SURGICAL INFECTIONS Volume 15, Supplement 1, 2014 ª Mary Ann Liebert, Inc. DOI: 10.1089/sur.2014.9990.abstracts

PROGRAM AND ABSTRACTS Thirty-fourth Annual Meeting of the Surgical Infection Society

Baltimore, Maryland May 1–3, 2014 Accreditation Statement This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the American College of Surgeons and the Surgical Infection Society. The American College Surgeons is accredited by the ACCME to provide continuing medical education for physicians. AMA PRA Category 1 Credits The American College of Surgeons designates this live activity for a maximum of 21 AMA PRA Category 1 Credits. This includes 17 hours for the general scientific sessions and 4 hours for the post-graduate course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Disclosure Information In compliance with ACCME Accreditation Criteria, the American College of Surgeons, as the accredited provider of this activity, must ensure that anyone in a position to control the content of the educational activity has disclosed all relevant financial relationships with any commercial interest. All reported conflicts are managed by a designated official to ensure a bias-free presentation. Please see the insert to this program for the complete disclosure list. Learning Objectives This activity is designed for physicians, research scientists, nurses, nurse practitioners, and pharmacists. Upon completion of this course, participants will be able to:      

Summarize results on the latest research relevant to the diagnosis and treatment of surgical infections Use antimicrobials for empiric treatment of VAP in trauma patients Debate current controversies in the diagnosis and treatment of surgical infections Use antimicrobials for a set course in the treatment of ventilator acquired pneumonia Discuss recent developments in the study of infection in cellular and molecular mechanisms Understand current treatment for secondary bacterial peritonitis

A MERICAN C OLLEGE OF S URGEONS Division of Education Inspiring Quality: Highest Standards, Better Outcomes


Wednesday, April 30, 2014 19:00–21:30

Presidential Dinner (By invitation) Thursday, May 1, 2014


Executive Council Breakfast (By invitation)



Executive Council Meeting (By invitation)






Surgical Infection Course Moderators: David Efron, MD and Stephanie Goldberg, MD


08:45–09:10 09:10–09:20 09:20–09:30

BIOLOGY OF SEPSIS and PHARMACOLOGY Microbiology of surgical pathogens Biology and metabolism of sepsis Organ physiology and multiple organ failure/dysfunction Antimicrobials and antibiotic pharmacodynamics Q and A session Break

09:30–10:00 10:00–10:20 10:20–10:30

RISK PREVENTION/PROPHYLAXIS Prevention of hospital-acquired infections Clostridium difficile Infections Q and A session

07:30–07:55 07:55–08:20 08:20–08:45

10:30–10:55 10:55–11:20 11:20–11:45

SPECIFIC INFECTIONS Necrotizing soft tissue infections Diagnosis and management of primary, secondary, and tertiary peritonitis High-risk patients: Who are they and how should they be managed? Q and A session

Lena Napolitano Timothy Billiar John Marshall Pamela Lipsett

E. Patchen Dellinger John Mazuski

Brian Harbrecht Mark Malangoni Soumitra Eachempati


Nominating Committee (By invitation)



LUNCHEON SYMPOSIUM (Industry sponsored, not part of scientific program)



PLENARY SYMPOSIUM The Art and Science of Surgical Infections (Papers 1–10) Moderators: William Cheadle, MD and Nicholas Namias, MD



O1. Replenishing the core gut microbiome via fecal microbiota transplant (FMT) can rescue mice from advanced-stage polymicrobial sepsis. Jennifer DeFazio (Resident), presenting. University of Chicago. Discussant: Greg Beilman, MD O2. The SIS study to optimize peritoneal infection therapy (STOP-IT) trial: Four days of antibiotics result in similar outcomes compared to duration. Robert Sawyer, presenting. University of Virginia. Discussant: Philip S. Barie, MD, MBA O3. Expression of MiR-21 is advantageous in the Immune Response to Peritonitis. Rebecca Barnett (Resident), presenting. University of Louisville. Discussant: Michael Morowitz, MD O4. A prospective randomized study to assess the optimal duration of antimicrobial prophylaxis in total gastrectomy. Ryoji Fukushima, presenting. Teikyo University School of Medicine. Discussant: J. Wesely Alexander, MD O5. Thrombin-processed Ecrg4 is chemotactic and recruits inflammatory monocytes to the injury site. Jisook Lee, presenting. University of California–San Diego. Discussant: Timothy Billiar, MD O6. Empiric azoles are not beneficial in surgical patients: A propensity-matched cohort study. Christopher Guidry (Resident), presenting. University of Virginia. Discussant: Pamela Lipsett, MD, MHE O7. TNF-Œ – , IL-6 and IL-8 cytokines in relation to TNF-Œ – -308 G/A polymorphism in postoperative sepsis. Kavita Baghel, presenting. King George’s Medical University, India. Discussant: John Marshall, MD O8. Obstructive sleep apnea: A risk factor for surgical site infection after colectomy. Spyridon Fortis (Resident-New Member), presenting. University of Minnesota. Discussant: E. Patchen Dellinger, MD O9. Are functional single nucleotide polymorphisms of proinflammatory cytokines associated with the development of necrotizing enterocolitis or spontaneous perforation in premature infants? Ashanti Franklin (Resident), presenting. Children’s National Medical Center. Discussant: Gary An, MD O10. Screening for ventilator-associated pneumonia in the surgical intensive care unit: Single-institution analysis of 1,013 bronchoalveolar lavages. Fredric D. Pieracci, presenting. Denver Health Medical Center/University of Colorado Health Sciences Center. Discussant: Lena Napolitano, MD


SIS Antibiotic Duration Study-Robert Sawyer, MD



Surgical Infections Editorial Reception (By Invitation)



SIS Foundation Board Meeting (By Invitation)



Welcome Reception

Pool Deck

Friday, May 2, 2014 07:00–08:00

BREAKFAST SYMPOSIUM (Industry-sponsored, not part of scientific program)



PARALLEL SESSION I Cellular and Molecular Mechanisms (Papers 11–15)

Ballroom I


O11. Cyclic adenosine monophosphate activation of protein kinase A may play a role in the pathogenesis of necrotizing enterocolitis. Catherine Hunter, presenting. Northwestern University. Discussant: Matthew Rosengart, MD O12. TNFR1 level in sepsis is dependent on MyD88-dependent upregulation of iNOS in hepatocytes. Meihong Deng (Resident/New Member), presenting. University of Pittsburgh. Discussant: Rachel Khadaroo, MD O13. Hepatic high motility group box-1 (HMGB1) levels are affected by invariant natural killer T-cells in polymicrobial sepsis. John Young (Resident), presenting. Brown University. Discussant: Ping Wang, PhD O14. Varying host response in different low-lethality models of murine abdominal sepsis. Lori Gentile (Resident), presenting. University of Florida. Discussant: Saman Arbabi, MD O15. Mitigation of splenocyte apoptosis by Th2-polarized invariant natural killer T-cells reduces disease severity in intraabdominal sepsis. Ram Anantha (Resident), presenting. Schulich School of Medicine and Dentistry, Western University. Discussant: Daithi Heffernan, MD


PARALLEL SESSION II Risk Factors and Surgical Infections (Papers 16–21) Moderators: E. Patchen Dellinger, MD and Heather Evans, MD

Ballroom II

O16. Can nasal methicillin-resistant Staphylococcus aureus screening be used to avoid empiric vancomycin use in intra-abdominal infection? Puja Shah (Resident), presenting. University of Virginia. Discussant: Reza Askari, MD O17. A randomized, prospective study of surgical site infections following vascular reconstructive surgery: Untreated vs. silverimpregnated dressings. Amani Politano (Resident), presenting. University of Virginia. Discussant: Jill Cherry-Bukowiec, MD O18. Microbial analysis to predict anastomotic leak in humans. Preston Luong (New Member), presenting. University of Chicago. Discussant: Brian Zuckerbraun, MD O19. Vancomycin-associated nephrotoxicity: The obesity factor. Stephen Davies (Resident/New Member), presenting. University of Virginia. Discussant: Heather Evans, MD O20. Hypoalbuminemia in obese surgical patients is disproportionately associated with infectious complications. Zachary Dietch (Resident), presenting. University of Virginia. Discussant: Sheryl M. Sahr, MD O21. Complex pelvic surgery and additional organ resection independently increase the risk of wound infection after elective colorectal surgery: An ACS-NSQIP analysis. Mary Kwaan (New Member), presenting. University of Minnesota. Discussant: John M. Davis, MD S-4


Break-Visit the Exhibits


William A. Altemeier Memorial Lecture ‘‘Warping disease space to improve recovery from infections’’ David S. Schneider, PhD and Associate Chair Associate Professor, Microbiology and Immunology Stanford University School of Medicine



Surgical Infection Society Presidential Address ‘‘The Wheel’’ Nicholas Namias, MD, MBA Professor and Chief, Division of Trauma and Acute Care Surgery Robert Zeppa Endowed Chair in Trauma Surgery Executive Vice Chairman, DeWitt Daughtry Family Department of Surgery University of Miami, Miller School of Medicine



LUNCHEON SYMPOSIUM (Industry-sponsored; not part of scientific program)



UPDATE SYMPOSIUM I GI Fistulae, Anastomotic Leak, and Other Abdominal Catastrophes Moderators: Tina Mele, MD and Samir S. Awad, MD


Topic 1: Endoscopic Approaches to Source Control: Rajeev Attam, MD—University of Minnesota Topic 2: Management of GI Fistulae, Soup to Nuts: David Efron, MD—The Johns Hopkins University Topic 3: Microbial Pathogenesis of Anastomotic Leaks: John Alverdy, MD—University of Chicago Topic 4: Closing the Infected Abdomen: If, When, How: Jose Diaz, MD—University of Maryland 15:15–13:30

Break-Visit the Exhibits


PARALLEL SESSION III Basic Mechanisms of Infection (Papers 22–27) Moderators: Timothy Billiar, MD and Daithi Heffernan, MD

O22. Oncostatin M modulates immune cell recruitment and bacterial translocation in a murine model of sepsis. Pang Young (Resident), presenting. University of Alberta. Discussant: Tina Mele, MD O23. Association of inflammasomes and caspase-1 mediated cardiac dysfunction with sepsis. Deborah Carlson, presenting. University of Texas–Southwestern. Discussant: Brian Eliceiri, PhD O24. Invariant natural killer T-cells modulate the gamma-delta-lymphocyte response to polymicrobial sepsis. Whitney Young (Resident), presenting. Brown University. Discussant: Ping Wang, PhD O25. Glutamine improves innate immunity and the intestinal barrier function during parenteral nutrition. Rebecca Busch (Resident/New Member), presenting. University of Wisconsin–Madison. Discussant: Todd Costantini, MD O26. Mesenchymal stem cells reverse chronic stress induced bone marrow dysfunction following traumatic injury. Amy Gore (Resident), presenting. New Jersey Medical School-Rutgers. Discussant: William Cheadle, MD O27. Wound infection after attenuating a key inflammatory signaling pathway. Saman Arbabi, presenting. University of Washington. Discussant: Olga Zaborina, PhD S-5

Ballroom I


PARALLEL SESSION IV Hospital Acquired and Skin/Soft Tissue Infections (Papers 28–33) Moderators: John Mazuski, MD, PhD and Addison May, MD

Ballroom II

O28. Reduction of infectious complications following trauma laparotomy through use of a perioperative antibiotic protocol. William Symons (New Member), presenting. Washington University. Discussant: Jeffrey Claridge, MD O29. Sustainability of a hospital-acquired pressure ulcer prevention bundle in surgical patients. Sylvia Martinez, presenting. Baylor College of Medicine. Discussant: Sandy Swoboda RN, MSN O30. Ventilator-associated events: Correlation with ventilator-associated pneumonia? Arek Wiktor (Resident/New Member), presenting. University of Michigan. Discussant: Fredric D. Pieracci, MD, MPH O31. Health-related quality of life among necrotizing soft tissue infection survivors and clinical predictors of poor outcome. Timo Hakkarainen (Resident), presenting. University of Washington. Discussant: Jeffrey G. Chipman, MD O32. A surgeon-directed peripherally inserted central catheter team utilizing a novel screening protocol to decrease infectious complications and associated cost. Vihas Patel (Resident), presenting. Brigham and Women’s Hospital, Harvard University. Discussant: Laura Moore, MD O33. Predictors of mortality among intravenous drug users with staphylococcus aureus bacteremia. Ram Anantha (Resident), presenting. Schulich School of Medicine and Dentistry, Western University. Discussant: Colin Braithwaite, MD


Annual Business Meeting (Members only)

Ballroom II


Committee Meetings (Attendance mandatory for committee members)


Saturday, May 3, 2014 07:00–08:00

Executive Council Meeting (By invitation)






UPDATE SYMPOSIUM II: PRO-CON DEBATES Moderators: Matthew R. Rosengart, MD


The Double X Chromosome: Does Gender Really Matter in Human Disease? Speakers: PRO: Jason Sperry, MD, MPH—University of Pittsburgh CON: Addison May, MD—Vanderbilt University Is Zero Achievable in CLABSI, CAUTI, and VAP? Speakers: PRO: Madhuri Sopirala, MD-University of Cincinnati CON: Zero Dark Dirty!-Robert Sawyer, MD-University of Virginia 09:00–10:00

UPDATE SYMPOSIUM III Advanced Platform Technologies: An Update Moderator: John Alverdy, MD


Topic 1: A metagenomic approach to understand surgical infection-The role of next generation technology-Jack Gilbert, PhD-Argonne National Laboratory Topic 2: Computational needs and approaches to manage metagenomic data-Scott Christley, PhD—University of Chicago Topic 3: Statistical analysis of megadatasets-managing terabytes of data? Paul Bankey, MD, PhD—University of Rochester S-6




SIS Foundation Resident Fellowship 2013 Kendall Sowards, MD SIS Foundation Junior Faculty Fellowship 2013 Jared Huston, MD 10:15–10:30

Break–Visit the Exhibits


PARALLEL SESSION V Proteins, Genes, and Pathogens (Papers 34–38) Moderators: John Marshall, MD and Rachel Khadaroo, MD, PhD

Ballroom I

O34. The enteric nervous system (ENS) neuropeptide, bombesin (BBS), maintains goblet cell function during parenteral nutrition (PN). Aaron Heneghan (New Member), presenting. University of Wisconsin–Madison. Discussant: Jared Huston, MD O35. Computational prediction of a novel transcriptional regulation for the PqsH encoding gene in Pseudomonas aeurginosa. Scott Christley, presenting. University of Chicago. Discussant: Kaysie Banton, MD O36. The genomic expression of aged murine hematopoietic stem cells after polytrauma indicates a failure to support development of innate immunity. Philip Efron, presenting. University of Florida. Discussant: Joseph Minei, MD O37. Ursodeoxycholic acid as a mediator of intestinal epithelial cell restitution. Stephanie Papillon (Resident), presenting. University of Southern California Children’s Hospital Los Angeles. Discussant: Celeste Finnerty, PhD O38. NEC as an infectious disease: Identifying strains of opportunistic pathogens. Debi Thomas, presenting. University of Southern California Children’s Hospital of Los Angeles. Discussant: Evan Nadler, MD


PARALLEL SESSION VI Clinical Issues in Surgical Infection (Papers 39–44) Moderators: Lillian Kao, MD and Jeffery Chipman, MD

O39. A systematic approach to preventing sharps injuries in the operative care line at an urban tertiary care center. Sylvia Martinez, presenting. Baylor College of Medicine. Discussant: Peter A. Burke, MD O40. Acute kidney injury (AKI) causes persistent dysregulation of the leukocyte transcriptome. Benjamin Szpila (Resident), presenting. University of Florida. Discussant: David Efron, MD O41. External validation of the ventral hernia risk score for predicting surgical site infections. Mike Liang (New Member), presenting. University of Texas Health Sciences Center, Houston. Discussant: Donald Fry, MD O42. Use of computed tomography to diagnose aspiration in trauma patients. Vanessa Fawcett, presenting. University of Washington. Discussant: Patrick J. O’Neill, PhD, MD O43. Predictors of monomicrobial necrotizing fasciitis. Rhett Willis (Resident/New Member), presenting. University of Virginia. Discussant: Addison May, MD S-7

Ballroom II

O44. Transforming growth factor beta induced epithelial-mesenchymal transition leads to persistent intestinal fistulae. Xiuwen Wu, presenting. Jinling Hospital, China. Discussant: Catherine Hunter, MD


LUNCHEON SYMPOSIUM (Industry-sponsored; not part of scientific program)


PARALLEL SESSION VII Pathophysiologic Mechanisms of Infection (Papers 45–49) Moderators: Marc Jeschke, MD, PhD and Catherine Hunter, MD


Ballroom I

O45. Genomic and proteomic survival biomarker profiles in severely burned children. Celeste Finnerty, presenting. University of Texas Medical Branch, Galveston Shriners Hospitals for Children. Discussant: Marc Jeschke, MD, PhD O46. Intestinal bile acids differentially control intestinal cell proliferation. Avafia Dossa (Resident), presenting. University of Southern California, Children’s Hospital Los Angeles. Discussant: Ziad Sifri, MD O47. The gut during prolonged critical illness harbors low membership pathogen communities that are less virulent as a group than individually. Olga Zaborina, presenting. University of Chicago. Discussant: Mary Kwaan, MD O48. Muscle injury and ischemia contribute to the pathogenesis of A. baumannii infection. Irma Fleming (Resident), presenting. University of Chicago. Discussant: Duane Hospenthal, MD O49. Differential immune and hormonal expression in cardiac versus hepatic blood after burn injury in rodents. Marc Jeschke (Resident), presenting. University of Toronto, Sunnybrook Health Sciences Centre. Discussant: Tina Palmieri, MD


PARALLEL SESSION VIII: The Surgical Infection Society Supreme Court (Papers 50–54) Moderators: Pamela Lipsett, MD, MHE, and Nicholas Namias, MD, MBA, John Alverdy, MD, Robert Sawyer, MD and E. Patchen Dellinger, MD

Ballroom II

O50. A Reappraisal of MRSA VAP in the surgical ICU: Not just a late infection any more. Jacquelyn Glenn, presenting. University of Colorado, Denver Health Medical Center. O51. Environmental contact versus patient contact in the ICU: What do we touch? Sandy Swoboda, presenting. Johns Hopkins University. O52. Early appropriate empiric antimicrobial prescribing in septic patients presenting to the emergency department does not lead to decreased mortality. James Gilmore (Resident), presenting. Brigham and Women’s Hospital, Harvard University. O53. CAUTIs and CLABSIs: Do physicians REALLY know what they are? Therese Duane, presenting. Virginia Commonwealth University. O54. A comparison of ICU infections in a United States trauma center and a teaching hospital in Ho Chi Minh City, Vietnam. Andrew Stephens, presenting. Brown University. S-8

Ballroom Foyer


POSTER SESSION (Posters 1–52) Basic and Clinical Studies in Surgical Infection


Group A: (P1–P8) Olga Zaborina, PhD and Patrick J. O’Neill, PhD, MD Group B: (P9–P17) Brian Elicieri, PhD and Celeste Finnerty, PhD Group C: (P18–P27) Jeffery Tessier, MD and Therese Duane, MD Group D: (P28–P33) Kaysie Banton, MD and David Blake, MD Group E: (P34–P43) Reza Askari, MD and Howard Belzberg, MD Group F: (P44–P52) Christine S. Cocanour, MD and Samir Awad, MD


New Member Reception

Ballroom Foyer


Awards Banquet





Oral Presentation Abstracts

O-01. REPLENISHING THE CORE GUT MICROBIOME VIA FECAL MICROBIOTA TRANSPLANT (FMT) CAN RESCUE MICE FROM ADVANCED-STAGE POLYMICROBIAL SEPSIS Jennifer DeFazio, Sangman Kim, Scott Christley, Irma Fleming, Baddr Shakhsheer, Bana Jabri, Olga Zaborina, John Alverdy, University of Chicago Background: During critical illness, the normal gut microbiota are replaced by virulent and multi-drug resistant (MDR) healthcare acquired pathogens (HAPs). Hypothesis: The aim of this study was to test the hypothesis that replenishing the microbiota with a fecal microbiota transplant (FMT) could rescue mice with advanced stage polymicrobial sepsis due to HAPs. Methods: We developed a novel model of lethal polymicrobial gut-derived sepsis due to MDR-HAPs in mice. Mice underwent a 30% hepatectomy with intestinal inoculation of a well characterized MDR human pathogen community (HPC) from the stool of a patient dying of sepsis. 100% of mice developed clinically apparent severe sepsis at 24 hours confirmed by positive cultures of the HPC in the lung, liver, spleen and blood (n = 24) with only 30% surviving to day 7. In reiterative experiments, when mice appeared frankly septic at 24 hours, they were assigned to receive either a fecal microbiota transplant (FMT- cecal contents of normal, healthy mice in H20) or an autoclaved (AC) FMT via enema. When moribund, mice were sacrificed and underwent 16S rRNA analysis of the gut microbiota on cecal contents and tissues. Filtered cecal lysates were inoculated onto bone marrow-derived dendritic cells (BMDCs) to assess the direct effect of the microbiota on immune function. Results: FMT resulted in an 87% survival rate as compared to AC which resulted in only 17% survival (n = 15/group, p < 0.001). FMT mice appeared completely healthy on POD 7. 16S rRNA showed a shift of the microbiota at the initiation of sepsis and in all groups through POD 7 (p < 0.05). There was also a significant decrease in Enterobacteriaceae and Enterococcus in FMT vs. AC (p < 0.05). The presence of Coprobacteriaceae was associated with survival during FMT treatment (p < 0.05). BMDC assays demonstrated differentially expressed cytokines between groups; IL-6 and IL-10 were increased in the FMT mice compared to AC mice (P < 0.05). Finally, the BMDC assays performed on healthy appearing surviving mice on POD7 from both groups demonstrated that FMT microbiota induced cytokines at a low baseline level compared to AC microbiota which remained proinflammatory as judged by IL-6, 10, 12, RANTES, and TNF (P < 0.01). Conclusions: Fecal microbiota transplant rescued mice from advanced stage polymicrobial sepsis due to MDR- HAPs possibly owing to its effect on both local and systemic immune function.

Hypothesis: The administration of four days of antibiotics after source control leads to outcomes equivalent to a strategy where antibiotics are administered for two days beyond resolution of physiologic abnormalities. Methods: The trial was a 23-center, randomized, controlled study of four days of antibiotics after source control (4 day) versus antibiotics given for two days beyond resolution of fever (T ‡ 38), leukocytosis (WBC ‡ 11), and ileus, with a maximum of 10 days (clinical response-CR). Antibiotic regimens adhered to SIS guidelines. The primary outcome was a composite of surgical site infection, recurrent intra-abdominal infection, and death within 30 days per group allocation (intent-to-treat). Secondary outcomes included rates of extra-abdominal infection and subsequent infections with resistant pathogens, including C. difficile. Results: 521 patients were enrolled: 263 in the CR group and 258 in the 4 day group. Colon/rectum was the most common source (159), followed by appendix (70), and small bowel (69). APACHE II was similar between groups: CR = 9.8 – 0.4 (SEM), 4 day = 10.1 – 0.4. Median duration of antibiotics with interquartile range (IQR) was 8 (5–10) days in the CR group and 4 (4–5) days in the 4 day group (p < 0.01 by MannWhitney U test). There was no difference in the composite or component endpoints. No difference was found in rates of subsequent infection with resistant pathogens or C. difficile. There were fewer patients with extra-abdominal infections (principally urinary tract infections) in the CR day group than the 4 day group (17/263 = 6.5% versus 31/258 = 12%, p = 0.028 by Pearson w2 test). Conclusions: Four days of antibiotics to treat intra-abdominal infections after source control yields outcomes similar to a longer course based on resolution of physiologic abnormalities and is associated with significantly fewer days of antibiotic exposure. We recommend this approach as standard of care.

O-03. EXPRESSION OF MIR-21 IS ADVANTAGEOUS IN THE IMMUNE RESPONSE TO PERITONITIS Rebecca Barnett, Ernesto Sepulveda, William Cheadle, University of Louisville Background: Peritonitis may trigger sepsis and organ failure, with most mortality due to the latter. Innate immune modulation allows a directed response to pathogens and minimal collateral organ injury. MicroRNA-21 (miR-21) is a short non-coding RNA

O-02. THESIS STUDY TO OPTIMIZE PERITONEAL INFECTION THERAPY (STOP-IT) TRIAL: FOUR DAYS OF ANTIBIOTICS RESULT IN SIMILAR OUTCOMES COMPARED TO DURATION BASED ON RESOLUTION OF PHYSIOLOGICAL RESPONSE Robert Sawyer, Jeffrey Claridge, Avery Nathens, Therese Duane, Heather Evans, Charles Cook, Patrick O’Neill, John Mazuski, Reza Askari, Mark Wilson, Lena Napolitano, Nicholas Namias, Preston Miller, E. Patchen Dellinger, Christopher Watson, Raul Coimbra, Daniel Dent, Stephen Lowry, Michael Moncure, Christine Cocanour, Michael West, Kaysie Banton, William Flynn, Pamela Lipsett, Kimberley Popovsky, University of Virginia Background: After source control, antibiotics are required to clear pathogens from the peritoneum. The most effective duration of antimicrobial therapy in this setting is unclear.

Survival from peritonitis in WT and miR-21 - / - mice


ORAL PRESENTATION ABSTRACTS with targets in the toll-like receptor (TLR) signaling pathway, and may facilitate the switch from pro- to anti-inflammatory phases of the innate response to peritonitis. Hypothesis: Macrophage miR-21 modulates the innate immune response, resulting in a reduction of pro-inflammatory cytokines. Methods: 8–12 week WT and miR-21 - / - C57BL/6 mice were given peritonitis by intra-peritoneal injection of lipopolysaccharide (LPS). Temperature, daily weight and survival were recorded. Bone marrow-derived macrophages from WT and miR-21 - / mice were plated and stimulated with LPS. MiR-21 and cytokine levels were measured at 0, 3, 6, 12, 24 and 48 hours. Peritoneal macrophages were transfected with miR-21 mimics and antagomirs for 24 hours, and stimulated with LPS. Cytokines were measured in the supernatant after 6 hours. Results: Knockouts did not express miR-21. Although WT mice began to die earlier, more miR-21 - / - mice died overall (p = 0.002). MiR-21 - / - macrophages produced significantly less IL-10 at 3, 6 and 12 hours after stimulation (p < 0.05). IL-6/TNF-a was significantly higher at 12 and 48 hours (p < 0.05) in the miR-21 - / - cultures. The increase in TNF-a/IL-6 were also seen after transfection with miR-21 antagomir and subsequent LPS stimulation (p = 0.02 and 0.1 respectively). An increase in IL-10 was seen after transfection of miR-21 mimic and LPS stimulation (p = 0.02). Conclusions: Expression of miR-21 conferred a survival benefit from LPS peritonitis, related to targets in the TLR pathway and ultimately cytokine production of the innate response. Identification of patients with overwhelming pro-inflammatory response could allow treatment to reduce the increased inflammatory load and improve organ damage and outcomes.

O-04. A PROSPECTIVE RANDOMIZED STUDY TO ASSESS THE OPTIMAL DURATION OF ANTIMICROBIAL PROPHYLAXIS IN TOTAL GASTRECTOMY Ryoji Fukushima, Toshiro Konishi, Yasuhiko Mohri, Tamaki Noie, Satoshi Ono, Kenji Omura, Susumu Sueyoshi, Akinori Takagane, Masato Kusunoki, Taro Shibata, Hidetaka Mochizuki, Yoshinobu Sumiyama, Teikyo University School of Medicine Background: Western guidelines state that the duration of antimicrobial prophylaxis (AMP) should be less than 24 hours postoperatively for most surgical procedures. However, some patients after gastrectomy especially in Japan still receive further extended AMP until 3–4 postoperative days. In contrast to Western countries, extended D2 lymphadenectomy has been a standard surgical treatment for gastric cancer in Japan (and in Eastern Asia) and high prevalence of drain use may be a potential risk for surgical site infections (SSI). There is not much information regarding the optimal duration of AMP in total gastrectomy with D2 lymphadenectomy. Hypothesis: A muti-center prospective, open-label, randomized controlled trial to assess the optimal duration of AMP in total gastrectomy was conducted. Methods: Patients with gastric cancer who underwent total gastrectomy (R0 resections) were randomly assigned (1:1) to group A: 24-hour AMP (ampicillin/sulbactam 1.5 g before the surgical incision and every 3 hour during surgery, 6 hours after wound closure and once on the next day) or group B: 72-hour AMP (ampicillin/sulbactam 1.5 g twice daily extended until postoperative day 3). The primary endpoint was the incidence of SSI and the secondary endpoint was the incidence of remote infections. We assessed non-inferiority of 24-hour prophylaxis with a margin of 9%. This study was registered in UMIN-CTR, UMIN000001062. Results: Between February 28, 2008, and March 31, 2012, 476 patients from 67 hospitals were included and 462 patients were analyzed (group A: n = 227, group B: n = 235). The two groups did not differ significantly in relation to age, sex, body mass index, cancer stages and operative procedures. Incidences of infections are presented in the table. The results showed statistically significant non-inferiority (p < 0.0001) of group A over group B in terms of the incidence rate of SSI. Conclusions: Antimicrobial prophylaxis should be limited to 24 hours postoperatively in total gastrectomy.

S-11 in mediating the injury response by characterizing its cleavage and determining whether shed Ecrg4 can recruit inflammatory monocytes. Hypothesis: We hypothesized that Ecrg4 is processed by thrombin and that monocyte recruitment to sites of injury will be impaired in Ecrg4 KO mice. Methods: To determine if Ecrg4 is processed by thrombin, recombinant Ecrg4 peptide was incubated with thrombin in vitro and cleavage was assessed by immunoblotting. To evaluate the effect of Ecrg4(133-148) on the recruitment of inflammatory monocytes to sites of brain injury, we performed stereotaxic injection of the Ecrg4(133148) peptide followed by dissociation of the brain and flow cytometry three days postinjury. To validate the role for Ecrg4 as a chemotactic factor, subcutaneous implants of polyvinyl alcohol (PVA) sponges were implanted into Ecrg4 WT and Ecrg4 KO mice, and infiltrated cells were isolated and analyzed by flow cytometry. Results: Incubation of recombinant Ecrg4 polypeptide with thrombin confirmed that thrombin cleavage released a C-terminal fragment of Ecrg4, Ecrg4(133-148). We observed a significant Ecrg4(133-148)-mediated recruitment of CD11b + CD45 high inflammatory monocytes following stereotaxic injection in the brain, while Ecrg4(133148) peptide did not affect recruitment of CD11b + CD45 low microglia at day 3. In Ecrg4 KO mice, there was a decreased recruitment of CD11b + Gr-1 high immature myeloid cells to the injury site in the Ecrg4 KO mice compared with Ecrg4 WT mice. Conclusions: Together, these findings suggest a chemotactic role for thrombinprocessed Ecrg4(133-148) to mediate a pro-inflammatory injury response by recruiting inflammatory myeloid cells.

O-06. EMPIRIC AZOLES ARE NOT BENEFICIAL IN SURGICAL PATIENTS: A PROPENSITY-MATCHED COHORT STUDY Christopher Guidry, Stephen Davies, Timothy McMurry, Zachary Dietch, Rhett Willis, Robert Sawyer, University of Virginia Background: Broad-spectrum empiric antibacterials are associated with an increased incidence of opportunistic infection, yet studies evaluating the impact of empiric azoles on the number and characteristics of future infections are lacking. Hypothesis: We hypothesized that empiric azole exposure would not significantly alter the rates of future infectious episodes or associated outcomes. Methods: We reviewed a prospectively collected and maintained surgical infection database from a tertiary hospital. All initial infectious episodes per patient per admission between Jan. 1, 2000 and Dec. 31, 2011 were identified and grouped according to the presence of a fungal isolate on initial culture and receipt of an empiric azole. Propensity score matching was performed using potential confounders (excluding initial culture results). The number and characteristics of subsequent infections, as well as mortality and length of stay were analyzed. Wilcoxon rank sum, chi-square, and fisher’s exact test were used as appropriate. Infection-free survival was evaluated using a Kaplan-Meier curve. Results: We identified 6,530 patients (9.6% with fungal infection, 11.6% with empiric azole exposure) as part of the initial cohort. Propensity matching identified 410 pairs of patients based upon empiric azole exposure (133 pairs with initial fungal infection). Peritoneal infection was the most common site in both groups (56.8% of fungal vs. 72.7% of non-fungal; 24.5 vs. 17.7% respectively from upper GI source). There were no differences in mortality (12.8 vs. 10.5% for fungal, p = 0.6; 11.9 vs. 8.7% for nonfungal, p = 0.2) or rate of subsequent infection with resistant pathogens. Empiric azole exposure was associated with a longer length of stay (median 11 vs. 9 days; p = 0.003) and lower rates of subsequent CRBSI (3.7 vs. 11.5%; p = 0.001) for those patients without an initial fungal infection. There were no differences in infection-free survival based on azole exposure regardless of fungal culture results. Conclusions: Our study did not identify a difference in the outcomes following initial infection or the characteristics of subsequent infectious episodes based upon receipt of empiric azole therapy. Empiric azole therapy appears to offer no benefit to surgical patients and should be avoided without culture-based evidence of fungal infection.

O-07. TNF-a, IL-6 AND IL-8 CYTOKINES IN RELATION TO TNF-a-308 G/A POLYMORPHISM IN POSTOPERATIVE SEPSIS Kavita Baghel, Rajeshwar Nath Srivastava, Abhijit Chandra, Jyotsna Agrawal, Hasan Raza Kazmi, Saloni Raj, King George’s Medical University

O-05. THROMBIN-PROCESSED Ecrg4 IS CHEMOTACTIC AND RECRUITS INFLAMMATORY MONOCYTES TO THE INJURY SITE Jisook Lee, Stu Knowling, Raul Coimbra, Vishal Bansal, Andrew Baird, Brian Eliceiri, Todd Costantini, University of California San Diego Background: Leukocytes utilize protease-mediated shedding of membrane-anchored factors as a mechanism to localize the release of chemotactic factors at sites of injury. We have recently shown that cell surface Ecrg4 is shed from granulocytes following LPS treatment, where shed Ecrg4 activates NF-kB signaling. These findings suggest that Ecrg4 may play an important role in recruiting inflammatory cells to sites of injury, which is consistent with our observations of loss of cell surface Ecrg4 expression in patients following trauma and brain injury. Here we further define the function of Ecrg4

Background: Early prediction of postoperative sepsis remains obscure. TNF-a also plays a major role in the clinical manifestations of sepsis, and serum levels inversely correlate with survival from severe sepsis. Inherited variability of cytokine production and genetic predisposition for fatal infectious diseases have been suggested. Several polymorphisms have been identified inside the TNF-a promoter, among which the G/A polymorphism at nucleotide position - 308 was found directly affecting TNF-a expression. In sepsis, interest has particularly focused on the promoter TNF-a-308 G/A single nucleotide polymorphism. We investigated association of TNF-a-308 G/A polymorphism and serum level of cytokine TNF-a, IL-6 and IL-8 with the development of sepsis following major surgery. Hypothesis: TNF-a-308 G/A polymorphism is associated with development of sepsis following surgery. Methods: 239 patients undergoing major elective gastrointestinal surgery were enrolled. Blood samples were drawn and genomic DNA was isolated. TNF-a-308 G/A polymorphism was studied using PCR-RFLP method. All patients were followed for 1 month following surgery for any evidence of sepsis. Serum cytokine TNF-a, IL-6 and IL-8 levels were measured pre and postoperatively by ELISA. Genotypes and cytokine levels were related to the occurrence of sepsis if any.

S-12 Results: 19.66% (n = 47) patients developed postoperative sepsis. Overall mortality was 3.34% (n = 8). The allele frequencies of G and A were 0.67 and 0.33 in patients with postoperative sepsis and 0.84 and 0.16 in patients without postoperative sepsis. Patients with postoperative sepsis were significantly (p = 0.002) more likely to possess AA homozygous genotype with higher capacity to produce cytokine TNF-a (p < 0.0001), IL-6 (p < 0.0001) and IL-8 (p < 0.0001) as compared to other genotypes. When compared with patients carrying at least one G allele (GG homozygous and GA heterozygous genotype), AA homozygous genotype was associated with an OR of 4.17 (p = 0.003; 95% CI = 1.5 to 11.48) for the development of sepsis. Compared with the homozygous GG genotype, the OR for the homozygous AA genotype was 5.18 (p = 0.0008; 95% CI = 1.82 to 14.76) for sepsis development. Conclusions: TNF-a-308 G/A polymorphism is significantly associated with the development of postoperative sepsis with increased expression of cytokine TNF-a, IL-6 and IL-8.

O-08. OBSTRUCTIVE SLEEP APNEA: A RISK FACTOR FOR SURGICAL SITE INFECTION AFTER COLECTOMY Spyridon Fortis, Kristin Colling, Catherine Statz, James Glover, Gregory Beilman, University of Minnesota Background: Obstructive sleep apnea (OSA) has not previously been identified as a risk factor for surgical site infection (SSI). OSA is associated with increased systemic oxidative stress, endothelial dysfunction and activation of pro-inflammatory cascades. Hypothesis: OSA is a risk factor for SSI after colectomy. Methods: We retrospectively reviewed data from all colectomies performed at the University of Minnesota Medical Center from August 2011 to September 2013 and identified patients with OSA undergoing colectomy. We matched patients with OSA to those without from the population of patients undergoing colectomy, with patient groups matched for age, body mass index (BMI), sex, open surgery, procedure time, diabetes mellitus (DM) and reason for surgery (e.g. cancer, inflammatory bowel disease or infection). Multivariate logistic regression and ANOVA were performed when appropriate. Results: Forty-two patients with preexisting OSA were identified from a total of 502 colectomies over the included time period. We matched these 42 patients to 68 patients from this population without OSA. The rate of SSI was 28.6% among the patients with OSA while the SSI in the control group was only 10.3% (p = 0.019). Compared to matched controls, multivariate regression analysis revealed the following risk factors for SSI: OSA (odds ratio [OR], 5.4; 95% confidence interval [CI], 1.19-24.58; p = 0.028), and DM (OR, 12.7; 95% CI, 2.08-77, p = 0.005). Age, BMI, sex, type of surgery and reason for surgery were not associated with an increased risk for SSI. OSA was associated with longer hospital stay in patients with SSI, but not in those that did not develop SSI (figure). Conclusions: OSA is an independent risk factor for SSI and is associated with longer hospital stay in patients that developed SSI after colectomy.

Length of hospital stay in days. *p < 0.05 vs OSA with SSI and no OSA with no SSI

ORAL PRESENTATION ABSTRACTS Methods: Institutional Review Board approval and parental/guardian consent was obtained. Buccal swabs for DNA extraction were collected from infants that were of the following clinical characteristics: £ 32 weeks gestation and/or a diagnosis of NEC ( ‡ Bell’s Stage II). Patients with congenital heart disease (except patent ductus arteriosus), major congenital anomalies, genetic disorders, and inherited blood/metabolic disorders were excluded. A TaqMan allelic discrimination assays were used to determine genotypes. Statistical analysis was completed utilizing logistic regression. Results: Ninety-two African-American infants were recruited for this study, of which 32 had NEC and 9 had spontaneous perforation. Allelic distribution for TNFa, NOS3, and IL1B were in Hardy-Weinberg equilibrium. Utilizing a dominant model, functional variants in TNFa, NOS3, IL1B, IL6, and IL12 were not associated with an increased risk of NEC, NEC totalis, or mortality. A copy of the rare allele for TNFa (rs1800629, -G308A) was associated with an increased risk of spontaneous perforation with an OR 5.97 [95% CI: 1.01 - 35.24, p 0.049]. Conclusions: In premature African-American infants, the functional variations in proinflammatory cytokine genes were not associated with an increased risk of NEC, NEC totalis, or mortality. The TNFa -G308A rare variant was associated with an increased risk of spontaneous perforation.

O-10. SCREENING FOR VENTILATOR-ASSOCIATED PNEUMONIA IN THE SURGICAL INTENSIVE CARE UNIT: SINGLE-INSTITUTION ANALYSIS OF 1,013 BRONCHOALVEOLAR LAVAGE CULTURES Fredric Pieracci, Maria Rodil, James Haenel, Robert Stovall, Clay Burlew, Jeffrey Johnson, Gregory Jurkovich, Ernest Moore, Denver Health Medical Center/University of Colorado Health Sciences Center Background: Refinement of criteria for both screening and initiation of empiric therapy in ventilator-associated pneumonia (VAP) will minimize antibiotic overuse. The aim of this study was to evaluate critically our current screening tools in order to develop evidence-based algorithms. Hypothesis: Clinical and gram stain (GS) variables used traditionally to screen for VAP have favorable test performance characteristics. Methods: Bronchoalveolar lavage (BAL) cultures obtained from surgical intensive care unit patients at attending discretion were abstracted (2009–2012). VAP was defined as ‡ 105 cfu/mL (not on antibiotics) and ‡ 104 cfu/mL (on antibiotics). The clinical pulmonary infection score both without (CPISclinical) and with (CPISclinical + GS) GS results was calculated. Data: median (range) or number (%). Stats: Wilcoxon rank, Fisher’s exact, receiver operator curve area under the curve (ROC AUC) and multivariable logistic regression. a = 0.05. Results: 1,013 lower respiratory tract cultures from 492 patients were analyzed; age 48 years (18–88), 823 (81.2%) from male patients and 719 (71.0%) from trauma patients. Number of respiratory cultures per patient was 2 (1–10) and days ventilated 11 (1–109). 310 of 492 patients (62.4%) had at least one episode of VAP. Both CPISclinical and CPISclinical + GS had poor discrimination for VAP (ROC AUC 0.55 and 0.66, respectively). Sensitivity of CPISclinical using a threshold of > 6 was 21%; the lowest threshold for CPISclinical for which the sensitivity was at least 85% was 3. The highest sensitivity among the individual CPIS components was new CXR infiltrate (91.1%). Among cultures sent during the early VAP window (days intubated < 5), organisms on GS had a sensitivity of 93.3%. CPISclinical, CPISclinical + GS, organisms, and neutrophils on GS all became less accurate in the late VAP window and when screening for recurrent VAP. Every case of VAP had at least one of the following 1) fever; 2) new CXR infiltrate or 3) organisms on GS (sensitivity = 100%). Conclusions: In this series, traditional screening tools for VAP missed over one-half of microbiologically-confirmed cases. Screening based on either new CXR infiltrate or fever yielded an acceptably high sensitivity. The only scenario identified in which empiric antibiotics could be withheld safely was the absence of organisms on GS in the early VAP window.


O-09. ARE FUNCTIONAL SINGLE NUCLEOTIDE POLYMORPHISMS OF PROINFLAMMATORY CYTOKINES ASSOCIATED WITH THE DEVELOPMENT OF NECROTIZING ENTEROCOLITIS OR SPONTANEOUS PERFORATION IN PREMATURE INFANTS? Ashanti Franklin, Mariam Said, Zoreh Tatari, Stanislav Vukmanovic, Khodayar RaisBahrami, Naomi Luban, Clint Cappiello, Joe Devaney, Anthony Sandler, Children’s National Medical Center Background: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal emergency that affects approximately 10% of premature neonates. There is an increased predilection in patients of African descent and males. Functional single nucleotide polymorphisms (SNPs) in nitric oxide synthase (NOS3) or proinflammatory cytokine genes, tumor necrosis factor (TNFa), IL1B, IL6, and IL12, lead to increased cytokine expression. Hypothesis: We evaluated whether African-American patients with polymorphisms in proinflammatory genes will have an increased susceptibility to NEC or spontaneous perforation.

Background: Necrotizing enterocolitis (NEC) is a deadly intestinal disease that affects newborn infants. Cronobacter sakazakii (CS) has been associated with outbreaks of NEC. Protein kinase A (PKA) is an abundant protein that is typically activated by cyclic adenosine monophosphate (cAMP). PKA has been associated both with cell survival and cell death pathways. Hypothesis: We hypothesized that cAMP and PKA mediated signaling may contribute to epithelial cell death in NEC. Methods: Three systems are used in this project: an in vitro cell line, a rat pup model of NEC and human tissue. After IRB approval, human intestinal segments were obtained from infants undergoing bowel resection for NEC (September 2012-November 2013), NEC strictures, or ostomy closures (controls). Protein was extracted for western blot analysis with antibodies for PKA, activated PKA and markers of apoptosis. Rat pups delivered near-term were subject to hypoxia (5%) and feeding with CS-inoculated formula, or dam fed. Intestinal samples were collected and processed for histology and protein extraction. Rat intestinal epithelial cells (IEC-6) were grown to 90% confluence and exposed to CS in vitro. PKA inhibitors (KT-5720 & SC-3010) were added at doses of 0.1 uM, 1 uM and 10 uM prior to CS infection. Cell and tissue lysates were assayed by

ORAL PRESENTATION ABSTRACTS western blot analysis of PKA, activated PKA and caspase-3. cAMP tissue levels were measured in all model systems by Elisa analysis. Results: Activated PKA was identified by Western blot analysis in human specimens with NEC (n = 4), as compared with controls (n = 6) p < 0.005. Increased caspase 3 activation was seen in patients with NEC as compared with controls. CS induces caspase 3 activation after 4 hours of co-culture in IEC-6 cells (P < 0.005). PKA is present in IEC6 and is activated by 4 hours of infection with CS. Furthermore, cAMP was increased in experimental NEC compared with breast milk fed controls (p < 0.005), and also in vitro after CS exposure. The addition of a PKA inhibitor prior to IEC-6 infection with CS prevents CS-induced apoptosis p < 0.005. Conclusions: We conclude that cAMP-PKA-mediated signaling may play an important role in CS-induced intestinal epithelial apoptosis. The prospect of PKA inhibitors presents an interesting potential therapeutic line of investigation.

O-12. TNFR1 LEVEL IN SEPSIS IS DEPENDENT ON MyD88-DEPENDENT UPREGULATION OF iNOS IN HEPATOCYTES Meihong Deng, Patricia Loughran, Liyong Zhang, Melanie Scott, Timothy Billiar, University of Pittsburgh Background: Our previous work showed that TLR4-dependent TNFR1 shedding from mouse hepatocyts (HCs) occurs via iNOS signaling in vivo and in vitro. However, the upstream signal for iNOS upregulation and TNFR1 shedding is unclear. MyD88 and Trif are two well-known signaling molecules downstream of TLR4. Hypothesis: Therefore, we hypothesized that HC-TNFR1 shedding might be MyD88 or Trif dependent in sepsis. Methods: WT (C57BL/6), MyD88KO, TrifKO mice were injected with LPS (5 mg/ kg, ip) for 6, and 12 h (n = 6 mice/group). Results: TNFR1 shedding was completely suppressed in the MyD88KO but not in TrifKO mice after LPS treatment. INOS mRNA level in the liver was significantly lower in MyD88KO than in WT and TrifKO mice. These findings using LPS as the activator show that HC-TNFR1 shedding and iNOS upregulation are MyD88-dependent. Several other relevant ligands can signal through MyD88. TNFR1 levels increased significantly in the media after 24 hrs treatment with Myddosome signals (HKLM-TLR2 ligand, LPSTLR4 ligand, HMGB1-TLR4 ligand, ST-FLA -TLR5 ligand, OD1669 -TLR9 ligand and IL-1-IL-1R ligand) compared with the no treatment controls. To further investigate the role of MyD88 in hepatocyte TNFR1 shedding, WT, MyD88KO, TrifKO, HCMyD88KO (HC MyD88 specific KO) and MyD88-flox mice (cell-specific KO controls) were subjected to a clinically relevant polymircrobial sepsis model (CLP with 5 mg/kg imipenem, 8 h, n = 6 mice/group). Likewise, TNFR1 shedding was MyD88-dependent (334 + / - 83 ng/mL in WT vs 179 + / - 36 ng/mL in MyD88KO, p < 0.05) but not Trifdependent (284 + / - 114 ng/mL) after CLP. Importantly, plasma TNFR1 level and iNOS mRNA level in the liver was significantly lower in HCMyD88KO than in MyD88flox mice. Conclusions: These data link systemic TNFR1 levels and TNFR1 shedding in sepsis to signaling pathways that upregulate iNOS through MyD88 in HCs.

O-13. INVARIANT NATURAL KILLER T-CELLS MODULATE THE GAMMA-DELTA-LYMPHOCYTE RESPONSE TO POLYMICROBIAL SEPSIS Whitney Young, John Young, Mai Tran, Shiang Chung, William Cioffi, Alfred Ayala, Daithi Heffernan, Brown University, Rhode Island Hospital Background: Lymphocytes and specifically innate lymphocytes cell subpopulations (ILCs) are emerging as central mediators in the response to and survival from sepsis. We have recently shown that among these ILCs, invariant natural killer T-cells (iNKT-cells) are key to survival from sepsis, and are critical modulators of neutrophil and macrophage function. Recent evidence suggests iNKT-cells may be capable of affecting other ILCs including the gamma-delta-T-cells (GDT-cell). Sepsis is associated with a divergent response; a preservation of iNKT-cells and a loss of GDT-cells in humans. Hypothesis: Sepsis will induce significant altertions in GDT-cell responses in a variety of tissue compartments, a response modulated by iNKT-cells. Methods: Both male wild type (WT) and iNKT-cell - / - mice underwent cecal ligation and puncture or sham. Liver, blood, and peritoneal fluid cell populations and circulating cytokines were assessed at 24 hours. Monoclonal antibodies directed against CD3, TCR-pan-dD (GDT-cells), and Va18-TCR were used. GDT-cell activation was evaluated using surface expression of CD69 and circulating levels of IL-17. Results: Following sepsis, wt and iNKT - / - mice displayed decreased circulating hepatic and peritoneal CD3 + lymphocytes. Sepsis was associated with increased hepatic GDT-cells in wt (1.64 vs 1.33 · 104; p = 0.04), which were more activated (47% vs 23%; p = 0.01). Further, in wt mice, sepsis was noted to induce an increase in absolute number of circulating GDT-cells (144 vs 89/100 microL; p = 0.02). Following sepsis, peritoneal GDT-cells were also increased (86.6 · 104 vs 4.08 · 104; p < 0.01) and more activated (78% vs 17%; p < 0.01). Conversely, iNKT - / - mice displayed decreased hepatic GDT-cells following sepsis (2.03 vs 4.02 · 104; p < 0.01) with lower activation (17% vs 32%; p < 0.01). This was associated with a decrease in peritoneal GDT-cells following sepsis in iNKT - / - mice (1.47 vs 3.01 · 104; p = 0.03). Compared to wt mice, iNKT - / - mice had markedly lower IL-17 levels (2.73 vs 12.12 pg/ml; p < 0.01). Conclusions: Sepsis induces priming and activation of GDT-cells in a variety of tissue sources. We demonstrate that iNKT - / - mice have the ability to alter sepsis

S-13 induced changes in the GDT-cell tissue populations and IL-17 expression. This data supports our previous observation of a divergent role of ILCs in human sepsis. iNKTcells may play a functional role in mediating the ILC response to sepsis.

O-14. HEPATIC HIGH MOTILITY GROUP BOX-1 (HMGB1) LEVELS ARE AFFECTED BY INVARIANT NATURAL KILLER T-CELLS IN POLYMICROBIAL SEPSIS John Young, Whitney Young, Shiang Chung, Yaping Chen, William Cioffi, Alfred Ayala, Daithi Heffernan, Brown University, Rhode Island Hospital Background: Invariant natural killer T-cells (iNKT) contribute to mortality in the murine model of polymicrobial sepsis. They play important roles in dampening the inflammatory response to sepsis, specifically neutrophils and macrophages. High motility group box 1 (HMGB1) is a highly conserved ubiquitous protein that has roles as a cytokine. It has been shown to be an early mediator of ischemic injury and a late mediator of experimental sepsis and is a potential target for immunomodulatory therapies. This study sought to clarify the role iNKT-cells in expression of hepatic HMGB1. Hypothesis: Hepatic HMGB1 will rise following CLP in WT mice with iNKT deficient mice showing a dampened HMGB1 response to sepsis. Methods: C57BL/6j (WT) mice or Ja18 - / - (iNK - / - ) mice were subjected to either sham laparotomy (sham) or cecal ligation and puncture (CLP). 24 (for WT mice) or 48 hours (for WT and iNKT - / - mice) later, liver samples were prepared and HMGB1 was assessed using western blot analysis. The integrated density value was measured and normalized by GAPDH. Results are expressed as a normalized HMGB1: GAPDH ratio. Circulating TNF-a and IFN-g (known stimulants of HMGB1 production) were measured using CBA cytometric analysis. Student’s t and ANOVAs were used for statistical analysis. Results: 24 h post CLP, WT mice displayed no statistically significant difference in HMGB1 expression as compared to their sham counterparts (0.61 + / - 0.09 vs. 0.49 + / - 0.08; p > 0.05). However, at 48 h post CLP, hepatic HMGB1 expression was increased in WT mice (1.01 + / - 0.07 vs. 0.49 + / - 0.08; p < 0.05). In contrast, iNKT - / - mice subjected to CLP did not show any change in expression of hepatic HMGB1 as compared to their sham counterparts (1.076 + / - 0.15 vs. 1.011 + / - 0.1; p = 0.7). iNKT - / - displayed significantly lower levels of TNF-a (15.3 + / - 1.4 vs 49.2 + / - 2.1 p = 0.01) and IFN-g (2.1 + / - 0.7 vs 12.3 + / - 1.7; p < 0.001). Conclusions: Congruent with our current understanding of HMGB1, we have shown that CLP leads to a late increased hepatic HMGB1 expression. iNKT - / - mice display lower cytokine levels of known drivers of HMGB1 expression in sepsis. Both baseline and the septic response of hepatic HMGB1 appears to be modulated by iNKT-cells.

O-15. MITIGATION OF SPLENOCYTE APOPTOSIS BY Th2-POLARIZED INVARIANT NATURAL KILLER T CELLS REDUCES DISEASE SEVERITY IN INTRA-ABDOMINAL SEPSIS Ram Anantha, Delfina Mazzuca, Stacey Xu, Brad Shrum, Tina Mele, Douglas Fraser, Claudio Martin, S.M. Mansour Haeryfar, John McCormick, Schulich School of Medicine and Dentistry, Western University Background: Invariant natural killer T (iNKT) cells are potent lymphocytes that can produce pro- and/or anti-inflammatory cytokines early in the course of an immune response. They present an attractive target for therapy in a wide range of human diseases. Because little is known about their role in sepsis, we sought to determine the frequency of iNKT cells in septic patients. We also employed a mouse model of intraabdominal sepsis (IAS) to test the effect of OCH, a Th2-polarizing agonist of iNKT cells that induces an anti-inflammatory phenotype, on disease severity. Hypothesis: We hypothesized that the frequency of iNKT cells would be elevated in septic patients, and that treatment with OCH would ameliorate disease severity in mice with IAS. Methods: Blood samples were drawn from patients with or without sepsis admitted to the intensive care unit within 48 hours. The frequencies of CD3 + conventional T cells and CD3 + CD1d tetramer + iNKT cells were determined by flow cytometry. A fecal solution was administered intraperitoneally to either OCH- or vehicle-treated C57BL/6 (B6) mice to induce IAS. After 24 hours, lymphocyte subsets (T cells and iNKT cells) were evaluated within the liver and spleen by flow cytometry. Organs were also harvested for histological and cytokine analyses. Results: Twenty-three septic and seven non-septic poly-trauma patients were identified. Peripheral blood iNKT cell frequency was higher (p = 0.047) in patients with sepsis (0.086% of T cells) compared to non-septic poly-trauma patients (0.014% of T cells). OCH-treated mice with IAS had significantly lower sepsis severity scores (p < 0.0001) and prolonged survival compared to vehicle-treated mice (p = 0.015). Treatment with OCH markedly reduced apoptosis of splenic macrophages, T cells, and B cells, but not natural killer (NK) cells. The expression of proinflammatory cytokines was also significantly reduced within the spleens of OCHtreated mice. Conclusions: Septic patients have an increased proportion of iNKT cells compared to non-septic patients. Polarizing iNKT cells towards a Th2 phenotype significantly reduces disease severity in IAS by mitigating splenocyte apoptosis, a novel finding that has not been previously reported. This study highlights iNKT cells as potentially important targets for therapy in sepsis.

S-14 O-16. CAN NASAL METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS SCREENING BE USED TO AVOID EMPIRIC VANCOMYCIN USE IN INTRA-ABDOMINAL INFECTION? Puja Shah, Sara Hennessy, Christopher Guidry, Robert Sawyer, Stephen Davies, Tjasa Hranjec, University of Virginia Background: Vancomycin is widely used as empiric therapy for gram-positive organisms in patients with an intra-abdominal infection (IAI), even in those with no history of methicillin-resistant Staphylococcus aureus (MRSA) infection or colonization. Potential adverse effects of vancomycin include nephrotoxicity, increased cost and bacterial resistance. Hypothesis: We hypothesized that nasal screening could be used to predict patients with MRSA IAI and used to avoid unnecessary empiric vancomycin use. Methods: A prospectively collected surgical infections database from a single institution was reviewed for all IAI between January 1, 2000 and December 31, 2011. Patients with and without MRSA obtained from abdominal cultures as either a monomicrobial or polymicrobial isolate were compared by univariate analysis using Wilcoxon rank sum, Chi-square, and fisher’s exact tests where appropriate. A multivariate logistic regression was performed to identify independent predictors of MRSA IAI. Results: MRSA nasal screening (pre-IAI) data were available for 387 patients of 2591 patients with an IAI. Patients with MRSA IAI (n = 48) had higher rates of diabetes, Crohn’s disease, and positive MRSA nasal screenings, along with lower white blood cell counts and rates of recent surgery compared to those with non-MRSA IAI. Mortality was similar between MRSA and non-MRSA IAI, 1/48 (2.1%) versus 18/339 (5.3%), respectively (p = 0.49). On multivariate analysis (c-statistic = 0.89), the strongest independent predictor of an MRSA IAI was a positive MRSA screen (OR 36.5, CI 14.4-92.4), followed by Crohn’s disease (OR 3.76, CI 1.2-11.6), and diabetes (OR 2.5, CI 1.1-5.7). The positive predictive value for a MRSA screen was 42% while the negative predictive value of MRSA screening was 98%. Conclusions: A negative MRSA nasal screen indicates with near certainty the absence of MRSA as part of intra-abdominal infection. In the setting of a recent screen, empiric vancomycin can be withheld. Further, rapid MRSA nasal screening could be used to forego or to rapidly discontinue vancomycin therapy in the setting of IAI. This change in empiric antibiotic management of intra-abdominal infections may lead to decreased morbidity, reduction in costs, and a decrease in bacterial resistance.

O-17. A RANDOMIZED, PROSPECTIVE STUDY OF SURGICAL SITE INFECTIONS FOLLOWING VASCULAR RECONSTRUCTIVE SURGERY: UNTREATED VS. SILVER-IMPREGNATED DRESSINGS Amani Politano, Margaret Tracci, David Strider, Robert Sawyer, John Kern, Gilbert Upchurch, Kenneth Cherry, University of Virginia Background: Surgical site infections (SSIs) can lead to significant comorbidities, especially in vascular patients, and particularly in the setting of synthetic conduits and distal incisions. Hypothesis: We hypothesized that post-operative placement of silver-impregnated dressings would decrease the incidence of SSIs following vascular reconstructions. Methods: This trial was a randomized controlled open label study of standard untreated surgical dressings (Primapore, smith&nephew, PP) versus silver-impregnated dressings (Therabond 3D, Choice Therapeutics, AG + ) in patients undergoing aortic or infrainguinal vascular procedures between August 2010 and November 2011. Randomization was performed by sequential block method. Prospective collection of patient demographics, operative and post-operative details, wound healing, and subsequent interventions were performed. Results: One-hundred-forty-five patients were enrolled; 70 received AG + , 75 PP. There were no differences in basic demographics or comorbid conditions, excepting more black patients in the AG + group. Type of operation did not differ significantly. Patients wore AG + longer than PP per the study protocol. The total number of infections in AG + was 25 (20.3%) compared to 19 (17.1%) in the PP group (NS), and did not vary by type of infection (table). Treatments for infection also did not differ. Conclusions: The use of silver in dressings, topical treatments, and other modalities reduces infections in some settings. However, in this study evaluating patients undergoing vascular reconstructive surgery with AG + compared to PP, no significant reduction in rates of SSI was noted. The addition of silver in this form to a wound dressing covering surgically closed wounds is unlikely to improve outcomes to a clinically significant degree.

ORAL PRESENTATION ABSTRACTS O-18. MICROBIAL ANALYSIS TO PREDICT ANASTOMOTIC LEAK IN HUMANS Preston Luong, Benjamin Shogan, Natalia Belogortseva, Simon Lax, Jack Gilbert, Olga Zaborina, John Alverdy, University of Chicago Background: Our laboratory has generated compelling evidence confirming that intestinal microbes are key causative agents in the pathogenesis of intestinal anastomotic leak. In a rat model, we identified two organisms, Pseudomonas aeruginosa and Enterococcus faecalis, that express a ‘‘leak-inducing phenotype’’ characterized by their capacity to produce collagenase and cleave host tissue matrix metalloproteinase MMP-9 that predicts leak. Hypothesis: The aim of this study was to determine if patients undergoing colon surgery harbor strains expressing the ‘‘leak-inducing phenotype’’ at the time of anastomotic construction. Methods: Eleven (11) patients undergoing colon surgery were studied under IRB protocol approved by the University of Chicago. To isolate microbes present at anastomotic tissues during surgery, we swabbed distal and proximal ends of resected colon segments immediately after removal. Microbial analysis was performed using standard culture techniques. Phenotype analysis of cultured microbes was performed using a fluorescein-based collagenase assay and a human recombinant MMP-9 cleavage assay developed in our lab. Finally, we performed 16S rRNA analysis to survey the background microbial community in which the cultured strains coexisted. Results: All 11 patients received IV cefoxitin prophylaxis according to the SCIP recommendations and all recovered from surgery. Among cultured strains tested, P. aeruginosa (only present in patient #10) and E. faecalis (only present in patient #11) produced high collagenase (n = 68, p < 0.001). Of strains tested, only P. aeruginosa and E. faecalis cleaved human recombinant MMP-9 from its inactive pro-form to its active collagen degrading form. 16S rRNA analysis at the phyla and genera level demonstrated a balanced and diverse community of microbiota in all except 1 patient (patient #10), where Gammaproteobacteria were abundant and the health-promoting Bacteroidetes were proportionally low. Only patient #10 developed a clinical course consistent with an anastomotic leak (collection on CT, percutaneous drainage, antibiotics). Conclusions: Data from the present study suggest that analysis of the species and phenotype of microbes that colonize anastomotic tissues, when coupled with an understanding of the background microbiota in which they coexist, might be a useful method to predict patients at risk for anastomotic leak. A larger clinical trial is underway that will be powered adequately to test this hypothesis formally.

O-19. VANCOMYCIN-ASSOCIATED NEPHROTOXICITY; THE OBESITY FACTOR Stephen Davies, Christopher Guidry, Zachary Dietch, Rhett Willis, Sara Hennessy, Robert Sawyer, University of Virginia Background: Current recommendations suggest vancomycin dosing utilize actual versus ideal body weight in obese patients due to accelerated renal clearance in this population. Additionally, an increase in multidrug resistant bacteria due to poor penetrance in certain tissues (e.g., lung) has resulted in higher vancomycin therapeutic ranges. Thus, obese patients may be at increased risk for nephrotoxicity. The purpose of this study was to compare the incidence of nephrotoxicity between vancomycin-treated, obese and lean patients at our institution where unadjusted, actual body weight-based dosing is used. Hypothesis: Obese patients will experience greater incidence of nephrotoxicity compared to lean patients. Methods: Patients treated with vancomycin for gram-positive or mixed infections in our facility from 1996–2008 were identified. Non-dialysis dependent patients were categorized by body mass index (BMI, lean < 30, obese ‡ 30). Categorical and continuous data were analyzed. Univariate, logistic regression was performed to evaluate each variable’s association with nephrotoxicity (i.e., 50% or 0.5 mg/dL increase in baseline creatinine). Results: 117 patients (lean = 72 vs obese = 45) with 211 separately identified infections (136 vs 75) met our inclusion criteria. Patient demographics, comorbidities (including initial creatinine levels), sites of infection, and organisms of infection were similar between groups. APACHE II scores (p = 0.0059) and Escherichia coli prevalence (p = 0.0002) were greater, while prevalence of nosocomial infection (p = 0.014) was less among obese compared to lean patients; however these differences were not associated with nephrotoxicity by logistic regression. Obese patients received vancomycin at similar trough levels (17 – 11 vs 14 – 8.3 mg/L; p = 0.10) for similar duration (9.8 – 9.9 vs 8.5 – 6.5 days; p = 0.92), and experienced similar maximum creatinine levels (1.6 – 1.3 vs 1.8 – 1.3; p = 0.092), incidences of nephrotoxicity [13(18%) vs 10(22%); p = 0.58], and mortality [10(14%) vs 8(18%); p = 0.57]. Conclusions: A difference in nephrotoxicity was not observed between lean and obese patients treated with vancomycin at our institution while using actual weightbased dosing. Additionally, similar trough levels (within the recommended target guidelines) were obtained. Unadjusted, actual weight-based dosing for vancomycin treatment among obese patients is appropriate, though larger sample sizes are needed to closely analyze this relationship among ‘‘at-risk’’ subsets of this population.

O-20. HYPOALBUMINEMIA IN OBESE SURGICAL PATIENTS IS DISPROPORTIONATELY ASSOCIATED WITH INFECTIOUS COMPLICATIONS Zachary Dietch, Christopher Guidry, Timothy McMurry, Rhett Willis, Stephen Davies, Robert Sawyer, University of Virginia

ORAL PRESENTATION ABSTRACTS Background: Protein-calorie deficiency (PCD) is a known risk factor for surgical complications, including surgical infections; however, the risks of PCD by weight class have not been well described. Hypothesis: We hypothesized that the combination of obesity and PCD is associated with increased surgical complications, including surgical infections, compared to normal weight patients. Methods: 89,718 general surgery patients undergoing elective operations within the 2011 National Surgical Quality Improvement Program were analyzed. Patients with conditions that could potentially confound serum albumin (SA) were excluded. Patients were stratified by normal ( > 3.0 g/dl) versus low ( < 3.0 g/dl) SA. The relative impact of SA and BMI (as individual and as combined variables) on surgical morbidity and mortality were assessed. Multivariate analyses were performed to identify independent risk factors for morbidity (overall and infectious) and mortality. Results: Overall, 2,933 (3.27%) of patients had low preoperative SA. 803 (27.4%) patients with low preoperative SA were obese (BMI > 30), versus 40,351 (46.5%) with normal preoperative SA. Importantly, the interaction of hypoalbuminemia and BMI was independently associated with infectious complications among hypoalbuminemic patients with BMI > 35, and mortality for patients with BMI > 30 (Table 1) after controlling for appropriate demographics, comorbidities, surgical wound classification, operation type and complexity (c-statistic: 0.768 and 0.874 respectively). Conclusions: PCD and hypoalbuminemia among obese surgical patients are associated with significantly increased morbidity and mortality compared to lean comparators. Paradoxically, malnutrition may be less easily recognized in obese individuals and surgeons may need to more carefully evaluate this population prior to surgery. Future studies should investigate therapy to correct PCD specifically among obese patients prior to surgery.

O-21. COMPLEX PELVIC SURGERY AND ADDITIONAL ORGAN RESECTION INDEPENDENTLY INCREASE THE RISK OF SURGICAL SITE INFECTION AFTER ELECTIVE COLORECTAL SURGERY: AN ACS-NSQIP ANALYSIS Mary Kwaan, Genevieve Melton, Robert Madoff, Jeffrey Chipman, University of Minnesota Background: Determining significant predictors of surgical site infection (SSI) in a large cohort is important for the design of accurate SSI surveillance programs. Hypothesis: Additional organ resection is independently associated with a higher risk of SSI. Methods: Patients in ACS-NSQIP (2005-12) were identified (n = 112,282). Infection (superficial or deep incisional SSI) at 30 days was the primary outcome (dependent variable). Using secondary CPT codes, additional organ resection was defined as: bladder resection/repair, hysterectomy, partial vaginectomy, additional segmental colon, small bowel, gastric, or diaphragm resection. Univariate analysis of patient and procedure factors identified significant (p < 0.05) predictors, which were modeled using stepwise logistic regression. Results: The rate of SSI was 9.2%. Strongest predictors of wound infection were high BMI (Table), bowel obstruction (OR) = 1.48), inflammatory bowel disease (OR = 1.35), open surgery (OR = 1.78), pelvic exenteration (OR = 1.48) and abdominoperineal resection (APR) (OR = 1.67). Additional organ resection was independently associated (OR = 1.19). Other risk factors are shown in the Table. Conclusions: In addition to other factors, complex pelvic surgery and additional organ resection are independently associated with a higher risk of SSI. In these established high-risk subgroups of patients, aggressive interventions to prevent SSI should be considered.

S-15 O-22. ASSOCIATION OF INFLAMMASOMES AND CASPASE-1 MEDIATED CARDIAC DYSFUNCTION WITH SEPSIS Deborah Carlson, Steven Wolf, University of Texas Southwestern Medical Center Background: Each year in the US, there are approximately 2.5 million episodes of sepsis requiring attention, accounting for > 100,000 hospitalizations and 12,000 deaths. Experimental and clinical studies have documented that patients with sepsis, experience cardiac dysfunction, and that non-survivors have significantly lower ventricular ejection fractions, and higher right ventricular end diastolic volumes than do survivors. We have shown that a family of cysteine proteases termed caspases, are directly associated with murine cardiac dysfunction following septic trauma. Caspase-1(Cas1) is known to induce apoptosis, and also cleave the precursor forms of IL-1 and IL-18 into active peptides, suggesting that Cas1 is a key player in the inflammatory response. Hypothesis: To investigate the involvement of Cas1 in cardiac dysfunction after septic injury. The role of Cas1 in the inflammatory response both systemically and in the myocardium following septic injury was also investigated. Methods: NOD.129S2(B6)-Casp1tm1Sesh/LtJ (Cas1 - / - ) and NOD/ShiLtJ (Cas1 + / + ) mice were injected IP with 4 mg/kg of E. coli 0111:B4 lipopolysaccharide (LPS) in a total of 0.5 ml, or PBS. Serum and hearts were collected at 4,8,12,18 and 24 hr post injection for analysis of serum IL-1, TNF, IL-6, MIF, and IL-10. qPCR analysis of myocardial IL-1, TNF, IL-6, MIF, and IL-10 expression. Fractional shortening was measured using M-mode echocardiography. TUNEL staining was performed from harvested hearts. Results: Loss of the Cas1 gene resulted in global changes in both circulating and cardiac specific cytokine expression at all time points examined post septic injury. A significant reduction in both TNF, as well as IL-1 was noted. mRNA expression in the heart significantly differed with the absence of Cas1. Specifically, there was no detectable increase over control at any time point besides 24 hrs for IL-6, IL-10, and IL-1 beta. There was a significant increase in fractional shortening in Cas1 - / - mice relative to Cas1 + / + mice at 2 hours (Cas1 + / + 52.7% vs. Cas1 - / - 65.9%, p = 0.042) and 24 hours (Cas1 + / + 46.8% vs. Cas1 - / - 63.6%, p = 0.032). Conclusions: Lack of Cas1 resulted in a decreased expression of known inflammatory cytokines during sepsis, and ameliorated myocardial dysfunction in septic mice. The increased cardiac function seen with the lack of upregulation of IL-1 beta in the myocardium suggests an important role for the inflammasome and its activation in sepsis.

O-23. VARYING HOST RESPONSE IN DIFFERENT LOW-LETHALITY MODELS OF MURINE ABDOMINAL SEPSIS Lori Gentile, Dina Nacionales, M. Cecilia Lopez, Angela Cuenca, Alex Cuenca, Benjamin Szpila, Ricardo Ungaro, Shawn Larson, Christiaan Leeuwenburgh, Frederick Moore, Henry Baker, Lyle Moldawer, Philip Efron, University of Florida College of Medicine Background: Animal models for the study of sepsis are being increasingly scrutinized. However, they remain essential for early translational research. In this report, we examined two different low-lethality murine models (20–40%) of polymicrobial intraabdominal sepsis at the level of the leukocyte transcriptome, and explored their overall effects on genes involved in innate and adaptive immunity. Hypothesis: We hypothesized that the cecal slurry (CS) model of sepsis would have more robust early inflammatory changes, whereas the cecal ligation and puncture (CLP) model would show greater changes involving adaptive immune suppression. Methods: 6–10 week old male C57BL/6j mice underwent either the ‘gold standard’ CLP model of intra-abdominal sepsis or the CS model of intra-abdominal sepsis, where cecal contents are injected i.p. Surviving mice were euthanized at 2 hrs, 1 or 3 days after sepsis. Whole blood was collected, and total RNA was isolated. Genome-wide expression analysis was performed on total blood leukocytes and expression patterns were compared between healthy control mice and septic mice (p < 0.001). Functional pathway analysis was performed using Ingenuity Pathway Analysis. Results: We found that the murine leukocyte transcriptomic response to CLP and CS models of sepsis were genomically dissimilar at 2 hours, 1, and 3 days after sepsis, with changes in gene expression in less than 1/3 of the probe sets overlapping. The Pearson correlation coefficient for the maximum change in expression for probe sets that changed significantly over time (n = 19,071) was R = 0.545 (R2 = 0.297). The CS model resulted in a greater magnitude of inflammatory gene expression changes in response to sepsis with an associated increased production of inflammatory chemokines and cytokines. Two hours after sepsis, the CLP pathway had more significant expression of genes associated with IL-10 signaling, whereas the CS pathway had greater expression of genes related to CD28, apoptosis, IL-1, and T-cell receptor signaling. By 3 days, the changes in gene expression from all pathways were returning to baseline in both the CS and CLP models. Conclusions: These analyses reveal that the murine blood leukocyte response to sepsis is markedly different depending on which model of intra-abdominal sepsis is employed, despite similar lethalities. Whereas the CS model favors the early proinflammatory changes, the CLP model is more evident of adaptive immune suppression.

O-24. GLUTAMINE IMPROVES INNATE IMMUNITY AND THE INTESTINAL BARRIER FUNCTION DURING PARENTERAL NUTRITION Rebecca Busch, Xinying Wang, Joseph Pierre, Aaron Heneghan, Kenneth Kudsk, University of Wisconsin, Madison

S-16 Background: PN patients are at increased risk for infectious complications compared to enteral feeding. Impaired mucosal immunity during PN provides a cogent explanation for part of this vulnerability. Adding glutamine (GLN) to PN has improved outcome in some clinical patient groups. Although GLN improves acquired mucosal immunity, its effect on innate mucosal immunity (defensins, mucus, lysozymes) has not been investigated. Hypothesis: We hypothesized addition of GLN to PN would improve innate immune function during PN. Methods: Forty-eight hours following venous cannulation, male ICR mice were randomized to receive chow (n = 10), PN (n = 12), or PN + GLN (2%) (n = 13) daily for 5 days. Small intestine wash fluid and ileum segments were collected for analysis of MUC2 and lysozyme density, and luminal levels of IL-4, IL-10 and IL-13. Tissue was also harvested for use in an ex vivo intestinal segment culture to assess susceptibility of the tissue to enteroinvasive Escherichia coli. Results: In both luminal and tissue samples, PN reduced MUC2 and lysozyme (P < 0.0001, respectively) compared with chow, whereas GLN addition increased MUC2 and lysozyme (luminal: P < 0.05 and tissue: P < 0.0001, respectively) compared with PN alone. PN significantly suppressed cryptdin 4 expression, while GLN supplementation significantly enhanced its expression. IL-4, IL-10 and IL-13 decreased significantly with PN compared with chow, whereas GLN significantly increased these 3 cytokines compared with PN. Functionally, bacterial invasion increased with PN compared with chow (P < 0.05), while GLN significantly decreased enteroinvasion similar to but not statistically different from chow levels (P < 0.05). Conclusions: GLN supplemented PN improves innate immunity and resistance to bacterial mucosal invasion that is lost with PN. This work confirms a clinical rationale for providing GLN for the protection of the intestinal mucosa with PN.

O-25. MESENCHYMAL STEM CELLS REVERSE CHRONIC STRESS INDUCED BONE MARROW DYSFUNCTION FOLLOWING TRAUMATIC INJURY Amy Gore, Letitia Bible, Walter Alzate, David Livingston, Alicia Mohr, Ziad Sifri, New Jersey Medical School, Rutgers Background: Bone marrow (BM) dysfunction following lung contusion (LC) resolves quickly, but the addition of chronic stress (CS) to LC results in persistent bone marrow dysfunction. Mesenchymal stem cells (MSC) have protective immunomodulatory effects which have not been tested in the setting of CS. Hypothesis: We hypothesize that MSC can protect the BM against the deleterious effect of CS following LC. Methods: Male Sprague-Dawley rats (n = 6-8/group) underwent LC or LC/CS – MSC injection. CS consisted of a daily 2 hour period of restraint with repositioning and exposure to alarms every 30 minutes to prevent habituation. A single iv dose of 5 · 106 MSC in 1 mL IMDM media was given ten minutes following LC. Animals were sacrificed at day seven and peripheral blood (PB) and BM were collected. Flow cytometry was used to assess HPCs mobilized to PB. BM cellularity and growth of BM HPC colonies (CFU-E, BFU-E, CFU-GEMM) were evaluated. Results: The addition of CS to LC resulted in a 32% decrease in BM cellularity, a significant decrease in CFU-GEMM, BFU-E, and CFU-E and marked increase in HPC in the PB as compared naı¨ve animals. The addition of MSC to LC/CS resulted in a 22% increase in BM cellularity and significant increase in CFU-GEMM, BFU-E, and CFU-E cultured from the BM. The addition of MSC to LC/CS prevented prolonged mobilization of HPC to PB and restored colony growth to naı¨ve levels. Conclusions: Chronic stress following LC results in persistent BM dysfunction manifested by a significant decrease in cellularity, HPC colony growth and increased HPC mobilization to the PB at seven days following injury. The addition of MSC following an acute traumatic injury reversed the deleterious effects of CS on BM function. Further study into the immunomodulatary effects of MSC in the setting of CS setting is warranted.

ORAL PRESENTATION ABSTRACTS Methods: Littermate OSMR + / + and OSMR - / - B6.129S-Osmr mice were studied in a fluid-resuscitated variant of the cecal ligation and puncture (CLP) model of sepsis. Using a standardized protocol of 50% cecal ligation and 18 gauge puncture, the mice were observed for a period of 12, 24, and 48 hours, with regular saline administration. Additional groups with shorter time points (0.5 and 1 hour), and standard time points (12–48 hours) without fluid resuscitation were carried out. Following the end point of the fluid-resuscitated groups, peritoneal lavage was performed. Tissue and blood samples were obtained. Cultures of spleen homogenate and whole blood were performed. Results: All animals (n = 42) survived to the standard end points with fluid resuscitation. Without fluid resuscitation, identical animal groups had 50% and 33% mortality at 48 hours, for OSMR + / + and OSMR - / - respectively (n = 6 each). Fluid resuscitation was demonstrated to be adequate, with no significant difference in serum blood urea nitrogen and renal Ngal between all fluid-resuscitated groups. Assessment of bacterial translocation in blood showed higher mean bacterial counts in OSMR - / - animals at 24 and 48 hours (65-fold and 25-fold higher colony counts, respectively). No trends were seen with cultures of spleen homogenate. Peritoneal lavage yielded no significant differences in overall cells counts. Serum levels of OSM increased rapidly after the onset of CLP, with > 2-fold increase compared to sham at 0.5 hours (p < 0.05). Conclusions: Signalling through the OSM/OSMR axis begins early in the onset of CLP. OSM deficiency results in increased bacterial translocation in the setting of intraabdominal sepsis, which is independent of the survival effects. Understanding this signalling cascade can provide novel strategies for treating intra-abdominal sepsis.

O-27. WOUND INFECTION AFTER ATTENUATING A KEY INFLAMMATORY SIGNALING PATHWAY Saman Arbabi, Adelaide Warsen, Nicolas Shubin, Megan Knoll, Joseph Cuschieri, Liang Qiao, Anne Hocking, University of Washington Background: Several investigators have proposed attenuating the innate immune response to injury to reduce the risk of subsequent systemic inflammatory response syndrome and organ failure. However, interfering with the innate immune response may increase the risk of subsequent infectious complication, such as wound infections. We have previously demonstrated that topical burn-wound inhibition of a key inflammatory signaling pathway, p38 MAPK, improved end-organ function and mortality in a rodent thermal injury model. Hypothesis: We hypothesized that while p38 MAPK inhibition significantly attenuates wound innate immune response, it does not increase the risk of subsequent wound infections. Methods: We used the female red Duroc pig wound model, which has been validated by us and others as a good model of human wound healing with a similar scarring phenotype. We performed three separate experiments with total of 12 pigs. Six pigs received dermatome wound injuries, and 6 received scald burn injuries. Each pig in the dermatome group received ten 4 · 5 cm deep dermal wounds in the dorsal paraspinal region. The pigs with burn injuries received deep partial thickness thermal injury in the paraspinal region using a hot water bottle technique. Out of the total of 12 pigs, 5 were treated with a topical p38 MAPK inhibitor and 7 were in the control group (5 with topical vehicle and 2 with no wound treatment). All the wounds were created after clipping the hair and scrubbing with chlorhexidine. The pigs did not receive any antibiotics or dressing. The experiments lasted up to 20 weeks after injury. Results: The topical p38 MAPK inhibition significantly attenuated wound innate immune response with improved healing. All pigs survived until the conclusion of the experiments with normal weight gain. The only wound infection was at a routine biopsy site in a pig that received the vehicle and was successfully treated with one dose of IM antibiotic. One pig had mild eye infection after corneal abrasion during general anesthesia, which was treated with eye drops. There were no other infectious complications. Conclusions: Topical p38 MAPK inhibition significantly attenuated wound innate immune response; however, none of the wounds treated with the inhibitor developed an infection. Using a porcine model, which closely resembles human wound healing, we demonstrated no infectious complication associated with inhibition of a key inflammatory signaling pathway.


O-26. ONCOSTATIN M MODULATES IMMUNE CELL RECRUITMENT AND BACTERIAL TRANSLOCATION IN A MURINE MODEL OF SEPSIS Pang Young, Saad Salim, Catherine Compston, Thomas Mueller, Rachel Khadaroo, University of Alberta Background: Sepsis is a major contributor to inpatient mortality and morbidity worldwide. Understanding the pathogenesis of sepsis is important in the development of new therapeutic modalities. Oncostatin M (OSM) is an immunomodulatory cytokine in the IL-6 family. Prior work in our laboratory demonstrated deficiency of OSM signalling is protective in sepsis, with improvement in survival and end organ injury. The mechanism of OSM in sepsis remains unclear. Hypothesis: We hypothesize that OSM signalling occurs early on in the onset of sepsis, and is involved in peritoneal immune cell recruitment.

William Symons, Keary Husain, Steve Jarman, Bryan Sato, Grant Bochicchio, Douglas Schuerer, John Mazuski, Washington University Background: Patients who undergo trauma laparotomy are at high risk for infectious complications, with up to 50% sustaining some type of postoperative infection. Use of perioperative antibiotics in this population has not been optimized, particularly with regard to antibiotic redosing for blood loss or length of operation. Hypothesis: A protocol for uniform use of antibiotics with long half-lives and appropriate spectrum of activity, coupled with scheduled redosing for high blood loss will decrease the rate of postoperative infections. Methods: A pre-/post-intervention trial was carried out from November 2009August 2013 in all patients undergoing laparotomy for acute trauma. No intervention was made during the first 24 months of the trial. During the subsequent 22 months, a protocol was implemented in which all trauma surgeons were requested to use ertapenem as the preferred antibiotic prior to incision, and to redose the antibiotic with each blood volume lost. Surviving patients were characterized as having no infection, a minor surgical site


infection only, an infection related to laparotomy, or an unrelated infection such as pneumonia. The pre-/post-intervention groups were compared using Fisher’s exact test. Results: A total of 134 patients were included in the pre-intervention cohort and 111 in the post-intervention cohort. The groups were similar with respect to demographics, mechanisms of injury, TRISS scores, and amount of blood transfused, with the post intervention group having a higher incidence of colonic injuries (28% vs 40%, p = .06). Use of ertapenem increased from 8% in the pre-intervention group to 55% in the postintervention group (p = .0001). As shown in the Table, overall incidence of infections decreased by 37% in the intervention cohort, with a 39% decrease in infections directly related to laparotomy. Conclusions: Use of the antibiotic protocol resulted in an overall reduction of all infectious complications, particularly in infections related directly to laparotomy.

O-29. SUSTAINABILITY OF A HOSPITAL-ACQUIRED PRESSURE ULCER PREVENTION BUNDLE IN SURGICAL PATIENTS Sylvia Martinez, Carla Braxton, Ryan Helmick, Samir Awad, Agueda Lara-Smalling, Baylor College of Medicine Background: Hospital-acquired pressure ulcers (HAPU) are associated with significant morbidity, mortality, and cost. However, HAPU represent a potentially preventable condition. On initial investigation, an evidence-based HAPU prevention bundle (HAPUB) was prospectively implemented with a reduction in HAPU rates in the first 6 months. We propose that HAPU-B can result in sustained decreased HAPU rates. Hypothesis: Implementation of an evidence-based HAPU-B can result in an early decrease in HAPU rates that is sustainable. Methods: A multidisciplinary prevention team created an evidence-based HAPU-B. Risk was assessed using the Scott Triggers (Age > 62 Albumin < 3.5 ASA > 3 Surgery > 3 hrs). From August 2012, for high risk patients ( ‡ 2 triggers), the HAPU bundle was applied: 1) Comprehensive skin assessment on admission, transfer and discharge 2) Placement on OR beds with pressure-redistributing mattress; careful positioning and padding of pressure points 3) Scheduled q2h turns with pressure points relief by adjusting devices, massage of bony prominences, pillows, heel pads, or wedges 4) Prevention hand-off between providers 5) HAPU assessment on daily rounds. Unit specific HAPU rates on the surgical service were collected 6 and 14 months post-HAPU-B and compared to rates at 6 month pre-HAPU-B implementation. Student’s ttest and Chi square test were used for statistical analysis. Results: Daily HAPU-B checklists were used for high-risk patients admitted to the surgical service. Six months after implementation, the mean surgical HAPU rate decreased from 3.37 – 0.19 to 1.45 – 0.33, p = 0.004. During the same time, mean VHA HAPU rate was unchanged (1.84 – 0.31 to 1.85 – 0.06, p = NS). By unit, the HAPU rates significantly decreased (ICU:Pre = 2.93 – 0.9, Post = 1.25 – 0.7; Ward: Pre = 2.93 – 0.6, Post = 0.83 – 0.3, p = 0.019). At 14 months post-implementation, HAPU rates remained at lower levels (Fig. 1). Conclusions: Implementation of an evidence-based HAPU-B resulted in significantly decreased HAPU rates on the surgical service. The reduced rates were sustained 14 months after implementation.

S-17 Background: Staphylococcus aureus bacteremia (SAB) and its complications remain a persistent and challenging problem among intravenous drug users (IVDUs) that has resisted advances in medical and surgical therapies. Hypothesis: We sought to determine the risk factors associated with mortality among IVDUs with SAB. Methods: We retrospectively reviewed all patients admitted with SAB between 2008 and 2012 at a tertiary-care centre in Southwestern Ontario. Hospital records were used to identify IVDUs, admissions to the intensive care unit (ICU), complications of SAB such as infective endocarditis (IE) and osteomyelitis, and mortality. Multivariable logistic regression was performed to determine predictors of mortality in all SAB patients, and particularly in IVDUs. P values less than 0.05 were considered statistically significant. Results: We identified 927 patients in our study: 167 (18%) were IVDUs. IVDUs were significantly younger than non-IVDUs (p < 0.0001), and had increased frequencies of IE (p < 0.0001), osteomyelitis (p < 0.0001), and sepsis (p = 0.022). Patients with IE were more likely to be infected by methicillin-sensitive, rather than methicillin-resistant, S. aureus (p = 0.0086). A similar proportion of IVDUs and non-IVDUs required ICU admission (23% and 30% respectively, p = 0.086). Although overall mortality in our study was 40%, we observed a significant (p = 0.019) decline in annual mortality. On multivariable analysis, sepsis (OR 1.83, 95% CI: 1.35-2.49, p < 0.0001) and mechanical ventilation (OR 3.46, 95% CI: 1.87-6.37, p < 0.0001) were independently associated with mortality among all patients with SAB. Among IVDUs, diagnosis of IE (OR 2.54, 95% CI: 1.13-5.68, p < 0.024) and prolonged ( > 21 days) mechanical ventilation (OR 19.8, 95% CI: 3.74-104.8, p < 0.0001) were independent predictors of mortality. Methicillin resistance was not predictive of mortality in either population. Conclusions: This study, to our knowledge, features the largest single-centre retrospective review of SAB in Canada. Identification of mortality predictors, combined with the characterization of antimicrobial resistance, may guide empiric therapy for patients with SAB, especially when there is clinical concern for complicated infections such as IE. This study also highlights the importance of reducing the duration of mechanical ventilation among patients with SAB, paving the way for future prospective studies.

O-31. VENTILATOR-ASSOCIATED EVENTS: CORRELATION WITH VENTILATOR-ASSOCIATED PNEUMONIA? Arek Wiktor, Christy Scipione, Laraine Washer, Pauline Park, Krishnan Raghavendran, Lena Napolitano, University of Michigan Background: The new ventilator-associated event (VAE) CDC surveillance definition algorithm was initiated in January 2013 to serve as objective measures of complications occurring in patients on mechanical ventilation utilizing a three tiered approach: ventilator-associated conditions (VAC), infection-related ventilator-associated complications (IVAC), and possible/probable ventilator-associated pneumonia (VAP). We sought to examine rates of VAEs in our surgical ICU and correlate with VAP rates. Hypothesis: VAEs are associated with VAPs. Methods: Prospective data were collected by APACHE and infection control providers for 11 months (1/2013–11/2013) in a 20-bed surgical ICU (SICU) that serves as an ARDS referral center at a University Hospital. VAC and IVAC were compared with possible VAP using the Fisher’s exact t-test. Ventilator bundle (HOB elevated, sedation holiday, wean assessment, SUP, chlorhexidine) compliance was 97–100%. Results: In this time period, the SICU had 1020 admissions with a total of 53 VAEs (29 VAC alone) in 44 patients. Patients with > 1 VAE ranged 2–4 events per ICU admission. Of all VAEs, 24 (45.2%) were IVACs, with an IVAC rate of 4.6/1000 ventilator days (VD). Possible VAP was confirmed in 11 (45.8%) of IVACs, with a possible VAP rate of 2.7/1000 VD. Possible VAP was not correlated with VAC (p = 0.67) but was strongly correlated with IVAC (p = 0.0056). Ventilator utilization ranged from 36–66% of total patient days. VAE and VAC rates significantly increased with ventilator utilization (R2 = 0.9139 for VAE, 0.7987 for VAC). Standardized mortality ratio (SMR) was 0.57 for ICU and 0.53 for hospital mortality. Conclusions: VACs identify episodes of sustained respiratory deterioration, are associated with increasing ventilator-utilization and commonly occur in ARDS and chronic ICU patients, but are not associated with increased VAP.



Ram Anantha, Januvi Jegatheswaran, Daniel Pepe, Johan Delport, John McCormick, Tina Mele, Schulich School of Medicine and Dentistry, Western University

Timo Hakkarainen, Tomio Tran, Nicole Burkette Ikebata, Eileen Bulger, Heather Evans, University of Washington

S-18 Background: Necrotizing Soft Tissue Infection (NSTI) is a devastating disease process with high morbidity and mortality. Treatment consists of wide surgical debridement and often, prolonged periods of ICU care. NSTI survivors are at risk for significant sequelae related to both disease and treatment. Information about the health-related quality of life (HRQOL) for NSTI survivors and clinical determinants of outcome is limited. Hypothesis: Survivors of NSTI will have reduced health-related quality of life (HRQOL). Clinical factors related to extent of surgical treatment, disease complications, and patient comorbidities will help predict outcomes. Methods: Retrospective cohort analysis of patients treated at a regional referral center for NSTI from 2007–2011. Patients were surveyed using the Short Form 36 (V2) between 22 and 73 months following admission. Additional information about return to prior employment, depression and PTSD symptoms was collected. Logistic regression analysis identified patient and clinical factors associated with poor outcome. Results: Of 345 patients discharged after treatment for NSTI, 279 were contacted. Surveys of 202 survivors (73% response rate) demonstrated lower summary scores for physical (35.1, 95% CI 27.2-43.0, p = < 0.001) and mental (34.3 [95% CI 29.8-38.8], p < 0.001) domains compared to the general population. Sub-scores were lower in all eight domains. There was a high incidence of depression (39% [95% CI 19-59%]) and PTSD symptoms (42% [95% CI 18-64%]). 48% (95% CI 37-59%) of patients were unable to return to previous level of employment. Upper extremity amputation, > 5 debridements, > 10 ICU days, renal failure without return of function prior to discharge, and/or involvement of the hand or face were independently associated with poor HRQOL. Wound coverage procedure, < 3 debridements, and involvement of the trunk or perineum were independently associated with better HRQOL. Conclusions: The majority of patients treated for NSTI have reduced HRQOL 22-73 months after discharge with impairments in physical, emotional, and social functioning. There is also high prevalence of PTSD and depression symptoms among survivors. A large proportion of survivors are unable to return to previous employment. Patient and clinical factors associated with long-term HRQOL and function may allow targeted follow-up and intervention with patients at high risk of poor outcomes. O-33. A SURGEON-DIRECTED PERIPHERALLY INSERTED CENTRAL CATHETER TEAM UTILIZING A NOVEL SCREENING PROTOCOL TO DECREASE INFECTIOUS COMPLICATIONS AND ASSOCIATED COST Hua Wang, Allan Peetz, Naomi Shimizu, Ali Salim, Vihas Patel, Brigham and Women’s Hospital, Harvard University Background: Since 2000, a selective screening protocol assessing appropriateness of peripherally inserted central catheters (PICC) was introduced by our hospital-wide surgeon-led PICC team. Hypothesis: We hypothesized that this process is associated with decreased infectious complications and cost. Methods: Retrospective review of a prospectively maintained database of PICC consults between 2000–2013. All PICC consults are captured by a computer order entry system and then evaluated by a highly specialized team member for indication, duration of intravenous therapy and contraindications. Consults are triaged by urgency and PICCs are inserted using ultrasound and electromagnetic tip imaging. Data regarding PICC indications, reasons for disapproval, location of procedure (bedside versus angiography suite), septic and phlebitic complications were analyzed. Comparisons between PICC and other central venous devices were made. Cost was conservatively estimated to be $491/PICC and supplies, $11,971/blood stream infection (BSI) episode and $7594/ DVT episode. Results: Over the 13-year study time period, 35,651 PICC consults were requested resulting in 24,638 insertions. Over 95% of insertions were successfully accomplished at the bedside within 0.5-day from approval. Comparing PICC with all other central devices, infection rate was 5.9% versus 7.0% (p = 0.26) and phlebitis rate was 1.9% versus 2.9% (p = 0.43). 30.8% of all the PICC consults were disapproved for reasons including duration of intravenous therapy < 3-days, existing central venous access, highly suspected or confirmed BSI, violation of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines, patients not approved by the Nutrition Support Service for TPN, and coagulopathy. Attributable cost saved from unnecessary procedures was $5,407,383 and complications avoided (BSI $7,778,361 and DVT $1,589,022) equaled $14,774,766. Conclusions: We demonstrate that implementing a hospital-wide surgeon-led PICC consult service can reduce the total number of PICC placements leading to significant healthcare cost savings. O-34. THE ENTERIC NERVOUS SYSTEM (ENS) NEUROPEPTIDE, BOMBESIN (BBS), MAINTAINS GOBLET CELL FUNCTION DURING PARENTERAL NUTRITION (PN) Aaron Heneghan, Rebecca Busch, Joseph Pierre, Xinying Wang, Kenneth Kudsk, University of Wisconsin–Madison Background: Parenteral a nutrition (PN) increases the risk of infection in critically ill patients. Recently, we identified a PN-induced decrease in GI tract innate mucosal immunity during PN which included lower production & secretion of the goblet cell protein, MUC2. MUC2 coats the mucosa concentrating defensive molecules made by the mucosal immune systems. The goblet cells produce and secrete other peptides as well, including trefoil factor 3 (TFF3). TFF3 is implicated in protection and repair of the mucosa & its release is governed by neuropeptides produced by the ENS. Experimentally, BBS, a gastrin-releasing neuropeptide analogue, reverses PN-induced defects in gut and respiratory acquired immunity.

ORAL PRESENTATION ABSTRACTS Hypothesis: Since PN reduces goblet cell function, we hypothesized that the ENS neuropeptide BBS would increase production & secretion of goblet cell products. Methods: 2 days after IV cannulation, randomized male ICR mice received Chow (n = 7), PN (n = 6), or PN + BBS (15 ug TID) (n = 7) for 5 days. Small intestine wash fluid (SIWF) was collected for analysis of the goblet cell products MUC2 and TFF3 by western blot. Defined segments of ileum were analyzed for tissue MUC2. Results: Compared to chow, PN significantly reduced levels of MUC2 (Chow: 34,543 + 6,535 vs PN: 8,232 + 762, p < 0.05) and TFF3 (Chow: 16,909 + 1,334 vs PN: 5,814 + 1,030, p < 0.05) in small intestinal fluid samples. Addition of BBS to PN significantly increased intestinal fluid levels of MUC2 (PN: 8,232 + 762 vs PN + BBS: 21,020 + 2,226, p < 0.05) and TFF3 (PN: 5,814 + 1,030 vs PN + BBS: 16,996 + 2,957, p < 0.05) compared to PN alone and back to Chow levels. There were no differences in tissue MUC2 levels between Chow and PN mice (Chow: 77,425 + 5,107 vs PN: 77,190 + 2,674, p > 0.05). However, PN + BBS significantly increased MUC2 tissue levels compared to chow and PN (PN + BBS: 94,189 + 5,374 vs Chow: 77,425 + 5,107). Conclusions: PN significantly impairs the goblet cell component of innate mucosal immune function. The ENS neuropeptide, bombesin, significantly improves this innate immune dysfunction and establishes the link between ENS and goblet cell function.

O-35. COMPUTATIONAL PREDICTION OF A NOVEL TRANSCRIPTIONAL REGULATION FOR THE PqsH ENCODING GENE IN PSEUDOMONAS AEURGINOSA Scott Christley, Olga Zaborina, John Alverdy, Gary An, University of Chicago Background: Pseudomonas aeruginosa is one of the most clinically significant microbes in healthcare associated infections, and is well known to transform into virulent phenotypes through host-pathogen interactions in conditions of host-stress. Quorum sensing is known to be involved in virulence transformation, however the ubiquitous challenge remains: The task of integrating vast amounts of data to generate new knowledge that can be tested in an efficient manner. Herein we present a novel approach using advanced computational modeling and bioinformatics to identify a novel putative regulatory interaction in P. aeruginosa quorum sensing. Hypothesis: Our computational analysis suggests the hypothesis that under low oxygen conditions, Anr is produced and suppresses transcription of PqsH. Methods: We developed a computational model from a literature survey that integrates the three primary P. aeruginosa quorum-sensing systems, LasRI, RhlRI, and MvfR-PQS. We performed large-scale simulations of the model ( > 25 million in 2 days using a desktop GPU machine) using novel computational algorithms developed by our group to extract useful predictions without requiring (typically unknown) kinetic rates. Bioinformatic search of DNA binding sites was performed using the motif search tool at Results: The computational simulations results suggest that the only currently known transcriptional regulation of the pqsH gene by the LasRI quorum system is insufficient to explain observed data under high phosphate (25 mM) conditions. Specifically, an inhibitory regulation of PqsH is required. PqsH encodes an enzyme for producing PQS from HHQ, and this metabolic reaction is limited by oxygen availability, which suggests that PqsH may be regulated by the oxygen-sensing system via its transcription factor Anr. A bioinformatic search of the Anr binding motif, TTGN{3,8}TCAA, reveals a potential binding site within the transcriptional unit of the pqsH gene. Conclusions: This research has shown that the compilation of biological knowledge from existing literature into a computational model, and then the use of dynamic simulations to analyze that model, can lead to novel and specific hypotheses. While the hypothesis that Anr suppresses transcription of PqsH is yet to be validated, the significant result is that computational analysis was able to pinpoint a gap in our current knowledge.

O-36. THE GENOMIC EXPRESSION OF AGED MURINE HEMATOPOIETIC STEM CELLS AFTER POLYTRAUMA INDICATES A FAILURE TO SUPPORT DEVELOPMENT OF INNATE IMMUNITY Philip Efron, Dina Nacionales, Donevan Westerveld, M. Cecilia Lopez, Fatima Needell, Lori Gentile, Erin Vanzant, Benjamin Szpila, Ricardo Ungaro, Angela Cuenca, Alex Cuenca, Azra Bihorac, Anna Joseph, Frederick Moore, Christiaan Leeuwenburgh, Henry Baker, Lyle Moldawer, University of Florida Background: Increased age is associated with worse outcomes after severe trauma. Our work using a mouse polytrauma (PT) model recapitulates this human phenotype - only aged mice have increased susceptibility to pseudomonal pneumonia after PT. In addition, bronchoalveolar lavages from these aged mice show myeloid cell dysfunction. Hypothesis: We hypothesize that dysfunctional emergency myelopoiesis by aged murine hematopoietic stem cells (HSCs) explains this phenomenon and is revealed at the genomic level. Methods: Young (6–12 wks) or old (18–24 mos) B6 mice underwent PT (90 mins shock + long bone fracture + cecectomy). Bone marrow (BM) samples were collected at 1 day. HSCs (Lin-sca-1 + ckit + ) were isolated through fluorescent cell sorting. Nucleic acids were collected and amplified. Genome-wide expression patterns were analyzed with a log2 transformed expression matrix using RMA. Then genes with significant expression differences were identified using BRB array tools (p < .001, t-test). Using Ingenuity Pathway Analysis (IPA), significant gene sets from PT mice were compared directly and with healthy controls (p < .001, f-test). Results: 593 probe sets representing 426 genes discriminated old vs young PT HSCs with 100% correct classification (leave one out cross validation). Functional analysis of

ORAL PRESENTATION ABSTRACTS these genes showed that only young PT had upregulation of genes involved in leukocyte recruitment and endotoxin shock response pathways (Z-score > 2), while only old mice downregulated the quantity of reactive oxygen species pathway (Z-score < 2). Only young PT were suggested by IPA as responsive to granulocyte colony stimulating factor as an upstream regulator. Individual gene analysis showed that young PT had significantly increased expression of innate immunity genes, such as chemokine receptor 2, caspase 12, toll-like receptor 1, and chemokine ligand 1; while interleukin (IL) 7, IL10 receptor a, and interferon receptor a/b 1 was reduced in the young. Finally, MHCII antigen presentation genes had significantly decreased fold expression in old PT. Conclusions: Transcriptomic analysis of murine HSCs after PT indicates the development of innate immunity myeloid cells in the elderly BM is significantly reduced. As HSCs are still plastic, therapies to alter the expression patterns of these cells in the elderly have the potential to improve emergency myelopoiesis in the aged after injury.

S-19 induced low-grade NEC at 106 cfu/mL and high-grade NEC at 108 cfu/mL. Strain 44 induced high-grade NEC at both doses. Conclusions: Our findings suggest that specific bacterial strains are implicated in the pathogenesis of NEC. Strain 22 did not promote NEC and thus may have been protective. Strain 44 strongly promoted NEC - an example of a true NEC pathogen. Further examination of these strains may provide useful insights into the pathogenesis, treatment, and prevention of NEC.


O-37. URSODEOXYCHOLIC ACID AS A MEDIATOR OF INTESTINAL EPITHELIAL CELL RESTITUTION Stephanie Papillon, Avafia Dossa, Annie Roberts, Henri Ford, Mark Frey, Christopher Gayer, University of Southern California, Children’s Hospital Los Angeles Background: Dysbiosis of the intestinal microbiota is implicated in a number of gastrointestinal inflammatory diseases, including necrotizing enterocolitis. While the mechanism is unknown, bile acids may play a role. Some intestinal bacteria can metabolize bile acids into ursodeoxycholic acid (UDCA), while others generate more injurious secondary bile acids, deoxycholic (DCA) and lithocholic (LCA). The epidermal growth factor receptor (EGFR) is a known signaling target of bile acids and may play a role in the differing effects of specific bile acid metabolites. Hypothesis: We hypothesize that UDCA modulates epithelial cell migration via regulation of EGFR. Methods: After 24 hours of serum-starvation, rat intestinal epithelial cell (IEC-6) monolayers were subjected to a modified wound restitution assay in the presence of bile acids, EGF, the EGFR inhibitor AG1478, the ADAM17 inhibitor TAPI-1 or a combination of these. Pictures were taken at zero and six hours and compared. Western blots were used to assess EGFR phosphorylation. Results: Most conjugated and unconjugated primary bile acids tested did not alter epithelial cell migration. DCA and LCA, meanwhile, decreased baseline migration (12% and 30%, respectively). This change was rescued by EGF administration. In contrast, UDCA and its glycine conjugate (GUDCA) stimulated cell migration at 6 hours (15% above control). UDCA reversed the inhibitory effects of DCA, while only partially reversing the LCA-induced decrease in cell migration. UDCA-stimulated cell migration was blocked by the EGFR inhibitor. Immunoblotting analysis revealed that IEC-6 treatment with UDCA led to EGFR phosphorylation at two hours. Inhibition of the metalloproteinase ADAM17 by TAPI-1 blocked both UDCA-stimulated migration and EGFR phosphorylation. Conclusions: These data demonstrate UDCA promotes epithelial cell migration via a mechanism involving metalloproteinase-induced release of EGFR ligand. This mechanism is capable of overcoming DCA-induced inhibition of migration. These results provide a possible mechanism through which intestinal dysbiosis can lead to disease via shifting the bile acid pool toward injurious metabolites. We also identify a potential therapeutic target via manipulation of the EGFR pathway.

Background: Percutaneous sharps injuries pose a significant occupational hazard for surgical personnel. Exposure to blood-borne pathogens from injuries can threaten a practitioner’s health, livelihood, and career, and often results in emotional distress. Despite well-documented consequences and increased awareness, an estimated 600 K to 800 K injuries occur per year in the US. The purpose of this study was to investigate the frequency, location, and contributing factors in sharps injuries in order to identify operational barriers and areas for improvement in the handling process. Hypothesis: Systematic analysis of the frequency, location, and personnel affected by sharps injuries can identify opportunities to implement interactive safe handling techniques and ongoing education to more effectively reduce injuries. Methods: A retrospective review of data from October 2009 to July 2012 was conducted identifying service lines and personnel most often affected by sharps injuries. The following interactive safe handling techniques were implemented from August 2012 to September 2013: creation of a safe zone in the operative field to allow use of handsfree technique for transfer of sharps, use of ‘Call and Response’ system when passing sharp instruments, and utilization of monthly training and education for residents and students. Results: Upon initial review, 184 sharps injuries were reported for all service lines. Eighty-two (44%) sharps injuries were reported within the Operative Care Line (OCL) alone. Residents reported 68 (37%) injuries, the largest number among all groups. Sharps injury data for August 2012 to September 2013 were then analyzed after implementation of interactive safe handling techniques and sharps injury education. During this period sharps injuries significantly decreased for the OCL (Fig. 1). Percent decreases for MD staff, residents, and students were 40%, 63%, and 42%, respectively. Conclusions: Interactive safe handling techniques and ongoing sharps education have a positive impact in reducing sharps injuries.

O-38. NEC AS AN INFECTIOUS DISEASE: IDENTIFYING STRAINS OF OPPORTUNISTIC PATHOGENS Debi Thomas, Brandon Bell, Stephanie Papillon, Anatoly Grishin, Henri Ford, University of Southern California, Children’s Hospital of Los Angeles Background: Despite significant improvements in neonatal intensive care, necrotizing enterocolitis (NEC) continues to be a significant cause of morbidity and mortality in premature infants. The pathophysiology of NEC remains poorly understood. Formula feeding, bacterial colonization and hypoxic/ischemic conditions are major risk factors. The role of bacterial pathogens as causative agents of NEC is suggested by hospital outbreaks of the disease secondary to contaminated formula. Hypothesis: While the premature gut is colonized with a variety of microbial species, we hypothesize that predominant species and strains acting as opportunistic pathogens are key in the pathogenesis of NEC. Methods: To test this hypothesis, we isolated bacteria from NEC animals, and assessed the ability of these bacteria to promote NEC upon introduction to naı¨ve rat pups. NEC was induced in neonatal rats by formula feeding, hypoxia (5% O2 for 10 min) and hypothermia (8C for 10 min), three times daily for four days. On day of life four, the rats were euthanized and a segment of the terminal ileum was resected for analysis. NEC was graded histologically. Intestinal microbiota were characterized by plating serially diluted homogenates of terminal ileum on blood agar. Bacterial colonies emerging after 48 h incubation at 37C were classified based on their appearance, and each class was enumerated. Bacterial species were identified by sequencing the variable region of the 16S rRNA gene and querying a nucleotide database. Suspected NEC pathogens were identified (designated numbers 4, 9, 22, 44, and 69) and introduced to rat pups subjected to the same NEC protocol. Formula was prepared daily with bacterial concentrations of 106 colony forming units per milliliter (cfu/mL) and 108 cfu/mL. After sacrifice on day of life 4, NEC was graded. Results: Bacterial strain 22 did not induce NEC. Bacterial strain 69 induced lowgrade NEC at 106 cfu/mL. Strain 4 induced low-grade NEC at 108 cfu/mL. Strain 9

O-40. ACUTE KIDNEY INJURY (AKI) CAUSES PERSISTENT DYSREGULATION OF THE LEUKOCYTE TRANSCRIPTOME Benjamin Szpila, Erin Vanzant, Lori Gentile, M. Cecilia Lopez, Angela Cuenca, Ricardo Ungaro, Dina Nacionales, Christiaan Leeuwenburgh, Henry Baker, Azra Bihorac, Mark Segal, Frederick Moore, Lyle Moldawer, Philip Efron, University of Florida Background: Following severe blunt trauma, patients often develop organ injury. AKI is a known risk factor associated with worse outcomes following trauma. The Inflammation and Host Response to Injury (Glue Grant) showed that patients with a ‘complicated’ clinical course ( > 14 ICU days with organ injury) had a prolonged and exacerbated genomic response involving innate and adaptive immunity, and that the expression of 63 specific genes could predict a complicated outcome. Hypothesis: We hypothesize that AKI will have a similar effect on these trauma patients’ genomic profile, looking at both genome-wide and the specific 63 genes. Methods: 244 severely traumatized patients (ISS > 15, no TBI, SBP hypotension or elevated BD, requirement for blood transfusion), genome-wide expressions were evaluated from blood neutrophils (PMN). The AKI cohort was based on RIFLE criteria (sCr increased · 2 or GFR decreased > 50% plus UO < 0.5 ml/kg/h · 12 h, n = 59) within 3 days. These were compared to non-AKI patients (n = 105). Samples were taken at 0.5, 1, 4, 7, 14, 21, and 28 days. Patients were cross-matched for gender, age, and ISS. Analysis

S-20 consisted of identifying gene expression differences among AKI, nonAKI, and healthy subjects (p < .001). Individual gene changes (compared as gene expression fold change to control), functional pathway, and Gene Ontologies were analyzed. Distance from reference (DFR) was calculated for all gene sets as a ln measure of aberration in gene expression. Results: At day 28, Gene Ontology showed that DFRs of pathways regarding inflammation/immunity were noted to be significantly greater (AKI vs non-AKI, respectively). These pathways include PMN and its surface molecules (4.3 vs 3.7), IL2 signaling (DFR 4.8 vs 4.3), and activation of the innate immune response (6.2 vs 5.8). Analysis of the 63 specific genes showed similar downregulation in immune response genes as seen in complicated patients, including: PDGF C, Prostaglandin-endoperoxide synthase 2, IFN-induced proteins, and Hect domain. Surprisingly, gene ontology analysis at 0.5 days also showed significantly different DFRs, indicating that genomic prediction of AKI early after trauma may be possible. Conclusions: The presence of AKI in trauma patients appears to lead to both early and late PMN genetic differences. Alterations in these genetic responses may prove useful in screening for predisposition to AKI and its long-term consequences, as well as possible therapies.


Conclusions: In the absence of an established gold standard, our chest CT aspiration score provides a new approach to the diagnosis of aspiration in trauma patients. The strong relationship between thoracic AIS scores and evidence of aspiration on chest CT reflects the challenge of discrimination between pulmonary aspiration and chest injury. However, higher CTAS was associated with worse clinical outcomes, including higher rates of pneumonia, reinforcing the negative impact of early injury-associated events.

O-43. PREDICTORS OF MONOMICROBIAL NECROTIZING FASCIITIS O-41. EXTERNAL VALIDATION OF THE VENTRAL HERNIA RISK SCORE FOR PREDICTING SURGICAL SITE INFECTIONS Mike Liang, Lillian Kao, Robert Martindale, Scott Roth, University of Texas Health Sciences Center, Houston Background: Previously, we reported that the Ventral Hernia Risk Score (VHRS) was more accurate in predicting surgical site infection (SSI) following open ventral hernia repair than other models such as the Ventral Hernia Working Group (VHWG) model in a Veterans Affairs population. VHRS was developed based on single-center data and stratifies SSI risk into five groups based on concomitant hernia repair, skin flaps created, American Society of Anesthesiologists score ‡ 3, body mass index ‡ 40 kg/m2, and wound class 4. The purpose of this study was to externally validate the VHRS in a twoinstitution cohort. Hypothesis: The VHRS has greater predictive accuracy of SSI following open ventral hernia repair compared to VHWG grade. Methods: A mixed prospective and retrospective database of all open ventral hernia repairs performed at two institutions from 2009–2012 was utilized. All patients with a follow-up of at least 1 month were included. The Center for Disease Control definition of SSI was utilized. Each patient was assigned a ventral hernia risk score and ventral hernia working group classification. Receiver operator characteristic curves (ROC) were used to assess predictive accuracy and the areas under the curve (AUCs) were compared between the two models. Results: A total of 311 patients underwent open ventral hernia repair; 69 (22.2%) patients developed a SSI. AUC of the VHRS (0.80) was greater than that of the VHWG (0.77); however both were highly accurate in predicting SSI. Conclusions: The VHRS provides a novel, externally validated risk assessment score of a patient’s likelihood to develop a SSI following open ventral hernia repair. Although the VHRS was developed in a Veterans Affairs population of largely high-risk, older men, this data provides evidence that the VHRS is generalizable to other populations. Elevating skin flaps, ASA score 3 or 4 patients, performing concomitant procedures, morbid obesity, and wound class all independently predict the likelihood of SSI. It remains to be seen if preoperative risk reduction, intra-operative surgical technique, and postoperative management can improve outcomes in the highest risk patients.

O-42. USE OF COMPUTED TOMOGRAPHY TO DIAGNOSE ASPIRATION IN TRAUMA PATIENTS Vanessa Fawcett, Joseph Cuschieri, Heemun Kwok, David Carlbom, Joel Gross, Heather Evans, University of Washington Background: While aspiration is linked to the development of respiratory complications following injury, the diagnosis remains challenging. Hypothesis: Chest computed tomographic (CT) scans can contribute to the diagnosis of aspiration and the prediction of poor clinical outcomes in trauma patients. Methods: We employed an existing dataset of ventilated adult trauma patients prospectively assessed for clinical evidence of aspiration during intubation. Patients who underwent chest CT imaging within 24 hours of hospital arrival were included in the analysis. A single radiologist, blinded to the clinical condition of the patients, retrospectively reviewed the CT images. Using the following pre-determined scoring system, the likelihood of aspiration was assessed: 0 = None, 1 = Possible, 2 = Probable, 3 = Definite. Descriptive statistics and univariate analyses were used to compare patient characteristics, injury severity, and outcome by CT aspiration score (CTAS). Results: 163 patients met the inclusion criteria. There were no differences in patient characteristics when compared by CTAS. Higher CTAS was associated with higher injury severity scores (mean group ISS 17.0 – 3.3 vs 21.8 – 1.5 vs 27.9 – 2.7 vs 45.0 – 5.0, p < 0.01 by ANOVA), especially severe thoracic injuries (mean group maximum thoracic AIS 0.5 – 0.2 vs 1.4 – 0.2 vs 2.2 – 0.3 vs 2.7 – 0.9, p < 0.01 by ANOVA). Table 1 displays patient outcomes. Patients with higher CTAS showed a trend towards increased hospital and ICU length of stay (LOS). As CTAS increased, the likelihood of developing pneumonia also increased. Using ordered logistic regression controlling for maximum thoracic AIS, we observed that evidence of clinical aspiration predicted CTAS (p < 0.001).

Rhett Willis, Christopher Guidry, Christopher Horn, Daniel Gilsdorf, Robert Sawyer, University of Virginia Background: Broad-spectrum antibiotic therapy is a cornerstone in the management of necrotizing fasciitis in the emergent setting. Clindamycin is often included empirically to cover monomicrobial gram-positive pathogens, but is associated with significant side effects, including the induction of Clostridium difficile colitis. However, there have been no studies predicting monomicrobial infections prior to obtaining cultures. The purpose of this study was to identify independent predictors of monomicrobial necrotizing fasciitis in order to avoid the use of clindamycin where unnecessary. Hypothesis: We hypothesized that monomicrobial infections are characterized by involvement of the upper extremities and fewer comorbid diseases. Methods: We reviewed all cases of potential necrotizing soft tissue infection occurring between 1996 and 2013 in a single tertiary care center. Necrotizing fasciitis was defined as rapidly progressing necrotic fascia upon debridement with positive tissue cultures. Univariate analysis was performed using T-test, Wilcoxon rank sum, Chi-sq., and Fisher’s exact test where appropriate. Multivariate logistic regression was used to identify independent variables associated with the outcome. Results: 151 patients with confirmed necrotizing soft tissue infections with complete data sets were used for this study. Of the monomicrobial infections, 61.8% were Group A streptococci, 20.1% S. aureus and 12.7% E. coli. Of the polymicrobial infections, E. coli was involved 13.7% of the time, followed by Candida species 12.9%, and B. fragilis 11.3%. On univariate analysis, immunosuppression, upper extremity infection, and initial serum sodium were associated with monomicrobial infection, while morbid obesity and perineum infection site were associated with polymicrobial infection. On multivariate analysis, the strongest predictor of monomicrobial infection was immunosuppression (OR: 7.00 95% CI 2.198-22.32) followed by initial serum sodium (OR: 1.1, 95% CI 1.032-1.236). Morbid obesity (OR: 0.055, 95% CI 0.007-0.45) and perineum infection site (OR: 0.32, 95% CI 0.134-0.765) were independently associated with polymicrobial infection. C-statistic for the model = 0.819. Conclusions: We identified independent risk factors associated with monomicrobial necrotizing fasciitis. We suggest empiric clindamycin coverage could potentially be limited to patients who are immunosuppressed, have an elevated serum sodium, or with upper extremity involvement.

O-44. TRANSFORMING GROWTH FACTOR BETA INDUCED EPITHELIAL-MESENCHYMAL TRANSITION LEADS TO PERSISTENT INTESTINAL FISTULAE Xiuwen Wu, Jianan Ren, Gefei Wang, Qin Wu, Jieshou Li, Jinling Hospital, China Background: Autologous glue can lessen closure times and promote closure rates in treatment of low-output enterocutaneous fistulas (ECFs). Factors affecting outcomes of the glue-assisted closure (GAC), however, are not clear. Hypothesis: The GAC-failed ECF might have a prolonged inflammatory phase modulated by excessive pro-inflammatory cytokines or proteases. Methods: A hospital based case-control study was performed. Blood samples and fistula tissues were collected before the autologous glue application. Protein or mRNA levels of biological markers (IL-6, IL-1b, TNF-a, IL-8, IL-10, GM-CSF, and TGF-b) were studied by multiplex xMAP immunoassay or real-time PCR. Those GAC-failed fistula patients turned to definite operations and surgical removed specimens were further analyzed by hematoxylin and eosin staining, and immunohistochemistry. Results: A total of 22 ECF patients with low-output volume were enrolled for the glue application. Elevated levels of pro-inflammatory cytokines (GM-CSF, IL-1b, IL-6, and TNFa), but decreased levels of anti-inflammatory cytokines (IL-8 and IL-10) from plasma as well as tissue samples were observed in GAC-failed fistulas (p > 0.05). Only TGF-b was significantly higher in open fistulas among all cytokines (p < 0.05). Besides, strong staining for b6-integrin, the mesenchymal marker, was found in transitional cells lining the tracts of surgically resected fistulas and in epithelial cells of deformed crypts adjacent to the fistulas. Conclusions: TGF-b was associated with the failure of GAC and provided a further hint that the growth factor was responsible for the epithelial-to-mesenchymal transition (EMT). Therefore, we speculate that EMT might take place in and around the majority of these GAC-failed fistulas.

ORAL PRESENTATION ABSTRACTS O-45. GENOMIC AND PROTEOMIC SURVIVAL BIOMARKER PROFILES IN SEVERELY BURNED CHILDREN Padma Nainar, Bernard Fongang, Xueling Li, Ronald Tompkins, Andrzej Kudlicki, David Herndon, Celeste Finnerty, University of Texas Medical Branch, Galveston/ Shriners Hospitals for Children Background: Following a severe burn injury, massive perturbations in the peripheral blood leukocyte genome and proteome occur. We have previously reported differential gene expression in severely burned children and adults. Abundance of proteins such as cytokines or acute phase proteins has been used to predict patient outcome and clinical course. Here we examine protein and gene expression in severely burned children to determine candidate proteins and genes for predicting patient outcome. Additionally we identify pathways that are implicated in the survival response due to significant differences in both gene and protein expression with respect to survival of the burn injury. Hypothesis: Both genes and proteins can be used to develop a biomarker profile that can be used to predict early identification of survival in children with large burn injuries. Methods: Gene expression in peripheral blood leukocytes from pediatric burn patients was measured using the Affymetrix HGU133 Plus 2.0 microarray. For this analysis, 254 gene chips were analyzed. These represented 101 pediatric patients with > 30% of total body surface area burned, admitted to our burn unit within 72 hours of injury, and requiring at least one operation. 58 analytes (cytokines, hormones, acute phase proteins, metabolic markers) were measured in the serum using techniques such as ELISA, nephelometry, and multi-plex analysis. T-tests were used to determine candidate biomarker genes. ANOVAs were used to identify candidate proteins. Significance was accepted at p < 0.05. Results: On the Affymetrix GeneChips, 14,489 probe sets were differentially expressed in survivors compared to non-survivors, p < 0.05. Changes in gene expression were similar to the modulations seen with cytokines and acute phase reactants. In both the proteomic and genomic data sets, the most significant differences associated with survival were found within the signaling pathways induced by IL17, IL10, IL4, and IL5. Conclusions: These results suggest that biomarker candidate proteins and genes which may enable improved prediction of patient outcome can be correlated with survival. Identification of signaling pathways via methods such as these may enable determination of mechanisms and therapeutic targets in patients not surviving major burn injuiry.

O-46. INTESTINAL BILE ACIDS DIFFERENTIALLY CONTROL INTESTINAL CELL PROLIFERATION Avafia Dossa, Stephanie Papillon, Henri Ford, Mark Frey, Christopher Gayer, University of Southern California, Children’s Hospital Los Angeles Background: Disruption of intestinal epithelial cell proliferation contributes to gut barrier failure in necrotizing enterocolitis. Certain enteric bacteria convert conjugated, primary bile acids (BAs) into more toxic, unconjugated secondary metabolites. Evidence suggests that while some bile acid metabolites may be beneficial to the intestine, secondary metabolites are injurious and lead to disease. Both the epidermal growth factor receptor (EGFR) and the farnesoid X receptor (FXR) are known molecular targets of bile acids and are thought to have opposing effects on intestinal cell proliferation. Hypothesis: We hypothesized that BAs differentially modulate intestinal epithelial cell proliferation via specific activation of either EGFR or FXR. Methods: We examined the effects of bile acids on the proliferation of rat intestinal cells (IEC-6) in vitro and confirmed these effects in a mouse colon cell line (YAMC) using both a crystal violet proliferation assay and a nucleic acid incorporation assay (EdU). Pharmacologic manipulation of both EGFR and FXR were used to determine their molecular contribution. Western blot analysis was used to assess EGFR phosphorylation. Results: Of all bile acids tested, only taurine-conjugated cholic acid (TCA, a primary bile acid) stimulated intestinal cell proliferation (119.3 – 3.6% above baseline) while glycine-conjugated cholic acid and unconjugated cholic acid did not. The TCAinduced increase in proliferation was blocked by the EGFR antagonist AG1478 and by the FXR agonist GW4064. Treatment with TCA stimulated EGFR phosphorylation (Tyr1068) at 6 hours on Western blot analysis. In contrast, the taurine-conjugated secondary bile acid deoxycholic acid had no effect on intestinal cell proliferation, while the unconjugated form (DCA) decreased intestinal cell proliferation (70.8 – 4.1% below baseline). The inhibitory effects of DCA were abolished in a dose dependent manner by blocking FXR activity with guggulsterone. Conclusions: These results suggest that specific bile acids can be either beneficial or injurious to intestinal epithelial cell proliferation via differential activation of EGFR and FXR. Since secondary bile acids increase during times of dysbiosis, this suggests a possible mechanism by which an altered microbiome may impair intestinal integrity and lead to disease.

O-47. THE GUT DURING PROLONGED CRITICAL ILLNESS HARBORS LOWMEMBERSHIP PATHOGEN COMMUNITIES THAT ARE LESS VIRULENT AS A GROUP THAN INDIVIDUALLY Olga Zaborina, Alexander Zaborin, Daniel Smith, Jack Gilbert, John Alverdy, University of Chicago Background: Loss of intestinal microflora emerges during critical illness under constant pressure from antibiotic use.

S-21 Hypothesis: Here we hypothesized that as low-membership communities adapt to the gut during critical illness, their virulence is repressed by each other as a mechanism of survival. Therefore the aim of this study was to examine the interdependence of individual pathogen community members on overall virulence among low membership communities. Methods: Using 16S rRNA and culture analyses, we examined the composition of 30 stool samples from 14 patients treated in the ICU at the University of Chicago for extended periods. We selected 2-member pathogen communities and determined their virulence, together and individually, using Caenorhabditis elegans killing assays as a model of intestinal infection. Results: Among 30 stool samples analyzed by 16S rRNA, 17 were determined to harbor low-membership pathogen communities (1–4) consisting at the genera level of Enterococcus or Staphylococcus, or at the family level of Enterobacteriaceae only. Culture analysis revealed Candida spp. in > 75% of samples (15/17). Surprisingly a subset of 4 samples contained only 2 members: Sample 1 had C. albicans + multi-drug resistant (MDR) Enterococcus faecium; sample 2- C. grabrata + MDR CoA- Staphylococcus; sample 3- C. glabrata + MDR Klebsiella pneumoniae, and sample 4- C. albicans + MDR K. pneumoniae. C. albicans and C. glabrata alone were highly lethal against C. elegans, however in each case their lethality was markedly attenuated in the presence of their bacterial community member (n = 40/group, p < 0.01). For example, C. albicans from the sample 1 killed 100% of C. elegans at 72 hrs while the same amount of C. albicans incubated with E. faecium, resulted in only 30% mortality. Phenotype analysis demonstrated that E. faecium completely suppressed hyphae formation of C. albicans. Conclusions: The survival, evolution, and virulence phenotype of intestinal microbes exposed to prolonged critical illness and their effect on outcome remains illdefined. As they adapt and survive, loss of one community member can affect the virulence of the other. Metagenomic interrogation of intestinal community structure, function, and virulence capacity is now possible and may offer surprising insight into the untoward effect of prolonged antibiotic use during critical illness.

O-48. MUSCLE INJURY AND ISCHEMIA CONTRIBUTE TO THE PATHOGENESIS OF A. BAUMANNII INFECTION Irma Fleming, Olga Zaborina, Natalia Belogortseva, Alexander Zaborin, Jennifer DeFazio, John Alverdy, University of Chicago Background: Acinetobacter baumannii wound infections are associated with high mortality in extensive military injuries involving deep extremity muscle trauma, but rarely cause wound infections in civilians. Hypothesis: We hypothesized that A. baumannii wound infections are a result of bidirectional cross-signaling between injured/ischemic host tissues and bacteria that make them particularly prevalent in blast injuries of major muscle groups. The aim of this study was to develop a model of A. baumannii infection that would allow for the identification of such signals. Methods: A muscle injury/ischemia model of A. baumannii infection was developed by exposing the rectus abdominus muscle via a skin incision and inoculating 100 mL of 105 CFUs to the rectus muscle for 2–3 min, followed by a saline wash, then skin closure. Acinetobacter baumannii (AC) infection to the rectus muscle was created in groups of mice with and without muscle injury (light crush injury) and with and without muscle ischemia (suture ligation of muscle). On post-operative day 7 (POD7), wounds were examined for purulence, HIF1a, AC colony counts, and AC virulence expression using Galleria mellonella virulence assays. Results: Gross infection (purulence) occurred in 100% of mice subjected to AC inoculation onto injured and ischemic muscle (n = 30, p < 0.01), which demonstrated a higher degree of HIF1a expression (see Figure). No infection/pus was noted in all other treatment groups, i.e. muscle injury alone, ischemia alone, no muscle injury, no ischemia. In treatment groups where AC was inoculated onto both ischemic and injured muscle, there was a higher bacterial count (10-fold) compared to all other groups. In this group we also noted that AC shifted its colony morphotype to a rough-edge colony appearance compared to the normal smooth edged colonies observed in all other groups. Rough colony morphotypes were more lethal to Galleria mellonella than smooth colonies (n = 15 p < 0.05). Conclusions: Muscle injury and ischemia may play a role in enhancing the virulence of A. baumannii and may explain its lethal effect in traumatic extremity injury. The role of HIF in this process remains to be elucidated.

O-49. DIFFERENTIAL IMMUNE AND HORMONAL EXPRESSION IN CARDIAC VERSUS HEPATIC BLOOD AFTER BURN INJURY IN RODENTS Mile Stanojcic, Elena Bogdanovic, Marc Jeschke, University of Toronto Sunnybrook Health Sciences Centre Background: Thermal injury is one of the most severe forms of trauma that a person can experience. The use of animal models of burn injury has enabled the ability to overcome clinical limitations through experimental design. Typically, the assessment of serological measures is limited to samples taken from cardiac puncture.

S-22 Hypothesis: The following study investigates the immune and hormonal profiles of control and burn mice by comparing blood collected from cardiac and hepatic portal vein blood. Furthermore, it will elucidate whether the portal system including small and large bowel as well as adipose tissue, has a different metabolic and inflammatory profile. Methods: Thirty-six balb/c mice (4–6 weeks old) were included in the study and divided into non-burn control (n = 14) and burn (n = 22) groups. Within each group, blood was collected from either cardiac (control, n = 12; burn, n = 17) or hepatic portal blood (control, n = 2; burn, n = 5). A multi-analyte Milliplex (Millipore, MA) platform was used to measure inflammatory and hormonal cytokines in plasma samples. Data was analyzed using mann-whitney, students t-test and ANOVA for differences in terms of collection location and experimental group. Results: There was a significantly greater concentration of several pro-inflammatory, metabolic and proliferative cytokine measures in burn cardiac blood than control: GM-CSF, IL-6, IP-10, CXCL1 and Peptide YY. When comparing the location of blood collection in burns exclusively, hepatic portal vein had a decreased proportion of IL-1a, IP-10, MCP-1, MIP-1a, MIP-1b and Rantes. Interestingly, the adipokine Leptin was significantly lower in burn hepatic blood than burn cardiac and control cardiac (62 – 42, 1032 – 281 and 2206 – 878, p < 0.05 respectively). Conclusions: The alterations in inflammatory cytokines and metabolic hormones between non-burn controls and burn mice differ depending on the collection site. These findings suggest that the portal hormonal and inflammatory profile is significantly different to cardiac derived and indicates localized responses in the intra-abdominal organs drained by the portal system. Thus, caution should be made when investigating such parameters exclusively from cardiac-derived blood and future studies should incorporate this collection practice to reflect this linear relationship.

O-50. A REAPPRAISAL OF MRSA VAP IN THE SURGICAL ICU: NOT JUST A LATE INFECTION ANY MORE Jacquelyn Glenn, Maria Rodil, Clay Burlew, Fredric Pieracci, University of Colorado, Denver Health Medical Center Background: Choice of empiric antibiotic(s) for early ventilator-associated pneumonia (VAP) involves weighing the risks of potential infection with multi-drug-resistant (MDR) pathogens against those of over-exposure to broad-spectrum agents, although early VAP is thought to be rarely caused by MDR pathogens, the overall incidence of all methicillin resistant Staphylococcus aureus (MRSA) infections is increasing. We questioned if MRSA VAP is becoming more common and if it these infections were occurring earlier in the patient’s hospital course. Hypothesis: We hypothesized that 1) early (2–7 days from intubation) VAP caused by MRSA is relatively uncommon and 2) those patients with early VAP due to MRSA had risk factors associated with a MDR organism infection. Methods: BALs from patients admitted to our SICU from 2010–2013 were reviewed. MRSA VAP was defined as growth of ‡ 105 cfu/mL from BAL. Risk factors included patient demographics or living conditions, prior recent hospitalization or transfer from long term care facility, and known prior colonization. Results: In the three year period, there were 438 cases of VAP. 47 specimens from 43 patients had quantitative microbiologic confirmation of early MRSA VAP for an overall prevalence of 10.7%. Of the 43 patients with MRSA VAP, 17 (39.5%) were early. Culture results were graphed according to ventilator days (Figure). The median days ventilated at the time of MRSA VAP were 11 days (range 2–81). None of the early MRSA VAP patients had identifiable risks for community or hospital-acquired MRSA infection. Conclusions: These data suggest that approximately 40% of cases of MRSA VAP occurred in the early window and without traditional or known risk factors. Since the rapid determination of the etiology of severe pneumonia is possible only in a limited number of cases, broad-spectrum antibiotic therapy that will treat infection with MRSA as well as other potential pathogens should be considered early in the course of treatment.

ORAL PRESENTATION ABSTRACTS Background: Hand hygiene (HH) for prevention of nosocomial infection has been the cornerstone for infection prevention for more than 20 years, however rates remain low. Recent emphasis on transmission of infection through contact with environmental surfaces has led to better efforts on daily and terminal cleaning. The CDC developed a checklist of ‘‘high touch surfaces’’ which include: Bedrails, bedside table, IV pole and pump, doorknobs, toilet, light switch, chair, telephone, call bell, monitor touch screen, cables, and ventilator control panel. Hypothesis: ICU health care workers (HCW) differ in HH practices and in contact with ‘‘high touch surfaces’’ during patient interactions. Methods: This was an observational study of HCW interactions in a surgical ICU on random weekdays. All contact with surfaces in the room and HH for each observation were recorded. Data analysis was performed as appropriate, p < 0.05. Results: 155 observations occurred over a 4 week period (49 MD and 106 RN observations). The majority of observations were in non-isolation patients for both groups (MD: 41 (83%), RN: 95 (90%). Only 48% MD and 81% RN performed entry and exit HH, p = 0.01. Of the 49 MD encounters, 212 contacts occurred (4 contacts/interaction, range 0–18) and 1,058 contacts for RNs (10 contacts/interaction, range 1–47), p = 0.01. RNs most frequently touched the patient (58%), IV lines (50%) and IV pumps (52%), the in-room computer (44%), and the bedrail (43%). MDs most frequently touched the patient (43%), the bedrail (36%), patient linen (26%) and the computer on wheels (12%). When compared to MDs, RNs were more likely to touch the supply cart, in room computer, monitor, glove box, IV pump and IV tubing, p < 0.04. The percent of all interactions listed as CDC high touch zones was only 18%. Conclusions: Despite decades of emphasis on HH, overall compliance for entry and exit HH is only 71%. Irrespective of HCW status, the majority of interactions are with environmental surfaces and not the patient, thus emphasizing the importance of environmental cleanliness. In our ICU, environmental surfaces are frequently touched by HCW, many of which are not part of the CDC surface cleaning checklist. Contact with environmental surfaces without HH may represent risk for disease transmission.

O-52. EARLY APPROPRIATE EMPIRIC ANTIMICROBIAL PRESCRIBING IN SEPTIC PATIENTS PRESENTING TO THE EMERGENCY DEPARTMENT DOES NOT LEAD TO DECREASED MORTALITY James Gilmore, Christopher Adams, Reza Askari, Brigham and Women’s Hospital, Harvard University Background: The 2012 Surviving Sepsis Campaign Guideline (SSC) recommends administration of broad-spectrum antimicrobials within 1 hour of recognition of severe sepsis and septic shock. The SSC also recommends that empiric regimens be composed of one or more drugs that have activity against all likely pathogens and that penetrate in adequate concentrations into the presumed source of sepsis. The purpose of this phase I analysis is to assess the appropriateness of empiric therapy based on culture results in patients presenting to the emergency department (ED) with sepsis, severe sepsis or septic shock at a tertiary academic medical center. Hypothesis: Appropriate empiric prescribing of antimicrobials improves survival in septic patients presenting to the emergency department. Methods: We conducted a retrospective, single-center analysis of adult patients admitted to our tertiary care academic medical center via the emergency department diagnosed with sepsis, severe sepsis or septic shock. We screened 786 patients identified by a hospital claims database discharged from the hospital with ICD-9 charge codes for sepsis, severe sepsis or septic shock between January 1st 2012 and December 31st 2012. Results: 271 patients met the criteria for inclusion. Overall mortality rate was 20.3%. 87 patients (32%) had no positive culture growth during admission and were excluded 100 cultures grew gram-positive organisms, 96 cultures grew gram (-) organisms, 11 anaerobic organisms, 15 fungal organisms, and 5 cultures with positive viral growth. Of patients with positive cultures, 113/ 184 (61%) were treated appropriately initially based on final culture results. Mortality of those treated appropriately was (23/ 113, 20%) and did not differ significantly from those who were not treated appropriately (16/71, 22%), p = 0.72. Mean time to antibiotic administration from bed placement was 2.2 hrs and 1.5 hrs from MD assessment. Conclusions: Our data failed to show a mortality benefit to early appropriate empiric antibiotic administration in patients with sepsis, severe sepsis, or septic, shock. Despite these findings our planned phase II analysis will focus on improving our overall appropriate antimicrobial prescribing.

O-53. CAUTIs AND CLABSIs: DO PHYSICIANS REALLY KNOW WHAT THEY ARE? Therese Duane, Rajesh Ramanathan, Patricia Leavell, Catherine Mays, Janis Ober, Virginia Commonwealth University Medical Center

O-51. ENVIRONMENTAL CONTACT VERSUS PATIENT CONTACT IN THE ICU: WHAT DO WE TOUCH? S Swoboda, Rebecca Adelman, Pamela Lipsett, Johns Hopkins University

Background: Considered preventable, CAUTIs and CLABSIs are being used to compare institutions and determine reimbursements. These data come from the United Healthcare Consortium (UHC) administrative database that relies almost exclusively on physician documentation as opposed to objective Centers for Disease Control (CDC) guidelines. Hypothesis: The rates of HACs are different depending on the guidelines used to determine infections. Methods: We performed a retrospective study from January 2012 through September 2013. We compared hospital acquired conditions (HACs), both CLABSI and CAUTI, as identified through our UHC database to those identified by the Department of Epidemiology using strict CDC guidelines. We performed subset analysis on those HACs identified by UHC but not CDC to determine causes for these discrepancies.


Results: There were a total of 221 discrete CAUTIs and 238 CLABSIs found between both UHC and CDC. Of these 16 CAUTIs (7.2%) and 44 (18.5%) CLABSIs were detected by both UHC and CDC. 72.4% (42/58) of the CAUTIs identified by UHC were not identified by CDC. 52.7% (49/93) of the CLABSIs identified by UHC were not identified by CDC. The etiology of the disparity in diagnosis for patients who were identified by UHC and not CDC are shown in Table 1. Conclusions: There is a major disconnect between definitions of infections depending on what process is used. This can lead to inappropriate treatment and inaccurate institutional comparisons which impact reimbursements. Educating providers regarding HAC definitions should result in more accurate recognition of infections thereby ensuring appropriate use of therapy.

O-54. A COMPARISON OF ICU INFECTIONS IN A UNITED STATES TRAUMA CENTER AND A TEACHING HOSPITAL IN HO CHI MINH CITY, VIETNAM Andrew Stephen, Minh Tran, Bich Sim, Stephanie Lueckel, Michael Connolly, Daithi Heffernan, Charles Adams, William Cioffi, Brown University, Rhode Island Hospital

S-23 Background: Infectious complications remain prominent causes of morbidity in Intensive care units (ICUs) worldwide. International collaborations allow establishment of common protocols. Despite isolation rooms and antibiotic stewardship, resistant organisms are increasing. To establish common practices it is critical to establish the microbiological flora of collaborating international ICUs. Hypothesis: Microbial patterns and resistant profiles vary vastly between international ICU’s. Methods: Prospectively gathered data from a Level 1 trauma center in Rhode Island (RIH) and patients in a mixed ICU in Ho Chi Minh City, Vietnam (HCM) over a one year period. Demographic, microbiologic and antibiotic resistant data of respiratory tract infections (RTIs), blood stream infections (BSIs) and urinary tract infections (UTIs) was collected. We compared logistics of isolation, patient distancing, cleaning practices and antibiotic tailoring between the two ICUs. Results: For both ICUs, RTIs were the most frequent infection. In HCM, BSIs were second followed by UTI. In RIH UTIs were second and BSIs third most frequent. Overall, in HCM gram neg organisms predominated, (Acinetobacter = 35.5% of all infections), whereas a greater frequency of gram pos organisms were noted at RIH (Acinetobacter < 2% of infections). The most common RTIs in HCM were Acinetobacter (43%) and Klebsiella (17%). Within RIH RTIs these were S. aureus (38.3%) and H. influenza (10.4%). In the UTIs there was no difference in common organisms between HCM and RIH-E.coli 31% vs 50%; p = 0.14 and enterococcus 21% vs 13%; p = 0.51. Again gram neg predominated BSIs in HCM (Acinetobacter-19% and Klebsiella-16%) with infrequent S. aureus, whereas S. aureus accounted for 50% of the RIH BSIs. In assessing resistance profiles of all infections no cases of either panresistant Acinetobacter or vancomycin resistant enterococcus (VRE) were noted in either ICU. Among S. aureus infections, there was no difference in MRSA infection rates (31% vs 40%; p = 0.15). Conclusions: RTIs are the most common ICU infection. Microbial profiles vary distinctly. Despite disparate set ups, including close patient proximity and poor contact precautions in HCM, there is no difference in antibiotic resistance profiles. Further work will address common international risk factors for infections in the critically ill.

Poster Presentation Abstracts

P-01. VAGUS NERVE SIGNALING MODULATES THE BALANCE BETWEEN REGULATORY T CELLS AND T-HELPER 17 CELLS IN THE MESENTERIC LYMPH NODE FOLLOWING TRAUMA/HEMORRHAGIC SHOCK Koji Morishita, Raul Coimbra, Vishal Bansal, Brian Eliceiri, Todd Costantini, University of California, San Diego Background: Dendritic cells (DCs) migrate from the gut to the mesenteric lymph node (MLN) and coordinate the response to injury. CD103 + DCs maintain tolerance by driving the development of regulatory T cells (Treg) in the MLN. Treg cells maintain homeostasis by suppressing excessive immune responses, while effector T-helper (Th) 17 cells drive a pro-inflammatory response. The relative expression of Treg and Th17 cells in the gut determine the balance between tolerance and immunity. We have shown that vagus nerve signaling (VNS) prevents gut injury and alters the DC profile in the mesenteric lymph after trauma/hemorrhagic shock (T/HS). Hypothesis: We hypothesized that 1) T/HS would decrease the CD103 + DC population in the MLN and alter the balance between Treg and Th17 cells, and 2) that VNS would promote tolerance to inflammation by increasing the Treg/Th17 ratio in the MLN after injury. Methods: Male rats were assigned to trauma/sham shock (T/SS) or T/HS. T/HS was induced by laparotomy and 60 min of HS followed by resuscitation. A cohort of animals underwent cervical VNS following HS. MLN samples were collected 24 hours after resuscitation. For flow cytometric analysis, MLN cells were stained with CD103, MHCII, CD4, CD25, Foxp3, IL-17A, and P-NFKB p65 antibodies. Results: The CD103 + MHCII + DC population in the MLN was decreased after T/ HS and demonstrated increased P-NFKB p65 expression. The Treg/Th17 cell ratio in the MLN was decreased after T/HS compared with T/SS suggesting a shift to an inflammatory response. VNS prevented the T/HS-induced decrease in MLN CD103 + DCs with P-NFKB p65 expression similar to T/SS. VNS increased the Treg/Th17 ratio compared to T/HS alone (*p < 0.05). Conclusions: VNS alters the immune response by altering the balance between Treg and Th17 cells in the MLN. The vagus nerve promotes tolerance to inflammation in the gut further supporting its ability to modulate the injury response.

Methods: The C57BL/6J mice (8–10 wk old, Jackson Laboratories) were divided into groups: ‘‘ALI’’ (n = 6) which received LPS (Escherichia coli O55:B5) via intratracheal injection; ‘‘Control’’ (n = 7) which received sterile water. Bronchoalveolar lavage (BAL) was performed at 72 h after treatment. Bacterial DNA was extracted, normalized to 1 ml BAL, and used for QPCR and 16S rRNA gene-tags (V3-V4) sequencing. Results: QPCR detected 5-fold increase of bacterial load in BAL samples from the ALI mice (p = 0.03). The community complexity remained unchanged after LPS treatment (p = 0.7), while Shannon diversity index indicated the increase of community evenness in response to ALI (p = 0.07). This analysis suggests that the observed bacterial growth is attributed to species existing within the lung ecosystem before the ALI. Principal coordinate analysis indicated that LPS treatment explained 66% of total variation in the dataset. The separation between control and ALI groups was significant (ANOSIM test, p = 0.005). The Metastats-based comparison of bacterial abundances between control and ALI groups revealed significant (p < 0.05) changes in the abundance of 6 bacterial genera: the genera Tumebacillus, Bradyrhizobium, Jeotgalicoccus, as well as the unclassified lineage from the class Betaproteobacreia lost the abundance in response to ALI; pathobionts Brucella (class Alfaproteobacteria) and Stenotrophomonas (class Gammaproteobacteria) were blooming (6–10 folds increase, p < 0.05) in response to ALI. Conclusions: The microbial community reaction to ALI is attributed to the loss of Firmicutes (genus Tumebacillus) and bloom of Proteobacteria (genera Brucella and Stenotrophomonas). We demonstrated that pathological transformation of lung microbiota is attributed to the set of inborn lung pathogens rather than the external infection. We further hypothesize that ARDS could be prevented via control of the pathobiontrelated lung microenvironment.

P-03. THE IMPACT OF ANTIBIOTICS ON NEONATAL RAT MICROBIOTA AND THE DEVELOPMENT OF EXPERIMENTAL NECROTIZING ENTEROCOLITIS Joanna Lim, Brandon Bell, Debi Thomas, Stephanie Papillon, Jin Wang, Larry Wang, Anatoly Grishin, Henri Ford, University of California, Children’s Hospital Los Angeles Background: Necrotizing enterocolitis (NEC) is the most lethal disorder affecting premature infants but the etiology is not understood. Cronobacter sakazakii is one of a few opportunistic pathogens that have been implicated in clinical and experimental NEC. In our previous studies, C. sakazakii dramatically increased the incidence and severity of NEC in neonatal rats. We sought to examine the effect of antibiotic therapy on the neonatal microbiome and putative opportunistic pathogens that have been implicated in the pathogenesis of NEC. Hypothesis: Antibiotic prophylaxis against opportunistic pathogens will decrease the incidence and severity of NEC. Methods: Newborn rats were fed conventional formula and subjected to hypoxia (5% O2 for 10 minutes) thrice daily. One group received untreated formula and the other received formula inoculated with C. sakazakii (107 CFU/100 ml). Each was further randomized to receive ampicillin (25–30 mg/kg) or an equivalent volume of untreated formula starting on day of life #1. The rats were sacrificed on day of life #4. The terminal ileum was examined histologically and by culture-based characterization of the

P-02. INNATE LUNG MICROBIOTA OF MICE UNDERGO MORBID TRANSFORMATION IN RESPONSE TO ACUTE LUNG INJURY Valeriy Poroyko, FanYong Meng, Taras Afonyushkin, Ekaterina Semenyuk, Vera Tesic, Mattew Perisin, Bergelson Joy, Konstantin Birukov, University of Chicago Background: Acute lung injury (ALI) and severe acute respiratory distress syndrome (ARDS) are among the risk factors associated with elective surgery. Understanding of interaction between lung injury and innate lung microbiota opens new modalities of treatment for ALI, ARDS and acute lung inflammation. Hypothesis: We hypothesize that ALI affects lung microbiota causing morbid transformation.

CS 0 showed a variety of NEC scores, mean 0.77. CS 107 showed a mean NEC score of 1.5. CS 107 + Amp showed a mean NEC score of 0.



S-25 cardiac contraction and diminished relaxation in the hsf - / - mice. However, lacking HSF-1 expression did not affect intracellular calcium and sodium responses in cardiomyocytes isolated from septic challenged mice, suggesting that ion loading was not a major or sustaining cause of the greater myocardial contractile defects in hsf - / - mice. Conclusions: In conclusion, our data indicated that HSF-1 and downstream heat shock proteins are essential components to support cardiac function in sepsis. Further studies are warranted to further define the precise mechanisms of HSF-1 mediated cardiac protection.


Celeste Finnerty, Xueling Li, Bernard Fongang, Padma Nainar, Nicole Gibran, Richard Gamelli, Andrzej Kudlicki, David Herndon, University of Texas Medical Branch, Galveston









microbiota, by sequencing a variable region of 16S rRNA. The maternal and neonatal stool microbiota were similarly examined. Results: Addition of C. sakazakii to the formula resulted in an overall paucity of organisms and increased incidence of NEC compared to rats that received untreated formula. Administration of ampicillin prevented the development of NEC. Stool cultures showed progressively greater counts of C. sakazakii with each day. Conclusions: Antibiotic prophylaxis prevented the development of NEC in a model that otherwise produced a 50% incidence of NEC. The paucity of bacteria may reflect that inoculation of C. sakazakii affected the microbiome but failed to colonize. Further studies should be done with antibiotic resistant strains to separate the effect of the antibiotic on the microbiome from that on specific opportunistic pathogens.


Background: The timeline of genomic response following burn injury may provide important information for refining therapeutic interventions during acute and rehabilitative stages. Time-series microarrays can capture dynamic profiles of the genome-wide gene expression. Hypothesis: Clustering the gene expression profiles according to the temporal response patterns will reveal the timing of the functionally related burn response genes. Also, considering the age and sex effects is expected to significantly improve the statistical capability in identifying genes response to burns. Methods: We obtained time-dependent gene expression profiles from peripheral blood leukocytes from burn patients 7–99 years old. The data were corrected for age and sex using expression profiles from control patients that were modeled using our generic linear model. After removing the age and sex specific effects on the gene expression in burn patients, we applied smoothing with moving median and subsequent hierarchical clustering to the burn time-course series. Results: Five distinct groups of the burn response genes were revealed by clustering the gene expression profiles on 0–39 post burn days according to the time-dependent response patterns. The five groups of the burn response genes are significantly enriched in distinct functions including immunity, metabolism, infection and wound healing. Three critical gene expression transitional timing points occur at approximately 3, 11, and 33 days post burn. Three interesting functional groups of genes correspond to temporal regulation. Metabolic genes are elevated between 1.5–11 days post burn. Immune genes are down regulated 3–33 days post burn. On the contrary, genes demonstrating a response to infection are up-regulated 3–33 days post burn. Genes involved in healing are modulated 3–33 days post burn as well. Conclusions: The timing of expression of different groups of genes identified by our approach reflects the distinct functions occurring in response to burn injury. Correcting for age and sex significantly improves the statistical accuracy in identifying genes response to burns. P-07. UNUSUAL HYPERACTIVITY OF A GLUCOCORTICOID RECEPTOR FRAGMENT IS AUTOMATIZED BY SPECIFIC DELETION OF THE 3¢UTR David Greenhalgh, Tajia Green, Debora Lim, Stacey Leventhal, Kelly Tung, Kiho Cho, University of California, Davis Medical Center

P-05. DEFICIENCY IN HEAT SHOCK FACTOR 1 (HSF-1) EXPRESSION EXACERBATES SEPSIS-INDUCED INFLAMMATION AND CARDIAC DYSFUNCTION Qun Zang, Robert Barber, David Maass, Steven Wolf, Joseph Minei, University of Texas, Southwestern Medical Center Background: In the heart, HSF1 deficiency reduces cardiac expression of Hsp25, alphaB-crystallin and Hsp70. The role of HSF-1/HSP70 in inflammation has been emphasized by the finding that HSF-1 deficient mice exhibit chronically elevated systemic TNF levels as well as increased susceptibility to LPS challenge. In this study, using HSF-1 knockout (hsf - / - ) mice as a model, we examined the role of HSF-1 in inflammation and cardiac function in response to septic challenge by lipopolysaccharide (LPS), gram-positive bacteria Streptococcus pneumoniae (S. pneumoniae), or gramnegative bacteria Klebsiella pneumoniae (K. pneumoniae). Hypothesis: We hypothesize that absence of heat shock factor 1 (HSF-1) and inability to increase myocardial expression of heat shock proteins alter septic responses of inflammatory cytokines and myocardial contractility. Methods: HSF-1 knockout (hsf - / - ) mice and wild type litter mates underwent a sterile (lipopolysaccharide; LPS) or infectious (S. pneumoniae or Klebsiella pneumoniae) septic challenge. Production of cytokines, TNF-a, IL-1b, IL-6 and IL-10, were examined in blood serum and in the culture medium of isolated cardiomyocytes. In addition, intracellular calcium and sodium responses in cardiomyocytes isolated from septic challenged mice were measured. Heart contractility was examined by Langendorf heart perfusions. Results: Production of cytokines, TNF-a, IL-1b, IL-6 and IL-10, in the blood and from cardiomyocytes was exaggerated in the hsf - / - mice compared to responses measured in wild type mice given an identical septic challenge. This enhanced compartmentalized myocardial inflammation was associated with significantly decreased

Background: The glucocorticoid receptor (GR) is essential to the response to stress. We have previously reported that a 118 amino acid fragment of the N-terminus of GR [hGRS1(-349A)] or ‘‘F1’’, which lacks ligand and DNA binding domains has a markedly enhanced response to steroids compared to the full-length GR (hGRa). To determine the mechanism of the augmentation we dissected the 3¢ untranslated region (3¢UTR) of the mRNA and retested its activity in response to steroids. Hypothesis: Elimination of the 3¢UTR from F1 will eliminate its hyperactivity. Methods: The 3¢UTR of F1 had 300 base pair (bp) segments removed and its activity tested for response to hydrocortisone (Hyd) using our standard luciferase reporter assay. Values are expressed as luciferase + :SEM.



Results: As usual, there was a dose response to adding hydrocortisone to the control hGRa. The F1 fragment had an increase in activity 5 times that of hGRa after treatment with hydrocortisone. When removing 300 bp segments from the F1 3¢UTR, all activity was lost until 1200 bps were removed. After eliminating these 1200 bps, which is near a poly A site, there was a doubling in activity beyond the highest F1 that did not require steroids. Conclusions: The 3¢UTR of F1 plays a major role in its hyperactivity. When 1200 bps are removed from the 3¢UTR there is an increase in activity that is independent of steroids. The role of the poly A site needs to be determined. P-08. GLOBAL BURDEN OF SURGICAL SITE INFECTIONS (SSIs) ASSOCIATED WITH KNEE ARTHROPLASTY Holly Yu, Harshila Patel, Hanane Khoury, Sharon Welner, Pfizer, Inc. Background: SSIs are post-surgical complications, comprising the third most frequent nosocomial infection (generally 15% of total). S. aureus is the major cause of SSIs worldwide, with a particular increase in methicillin-resistant S. aureus (MRSA) prevalence in the past decade. Patients who undergo knee arthroplasty are among those susceptible of developing SSIs. Hypothesis: To review the global epidemiology, mortality, costs and healthcare resource utilization of SSIs following knee arthroplasty. Methods: A comprehensive search was conducted in PubMed and of relevant conference proceedings; 236 full-text publications were reviewed to identify the epidemiology and burden of SSIs related to knee arthroplasty published from 2003 to 2013. Results: Median SSI infection rate (as percentage of all knee arthroplasty procedures) was 1.35% (range: 0.3%–19%). Median 39% (27%–71%) of SSIs after knee arthroplasty were attributed to S. aureus. MRSA infection rates (as percentage of all S. aureus infections) vary widely by region, ranging from 1.2% to 47%; the lowest value was reported for Sweden, a country with usually low MRSA infection rates. Few studies evaluated mortality, resource utilization and costs due to SSIs associated with knee arthroplasty; however, differences in studies, populations and outcome measures precluded group analysis. SSI mortality rates following knee arthroplasty were reported by a UK study as 0.4 deaths per 100 procedures and by a US study as a 6-month rate of 29%. A US study (2007–2011) reported that within 1 year after primary total knee arthroplasty, patients with periprosthetic infection had on average 3.6 readmissions as compared to 0.1 readmissions for controls. It also reported a mean annual cost of $116,383 per patient with infection, over 4 times higher than matched controls. Conclusions: Despite gaps in the literature, including insufficient data from South America, Asia, and Africa, and inconsistent use of outcome measures, evidence to date indicates marked variation in SSI infection rates after knee arthroplasty that result in significant healthcare resource utilization and increased costs. Since the majority of these SSIs are attributed to S. aureus, it may be a worthwhile target for preventive strategies.

Dose-dependent inhibition of gp96 ATPase by Semapimod of action of Semapimod has not been unambiguously established. We have previously demonstrated that Semapimod blocks TLR4 signaling and interferes with the ATPbinding activity of the HSP90 family chaperone gp96, which plays a critical role in the biogenesis of Toll-like receptors. Hypothesis: Semapimod blocks TLR4 signaling by inhibiting gp96. Methods: Activation of p38 MAPK and NF-kB was examined by Western blotting with activation-specific antibodies. ATP-binding proteins were pulled down using ATPdesthiobiotin agarose. gp96 was identified using mass spectroscopy of tryptic digest and Western blotting with anti-gp96 antibody. ATPase activity of gp96 was measured using g-32P ATP. Results: Semapimod blocks LPS-induced activation of both p38 and NF-kB, indicating that the blockade is upstream in the TLR4 pathway. Moreover, this blockade is partially alleviated by high concentrations of LPS, which is consistent with Semapimod targeting the interaction between LPS and its cognate receptor. Semapimod also blocks gp96 pulldown by desthiobiotin-agarose and inhibits the ATPase activity of purified gp96 in a dose-dependent manner. Conclusions: Semapimod blocks TLR4 interaction with LPS by inhibiting gp96. gp96 is an essential component of the TLR4 signaling complex.



Joshua Gatson, Ming-Mei Liu, Joseph Minei, Steven Wolf, University of Texas, Southwestern, Southwestern Medical Center

Fangming Xiu, Michael Li Diao, Marc Jeschke, University of Toronto, Sunnybrook Health Sciences Centre

Background: Following a mild traumatic brain injury (TBI) event, the secondary brain injury that persists after the initial blow to the head consists of excitotoxicity, decreased cerebral glucose levels, oxidant injury, mitochondrial dysfunction, inflammation, and neuronal cell death. With respect to inflammation, increased activation of the transcription, factor serum amyloid A factor-1 (SAF-1), results in increased levels of inflammation and degradation of the extracellular matrix in various tissue types. Hypothesis: Here, we hypothesized that activation of SAF-1 increases in the brain after mild TBI and results in heightened neuro-inflammation during both acute and chronic time points. Methods: In the current study, male mice were injured using the controlled cortical impact device. Using a closed-head mild TBI model, a midline incision was made to access the skull and the impactor tip was aligned directly on the skull on the sagittal suture midway between the bregma ( - 2.12 mm) and lambda sutures. The mice were injured at a depth of 1.5 mm, velocity of 3.5 m/sec, and a delay time of 100 msec. At 1, 3, 7, 14, and 30 days after injury, the animals were intra-cardially perfused with 0.9% saline followed by 10% phosphate-buffered formalin. The whole brain was removed, sliced, and stained for total and phosphorylated serum amyloid A factor-1 (SAF-1), microglial activation, and astrocyte activation/infiltration in the brain. Results: In this study we found that following mild TBI an increase in the levels of phosphorylated SAF-1 was increased in the cortex and hippocampus at day 7 (p = 0.05) and 30 (p = 0.03) after injury. No increase was observed in the brain on day 1 and 3 after injury. The levels of SAF-1 correlated with an increase in the levels of activated microglia (p = 0.05) and astrocytes (p = 0.04) in the injured animals. Conclusions: An increase in phosphorylated SAF-1 levels in the brain may result in chronic inflammation and cognitive decline after mild TBI. SAF-1 may be target to reduce chronic inflammation and improve neurological outcomes after TBI.

Background: The hypermetabolic stress response occurs in almost every burn patient with burns over 20% of their body surface area is associated with severe inflammation and immune dysfunction. As opposed to a chronic low-grade inflammatory state of M1macrophage (M1MF) dominant in metabolic diseases, adipogenesis and accumulation of tissue, M2MF are hallmarks of prolonged critical illness. M2MF are shown to be predominantly present in humans with severe trauma including burn injuries, sepsis in the peripheral blood and adipose tissues as well as the liver and lungs. Although increased protein levels of PPARg is a key signal in M2MF polarization, it has been found in adipose tissue of critically-ill patients and no study has identified the trigger for the M2 polarization. Hypothesis: We hypothesize that palmitate with our without glucose will induce a shift towards type 2 macrophages. Methods: In this study we explored the long-term effects of glucose and palmitate on macrophage differentiation and function by using ex vivo bone marrow-derived macrophage (BMM) culture. The doses of glucose and palmitate were 4.5 mM, 7.5 mM, 10 mM and 12.5 mM for glucose, and 0.25 mM, 0.5 mM for palmitate, respectively. Results: At the end of 7 days culture, we found both glucose and palmitate decreased the phagocytosis and HLA-DR expression of BMM. What is more interesting is that palmitate alone or in combination with glucose (10 mM) led to an alternative macrophage polarization (M2MF) as defined by increased production of IL-10 and decreased IL-12 and TNF-a. Conclusions: Our findings are that glucose and palmitate enhance the macrophage polarization towards M2MF suggest that dominant accumulation of M2MF in adipose tissues and liver may be resulted from increased concentrations of blood glucose and free fatty acids in critical illness. P-10. THE ANTI-INFLAMMATORY DRUG SEMAPIMOD (CNI-1493) BLOCKS RESPONSES TO LPS BY INHIBITING THE ATPase ACTIVITY OF THE TLR CHAPERONE gp96 Anatoly Grishin, Rudolph Davis, Mary Beth Amrine, Jin Wang, Henri Ford, University of Southern California Keck School of Medicine Background: Semapimod, an experimental anti-inflammatory drug, is effective against a variety of inflammatory disorders including necrotizing enterocolitis. The mechanism

P-12. EFFECT OF LAURIC ACID ON STAPHYLOCOCCUS AUREUS BIOFILM DEVELOPMENT Donavon Hess, Michelle Henry-Stanley, Carol Wells, University of Minnesota Background: Biofilms develop in a variety of clinical situations and the majority of infections are thought to involve biofilms, defined as microbial communities attached to a surface and encased in an extracellular polymeric substance. Biofilm-associated bacteria are less susceptible to antibiotics, often complicating treatment and necessitating removal of implanted devices. In Staphylococcus aureus biofilms, we have

POSTER PRESENTATION ABSTRACTS observed lipid structures which appear to play an important role in biofilm structure and antibiotic susceptibility of biofilm-associated bacteria. Hypothesis: Because lipid structures can be disrupted by surfactants, we hypothesized that surfactants may disrupt biofilm development, and we noted that glycerol monolaurate (GML), a natural surfactant found in human breast milk, can prevent development of S. aureus biofilms. Because GML is made up of glycerol and lauric acid, experiments were designed to test the effect of lauric acid on S. aureus biofilm development. Methods: S. aureus RN6390 or ATCC 25932 was inoculated onto 1-cm segments of 3-0 silk suture and incubated 16 hr in biofilm growth medium (66% tryptic soy broth plus 0.2% glucose) with or without lauric acid. Growth was assessed as viable colony forming units quantified from sonicated biofilms, and biomass was quantified with crystal violet staining. Data were analyzed by ANOVA with Fisher’s post hoc test. Results: Following incubation with 0, 0.313, 0.625, 1.25, 2.5 and 5 mM lauric acid, the numbers of viable biofilm-associated bacteria decreased resulting in avg log10 of 7.1, 6.1, 6.2, 3.9, 3.0, and < 1.7, respectively, with all numbers decreased from control (no lauric acid) at P < 0.01, and reflecting a 90% decrease with 0.313 mM lauric acid. Biofilm biomass was similarly decreased at P < 0.01 in samples incubated with all concentrations of lauric acid. Similar results were obtained with S. aureus ATCC 25923 indicating that lauric acid-mediated inhibition of biofilm development was not limited to a single S. aureus strain. Conclusions: Lauric acid effectively prevented biofilm development as noted by a decrease in viable numbers of bacteria as well as in biofilm biomass. The mechanism of biofilm inhibition by lauric acid at the tested concentrations remains unclear, but could relate to disruption of biofilm structure formation (e.g. lipid structures), or interfere with bacterial attachment. These findings suggest potential preventative or therapeutic adjuncts.

P-13. INCREASED MURINE MYOBLAST PROLIFERATION IN VITRO WITH URINARY BLADDER MATRIX: A MECHANISM OF TISSUE REGENERATION AND WOUND HEALING Melody Saeman, Juquan Song, Kevin Despain, Ming-Mei Liu, Joseph Minei, Steven Wolf, University of Texas Southwestern Background: Porcine-derived urinary bladder matrix (UBM) is a biological scaffold used clinically for wound healing and tissue regeneration after injury. A case report showed the application of UBM to an injured muscle site increased muscle mass and function in a trauma patient. Hypothesis: The aim of this study was to investigate mechanisms of UBM in regulating muscle regeneration of progenitor cells. Methods: C2C12 cells from American Tissue and Cell Culture (AATCC) biological resource center were cultured in medium containing Dulbecco’s Modified Eagle Medium (DMEM), 10% fetal bovine serum and 1% glutamine. The cultures were maintained in a humidified atmosphere of 5% CO2 at 37 degrees Celsius. Cells were treated with 0, 5, 50, or 250 ug/mL of UBM (Matricel, Acell Inc.) in culture medium for 18 hours. Sample proteins were extracted from cell lysate and analyzed with SDS-PAGE and Western blot. Samples were normalized to controls and then analyzed by Mann-Whitney test. Results: Proliferating cell nuclear antigen (PCNA) increases leading strand synthesis in DNA replication, and is a marker of cell proliferation. After normalized to b-actin, we found an increase in PCNA band intensity at higher concentrations of UBM with a median of 1.7 (1.5-3.2, IQR) at 250 ug/mL concentration compared to control, median of 0.9 (0.81.2, IQR) (p < 0.05). We found no differences at lower concentrations of UBM. Conclusions: We showed that urinary bladder matrix stimulates proliferation in C2C12 murine myoblast progenitor cells in vitro in a dose response manner demonstrated by an increase in PCNA after 18 hours of treatment. Urinary bladder matrix increases activation of progenitor cells, potentially useful in tissue regeneration after injury.

P-14. GALLERIA MELLONELLA-A HIGH THROUGHPUT INEXPENSIVE MODEL TO SCREEN FOR THE PRESENCE OF LETHALITY FACTORS IN THE STOOL OF ANIMALS AND HUMANS Alexander Zaborin, Jennifer DeFazio, Olga Zaborina, John Alverdy, University of Chicago Background: There is an unmet need to identify the factors present in the human gut that drive lethal gut derived sepsis. Here we propose to use Galleria mellonella larvae as an inexpensive, high-throughput screening platform to determine whether lethality factors are present in stool samples of critically ill humans. In G. mellonella larvae, there is a hemocoelic compartment filled with hemolymph that is functionally comparable to the peritoneal fluid of mammals. In the hemocoel, hemocytes and humoral immune factors are located with granulocytes being the most abundant phagocytic cells analogous to neutrophils. Humoral factors include signaling cascades initiated by hemocytes that lead to melanization. Melanization precedes death when the hemocoelic cavity is exposed to pathogens or their secreted toxins. Hypothesis: We hypothesized that G. mellonella is a reliable intraperitoneal infection model that can discriminate between stool filtrates from healthy vs septic host. Methods: Four sources of samples were screened in Galleria mellonella via direct intrahemocoelic injection: filtered stool contents from healthy volunteers; filtered stool samples from septic critically ill human harboring well characterized human pathogen communities (HPCs); filtered cecal contents of septic appearing and non-septic appearing mice intestinally inoculated with the characterized HPC; and filtered contents from the above HPC grown under low and high phosphate conditions, a critical factor for microbial virulence expression. Larvae were observed for melanization and death over 24 hours.

S-27 Results: Filtered stool samples from 5 healthy volunteers caused no mortality, whereas filtered stool samples from 4 patients dying of severe sepsis caused > 50% melanization and subsequent death in larvae (n = 20, p < 0.001). Filtered cecal contents of 5 septic mice but not cecal contents of 5 healthy appearing mice intestinally inoculated with the HPC resulted in 40% melanization and subsequent death in larvae (n = 20, p < 0.01). Filtered contents from the HPC grown in low phosphate media caused 45% melanization and mortality in larvae (n = 20, p < 0.01) whereas there was no mortality when the HPC was grown in high phosphate media. Conclusions: The G. mellonella model can narrow down the search for gut factors that drive inflammation and lethality in a stringent and high throughput manner.

P-15. ENDOPLASMIC RETICULUM STRESS IN ADIPOSE TISSUE STIMULATES LIPOLYSIS IN VIVO Elena Bogdanovic, Nicole Kraus, Abdikarim Abdullahi, Marc Jeschke, University of Toronto Sunnybrook Health Sciences Centre Background: Endoplasmic reticulum stress (ER stress) or ER dysfunction affects numerous cellular processes and has been implicated as a contributing factor in several pathophysiological conditions. The antibiotic tunicamycin induces ER stress in a variety of cell types in vitro and has been used as a tool to induce ER stress in vivo. In mice, tunicamycin induces a robust ER stress response within the liver and kidney, accompanied by lipid accumulation and cell apoptosis. Recently, ER stress in adipocytes has been shown to stimulate lipolysis in vitro. Hypothesis: We hypothesized that hepatic ER stress and the development of fatty livers induced by tunicamycin was due to increased lipolysis from adipose tissue. Methods: Male Balb/c mice were injected intraperitoneally with tunicamycin. The liver and adipose tissue was dissected at various times post injection and ER stress was evaluated by Western blotting and quantitative real-time PCR. Plasma glycerol levels were determined using a colourimetric assay. Results: We examined whether tunicamycin stimulated ER stress in adipose tissue in vivo and whether ER stress induced lipolysis was associated with fatty infiltration of the liver and hepatic ER stress. We show that tunicamycin administration in male mice rapidly induced an ER stress response in adipose tissue that correlated with increased lipolysis, fatty infiltration of the liver, increases in liver density and hepatic ER stress. The stimulation of lipolysis by tunicamycin was rapid, detectable after 2 h both in vitro and in vivo and did not involve increased phosphorylation of hormone sensitive lipase (HSL). Prolonged (18–21 h) incubation of primary adipocytes with tunicamycin induced widespread changes in protein expression such as decreased phosphorylation of HSL and reduced expression of perilipin. Conclusions: Our results highlight a possible role for ER stress induced lipolysis in adipose tissue as an underlying mechanism leading to increases in serum free fatty acids (FFAs), fatty infiltration of the liver, hepatic ER stress and hepatic apoptosis.

P-16. ANTIBACTERIAL EFFECT OF A NITRIC OXIDE RELEASING SACHET Michael Neidrauer, Aparna Bhattacharyya, Sarah Julius, Carli Moorehead, Jonell Belle, Kenneth Barbee, Suresh Joshi, Zeomedix, Inc. Background: Nitric oxide is a broad spectrum antimicrobial agent that has the potential to reduce surgical infections when delivered at controlled rates. Hypothesis: The rate of nitric oxide released from sachets containing nitric oxide loaded zeolite powder can be controlled by altering the formulation of the sachet, and antibacterial amounts of nitric oxide can be released from some sachet formulations. Methods: Single-use sachets containing nitric oxide loaded zinc-exchanged zeolite A in an emulsifying ointment base were developed using polyurethane and ethylene vinyl acetate (EVA) films. The rate at which nitric oxide is released from the sachets upon contact with water was characterized using a chemiluminescence detection system. The antimicrobial efficacy of the sachets was tested in vitro by inoculating agar slurry with methicillin-resistant Staphylococcus aureus (MRSA) to a final concentration of 108 c.f.u./ml. Inoculated agar was placed on moistened nitric oxide sachets and control sachets (containing zeolite ointment without nitric oxide). The sachets were incubated for 24 hours, the agar was removed, and a colony count assay was performed. Logreductions were calculated by comparing nitric oxide sachets to control sachets. Results: Nitric oxide was released from the sachets at rates ranging from 0.250 to 1.50 micromole per square cm of surface area. Log reductions of MRSA ranged from 0 to 6, and increased as the rate of nitric oxide release from each sachet increased. Conclusions: This work demonstrates that antibacterial amounts of nitric oxide can be released from single-use sachets that could potentially be applied to infected skin or wounds.

P-17. THE IMMUNOPHENOTYPE OF CULTURE-POSITIVE BRONCHOALVEOLAR LAVAGE FROM MECHANICALLY VENTILATED TRAUMA PATIENTS Ryan Huebinger, Ashley Smith, Ding Chen, Sara Ireland, Christian Minshall, Joseph Minei, Steven Wolf, Michael Allen, Robert Barber, Nancy Monson, University of Texas Southwestern Medical Center

S-28 Background: Mechanically ventilated trauma patients have a variety of bacterial flora that are often undetectable. To address this problem, we have used next generation sequencing to query the microbiome of such patients as a means to identify the source of infection. In addition, we have initiated a series of experiments to address the immunophenotype in bronchoalveolar lavage (BAL) samples from these same patients. We anticipate this data will allow us to characterize immune responses to particular bacteria in the lung that we identify by next generation sequencing. Hypothesis: Different immune cell response and phenotypes exist that correlate with the type of bacterial pathogen(s) indentified in bronchoalveolar lavage. Methods: Bronchoalveolar lavage samples were collected in the SICU as a part of standard of care for intubated individuals that had a CPIS > 6. BALs were filtered through a 70 micron filter and centrifuged to pellet cells. Cells were resuspended in human freezing media and stored at - 80 until flow cytometric analysis. BAL samples were stained with an 11-color flow cytometry panel that identifies both innate and adaptive immune components. BAL cells were analyzed on a FACS Aria flow cytometer. Results: Our initial analysis of culture positive BALs (CPIS > 6) indicates that the vast majority of CD45 + lymphocytes in the BAL samples are CD16 + monocytes, followed by fairly equal frequencies of CD4 + T cells and CD8 + T cells. Some CD19 + B cells are also present, but the majority of these tend to be CD27- naı¨ve B cells rather than the antigen experienced CD27 + B cells. Conclusions: Understanding the immunophenotype of BAL samples from patients with pulmonary infections will provide a foundation for classifying the genetics of the adaptive immune response that emerge in response to particular bacterial infections of the lung.

P-18. IMPACT OF SEPSIS ACROSS SURGICAL SPECIALTIES Rajesh Ramanathan, Patricia Leavell, Catherine Mays, Therese Duane, Virginia Commonwealth University Background: Sepsis is among the leading causes of death and rates of sepsis are tracked by the Agency for Healthcare Research and Quality (AHRQ) through administrative billing code data. Sepsis is a quality indicator and public reporting benchmark for the Centers of Medicare and Medicaid Services. Surgical patients undergoing procedures are at increased risk for infectious complications. Hypothesis: To investigate the incidence of sepsis and its impact on outcomes amongst surgical patients undergoing procedures. To additionally study the specific impact of sepsis across various surgical specialties. Methods: Patients undergoing procedures performed by a surgical service at our academic medical center between January 2010 and June 2013 were reviewed for sepsis by the presence of AHRQ sepsis-related procedural and diagnostic billing codes. Patient outcomes included hospital length of stay, intensive care unit (ICU) admission, ICU length of stay, mortality, and early mortality. Subgroup analysis investigated the incidence and impact of sepsis in procedures performed by various surgical specialties. Results: 25,869 patients underwent a procedure by a surgical service and 858 (3.3%) patients developed sepsis during their hospital stay. Compared to all patients, patients with sepsis had significantly longer hospital stays, increased ICU admission and longer ICU stays. Patients who developed sepsis also had increased mortality and higher rates of early mortality (Table). The incidence of sepsis was highest in patients with procedures performed by cardiothoracic surgery (8.0%), trauma/emergency surgery (7.6%) and plastic/reconstructive surgery (5.4%). Sepsis was associated with the greatest incidence of mortality amongst patients undergoing procedures by vascular surgery (36.8%), gastrointestinal/bariatric surgery (31.2%), and trauma/emergency surgery (27.1%). Conclusions: Sepsis is not an uncommon condition and is associated with increased hospital stays, ICU admissions, ICU stays and mortality. Accurate benchmarking of sepsis is essential for development and monitoring of sepsis-reduction quality improvement initiatives.

P-19. TOTAL ABDOMINAL HYSTERECTOMY: REDUCED RISK OF SURGICAL SITE INFECTION ASSOCIATED WITH ROBOTIC AND LAPAROSCOPIC TECHNIQUE Kristin Colling, James Glover, Melissa Geller, Catherine Statz, Gregory Beilman, University of Minnesota Background: Total abdominal hysterectomy (TAH) is one of the most common procedures performed in the US. New techniques utilizing laparoscopic and robotic technology are becoming increasingly common. It is unknown if these minimally invasive surgical (MIS) techniques alter the risk of surgical site infections (SSI). Hypothesis: MIS techniques are associated with decreased SSI following TAH.


Fig. 1. In multivariate analysis: Open technique, ASA score and wound class were all independently associated with increased risk of SSI after TAH.

Methods: We performed a retrospective review of all TAH performed at our institution January 2011 through June 2013. ICD-9 codes and chart review were used to identify patients undergoing TAH by open, laparoscopic or robotic approach and to identify patients that subsequently developed SSI. Univariate analysis was performed with Chi-square and ANOVA tests. Logistic regression was used to perform multivariate analysis. Results: During this time, 986 patients underwent TAH: 433 with open technique (44%), 116 laparoscopic (12%), 407 robotic (41%) and 30 cases converted to open (3%). Patients undergoing laparoscopic TAH were significantly younger and had lower BMI and ASA score than those undergoing open or robotic TAH. There were no significant differences in patients undergoing open and robotic TAH. Open TAH was associated with significantly longer hospital stay than laparoscopic or robotic TAH (5.1, 1.7 and 1.6 days respectively; p < 0.0001). The rate of SSI after any TAH was 4%. Significantly more SSI occurred in open cases (7%) than laparoscopic (0) or robotic (2%) (p < 0.0001). Cases converted to open also had an increased rate of SSI (13%). In univariate analysis: Open technique, ASA ‡ 3, wound class of III/IV and obesity were all associated with increased risk of SSI. In multivariate analysis: wound class of III/IV, ASA score of ‡ 3 and open technique were all independently associated with increased risk of SSI. Conclusions: Laparoscopic and robotic TAH were associated with a significantly lower risk of SSI and shorter hospital stay. ASA score and wound class were also independent risk factors for SSI.

P-20. PANCREATITIS MANAGED BY AN ACUTE CARE SURGERY SERVICE: ETIOLOGY, RESOURCE UTILIZATION, AND OUTCOMES Arek Wiktor, Kathleen To, Andrew Rosenberg, Lena Napolitano, University of Michigan Background: The management of acute pancreatitis (AP) has evolved substantially. Necrotizing pancreatitis (NP) develops in 15–20% of AP, with secondary infection carrying an 8–39% mortality risk and risk for multidrug resistant bacteria (MDR). The randomized trial comparing step-up to open necrosectomy reported mortality rates of 19% vs. 16% (1). Pancreatitis managed by an acute care surgery service (ACS), has not been fully examined. Hypothesis: AP complicated by NP or MDR infection results in increased resource utilization and worse outcomes. Methods: Retrospective review of all adult ( ‡ 18 years old) ACS admissions from 11/2007- 3/2012, with AP (ICD-9 code 577.0). Clinical characteristics, AP etiology, number/type of procedures performed, hospital and ICU length of stay (LOS), ventilator days, microbiology, disposition and mortality were examined. Results: 148 ACS patients had 169 admissions for AP (mean age 52 years, 43.9% male); hospital LOS was 15.5 days ( – 19.39), and all-cause mortality was 3.3% (2 NP, 3 non-NP). Most AP was from gallstone pancreatitis (54.4% of admissions, 58.8% of patients). 141 (83.4%) admissions resulted in home discharge, 36 (21.3%) required home health care. NP was diagnosed in 38 (25.7%) of patients; 52 (30.8%) of admissions. Readmissions were significantly greater for NP patients compared to those without [14 (36.8%) vs. 4 (3.6%) (p < 0.001)]. NP patients had longer hospital LOS [26.7 – 14.4 vs. 10.6 – 24.4 days (p < 0.001)], and ICU LOS [4.1 – 7.4 vs. 1.5 – 7.1 days (p = 0.03)]; but no difference in ventilator days [1.44 – 3.9 vs. 1.09 – 5.3 (p = 0.67), respectively]. Sterile necrosis was diagnosed in 13 (25%) of NP admissions. Patients with infected NP required: Open necrosectomy 18 (47.4%), percutaneous drainage 6 (15.8%), and cystgastrostomy 3 (7.9%). MDR pathogens were present in 26 (66%) of total isolates, 21 (80%) of patients with infected NP. MDR infection was associated with increased hospital LOS [34.3 – 29.6 vs. 19.1 – 15 days (p = .02)]. Neither infected NP nor MDR were associated with discharge disposition (p = 0.30). Conclusions: NP poses an increased burden on inpatient health care resources by increased LOS, readmission rates, and incidence of MDR infections, but was not associated with increased mortality. Management of NP by an ACS service was associated with decreased mortality compared to published studies.

POSTER PRESENTATION ABSTRACTS P-21. BILATERAL PECTORALIS ADVANCEMENT FLAPS AND TRANSVERSE PLATE FIXATION SYSTEM FOR STERNAL RECONSTRUCTION IN THE COMPLICATED STERNAL WOUND Jan De Raet, Herbert De Praetere, Paul Sergeant, Heart Center Leipzig, University of Leipzig Background: Complicated sternal wound infection after cardiac surgery has an incidence of 0.4–6.9% and a mortality of 7–80%. The ideal reconstructive procedure is still a matter of debate. Many reconstructive flaps (LD, PM, RA, pedicled omentum) and osteosyntheses have been published for sternal reconstruction. Hypothesis: To report our experience with bilateral pectoralis advancement flaps and a transverse plate fixation system for sternal reconstruction in the complicated sternal wound. Methods: Between 2008 and 2012, 24 patients with a complicated sternal wound underwent a sternal reconstruction with bilateral pectoralis advancement flaps and a transverse plate fixation system. The median age of the cohort (4 female and 20 males), was 65.8 years (range: 33–83 years). In 19 patients, a bilateral internal thoracic artery had been used. Considerable preoperative risk factors were present: morbid obesity with Body Mass Index (BMI) ‡ 35 (range: 35–49.7: 13 patients); chronic obstructive pulmonary disease (COPD) without steroid therapy preoperatively (7 patients); Diabetes mellitus (7 patients). Concomitant laparoscopically harvested omentoplasty was performed in case of overt mediastinits (4 patients). In 14 cases, the mediastinal wound was prepared with negative pressure wound therapy following surgical debridement. An internal fixation of the sternum by titanium locking plates with sternal and rib-to-rib fixation and bilateral pectoralis advancement flaps were performed in all patients. The postoperative course was followed by clinical follow-up. Results: Early postoperative sternal stability was seen in all 24 patients. The 30-day perioperative mortality rate was zero, with an overall survival of 100% until today. Postoperatively 2 (8.3%) small superficial and 1 (4.1%) deep surgical site infection (SSI) were appreciated. Follow-up ranged from 12 to 60 months (median: 31 months). Conclusions: Combination of bilateral pectoralis advancement flaps and a transverse plate fixation system for sternal reconstruction can contribute to a successful outcome following a complicated sternal wound.

S-29 risk secondary to ongoing immunosuppression. This study evaluates the hematological safety of linezolid for the treatment of infections in transplant recipients compared to transplant patients treated with a control antibiotic, daptomycin. Hypothesis: The incidences of hematological toxicity are increased in transplant patients treated with linezolid compared to transplant patients treated with daptomycin. Methods: We performed a retrospective study from 1/08 through 6/12 of transplant inpatients on immunosuppression treated with linezolid (LZD) or daptomycin (DAP) excluding patients: < 18 years old, pre-engraftment after HSCT, relapsed cancer, aplastic anemia, or those who had received cytotoxic therapy or antibodies within 30 days preceding treatment. Outcomes included the incidences of anemia, leukopenia, or thrombocytopenia at the end of antimicrobial treatment, and blood product transfusions. Results: The LZD cohort included 126 incidences, while the DAP cohort included 130 incidences of treatment. The demographic and baseline clinical variables were similar between cohorts. DAP cohort were more likely to be treated for blood stream infections (46.15% vs 31.75%; P = .02), while LZD group received more linezolid doses (15.8 vs 9.74; P < 0.0001) than daptomycin doses received by the DAP group. LZD patients were more likely to receive red blood cell (68% vs 50.8%; P = 0.007) and platelet transfusions (38.4% vs 20.8%; P = 0.002) during course of treatment. For patients receiving thrombocytopenic drugs, mycophenolate and/or chemotherapeutic agents, end of treatment (EOT) platelet < 150 K was not statistically significant in the LZD cohort compared to DAP (54.8% vs 40%; P = 0.09). Conclusions: Transplant patients who received linezolid had a higher incidence of blood product transfusions, compared to transplant patients who received daptomycin. Although there was no statistically significant EOT thrombocytopenia between cohorts, LZD patients were more likely to receive platelet transfusion during the course of treatment. The difference may be related to greater drug exposure (number of doses) in the LZD cohort. Clinicians caring for transplant patients should account for the need for blood products when considering the use of linezolid.


P-22. ACUTE CHOLECYSTITIS IN THE PEDIATRIC POPULATION Katherine Davenport, Timothy Fairbanks, Nicholas Saenz, Mary Hilfiker, Stephen Bickler, Karen Kling, Julia Grabowski, University of California-San Diego, Rady Children’s Hospital Background: Gallbladder disease in children is increasing in prevalence, but little has been written specifically about acute cholecystitis (AC) in the pediatric population. The presentation, imaging findings, surgical management, and pathologic findings of AC in children are not well described. Hypothesis: The presentation and course of AC in children differ from that in adults. Children with AC may be treated with laparoscopic cholecystectomy even when there is delayed presentation and prolonged symptoms. Methods: We performed a retrospective review of all cholecystectomies performed at our institution between 10/2009 and 10/2013. We identified those with the pathologic diagnosis of AC and reviewed their preoperative data (demographics, diagnostic tests and preoperative length of symptoms), procedural data and outcomes. Results: 277 patients underwent cholecystectomy during this 4 year period, with 25 patients having pathologic evidence of AC. Of these 25, 72% were female, the average age was 14 years old (2–19 y) and average BMI was 28.3 kg/m2 (range, 15.0–43.2). All patients presented with abdominal pain. The duration of symptoms ranged from 1–90 days (avg 16 d). Only 40% of patients had leukocytosis at time of admission. All 25 patients had imaging (US, MRI, CT or HIDA) reviewed by a radiologist. A radiographic diagnosis of AC was made in only 39% of those who had US (n = 22), and 71% of those who had MRI (n = 7); however 100% of those who had CT (n = 5) or HIDA (n = 2). Sixteen patients (64%) had a preoperative diagnosis of AC, and these patients underwent cholecystectomy during the initial hospitalization. The remaining 9 underwent elective cholecystectomy for cholelithiasis and were found to have AC on pathology. Twentyfour patients underwent laparoscopic cholecystectomy, 2/24 patients required conversion to open operation and one patient had an initial open cholecystectomy. Upon review of pathology, 16/25 had evidence of chronic as well as AC, 4/25 had necrosis, and 2/25 were gangrenous. 22/25 had cholelithiasis, while 3 were acalculous. Conclusions: AC in the pediatric population is a clinical entity with a different spectrum of findings than those reported in adults. US underestimates AC, and pathology often shows concomitant acute and chronic inflammation, a combination less frequently seen in adults. Cholecystectomy should be considered in pediatric patients with acute cholecystitis even in patients with prolonged symptoms and advanced pathology.

P-23. INCREASED INCIDENCE OF BLOOD PRODUCT TRANSFUSIONS AMONG TRANSPLANT PATIENTS TREATED WITH LINEZOLID COMPARED TO DAPTOMYCIN Ashley Limkemann, Jeffery Tessier, Leahna Haldeman, Andrew Young, Teddy Puzio, Luke Wolfe, Jinfeng Han, Therese Duane, Virginia Commonwealth University Background: Thrombocytopenia is a known complication of prolonged linezolid use although little data exist specifically in the transplant population who may be at higher

Background: The purpose of this study was to evaluate the factors associated with survival of patients who had CPR at the scene or within one hour of arrival to the trauma center. Hypothesis: Odds of survival of traumatic injured patient depends upon severity of injury Methods: Data was retrieved from the National Trauma Data Bank (NTDB) data set (RDS_2007-RDS_2010). Patients were identified cardio-pulmonary resuscitation (CPR) with Pcode (99.6) with 0 and 1 hour of hospital arrival. In-hospital survival was the main outcome variable. Multiple logistic regression analysis was performed to assess the association between survival and the study groups. All of the tests were two-sided. A pvalue of 0.05 or less was considered statistical significance. Results: Two-thousand-eight-hundred-fifty-eight CPR were performed in 2,733 trauma patients within one hour of hospital arrival. Two-thousand-three-hundred-ninetyseven out of 2,733 (88%) died (Group I) and 336/2733 (12%) survived (Group II). There were no differences between the groups regarding age (p = 0.38) and gender (p = 0.89). There were significant differences between the groups in terms of race (p < 0.001), Injury Severity Score (ISS) [P < 0.001], Glasgow Coma Scale (GCS) [p < 0.001], and American College of Surgeon (ACS) level of trauma center (p < 0.001). However, in multiple logistic regression analysis low ISS (p < 0.001), high GCS (p < 0.001), were significantly associated with survival. For each unit increase in total GCS, there was a 15% increase in survival. Similarly for each unit decrease in ISS there was a 2% increase in survival. Conclusions: Approximately 12% of patients who had cardiopulmonary resuscitation within an hour of arrival to trauma center survived their injury. High GCS and lower ISS were associated with increased survival.

P-25. HIDRADENITIS SUPPURATIVA OF THE BREAST: A CASE REPORT OF A LESS COMMON SITE OF MANIFESTATION Whitney Young, Stephanie Lueckel, William Cioffi, Daithi Heffernan, Brown University Background: Hidradenitis suppurtiva (HS) is a chronic disease characterized by inflammation, infection with abscesses, and sinus tract formation and scarring. It most often affects the apocrine gland baring skin of axillary, inguinal and genital regions. Breast HS is a less well described entity and often confined to the infra-mammary fold (IMF). Wide local excision is recommended for axillary or groin HS. However, for breast HS this may require mastectomy because of the more diffuse nature of breast apocrine glands.


Hypothesis: Recent case reports of breast reduction techniques with or without nipple re-implantation for breast HS have been described allowing preservation of the breast. Methods: We describe a case of bilateral sub-mammary and mammary hidradenitis suppurativa compounded by poor socioeconomic status. Results: A 44 year old woman presented with recurrent breast abscesses. Her medical history was significant for obesity, smoking, and axillary HS requiring excision and grafting. She ascribed her acute worsening of the breast HS being due to worsening socioeconomic status resulting in no running water leading to inability to bathe. Examination revealed bilateral sinus tracts, abscesses and scarring in the submammary and inframmary folds with tracking onto the breast approximating the areolar complex on the right (Image). Incision and drainage obtained a large amount of purulence, resolving the immediate problem. Wound care and social work assistance with personal hygiene were the mainstay of early therapy. Following infection resolution, surgical planning included bilateral reduction mammoplasty with re-implantation of the nipple areolar complex allowing for breast conservation. Conclusions: Breast HS is relatively rare though reported. Non-clinical socioeconomic factors may worsen this disease. Mastectomy removes all the apocrine gland tissue and minimizes recurrence. However, surgeons need to be aware of the potential role of breast preservation techniques in breast HS.

P-26. FACTORS ASSOCIATED WITH POSTOPERATIVE CARDIAC COMPLICATION IN PATIENTS WITH MALIGNANT NEOPLASM OF ASCENDING COLON WHO UNDERWENT ELECTIVE RIGHT HEMICOLECTOMY Yen-Hong Kuo, Yen-Liang Kuo, Nasim Ahmed, John Davis, Jersey Shore University Medical Center Background: Postoperative cardiac complication is associated with prolonged length of hospital stay, high mortality, and increased cost of health care. Identifying the risk factors associated with postoperative cardiac complications will improve patient care. The purpose of this study was to assess the factors which associated with the risk of developing postoperative cardiac complication in patients with malignant neoplasm of ascending colon who underwent elective right hemicolectomy. Hypothesis: Patient and hospital characteristics impact the chance of developing postoperative cardiac complication. Methods: A retrospective cohort study was conducted by using the 2001–2006 Nationwide Inpatient Sample. Adult patients (age ‡ 18 years) with malignant neoplasm of ascending colon and scheduled for right hemicolectomy are the population of interest. Patients with a primary diagnosis of malignant neoplasm of the ascending colon (ICD-9CM code: 153.6), with primary procedure of open and other right hemicolectomy (ORH, ICD-9-CM code: 45.73) were included for this study. Postoperative cardiac complication is the primary outcome (ICD-9-CM code: 997.1). Results: There were an estimated 66,789 patients with malignant neoplasm of the ascending colon admitted for elective ORH in 2001–2006. Among them, 2.3% experienced postoperative cardiac complication after the surgery. Patients with postoperative cardiac complication were older (mean [standard error]: 77.1 [0.5] vs. 71.4 [0.1] years, p < 0.0001), but no difference in gender distribution (54.3% vs. 56.3%, p = 0.49). They had a significantly higher in-hospital mortality rate (5.5% vs. 1.2%, p < 0.0001). From a multiple logistic regression model, the risk of experiencing postoperative cardiac complication increased with older age (adjusted odds ratio{AOR}[95% confidence interval {CI}]: 1.04 [1.03, 1.06], p < 0.0001), male gender (1.35 [1.05, 1.73], p = 0.02), congestive heart failure (3.00 [2.20, 4.10], p < 0.0001), coagulopathy (2.22 [1.05, 4.71], p = 0.04), fluid and electrolyte disorders (1.71 [1.26, 2.32], p = 0.001), and being treated in a teaching hospital (1.48 [1.13, 1.96], p = 0.005). Conclusions: This study identified factors which associated with increased risk of postoperative cardiac complication. Strategy on managing patients with those conditions can reduce the cost of health care.

POSTER PRESENTATION ABSTRACTS Background: Pneumonia is a major cause of morbidity and mortality in ventilated trauma patients. It is difficult to determine the true etiology of pneumonia during the first 24–72 hours in ventilated trauma patients as these patients can present with a variety of diagnoses such as aspiration in the field, systemic inflammatory response syndrome (SIRS), pulmonary contusion, and true-ventilator-associated pneumonia (VAP). Trauma associated pneumonia (TAP) is a term that has been coined in an attempt to make the point clear that traditional definitions of VAP in ventilated trauma patients should not be applied. Hypothesis: The aim of this study is to assess the true etiology of TAP using the mini-bronchoalveolar lavage (mini-BAL) to detect early aspiration in emergently intubated trauma patients. Methods: Patients who were emergently intubated either in the field or trauma bay were prospectively assessed on a daily basis for clinical signs of pneumonia, and if suspected underwent a mini-BAL. Cultures were defined as positive when they showed bacterial growth > 1 · 104 colony-forming unit (cfu)/mL. Positive cultures on mini-BAL at < 48 hours were defined as an aspiration pneumonia and after 48 hours were defined as VAP. Results: Forty patients were identified that were intubated at the scene or after evaluation in the trauma center. Median GCS was 9, mean age was 38.6, 64% of patients were male, 60% loss of consciousness and 60% had illegal substances on board or blood alcohol level over 80. Twenty-five patients (62.5%) met clinical indications to receive a mini-BAL during their hospital stay, 17 (68%) of these being in the first 48 hours from injury. Of these patients 47.1% had culture proven pneumonia. Of the 15 patients who were never cultured 80% were extubated within 24 hours, one patient died and one patient never met clinical indication for culture prior to 48 hours. Conclusions: In trauma patients requiring emergent intubation 47% with clinical suspicion of pneumonia have culture-proven aspiration prior to 48 hours. Organisms isolated in these patients are consistent with bacteria from a patient derived source. Early diagnosis based on mini-BAL culture facilitates identification of these patients early, which allows for early antibiotic coverage and evaluation of sensitivities. Early diagnosis of TAP versus VAP may help in clarification of quality indicator standards for pneumonia in ventilated trauma patients.

P-28. TEDIZOLID (TZD) VERSUS LINEZOLID (LZD) IN PATIENTS (PTS) WITH WOUND INFECTION OR MAJOR ABSCESS: POOLED ANALYSIS OF TWO PHASE 3 DOUBLE-BLIND STUDIES Philip S. Barie, Edward Fang, Sonia Minassian, Philippe Prokocimer, Weill Cornell Medical College Background: TZD is a novel oxazolidinone antibacterial under investigation for the treatment of gram-positive infections, including methicillin-resistant S. aureus. Hypothesis: TZD results in similar treatment outcomes as LZD in pts with wound infection or cutaneous abscess. Methods: ESTABLISH-1 and ESTABLISH-2 were randomized, double-blind, phase 3 non-inferiority trials evaluating TZD (200 mg once daily for 6 d) versus LZD (600 mg twice daily for 10 d) for treatment of acute bacterial skin and skin structure infections. This post-hoc analysis included all pts with wound infection or major cutaneous abscess and excluded those with cellulitis/erysipelas (46% of intent-to-treat [ITT] pts). The primary outcome was early clinical response rate (defined as a > 20% reduction in lesion area compared to baseline) at 48–72 h in the ITT population. Secondary outcomes (also in ITT pts) included programmatic clinical response at end of therapy (EOT) and investigator-assessed response at a post-therapy evaluation (PTE) 7–14 days after the EOT visit. Results: Overall, 725 pts had a wound infection (N = 391; n = 377 post-traumatic, n = 14 superficial incision surgical site infection) or major cutaneous abscess (N = 334). Mean age was 41 years, and 66% were male. The primary infection site was mostly on the lower (32% of patients) or upper extremities (39%); 63% of pts overall underwent an incision and drainage (I&D) procedure in addition to study treatment. Early clinical response was seen in 86.5% and 83.7% of pts treated with TZD and LZD, respectively (difference 2.8%, 95% CI: - 2.4, 8.0); outcomes by I&D status were similar. Response rates at EOT were 87.1% and 89.8%, respectively, and at PTE were 85.7% and 87.8%, respectively. Most adverse events (AEs) were mild to moderate in both treatment arms. Gastrointestinal disorders were the most frequent type of AEs (15.2% of TZD and 24.9% of LZD pts; odds ratio 0.54, 95% CI: 0.37, 0.78), including nausea (7.2% and 11.8%, respectively), diarrhea (3.6%, 5.9%), and vomiting (3.0%, 5.0%). Conclusions: For the treatment of major cutaneous abscesses or wound infections (almost all of which were post-traumatic wounds), a short 6-d course of once-daily TZD demonstrated similar response rates to 10 d of twice-daily LZD at 48–72 h and all later time points evaluated. Both agents were well tolerated, but gastrointestinal disorders were more frequent with LZD.

P-29. PATHOGEN-DEPENDENT DURATION OF ANTIMICROBIAL THERAPY REDUCES RECURRENT PNEUMONIA IN TRAUMA PATIENTS Anastasia Kunac, Alicia Mohr, Miguel Matos, Helen Horng, Ziad Sifri, Robert Lavery, David Livingston, Rutgers-New Jersey Medical School

P-27. TAP VERSUS VAP: EARLY DIAGNOSIS OF PNEUMONIA IN TRAUMA PATIENTS Nicole Hooft, Christine Lovato, Pam Goslar, Kristina Kahzeni, Tom Gillespie, Scott Petersen, St. Joseph’s Hospital and Medical Center

Background: Ventilator associated pneumonia (VAP) is a frequent occurrence in severely injured patients. Patients with prolonged respiratory failure often suffer multiple bouts of VAP; previous studies have shown certain organisms are more likely to be associated with recurrent pneumonia. The optimal duration of antibiotic therapy for VAP remains unknown.

POSTER PRESENTATION ABSTRACTS Hypothesis: We hypothesized that treating patients infected with nonfermenting gram negative bacilli (NFGNB), MRSA, and multi-drug resistant (MDR) Enterobacteriaciae for 10 days would mitigate the risk of recurrent VAP. Methods: Data were collected prospectively and reviewed retrospectively for trauma patients with VAP from 7/12–6/13 following institution of a VAP treatment protocol. VAP was defined as a clinical pneumonia with positive respiratory cultures (BAL with ‡ 10 K organisms). Recurrence was defined as a positive respiratory culture following a full course of antibiotic therapy. The protocol mandated a 10-day course of therapy for NFGNB, MRSA, and MDR Enterobacteriaciae; and a 7-day course for other organisms. Demographic data, ISS, transfusion and microbiology were reviewed. Outcome included ICU and hospital length of stay, ventilator days and survival. A student ttest, chi-square test or logistic regression was used as appropriate. Results: Following implementation of the VAP protocol, 1,420 trauma admissions over a 1-year period were reviewed. Of these, 103(7%) were diagnosed with VAP, and a total of 28(27%) had recurrent VAP. Adherence to the protocol was noted in 75 patients (73%). Outcome data based on compliance with the protocol are compared in the summary table. There was no difference in age, gender, ISS, units of PRBC transfusion, or mortality between groups. Conclusions: Protocol driven treatment of post-traumatic VAP is associated with a reduced rate of recurrent VAP, reduced duration of mechanical ventilation, and decreased hospital and ICU length of stay. These data suggest that duration of antimicrobial therapy should be tailored to the offending pathogen. Further prospective studies are warranted to validate these results and to more clearly elucidate the ideal duration of treatment for VAP.

S-31 Background: Nosocomial infections increase morbidity, mortality, length of stay and treatment cost. The SMART program tracks susceptibility of hospital- (HA) and community-associated (CA) intra-abdominal infection (IAI) gram-negative pathogens (GNP) globally. This report summarizes susceptibility differences of HA IAI GNP between surgical and medical wards in the US. Methods: 23 labs in the US each collected up to 100 consecutive isolates yearly of aerobic GNP from IAI. From 2010 to 2012, 3,778 GNP were collected, of which 1,713 were from HA IAI. An IAI was defined as HA if cultured ‡ 48 hours post-admission. Antimicrobial susceptibility and extended-spectrum b-lactamase (ESBL) phenotypes were determined using the CLSI broth microdilution method. Results: ESBL + rates in surgical and medical wards were 7% and 11%, respectively, for E. coli (p > 0.05, chi-square test) and 20% and 8% for K. pneumoniae (p < 0.05). Prevalence and susceptibility (%S) of the top 3 species and of all GNP combined are shown below for selected drugs. AMK = amikacin, FEP = cefepime, CTX = cefotaxime, FOX = cefoxitin, CAZ = ceftazidime, CRO = ceftriaxone, ETP = ertapenem, IMP = imipenem, LVX = levofloxacin, TZP = piperacillintazobactam, NB = no breakpoint. Conclusions: On both surgical and medical wards, the top 3 species–E. coli, K. pneumoniae, and P. aeruginosa–made up almost 70% of IAI pathogens. K. pneumoniae ESBL rates were significantly higher in surgical wards. Overall susceptibility for all GNP combined was usually 3–6% lower in surgical wards. This decrease appears partly driven by both lower susceptibility and higher prevalence of typically less susceptible K. pneumoniae and P. aeruginosa in surgical wards. Knowledge of the epidemiology of IAI pathogens, ESBL + rates, and susceptibility patterns–not only by geographic location but also by patient location in the hospital– may be helpful for empiric therapy decisions for HA IAI.

P-30. ANTIBIOTIC TREATMENT OUTCOMES IN COMPLICATED INTRA-ABDOMINAL INFECTION (cIAI)—RESULTS FROM A PROPENSITY-MATCHED COHORT STUDY Joseph Solomkin, C. Mullins, Alvaro Quintana, Christian Eckmann, Ahmed Shelbaya, Mingfang Zhao, Frank Ernst, Michelle Krukas, Arlene Reisman, University of Cincinnati College of Medicine Background: Treatment outcomes for patients suffering from cIAI are known to depend on various severity- and treatment-related variables. To examine 3M APR-DRG severity of illness the effectiveness of tigecycline and other antibiotic treatments, we constructed a propensity score using the Premier research database. We then matched patients with this score to examine outcomes of tigecycline vs. other antibiotic therapy. Hypothesis: Severity of illness descriptors predict outcomes in patients receiving broad-spectrum antimicrobial therapy. Methods: Retrospective, observational study using a large clinical database maintained by Premier. Success was defined as 1 operation, no additional antibiotics for the cIAI, and survival to 30 days. Results: The final propensity score model included: APR-DRG severity of illness, APR-DRG risk of mortality, ICU admission, vasopressor use, mechanical ventilation, site of infection, and a range of demographic data for patients and hospitals. The cstatistic for this model was 0.7. A total of 2,424 patients were matched (tigecycline [606]; other antibiotic therapy [1818]). Organ site of infection (combined treatment procedure groups): stomach (61), gallbladder (134), appendix (29), small intestine (670), large bowel (1040), and other (875). Treatment was successful in 426 (70.3%) tigecycline-treated patients and 1294 (71.2%) patients receiving other antibiotic therapy. Similar treatment success occurred across all infection sites. Of those survivors, allcause rehospitalization within 180 days was 45.2% for those considered ‘‘cured’’, and 49.6% for those considered ‘‘failed’’. cIAI-related hospitalization was 6.4% for cures and 7.8% for failures. Conclusions: These data demonstrate the association between severity of acute illness and outcome. Tigecycline and other antibiotic therapies were similar in effectiveness in the overall matched population, and among those in the extreme severity of illness category.

P-32. EVALUATION OF ANTIMICROBIAL PROPHYLAXIS AMONG PATIENTS RECEIVING MEDICINAL LEECH THERAPY Brian Gilbert, Rachel Kruer, University of Florida, Jacksonville Background: Medicinal leeches (Hirudo medicinalis) are an important therapy in plastic and reconstructive surgery. Leeches are indicated for salvage of tissue flaps, grafts, or replants. The use of medicinal leeches does not come without risk; infection threatens graft survival. Antimicrobial prophylaxis is recommended. Hypothesis: Prophylactic antimicrobial administration will prevent leech-associated Aeromonas spp. infections. Methods: Patients 18 years or older were included if they received leech therapy and were admitted to the hospital between December 2009–February 2013. A query of patients with orders for medicinal leeches was performed via the pharmacy electronic medication order management system. The primary outcome of this study was to describe the incidence of wound site infection or bacteremia associated with leech therapy in patients receiving prophylaxis and the associated pathogens isolated from cultures within 48 hours of receiving leech therapy. Secondary objectives were to describe antimicrobials utilized for prophylaxis, and evaluate adverse effects associated with antimicrobials. Results: Thirty-two patients received leech therapy and 31 met inclusion criteria. The mean age of patients included was 58 ( + / - 13). Fifty-five percent of patients were male. The mean number of days of leech therapy was 5.2 ( + / - 2.9). Thirty patients received antibiotic prophylaxis; 17 received trimethoprim/sulfamethoxazole, 12 received ciprofloxacin, and one received ceftriaxone. Of the patients who received antimicrobial prophylaxis, four patients had positive cultures. One patient had a Proteus vulgaris surgical site infection, resistant to the prophylactic agent utilized. One patient had a Candida parapsilosis surgical wound site infection. Two patients had urine cultures positive for Enterococcus; one patient was treated for an infection and one was not. trimethoprim/sulfamethoxazole was discontinued in one patient due to rash. Conclusions: Given antimicrobial prophylaxis with trimethoprim/sulfamethoxazole, ciprofloxacin, or ceftriaxone, no patients in this study developed an infection with Aeromonas spp. One patient developed a surgical site infection with Proteus vulgaris, resistant to the prophylactic agent used. The antimicrobial agents utilized in this study were associated with minimal adverse effects.



Samuel Bouchillon, Robert Badal, Sibylle Lob, Meredith Hackel, Daryl Hoban, International Health Management Associates, Inc.

Erik Askenasy, David Berger, Bradford Scott, Lillian Kao, Mike Liang, Baylor College of Medicine



Background: Operative reports which do not reflect the key components required by payors and current procedural terminology (CPT) may lead to significant reductions in reimbursement. Often the requirements and CPT codes are complicated and nebulous such as for skin and soft tissue (SST) procedures. Hypothesis: Surgeon operative reports do not accurately reflect the key components of the procedure performed and consequently results in a significant decrease in potential reimbursement for skin and soft tissue surgeries. Methods: Fifty consecutive patients undergoing SST procedures at an urban safety net hospital were evaluated. The operative reports were reviewed and assessed for five elements necessary to meet criteria for excisional debridement. Original relative value units (RVU) and charge values were obtained and compared to ideal RVU and charge value had the operative report been complete. Results: The overall accuracy of the dictated operative report for SST surgeries was 30%. When looking specifically at excisional debridements the accuracy rate dropped to 13%. Size and depth of the wound were elements most likely left off the operative report. Had the operative reports included all necessary components, RVU generation and charges would have doubled. Conclusions: The dictated operative report for SST surgeries does not contain many of the necessary elements. A potential increase in productivity measures can be accomplished by more complete and thorough dictations.

P-34. SURGICAL SITE INFECTION IN VENTRAL HERNIA PATIENTS WITH OPEN INCISIONAL HERNIA REPAIR Yen Hong Kuo, Yen-Liang Kuo, Nasim Ahmed, John Davis, Jersey Shore University Medical Center Background: The purpose of this study was to evaluate the rate of surgical site infection in patients undergoing open incisional hernia repair. Hypothesis: Patient characteristics contribute to surgical site infection. Methods: A retrospective cohort study was conducted by using the 2006 Nationwide Inpatient Sample to evaluate adult patients with ventral hernias. The disease status and procedures were categorized according to the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Patients with a primary diagnosis of hernia with or without obstruction, with procedure of incisional hernia repair with graft or prosthesis were included for this study. The primary measured outcome for the study was surgical site infection as defined by a patient who had record of cellulitis or abscess, peritoneal abscess, infection postoperative seroma (ICD-9 code 998.51), or other postoperative infection. The weighted number of procedures and rates were calculated to take into consideration the stratified sampling design of NIS data. Results: An estimated 47,007 procedures were performed in U.S. in 2006; 50.5% of the patients had hypertension, 20.2% were obese, 19.3% had chronic pulmonary disease, 18.6% had diabetes, and 6.5% had fluid and electrolyte disorders. Postoperatively 1.1% had a surgical site infection (SSI). Age and gender did not differ in those who did and did not experience SSI (mean [standard error]: SSI vs. no SSI = 58.7 [1.34] vs. 58.2 [0.22] years, P = 0.89 and female %: SSI vs. no SSI = 63.7% vs. 64.7%, P = 0.84). However, a higher proportion of patients had fluid and electrolyte disorders (SSI vs. no SSI = 19.1% vs. 6.4%, P < 0.0001). From a multiple logistic regression model, patients with fluid and electrolyte disorders had an increased chance of experiencing SSI (adjusted odds ratio {AOR} [95% confidence interval {CI}] = 3.29 [2.03, 5.34], p < 0.0001). Chronic pulmonary disease also associated with an increased chance (AOR[95% CI] = 1.54 [1.03, 2.30], p = 0.03). However, obesity did not show a significant association with SSI (AOR[95% CI] = 1.12[0.72, 1.73], p = 0.63). Conclusions: The SSI rate reported was low compared to current publications not using the NIS database. Patients with fluid and electrolyte disorders or chronic pulmonary disease had a higher chance of experiencing surgical site infection.

P-35. PREDICTIVE VALUE OF PROCALCITONIN FOR SURGICAL SITE INFECTION FOLLOWING CROHN DISEASE RESECTION Dong Hu, Jianan Ren, Song Liu, Guanwei Li, Xiuwen Wu, Gefei Wang, Guosheng Gu, Jieshou Li, Jinling Hospital, Nanjing University, China Background: Patients with Crohn disease (CD) usually receive immunosuppressants or complicating with malnutrition, which contribute to a high incidence of surgical site infection (SSI) following CD resection. Hypothesis: Procalcitonin (PCT) is a biomarker of bacterial infection and systemic inflammation. We hypothesized that PCT may be useful for early diagnosis of SSI after CD resection. Methods: Sixty-six patients undergoing segmental bowel resection for CD were evaluated prospectively. PCT, C-reactive protein (CRP), and white blood cell count (WBC) were measured on postoperative days (POD) 1, 2, and 3. Patients were followed for postoperative complications. Results: Between December 2011 and October 2013, a total of 66 patients were enrolled, among which 30 (45.4%) patients received ileocaecal resection, 26 (39.4%) patients received ileocolonic resection, and 10 (15.2%) patients received partial small bowel resection. SSIs were proven in 13 (19.7%) patients, among which 10 (15.2%) patients with incisional SSI and 4 (6.1%) patients with organ/space SSI. Significant higher PCT levels (on PODs 1, 2 and 3) and CRP levels (on POD 3) were observed in patients with SSI compared to those without SSI. Receiver-operating characteristic (ROC) analysis showed that PCT counts for the highest area under the curve (AUC) for

Figure 1. Box plots of PCT (a), CRP (b), and WBC (c) of patients with or without SSI in different post-operative days. Significantly higher PCT levels (on PODs 1, 2 and 3) and CRP levels (on POD 3) were observed in patients with SSI compared to those without SSI. SSI, surgical site infection; PODs, post-operative days.

predicting SSI on both PODs 1, and 2 (AUC, 0.758 and 0.750, respectively), while PCT and CRP had similar predictive values for the development of SSI on POD 3 (AUC, 0.734 and 0.739, respectively). Conclusions: Compared with conventional inflammatory markers, PCT is more reliable in detecting SSI on early postoperative days after CD resection.

P-36. VALUE OF C-REACTIVE PROTEIN IN PREDICTING ABSCESS IN PEDIATRIC APPENDICITIS Katherine Davenport, Timothy Fairbanks, Stephen Bickler, Karen Kling, Mary Hilfiker, Nicholas Saenz, Julia Grabowski, University of California, San Diego, Rady Children’s Hospital Background: Appendicitis is the most common pediatric surgical emergency. Abscess formation is a frequent complication of appendicitis and can occur both pre-operatively or post-operatively. Though the management of an abscess depends on the clinical situation, its diagnosis typically requires cross- sectional imaging, often a CT scan. In an effort to minimize radiation, exclusion of an abscess with lab markers may mitigate the need for imaging. Hypothesis: We predict that CRP level correlates with appendicitis-related abscesses.






Methods: We performed a retrospective review of all appendectomies performed for presumed appendicitis from 10/2011–10/2013 in our university practice. We identified patients who had a CT scan and CRP drawn concurrently either preoperatively or post-operatively. We reviewed demographic data, CT scan findings, and CRP. For those who underwent surgery, we correlated CT findings to pathology and operative details. We compared the weighted mean of CRP of those who had an abscess to those who did not and calculated statistical significance using the ranksum test. Results: 1,333 patients underwent appendectomy in this 24 month period. 548 had a CT scan and CRP drawn simultaneously. The average age was 10 years (1–20 years). 56% were male. There were 91 abscesses identified in 87 patients. 61 abscesses were identified pre-operatively, 30 were post-operative. The weighted mean of CRP was significantly higher in those with an abscess (17.0 mg/dL) compared to those without an abscess (6.0 mg/dL), both pre-operatively and post-operatively (p < 0.05). Furthermore, of the 91 abscesses recognized, none had a normal CRP. Conclusions: CRP is significantly higher in the presence of an abscess, both preoperatively and post-operatively. Additionally, an abscess was never diagnosed in any patient with a normal CRP. CRP value may be helpful in guiding the diagnostic algorithm in patients with a presumed appendicitis-related abscess. A normal CRP level may obviate the need for imaging, thereby reducing radiation exposure in children.


Song Liu, Jianan Ren, Guosheng Gu, Gefei Wang, Gang Han, Xiuwen Wu, Jieshou Li, School of Medicine, Nanjing University, China Background: Intra-abdominal abscess (IAA) is a common complication in Crohn’s disease (CD). Traditional percutaneous catheter drainage (PCD) and surgical intervention could not obtain satisfactory results in a certain number of cases. Hypothesis: We herein demonstrated a novel strategies (trocar puncture with sump drain) for the management of IAA in CD, and compared it with traditional PCD and surgical options. Methods: 77 patients were collected into three groups. Postoperative complication, postoperative recurrence of abscess, subsequent surgery, ultimate stoma creation rate and survival rate were analyzed. Potential risk factors that correlate with postoperative complication, recurrence of abscess and ultimate stoma creation were analyzed as well. Results: Patients were divided into trocar (n = 21), PCD (n = 25) and surgery group (n = 31). Incidence of postoperative complication (0/21 vs. 6/25, 8/31), incidence of recurrent abscess (6/21 vs. 16/25, 18/31) and ultimate stoma creation rate (2/21 vs. 5/25, 18/31) were all lowest with statistical significance in trocar group. Subsequent surgery rate (10/21 vs. 17/25, 22/31) and survival rate (0/21 vs. 0/25, 2/31) were also lowest in trocar group as well, but without statistical differences. Drainage strategy was confirmed as a risk factor of postoperative complication and recurrence of abscess in the management of IAA in CD. Conclusions: This novel technique might be an optimal option in the management of IAA in CD.

A diagram of trocar puncture with sump drain for intra-abdominal abscess in Crohn’s disease. (A) local anesthesia (B) skin incision and blunt dissection of subcutaneous tissues (C) a 12-mm laparoscopic trocar was placed into the abscess cavity (D) purulence was aspirated from abscess cavity (E) a 10-mm sump drain, consisting of an irrigation tube (red tube) and a suction tube (white tube), was inserted through the trocar cannula (F) the trocar was removed, leaving the sump drain in situ.

P-39. FINGERSTICK CAPILLARY LACTATE TRENDS CLOSELY WITH ARTERIAL LACTATE IN PATIENTS WITH SEPTIC SHOCK: POINTING SEPSIS RESUSCITATION IN A NEW DIRECTION Simon Eiref, Asaf Gave, Scott Gould, Ezra Gillego, Anita Hariprashad, Shailyn Almonte, Christine Wiest, Michael Leitman, Beth Israel Medical Center Background: Interest in the application of capillary (CAP) whole blood lactate (LAC) has led to the development of handheld point-of-care devices that use test strip tech-

S-34 nology similar to glucometers. These devices can process tiny ml aliquots of CAP blood from patient fingersticks, with rapid result turnaround time. As such, the use of CAP blood may have advantages over arterial (ART) blood in LAC determination. Hypothesis: We hypothesized that changes in CAP LAC trend closely with ART LAC levels in patients undergoing resuscitation for severe sepsis and septic shock. Methods: The study took place in the surgical ICU of an urban teaching hospital. Fingerstick CAP whole blood specimens were obtained via lancet every 4–6 hours, and assessed for LAC using a handheld LAC analyzer (StatStrip, Nova Biomedical, MA). Comparison was made to ART blood specimens that were assessed for LAC both by blood gas analyzer and core lab. Results: Six patients with severe sepsis (A, B) and septic shock (C, D, E, F) were included from Sep to Oct 2013. The group had an average age 81 years, and mean APACHE II score of 20. Changes in CAP and ART LAC over time are shown for each patient (x-axis = 24-hour clock time, y-axis = LAC mmol/L, blue = CAP LAC, red = ART LAC). Patient A had colitis, B perforated ulcer, C cholangitis, D strangulated hernia, E anastomotic leak, and F pneumonia. CAP and ART LAC trended closely together over time: rising (E, F), peaking (E, F), and falling (A, B, C, D, F) in tandem. Resolution of elevated CAP and ART LAC levels mirrored clinical improvement. High LAC normalized in all cases except for patient E, who did not recover. Conclusions: Fingerstick CAP LAC trends closely with ART LAC in patients undergoing resuscitation for severe sepsis and septic shock - suggesting a new guide for goal-directed therapy.


POSTER PRESENTATION ABSTRACTS Background: Emergently intubated patients are at significant risk of developing ventilator-associated pneumonia (VAP). Pre-intubation chlorhexidine gluconate (CHX) mouth cleansing is effective in preventing pneumonia in electively intubated surgical patients, but it is unknown whether this procedure can be safely and effectively performed in a prehospital setting. Hypothesis: We hypothesize that an instructional video can be used to teach preintubation oral cleansing to providers with different airway training backgrounds. Methods: We created a brief instructional video to demonstrate preparation of a 0.05% CHX swab and appropriate oral swabbing technique and duration. We then evaluated the teaching effectiveness of this video-based training in 10 care providers who were asked to view the video. Participants were observed demonstrating the oral cleansing procedure in volunteer subjects undergoing intubation prior to elective surgery. Performance was measured by an observer and self-reported according to the following parameters: 1) use of the entire 5 mL of solution, 2) adequate oropharyngeal coverage of 6 pre-defined areas, and 3) duration of cleansing between 10–15 seconds. Results: Nine of 10 (90%) participants covered all 6 required oropharyngeal areas. One paramedic student failed to swab under the tongue. Four paramedic students and 1 respiratory therapist self-reported that they failed to use the entire 5 mL of fluid, but the study observer only confirmed this in one subject. All of the participants completed the task in less than 15 seconds. The subjects uniformly reported that they felt adequately prepared by the training for both the current study setting and the proposed prehospital setting. There were no adverse events and there were no observed or perceived delays in intubation as a result of the study procedure. Participants remarked that the procedure would be significantly easier by improved packaging of the swab. Conclusions: Our study participants effectively performed pre-intubation oral cleansing after watching a brief instructional video without delaying intubation. This suggests that wider-scale implementation of this video-based teaching method is feasible for future studies investigating the effect of pre-intubation mouth cleansing on VAP rates. This approach is particularly relevant and efficient for training providers in a multicenter trial setting where procedure standardization and scalability are essential.

Background: CLABSI is a serious complication for hospitalized patients. Numerous advances and practices have been advocated to decrease CLABSI rate with varying degrees of success. In 2008, the University of Kentucky formed a multi-disciplinary group that aimed to reproduce the excellent results published by Dr. Pronovost in the Keystone Project. The five elements were: hand hygiene, maximal barrier precautions, chlorhexidine skin antisepsis, optimal site selection and daily review of necessity with early removal of unnecessary lines. Hypothesis: For practical reasons, we were unable to fully implement the entire bundle. We therefore hypothesized that the last element of the bundle, which is early removal of unnecessary lines, is the most impactful one. Methods: In March of 2009, early removal of unnecessary central lines was implemented, while the remaining bundle elements were strongly encouraged but not enforced. Early line removal was achieved with diligent daily rounding of unit managers with the bedside care teams. In April of 2010, the full bundle was implemented and tracked. Results: In the twelve months following implementation of just a single component of the bundle, the CLABSI rate dropped from a six-month average of 5.6 infections per 1,000 line days to a rate of 2.6 per 1,000 line days, using the same months to account for seasonable variation (p = 0.037). Our infection rates were tracked by utilizing surveillance techniques and NHSN (National Healthcare Safety Network) definitions and benchmark. Surprisingly, we were not able to demonstrate further decrease in CLABSI rate after implementing of the rest of the bundle. The twelve-month CLABSI rate did not show any statistically significant decrease in rate, from 2.6 to 2.3 (p = 0.263). Conclusions: While all elements of the bundle are important, our single-institution experience suggests that the most important element of the 5-element bundle as described by Keystone ICU project is to diligently remove central lines when they are no longer necessary.




Courtney Sommer, Gareth Gilna, Peter Louras, Miriam Treggiari, David Carlbom, Eileen Bulger, Heather Evans, University of Washington, Harborview Medical Center

John Young, Andrew Stephen, Charles Adams, William Cioffi, Daithi Heffernan, Brown University

Zain Nasim, Nasim Ahmed, Johnson Victor, Yen-Hong Kuo, John Davis, Jersey Shore Medical Center Background: The purpose of the study was to see the neurologic improvement in patients with traumatic brain injury (TBI) who received platelet transfusion. Hypothesis: Platelet transfusion does not help in-hospital neurological outcome in TBI. Methods: A total of 516 consecutive patients were studied for last two years. The subjects’ were selected based on all adult patients that sustained TBI and computerized tomography (CT) scan showed of an intracranial hemorrhage. The patients were divided into a group (1), those who received platelet transfusions within 24 hours and a group (2), those who did not receive platelets. Patient demographic characteristics and the neurological outcome, analyzed by the Glasgow Coma scale (GCS) at the time of admission and discharge, were assessed. Statistical analysis was performed using Pearson Chi-squared test, Fisher’s exact test and Wilcoxon rank sum test. Results: Ninety-two of 516 patients (18%) received platelet transfusion. There were no significant differences between the groups in terms of male gender ((p = 0.25). However, there were significant differences regarding age (p < 0.001), and the Injury Severity Score (ISS) (p = 0.001). Results showed that Median GCS scores at admission between the groups were significantly different (p = 0.008). However, the discharge GCS scores were not significantly different (p = 0.11). There was no improvement regarding the initial and discharge GCS score between the groups (p = 0.45). The mortality was higher in Group 1 (21.7%) than that of Group 2 (8.7%) (p < 0.001). The disposition to home was significantly higher in Group 2 (p < 0.001) whereas disposition to rehabilitation was higher in Group 1 (p < 0.001). Multivariate analysis showed higher mortality in Group 1 and was significantly associated with higher ISS (P < 0.001). Conclusions: Platelet transfusion within 24 hours of admission following TBI shows no positive GCS improvement compared with no platelet transfusion. Mortality in platelet transfusion group was significantly higher and was associated with higher ISS in the platelet transfusion group.

POSTER PRESENTATION ABSTRACTS Background: Necrotizing fasciitis (Nec Fasc) is a rapidly spreading necrotizing infection of soft tissues and fascia requiring surgical debridement. Sweet syndrome (acute febrile neutrophilic dermatosis) is characterized by fevers and tender erythematous skin lesions with dermal neutrophil infiltration, often paraneoplastic, responding to systemic corticosteroids. The necrotizing Sweet Syndrome (NSS) subtype, has rapidly progressive lesions, deep-tissue neutrophilic infiltration and soft-tissue necrosis in the absence of an infection. Hypothesis: NSS mimics Nec Fasc both clinically and pathologically and may lead to harmful surgical debridements. Methods: We present a case of NSS masqueading as Nec Fasc. Results: A 34 yr old female presented with a presumed thigh abscess. Despite drainage and antibiotics, she developed shock, rapid wound progression, prompting surgical debridement. Clinical and pathologic features were consistent with Nec Fasc. However culture data were negative. Despite initial wound healing, multiple areas of skin necrosis occurred - original wound, peripheral and central (Image) IV sites, requiring debridement. Pathology was consistent with Nec Fasc. The development of pancytopenia with greater than 70% blasts raised concern for acute myeloid leukemia, confirmed by bone marrow biopsy. The diagnosis of AML, negative cultures and multifocal nature of soft tissue necrosis, led to the consideration of Sweet syndrome. Further pathology review noted dermal neutrophilic and atypical mononuclear infiltrate epidermal hyperplasia, spongiosis and neutrophil exocytosis, consistent with Sweet syndrome. Steroids were started with prompt fever resolution and wound improvement, and she was transitioned to chemotherapy. Conclusions: Operative intervention in NSS can lead to disease progression. NSS and Nec Fasc both display rapidly expanding erythematous painful skin bullae. In culture negative patients with delayed progression of necrotizing wounds, alternate diagnoses, such as NSS need to be considered. Communication between surgeon and pathologist is critical.

S-35 P-45. MICROBIOLOGY AND RESISTANCE PATTERNS IN SURGICAL SITE INFECTIONS AFTER OPEN REDUCTION AND INTERNAL FIXATION (ORIF) Neil Pathak, Vanessa Ho, Taylor Klein, Nisha Iyer, Arun Kottarathara, Sebastian Schubl, Farshad Bagheri, Jamaica Hospital Medical Center Background: Infectious complications after ORIF lead to increased hospital length of stay, long-term physical limitations, and reduced overall quality of life. Greater understanding of the microbiology and resistance patterns of these infections is required to guide appropriate empiric antibiotic therapy and preoperative prophylaxis regimens. Hypothesis: We hypothesize that the most common pathogens isolated would be sensitive gram-positive organisms. We secondarily hypothesize that patients with chronic medical conditions or recent hospitalization would be more likely to exhibit more virulent pathogens. Methods: A retrospective review was performed on patients who received ORIF between 2009–2011 at a community teaching hospital and developed a surgical site infection. Patient demographics, clinical risk factors, microbiology, and outcome data were collected. The Chi square test was utilized to determine association between risk factors and specific microorganisms. Results: Fifty-nine patients (35 male) were included in the study (mean age 52.7 y, SD 19.9). The most common ORIF performed was hip/knee with 17 cases (29%). Fortyfour patients (75%) required antibiotics at discharge. Two patients died (4%). Twentyseven (46%) patients had gram positive and 12 (20%) had gram negative organisms identified. S. aureus was the most common causative agent, in 23 patients (39%): 12 methicillin resistant (MRSA), 10 methicillin sensitive (MSSA), and 1 with both. Other causative agents isolated included Enterobactericeae (9%), pseudomonas (8%), enterococcus (7%), acinetobacter (3%), and fungi (3%). Isolation of MRSA was associated with prolonged preoperative hospital stay and recent antibiotic use (p < 0.05). Isolation of MSSA was associated with a history of a chronic skin condition (p < 0.05). Conclusions: The treatment of infectious complications following ORIF is an ongoing challenge. Patients with a prolonged hospital stay or recent antibiotic use are at risk of MRSA infection. Consideration should be given to routine MRSA prophylaxis or MRSA eradication in high risk patients with mupirocin or chlorhexidine baths. Patients with presumed infection following ORIF should be treated with empiric antibiotics active against MRSA and gram-negative organisms until final culture results are available.


Debrided central line site

P-44. THE MICROBIOLOGIC SPECTRUM AND PATIENT CHARACTERISTICS OF PARAPNEUMONIC AND POST-SURGICAL EMPYEMA Christopher Towe, Nathaly Llore, Nathalie Hirsch, Jessica Donington, Harvey Pass, Vanessa Ho, New York University Langone Medical Center Background: Empyema can result as a complication of bacterial pneumonia or thoracic surgery procedures with mortality as high as 15%. Empyema pathogens are poorly described in the modern era. Greater understanding of common pathogens and risk factors is required to improve empiric treatment. The primary aim of this study is to describe the microbiology of empyema in the modern era. Hypothesis: We hypothesize that parapneumonic empyema (PNE) and post-surgical empyema (PSE) will be clinically and microbiologically distinct. Methods: All patients with positive pleural cultures between 4/2007 and 6/2012 were identified from microbiological records. Patient demographics, clinical course and microbiological information were collected. Each acute empyema was classified as PNE or PSE and differences between groups were assessed using the Chi-square test. Results: A total of 227 microorganisms from 28 genus classes were isolated from 125 patients (74 (64%) male, mean age 61). 120 (97%) required drainage or decortication, while 5 were treated with antibiotics alone. Common comorbidities included: A history of immunosuppression (29%), diabetes (19%), and renal disease (14%). Mortality was 15%. Half (47.7%) of the index cultures were polymicrobial. 152 isolates (67%) were gram positive, 56 (25%) were gram-negative, 16 (7%) were fungal, and 3 (1%) were unclassified. Only 7% of isolates were obligate anaerobes. The most common organisms were Streptococcus spp (27%) and Staphylococcus spp (25%), followed by Enterococcus spp (9%), Candida (6%), and Pseudomonas (6%). Of 31 isolates of S. aureus, 14 (45%) were methicillin-resistant. 29% of the infections were postoperative. Patients with PSE were less likely to have had a preceding pneumonia (28% vs 65%, p < 0.05). Patients with PSE had a slightly higher incidence of gram-negative pathogens but this did not reach statistical significance (40% vs 26%, p = 0.1). There was no difference in outcome between the PNE and PSE patients. Conclusions: A wide variety of pathogens were isolated from infected pleural cultures. The most common pathogens isolated were aerobes and gram-positives. Polymicrobial infections were common. There was no significant difference in clinical course or pathogens isolated from parapneumonic and post-surgical empyema.

Background: Diarrhea is a common condition after solid organ transplant (SOT); Clostridium difficile-associated colitis (CDAC) is one of the most common infection following SOT. We previously documented that some types of enteritis are associated with an elevation of tacrolimus (TAC) trough levels by interfering with the drug’s complex metabolism. Hypothesis: To investigate if TAC trough levels rise during CDAC post transplant. Methods: TAC levels of 25 SOT recipients including 12 renal and 13 liver recipients before, during and after CDAC were retrospectively analyzed. Results: Median age of the 25 patients was 54 years (range 36–71), there were 15 men and 10 women. CDAC developed at a median of 55 days (range 2–4551) post-SOT. Median TAC levels prior to the outbreak of CDAC were 6.9 (range < 1.5–17.2) ng/mL, 5.6 (range < 1.5–13.2) ng/ml during diarrhea and 7.4 (range < 1.5–24.3) ng/mL after resolution of diarrhea (p > 0.05, n.s.). Treatment of CDAC consisted of metronidazole for 14 days in all cases. All patients recovered from CDAC but 7 patients had CDAC relapse. Conclusions: In contrast to other types of infectious diarrhea such as Rota virus enteritis and cryptosporidiosis, CDAC is not associated with a rise in TAC levels. This is due to the fact that C. difficile causes primarily colitis as opposed to other organisms, which are associated with enteritis.

P-47. HPV-ASSOCIATED ANAL LESIONS: A SURGICAL INFECTION? Hugo Bonatti, B. Bruene, J. Wehnemann, Michael Oberwalder, Irmgard Kronberger, Friedrich Conrad, Felix Aigner, Easton Memorial Hospital Background: Treatment concepts of human papilloma virus (HPV) associated anogenital infections include conservative treatment with local chemotherapy, immunomodulatory agents and antivirals but surgical management is still the most common approach. Hypothesis: Anogenital HPV lesions are common and have a high recurrence rate. Methods: Data of 433 patients (320 female, 73.9%) with a mean age of 30.1 – 11.8 years treated at our proctology clinic for anogenital warts during a five year period were retrospectively analyzed. Patients were divided into three groups: Predominant genital, anal, perianal lesions. 25 individuals had HIV infection; there were 32 pregnant women and 10 transplant recipients. Results: A total of 410 patients (94.8%) presented with condylomata accuminata. In 263 individuals (60.8%) both the genital and the anal region were involved, in 90% both areas were treated simultaneously using electrocautery. A total of 646 lesions (231 in the anal canal, 282 in the perianal region and 133 genital) were recorded and followed for an

S-36 average of 10 (range 1–87) months. Of those having anal HPV infection, most lesions were found in the anal canal spreading to the perianal area (n = 225, 52%). Isolated affection of the anal canal was seen in 26 patients (6%) and of the perianal region in 139 patients (32.1%). Anal intraepithelial neoplasia was diagnosed in 18 patients (4.1%) and anal squamous cancer in 19 patients (4.3%) including one giant condyloma (BuschkeLowenstein). Primary non-operative treatment of HPV associated lesions with imiquimod (n = 11), trichloroacetic acid (n = 1), podophyllotoxin (n = 1) and the antiviral agent cidofovir (n = 1) was exclusively used in the anal region for subsets of patients with either comorbidities precluding surgery and, in transplant recipients. Recurrence rates were 32% for genital, 28% for perianal and 23% for lesions in the anal canal. Recurrence rates for HIV infected individuals, pregnant women and transplant recipients exceeded 50%. Recurrent conylomata accuminata (n = 176) were predominantly treated by repeat surgical intervention (66.8%). Conclusions: Recurrence rates of anogenital HPV lesions remain high. Universal immunization against HPV may reduce incidence and prevalence of the disease, however, the available vaccines do not cover many HPV strains causing conylomata accuminata. Imiquimod and cidofovir represent promising new agents for subsets of patients.

P-48. ACUTE CARE SURGERY - INFECTIOUS COMPLICATIONS AND MORTALITY Brandon Bruns, Matthew Lissauer, Ronald Tesoriero, Laura Buchanan, Mayur Narayan, Samuel Galvagno, Jose Diaz, University of Maryland; R Adams Cowley Shock Trauma Center Background: Acute care surgery (ACS) has evolved in an effort to provide 24-hour surgical services for an array of general surgical emergencies. ACS services have been shown to improve outcomes and lead to more timely care. Yet, the etiology and timing of patient mortality has not been described. Hypothesis: We hypothesized that infectious complications occur more frequently in ACS patients that die during their hospitalization. Methods: Retrospective review of a prospectively collected institutional ACS (nontrauma) repository was performed (12/2009–12/2012). Demographic, admission, and discharge variables were collected. ICD-9 codes were used to identify patients with sepsis, shock, GI perforation, and/or peritonitis that was present on admission. Other hospital acquired infections (UTI, BSI, VAP) were also captured. The primary outcome was in-hospital mortality. Survivors were compared to those that died utilizing Fischer’s exact test to determine differences between the groups. Results: 1,329 patients were included in the study. 53% were male with a mean age of 52 – 17 years and an average length of stay of 13 – 20 days. Overall mortality inhospital was 8% (n = 106). Of the patients who died, 32% (n = 34) died within 7 days of admission. The majority of mortalities (56%) occurred after hospital day 14. Patients that died had sepsis, shock, perforation, and/or peritonitis on admission in 73% of cases (Table 1). Conclusions: In the current study, infectious complications present on admission occurred frequently in patients who went on to die. The addition of a subsequent HAI had little effect on mortality. Early identification of infectious complications and emergent source control with anti-microbial therapy holds promise for future efforts to improve outcomes in the ACS patient.

POSTER PRESENTATION ABSTRACTS procedures. We noted occasional patients after sleeve gastrectomy with H. pylori detected in their pathologic specimen after surgery, despite very few patients with preoperative symptoms. We reviewed our experience with our adolescent sleeve gastrectomy cohort to determine the prevalence of H. pylori infection, its predictive factors, and any association with outcomes. Hypothesis: We hypothesized that H. pylori infection would be associated with preoperative symptoms and surgical outcomes. Methods: All patients undergoing sleeve gastrectomy at our hospital were included. We conducted a chart review to determine pre- or post-operative symptoms of GERD or gastritis, as well as any operative complications, including staple-line leak and wound infection. Chart review was also conducted to determine any patient requiring long-term anti-reflux therapy after surgery. Pathology reports were reviewed for H. pylori status and evidence of gastritis. Results: 61 adolescents had laparoscopic sleeve gastrectomy from January 2010 through November 2013. The prevalence of chronic gastritis was 32.8% (20/61), and 15.0% of those patients had H. pylori (3/20). No patient with H. pylori had preoperative symptoms, and only 30.0% of patients with pathology-proven gastritis had symptoms (6/20). No complications occurred, and no patient required long-term antireflux therapy. Conclusions: There is a considerable prevalence of gastritis among adolescents undergoing sleeve gastrectomy, but only a small number of these patients had H. pylori infection. Neither presence of chronic gastritis nor H. pylori infection correlated with pre- or post-operative symptoms. Thus in the absence of predictive symptomology or any adverse outcome in those who are infected, we advocate for continued routine pathologic evaluation without the need for pre-operative determination.

P-50. OUTCOME OF HUMAN DEFICIENCY VIRUS-INFECTED PATIENTS FOLLOWING TRAUMATIC BRAIN INJURY Nasim Ahmed, Yen-Hong Kuo, John Davis, Jersey Shore University Medical Center Background: Recent reports showed no significant difference in mortality following traumatic injuries whether the patient had HIV infection or not. The purpose of this study was to evaluate the mortality of HIV-infected patients who sustained traumatic brain injury. Hypothesis: No difference in outcome following head injury regardless of HIV infection. Methods: Last ten years data of all adult head injury patients who were admitted to our institution was analyzed. Demography and clinical information of HIV infected patients (Group1) were compared with non-HIV-infected patients (Group 2). Outcome was in-hospital mortality and hospital length of stay (LOS). Data was analyzed using Wilcoxon rank sum test, Chi-square test and Fisher exact test. The median total hospital days were estimated using the Kaplan-Meier procedure. The standard errors were estimated using the Greenwood formula. The log-rank test was used to compare the total hospital days between groups. A p-value of 0.05 or less was considered an indication of statistical significance. Results: One thousand eight hundred ten adult patients were admitted to the hospital following traumatic head injury in last ten years. The prevalence of HIVinfected patients in this cohort was 16 out of 1810 (0.88%). There were no significant differences between the groups regarding the distribution of traumatic brain injury [Subdural hematoma (p = 0.35), Epidural hematoma (p = 1.00), Subarachnoid hemorrhage (p = 1.00), Brain contusion (p = 1.00), Diffuse axonal injury (p = 1.00)], female gender [(43.5%) versus (18.8%), p = 0.08] and initial Glasgow Coma Scale (GCS) (p = 0.32). However, there were significant differences between the groups regarding age [48.5 {44.3, 55.3} versus 67.5 {45,82}, p = 0.005], and race, black or African American [31.2% versus 7.3%, p = 0.06]. There were no significant differences in terms of mortality (p = 0.24), LOS (p = 0.87), or development of Acute respiratory distress syndrome (p = 1.00). Conclusions: HIV status did not impact in-hospital mortality and hospital length of stay following traumatic brain injury.



Background: In adult patients undergoing gastric bypass surgery, it is routine practice to perform pre-operative testing for Helicobacter pylori (H. pylori) infection, given the difficulty in accessing the stomach after surgery. Furthermore, there is evidence that infection impairs anastomotic healing and contributes to complications. Long-term, untreated infection increases the risk of gastroesophageal reflux disease (GERD) and gastric cancer. However, there are currently no data for adolescents undergoing bariatric

Tanaz Vaghaiwalla, Shevonne Satahoo, Rolla Zarifa, Marc Dauer, James Davis, Doreann Dearmas, Nicholas Namias, Louis Pizano, Carl Schulman, Jackson Memorial Hospital/ University of Miami Miller School of Medicine Background: Infection is the leading cause of death in burn patients. Historically, this was due to burn wound sepsis but pneumonia has now emerged as the most common

POSTER PRESENTATION ABSTRACTS source. In light of the increasing incidence of multi-drug resistant organisms, the description of rare infections is paramount to continuing the fight against deadly pathogens. Hypothesis: We aim to describe the second case of non-tuberculous mycobacterium (NTM) reported in a burn patient. Difficulties in diagnosis and management will also be highlighted. Methods: A 70 year-old Caucasian female, with a past medical history significant for diabetes mellitus type 2, was transferred to our facility after a house fire. She had sustained a 28% TBSA flame burn to her neck, torso, and all 4 extremities. She underwent excision and grafting on hospital day (HD) 5 with multiple subsequent attempts at excision and grafting due to graft loss. On HD 14, she had a tracheostomy performed. Her hospital course was complicated by ongoing respiratory failure, renal injury and sepsis. Results: Mycobacterium abscessus was found on blood cultures from central venous catheters and arterial line catheters; as well as on tracheal aspirate and bronchial alveolar lavage on HD 86. Imaging then revealed multiple pulmonary nodular densities with patchy ground-glass opacities. After multiple adjustments to the antibiotic regimen, she was placed on tigecycline, clarithromycin, and cefoxitin therapy. She remained on this regimen for almost 4 weeks. Her other infections included Acinetobacter baumannii treated with tobramycin and colistin, as well as Candida albicans for which she received Fluconazole. Ultimately, her clinical state worsened leading to withdrawal of care. Conclusions: NTM sepsis is rare in burn patients with only one other case described in the English language literature. Both cases reflect differences in diagnosis and management. This highlights the need to discuss rare infections in an attempt to broaden the clinician’s awareness of such pathogens, as well as to collaborate to form a consensus about their management.

S-37 P-52. EXTENSIVE BILATERAL GLUTEAL NECROTIZING MYOSITIS AFTER INTERNATIONAL COSMETIC TOURISM Robel Beyene, Jeffrey Shupp, Anthony Shiflett, Chadi Abouassaly, MedStar Washington Hospital Center Background: International cosmetic tourism, the practice of travelling outside of one’s home country to pursue low-cost cosmetic surgery in developing nations, is a growing concern in many developed nations. As the popularity of cosmetic tourism increases, an increasing number of patients are presenting to healthcare providers in the developed world with complications from these surgeries. Among the most concerning complications is the potential for surgical infections. Necrotizing soft tissue infections secondary to cosmetic tourism, which has not previously been described in the literature, represents a rare, but life-threatening complication. Hypothesis: Case report. Methods: Case report and literature review. Results: We report a case of a necrotizing myositis related to abdominoplasty, bilateral thigh liposuction, and gluteal fat injections. Cultures from the necrotic tissue grew Peptostreptococcus spp. and coagulase-negative staphylococci. The virulence factor profiles of these pathogens were investigated. Additionally we review the literature on cosmetic tourism and infectious disease complications of medical tourism, as well as discussing the potential incentives and unforeseen consequences of medical tourism. Conclusions: Cosmetic tourism represents an enticing financial option for patients who cannot afford aesthetic surgery in the developed world. However, the public should be made aware of the potential lack of set standards of care and reporting of complications in surgical tourism.

Abstracts Thirty-fourth Annual Meeting of the Surgical Infection Society, May 1-3, 2014, Baltimore, Maryland .

Abstracts Thirty-fourth Annual Meeting of the Surgical Infection Society, May 1-3, 2014, Baltimore, Maryland . - PDF Download Free
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