ABC and microsatellite genotyping of 51 strains of C. albicans revealed that patients who did not develop candidaemia were multiply colonised by at least two ABC genotypes of C. albicans, whereas candidaemic patients had highly related microsatellites and the same ABC genotype in colonising and bloodstream isolates that were probably present in different body sites before the onset of candidaemia.
Our aim was to assess the effect of genetic variations in the ATG16L1 and IRGM autophagy genes on the susceptibility of patients with candidemia and oropharyngeal candidiasis.
Based on logistic regression modelling, admission to north Indian ICUs [OR 2.1 (1.2-3.8); P = 0.012], public-sector hospital [OR 2.2 (1.2-3.9); P = 0.006], underlying respiratory illness [OR 2.1 (1.3-3.6); P = 0.002], vascular surgery [OR 2.3 (1.00-5.36); P = 0.048], prior antifungal exposure [OR 2.8 (1.6-4.8); P < 0.001] and low APACHE II score [OR 0.8 (0.8-0.9); P = 0.007] were significantly associated with C. auris candidaemia.
We observe significant association between candidaemia and SNPs in the CD58 (P = 1.97 × 10(-11); odds ratio (OR) = 4.68), LCE4A-C1orf68 (P = 1.98 × 10(-10); OR = 4.25) and TAGAP (P = 1.84 × 10(-8); OR = 2.96) loci.
No significant association between the single-nucleotide polymorphisms DECTIN-1 Y238X and CARD9S12N and the prevalence of candidemia was found, despite the association of the DECTIN-1 238X allele with impaired in vitro and in vivo cytokine production.
Rezafungin (CD101) is a novel echinocandin antifungal agent currently in clinical development for the treatment of candidemia and invasive candidiasis.
CD101 IV is a novel echinocandin with distinctive pharmacokinetic properties that is being developed as a once-weekly treatment for candidemia and invasive candidiasis.
CD101, a novel echinocandin with a long plasma half-life and enhanced stability, is in development for once-weekly IV administration for the treatment of candidemia and invasive candidiasis.
We observe significant association between candidaemia and SNPs in the CD58 (P = 1.97 × 10(-11); odds ratio (OR) = 4.68), LCE4A-C1orf68 (P = 1.98 × 10(-10); OR = 4.25) and TAGAP (P = 1.84 × 10(-8); OR = 2.96) loci.
CD82 knockout mice were more susceptible to <i>C. albicans</i> as compared with wild-type mice.Furthermore, patient <i>C. albicans</i>-induced cytokine production was influenced by two human CD82 single nucleotide polymorphisms, whereas an additional CD82 single nucleotide polymorphism increased the risk for candidemia independent of cytokine production.
Candidemia following NCA in neonates (p = 0.02), infants (p = 0.04) and adults (p = 0.02) in ICU and immunocompromised patients were significantly higher.
Candidemia following NCA in neonates (p = 0.02), infants (p = 0.04) and adults (p = 0.02) in ICU and immunocompromised patients were significantly higher.
Whereas the dectin-1/CARD9 signaling pathway is nonredundant in mucosal immunity to C. albicans, a partial deficiency of β-glucan recognition has a minor impact on susceptibility to candidemia.
The role of Candida species herein has recently been rediscovered since a 'loss-of-function' Y238X polymorphism in dectin-1, a C-type lectin receptor recognizing the β-1,3-glucan motif of Candida, resulted in diminished membrane expression and lower cytokine responses upon β-1,3-glucan recognition, and was associated with increased Candida colonization of SCT recipients, rendering them at risk for candidaemia.
Among them, a cytokine QTL at the NAA35-GOLM1 locus markedly modulated interleukin (IL)-6 production in response to multiple pathogens and was associated with susceptibility to candidemia.
Administration of miR-204/miR-211 mimics substantially downregulated Hmx1 and mitigated the severity of the kidney injuries induced by Candidemia, as reflected by improved renal glomerular filtration rate (GFR) determined by serum cystatin C (CysC), serum β2-microglobulin (β2-MG) and blood urea nitrogen (BUN).