Posterior trans-mediastinal lung herniation in a postoperative Marfan's patient.

Thoracic hernias are defined as the protrusion of contents either into or outside of the thoracic cavity. These hernias can be acquired or congenital and occur in varying locations. Acquired thoracic hernias typically develop after surgery or trauma. The most common form is intercostal herniation due to thoracotomy. Trans-mediastinal herniation of the lung is even less common, typically seen in patients with sequestration, scimitar syndrome, or pneumonectomy, and, when present, commonly occurs across the anterior mediastinum. Here, we present to our knowledge the first known case of posterior trans-mediastinal lung herniation diagnosed on CT after thoracoabdominal aneurysm repair in a patient with Marfan's disease, highlighting the importance of evaluating for rare anatomic complications in the post-operative setting. (1).

Enterococcus faecalis inhibits hyphal morphogenesis and virulence of Candida albicans.

The Gram-positive bacterium Enterococcus faecalis and the fungus Candida albicans are both found as commensals in many of the same niches of the human body, such as the oral cavity and gastrointestinal (GI) tract. However, both are opportunistic pathogens and have frequently been found to be coconstituents of polymicrobial infections. Despite these features in common, there has been little investigation into whether these microbes affect one another in a biologically significant manner. Using a Caenorhabditis elegans model of polymicrobial infection, we discovered that E. faecalis and C. albicans negatively impact each other's virulence. Much of the negative effect of E. faecalis on C. albicans was due to the inhibition of C. albicans hyphal morphogenesis, a developmental program crucial to C. albicans pathogenicity. We discovered that the inhibition was partially dependent on the Fsr quorum-sensing system, a major regulator of virulence in E. faecalis. Specifically, two proteases regulated by Fsr, GelE and SerE, were partially required. Further characterization of the inhibitory signal revealed that it is secreted into the supernatant, is heat resistant, and is between 3 and 10 kDa. The substance was also shown to inhibit C. albicans filamentation in the context of an in vitro biofilm. Finally, a screen of an E. faecalis transposon mutant library identified other genes required for suppression of C. albicans hyphal formation. Overall, we demonstrate a biologically relevant interaction between two clinically important microbes that could affect treatment strategies as well as impact our understanding of interkingdom signaling and sensing in the human-associated microbiome.