Candida glabrata intra-abdominal candidiasis is characterized by persistence within the peritoneal cavity and abscesses.
Infect Immun. 2014 May 5;
Authors: Cheng S, Clancy CJ, Hartman DJ, Hao B, Nguyen MH
The pathogenesis of Candida glabrata infections is poorly understood. We studied pathogenesis of intra-abdominal candidiasis (IAC) in mice that were infected intra-peritoneally with C. glabrata and sterile stool. C. glabrata BG2 (5×10(8) CFU) caused 100% mortality. Sublethal inocula of BG2 (1×10(8) or 1×10(7) CFU) caused peritonitis that progressed to abscesses. Three clinical C. glabrata strains (5×10(8) CFU) caused 80-100% mortality, compared to 29% for a fourth strain (#346). Following sublethal inocula (1×10(7) CFU), intra-abscess burdens of virulent strain #356 were ∼ 1-log higher than those of #346. C. glabrata Δplb1-2 (disruption of phospholipase B genes) killed mice as well as BG2. Following sublethal inocula, however, Δplb1-2 was associated with more rapid abscess resolution and lower intra-abscess burdens; these findings were reversed by PLB1-2 re-insertion. Δplb1-2 was also more susceptible than BG2 to killing by human neutrophils in vitro. BG2 and Δplb1-2 were indistinguishable during hematogenously disseminated candidiasis. C. albicans SC5314 was more virulent than C. glabrata BG2 during IAC, causing 100% mortality following challenge with 5×10(7) CFU. In contrast, sublethal inocula (1×10(7) CFU) of BG2 caused less neutrophil infiltration and higher burdens in peritoneal fluid than SC5314, and abscesses that persisted longer and contained higher burdens. In conclusion, a mouse model of C. glabrata IAC mimics disease in humans and distinguishes the relative virulence of clinical and gene disruption strains. C. glabrata differed from C. albicans during IAC by causing attenuated mortality and eliciting dampened neutrophil responses, but resulting in more persistent peritonitis and abscesses.
PMID: 24799629 [PubMed - as supplied by publisher]