To assess the clinical utility of an enzyme-linked immunosorbent assay method for the quantitative detection of Candida species antigen (Candigen; Biomerica Inc, Newport Beach, Calif) in patients with suspected disseminated candidiasis.
Recently, a candidal strain deleted for PLB1, the gene encoding the predominant phospholipase B (Plb1) secreted by C. albicans, was constructed and its virulence in an intravenous murine model of disseminated candidiasis was evaluated.
We previously demonstrated that genes encoding a putative two-component histidine kinase (CHK1) or a response regulator (CSSK1) are each required for virulence in a murine model of hematogenously disseminated candidiasis and that strains with each gene deleted are also defective in morphogenesis under certain growth conditions.
The first recombinant antibody fragment, Mycograb (Neu Tec Pharma plc), against Candida HSP90 is now in clinical trials in patients with disseminated candidiasis in Europe and the US.
SPI3-deficient mice were equally susceptible as wild-type mice to systemic Candida albicans infection, although there was a slight decrease in the ability of neutrophils from SPI3-deficient mice to kill C. albicans in vitro.
Compared to wild-type (CAF2-1) and gene-reconstituted (SSK23) strains, the ssk1 null strain (SSK21) was avirulent in a murine model of hematogenously disseminated candidiasis and less able to adhere to human esophageal cells.
Candida albicans PALS-green fluorescent protein (GFP) reporter strains were inoculated into mice in a disseminated candidiasis model, and GFP production was monitored by immunohistochemistry and reverse transcription-PCR (RT-PCR).
IRS4's effects on hyphal formation and virulence during DC were not evident on the first day after intravenous inoculation, even though transcripts were detected within murine kidneys.
However, the cytokine defect in TLR9-/- mice is compensated by alternative pathways, and the TLR9-dependent pathway seems to be redundant in the disseminated candidiasis model in mice.
The finding that DECTIN-1 polymorphisms rendered HSCT recipients at increased risk for fungal complications may contribute to the selection of high-risk patients who should be considered for antifungal prophylaxis to prevent systemic candidiasis.
Anti-Als1 immunolabelling patterns vary depending on the source of the C. albicans cells, with obvious differences between cells recovered from culture and those from a murine model of disseminated candidiasis.