Association of Clinical Disease with Genomic Features of Bacillus cereus
Bacillus cereus infections are rare in the general population but can cause serious invasive bacterial disease in the immunocompromised. Chang et al. (e00574-17) report an investigation of the genetic features of B. cereus from immunocompromised patients with distinct disease manifestations. These data underscore the importance of secreted toxins in invasive disease and allelic differences in transcriptional regulators in isolates from different infection sites. These data provide the first whole genome-based genetic snapshot of B. cereus infections and provide a framework for understanding clinical infections caused by these species in highly susceptible patient populations.
Candidalysin, the Key Virulence Determinant in the Immunopathogenesis of Vulvovaginal Candidiasis
Candida albicans is the primary etiological agent of vulvovaginal candidiasis (VVC), causing significant quality of life issues for women worldwide. However, until now, the fungal factor(s) contributing to symptomatic inflammation during VVC has been poorly understood. Using a murine model of VVC and C. albicans deletion mutants, Richardson et al. (e00645-17) identified a requirement for the hypha-associated peptide toxin Candidalysin to elicit vaginal mucosal damage, proinflammatory cytokine signaling, and neutrophil recruitment. Moreover, treatment of human vaginal epithelium with Candidalysin toxin alone largely recapitulated these responses. Thus, Candidalysin is the major virulence factor driving the pathogenesis of this most prevalent fungal infection.
Calprotectin and Metal Starvation Stress in a Fungal Pathogen
An important component of the innate immune response involves host withholding of metal micronutrients from pathogens. Besold et al. (e00779-17) show that the host metal binding protein calprotectin can withhold both zinc and copper from the opportunistic fungal pathogen Candida albicans, providing the first evidence of copper sequestration by calprotectin. This metal withholding by calprotectin occurs during fungal invasion of the kidney, but only in early stages of infection. Remarkably, the fungus recovers from calprotectin metal starvation stress at later stages, underscoring the complexity of metals at the host-pathogen interface.