Characterization of putative virulence determinants encoded on the lp17 plasmid of the Lyme disease agent, Borrelia burgdorferi, has only recently begun. In this report, mutation of an intergenic region of lp17 was found to significantly impair tissue colonization and pathology by B. burgdorferi, and the tissue colonization defect was alleviated in mice lacking an adaptive immune response. Interestingly, our results suggest that the intergenic region affects the expression of genes that code for immunogenic proteins normally repressed during host infection.

The vitamin biotin is essential for all organisms, including the opportunistic fungal pathogens Candida albicans and C. glabrata. Both species are auxotrophic for this vitamin and acquire host biotin during infection by using a conserved system, consisting of the biotin transporter Vht1 and the transcriptional regulator Vhr1. We show that Vht1-mediated biotin acquisition is critical for both species during intracellular proliferation within and escape from macrophages, and systemic infections. We conclude that biotin access is limited in phagosomes containing fungi.

The molecular pathophysiology of cryptosporidiosis, a widespread diarrheal disease caused by infection with the protozoan parasite Cryptosporidium parvum, is incompletely understood. Impaired intestinal epithelial barrier function and increased permeability are most commonly associated with diarrheal diseases caused by enteric infections. Our studies for the first time demonstrated disruption of epithelial barrier function following C. parvum infection via extensive downregulation of key tight junction and adherens junction proteins that could be a major mechanism of cryptosporidiosis.