This study compared the YeastOne and reference CLSI M38-A2 broth microdilution methods for antifungal susceptibility testing of species. The MICs of antifungal agents were determined for 100 isolates, including 54 (24 TR/L98H isolates), 23 , 13, and 10 isolates. The overall agreement (within 2 2-fold dilutions) between the two methods was 100%, 95%, 92%, and 90% for voriconazole, posaconazole, itraconazole, and amphotericin B, respectively. The voriconazole geometric mean (GM) MICs were nearly identical for all isolates using both methods, whereas the itraconazole and posaconazole GM MICs obtained using the YeastOne method were approximately 1 dilution lower than those obtained using the reference method. In contrast, the amphotericin B GM MIC obtained using the YeastOne method was 3.3-fold higher than that observed using the reference method. For the 24 TRL98H isolates assayed, the categorical agreement (classified according to the CLSI epidemiological cutoff values) was 100%, 87.5%, and 83.3% for itraconazole, voriconazole, and posaconazole, respectively. For four isolates, the itraconazole MICs were>8 μg/ml using the M38-A2 method due to trailing growth, whereas the corresponding itraconazole MICs obtained using the YeastOne method were all ≤0.25 μg/ml without trailing growth. These data suggest that the YeastOne method can be used as an alternative for azole susceptibility testing of species and for detecting the TR/L98H isolates but that this method fails to detect isolates exhibiting trailing growth with itraconazole. Additionally, for isolates with azole MICs that approach or that are at susceptibility breakpoints or with high amphotericin B MICs detected using the YeastOne method, further MIC confirmation using the reference CLSI method is needed.
Genetic and antigenic analyses of influenza B virus field strains isolated in Taiwan
Summary Poor clinical outcomes for invasive aspergillosis are associated with antifungal resistance. Performing antifungal susceptibility tests on clinically relevant Aspergillus isolates from patients and environmental regions with known azole resistance is recommended. The aim of the study was to assess the presence of azole resistance in clinical Aspergillus spp. isolates and those from hospital environments and farmlands within a 40 km radius of the hospital. Clinical Aspergillus spp. isolates were cultured, as well as environmental Aspergillus spp. isolates obtained from air samples. Samples were subcultured in azole‐containing agar plates. Isolates with a positive screening test were subjected to YeastOne methods to determine their minimum inhibitory concentrations of antifungals. Resistance mechanisms were investigated in the azole‐resistant Aspergillus spp. isolates. No azole‐resistant clinical or environmental A flavus, A oryaze, A niger or A terreus isolates were found in the present study. All A fumigatus clinical isolates were azole‐susceptible. Seven A fumigatus environmental isolates were associated with cyp51A mutations, including two that harboured TR34/L98H mutations with S297T/F495I substitutions, two with TR34/L98H mutations and three with TR46/Y121F/T289A mutations. One of these isolates was collected from farmland, one was from A ward and five were from B ward. The proportion of azole‐resistant A fumigatus was 10.2% (6/59) and 3.2% (1/31) in the hospital environments and the farmlands near the hospital, respectively. The results showed that azole‐resistant A fumigatus existed within hospital environments. This emphasises the importance of periodic surveillance in hospital environments and monitoring for the emergence of azole‐resistant A fumigatus clinical isolates.
This study delineated the characteristics of 24 (11.2%) culture-positive, influenza-associated pulmonary aspergillosis (IAPA) patients out of 215 patients with severe influenza during 2016–2019 in a medical center in southern Taiwan. Twenty (83.3%) patients did not have EORTC/MSG-defined host factors. The mean time from influenza diagnosis to Aspergillus growth was 4.4 days, and 20 (83.3%) developed IAPA within seven days after influenza diagnosis. All patients were treated in intensive care units and all but one (95.8%) received mechanical ventilation. Aspergillus tracheobronchitis was evident in 6 (31.6%) of 19 patients undergoing bronchoscopy. Positive galactomannan testing of either serum or bronchoalveolar lavage was noted in all patients. On computed tomography imaging, IAPA was characterized by peribronchial infiltrates, multiple nodules, and cavities superimposed on ground-glass opacities. Pure Aspergillus growth without bacterial co-isolation in culture was found in 17 (70.8%) patients. A. fumigatus (15, 62.5%), A. flavus (6, 25.0%), and A. terreus (4, 16.7%) were the major causative species. Three patients had mixed Aspergillus infections due to two species, and two had mixed azole-susceptible and azole-resistant A. fumigatus infection. All patients received voriconazole with an all-cause mortality of 41.6%. Of 14 survivors, the mean duration of antifungal use was 40.5 days. In conclusion, IAPA is an early and rapidly deteriorating complication following influenza that necessitates clinical vigilance and prompt diagnostic workup.
Three sequences similar to that of the consensus binding sequence of the cyclic AMP (cAMP)-cAMP receptor protein (CRP) complex were found in the major IS2 promoter region. Experiments were performed to determine whether the cAMP-CRP complex plays a role in the regulation of IS2 transposition. In the gel retardation assay, the cAMP-CRP complex was found to be able to bind the major IS2 promoter. A DNA footprinting assay confirmed that the cAMP-CRP complex binds to the sequences mentioned above. With an IS2 promoter-luciferase gene fusion construct, the cAMP-CRP complex was shown to inhibit transcription from the major IS2 promoter. IS2 was found to transpose at a frequency approximately 200-fold higher in an Escherichia coli host defective for CRP or adenyl cyclase than in a wild-type host. These results suggest that the cAMP-CRP complex is a negative regulator of IS2 transposition.
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