Candida infections are a significant source of patient morbidity and mortality. Candida albicans is the most common pathogen causing Candida infections. Candida auris is a newly described pathogen that is associated with multi-drug-resistant candidiasis and candidaemia in humans. The antifungal effects of various essential oils and plant compounds have been demonstrated against human pathogenic fungi. In this study, the effect of cinnamon leaf and bark essential oils (CEOs) was determined against both C. albicans and C. auris. The disc diffusion (direct and vapour) and broth microdilution method was used to determine antifungal activity of the EOs against selected strains (C. albicans ATCC 10231, C. albicans ATCC 2091 and C. auris NCPF 8971) whilst the mode of action and haemolysin activity of the CEOs were determined using electron microscopy and light microscopy. Direct and vapour diffusion assays showed greater inhibitory activity of bark CEO in comparison with leaf CEO. The minimum inhibitory concentrations (MICs) and minimum fungicidal concentrations (MFCs) of bark CEO for all tested strains was below 0.03% (v/v), which was lower than the MICs of the leaf CEO (0.06–0.13%, v/v) dependent on the strain and the MFCs at 0.25% (v/v). In the morphological interference assays, damage to the cell membrane was observed and both CEOs inhibited hyphae formation. The haemolysin production assay showed that CEOs can reduce the haemolytic activity in the tested C. albicans and C. auris strains. At low concentrations, CEOs have potent antifungal and antihaemolytic activities in vitro against C. albicans and C. auris.
Key points
• Essential oils from Cinnamomum zeylanicum Blume bark and leaf (CBEO and CLEO) demonstrated fungicidal properties at very low concentrations.
• The antifungal activity of CBEO was greater than that of CLEO consistent with other recent published literature.
• The mode of action of CBEO and CLEO was damage to the membrane of C. albicans and C. auris.
• Both CBEO and CLEO inhibited the formation of hyphae and reduced haemolysin production in C. albicans and C. auris.
Fluoroquinolone resistance in bacteria is multifactorial, involving target site mutations, reductions in fluoroquinolone entry due to reduced porin production, increased fluoroquinolone efflux, enzymes that modify fluoroquinolones, and Qnr, a DNA mimic that protects the drug target from fluoroquinolone binding. Here we report a comprehensive analysis using transformation and in vitro mutant selection, of the relative importance of each of these mechanisms in fluoroquinolone resistance and non-susceptibility, using Klebsiella pneumoniae, one of the most clinically important multi-drug resistant bacterial species known, as a model system. Our improved biological understanding was then used to generate rules that could be predict fluoroquinolone susceptibility in K. pneumoniae clinical isolates. Key to the success of this predictive process was the use of liquid chromatography tandem mass spectrometry to measure the abundance of proteins in extracts of cultured bacteria, identifying which sequence variants seen in the whole genome sequence data were functionally important in the context of fluoroquinolone susceptibility.
Fluoroquinolone resistance in Gram-negative bacteria is multifactorial, involving target site mutations, reductions in fluoroquinolone entry due to reduced porin production, increased fluoroquinolone efflux, enzymes that modify fluoroquinolones, and Qnr, a DNA mimic that protects the drug target from fluoroquinolone binding. Here we report a comprehensive analysis, using transformation and mutant selection, of the relative importance of each of these mechanisms for fluoroquinolone nonsusceptibility using as a model system. Our improved biological understanding was then used to generate 47 rules that can predict fluoroquinolone susceptibility in clinical isolates. Key to the success of this predictive process was the use of liquid chromatography-tandem mass spectrometry to measure the abundance of proteins in extracts of cultured bacteria, identifying which sequence variants seen in the whole-genome sequence data were functionally important in the context of fluoroquinolone susceptibility.
The annotation of six cluster N Mycobacterium smegmatis phages (Kevin1, Nenae, Parmesanjohn, ShrimpFriedEgg, Smurph, and SpongeBob) reveals regions of genomic diversity, particularly within the central region of the genome. The genome of Kevin1 includes two orphams (genes with no similarity to other phage genes), with one predicted to encode an AAA-ATPase.
Macrophages (mφ) from pre-diseased mice of the major murine inbred models of spontaneous autoimmunity (AI), including multiple lupus-prone strains and the type I diabetes-prone NOD (non-obese diabetic) strain, have identical apoptotic target-dependent abnormalities. This characteristic feature of mφ from AI-prone mice suggests that abnormal signaling events induced within mφ following their interaction with apoptotic targets may predispose to AI. Such signaling abnormalities would affect predominantly the processing and presentation of self-antigen (i.e., derived from apoptotic targets), while sparing the processing and presentation of foreign antigen (i.e., derived from non-apoptotic sources). Here, we used DNA microarrays to test the hypothesis that mφ from AI-prone mice (MRL/MpJ [MRL/+] or MRL/MpJ-Tnfrsf6lpr [MRL/lpr]) differentially express multiple genes in comparison to non-AI mφ (BALB/c), but do so in a largely apoptotic cell-dependent manner. Mφ were stimulated with lipopolysaccharide, a potent innate stimulus, in the presence or absence of serum (an experimental surrogate for apoptotic targets). In accord with our hypothesis, the number of genes differentially expressed by MRL mφ was significantly increased in the presence vs. the absence of serum, the apoptotic target surrogate (n=401 vs. n=201). Notably, for genes differentially expressed by MRL mφ in the presence of serum, serum-free culture normalized their expression to a level statistically indistinguishable from that by non-AI mφ. Comparisons of mφ from AI-prone NOD and non-AI C57BL/6 mice corroborated these findings. Together, these data support the hypothesis that mφ from MRL and other AI-prone mice are characterized by a conditional abnormality elicited by serum lipids or apoptotic targets.
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