 60. Another limitation for determining the MIC is that MIC level is not the best indicator of resistance times. Some reports, minimum effective concentration is defined as the drug concentration resulted in a morphological change of the hyphal cells indicates that it may be more appropriate than MIC endpoint for susceptibility testing of filamentous bacteria echinocandin. In addition, infection antifungal activity of exposure to mold can detect conidia for activity against mycelial structure of many clinically important.
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