title: The intestinal environment of surgical injury transforms Pseudomonas aeruginosa into a discrete hypervirulent morphotype capable of causing lethal peritonitis.
abstract: BACKGROUND
  Secondary peritonitis continues to carry a high mortality rate despite the aggressive use of imaging, drainage, and antibiotics. Although host factors and microbial burden contribute to the outcome of peritonitis, we propose a role for bacterial virulence as a determinant of outcome from peritonitis. Bacterial virulence is an inducible trait that is activated in response to specific local "cues" that we have previously shown to be present in the mouse gut exposed to surgical stress and injury.
  
  
  METHODS
  Pseudomonas aeruginosa was harvested after its intestinal inoculation into the cecum of mice subjected to surgical injury (30% hepatectomy) or sham surgery (controls). Harvested strains were then injected into the peritoneum of noninjured (naïve) mice and mortality determined.
  
  
  RESULTS
  P. aeruginosa harvested from the intestines of surgically injured mice caused 100% mortality, whereas strains harvested from control mice caused no mortality. Among recovered strains, a distinct P. aeruginosa morphotype (wrinkled shape) was shown to cause lethal peritonitis compared to smooth-shaped strains, which were nonlethal. Wrinkled strains were associated with a tendency to elicit a more proinflammatory response in mice compared to smooth-shaped strains.
  
  
  CONCLUSIONS
  Surgical injury transforms the morphotype of intestinal P. aeruginosa to express a hypervirulent response in the peritoneum of mice. Enhanced virulence of intestinal pathogens in response to surgical injury may play an important role in predicting the outcome of peritonitis.
authors.affiliation: Center for Surgical Infection Research and Therapeutics, University of Chicago Pritzker School of Medicine, Chicago, IL, USA.
authors.forename: Trissa
authors.initials: T
authors.lastname: Babrowski
authors.forename: Kathleen
authors.initials: K
authors.lastname: Romanowski
authors.forename: David
authors.initials: D
authors.lastname: Fink
authors.forename: Moses
authors.initials: M
authors.lastname: Kim
authors.forename: Vissagan
authors.initials: V
authors.lastname: Gopalakrishnan
authors.forename: Olga
authors.initials: O
authors.lastname: Zaborina
authors.forename: John C
authors.initials: JC
authors.lastname: Alverdy
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006498:Hepatectomy; D007422:Intestines / Q000382:microbiology*; D053208:Kaplan-Meier Estimate; D051379:Mice; D008810:Mice, Inbred C57BL; D009894:Opportunistic Infections / Q000209:etiology / Q000378:metabolism / Q000382:microbiology* / Q000401:mortality; D010538:Peritonitis / Q000209:etiology / Q000378:metabolism / Q000382:microbiology* / Q000401:mortality; D010641:Phenotype; D011183:Postoperative Complications / Q000378:metabolism / Q000382:microbiology* / Q000401:mortality; D011552:Pseudomonas Infections / Q000209:etiology / Q000378:metabolism / Q000382:microbiology* / Q000401:mortality; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity*; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms; D014774:Virulence
chemical_list: D015415:Biomarkers; D016207:Cytokines