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.
The proportion of patients receiving treatment increased (65.5%, 79.4% and 74.7% in periods 1, 2 and 3, respectively, p = 0.04), and the median time from candidemia to treatment initiation decreased from 4 days in period 1 (range 0-32 days) to 2 days in period 2 (range 0-33 days) and 2 days in period 3 (range 0-14 days, p < 0.001).
The study period was split into two periods, 2007 to 2010 (period 1) and 2011 to 2014 (period 2).The number of episodes of <i>C. albicans</i> and <i>C. parapsilosis</i> candidemia (<i>n</i> = 262 versus <i>n</i> = 170, respectively), the mean incidence (1.62 versus 1.36 episodes per 1,000 admissions, respectively), and the percentage of episodes caused by clusters (overall clusters [40% versus 12%] and tracking clusters [18% versus 3%], respectively) were significantly lower in period 2 than in period 1.
In the multivariable model, persistent candidemia was significantly associated with (odds ratio [95% confidence interval]): total parenteral nutrition (2.79 [1.26-6.17]), dialysis dependence (3.76 [1.46-8.64]), and the SNPs IL10rs1800896 (3.45 [1.33-8.93]) and IL12B rs41292470 (5.36 [1.51-19.0]).
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.
IL-10 production was higher in C. albicans-stimulated PBMC from volunteers bearing the TLR4 Asp299Gly polymorphism, and a similar tendency was observed in TLR4 Asp299Gly heterozygous patients who had recovered from candidemia.
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.
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.