2008 Conference on Antimicrobial Resistance

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1 1 Table of Contents Conference Objectives Acknowledgments Conference Co-Chairs Conference Committee Members NFID Staff Invited Presenters Disclosure Index General Information Americans with Disabilities Act Conference Information Desk Conference Language Conference Location Continuing Education Messages No Smoking Policy Poster Session Press Room Program and Abstract Book Registration Fees and Hours Speaker Ready Room and Audiovisual Equipment Verification of Attendance Affiliated Events and Other Meetings Program At-A-Glance Hotel Floor Plan Final Program Meet the Expert Presenters Abstracts Abstracts of Invited Presentations Abstracts of Submitted Oral Presentations Abstracts of Submitted Poster Presentations Author Index

2 Conference on Antimicrobial Resistance Conference Objectives Overall Conference Objectives: At the conclusion of this conference, participants should be able to meet the following objectives: Discuss the science, prevention and control of antimicrobial resistance Define issues and potential solutions to the problem of antimicrobial resistance. Symposium Objectives: Keynote Address Assess the validity and pitfalls of published resistance surveys and determine which infected patients are more or less likely to harbor resistant bacteria Symposium 1: C. Difficile Discuss the current issues related to the pathogenesis of Clostridium difficile infection Review C. difficile infection and colonization in various animal species, and describe zoonotic transmission of C. difficile and the limitations of knowledge regarding public health risks Discuss the distribution of Clostridium difficile in food animals and retail meats and describe the potential for transmission to humans Discuss how rates and severity of Clostridium difficile infections (CDI) are continuing to increase and the role of an epidemic strain in this increase; describe major risk factors for CDI and how modifying these factors may decrease rates; recognize cases of CDI in previously low risk populations Symposium 2: The Growing Clinical Problem of Resistance Among Gram-negative Bacteria Discuss the occurrence of infection with gram-negative bacteria resistant to multiple classes of antimicrobial agents in US hospital patients and the challenges to treatment Discuss the current state of leishmaniasis, multi-drug resistant Acinetobacter infections and Q fever infections associated with the global war on terrorism (GWOT) Review the epidemiology and management strategies for P. aeruginosa in cystic fibrosis Discuss the contribution of the food supply to antimicrobial resistance among enteric bacteria and the challenges that remain in developing mitigation strategies to reduce contamination of foods with antimicrobial resistant foodborne bacteria and protecting public health Symposium 3: Collateral Damage of Antibiotic Use Discuss the collateral damage of antibiotic use due to emergence of new resistance clones; describe the levels of surveillance and response that would be needed for their early detection and possible containment

3 SCIENCE PREVENTION CONTROL 3 Review the risks of antibiotic use in animals with respect to selective pressures for resistance among nontargeted pathogens and bacteria associated with treated animals Describe the limitations of correlations between in vitro testing and clinical outcomes; discuss the unintended consequences of misdiagnosis and other forms of injudicious use on humans, commensal organisms and the environment Symposium 4: Innovative Practices for Prevention of Resistance Describe the basis for clinician overuse and spiraling empiricism of antibiotics in the ICU; discuss the outcomes for those patients who receive empiric antibiotics but are later found not to be infected Discuss methods of limiting antibiotic use in neonates that may lead to prevention of antimicrobial resistance Discuss types of interventions to reduce or improve antimicrobial use that have been implemented in healthcare settings and the association between these interventions and reductions in antimicrobial resistance Discuss how in vitro susceptibility measurements (MPC) can be combined with pharmacokinetic data to determine antimicrobial doses that will restrict the selective amplification of bacterial subpopulations of resistant mutants Symposium 5: Risk versus Benefits Discuss the history of the evaluation of adverse events with antimicrobials; describe the modern evaluation of the potential harms of antimicrobials and how they are compared to the potential benefits in an overall risk benefit assessment Discuss the risk of antibiotic use from an individual as well as a population perspective; describe the evidence of benefit or the lack of evidence of benefit for antibiotic use in the most commonly prescribed outpatient indications Discuss how the use of antimicrobial agents in food animals is associated with antimicrobial resistance among bacteria isolated from humans, and how such resistance results in adverse human health consequences Symposium 6: Resistant Pathogens in the Food We Eat Discuss the principal outlines of the flow of food through the food industry, how microbes contaminate food along the way, and the importance of the links between ecologies on farms and in food factories, and the public health Describe the broad range of interventions that can be used throughout the food industry to prevent food contamination by antibiotic-resistant microbes Symposium 7: The Role of Ecology in the Spread of Resistant Pathogens Discuss the factors underlying the evolution of antibiotic resistance and the relationship between resistance as manifested in the clinic and in the outside environment, as well as the application of this knowledge in new antibiotic development Discuss the global nature of dust storms and how they can impact human health in communities far removed from their point of origin

4 Conference on Antimicrobial Resistance Discuss the routes by which antibiotics and antibiotic resistance genes are entering the water supply and the subsequent human health impacts of the presence of these antibiotics and antibiotic resistance genes Acknowledgments (as of June 1, 2008) This conference is supported, in part, through unrestricted educational grants from: Achaogen, Inc. AdvanDx, Inc. Arpida, Ltd Astellas Pharma US, Inc. AstraZeneca Becton Dickinson Cubist Pharmaceuticals GangaGen, Inc. Generic Pharmaceutical Association Gilead Sciences Merck & Co., Inc. Paratek Pharmaceuticals Pfizer, Inc. PriCara, Unit of Ortho-McNeil, Inc. Quidel Corporation Rib-X Pharmaceuticals Schering-Plough Corporation ViroPharma, Inc. Wyeth Pharmaceuticals

5 SCIENCE PREVENTION CONTROL 5 NFID recognizes the following individuals for their support and contributions in planning this event. Lisa Becton, D.V.M. Conference Organizing and Scientific Program Committees American Veterinary Medical Association Harris, MO John S. Bradley, M.D. Conference Organizing and Scientific Program Committees Children s Hospital, San Diego San Diego, CA Mitchell L. Cohen, M.D., U.S.P.H.S. Conference Organizing and Scientific Program Committees Centers for Disease Control and Prevention Atlanta, GA Stuart H. Cohen, M.D. Conference Organizing and Scientific Program Committees University of California, Davis Medical Center Sacramento, CA Kathryn M. Edwards, M.D. NFID CME Committee Vanderbilt University Medical Center Nashville, TN Barry I. Eisenstein, M.D. Scientific Program Committee Cubist Pharmaceuticals, Inc. Washington, D.C. George M. Eliopoulos, M.D. Scientific Program Committee Beth Israel Deaconess Medical Center Boston, MA Paula J. Fedorka-Cray, Ph.D. Scientific Program Committee U.S. Department of Agriculture Athens, GA Thomas M. File, Jr., M.D. NFID CME Committee Summa Health System Akron, OH Cindy Friedman, M.D. Scientific Program Committee Centers for Disease Control and Prevention Atlanta, GA Dale N. Gerding, M.D. Conference Organizing Committee ACOS/Research and Development Hines VA Hospital Hines, IL Gayle K. Gilmore, R.N., M.A., M.I.S., C.I.C. Conference Organizing and Scientific Program Committees Association for Professionals in Infection Control and Epidemiology Duluth, MN George C. Hill, Ph.D. NFID CME Committee Vanderbilt University School of Medicine Nashville, TN Marguerite Jackson, Ph.D., R.N., F.A.A.N. NFID CME Committee University of California, San Diego School of Medicine San Diego, CA Susan Jennings, M.S. Conference Organizing and Scientific Program Committees Environmental Protection Agency Washington, D.C. Mark Kunkel, M.D. Scientific Program Committee Pfizer Global Pharmaceuticals New York, NY

6 Conference on Antimicrobial Resistance Stuart B. Levy, M.D. Conference Organizing Committee Tufts University School of Medicine Boston, MA Sasha Madison, M.P.H., C.I.C. NFID CME Committee Stanford Hospital and Clinics Stanford, CA June E. Osborn, M.D. NFID CME Committee Falls Church, VA George A. Pankey, M.D. NFID CME and Scientific Program Committees Ochsner Clinic Foundation New Orleans, LA Georges Peter, M.D. NFID CME Committee Warren Alpert Medical School of Brown University Brookline, MA N. Kent Peters, M.A., Ph.D. Conference Organizing and Scientific Program Committees National Institute of Allergy and Infectious Diseases/NIH Bethesda, MD John H. Powers, III, M.D., F.A.C.P., F.I.D.S.A. Conference Organizing Committee Scientific Applications International Corporation Bethesda, MD Susan J. Rehm, M.D. Conference Co-Chair, Conference Organizing, Scientific Program, and NFID CME Committees National Foundation for Infectious Diseases Bethesda, MD John H. Rex, M.D., F.A.C.P. Scientific Program Committee AstraZeneca Pharmaceuticals Cheshire, United Kingdom Mary E. Singer, M.D. Conference Organizing and Scientific Program Committees U.S. Food and Drug Administration Silver Spring, MD Alan D. Tice, M.D. NFID CME Committee John A. Burns School of Medicine University of Hawaii Honolulu, HI Mary E. Torrence, D.V.M, Ph.D. Conference Organizing and Scientific Program Committees U.S. Department of Agriculture Beltsville, MD J. Todd Weber, M.D. Conference Co-Chair, Conference Organizing and Scientific Program Committees Centers for Disease Control and Prevention Stockholm, Sweden NFID Staff Bethesda, MD Sharon Cooper-Kerr Director, Events Planning Lauren Ero Director, Continuing Medical Education Charlotte Lazrus Executive Assistant Len Novick Executive Director Natasha L. Patterson Continuing Medical Education Coordinator

7 SCIENCE PREVENTION CONTROL 7 Invited Presenters* Frederick Angulo, D.V.M., Ph.D. Medical Epidemiologist, Division of Foodborne, Bacterial and Mycolic Diseases Centers for Disease Control and Prevention Atlanta, GA Stuart H. Cohen, M.D. Professor, Division of Infectious and Immunologic Diseases University of California, Davis Medical Center Sacramento, CA Sara E. Cosgrove, M.D., M.S. Assistant Professor of Medicine, Division of Infectious Diseases Director, Antibiotic Management Program Johns Hopkins Medical Institutions Baltimore, MD Michael P. Doyle, Ph.D. Regents Professor and Director, Center for Food Safety University of Georgia Griffin, GA Karl Drlica, Ph.D. Professor, Department of Microbiology & Molecular Genetics Public Health Research Institute New Jersey Medical School Newark, NJ George M. Eliopoulos, M.D. Chief, James L. Tullis Firm Department of Medicine Beth Israel Deaconess Medical Center Boston, MA Dale W. Griffin, Ph.D., M.S.P.H. Environmental/Public Health Microbiologist United States Geological Survey Tallahassee, FL Rosemary Johann-Liang, M.D., F.A.A.P. Chief Medical Officer U.S. Department of Health and Humans Services Bethesda, MD Susan F. Kotarski, Ph.D. Research Fellow, Veterinary Medicine Pfizer, Inc. Kalamazoo, MI David M. Livermore, Ph.D. Director, Antibiotic Resistance Monitoring and Reference Laboratory Health Protection Agency London, United Kingdom L. Clifford McDonald, M.D. Chief, Prevention and Response Branch Centers for Disease Control and Prevention Atlanta, GA Thomas F. O Brien, M.D. Senior Physician in Medicine Medical Director, Microbiology Brigham and Women s Hospital Boston, MA John H. Powers, III, M.D., F.A.C.P., F.I.D.S.A. Senior Medical Scientist Scientific Applications International Corporation Bethesda, MD Lisa Saimin, M.D., M.P.H. Professor of Clinical Pediatrics Hospital Epidemiologist Morgan-Stanley Children s Hospital of New York Presbyterian, Columbia University Medical Center New York, NY Pablo J. Sanchez, M.D. Professor of Pediatrics UT Southwestern Medical Center Dallas, TX Randall Singer, D.V.M., M.P.V.M., Ph.D. Associate Professor, Epidemiology College of Veterinary Medicine University of Minnesota St. Paul, MN J. Glenn Songer, Ph.D., F.A.A.M., D.A.C.V.M. Professor, Department of Veterinary Science and Microbiology The University of Arizona Tucson, AZ

8 Conference on Antimicrobial Resistance Robert V. Tauxe, M.D., M.P.H. Deputy Director, Division of Foodborne, Bacterial and Mycotic Diseases Centers for Disease Control and Prevention Atlanta, GA J. Scott Weese, D.V.M., D.V.Sc. Associate Professor, Department of Pathobiology Ontario Veterinary College University of Guelph Guelph, ON, Canada David G. White, Ph.D. Director, Division of Animal and Food Microbiology Director, National Antimicrobial Resistance Monitoring System (NARMS) U.S. Food and Drug Administration Laurel, MD Glenn Wortmann, M.D. Acting Chief, Infectious Disease Service Program Director, National Capital Consortium Infectious Disease Fellowship Walter Reed Army Medical Center Washington, DC Gerry Wright, Ph.D. Director, M.G. DeGroote Institute for Infectious Disease Research McMaster University Hamilton, ON, Canada Victor L. Yu, M.D. Chief, Infectious Disease Section University of Pittsburgh Pittsburgh, PA *Speakers and presentations subject to change

9 SCIENCE PREVENTION CONTROL 9 DISCLOSURE AUTHOR INDEX As a sponsor accredited by the Accreditation Council for Continuing Medical Education (ACCME) the National Foundation for Infectious Diseases must insure balance, independence, objectivity, and scientific rigor in all its educational activities. All presenters participating in a sponsored activity and all Scientific Program Committee members are expected to disclose any relevant financial interest or other relationship with the manufacturer(s) of any commercial product(s) and/or provider(s) of commercial services discussed in an educational presentation and/or with the commercial supporters of the conference. They also will disclose any intention to discuss offlabel uses of regulated substances or devices. Disclosure information is reviewed in advance to manage and resolve any conflict of interest that may affect the balance and scientific integrity of an educational presentation. The intent of this disclosure is not to prevent a speaker or a Scientific Program Committee member with a financial or other relationship from making a presentation or assisting in conference organization. The intent is to provide attendees with information on which they can make their own judgments. It remains for the audience to determine whether the speaker's interests or relationships have influenced the presentation with regard to exposition or conclusion. The following speakers have no relationships to disclose: Aiello, Allison Angulo, Frederick Barbosa-Cesnik, Cibele Bravo, Lulette Tricia Cho, Yong Kyun Cohen, Stuart H. Doi, Yohei Essack, Sabiha Griffin, Dale W. Hearn, Michael Howie, Rebecca Jacobs, Micah Jimenez, Humberto Johann-Liang, Rosemary Khan, Wasif Krueger, Amy Lazzar, Megan McDonald, L. Clifford Murillo, Jeremias O Brien, Thomas F. Pankey, George A. Raju, Venkedesh Ranallo, Ryan Safdar, Nasia Saiman, Lisa Sarwari, Arif Shaheen, Bashar Singer, Randall Smith, Jacinta Tauxe, Robert V. Weese, J. Scott White, David G. Wortmann, Glenn Yu, Victor L. The remaining speakers have disclosed the following: Presenter Company Relationship* Cosgrove, Sara E. AdvanDx, Inc, Merck B Astellas, Cubist, Ortho McNeil E Doyle, Michael P. GangaGen E Drlica, Karl Bayer Corp., Bristol-Myers-Squibb, Cubist, Mylan B Eliopoulos, George M. Achaogen, Ortho McNeil E Kotarski, Susan F. Pfizer A, C Lamp, Kenneth Cubist A,C Lindfield, Kimberly Cubist A, C Livermore, David M. Ortho McNeil, Pfizer, Schering-Plough A AstraZeneca A, E Merck, Wyeth B, E Achaogen E Marx, Melissa Pfizer B Perez, Federico Wyeth B Powers, John H. Cubist, AstraZeneca, Merck, Wyeth E Rieder, Ronald BioSense Technologies, Inc. C Robberts, Frans BD Diagnostics H

10 Conference on Antimicrobial Resistance Rogelj, Snezna Cellular Bioengineering, Inc. B Sanchez, Pablo J. Astellas B Scholl, Dean AvidBiotics A Songer, J. Glenn Schering-Plough B, E Wright, Gerry Cubist B The following Scientific Program Committee members have no relationships to disclose: Becton, Lisa Cohen, Mitchell L. Cohen, Stuart H. Gilmore, Gayle K. Jennings, Susan Pankey, George A. Peters, N. Kent Singer, Mary E. Torrence, Mary E. Weber, J. Todd The remaining Scientific Program Committee members have disclosed the following: Member Company Relationship* Bradley, John S. Cubist, Pfizer, Schering-Plough, Trins E Johnson & Johnson, Wyeth B, E Eisenstein, Barry I. Cubist A, C Eli Lilly, Middlebrook, Replidyne A Eliopoulos, George M. Cubist, Novexel, Theravance B Johnson & Johnson, Pfizer, Achaeogen E Fedorka-Cray, Paula J. Intervet, Novartis, Bio Meriuex, National Pork Board B Kunkel, Mark Pfizer C Rehm, Susan J. Cubist, Wyeth, Pfizer E Rex, John H. AstraZeneca A, C *Please refer to the following relationship table Label A B C D E F G Relationship I have stocks, stock options, and/or bond holdings in this company I have a research grant, stipend, and/or fellowship from this company I am employed by this company, or it employs a member of my immediate family I or a member of my immediate family own or is a partner in this company I or a member of my immediate family receive consulting fees, honoraria, paid meeting registration fees, paid travel, speaking fees, or other financial compensation from this company I or a member of my immediate family hold a nonrenumerative position of influence with this company such as officer, board member, trustee, or public spokesperson. I or a member of my immediate family hold a patent for and/or receive royalties from this company s product

11 General Information SCIENCE PREVENTION CONTROL 11 Americans with Disabilities Act The Hyatt Regency Bethesda is fully accessible to the public in accordance with the Americans with Disabilities Act guidelines. If you have any special meeting needs or requirements, please contact either Sharon Cooper-Kerr or a member of the hotel staff. Conference Information Desk The Conference Information Desk is located in the Waterford Lobby area outside the Crystal Ballroom. Conference staff will be available at the desk throughout the conference. Conference Language The official language for the conference is English. Conference Location All sessions of the conference will be held at: Hyatt Regency Bethesda One Bethesda Metro Center Wisconsin Avenue at Old Georgetown Road Bethesda, Maryland (301) Meeting rooms for specific sessions are listed in the Final Program (see Table of Contents). Continuing Education Continuing Medical Education The National Foundation for Infectious Diseases (NFID) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide Continuing Medical Education (CME) for physicians. NFID takes responsibility for the content, quality, and scientific integrity of this CME activity. NFID designates this CME activity for a maximum of 16.5 AMA PRA Category 1 credits. Each physician should only claim credit commensurate with the extent of their participation in the activity. Continuing Nursing Education NFID is an approved provider of continuing nursing education by the Maryland Nurses Association, an accredited approver by the American Nurses Credentialing Center s Commission on Accreditation. This educational activity has been approved for 16.5 contact hours. To earn contact hours, each participant must attend the entire conference, sign in daily, and complete the conference evaluation form.

12 Conference on Antimicrobial Resistance Designated Continuing Education Activities Sessions designated with a hours. CME and Nursing Certificates CE symbol have been approved for credit. No other sessions are eligible for credit In order to ensure that you receive the credits to which you are entitled, please complete and return the Continuing Education and Evaluation form to conference staff at the Conference Information Desk, or mail to: NFID, Office of CME 4733 Bethesda Avenue, Suite 750 Bethesda, MD FOR NURSES ONLY: you must also sign in daily and attend the entire conference to receive credit for attendance. Disclosures As a sponsor accredited by the ACCME, NFID must ensure balance, independence, objectivity, and scientific rigor in its educational activities. All faculty and Scientific Planning Committee members are required to disclose any relevant financial interest or other relationship with the manufacturer(s) of any product or service discussed in an educational presentation and with the commercial supporters of this activity. Disclosure information is reviewed in advance to manage and resolve any conflict of interest that may affect the balance and scientific integrity of an educational presentation. A summary of the disclosure information is printed separately in this book under the heading Disclosure Index (see Table of Contents). Messages All sleeping rooms in the Hyatt Regency Bethesda are equipped with a voice mail system. This system is accessible via the hotel operator using the house phone. In case of emergencies requiring immediate attention, your party should call the general hotel number listed below and instruct the switchboard to deliver a message to Sharon Cooper-Kerr or Lauren Ero at the Antimicrobial Resistance Conference Information Desk outside of the Crystal Ballroom. The general hotel number is No Smoking Policy The Hyatt Regency Bethesda is a non-smoking facility. No smoking is allowed in any of the sleeping rooms, session rooms, coffee break area, or in the foyer adjoining the session rooms. Poster Session The Poster Session and Reception will be held on Monday, June 23, 5:15 p.m. in the Waterford/Lalique Room. Presenters will be at their posters to answer questions and discuss their research. The Posters will continue to be on display throughout the conference. Press Room NFID will have a Press Room located in the Cartier Room. Press should sign in at the Conference Information Desk during registration hours.

13 SCIENCE PREVENTION CONTROL 13 Program and Abstract Book and Handouts Each registered participant will receive one complimentary copy of the Final Program and Abstract Book as part of his/her registration fee. Additional copies, if available, may be purchased for $25. Orders for additional copies can be taken at the Conference Information Desk and after the conference, by to or by calling (301) , ext 19. PLEASE NOTE THAT WE ARE UNABLE TO REPLACE LOST OR STOLEN PROGRAMS. Handouts of the symposia presentations will also be available as provided by the speaker. Due to the advance printing of the handouts, presentations are subject to change. The conference is unable to provide revised copies of handouts. Registration Fees and Hours Onsite registration fee: US $ (Non Member) and $450 (NFID Supporting Member) The registration fee includes a program and abstract book, continental breakfast on each day of the conference, all scheduled coffee breaks, and the reception on Monday. Accommodations and additional meals are not included. Individuals interested in registering onsite may do so at the Conference Information Desk between the following times: Sunday, June :00 p.m. - 8:00 p.m. Monday, June :00 a.m. - 5:00 p.m. Tuesday, June :00 a.m. - 5:00 p.m. Wednesday, June :00 a.m. - 8:00 a.m. Speaker Ready Room and Audiovisual Equipment A room has been set aside for speakers to preview their slides. All speakers should check in at the Conference Information Desk to be directed to the room, which will be open during the registration hours and equipped with a laptop for preview of your PowerPoint presentation. Standard session room setup includes a PC, LCD projector, laser pointer, podium microphone, lavaliere microphone, and aisle microphones. Verification of Attendance Attendees may obtain a letter of attendance verification from the staff at the Conference Information Desk during registration hours.

14 Conference on Antimicrobial Resistance Affiliated Events and Other Meetings Tuesday, June 24, 2008 Conference on Antimicrobial Resistance Organizing and Scientific Program Committee Meeting (Closed meeting) 5:00pm 8:00pm., Diplomat/Ambassador Rooms Wednesday, June 25, 2008 Interagency Task Force on Antimicrobial Resistance Sponsored by the Centers for Disease Control and Prevention, U.S. Food and Drug Administration, and the National Institutes of Health 12:00pm-1:00pm., Haverford/Baccarat Ballroom The Centers for Disease Control and Prevention (CDC), Food and Drug Administration (FDA), and National Institutes of Health (NIH), co-chairs of the Interagency Task Force on Antimicrobial Resistance, will hold an open meeting to present the annual report of progress by Federal agencies in accomplishing activities outlined in A Public Health Action Plan to Combat Antimicrobial Resistance (Part I: Domestic Issues) and solicit comments from the public regarding the annual report. The Action Plan serves as a blueprint for activities of Federal agencies to address antimicrobial resistance. The agenda will consist of welcome and introductory comments, an executive summary, and brief reports in four focus areas: Surveillance, Prevention and Control, Research, and Product Development. The meeting will then be open for general discussion. The Action Plan and Annual Report are available at The public meeting is sponsored by the CDC, FDA, and NIH in collaboration with seven other Federal agencies and departments that were involved in developing and writing the report.

15 SCIENCE PREVENTION CONTROL 15 PROGRAM-AT-A-GLANCE FINAL SUNDAY, JUNE 22 MONDAY, JUNE 23 TUESDAY, JUNE 24 WEDNESDAY, JUNE 25 7:00am Registration Registration Meet the Experts Breakfast Session Meet the Experts Breakfast Session 7:30am Continental Breakfast Continental Breakfast 8:00am Registration Symposium 4: Symposium 7: Poster Set-up Innovative Practices for Prevention The Role of Ecology in the Spread of Resistance of Resistant Pathogens of Resistance 8:30am 8:50am 9:00am Continental Breakfast Welcome and Introductions Keynote Address 10:00am Coffee Break Coffee Break Coffee Break 10:30am Symposium 1: Symposium 5: Submitted Presentations C. Difficile Risk versus Benefits of Antimicrobial Resistance 12:00pm Adjournment/Conference Evaluation 12:30pm Lunch (on your own) Lunch (on your own) 1:30pm Symposium 2: Submitted Presentations The Growing Clinical Problem of Resistance Among Gram-negative Bacteria 2:30pm Coffee Break 2:45pm Symposium 6: Resistant Pathogens in the Food We Eat 3:30pm Coffee Break 3:45pm Symposium 3: Collateral Damage of Antibiotic Use 4:45pm Adjournment 5:15pm Poster Session and Reception 6:00pm Registration

16 Conference on Antimicrobial Resistance HOTEL FINAL FLOOR PROGRAM PLAN

17 SCIENCE PREVENTION CONTROL 17 Sunday, June 22, 2008 FINAL PROGRAM 6:00 p.m. 8:00 p.m. Registration Crystal Ballroom Foyer Monday, June 23, :00 a.m. 5:00 p.m. Registration Crystal Ballroom Foyer 8:00 a.m. Poster Set-Up Waterford/Lalique Ballroom 8:30 a.m. Continental Breakfast Crystal Ballroom Foyer 8:50 a.m. Welcome and Introductions Haverford/Baccarat Ballroom Susan J. Rehm, M.D. National Foundation for Infectious Diseases Bethesda, MD Keynote Address CE Haverford/Baccarat Ballroom Moderator: Susan J. Rehm, M.D. National Foundation for Infectious Diseases Bethesda, MD 9:00 a.m. 1. Antibiotic Resistance: Location, Location, Location! David M. Livermore, Ph.D. Health Protection Agency London, United Kingdom 9:45 a.m. Questions and Answers 10:00 a.m. Coffee Break Crystal Ballroom Foyer Symposium 1. C. Difficile CE Haverford/Baccarat Ballroom Moderator: Mary E. Torrence, D.V.M., Ph.D. U.S. Department of Agriculture Beltsville, M.D. 10:30 a.m. 2. Pathogenesis of Clostridium difficile Infection Stuart H. Cohen, M.D. University of California, Davis Medical Center Sacramento, CA 10:55 a.m. Questions and Answers

18 Conference on Antimicrobial Resistance FINAL PROGRAM Monday, June 23, 2008 (continued) 11:00 a.m. 3. Clostridium difficile in Animals: Public Health and Veterinary Consequences J. Scott Weese, D.V.M., D.V.Sc. Ontario Veterinary College University of Guelph Guelph, ON, Canada 11:25 a.m. Questions and Answers 11:30 p.m. 4. Human and Food Animal Genotypes of Clostridium difficile in the Food Supply J. Glenn Songer, Ph.D., F.A.A.M., D.A.C.V.M. The University of Arizona Tucson, AZ 11:55 a.m. Questions and Answers 12:00 p.m. 5. The Epidemiology of Clostridium difficile Infection in Humans L. Clifford McDonald, M.D. Centers for Disease Control and Prevention Atlanta, GA 12:25 p.m. Questions and Answers 12:30 p.m. Lunch (on your own) Symposium 2. The Growing Clinical Problem of Resistance Among Gram-Negative Bacteria Moderator: John S. Bradley, M.D. Children s Hospital, San Diego San Diego, CA CE Haverford/Baccarat Ballroom 1:30 p.m. 6. The Clinical Challenge of Multi-Resistant Gram-negative Pathogens in U.S. Hospitals George M. Eliopoulos, M.D. Beth Israel Deaconess Medical Center Boston, MA 1:55 p.m. 7. The Clinical Challenge of MDR Acinetobacter in Iraq Glenn Wortmann, M.D. Walter Reed Army Medical Center Washington, DC 2:20 p.m. 8. The Clinical Challenge of MDR Pseudomonas in Cystic Fibrosis Lisa Saimin, M.D., M.P.H. Columbia University Medical Center New York, NY

19 SCIENCE PREVENTION CONTROL 19 FINAL PROGRAM 2:45 p.m. 9. The Challenge of MDR Foodborne Gram Negative Pathogens David G. White, Ph.D. U.S. Food and Drug Administration Laurel, MD 3:10 p.m. Questions and Answers 3:30 p.m. Coffee Break Crystal Ballroom Foyer Symposium 3. Collateral Damage of Antibiotic Use Moderator: Lisa Becton, D.V.M. National Pork Board Des Moines, IA CE Haverford/Baccarat Ballroom 3:45 p.m. 10. Early Detection and Containment of New Antimicrobial Resistance Clones Thomas F. O Brien, M.D. Brigham and Women s Hospital Boston, MA 4:10 p.m. Questions and Answers 4:15 p.m. 11. Collateral Damage of Antiobiotic Use in Animals: Impact on Secondary Pathogens and Commensals Susan F. Kotarski, Ph.D. Pfizer, Inc. Kalamazoo, MI 4:40 p.m. Questions and Answers 4:45 p.m. 12. Evaluating the Human Public Health Impact of In Vitro Resistance John H. Powers, III, M.D., F.A.C.P., F.I.D.S.A. Scientific Applications International Corporation Bethesda, MD 5:10 p.m. Questions and Answers 5:15 p.m. Poster Session and Reception Waterford/Lalique Ballroom (Posters will remain on display throughout the conference) P1 Use of Cefepime versus Gentamicin as Empiric Therapy in Catheter-related Bloodstream Infections in Hemodialysis Patients H. R. Jimenez 1, J. Slim 1, R. Khan 2, K. Patel 2 1Infectious Disease, St. Michael s Medical Center, Newark, NJ, 2 Ernest Mario School of Pharmacy, Rutgers University

20 Conference on Antimicrobial Resistance FINAL PROGRAM Monday, June 23, 2008 (continued) P2 P3 P4 P5 P6 P7 P8 P9 Staphylococcus aureus from Public Hospitals in Kwa-Zulu Natal: Infection Detection and Strain Typing Z. Essa, S. Y. Essack Pharmacy, University of Kwazulu-Natal, Durban, South Africa Treatment Guidelines and Nosocomial Infections: The KwaZulu-Natal Experience S. Y. Essack Pharmacy, University of Kwazulu-Natal, Durban, South Africa Azithromycin Minimum Inhibitory Concentration (MICs) for Shigella sonnei Isolated from Humans in the United States R. L. Howie 1, J. Folster 1, A. Bowen 2, E. Barzilay 2, K. Joyce 1, J. Whichard 2 1Atlanta Research and Education Foundation, Atlanta, GA, 2 Centers for Disease Control and Prevention, Atlanta, GA Cost of Methicillin-resistant Staphylococcus aureus (MRSA) Infection in the Neonatal Intensive Care Unit J. L. Murillo 1, Y. Xavier 2, M. Cohen 3 1Clinical Services, Saint Barnabas Health Care System, West Orange, NJ, 2 Decision Support, Saint Barnabas Health Care System, West Orange, NJ, 3 Neonatal Medicine, Children s Hospital of New Jersey, Newark, NJ New Derivatives of para-aminosalicylic Acid and Their Activities against Drug- Resistant Mycobacterium tuberculosis M. Hearn 1, M. Chen 1, M. Cynamon 2, C. Schlemme 1, R. Wang ondu 1 1Department of Chemistry, Wellesley College, Wellesley, MA, 2 Veterans Affairs Medical Center, Syracuse, NY Comparison of Three Methods used for the Identification of Campylobacter spp., NARMS Human Isolates, 2005 J. Smith 1, J. Pruckler 2, A. Stuart 1, K. Joyce 1, F. Medalla 2, E. Barzilay 2, J. Whichard 2, C. 1Atlanta Research and Education Foundation (AREF), Decatur, GA, 2 Centers for Disease Control and Prevention, Atlanta, GA The Detection of Synergy Between Meropenem (MER) and Polymyxin B (PB) Against MER-Resistant Acinetobacter baumannii using Etest and Time-Kill Assay (TKA) G. A. Pankey, D. S. Ashcraft Infectious Disease Research, Ochsner Clinic Foundation, New Orleans, LA Impact of Methicillin Resistance on Patient Response to Daptomycin for Treatment of Skin and Skin Structure Infections K. Lamp Cubist Pharmaceuticals, Lexington, MA

21 SCIENCE PREVENTION CONTROL 21 FINAL PROGRAM P10 Resistance to Third-Generation Cephalosporins in E. coli Isolates from Outpatients, A. L. Krueger Enteric Diseases Epidemiology Branch, Centers for Disease Control and Prevention, Atlanta, GA P11 Surveillance for Mupirocin Resistance among MRSA Clinical Isolates V. Raju, K. Mongkolrattanothai, P. Mankin, B. Gray Pediatrics, University of Illinois College of Medicine at Peoria and The Children s Hospital of Illinois at OSF St. Francis Medical Center, Peoria, IL P12 Prevalence of Antibiotic Resistance of Escherichia coli Blood Isolates Y. Cho 1, Y. Park 1, J. Kim 1, L. Zhang 2, B. Foxman 3 1Department of Internal Medicine, Gil Medical Center, Incheon, Republic of Korea, 2Department of Epidemiology University of Michigan School of Public Health, Center for Molecular and Clinical Epidemiology of Infectious Diseases, Ann Arbor, MI, 3 Department of Epidemiology, Center for Molecular and Clinical Epidemiology of Infectious Diseases, Ann Arbor, MI P13 Rapid Antimicrobial Susceptibility Testing of Human Pathogens R. Rieder, B. Zavizion BioSense Technologies, Inc., Woburn, MA P14 Engineering the Bactericidal Spectra of R-type Pyocins for Use as Antimicrobial Agents D. Scholl, S. Williams, D. Gebhart, D. Martin AvidBiotics, South San Francisco, CA P15 E. coli Resistance to Targeted R-type Pyocins Forces Loss of Virulence Factor D. Scholl, D. Martin AvidBiotics, South San Francisco, CA P16 Differences in Outpatient Antibiotic Treatment Perception Among Health Care Providers K. C. Lindfield, L. A. Scoppettuolo, W. J. Martone, D. E. Katz Clinical Development/Medical Affairs, Cubist Pharmaceuticals, Lexington, MA P17 Antibacterial Properties of a Novel Polymer Hydrogel-Decon Gel H. Tang 1, S. Shors 1, S. Rogelj 1, G. Edgington 2, M. O Neill 2 1Biology Department, New Mexico Institute of Mining and Technology, Socorro, NM, 2Cellular Bioengineering, Inc., Honolulu, HI P18 Impact of an Antimicrobial Stewardship Program on Antimicrobial Use and Resistance in Intensive Care Units (ICU) A. R. Sarwari 1, K. O. Petros 2, R. B. Sager 2, A. Wilson 3, H. V. Dedhia 4, C. J. Mullett 5, J. Thomas 6, P. Miller-Canfield 6, D. Slain 7, K. Moffett 5, H. C. Palmer, Jr. 8 1Infectious Diseases, West Virginia University, Morgantown, WV, 2 Pharmacy, West Virginia University Hospitals, Morgantown, WV, 3 Surgery, West Virginia University, Morgantown, WV, 4 Pulmonary Critical Care Medicine, West Virginia University, Morgantown, WV, 5 Pediatrics, West Virginia University, Morgantown, WV, 6 Clinical Microbiology, West Virginia University, Morgantown, WV, 7 School of Pharmacy, West Virginia University, Morgantown, WV, 8 Internal Medicine, West Virginia University, Morgantown, WV

22 Conference on Antimicrobial Resistance FINAL PROGRAM Monday, June 23, 2008 (continued) P19 The Phenotypic Expression of Multidrug Resistant Escherichia coli Recovered from Spontaneous Diseased Dogs and Cats B. W. Shaheen, D. M. Boothe, T. Smaha Anatomy, Physiology and Pharmacology, Auburn University, Auburn, AL P20 Antimicrobial Resistance and Class 1 Integrons in Resistant Escherichia coli Recovered from Spontaneous Diseased Dogs and Cats B. W. Shaheen 1, D. M. Boothe 1, O. A. Oyarzabal 2, T. Smaha 1 1Anatomy, Physiology and Pharmacology, Auburn University, Auburn, AL, 2 Poultry Science, Auburn University, Auburn, AL P21 Antibiotic Resistance among Uropathogenic E.coli (UPEC) in a College Population in Michigan C. Barbosa-Cesnik, M. Buxton, J. Debusscher, M. LaFontaine, L. Zhang, B. Foxman University of Michigan, Ann Arbor, MI P22 Pyrosequencing for Rapid Detection of Fluoroquinolone Resistance among Mycobacterium Tuberculosis Isolates from the Philippines L. C. Bravo 1, M. Tuohy 2, C. Ang 3, N. Shrestha 1 1Infectious Disease, Cleveland Clinic Foundation, Cleveland, OH, 2 Pathology and Lab Medicine, Cleveland Clinic Foundation, Cleveland, OH, 3 Philippine General Hospital, University of the Philippines Manila, Philippines Tuesday, June 24, :00 a.m. - Registration Crystal Ballroom Foyer 5:00 p.m. 7:00 a.m.- Meet the Experts Breakfast Session Waterford/Lalique Ballroom 7:45 a.m. Implementing an Antimicrobial Stewardship Program Sara E. Cosgrove, M.D., M.S. John Hopkins Medical Institutions Baltimore, MD MRSA in Adults George M. Eliopoulos, M.D. Beth Israel Deaconess Medical Center Boston, MA MDR-GNB: Lessons from Cystic Fibrosis Lisa Saiman, M.D., M.P.H. Morgan-Stanley Children s Hospital of New York Presbyterian, Columbia University Medical Center New York, NY

23 SCIENCE PREVENTION CONTROL 23 FINAL PROGRAM 7:30 a.m. Continental Breakfast Crystal Ballroom Foyer Symposium 4: Innovative CE Practices for Prevention of Resistance Haverford/Baccarat Ballroom Moderator: Barry I. Eisenstein, M.D. Cubist Pharmaceuticals, Inc. Washington, DC 8:00 a.m. 13. Antibiotic Resistance Starts in the ICU: An Innovative Approach for Limiting Empiric Therapy Victor L. Yu, M.D. University of Pittsburgh Pittsburgh, PA 8:25 a.m. Questions and Answers 8:30 a.m. 14. Prevention of Resistance by Limiting Antibiotic Exposure: Innovative Approaches in the Neonate Pablo J. Sanchez, M.D. UT Southwestern Medical Center Dallas, TX 8:55 a.m. Questions and Answers 9:00 a.m. 15. Prevention of Resistance by Optimizing Antibiotic Usage: Antimicrobial Stewardship Sara E. Cosgrove, M.D., M.S. Johns Hopkins Medical Institutions Baltimore, MD 9:25 a.m. Questions and Answers 9:30 a.m. 16. Prevention of Resistance by Optimizing Antibiotic Exposure: The Mutant Prevention Concentration Karl Drlica, Ph.D. Public Health Research Institute New Jersey Medical School Newark, NJ 9:55 a.m. Questions and Answers 10:00 a.m. Coffee Break Waterford/Lalique Ballroom

24 Conference on Antimicrobial Resistance FINAL PROGRAM Tuesday, June 24, 2008 (continued) Symposium 5. Risk versus Benefits of Antimicrobial Resistance CE Haverford/Baccarat Ballroom Moderator: Mary E. Singer, M.D. U.S. Food and Drug Administration Silver Spring, MD 10:30 a.m. 17. Antibiotic Resistance as an Adverse Event and Risk Perception John H. Powers, III, M.D., F.A.C.P., F.I.D.S.A. Scientific Applications International Corporation Bethesda, MD 10:55 a.m. Questions and Answers 11:00 a.m. 18. Risk versus Benefit of Antibiotics Rosemary Johann-Liang, M.D., F.A.A.P. U.S. Department of Health and Humans Services Bethesda, MD 11:25 a.m. Questions and Answers 11:30 a.m. 19. The Human Health Consequences of Antibiotic Use in Animals Frederick Angulo, D.V.M., Ph.D. Centers for Disease Control and Prevention Atlanta, GA 11:55 a.m. Questions and Answers 12:00 p.m. Roundtable Discussion 12:30 p.m. Lunch (on your own) Submitted Presentations 1: CE Resistant Gram-negative Bacteria: Mechanisms, Susceptibility Testing and Clinical Significance Haverford/Baccarat Ballroom Moderator: Gayle K. Gilmore, R.N., M.A., M.I.S., C.I.C. Association for Professionals in Infection Control and Epidemiology Duluth, MN 1:30 p.m. S1 ESBL Obfuscation by Concomitant Expression of Plasmid-mediated AmpC β-lactamases in Escherichia Coli F. J. L. Robberts, P. C. Kohner, R. Patel Clinical Microbiology, Mayo Clinic, Rochester, MN

25 SCIENCE PREVENTION CONTROL 25 FINAL PROGRAM 1:45 p.m. S2 Establishing in vitro Susceptibility Standards for Ciprofloxacin against V. cholerae O1 W. A. Khan 1, S. Ahmed 1, M. A. Salam 1, M. L. Bennish 2,3 1Clinical Sciences Division, International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh, 2 Mpilonhle, Mtubatuba, South Africa, 3 Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 2:00 p.m. S3 Genetic Basis of Multidrug Resistance in Acinetobacter baumannii Clinical Strains Isolated at a Tertiary Medical Center in Pennsylvania J. M. Adams-Haduch, H. E. Sidjabat, A. W. Pasculle, B. A. Potoski, D. L. Paterson, Y. Doi Division of Infectious Diseases, University of Pittsburgh Medical Center, Pittsburgh, PA 2:15 p.m. S4 Multi-Drug Resistant Acinetobacter sp. Isolates from the Walter Reed Army Medical Center: Correlation of Antibiotic Resistance with Adverse Clinical Outcomes F. Perez 1, A. M. Hujer 2, K. M. Hujer 2, E. A. Hulten 3, D. J. Ecker 4, D. Aron 2, K. Thweatt 2, C. Donskey 2, J. Adams 5, D. L. Paterson 5, R. A. Bonomo 6 1Division of Infectious Diseases and HIV Medicine, University Hospitals Case Medical Center, Cleveland, OH, 2 Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, OH, 3 Department of Internal Medicine, Walter Reed Army Medical Center, Bethesda, MD, 4 Ibis Biosciences Inc., Carlsbad, CA, 5 Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, 6Section of Infectious Diseases, Louis Stokes Cleveland VAMC, Cleveland, OH 2:30 p.m. Coffee Break Waterford/Lalique Ballroom Symposium 6. Resistant CE Pathogens in the Food We Eat Haverford/Baccarat Ballroom Moderator: Mitchell L. Cohen, M.D., U.S.P.H.S. Centers for Disease Control & Prevention Atlanta, GA 2:45 p.m. 20. Food Safety and Infectious Diseases: A Microbe s View of the Food Industry Robert V. Tauxe, M.D., M.P.H. Centers for Disease Control and Prevention Atlanta, GA 3:10 p.m. Questions and Answers 3:15 p.m. 21. Interventions to Prevent Contamination of Foods We Eat Michael P. Doyle, Ph.D. Center for Food Safety University of Georgia Griffin, GA 3:40 p.m. Questions and Answers

26 Conference on Antimicrobial Resistance FINAL PROGRAM Tuesday, June 24, 2008 (continued) 3:45 p.m. Panel Discussion 4:45 p.m. Adjournment Wednesday, June 25, :00 a.m. Registration Crystal Ballroom Foyer 8:00 a.m. 7:00 a.m. Meet the Experts Breakfast Session Waterford/Lalique Ballroom 7:45 a.m. MRSA in Children John S. Bradley, M.D. Children s Hospital, San Diego San Diego, CA Epidemiology of Antimicrobial Resistance Thomas F. O Brien, M.D. Brigham and Women s Hosptial Boston, MA How Can We Overcome Antibiotic Resistance? Gerry Wright, B.Sc., Ph.D. M.G. DeGroote Institute for Infectious Disease Research McMaster University Hamilton, ON, Canada 7:30 a.m. Continental Breakfast Crystal Ballroom Foyer

27 SCIENCE PREVENTION CONTROL 27 FINAL PROGRAM Symposium 7. The Role of Ecology in the Spread of Resistant Pathogens Moderator: George A. Pankey, M.D. Ochsner Clinic Foundation New Orleans, LA 8:00 a.m. 22. The Antibiotic Resistome: Scope and Impact Gerry Wright, Ph.D. McMaster University Hamilton, ON, Canada 8:30 a.m. Questions and Answers CE Haverford/Baccarat Ballroom 8:40 a.m. 23. Intercontinental Transport of Microorganisms in Clouds of Desert Dust: A Global Human Health Perspective Dale W. Griffin, Ph.D., M.S.P.H. United States Geological Survey Tallahassee, FL 9:10 a.m. Questions and Answers 9:20 a.m. 24. Potential Impacts of Antibiotics and Antibiotic Resistance on the Water Supply Randall Singer, D.V.M., M.P.V.M., Ph.D. University of Minnesota St. Paul, MN 9:50 a.m. Questions and Answers 10:00 a.m. Coffee Break Waterford/Lalique Ballroom Submitted Presentations 2: CE Epidemiology of Resistance and Antibiotic Use Haverford/Baccarat Ballroom Moderator: J. Todd Weber, M.D. Centers for Disease Control and Prevention Stockholm, Sweden 10:30 a.m. S5 Use of Household Cleaning Products Containing Benzalkonium Chloride and Antibiotic Resistance in the Community A. E. Aiello 1, R. Carson 2, S. B. Levy 3, B. Marshall 3, E. L. Larson 4 1Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, 2Epidemiology, Columbia University, New York, NY, 3 Medicine, Tufts University Medical School, Boston, MA, 4 Epidemiology and Nursing, Columbia University, New York, NY

28 Conference on Antimicrobial Resistance FINAL PROGRAM Wednesday, June 25, 2008 (continued) 10:45 a.m. S6 Mupirocin Resistance Among Staphylococcus aureus Isolates After Implementation of a Decolonization Program M. A. Jacobs 1, N. K. Shrestha 1, T. G. Fraser 1, D. A. Wilson 2, G. S. Hall 2 1Infectious Disease, Cleveland Clinic Foundation, Cleveland, OH, 2 Clinical Pathology - Microbiology, Cleveland Clinic, Cleveland, OH 11:00 a.m. S7 Results of a Case-control Investigation of Risk Factors for CA-MRSA in New York City, M. A. Marx 1, H. Cook 1, Z. Rehana 1, D. Krieger 1, A. Yeung 1, Y. Lue 2, A. John 2, D. Duquaine 1, D. Kapell 1, D. Ip 3, J. Mediavilla 4, J. Kornblum 3, B. Kreiswirth 4, D. Weiss 1 1Communicable Diseases, NYC Department of Health and Mental Hygiene, New York, NY, 2 Quest Diagnostics, Teterboro, NJ, 3 Public Health Laboratory, NYC Department of Health and Mental Hygiene, New York, NY, 4 The Public Health Research Institute of New Jersey Medical School/UMDNJ, Newark, NJ 11:15 a.m. S8 Trends in QRNG and Antibiotic Resistance for Gonorrhea in Los Angeles County: M. Lazzar Los Angeles County Public Health Department, Los Angeles, CA 11:30 a.m. S9 Antibiotic Prescribing by Emergency Room Physicians N. Safdar 1, B. Fox 1, J. E. Svenson 1, R. Wigton 2 1University of Wisconsin, Madison, WI, 2 University of Nebraska, Omaha, NE 11:45 a.m. S10 Efforts to Influence Antimicrobial Use and Resistance at a Tertiary Care Institution Using Collaborative Multifaceted Interventions A. R. Sarwari 1, K. O. Petros 2, R. B. Sager 2, C. J. Mullett 3, J. Thomas 4, P. Miller-Canfield 4, H. V. Dedhia 5, A. Wilson 6, D. Slain 7, K. Moffett 3, H. C. Palmer, Jr 8 1Infectious Diseases, West Virginia University, Morgantown, WV, 2 Pharmacy, West Virginia University Hospitals, Morgantown, WV, 3 Pediatrics, West Virginia University, Morgantown, WV, 4 Clinical Microbiology, West Virginia University, Morgantown, WV, 5Pulmonary Critical Care Medicine, West Virginia University, Morgantown, WV, 6Surgery, West Virginia University, Morgantown, WV, 7 School of Pharmacy, West Virginia University, Morgantown, WV, 8 Internal Medicine, West Virginia University, Morgantown, WV 12:00 p.m. Adjournment/Participant Evaluation 12:00 p.m. Meeting of the Interagency Task Force on Antimicrobial Resistance Sponsored by the Centers for Disease Control and Prevention, U.S. Food and Drug Administration, and the National Institutes of Health

29 SCIENCE PREVENTION CONTROL 29 MEET THE FINAL EXPERT PROGRAM PRESENTERS MEET THE EXPERT PRESENTERS

30 Conference on Antimicrobial Resistance MEET THE FINAL EXPERT PROGRAM PRESENTERS Sara E. Cosgrove, M.D., M.S. Tuesday, June 24, :00 am 7:45 am Dr. Cosgrove is an Assistant Professor of Medicine in the Division of Infectious Diseases at Johns Hopkins University School of Medicine. She serves as the Director of the Antibiotic Management Program and as an Associate Hospital Epidemiologist at The Johns Hopkins Hospital in Baltimore, Maryland. Dr. Cosgrove received her undergraduate degree from Columbia College in New York, her medical degree from Baylor College of Medicine in Houston, Texas, and her Master of Science degree in epidemiology from Harvard School of Public Health in Boston, Massachusetts. She completed her postgraduate training in internal medicine at Johns Hopkins Hospital, and underwent subsequent training in infectious disease at Beth Israel Deaconess Medical Center in Boston. She is board certified in both internal medicine and infectious diseases. Dr. Cosgrove s research interests include the epidemiology and outcomes of antimicrobial resistance, the development of tools and programs to promote the rational use of antimicrobials, and the prevention of hospital-acquired infections, particularly device-related infections. She has published several articles in peer-reviewed journals on these topics. Dr. Cosgrove is a member of the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. She will be serving on the SHEA Board of Directors starting in 2008 as an Academic Councilor. George M. Eliopoulos, M.D. Tuesday, June 24, :00 am 7:45 am Dr. Eliopoulos is an infectious diseases physician at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, and Professor of Medicine at Harvard Medical School. Dr. Eliopoulos is Editor in Chief of Antimicrobial Agents and Chemotherapy and special section editor for Clinical Infectious Diseases. He serves on the Antimicrobial Susceptibility Testing subcommittee of the Clinical and Laboratory Standards Institute. He is a fellow of the American College of Physicians and of the Infectious Diseases Society of America. Dr. Eliopoulos received his bachelor s degree from Harvard College and his medical degree from Harvard Medical School. He completed his residency in internal medicine at Columbia Presbyterian Medical Center in New York, and his fellowship in infectious diseases at the Massachusetts General Hospital and Beth Israel Deaconess Medical Center in Boston. Dr. Eliopoulos has co-authored more than 130 research papers. His primary interest is the action of antimicrobial agents and mechanisms of resistance of clinically important bacteria to these agents. Lisa Saiman, M.D., M.P.H. Tuesday, June 24, :00 am 7:45 am Dr. Saiman is Professor of Clinical Pediatrics in the Department of Pediatrics at Columbia University, and an attending physician and Hospital Epidemiologist at Morgan Stanley Children s Hospital of New York Presbyterian. Dr. Saiman s primary research and clinical interests are in cystic fibrosis (CF), healthcareacquired infections and hospital epidemiology and multidrug-resistant organisms. She is the director of the CF Referral Center for Synergy Studies in Multidrug-resistant Organisms isolated from Patients with CF. She also serves as an advisor to the CF Foundation on infectious diseases, clinical microbiology, and infection control issues, and is a member of the CF Foundation s Data Safety and Monitoring Board, the Clinical Research Committee, and annual meeting planning committee. She has served as a division chair for the American Society of Microbiology, is active in the local chapter of the American Academy of Pediatrics, and serves on the Editorial Boards of the Pediatric Infectious Diseases Journal, Infection Control and Hospital Epidemiology, and the American Journal of Infection Control. Dr. Saiman s other research interests include infection control in pediatric healthcare settings, particularly the neonatal ICU. She has studied risk factors and the molecular epidemiology of hospital-acquired infections. Dr. Saiman has co-authored more than 150 research papers, review articles and chapters.

31 SCIENCE PREVENTION CONTROL 31 MEET THE FINAL EXPERT PROGRAM PRESENTERS John S. Bradley, M.D. Wednesday, June 25, :00 am 7:45 am Dr. Bradley is the Director of the Division of Infectious Diseases at Children s Hospital and Health Center, San Diego, California. He holds a teaching faculty appointment with the University of California, San Diego. He is a member of the American Academy of Pediatrics Committee in Infectious Diseases, and sits on the Antimicrobial Drug Availability Task Force of the Infectious Diseases Society of America (IDSA). He has served on the FDA s Anti-Infective Drug Advisory Committee for the past four years. Dr. Bradley has participated in the NIH Collborative Antiviral Study Group for the past 25 years, and has been involved in anti-infective drug development through the National Institute of Child Health and Human Development (NICHD) Pediatric Pharmacology Research Unit Network for the past 10 years. He is a member of the SubBoard for Pediatric Infectious Diseases of the American Board of Pediatrics. He is involved in creating IDSA National Guidelines for Outpatient Parenteral Therapy of Infectious Diseases, Treatment and Prophylaxis of Influenza Infections, and Treatment of Intra-Abdominal Infections. Dr. Bradley received his pediatric infectious diseases training at Stanford University and has focused his clinical research on therapeutic agents for infectious diseases, with phase I through IV investigations of antibacterial, antiviral and antifungal agents. He has authored or coauthored more than 120 publications. His focus is the treatment of serious infections caused by antibiotic-resistant pathogens. Thomas F. O Brien, M.D. Wednesday, June 25, :00 am 7:45 am Dr. O Brien is Senior Physician in the Division of Infectious Diseases of the Department of Medicine and Medical Director of the Microbiology Laboratory, Brigham and Women s Hospital, and Associate Professor of Medicine at Harvard Medical School, Boston, MA. He is Co-Director of the World Health Organization Collaborating Center for Surveillance of Antimicrobial Resistance and Vice President of the Alliance for the Prudent Use of Antibiotics (APUA), both based in Boston. He is a Fellow of the American Academy of Microbiology and of the Infectious Diseases Society of America. Dr. O Brien received his medical degree from the Harvard Medical School and internal medicine training at Peter Bent Brigham Hospital. He completed research fellowships at Cambridge University, United Kingdom, Harvard Medical School and the University of Washington. He served in the U.S Army Medical Corps and has authored or co-authored more than a hundred research papers and book chapters on topics in microbiology and infection. Gerry Wright, B.Sc., Ph.D. Wednesday, June 25, :00 am 7:45 am Dr. Wright is the Director of the Michael G. DeGroote Institute for Infectious Disease Research, a Professor in the Department of Biochemistry and Biomedical Sciences and Associate member of the Department of Chemistry at McMaster University. He was Chair of the Department of Biochemistry and Biomedical Sciences from , and is the founding director of the McMaster Antimicrobial Research Centre. Dr. Wright received his B.Sc. in biochemistry in 1986 and his Ph.D. in chemistry from the University of Waterloo in He completed his post doctoral research at Harvard Medical School, and joined the Department of Biochemistry at McMaster in Dr. Wright is co-founder, with Dr. Eric Brown, of the McMaster High Throughout Screening Facility. He is a member of the editorial boards of the scientific peer-reviewed journals Chemistry and Biology and the Journal of Antibiotics, and is the author of over 100 published papers and book chapters. Dr. Wright s laboratory conducts research on the chemical biology of antibiotic resistance including resistance to aminoglycoside, glycopeptide and streptogramin families of antibiotics, on the mechanisms of antibiotic biosynthesis, and on the discovery of new antimicrobial targets, in particular antifungal agents.

32 Conference on Antimicrobial Resistance ABSTRACTS OF FINAL INVITED PROGRAM PRESENTATIONS ABSTRACTS OF INVITED PRESENTATIONS

33 SCIENCE PREVENTION CONTROL 33 ABSTRACTS OF INVITED PRESENTATIONS 1 Antibiotic Resistance: Location, Location, Location! D. M. Livermore Health Protection Agency, London, United Kingdom Objective: Assess the validity and pitfalls of published resistance surveys and determine which infected patients are more or less likely to harbor resistant bacteria. Summary: Numerous antibiotic surveys are published, presenting percentage rates for this or that pathogen and often based on sampling at just a few hospitals in each country or continent. Such data seem beguilingly straightforward, but hide great complexity. In reality, resistance rates vary greatly between contiguous countries or regions, reflecting (i) the emphasis placed on infection control, (ii) the weight of antibiotic usage and availability in the community, which, in turn, depend on the cultural environment and on how medical services are organized and (iii) whether or not internationally successful clones or mechanisms have reached the locale. Within countries, resistance varies between hospitals and hospital units, again reflecting hygiene and antibiotic policies, but also case-mix: in general, resistance rates are higher in tertiary care than district general hospitals, and are particularly high in intensive care units and in those managing chronic infections. Finally, the likelihood of resistance varies with the patient: those from nursing homes and with underlying disease, recent antibiotics, and hospitalization are more likely to harbor resistant pathogens than are antibiotic-naïve real community patients. These factors should be considered when choosing the appropriate antibiotic for a seriously-ill patient admitted via the emergency room, as should any history of foreign travel: patients admitted after hospitalization overseas may harbor very different bacteria from those locally prevalent. In short, published national or international resistance statistics illustrate trends and provide benchmarks, but local surveillance data are essential to guide usage and infection control. Which units are most affected? Are the resistant infections locally acquired or imported? Are the resistant isolates clonal, indicating cross-infection, or diverse, indicating repeated selection? Unless these aspects are considered, interventions are likely to be misdirected. Reference: 1. Livermore DM, Pearson A. Antibiotic resistance: location, location, location. Clin Microbiol Infect. 2007;13(Suppl 2): Pathogenesis of Clostridium difficile Infection S. H. Cohen University of California, Davis Medical Center, Sacramento, CA Objective: Discuss the current issues related to the pathogenesis of Clostridium difficile infection. Summary: Clostridium difficile is an anaerobic, spore-forming, gram-positive rod responsible for the majority of infectious diarrhea in the healthcare setting. The clinical manifestations range from minor diarrhea to severe life-threatening disease with colitis. Additionally, persons can be asymptomatically colonized with C. difficile. The majority of strains of C. difficile that cause disease produce two toxins, toxin A and toxin B. The genes for these two toxins reside in the pathogenicity locus (PaLoc) along with several regulatory genes and a gene producing a porin protein. The toxins glycosylate rho proteins to disrupt cell signaling, leading to actin disintegration and apoptosis. A third toxin called the binary toxin is expressed by a minority of C. difficile strains and may have a role in the pathogenesis of C. difficile infection (CDI). The current epidemic strain has a functional mutation in the tcd. A negative regulatory gene in the PaLoc is thought to be responsible for increased toxin production in addition to production of the binary toxin. The immune response to toxin A appears to be important in protecting against disease and in decreasing risk for recurrent disease. There may also be genetic determinants that increase an individual s risk for CDI. A polymorphism in IL-8 was associated with a two-fold increase in risk of CDI. The discussion will review the literature in relation to these important factors. Reference: 1. Cloud J, Kelly CP. Update on Clostridium difficile associated disease. Current Op Gastroenterol 2007;23: Clostridium difficile in Animals: Public Health and Veterinary Consequences J. S. Weese Ontario Veterinary College, University of Guelph, Guelph, Ontario Objective: Review C. difficile infection and colonization in various animal species, and describe zoonotic transmission of C. difficile and the limitations of knowledge regarding public health risks. Summary: Clostridium difficile is an important pathogen in human hospitals, and there is concern that community-associated disease may be on the rise. Clostridium difficile is also known to be a cause of enteric disease in species such as horses and pigs. Further, colonization of dogs, cats, cattle and other domestic animals has been reported; the role of C. difficile in disease is still unclear. There are also reports of contamination of retail meat with C. difficile spores. Isolates found in animals and food are often indistinguishable from those that cause disease in humans, and there have been recent suggestions that strains most commonly found in food animals in some regions may be over-represented in community-associated C. difficile. It is plausible that C. difficile is transmitted between humans and animals via direct contact and perhaps through food. When one considers the frequency and closeness of contact that may people have with animals, especially pets, and the potential for foodborne or environmental exposure, it is not surprising that concerns have been raised that C. difficile may be a zoonotic pathogen. 1 Reference: 1. Rupnik M. Is Clostridium difficile-associated infection a potentially zoonotic and foodborne disease? Clin Microbiol Infect. 2007;13(5): Human and Food Animal Genotypes of Clostridium difficile in the Food Supply J.G. Songer The University of Arizona, Tucson, AZ Objective: Discuss the distribution of Clostridium difficile (CD) in food animals and retail meats and describe the potential for transmission to humans. Summary: CD genotypes from colitis in neonatal pigs and calves [primarily ribotype 078/toxinotype (TT)V] are becoming common in human disease, especially cases which are neither nosocomial nor antimicrobial-associated. Phylogenomic data suggest that human strains originate in animals, and we hypothesized transmission via meats. CD was isolated from > 42% of beef, pork, and turkey. Most (73.0%) isolates were ribotype 078/ (TT)V, from ground beef, ground pork, pork braunschweiger, pork chorizo, pork sausage, and ground turkey. Human epidemic strain ribotype 027/toxinotype III accounted for >1/4 of isolates (from braunschweiger, beef summer sausage, ground beef, ground pork, and pork chorizo). Most were % related (continued)

34 Conference on Antimicrobial Resistance ABSTRACTS OF INVITED PRESENTATIONS to human isolates (via PFGE typing), supporting a contention that domestic animals may be a source of CD for human infection. Reference: 1. Songer JG. The emergence of Clostridium difficile as a pathogen of food animals. Anim Health Res Rev. 2004;5(2): The Epidemiology of Clostridium difficile Infection in Humans L. C. McDonald Centers for Disease Control and Prevention, Atlanta, GA Objective: Discuss how rates and severity of Clostridium difficile infections (CDI) are continuing to increase and the role of an epidemic strain in this increase; describe major risk factors for CDI and how modifying these factors may decrease rates; recognize cases of CDI in previously low risk populations. Summary: Although not a reportable disease, national hospital discharge and death certificate data indicate that the incidence and mortality associated with Clostridium difficile infection is increasing. Increased CDI incidence and mortality appears due to spread of an epidemic strain known variously as North American pulsed-field type 1 (NAP1), restriction endonuclease analysis type BI, or PCR ribotype 027. NAP1/BI/027 carries an extra toxin in addition to toxins A and B, known as binary toxin, and possesses polymorphisms in the toxin negative regulatory gene, tcdc. The latter may be in part or wholly responsible for toxin hyper-production with 16-fold increased toxin A production and 23-fold increased toxin B production documented in vitro. This strain, although historically uncommon, has become an epidemic strain coincident with it becoming more resistant to the fluoroquinolones. Outbreaks caused by NAP1/BI/027 continue to be reported in association with a variety of antimicrobials but especially fluoroquinolones. Previously low-risk populations in which CDI may be becoming more common include peri-partum women, in whom disease may be life threatening, and persons living in the community including, but not limited to, otherwise healthy persons. There are now several reports suggesting antimicrobial exposure, a ubiquitous factor for CDI in hospitalized patients, may be absent in a significant proportion of patients with community-associated CDI. Reference: 1. Blossom DB, McDonald LC. The challenges posed by re-emerging Clostridium difficile. Clin Infect Dis. 2007;45(2): The Clinical Challenge of MDR Gram-negative Pathogens in US Hospitals G. M. Eliopoulos Beth Israel Deaconess Medical Center, Boston, MA Objective: Discuss the occurrence of infection with gram-negative bacteria resistant to multiple classes of antimicrobial agents in US hospital patients and the challenges to treatment. Summary: In recent years, Acinetobacter spp. have joined Pseudomonas aeruginosa and Stenotrophomonas maltophilia as prototypic multi-drug resistant pathogens in US hospitals. The emergence of resistance, either by mutation or acquisition of resistance elements (e.g., carbapenemase genes), superimposed on broad intrinsic drug resistance, renders some isolates nonsusceptible to virtually all available treatment options. Isolates of the family Enterobacteriaceae producing extended-spectrum β-lactamases (ESBLs) are widely distributed in the US, but still account for a small proportion of isolates. The CTX-M β-lactamases, which have spread globally, have now begun to appear in the US as well. In contrast, the KPC carbapenemases that have plagued hospitals in New York City, and which can be difficult to detect using current techniques, have now emerged elsewhere in the US and abroad. The proportion of gram-negative bacterial isolates resistant to fluoroquinolones has reached disturbing levels. These and other resistance traits, together with host factors such as allergy or intolerance to certain antimicrobial classes, frequently limits severely the options for treating infections, including those seen in the outpatient setting. As a result, for some patients the only remaining options may include individual agents or combination regimens for which optimal dosing and specific indications have not been established and which may be associated with significant toxicity. 1. Paterson DL, Doi Y. A step closer to extreme drug resistance (XDR) in gram-negative bacilli. Clin Infect Dis. 2007;45: Munoz-Price LS, Weinstein RA. Acinetobacter infection. N Engl J Med. 2008;358: The Clinical Challenge of MDR Acinetobacter in Iraq G. Wortmann Walter Reed Army Medical Center, Washington, DC Objective: Discuss the current state of leishmaniasis, multi-drug resistant Acinetobacter infections and Q fever infections associated with the global war on terrorism (GWOT). Summary: Infectious disease rates associated with the GWOT have fortunately been low. However, infection with leishmaniasis, the emergence of multi-drug resistant Acinetobacter as a nosocomial pathogen and scattered cases of Q fever have marked the conflict. Although cases of leishmaniasis were high after the initial invasion, they have dropped to a low, but steady, rate. Multi-drug resistant Acinetobacter infections have proven to be problematic throughout the evacuation chain, and have lead to significant changes in antibiotic use and in the ecology of the hospital flora. Q fever has been diagnosed sporadically throughout the war, and may be a more widespread infection than initially appreciated. The current state of each of these infections will be reviewed. Reference: 1. Zapor MJ, Moran KA. Infectious diseases during wartime. Curr Opin Infect Dis. 2005:18(5): The Clinical Challenge of Multi-drug Resistant (MDR) Pseudomonas in Cystic Fibrosis L. Saimin Columbia University Medical Center, New York, NY Objective: Review the epidemiology and management strategies for P. aeruginosa in cystic fibrosis. Summary: Pseudomonas aeruginosa is the most common pathogen in patients with cystic fibrosis (CF). Approximately 30% of infants and 80% of adults with CF are infected with this pathogen. Initial strains of P. aeruginosa are relatively susceptible to most anti-pseudomonal antibiotics but over time, due to the selective pressure of oral, intravenous, and aerosolized antibiotics, P. aeruginosa becomes progressively resistant to antibiotics. Antimicrobial treatment strategies for P. aeruginosa include: management of pulmonary exacerbations, chronic suppressive therapy, and most recently, early eradication of colonization/infection. Management of pulmonary

35 SCIENCE PREVENTION CONTROL 35 ABSTRACTS OF INVITED PRESENTATIONS exacerbations has been traditionally guided by in vitro susceptibility testing, but such testing may not predict the optimal management for organisms that grow within a biofilm, which is thought to be the mode of growth of CF endobronchial disease. Synergy testing of MDR strains has been performed, but clinical trials supporting the efficacy of such an approach are lacking. Chronic suppressive therapy consists of oral azithromycin and/or aerosolized antibiotics, such as tobramycin and more recently aztreonam, which can achieve high concentrations within the lung and therefore overwhelm some mechanisms of resistance such as efflux pumps. Traditional susceptibility testing is not useful to predict the efficacy of chronic suppressive therapy. Prevention strategies for MDR P. aeruginosa are very limited. Infection control strategies are critically important to prevent patient-to-patient spread of P. aeruginosa within the healthcare setting. To date, vaccines have not been shown to be efficacious, primary prevention with antibiotics has not been attempted, and effective antimicrobial stewardship has not been attempted. 1. Aaron SD, Vandemheen KL, Ferris W, et al. Combination antibiotic susceptibility testing to treat exacerbations of cystic fibrosis associated with multiresistant bacteria: a randomised, double-blind, controlled clinical trial. Lancet. 2005;366(9484):: Blumer JL, Saiman L, Konstan MW, Melnick D. The efficacy and safety of meropenem and tobramycin vs ceftazidime and tobramycin in the treatment of acute pulmonary exacerbations in patients with cystic fibrosis. Chest. 2005;128(4): Gibson RL, Burns JL, Ramsey BW. Pathophysiology and management of pulmonary infections in cystic fibrosis. Am J Respir Crit Care Med. 2003;168(8): Saiman L, Marshall BC, Mayer-Hamblett N, et al. Azithromycin in patients with cystic fibrosis chronically infected with Pseudomonas aeruginosa: a randomized controlled trial. JAMA. 2003;290(13): Saiman L, Siegel J, Cystic Fibrosis Foundation. Infection control recommendations for patients with cystic fibrosis: microbiology, important pathogens, and infection control practices to prevent patient-to-patient transmission. Infect Control Hosp Epidemiol. 2003;24(Suppl 5):S1-S52. 9 The Challenge of Multi-drug Resistant (MDR) Foodborne Gram Negative Pathogens D. G. White U.S. Food and Drug Administration, Laurel, MD Objective: Discuss the contribution of the food supply to antimicrobial resistance among enteric bacteria and the challenges that remain in developing mitigation strategies to reduce contamination of foods with antimicrobial resistant foodborne bacteria and protecting public health. Summary: An undesired consequence of antimicrobial use in animals is the development of antimicrobial-resistant (AMR) foodborne bacteria pathogens and the subsequent transmission of those bacteria to humans via contaminated food and water. Over the past two decades, we have observed a steady loss of antimicrobial efficacy against many foodborne pathogens, with resistance to the most potent agents also appearing. The evolution and propagation of transmissible plasmids in Salmonella and E. coli carrying resistance to eight or more antimicrobials is particularly worrisome. Sequence data shows that many different resistance determinants can amass in linked clusters on plasmids, such that antimicrobials of a different class, including substances such as disinfectants or heavy metals, may select for multidrug resistant foodborne bacteria. As intensive food production systems become more common and as expanding trade in food animals and their derived products evolve to meet global demands, national and regional surveillance systems to measure and track drug resistance in these and other enteric organisms will become more important. Developing effective ways to characterize and mitigate resistance requires continued exploitation of basic research on the ecology and epidemiology of the major foodborne pathogens, and improved surveillance of food animals and derived retail products, including imports. Reference: 1. Welch TJ, Fricke WF, McDermott PF, et al. Multiple antimicrobial resistance in plague: an emerging health risk. PLoS One. 2007;2(3):e Early Detection and Containment of New Antimicrobial Resistance Clones T. F. O Brien Brigham and Women s Hospital, Boston, MA Objective: Discuss the collateral damage of antibiotic use due to emergence of new resistance clones, and describe the levels of surveillance and response that would be needed for their early detection and possible containment. Summary: After a strain of bacteria or a mobile genetic element expressing significant new antimicrobial resistance emerges somewhere in the world, its progeny may then first appear and later spread in stages through any country and its hospitals. Intensive containment efforts (e.g. screening for and furloughing caregiver carriers, closing wards, banning some antimicrobials, etc.) could be more cost-effective at early stages because carriers and sites would be fewer and early progeny may be less competitive. Examples at early stages in the U.S. now are VRSA (a few patients) and KPC-2 (a few states). Early containment would need advance planning for automated ongoing surveillance of all clinical isolates and for provision of prompt emergency funding by a government or private insurance program to support intensive containment at the earliest sites. Reference: 1. O Brien, TF. The global epidemic nature of antimicrobial resistance and the need to monitor and manage it locally. Clin Infect Dis. 1997;24 (Suppl 1):S2-S8. 11 Collateral Damage of Antibiotic Use in Animals: Impact on Secondary Pathogens and Commensals S. F. Kotarski Pfizer, Inc., Kalamazoo, MI Objective: Review the risks of antibiotic use in animals with respect to selective pressures for resistance among non-targeted pathogens and bacteria associated with treated animals. Summary: People are dependent on domesticated animals for food and other animal-derived products (e.g., wool, leather), companionship, and various types of activities (e.g., seeing-eye dogs, sporting activities). Thus, when antibiotics are used to treat infections in an animal, there are implications for the treated animal, individuals housed with the treated animal, the caretaker, and the public health at large. Each antibiotic may exert selective pressure for antimicrobial resistance for targeted pathogens, and collateral selective pressure for resistant or inherently insensitive commensal organisms and pathogens when present. Antibiotics may also co-select for resistance determinants against other drug classes in cases where multi-drug resistant organisms are present. Additionally, antibiotic use may result in ecological changes in microbial communities associated with the treated animal. This, in turn, may allow colonization by new organisms, including secondary and (continued)

36 Conference on Antimicrobial Resistance ABSTRACTS OF INVITED PRESENTATIONS zoonotic pathogens. Ultimately, the number of antibiotic drugs available for use in each animal species is restricted by both human and animal safety constraints, including resistance concerns as addressed by national regulatory authorities in the drug approval process. As sick animals require treatment for the health and welfare of both animals and humans, these circumstances reinforce the need for continued vigilance in appropriate antibiotic use, surveillance and infection control programs for animals. Reference: 1. Boerlin P. Antimicrobial resistance and its epidemiology. In: Giguerem S, Prescott J, Baggot J, Walker R, Dowling P, eds. Antimicrobial Therapy in Veterinary Medicine. Fourth ed. Ames, Iowa: Blackwell Publishing; 2006: Evaluating the Human Public Health Impact of In Vitro Resistance J. H. Powers Scientific Applications International Corporation, Bethesda, MD Objective: Describe the limitations of correlations between in vitro testing and clinical outcomes; discuss the unintended consequences of misdiagnosis and other forms of injudicious use on humans, commensal organisms and the environment. Summary: When discussing antimicrobial resistance, it is important to define exactly what we mean by resistance before we can evaluate its public health impact. While clinicians often use in vitro assessments of the amount of drug needed to inhibit the growth of microorganisms, it is necessary to link these changes in the biology of organisms to changes in clinical effectiveness of an antimicrobial in humans in a given disease or range of diseases. The impact of resistance may differ in different diseases or in different hosts. The potential collateral damage caused by antimicrobials relates to both the human host who receives the drugs as well as undesirable effects on both pathogenic microorganisms and commensal organisms in both the human body and the environment. Not all bacteria are pathogens. Colonizing bacteria play several important roles in the human body. For instance, recent evidence points to interactions between bacteria in the gut and intestinal cells which appear necessary to appropriate maturation and differentiation of these cells. Decreased exposure to microorganisms early in life may also be a potential factor in the increase in atopic diseases over the last three decades. The commensal bacteria also may play an important role in preventing colonization with organisms that may be more pathogenic in terms of their capacity to cause disease. Secondary infections caused by the receipt of antimicrobials are well-documented, both for potentially life-threatening diseases such as Clostridium difficile associated disease as well as other non-life threatening diseases like vaginal candidiasis. Treatment of an infection in a human being with antimicrobials can affect both the infecting pathogen as well as other bacteria present in the body. When discussing interventions to prevent the development of resistance, one should take into account not only the effect on the primary pathogen but also the effect on other bacteria as well. Non-pathogenic bacteria may act as reservoirs to pass on resistance determinants to other bacteria as well. In addition, organisms which are pathogens in humans may be commensals in animals who may act as a reservoir to pass on resistant organisms or their resistance determinants to humans, either directly or through the environment. One should take into account the effects of antimicrobial resistance during the development process of new drugs as well as their judicious use once they become widely available. This assessment should include both the effects of an antimicrobial on the disease state under study as well as broader potential effects on commensals and the environment as part of the overall assessments of risks and benefits of antimicrobials. The overall risk and benefit assessments depends on both the nature and frequency of both the benefits and the harms of interventions. More research is needed to evaluate the predictors of when resistance will occur and therefore how to mitigate this risk. 1. Madara J. Building an intestine architectural contributions of commensal bacteria. N Engl J Med 2004;351(16): Baker BS. The role of antibiotics in atopic dermatitis. Clin Exp Immunol. 2006:144(1): Antibiotic Resistance Starts in the ICU: An Innovative Approach for Limiting Empiric Therapy V. L. Yu University of Pittsburgh, Pittsburgh, PA Objective: Describe the basis for clinician overuse and spiraling empiricism of antibiotics in the ICU; discuss the outcomes for those patients who receive empiric antibiotics but are later found not to be infected. Summary: ICU prescription of antibiotics constitutes a disproportionately high percentage of antibiotics in the hospital, and empiric antibiotic prescription is rampant in the ICU. The necessity for early, active in vitro ( appropriate ) antibiotic therapy has been emphasized for severely-ill infected patients. What has been overlooked is that an indiscriminate approach of empiric broad-spectrum combination antibiotics is also being applied to patients who are neither severely-ill nor likely to have an infection. Pulmonary infiltrates are a common indication for empiric antibiotics despite the fact that pneumonia is less likely than other causes of infiltrates. We devised an approach using a Clinical Pulmonary Infection Score (CPIS) to select those ICU patients who were sufficiently stable that a 3-day course of monotherapy might suffice as adequate therapy. This approach allowed the concerned clinician the flexibility of administering an antibiotic in a severely-ill patient, but limited the number and duration of antibiotics. In a prospective randomized study of standard therapy (multiple antibiotics for prolonged duration vs monotherapy for 3 days) in patients with low CPIS, 74% of patients with pulmonary infiltrates were prospectively enrolled. Patients enrolled into the 3-day monotherapy group encountered fewer adverse effects of antibiotics, lower incidence of antibiotic resistance or superinfection (p=.017), and lower antibiotic costs (p=.0001) as compared to standard therapy. Clearing of pulmonary infiltrates was identical in both groups. Unexpectedly, length of stay (p=.04) and 30 day mortality (p=.059) were less in the 3-day monotherapy group. Nevertheless, despite the logic of the concept, the almost universal acceptance by ID specialists, and the endorsement in the ATS/IDSA Guidelines for Healthcare Pneumonia, this approach has not been widely adopted. The reasons for the lack of implementation will be discussed and a solution proposed. 1. Yu VL, Singh N. Excessive antimicrobial usage causes measurable harm to patients with suspected ventilator-associated pneumonia. Intensive Care Med. 2004;30(5): Singh N, Rogers P, Atwood CW, Wagener MM, Yu VL. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med. 2000;162(2 Pt 1):

37 SCIENCE PREVENTION CONTROL 37 ABSTRACTS OF INVITED PRESENTATIONS 14 Prevention of Resistance by Limiting Antibiotic Exposure: Innovative Approaches in the Neonate P. J. Sanchez UT Southwestern Medical Center, Dallas, TX Objective: Discuss methods of limiting antibiotic use in neonates that may lead to prevention of antimicrobial resistance. Summary: Antimicrobial resistance has emerged as a major problem in the neonatal intensive care unit (NICU). It has been associated with an increase in morbidity and mortality, and its occurrence results in increased costs of health care. It is imperative that strategies be developed that will prevent emergence of resistance and dissemination of resistant organisms. The public health of our NICUs are at stake! Antimicrobial utilization practices impact on the types of microorganisms responsible for neonatal sepsis and their antibiotic resistance patterns. The use of third generation cephalosporins has been associated with increased mortality when used for empiric therapy of early-onset infections, as well as with the occurrence of systemic candidiasis in preterm infants. Aminoglycosides have the distinct advantage of exerting less selective pressure for development of resistance in closed units like the NICU, thus minimizing the risk of emergence of resistant bacteria and fungi. For late-onset sepsis, vancomycin often is recommended along with an aminoglycoside since approximately 50% of all bloodstream infections are due to coagulase-negative staphylococci. This practice has led to widespread use of vancomycin in NICUs with its attendant risk for emergence of vancomycin resistant organisms. Clinical experience with the use of oxacillin or nafcillin rather than vancomycin suggests that these antibiotics may be used safely in the NICU. Bloodstream infections due to cagulase-negative staphylococci are rarely fulminant or fatal, and they are not associated with an increased case-fatality rate over that seen among uninfected very-low-birth-weight infants. The emergence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) in NICUs may limit the use of such a policy in NICUs where the prevalence of CA-MRSA is high. However, by routine screening for MRSA and appropriate isolation precautions for colonized infants, MRSA can be controlled if not eradicated in NICUs Duration of antibiotic therapy is dependent on the causative organism, site(s) of infection, clinical severity and course. This is usually 5 days for uncomplicated pneumonias, 7 days for uncomplicated bacteremia, 10 days for sepsis and pneumonia, and 14 to 21 days for meningitis. Normalization of the CRP and/or other inflammatory markers such as IL-8, also has been utilized to discontinue antibiotic therapy. In infants evaluated for early- and late-onset infections, antibiotics may be safely discontinued if the blood cultures remain sterile after 36 and 48 hours of incubation, respectively. The increasing prevalence of antibiotic resistance among hospitalized patients has prompted a national and international campaign by healthcare associations and agencies to prevent antimicrobial resistance. In the NICU, neonatologists hold the solution, and they must be vigilant in their antibiotic choices for the sake of our preemies. 1. Franz AR, Steinbach G, Kron M, Pohlandt F. Reduction of unnecessary antibiotic therapy in newborn infants using interleukin-8 and C-reactive protein as markers of bacterial infections. Pediatrics. 1999;104(3 Part 1): Franz AR, Bauer K, Schalk A, et al. Measurement of interleukin 8 in combination with C-reactive protein reduced unnecessary antibiotic therapy in newborn infants: a multicenter, randomized, controlled trial. Pediatrics. 2004;114(1): Jardine L, Davies MW, Faoagali J. Incubation time required for neonatal blood cultures to become positive. J Paediatr Child Health. 2006;42(12): Engle WD, Jackson GL, Sendelbach D, et al. Neonatal pneumonia: Comparison of 4 vs 7 days of antibiotic therapy in term and near-term infants. J Perinatol. 2000;20(7): Jackson GL, Engle WD, Sendelbach DM, et al. Are complete blood cell counts useful in the evaluation of asymptomatic neonates exposed to chorioamnionitis? Pediatrics. 2004;113(5): Prevention of Resistance by Optimizing Antibiotic Usage: Antimicrobial Stewardship S. E. Cosgrove Johns Hopkins Medical Institutions, Baltimore, MD Objective: Discuss types of interventions to reduce or improve antimicrobial use that have been implemented in healthcare settings and the association between these interventions and reductions in antimicrobial resistance. Summary: Antimicrobial use in the healthcare setting is frequent, often unnecessary, and a contributing factor to the increasing rates of antimicrobial resistance in gram positive and gram negative organisms that have emerged over the past twenty years. Rates of resistance continue to increase in the face of a dwindling stream of new antimicrobial agents, particularly those with activity against multidrug resistant gram negative organisms. Antimicrobial stewardship is an important approach to ensuring more rational antimicrobial use. Although there is ample evidence that various interventions can decrease or improve antimicrobial use, there is less evidence that they can lead to sustained decreases in antimicrobial resistance. Types of interventions to decrease or improve antimicrobial use include pre-prescription approval for antimicrobials, post-prescription review of the appropriateness of therapy after additional clinical data are available, computer assisted decision support, education regarding antibiotics, antibiotic cycling, use of prediction rules for early discontinuation of therapy, and use of rapid diagnostic testing to direct antimicrobial therapy. Reference: 1. Dellit TH, Owens RC, McGowan JE Jr, et al. Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship. Clin Infect Dis. 2007;44(2): Prevention of Resistance by Optimizing Antibiotic Exposure: The Mutant Prevention Concentration (MPC) K. Drlica Public Health Research Institute, New Jersey Medical School, Newark, NJ Objective: Discuss how in vitro susceptibility measurements (MPC) can be combined with pharmacokinetic data to determine antimicrobial doses that will restrict the selective amplification of bacterial subpopulations of resistant mutants. Summary: The mutant selection window hypothesis provides a conceptual framework for restricting the emergence of antimicrobial resistance through the design of dosing regimens and through screening of new compounds for exceptional activity with resistant mutants. The window hypothesis maintains that for each antimicrobial and each pathogen, a concentration range exists in which single-step mutants grow while wild-type cells do not. Placing antimicrobial concentrations inside the window, which is common practice, leads to selective amplification of resistant mutant subpopulations that are (continued)

38 Conference on Antimicrobial Resistance ABSTRACTS OF INVITED PRESENTATIONS present prior to therapy or arise during therapy. In vitro assays using agar plates, liquid cultures, and dynamic models support the hypothesis, as do animal studies and a small clinical experiment. Dose-escalation modeling, which is used to establish PK/PD targets and then to determine how well particular doses achieve those targets in human populations, can be modified for restricting emergence of resistance by substituting MPC (mutant prevention concentration) for MIC (minimal inhibitory concentration). This substitution is necessary because the two parameters are discordant when large numbers of clinical isolates are examined. New compounds can be examined for a narrow selection window by seeking a low ratio of resistant mutant MIC to wild-type MIC using a battery of known mutants. An example is presented in which the ratio approaches unity. Reference: 1. Drlica K, Zhao X. Mutant selection window hypothesis updated. Clin Infect Dis. 2007;44(5): will discuss the issues of defining resistance and measuring harms and benefits of antimicrobials, including the impact of resistance. We also will discuss the issues of risk communication and perception. This presentation will also discuss issues related to development of medical interventions to prevent or counter resistance, and how investigators should consider the potential societal impact of these interventions in light of the harms or benefits for individual patients. 1. Lepper MH, Dowling HF, Robinson JA, et al. Studies on hypersensitivity to penicillin. I. Incidence of reactions in 1303 patients. J Clin Invest. 1949;28(5 Part 1): Finland M. Controlling clinical therapeutic experiments with specific serums. N Engl J Med 1941;225(13): Starr C. Social benefits versus technological risks. Science 1969:165(3899): Antibiotic Resistance as an Adverse Event and Risk Perception J. H. Powers Scientific Applications International Corporation, Bethesda, MD 18 Risk versus Benefit of Antibiotics R. Johann-Liang U.S. Department of Health and Humans Services, Bethesda, MD Objective: Discuss the history of the evaluation of adverse events with antimicrobials; describe the modern evaluation of the potential harms of antimicrobials and how they are compared to the potential benefits in an overall risk benefit assessment. Summary: The first therapies used to treat infections were immune therapies, such as serum therapy in pneumonia. While showing large decreases in mortality in serious disease, serum therapy caused serum sickness and even drug related deaths in a substantial proportion of patients, demonstrating a need for interventions with less risk. In the 1930 s sulfonamides were introduced, followed shortly thereafter by penicillin and various tetracycline derivatives. While the effects of these drugs in curing disease seem obvious today, early investigators noted that given the variability of human disease there was a need to compare outcomes with control patients treated with no specific therapy to evaluate both the benefits and the harms of therapy. Concurrently with the demonstration of effectiveness of antimicrobials in serious disease, clinicians began to use the drugs in viral infections in attempts to prevent bacterial infections, despite the admonitions of experts in the field. While associated with less risks that serum therapy, investigators still noted serious adverse reactions with antimicrobials as well. Initially, investigators believed that resistance in certain organisms, such as Streptococcus pneumoniae would be rare. Therefore, they concentrated on the direct adverse events caused by antimicrobials as causing harm to patients in settings where the benefits were unclear. More recent evaluation of the potential harms of antimicrobials shows that they are associated with the potential for long term, as well as acute toxicities. Over time, clinicians noted that resistance could occur, and could results in clinical failures in patients, adding an additional dimension to the potential harm caused by injudicious use of antimicrobials. The safety of a medical intervention is defined by an evaluation of the balance of the risks and benefits of a medical intervention under the intended conditions of use. Since no intervention is devoid of potential harm, it is important to have accurate and precise evaluations of the nature and frequency of both the benefits and harms of medical interventions. Adverse reactions are defined as undesirable effects reasonably associated with use of a medical intervention. In this regard, antimicrobial resistance is an adverse event, since it is an undesirable consequence associated with the use of antimicrobials. Measuring harms and benefits requires accurate data upon which to base analyses. It is also important to clearly communicate the risks and benefits to clinicians and patients. A key consideration in risk communication is risk perception by those for whom the information is intended. This presentation Objective: Discuss the risk of antibiotic use from an individual as well as a population perspective; describe the evidence of benefit or the lack of evidence of benefit for antibiotic use in the most commonly prescribed outpatient indications. Summary: Antibiotics are prescribed most commonly for respiratory tract infections in the outpatient setting under the indications of sinusitis, bronchitis, and otitis media. These are illnesses which mainly self-resolve. Whether there are added benefits of antibiotic therapy for these indications still remain unclear after decades of clinical trials comparing one antibiotic to another for these indications. This is because the large margin of benefit of antibiotic therapy observed over no antibiotic therapy when treating severe conditions such as meningitis or bacteremic pneumonia were never reproduced in self-resolving diseases. One antibiotic after another has been approved for common respiratory tract infections in non-inferiority test setting (which means no worse than the control antibiotic by a certain margin), rather than in superiority setting (that is, better than the older control antibiotic or placebo). Thus, over the last several decades, all antibiotics have been approved for use in self-resolving illnesses without actually showing that they add benefit for the patient in these indications. While the benefit of antibiotic use in commonly prescribed outpatient indications is unclear, it is quite clear that antibiotic use poses risks to the patient. No drug therapy is without the potential to harm, antibiotics included. Depending on the type of antibiotic used, in clinical trials and in clinical practice, one can generate a large and variable list of mild to serious adverse drug reactions which may be experienced by individuals taking antibiotics for self-resolving respiratory infections. It is important before prescribing antibiotics to patients with self-resolving diseases to examine the potential risks of drug therapy in the context of what actual benefit evidence is available in that indication (i.e. the risk versus benefit). Moreover, unique to antimicrobials among all drugs, is the safety concern that extends beyond the individual risk. Antibiotic use promotes antibiotic resistance for the community. Inappropriate antibiotic use, that is, use in indications where the benefit is not clear, translates into societal harm. Risk versus benefit analysis is needed before every antibiotic prescription in the context of what is being treated. Reference: 1. Mölstad S, Erntell M, Hanberger H, et al. Sustained reduction of antibiotic use and low bacterial resistance: 10-year follow-up of the Swedish Strama programme. Lancet Infect Dis. 2008;8(2):

39 SCIENCE PREVENTION CONTROL 39 ABSTRACTS OF INVITED PRESENTATIONS 19 The Human Health Consequences of Antibiotic Use in Animals F. Angulo Centers for Disease Control and Prevention, Atlanta, GA Objective: Discuss how the use of antimicrobial agents in food animals is associated with antimicrobial resistance among bacteria isolated from humans, and how such resistance results in adverse human health consequences. Summary: Several lines of evidence indicate that the use of antimicrobial agents in food animals is associated with antimicrobial resistance among bacteria isolated from humans. The use of antimicrobial agents in food animals is most clearly associated with antimicrobial resistance among Salmonella and Campylobacter isolated from humans, but also appears likely among enterococci, Escherichia coli and other bacteria. Evidence is also accumulating that the antimicrobial resistance among bacteria isolated from humans resulting from using antimicrobial agents in food animals is leading to human health consequences. These human health consequences include: (i) infections that would not have otherwise occurred and (ii) increased frequency of treatment failures and increased severity of infection. Increased severity of infection includes longer duration of illness, increased frequency of bloodstream infections, increased hospitalization and increased mortality. Continued work and research efforts will provide more evidence to explain the connection between the use of antimicrobial agents in food animals and antimicrobial-resistant infections in humans. One particular focus, which would solidify this connection, is to understand the factors that dictate spread of resistance determinants, especially resistant genes. With continued efforts on the part of the medical, veterinary and public health community, such research may contribute to more precise guidelines on the use of antimicrobials in food animals. Reference: 1. Angulo FJ, Nargund VN, Chiller TC. Evidence of an association between use of anti-microbial agents in food animals and anti-microbial resistance among bacteria isolated from humans and the human health consequences of such resistance. J Vet Med B Infect Dis Vet Public Health. 2004;51 (8-9): Food Safety and Infectious Diseases: A Microbe s View of the Food Industry R. V. Tauxe Centers for Disease Control and Prevention, Atlanta, GA Objective: Discuss the principal outlines of the flow of food through the food industry, how microbes contaminate food along the way, and the importance of the links between ecologies on farms and in food factories, and the public health. Summary: Foodborne infections affect an estimated 76 million persons each year in the United States, with 323,000 hospitalizations and 5,000 deaths. Bacterial, viral and parasitic agents can contaminate foods at many points in the food chain from farm to table. On the farm, colonized food animals are a source of infection for Salmonella, Shiga toxin producing E. coli (STEC), and Campylobacter. Complex ecologies link animal and plant production. At slaughter and food processing plants, those microbes can persist and amplify in raw meat, poultry and produce. Fish and shellfish reflect contamination of the environments in which they are caught or raised, including Vibrio spp. When Listeria monocytogenes and Salmonella find sustained niches in the factory environment, they may contaminate finished food products, even after a high temperature cooking step has taken place. Microbes can often contaminate foods during preparation in the kitchen, by cross-contamination from other foods (Salmonella and Campylobacter), or from an infected food handler (norovirus or hepatitis A). 11% of the food supply is imported, and fresh foods grown in the developing world may be contaminated with pathogens from human and animal sources. The spectrum of pathogens and of contaminated foods can change. Robust public health surveillance, vigorous multi-disciplinary investigations, and applied research can help improve control and prevention. Reference: 1. Tauxe RV. The burden of illness associated with foodborne threats to health, and the challenge of prevention. In: Addressing Foodborne Threats to Health: Policies, Practices and Global Coordination, Workshop Summary, Forum on Microbial Threats, Board on Global Health and Institute of Medicine of the National Academies. Washington DC, The National Academies Press, 2006, pp Interventions to Prevent Contamination of Foods We Eat M. P. Doyle Center for Food Safety, University of Georgia, Griffin, GA Objective: Describe the broad range of interventions that can be used throughout the food industry to prevent food contamination by antibioticresistant microbes. Summary: The food industry throughout the food chain uses a variety of antimicrobials for many purposes. These range from using antibiotics to treat diseases in animals to using sanitizers to kill pathogens on equipment surfaces or on raw foods such as produce or meat. A recent Institute of Food Technologists expert report concluded that a Hazard Analysis Critical Control Point (HACCP) system using interventions (critical control points) throughout the food chain would be the most effective measure to control foodborne pathogens and reduce foodborne illnesses. Since most interventions are equally effective in killing foodborne pathogens, whether antibiotic-resistant or not, applying interventions to pathogens in general rather than focusing on antibiotic-resistant strains specifically would have the greatest impact in reducing foodborne illnesses. On the farm, livestock and poultry are major sources of foodborne pathogens, transmitting these microbes through contaminated manure. A wide array of interventions has been developed to reduce pathogens carried in these animals, ranging from sanitation practices to biological treatments that would inactivate the pathogen within the host. Recent innovations for controlling pathogens on foods include packaging in modified atmospheres, irradiation, competitive exclusion microbes, and chemical treatments to kill or inhibit growth. 1. Council for Agricultural Science and Technology (CAST) Expert Panel. Intervention strategies for the safety of foods of animal origin. CAST, Ames, IA. Issue Paper No ;January: Doyle MP, Erickson MC. Reducing the carriage of foodborne pathogens in livestock and poultry. Poult Sci. 2006;85(6): Institute of Food Technologists Expert Panel. Antimicrobial resistance: Implications for the food system. Comprehensive Reviews in Food Science and Technology 2006;5(3):

40 Conference on Antimicrobial Resistance ABSTRACTS OF INVITED PRESENTATIONS 22 The Antibiotic Resistome: Scope and Impact G. Wright McMaster University, Hamilton, ON, Canada Objective: Discuss the factors underlying the evolution of antibiotic resistance and the relationship between resistance as manifested in the clinic and in the outside environment, as well as the application of this knowledge in new antibiotic development. Summary: The past century of antimicrobial chemotherapy has shown that resistance to antibiotics is inevitable and generally emerges rapidly in the clinic, often within a few years of launch. We also now know that for antibiotics of natural origin, resistance has necessarily co-evolved with their biosynthesis and that microbial genome sequences have revealed that even non-producers can harbor highly efficient resistance genes. Antibiotic producers and other bacteria, therefore, have developed an innate ability to overcome antibiotics; collectively termed the Resistome. What drives this process and what are the molecular origins of resistance? The answers may lie in the diversity of environmental chemicals that are produced by living organisms. The selective pressure of bioactive molecules has primed the evolution of the Resistome and provides a challenge for the development of new antibiotics that are not susceptible to resistance. Nevertheless, the Resistome can also provide guidance for the development of new generations of antibiotics and antimicrobial strategies. Reference: 1. Wright GD. The antibiotic resistome: the nexus of chemical and genetic diversity. Nat Rev Microbiol. 2007;5(3): Intercontinental Transport of Microorganisms in Clouds of Desert Dust: A Global Human Health Perspective D. W. Griffin United States Geological Survey, Tallahassee, FL Objective: Discuss the global nature of dust storms and how they can impact human health in communities far removed from their point of origin. 24 Potential Impacts of Antibiotics and Antibiotic Resistance on the Water Supply R. Singer University of Minnesota, St. Paul, MN Objective: Discuss the routes by which antibiotics and antibiotic resistance genes are entering the water supply and the subsequent human health impacts of the presence of these antibiotics and antibiotic resistance genes. Summary: The emergence and spread of antimicrobial resistance among bacterial populations has major health and economic consequences in both human and animal populations. The purpose of this presentation is to discuss the ways in which antibiotic resistant bacteria and resistance genes are disseminated via water. Of particular concern is the finding of low concentrations of antibiotics in water supplies and the impacts that these levels might have on the selection of antibiotic resistant bacteria. Some studies have found a correlation between increased concentrations of antibiotics and higher levels of antibiotic resistant bacteria and antibiotic resistance genes. However, in laboratory based studies, low levels of antibiotics, such as those found in environmental samples, do not appear to select for resistance. Because the pressures that can select for antibiotic resistance in the environment have considerable spatial and temporal heterogeneity, studies that investigate the emergence and spread of antibiotic resistance in water must be carefully designed. In conclusion, there are many factors that can affect antibiotic resistance in the water supply. An ecosystembased approach to antibiotic resistance is the only way in which the myriad of selection pressures and other determinants can be taken into account. 1. Muñoz-Aguayo J, Lang KS, LaPara TM, González G, Singer RS. Evaluating the effects of chlortetracycline on the proliferation of antibiotic-resistant bacteria in a simulated river water ecosystem. Appl Environ Microbiol. 2007;73(17): Singer RS, Ward MP, Maldonado G. Can landscape ecology untangle the complexity of antibiotic resistance? Nat Rev Microbiol. 2006;4(12): Summary: Dust storms move an estimated 3 x grams of soil vast distances in the Earth s atmosphere each year. Large dust events are capable of global dispersion. Microbial ecology studies in soil have shown that there are approximately 1 million to 1 billion bacteria cells (pathogens and nonpathogens) per gram, and that this community is composed of approximately 10,000 genotypes. Other microorganisms present in a typical gram of soil include ~ 10 thousand to 10 million viruses, ~ 1 million fungi, and ~ 10 thousand protozoa. This presentation will cover our current state of knowledge in this emerging research field to include historical and current observations, and how specific organisms within these clouds may impact human health. Reference: 1. Griffin DW. Atmospheric movement of microorganisms in clouds of desert dust and implications for human health. Clin Microbiol Rev. 2007;20(3):

41 SCIENCE PREVENTION CONTROL 41 ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS

42 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS S1 ESBL Obfuscation by Concomitant Expression of Plasmid-mediated AmpC β-lactamases in Escherichia Coli F. J. L. Robberts, P. C. Kohner, R. Patel Clinical Microbiology, Mayo Clinic, Rochester, MN Objective: Describe how AmpC expression may obfuscate ESBL detection in E. coli Background: Accurate ESBL detection guides antimicrobial susceptibility reporting, treatment and infection control measures. The increased frequency of plasmid-mediated AmpC resistance is concerning; there is little available data on in vitro detection of ESBL enzymes in the setting of pampcproduction. Aim: We evaluated in vitro detection of ESBL enzymes in the setting of concomitant pampc-production. Methods: Twenty six consecutive E. coli clinical isolates were selected for analysis based on a positive ESBL screen (cefpodoxime MIC > 4μg/ml) and susceptibility pattern suggestive of AmpC-mediated resistance (decreased susceptibility to cefoxitin). ESBL confirmation employing disk augmentation and Etest (CAZ, CAZ-CLA; CTX, CTX-CLA), and phenotypic screening of pampc with aminophenylboronic acid (BA) were evaluated. Results were confirmed by amplification and sequencing of TEM, SHV and pampc genes. Results: Of 26 isolates studied 22 harbored pampc genes (20 CMY- and 2 FOX-type) of which 12 were confirmed ESBLpositive by amplification and sequencing (9 TEM, 1 SHV, 2 TEM+SHV). ESBL Etest results were positive for only 1/12 isolates. ESBL disk augmentation results were positive in only five of the 12 isolates (5/12 CAZ-positive, 2/12 CTX-positive). Phenotypic detection of pampcs employing BA was successful in 21/22 PCR confirmed isolates. Addition of BA to ESBL augmentation disks did not assist in revealing cryptic ESBL expression. Conclusion: In E. coli, expression of pampc may obfuscate ESBL enzyme expression leading to falsenegative ESBL detection with subsequent release of inappropriate thirdgeneration cephalosporin results. Strains escaping ESBL infection control practices may be a reservoir for ESBL enzymes in the hospital environment, undermining control and eradication efforts. Improved laboratory detection of ESBL genes is required in the setting of concomitant pampc genes. 1. Park Y, Park YS, Oh E, et al. Occurence of extended-spectrum B-lactamases among chromosomal AmpC-producing Enterobacter cloacae, Citrobecter freundii, and Serratia marcescens in Korea. Diagn Microbiol Infect Dis. 2005;51(4): Deshpande LM, Jones RN, Fritsche TR, Sader HS. Occurence of plasmidic AmpC type B-lactamase-mediated resistance in Eschericia coli: report from the SENTRY antimicrobial surveillance program (North America, 2004). Int J Antimicrob Agents. 2006;28(6): S2 Establishing In Vitro Susceptibility Standards for Ciprofloxacin against V. cholerae O1 W. A. Khan 1, S. Ahmed 1, M. A. Salam 1, M. L. Bennish 2,3 1Clinical Sciences Division, International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh, 2 Mpilonhle, Mtubatuba, South Africa, 3 Johns Hopkins Bloomberg School of Public Health, Baltimore, MD Objective: Determine appropriate thresholds for ciprofloxacin susceptibility for V. cholerae O1 Background: Current thresholds used for determining in vitro susceptibility of V. cholerae O1 to ciprofloxacin susceptibility are no longer predictive of clinical response. Methods: We correlated clinical response in 242 patients with cholera treated with ciprofloxacin from 1994 to 2003 to in-vitro susceptibility testing of V. cholerae O1 isolates using both disc-diffusion and e-test methods. Results: The 242 V. cholerae O1 isolates were all susceptible to ciprofloxacin when using the disc-diffusion cutoff for susceptibility of zone of inhibition of > 20 mm. In 1994 the MIC90 to CIP of V. cholerae O1 was 0.012µg/ml with clinical success of therapy (resolution of diarrhea in 48 h) occurring in 62/66 (94%) patients, and microbiologic resolution of therapy (inability to isolate V. cholerae O1 after 48 h) in 63/66 (95%) patients. In 2001 the MIC90 was µg/ml, clinical success occurred in 41/78 (60%), and microbiologic success in 33/78 (42%) patients (P < when compared to both clinical and bacteriologic response in 1994). In 2004 the MIC90 was µg/ml, clinical success occurred in 26/98 (27%) of patients, and microbiologic success in 10/98 (98%) of patients (P < when compared to both clinical and bacteriologic response in 2001). Conclusions: V. cholerae O1 strains with diminished susceptibility to ciprofloxacin are deemed susceptible using current susceptibility thresholds. Clinical response is poor, however; and new thresholds need to be defined for use of ciprofloxacin in the treatment of cholera. 1. Saha D, Karim MM, Khan WA, Ahmed S, Salam MA, Bennish ML. Singledose azithromycin for the treatment of cholera in adults. N Engl J Med. 2006;354(23): Das S, Goyal R, Ramachandran VJ, Gupta S. Fluoroquinolone resistance in Vibrio cholerae O1: emergence of El Tor Inaba. Ann Trop Paediatr. 2005;25(3): S3 Genetic Basis of Multidrug Resistance in Acinetobacter baumannii Clinical Strains Isolated at a Tertiary Medical Center in Pennsylvania J. M. Adams-Haduch, H. E. Sidjabat, A. W. Pasculle, B. A. Potoski, D. L. Paterson, Y. Doi Division of Infectious Diseases, University of Pittsburgh Medical Center, Pittsburgh, PA Objective: Discuss the evolving antimicrobial resistance mechanisms in Acinetobacter baumannii Background: Several outbreaks caused by multidrug-resistant (MDR) A. baumannii have been reported in the United States. We recently reported the emergence of A. baumannii producing OXA-23 carbapenemase and ArmA 16S ribosomal RNA methylase at our facility. Methods: Approximately half of all A. baumannii clinical strains isolated between August 2006 and September 2007 qualified as MDR. Of those, 50 non-duplicate MDR strains were available for this study. PCR was performed for various genes encoding imipenem, amikacin and ciprofloxacin resistance genes. Pulsed-field gel electrophoresis was performed to determine the genetic relatedness of the MDR strains. Results: Resistance to imipenem, amikacin and ciprofloxacin were observed in 18%, 38% and 94%, respectively. All strains remained susceptible to colistin and tigecycline. The presence of bla OXA-23 and arma predicted high-level resistance to imipenem and amikacin, respectively. bla OXA-23 was preceded by insertion sequence ISAba1 which likely provided a potent promoter activity. ESBL gene bla CTX-M-2 was also identified in some strains, but its presence did not predict cephalosporin or carbapenem resistance. Typical resistance substitutions in the quinolone resistance-determining regions (QRDRs) of gyra and parc were observed in the ciprofloxacin-resistant strains. Plasmidmediated quinolone resistance genes (qnrs) were not identified. 58% of the MDR strains belonged to a single clonal group. Conclusions: Production of OXA-23, arma and substitutions in QRDRs played a crucial role in development of multidrug resistance among A. baumannii at our facility. 1. Doi Y, Adams JM, Yamane K, Paterson DL. Identification of 16S ribosomal RNA methylase-producing Acinetobacter baumanii clinical strains in North America. Antimicrob Agents Chemother. 2007;51(11):

43 SCIENCE PREVENTION CONTROL 43 ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS S4 Multi-Drug Resistant Acinetobacter sp. Isolates from the Walter Reed Army Medical Center: Correlation of Antibiotic Resistance with Adverse Clinical Outcomes. F. Perez 1, A. M. Hujer 2, K. M. Hujer 2, E. A. Hulten 3, D. J. Ecker 4, D. Aron 2, K. Thweatt 2, C. Donskey 2, J. Adams 5, D. L. Paterson 5, R. A. Bonomo 6 1Division of Infectious Diseases and HIV Medicine, University Hospitals Case Medical Center, Cleveland, OH, 2 Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, OH, 3 Department of Internal Medicine, Walter Reed Army Medical Center, Bethesda, MD, 4 Ibis Biosciences Inc., Carlsbad, CA, 5 Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, 6 Section of Infectious Diseases, Louis Stokes Cleveland VAMC, Cleveland, OH Objective: Describe the link between multi-drug-resistant (MDR) phenotype and adverse outcomes in patients infected with Acinetobacter baumannii. Background: The clinical significance of isolating multi-drug resistant (MDR) Acinetobacter sp. in hospitalized patients merits increasing attention. Here, we evaluated the impact of Acinetobacter sp. infection and/or colonization on the outcomes of 75 patients at the Walter Reed Army Medical Center (WRAMC). Our goal was to determine if certain resistance phenotypes, genes, or clonal types were more likely associated with increased morbidity or mortality. Methods: The medical records of 75 patients were retrospectively examined. They had Acinetobacter sp. infection and/or colonization of the blood, respiratory tract, skin, urinary tract, meninges, and soft tissues. Association between selected resistance determinants and clinical outcomes was investigated through Mann-Whitney U test and chi-square analyses. Isolates from these patients were previously characterized by susceptibility testing, PCR amplification of resistance genes, and two molecular typing methods. There were 73 A. baumannii isolates, 1 Acinetobacter johnsonii, and 1 Acinetobacter genome species 3. Results: Our analysis revealed: 1) an association between the recovery of a carbapenem resistant A. baumannii isolate and requiring mechanical ventilation; and 2) possession of an isolate containing a blaoxa carbapenemase and requiring mechanical ventilation. A link was also uncovered between carbapenem resistance and the duration of this outbreak (i.e., patients with longer lengths of stay were more likely to have a carbapenem resistant Acinetobacter sp. isolate). Lastly, amikacin resistant A. baumannii were associated with hospital acquired infections. Conclusion: The associations between the presence or absence of certain resistance phenotypes or genes and clinical outcomes serve as an important starting point to devise strategies to examine the impact of MDR Acinetobacter sp. on health care delivery systems. 1. Hujer KM, Hujer AM, Hulten EA et al. Analysis of antibiotic resistance genes in multidrug-resistant Acinetobacter sp. isolates from military and civilian patients treated at the Walter Reed Army Medical Center. Antimicrob. Agents Chemother. 2006;50(12): Abbo A, Carmeli Y, Navon-Venezia S, Siegman-Igra Y, Schwaber MJ. Impact of multi-drug-resistant Acinetobacter baumannii on clinical outcomes. Eur J Clin Microbiol Infect Dis. 2007;26(11): S5 Use of Household Cleaning Products Containing Benzalkonium Chloride and Antibiotic Resistance in the Community A. E. Aiello 1, R. Carson 2, S. B. Levy 3, B. Marshall 3, E. L. Larson 4 1Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, 2 Epidemiology, Columbia University, New York, NY, 3Medicine, Tufts University Medical School, Boston, MA, 4Epidemiology and Nursing, Columbia University, New York, NY Objective: Discuss the epidemiological links between biocides use in household cleaning products and emergence of antibiotic resistance in the community setting. Background: Widespread use of antibacterial products containing ingredients such as triclosan or quaternary ammonium compounds such as benzalkonium chloride (BZK) has raised concern about emergence of biocide and antibiotic resistant bacteria in the community setting. We assessed whether antibacterial use influenced susceptibility to BZK among bacteria isolated from individuals in the home over a one year period. Methods: Households (n=238) were randomized to either antibacterial or non-antibacterial cleaning products and bacterial isolates (n=645), including gram negative and staphylococcal species, were isolated from hands of participants at baseline and one year later. Hand isolates were tested for MICs to BZK, triclosan, and several antibiotics. All gram negative bacteria (GNB) were tested against gentamicin, imipenem and ciprofloxacin. Other antibiotics tested with certain species included: amikacin, ticarcillin/clavulanate for Acinetobacter baumannii and A. lwoffii; trimethoprim/sulfamethoxazole for Enterobacter agglomerans and E. cloacae; trimethoprim/sulfamethoxazole, piperacillin/tazobactam, ceftriaxone for Klebsiella pneumoniae; piperacillin/tazobactam, ceftazidime for Pseudomonas fluorescens/putida. Staphylococcal species were tested against oxacillin for methicillin resistance. Logistic regressions with generalized estimating equations were used to assess the relationship between BZK, triclosan, and antibiotic resistance among bacterial species. Results: There were no significant differences between assigned product use and BZK susceptibility for all species combined. However, after one year, there was an association between decreased susceptibility to BZK and triclosan for all species combined (OR = 2.18, 95% CI = 1.44 to 3.29) and between decreased susceptibility to BZK and antibiotic resistance to a combination of several antibiotics (OR = 2.45, 95% CI = 1.38 to 4.36). Conclusions: These findings suggest antibacterial product use may lead to decreased susceptibility to other antibacterial ingredients and antibiotic resistance in the home. 1. Aiello AE, Larson EL, Levy SB. Consumer antibacterial soaps: Effective or just risky? Clin Infect Dis. 2007;45(Suppl 2):S137-S Joynson JA, Forbes B, Lambert RJW. Adaptive resistance to benzalkonium chloride, amikacin and tobramycin: the effect on susceptibility to other antimicrobials. J Appl Microbiol. 2002;93(1): S6 Mupirocin Resistance Among Staphylococcus aureus Isolates After Implementation of a Decolonization Program M. A. Jacobs 1, N. K. Shrestha 1, T. G. Fraser 1, D. A. Wilson 2, G. S. Hall 2 1Infectious Disease, Cleveland Clinic Foundation, Cleveland, OH, 2Clinical Pathology-Microbiology, Cleveland Clinic, Cleveland, OH Objective: Examine the effect of implementation of a selective decolonization program on mupirocin resistance among Staphylococcus aureus (SA) isolates Background: Jones et al. 1 showed a high baseline rate of mupirocin resistance among methicillin resistant SA (MRSA) in the setting of low hospital usage. (continued)

44 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS Since 2007, all SA carriers admitted to our medical intensive care unit (MICU) have been decolonized with mupirocin. We hypothesized that increased mupirocin use might lead to increased mupirocin resistance. Methods: Consecutive isolates of SA were tested, from 99 unique patients each year, in 2006 and Of these, 52 and 54 of 99, respectively, were MRSA isolates. SA was isolated using a selective medium from residual frozen broth previously used for SA PCR testing for colonization. After transferring to verify purity the isolates were suspended in broth to a 0.5 McFarland density and plated on Mueller-Hinton agar. Mupirocin E-test and cefoxitin disks were then placed and the plates incubated at 35 o C for hours. MIC and inhibition zones were read for each isolate and interpreted according to product inserts and previous literature 2. Appropriate control strains were also tested. P-values were computed using the Fisher s exact test. Results: In 2006 one of 99 isolates (1%) had high-level mupirocin resistance, compared with five of 99 (5%) in 2007 (p-value 0.212). All high-level mupirocin resistance occurred in MRSA isolates (2% in 2006 vs. 9% in 2007, p-value 0.206). Total resistance went from 4% in 2006 to 9% in 2007 (p-value 0.251). Conclusions: There was no significant increase in high-level mupirocin resistance in SA one year after beginning selective decolonization in the MICU. However, continued monitoring will be necessary to determine if these findings hold with continued mupirocin use. 1. Jones JC, Rogers TJ, Brookmeyer P, et al. Mupirocin resistance in patients colonized with methicillin-resistant Staphylococcus aureus in a surgical intensive care unit. Clin Infect Dis. 2007;45(5): Palepou MFI, Johnson AP, Cookson BD, Beattie H, Charlett A, Woodford N. Evaluation of disk diffusion and Etest for determining the susceptibility of Staphylococcus aureus to mupirocin. J Antimicrob Chemother. 1998;42(5): S7 Results of a Case-control Investigation of Risk Factors for CA-MRSA in New York City, M. A. Marx 1, H. Cook 1, Z. Rehana 1, D. Krieger 1, A. Yeung 1, Y. Lue 2, A. John 2, D. Duquaine 1, D. Kapell 1, D. Ip 3, J. Mediavilla 4, J. Kornblum 3, B. Kreiswirth 4, D. Weiss 1 1Communicable Diseases, NYC Department of Health and Mental Hygiene, New York, NY, 2 Quest Diagnostics, Teterboro, NJ, 3 Public Health Laboratory, NYC Department of Health and Mental Hygiene, New York, NY, 4 The Public Health Research Institute of New Jersey Medical School/UMDNJ, Newark, NJ Objective: Discuss risk factors for community-associated (CA) Methicillin resistant Staphylococcus aureus (MRSA) in New York City (NYC) men who have sex with men (MSM) Background: Community-associated (CA) Methicillin resistant Staphylococcus aureus (MRSA) incidence is increasing worldwide. Studies have suggested high incidence among men who have sex with men (MSM). We conducted a casecontrol investigation to determine risks for CA-MRSA among MSM. Methods: We received reports of New York City residents diagnosed with Staphylococcus aureus skin, soft tissue infections by a commercial laboratory serving private physicians (Lab A) from April 2005 to September Cases were characterized as CA if they had not: been exposed to a hospital, dialysis, or had an outpatient procedure in 3 months before infection. Controls were all adult men diagnosed with amebiasis or giardiasis July 2006-October 2007 by Lab A. We administered structured questionnaires by phone, addressing demographics and risk behaviors, and determined risks for CA-MRSA among MSM. Results: Of 2813 patients diagnosed with Staphylococcus aureus, 1069 (38%) had MRSA. We interviewed 687 (64%) MRSA patients, 574 (84%) of whom had CA-MRSA. Among CA-MRSA, 373 (65%) were male. Of 347 men reporting sex behaviors, 186 (55%) identified as MSM. We interviewed 295 (70%) controls, 196 (66%) of whom were MSM. Compared to MSM controls, CA-MRSA MSM were more likely to use crystal methamphetamine (OR= 4.0, CI: ) and have physical contact with someone with a skin infection (OR=3.4 CI: ) in 3 months before infection, have sex at private parties in the year before infection (OR=2.9 CI: ), routinely wait to wash >30 minutes after sex (OR=1.8; CI: ), and have HIV/AIDS (OR=2.1, CI: ). Conclusions: Results suggest reduced hygiene and drug use are associated with CA-MRSA in MSM seeking care at private physicians offices. Further investigation is needed to elucidate other mechanisms of transmission. 1. Diep BA, Chambers HF, Graber CJ, et al. Emergence of multidrugresistant, community-associated, methicillin-resistant Staphylococcus aureus clone USA300 in men who have sex with men. Ann Intern Med. 2008;148(4): Lee NE, Taylor MM, Bancroft E, et al. Risk factors for communityassociated methicillin-resistant Staphylococcus aureus skin infections among HIV-positive men who have sex with men. Clin Infect Dis. 2005;40(10): S8 Trends in QRNG and Antibiotic Resistance for Gonorrhea in Los Angeles County: M. Lazzar Los Angeles County Public Health Department, Los Angeles, CA Objective: Describe the importance for ongoing gonococcal antibiotic susceptibility surveillance on a local level Background: The rates of fluoroquinolone-resistant Neisseria gonorrhoeae (QRNG) have increased in California and nationwide over the past several years 1. Multidrug-resistant (MDR) isolates with decreased susceptibility to ceftriaxone are emerging 2. The objective of this study was to identify trends in and characteristics associated with QRNG and MDR-isolates identified in Los Angeles County. Methods: The Gonococcal Isolate Surveillance Project (GISP) monitors trends in antimicrobial susceptibilities throughout the United States. Local sentinel surveillance for gonococcal isolate susceptibility through GISP collected 1021 isolates between Aug and Dec from two clinics - the Los Angeles Gay & Lesbian Center (LAGLC) clinic that primarily serves men who have sex with men (MSM) and South Health Center (SHC) that primarily serves low-income, African-American and Hispanic heterosexuals. Trend analysis by year was completed using correlation coefficients. Multiple-logistic regression was computed to examine the association between QRNG/MDR isolates and sociodemographics and sexual partnership information. Results: From 2003 to 2007 the percentage of QRNG isolates increased from 12% to 21% (correlation 0.11, p<0.01). The percentage of MDR-isolates increased from 13%-24% (correlation 0.11, p<0.01). Five of the seven isolates with alert values to ceftriaxone were also MDR (71%). Increased number of isolates resistant to any antibiotic was associated with younger age (OR=0.69, 95% CI: 0.48, 0.99) and African-American (OR=5.6, 95% CI: 1.6, 19.9). Conclusion: The percentage of QRNG and MDR isolates in Los Angeles are increasing and MDR isolates with alert values to ceftriaxone are emerging. Ongoing gonococcal susceptibility surveillance in Los Angeles, a major gateway into the United States from the Pan-Pacific region, is crucial to monitor the prevalence of emerging resistance and ensure successful treatment and control of gonorrhea. 1. Bauer HM, Mark KE, Samuel M, Wang SA, et al. Prevalence of and associated risk factors for fluoroquinolone-resistant Neisseria gonorrhoeae in California, Clin Infect Dis. 2005;41(6):

45 SCIENCE PREVENTION CONTROL 45 ABSTRACTS OF SUBMITTED ORAL PRESENTATIONS 2. Wang SA, Harvey AB, Conner SM, et al. Antimicrobial resistance for Neisseria gonorrhoeae in the United States, 1988 to 2003: the spread of fluoroquinolone resistance. Ann Intern Med. 2007;147(2): S9 Antibiotic Prescribing by Emergency Room Physicians N. Safdar 1, B. Fox 1, J. E. Svenson 1, R. Wigton 2 1University of Wisconsin, Madison, WI, 2 University of Nebraska, Omaha, NE Objective: Discuss the prescribing decisions of ER physicians Background: Antibiotics are frequently prescribed for treatment of upper respiratory tract infections in the emergency room. To reduce inappropriate overprescribing, it is necessary to understand the factors influencing physicians decision to prescribe antibiotics. Objective: To analyze the judgment policies of emergency room physicians to determine factors predicting antibiotic use. Design: Paper case vignette study. Participants: 104 emergency room practitioners from Wisconsin. Measurements: We used judgment analysis to derive the policies of 104 emergency room practitioners from their responses to 20 case vignettes. We designed the cases such that each practitioner s use of clinical findings and patient factors could be inferred from the decisions they made about each case. Results: Practitioners reported they would prescribe antibiotics in 51% of cases. The majority of practitioners gave the greatest weight to duration of illness (51%, 57/110) followed by temperature (20%, 22/110) and cough (12%, 13/110). Limitations: Prescribing decisions were made in response to paper case vignettes limited to 9 features and not actual patients. Conclusions: Based on hypothetical cases of acute respiratory tract infections, ER physicians appear to prescribe antibiotics far more frequently than recommended by CDC guidelines. Practitioners were most strongly influenced by duration of illness. Further research is needed to determine strategies to reduce overprescribing of anti-infectives. teaching hospital developed a scope of work that was implemented over the ensuing 5 years (2003 to 2007). General interventions included: 1. monitoring antimicrobial use by a) following defined daily doses per 1000 patient days, and b) tracking pharmacy drug procurement budget represented by antimicrobials; 2. monitoring antimicrobial resistance by a) observing trends for select bug/drug combinations, and b) tracking C. difficile rates and rates of nosocomial bacteremia/candidemia; 3.Institution-wide discouragement of quinolone and ceftazidime use; and 4. educational and infection control strategies e.g., Pocket Card, website, alcohol hand sanitizers. Specific interventions included the development and implementation of febrile neutropenia and ventilator associated pneumonia protocols, both centered on antimicrobial cycling. Results: Time trends revealed that quinolone and ceftazidime use declined by 81% and 37% respectively; the proportion of pharmacy budget attributed to antimicrobials decreased from 16% in 2003 to 10% in Ciprofloxacin resistant Pseudomonas and Acinitobacter decreased but E. coli increased (from 2% to 17%). Ceftazidime resistant Klebsiella remained stable at around 5%. The proportion of nosocomial bacteremia due to MRSA decreased (from 20% to 10%) while VRE bacteremia, candidemia, and C. difficile rates remained stable. Conclusions: Multifaceted, institution wide and unit specific programs centered on collaboration and educational strategies appear reasonably successful in affecting institutional antimicrobial use and resistance but appear not to influence the problem of imported resistance. 1. Dellit TH, Owens RC, McGowan JE, et al. Infectious Disease Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship. Clin Infect Dis. 2007;44(2): Tamayo-Sarver JH, Dawson NV, Cydulka RK, Wigton RS, Baker DW. Variability in emergency physician decision making about prescribing opioid analgesics. Ann Emerg Med. 2004;43(4): S10 Efforts to Influence Antimicrobial Use and Resistance at a Tertiary Care Institution Using Collaborative Multifaceted Interventions A. R. Sarwari 1, K. O. Petros 2, R. B. Sager 2, C. J. Mullett 3, J. Thomas 4, P. Miller-Canfield 4, H. V. Dedhia 5, A. Wilson 6, D. Slain 7, K. Moffett 3, H. C. Palmer, Jr 8 1Infectious Diseases, West Virginia University, Morgantown, WV, 2Pharmacy, West Virginia University Hospitals, Morgantown, WV, 3Pediatrics, West Virginia University, Morgantown, WV, 4 Clinical Microbiology, West Virginia University, Morgantown, WV, 5Pulmonary Critical Care Medicine, West Virginia University, Morgantown, WV, 6 Surgery, West Virginia University, Morgantown, WV, 7 School of Pharmacy, West Virginia University, Morgantown, WV, 8 Internal Medicine, West Virginia University, Morgantown, WV Objective: Discuss the complex interaction between antimicrobial use and antimicrobial resistance Background: The relationship between antimicrobial use and resistance is complex and influenced by antimicrobial stewardship and infection control programs. General and specific interventions need to be multifaceted and collaborative to affect the overall resistance patterns in an institution. Methods: The Antimicrobial Stewardship Program at a tertiary care university

46 Conference on Antimicrobial Resistance ABSTRACTS OF OF SUBMITTED POSTER ORAL PRESENTATIONS ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS

47 SCIENCE PREVENTION CONTROL 47 ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P1 Use of Cefepime versus Gentamicin as Empiric Therapy in Catheter-related Bloodstream Infections in Hemodialysis Patients H. R. Jimenez 1, J. Slim 1, R. Khan 2, K. Patel 2 1Infectious Disease, St. Michael s Medical Center, Newark, NJ, 2Ernest Mario School of Pharmacy, Rutgers University Background: Gram-negative bacteremia now represents approximately one-third of catheter-related bloodstream infections in hemodialysis patients. At our institution, patients admitted with suspected line infections are empirically treated with vancomycin and cefepime. We sought to review the susceptibility of gram-negative bacteria (GNB) in hemodialysis patients to cefepime, and determine if gentamicin would be a suitable alternative. Methods: The study was a retrospective review of all patients on hemodialysis who developed gram-negative bacteremia between August, 2006 and December, The primary endpoint was to compare the susceptibility of cefepime and gentamicin using the MicroScan WalkAway system. Intermediate susceptibility was recorded as resistant. Secondary measures were percentage of bacteria resistance or susceptibility to both and identification of common pathogens. Duplicate cultures (within 30 days) were not included. Results: There were a total of 67 isolates. The most common organisms were Klebsiella pneumonia (26.9%), Escherichia coli (16.4%), Enterobacter cloacae (14.9%), Proteus mirabilis (9.0%), and Acinetobacter baumanni (9.0%). The GNB cultured was sensitive to cefepime 61.2% of the time. Gentamicin susceptibility was 56.7%. Pathogens were usually sensitive or resistant to both agents (44.8% and 26.9%, respectively). Discussion: This study illustrated that the use of cefepime as part of empirical therapy for line infections is not appropriate for hemodialysis patients at our institution. Gentamicin, however, would not be an acceptable alternative due to its lower susceptibility rate. Since most of the isolates demonstrated either susceptibility or resistance to both agents (71.7%), combining these agents would not be suitable either. Conclusion: Empiric treatment strategies will be changed at our institution for this subpopulation. Further studies are needed to determine the best antimicrobial option. 1. Sullivan R, Samuel V, Le C, et al. Hemodialysis vascular catheter-related bacteremia. Am J Med Sci. 2007;334(6): Alexandraki I, Bhatt MD, Plott DT, et al. Hemodialysis vascular catheterrelated bacteremia: five year epidemiologic shift in organism isolates. J Am Soc Nephrol. 2005; 16:435A. P2 Staphylococcus aureus from Public Hospitals in Kwa-Zulu Natal: Infection Detection and Strain Typing Z. Essa, S. Y. Essack Pharmacy, University of Kwazulu-Natal, Durban, South Africa Staphylococci have demonstrated a remarkable ability to adapt to antibiotic treatment protocols. The continuous dissemination of strains resistant to methicillin and other antibiotics has implicated S. aureus particularly methicillin resistant Staphylococcus aureus (MRSA) in many fatal infections. Rapid, reliable, reproducible and cost-effective methods for the detection of MRSA are thus particularly important for the containment of this organism. 242 S. aureus isolates collected from 16 hospitals in Kwa-zulu Natal were subjected to antibiotic susceptibility testing using the CLSI disc sensitivity testing method. 24 randomly selected putative MRSA and matched control of MSSA isolates were subjected to agar based methods, the E-test and Screen Latex Agglutination methods for MRSA detection using PCR as the gold standard. Multi-locus strain typing (MLST) was carried out on the 48 isolates to determine the relatedness of clones to those seen worldwide. S. aureus was implicated in a range of infections. Sensitivity, specificity, positive-predictive values, negative-predictive values and costs of the various detection tests showed that the use of oxacillin disk agar diffusion and oxacillin screening salt agar was appropriate for routine laboratory testing for the identification of MRSA in resource constrained healthcare settings. MLST identified the ST5 (paediatric), ST8 (EMRSA-2, EMRSA-6 and Irish-1), ST45 (Berlin), and ST239 (EMRSA-1, EMRSA-4, EMRSA-11Por/Bra, Vienna) clones. Infections by MRSA are a public health concern in South Africa as is the case worldwide. Antibiotic prescribing trends may account for the de novo evolution of strains identified globally. Prudent antibiotic use and routine surveillance for MRSA is advocated in a South African healthcare system experiencing increasing incidence and prevalence of infections as a result of HIV and AIDS. 1. Nagarajan V, Elasri MO. SAMMD: Staphylococcus aureus microarray metadatabase. BMC Genomics. 2007;8: de Lencastre H, Oliveira D, Tomasz A. Antibiotic resistant Staphylococcus aureus: a paradigm of adaptive power. Curr Opin Microbiol. 2007;10(5): P3 Treatment Guidelines and Nosocomial Infections: The KwaZulu-Natal Experience S. Y. Essack Pharmacy, University of Kwazulu-Natal, Durban, South Africa Nosocomial infections are highly communicable in under-resourced hospital settings and are amongst the major causes of morbidity and mortality in hospitalized patients where intensive antimicrobial use, overcrowded conditions and large numbers of ill people drive the emergence and dissemination of multi-resistant pathogens. This study evaluated nationallydevised standard treatment guidelines (STGs) for nosocomial infections in the context of antibiotic resistance within the public health care system in Kwazulu-Natal. A multi-centre surveillance study was undertaken in 3 hospitals (district, regional, and tertiary) where 100 isolates commonly implicated in nosocomial infections were subjected to susceptibility testing using the CLSI disc diffusion method. Susceptibility to antibiotics recommended in the STGs and hence potentially successful empiric therapy ranged from 2% to 81% with multi-resistance evident in all isolates. Statistically significant (p<0.05) differences in susceptibility against antibiotics recommended as empiric therapy were evident as were differences in the susceptibilities of common nosocomial organisms. This study showed that resistance profiles amongst bacteria vary too much to allow a national antibiotic policy as proposed in the STGs. Rather, such guidelines should be directed to specific profiles found in different hospitals and at different levels of health care. Regular surveillance to adjust such guidelines in combination with stringent infection control is essential to the containment of nosocomial infections. 1. Ducel G, Fabry J, Nicolle L (eds). Prevention of Hospital-Acquired Infections: A Practical Guide, 2nd edition. Geneva, Switzerland:World Health Organization, 2002, pp Blondeau JM, Tillotson GS. Formula to help select rational antimicrobial therapy (FRAT): its application to community- and hospital-acquired urinary tract infections. Int J Antimicrob Agents. 1999;12(2):

48 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P4 Azithromycin Minimum Inhibitory Concentration (MICs) for Shigella sonnei Isolated from Humans in the United States R. L. Howie 1, J. Folster 1, A. Bowen 2, E. Barzilay 2, K. Joyce 1, J. Whichard 2 1Atlanta Research and Education Foundation, Atlanta, GA, 2Centers for Disease Control and Prevention, Atlanta, GA Although azithromycin is not currently labeled by the Food and Drug Administration to treat Shigella infections, the American Academy of Pediatrics recommends azithromycin for multidrug-resistant shigellosis due to the drug s properties of concentrating in the gastrointestinal tract, high tissue concentration level, and relatively long half-life. Concerns have recently arisen over the emergence of resistance in outbreaks where azithromycin has been used. These concerns are complicated by the fact that, as it is not currently an antibiotic labeled for use against gram negative organisms, there are no guidelines for what constitutes resistance of Shigella to azithromycin. This study examined the azithromycin MICs of recent outbreak and routine Shigella sonnei isolates. Fifty-six representative isolates from outbreaks were received by CDC in 2006 and 2007 (outbreak study, OS); 336 routine isolates submitted by 54 state and local public health laboratories to the National Antimicrobial Resistance Monitoring System (NARMS) in 2005 were included. Isolates were tested by broth microdilution using frozen azithromycin panels from Trek Diagnostics (Westlake, Ohio), according to manufacturer s instructions. MIC 50 and MIC 90 were calculated as the concentrations required for inhibition of 50% and 90% of strains, respectively. MIC 50 for both groups was 8µg/mL; the MIC 90 was 16µg/mL for OS and 8µg/mL for NARMS isolates. One OS and two NARMS isolates showed unexpectedly high MICs ( µg/mL). Azithromycin MIC distributions are similar for OS and NARMS Shigella sonnei. The MIC 50 for both groups was higher than previously reported (1µg/mL in 1987 and 1993). Different methodologies including the previous use of E-test and disk diffusion methods may have contributed, or this may indicate an increase in azithromycin MICs for Shigella sonnei over time. 1. Retsema J, Girard A, Schelkly W, et al. Spectrum and mode of action of azithromycin (CP-62,993), a new 15-membered-ring macrolide with improved potency against gram-negative organisms. Antimicrob Agents Chemother. 1987;31(12): Gordillo ME, Singh KV, Murray BE. In vitro activity of azithromycin against bacterial enteric pathogens. Antimicrob Agents Chemother. 1993;37(5): P5 Cost of Methicillin-resistant Staphylococcus aureus (MRSA) Infection in the Neonatal Intensive Care Unit J. L. Murillo 1, Y. Xavier 2, M. Cohen 3 1Clinical Services, Saint Barnabas Health Care System, West Orange, NJ, 2 Decision Support, Saint Barnabas Health Care System, West Orange, NJ, 3 Neonatal Medicine, Children s Hospital of New Jersey, Newark, NJ Background: While the attributable cost of MRSA infection is frequently reported in adult infections, very little data is available for neonatal infections. We report our estimate of the cost of MRSA infection in premature infants. Method: Financial data was retrospectively collected for MRSA-infected neonates admitted to an inner-city Level 3 neonatal intensive care unit in 2005 and compared with non-infected controls matched for birth weight and gestational age. Length of stay was also compared between the two groups. Results: Mean cost of hospitalization for 17 infected infants was $106,359 (95% CI $79,967-$132,750) versus $58,337 (95% CI $40,912-$75,762), p<0.01 for non-infected infants. The attributable cost of MRSA infection was estimated to be $48,022 per infected case. The length of stay was significantly different with 63.9 days (95% CI ) for MRSA-infected infants versus 42.4 days (95% CI ), p=0.02 for non-infected neonates. Conclusion: MRSA-infected neonates stay longer in the hospital and consume more resources resulting in increased cost of hospitalization. 1. Rubin RJ, Harrington CA, Poon A, Dietrich K, Greene JA, Moiduddin A. The economic impact of Staphylococcus aureus infections in New York City hospitals. Emerg Infect Dis. 1999;5(1): Reed SD, Friedman JY, Engemann JJ, et al. Cost and outcomes among hemodialysis-dependent patients with methicillin-resistant or methicillinsusceptible Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol. 2005;26(2): P6 New Derivatives of para-aminosalicylic Acid and Their Activities against Drug-Resistant Mycobacterium tuberculosis M. Hearn 1, M. Chen 1, M. Cynamon 2, C. Schlemme 1, R. Wang ondu 1 1Department of Chemistry, Wellesley College, Wellesley, MA, 2Veterans Affairs Medical Center, Syracuse, NY Background: Para-Aminosalicylic acid (PAS) is frequently included in therapeutic regimens against infection with multiple-drug resistant (MDR) tuberculosis (TB). Such amine-containing antituberculars are subject to chemical modification by N-arylaminoacetyl transferases, found in both mycobacteria and their mammalian hosts. At present, very little is known about the general effects of acylation on either drug properties or antimicrobial activities of PAS derivatives. We were thus interested in evaluating in vitro the results of such acylation on the antitubercular activities of these compounds. Methods: A series of the title compounds was prepared using the methods of synthetic organic chemistry. MTB ATCC (strain Erdman) was obtained from the American Type Culture Collection, Manassas, Virginia. Other strains included drug-resistant clinical isolates, for which the mutational origins of resistance were well-defined. The minimum inhibitory concentrations (MICs) were determined by a broth dilution method in modified 7H10 broth. Positive controls included PAS (MIC µg/ml) and isoniazid (MIC 0.03 µg/ml). Results: By management of reaction conditions, controlled chemoselective functionalization was readily achieved in good yields at either the amine function or at both the amine and phenol functions of methyl 4-aminosalicylate. A representative compound displayed in vitro activities of less than 0.2 µg/ml against the following organisms: H37Rv, Erdman, EMB-R, INH-R, RMP-R, ETA-R and TAC-R. Conclusions: The structural variety made possible by our chemoselective acylation reactions permits exploration of activity factors in these compounds. A number of these substances had substantial inhibition against TB. 1. Hearn MJ, Cynamon MH. In vitro and in vivo activities of acylated derivatives of isoniazid against Mycobacterium tuberculosis. Drug Des Discov. 2003;18(4): Hearn MJ, Chen MF, Cynamon MH, Wang ondu R, Webster E. Preparation and properties of new antitubercular thioureas and thiosemicarbazides. J Sulfur Chem. 2006;27(2):

49 SCIENCE PREVENTION CONTROL 49 ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P7 Comparison of Three Methods used for the Identification of Campylobacter spp., NARMS Human Isolates, 2005 J. Smith 1, J. Pruckler 2, A. Stuart 1, K. Joyce 1, F. Medalla 2, E. Barzilay 2, J. Whichard 2, C. Fitzgerald 2 1Atlanta Research and Education Foundation (AREF), Decatur, GA, 2Centers for Disease Control and Prevention (CDC), Atlanta, GA Background: Campylobacter is a leading cause of gastroenteritis in humans; almost all infections are caused by C. jejuni or C. coli. There are several phenotypic and genotypic methods available for the identification of Campylobacter species. The objective of this study was to compare three methods for the identification of species of presumptive Campylobacter isolates submitted to the National Antimicrobial Resistance Monitoring System (NARMS). Methods: In 2005, 10 states participating in the Foodborne Diseases Active Surveillance Network (FoodNet) submitted a representative sample of Campylobacter isolates received from clinical/reference laboratories. One hundred and sixteen presumptive Campylobacter isolates were selected from among 981 isolates submitted to NARMS in The species was identified for each selected isolate using three methods. Method A involved traditional biochemical testing (hippurate, oxidase, and catalase) in combination with dark-field microscopy and Campylobacter species-specific PCR assays. Method B was a C. jejuni and C. coli specific BAX PCR (DuPont Qualicon, Wilmington, DE). Method C was a multiplex real-time PCR assay targeting the 16S rrna gene, ceue gene, and mapa gene for the identification of Campylobacter genus, C. coli, and C. jejuni respectively. Results: All three methods agreed 100% of 116 selected isolates; 102 (88%) isolates were identified as C. jejuni and 11 (9%) isolates as C. coli. Three isolates were negative by all three methods and determined not to be Campylobacter isolates. Conclusions: Methods A, B, and C can be used to accurately identify C. jejuni and C. coli without major discrepancies. However, further validation of these methods with other Campylobacter species and sample sources is warranted. Factors such as cost and time should also be assessed for determining the method of choice. 1. Fitzgerald C, Nachamkin I. Campylobacter and Arcobacter, Chapter 59 in Manual of Clinical Microbiology, 8th edition. Washington, DC, ASM Press, 2006, pp Pruckler J, Fields PI, Fitzgerald C. Comparison of four real-time PCR methods for the identification of the genus Campylobacter and speciation of C. jejuni and C. coli. American Society for Microbiology 106th General Meeting; PosterC282. P8 The Detection of Synergy Between Meropenem (MER) and Polymyxin B (PB) Against MER-Resistant Acinetobacter baumannii Using Etest and Time-Kill Assay (TKA) G. A. Pankey, D. S. Ashcraft Infectious Disease Research, Ochsner Clinic Foundation, New Orleans, LA Background: The incidence of multi-drug resistant A. baumannii infections is increasing. Antimicrobial synergy might be useful, but there is no standardized method for in vitro synergy testing. We elected to compare two methods. Methods: Eight genetically unique U.S. MER-resistant (Etest MICs: 24- >32μg/ml) A. baumannii isolates were collected in All isolates were resistant to beta-lactams and fluoroquinolones but susceptible to PB (Etest MICs: all 0.5 μg/ml). Synergy testing, using a concentration equal to the MIC, was performed in duplicate by standard TKA at 0h and 24h (synergy: > 2 log 10 decrease in CFU/ml after 24h by the combination compared to the most active single agent) and in triplicate by Etest (synergy: summation fractional inhibitory concentration > 0.5). TKA was also performed using ¼ and ½ the MIC of PB in combination with MER. Results: TKA showed synergy (100%) with all combinations of PB and MER for all 8 isolates. The Etest method showed synergy in 63% (5/8) isolates. Two of three isolates not showing synergy by Etest had a MER MIC >32μg/ml. The concentration on the Etest strip may limit the use of the Etest synergy method to isolates with a MIC not exceeding the strip concentration. There was no antagonism found. Conclusions: In vitro synergy may or may not translate into in vivo benefit, but if so, a lower dose of PB combined with MER might prove both efficacious and less toxic. 1. Pankey GA, Ashcraft DS. In vitro synergy of ciprofloxacin and gatifloxacin against ciprofloxacin-resistant Pseudomonas aeruginosa. Antimicrob Agents Chemother. 2005; 49(7): Pankuch GA, Gengrong L, Seifert H, Appelbaum PC. Activity of meropenem with and without ciprofloxacin and colistin against Pseudomonas aeruginosa and Acinetobacter baumannii. Antimicrob Agents Chemother. 2008;52(1): P9 Impact of Methicillin Resistance on Patient Response to Daptomycin for Treatment of Skin and Skin Structure Infections K. Lamp Cubist Pharmaceuticals, Lexington, MA Background: Methicillin resistance (MR) is frequently identified as a contributor to clinical failure and increased hospitalization costs for skin and other infections. 1 Daptomycin has equivalent activity against methicillinresistant (MRSA) and -susceptible S. aureus (MSSA). Methods: Patients with only skin and skin structure infections (SSSI) and S. aureus identified as the primary pathogen were identified in a registry - The Cubicin Outcomes Registry and Experience (CORE) Patients nonevaluable for outcome (52 of 486, 11%) were excluded. Outcome was assessed at the end of daptomycin therapy. Success was defined as cure or improved. Results: Four hundred thirty-four patients were identified; 338 (78%) MRSA and 96 (22%) MSSA. An analysis of demographics identified differences in the MRSA cohort; lower incidence of diabetes (28% vs 41%, P=0.02), fewer patients on dialysis at the initiation of daptomycin (1.5% vs 7.3%, P=0.008) and higher incidence of uncomplicated SSSI (29% vs 18%, P=0.04). These characteristics had no effect on clinical outcomes. Clinical success was achieved in 96% of MRSA and 95% of MSSA pts; P=0.5. Daptomycin was begun as first line therapy in 95 patients (22%). The most frequent prior antibiotic therapy was vancomycin (MRSA, 46%, MSSA, 45%); about one-third of these switched to daptomycin due to vancomycin failure. The median daptomycin dose was similar for MRSA (4 mg/kg, range mg/kg; 56% 4mg/kg) and MSSA (4 mg/kg, range mg/kg; 59% 4mg/kg). The median daptomycin duration was 13 days for MRSA (range 1-243) and 11 days for MSSA (range 1-64) days); P=0.4. Adverse events possibly related to daptomycin; MRSA 18 (5%) patients and MSSA 9 (9%) patients. Conclusions: In this population, daptomycin was effective for SSSI with similar outcomes for MRSA and MSSA. 1. Engemann JJ, Carmeli Y, Cosgrove SE, et al. Adverse clinical and economic outcomes attributable to methicillin resistance among patients with Staphylococcus aureus surgical site infection. Clin Infect Dis. 2003;36(5): Kopp BJ, Nix DE, Armstrong EP. Clinical and economic analysis of methicillin-susceptible and -resistant Staphylococcus aureus infections. Ann Pharmacother. 2004;38(9):

50 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P10 Resistance to Third-Generation Cephalosporins in E. coli Isolates from Outpatients, A. L. Krueger Enteric Diseases Epidemiology Branch, CDC, Atlanta, GA Background: In recent years, human E. coli isolated from urinary tract infections and bloodstream infections have been increasingly resistant to third-generation cephalosporins such as ceftriaxone. The source of these resistant isolates is not well described and may be associated with the use of third-generation cephalosporins in humans. However, questions have been raised about the possible carriage of resistant E. coli in the human intestinal flora of healthy people, which may reflect the prevalence of resistant E. coli in the food supply. This may be influenced by the use of ceftiofur, a thirdgeneration cephalosporin in food animals. Methods: Each month, , participating sites in Maryland and Michigan collected 10 stool samples from outpatients who were not residents of a nursing home or hospitalized in the previous six months and cultured the samples on a selective plate of 2µg/mL cefotaxime for E. coli. E. coli isolates were susceptibility tested at CDC to 15 antimicrobial agents using broth microdilution (Sensititre ). CLSI interpretation criteria were used for ceftriaxone; ceftiofur resistance was defined as MIC>8µg/mL, decreased susceptibility to ceftriaxone as MIC?2µg/mL. Results: Of 553 stool specimens submitted, 350(63.3%) yielded E. coli. Of 350 E. coli isolates, 4(1%) were ceftiofur-resistant. All 4 ceftiofur-resistant isolates had decreased susceptibility to ceftriaxone. Conclusion: The human intestinal tract may be an important reservoir of E. coli resistant to third-generation cephalosporins. Further studies are needed to understand the contribution of the food supply and the potential contribution of ceftiofur use in food animals to this resistance. 1. van den Bogaard AE, Stobberingh EE. Epidemiology of resistance to antibiotics. Links between animals and humans. Int J Antimicrob Agents. 2000;14(4): Srinivasan V, Gillespie BE, Nguyen LT, Headrick SI, Murinda SE, Oliver SP. Characterization of antimicrobial resistance patterns and class 1 integrons in Escherichia coli O26 isolated from humans and animals. Int J Antimicrob Agents. 2007;29(3): P11 Surveillance for Mupirocin Resistance among MRSA Clinical Isolates V. Raju, K. Mongkolrattanothai, P. Mankin, B. Gray Pediatrics, University of Illinois College of Medicine at Peoria and The Children s Hospital of Illinois at OSF St. Francis Medical Center, Peoria, IL Background: Mupirocin is widely used to reduce MRSA colonization as a measure to control the spread of MRSA. However, there are few data on actual resistance rates and no approved methods for testing mupirocin susceptibility. Although the importance of low level resistance may be subject to debate, high level resistance is regularly associated with treatment failure. We undertook this survey in anticipation of the possibility that the emergence of mupirocin resistance could limit therapeutic options available for control of MRSA. Methods: We evaluated 156 MRSA clinical isolates, collected from July to October, 2007, for mupirocin resistance by disk diffusion using 5-μg and 20-μg disks, and for minimal inhibitory concentrations (MICs) by E-test. High level resistance was defined by an MIC > 512 μg/ml and confirmed by the detection of the mupa gene by PCR. Isolates with low level resistance had MICs of μg/ml. Results: Mupirocin resistance was detected in 37 isolates (24%). High level resistance was found in 8 strains (5%), all of which were confirmed to have the mupa gene. Low level resistance was found in 29 (19%), of which none had the mupa gene. The 5-μg disk was fairly reliable in detecting resistance, depending on the breakpoint used. Only the Etest accurately distinguished high from low level resistance. Mupirocin-resistant MRSA isolates were more likely to be resistant to clindamycin and levofloxacin. Conclusions: A relatively high rate of mupirocin resistance was revealed in our survey, possibly reflecting our hospital policy of treating most MRSA carriers in high-risk nursing units. Ongoing accurate surveillance will be needed to monitor resistance rates, inform our drug use policies, and preserve the utility of an important antibiotic. 1. Cookson BD. The emergence of mupirocin resistance: a challenge to infection control and antibiotic prescribing practice. J Antimicrob Chemother. 1998;41(1): Deshpande LM, Fix AM, Pfaller MA, Jones RM; SENTRY Antimicrobial Surveillance Program Participants Group. Emerging elevated mupirocin resistance rates among staphylococcal isolates in the SENTRY Antimicrobial Surveillance Program (2000): correlations of results from disk diffusion, Etest and reference dilution methods. Diagn Microbiol Infect Dis. 2002;42(4): P12 Prevalence of Antibiotic Resistance of Escherichia coli Blood Isolates Y. Cho 1, Y. Park 1, J. Kim 1, L. Zhang 2, B. Foxman 3 1Department of Internal Medicine, Gil Medical Center, Incheon, Republic of Korea, 2 Department of Epidemiology University of Michigan School of Public Health, Center for Molecular and Clinical Epidemiology of Infectious Diseases, Ann Arbor, MI, 3Department of Epidemiology, Center for Molecular and Clinical Epidemiology of Infectious Diseases, Ann Arbor, MI Background: Even when community acquired (CA), Escherichia coli causing blood stream infections (BSIs) are increasingly resistant to newer antibiotics. Methods: We conducted a retrospective cohort study of patients in Korea diagnosed with E. coli BSI between We classified community-onset (CO) E. coli BSIs into CA and healthcare-associated (HCA) BSI. Results: A total of 462 first isolates from 460 patients with E. coli BSI were enrolled (median age[range], 65[19-101] years; male/female, 148/314). Urinary (245) and hepatobiliary (132) pathogens accounted for 81.6% of all E. coli BSIs. The proportion resistant to TMP/SXT, gentamicin, ciprofloxacin and cefotaxime was 29.2%, 21.8%, 27.6% and 10.6% respectively. Prevalence of antibiotic resistance was significantly higher among hepatobiliary than urinary isolates (ciprofloxacin 36.4% versus 22.9%, P<0.01; cefotaxime 23.5% versus 3.7%, P<0.01). Both isolates of urinary and hepatobiliary origin from patients with HA or HCA BSI had significantly higher prevalence of ciprofloxacin (urinary: 44.8% and 26.2% vs. 17.4%; hepatobiliary: 52.9% and 40.9% vs. 20.4%) and cefotaxime resistance (urinary: 17.2% and 6.6% vs. 0%; hepatobiliary: 35.3% and 25.0% vs. 5.6%) than CA isolates. Gentamicin resistance was significantly higher among HA or HCA BSIs of hepatobiliary origin, but there was no difference in resistance among BSI of urinary origin. Almost 6-9% of HA and HCA isolates from both sites were ESBL positive; only 1 community isolate was and it was of hepatobiliary origin. TMP/SMX resistance levels were similar in all groups. Conclusions: Even in an area with high rates of antibiotic resistance, patterns of resistance vary strongly among patient populations. To minimize selection pressure on CA organisms, patient population should be taken into account when choosing BSI therapy. Reference: 1. Peralta G, Sánchez MB, Garrido JC, et al. Impact of antibiotic resistance and of adequate empirical antibiotic treatment in the prognosis of patients with Escherichia coli bacteraemia. J Antimicrob Chemother. 2007;60(4):

51 SCIENCE PREVENTION CONTROL 51 ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P13 Rapid Antimicrobial Susceptibility Testing of Human Pathogens R. Rieder, B. Zavizion BioSense Technologies, Inc., Woburn, MA Background: A novel method for the antibiotic susceptibility testing (AST) of infectious bacteria is presented that provides results in under one hour. Currently used culture-based AST methods require up to several days to obtain results for many bacteria because of their reliance on bacterial population growth to reach detectable changes in the total biomass. The long time required to acquire test results can result in the prescription of inappropriate drug therapies and the consequential spread of antibiotic resistance. Methods: The susceptibility of bacteria to antimicrobial compounds was measured using a new approach that relies on quantitative measurements of the bacterial stress response during exposure to antibiotics. Measurements of the stress response are optimally implemented by monitoring subtle changes in the dielectric properties of the suspension using impedance sensing. The stress response is both immediate and more intense than the response from normal growth enabling test results to be obtained rapidly. Results: Data were obtained for Escherichia coli, Neisseria gonorrhoeae, Staphylococcus aureus, and other common pathogens. Stress responses were measured for strains of these species known to be both resistant and susceptible to first line antibiotics in less than one hour and were correlated with known susceptibilities (MIC). Conclusions: Monitoring the stress response of pathogenic bacteria treated with antibiotics in contrast to monitoring changes in the biomass of the population is an effective way to obtain antibiotic susceptibility/resistance profiles rapidly. The ability to measure susceptibility and identify drug resistance in less than one hour for pathogenic organisms has been successfully demonstrated for several first-line antibiotics commonly prescribed. 1. Centers for Disease Control and Prevention. Update to CDC s sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. 2007:56(14): Manges AR, Johnson JR, Foxman B, et al. Widespread distribution of urinary tract infections caused by a multidrug-resistant Escherichia coli clonal group. N Engl J Med. 2001;345(14): P14 Engineering the Bactericidal Spectra of R-type Pyocins for Use as Antimicrobial Agents D. Scholl, S. Williams, D. Gebhart, D. Martin AvidBiotics, South San Francisco, CA Background: R-type pyocins are high molecular weight Pseudomonas aeruginosa bacteriocins that resemble the tail apparatus of Myoviridae bacteriophages. These structures have a narrow bactericidal spectrum, typically killing a subset of other P. aeruginosa strains. R-type pyocins have many desirable properties for antibacterial applications; they are potent, MICs are extremely low (pg/ml), they have no known toxicities, are composed entirely of proteins, their mechanism of action is unrelated to known antibiotic resistance mechanisms, and they are effective in vivo. However their species-specific spectra severely limit the applications of natural R-type pyocins. To be useful antimicrobials pyocins require retargeted killing spectra. Methods: The killing spectrum of an R-type pyocin is determined primarily by the tail fiber proteins which bind to specific bacterial surface structures. By making molecular fusions of the baseplate binding region of the R2 tail fiber to the receptor recognizing region of different bacteriophage tail proteins, we changed the binding specificity, and thereby killing spectrum, of the pyocin to that of the donor bacteriophage. Results: We have made R2 pyocin tail fiber/phage tail spike or fiber fusions using donor phages specific for E. coli O157:H7, several Salmonella serovars, and Yersinia pestis, all of which, when incorporated into the pyocin structure, change the spectrum of the pyocin to the targeted bacteria. Conclusions: Changing the binding specificity of R-type pyocin tail fibers is sufficient to change its killing spectrum to other bacterial species and therefore can be targeted to a pathogen of interest. These agents may be effective for treating specific pathogenic bacteria without causing collateral damage to commensals. Reference: 1. Scholl D, Martin DW Jr. Antibacterial efficacy of R-type pyocins towards Pseudomonas aeruginosa in a murine peritonitis model. Antimicrob Agents Chemother Mar 10; [Epub ahead of print]. P15 E. coli Resistance to Targeted R-type Pyocins Forces Loss of Virulence Factor D. Scholl, D. Martin AvidBiotics, South San Francisco, CA Background: R-type pyocins are high molecular weight, phage tail-like bacteriocins of Pseudomonas aeruginosa. We have shown that it is possible to retarget the bactericidal spectra of these protein complexes by altering the tail fiber, the main spectrum determinant. In one such construct, termed R2-V10, we fused a tail spike protein from E. coli O157:H7-specific bacteriophage phiv10 to the baseplate-binding region of the R2 pyocin tail fiber. Pyocin particles that incorporate this fusion specifically kill E. coli that produce the O157 antigen. We have shown that R2-V10 pyocin specifically degrades the O157 LPS. Methods: Mutants of E. coli EDL933 (O157:H7) selected for resistant to R2-V10 were isolated spontaneously, after chemical mutagenesis, or after transposon mutagenesis. LPS from the R2-V10 resistant mutants were extracted and analyzed by SDS PAGE. Results: Of 12 independently isolated R2-V10 resistant mutants, all had lost or had greatly reduced high molecular weight O antigen. Transposon mutants mapped either in the O-antigen gene cluster itself or some metabolic gene that likely knocks out an LPS precursor. Conclusions: The engineered R-type pyocin R2-V10 is a candidate antimicrobial agent for E. coli O157:H7 that specifically targets the O157 antigen as its receptor. All isolated resistant mutants have lost the O antigen receptor. Since this polysaccharide is a known virulence factor that is necessary for intestinal colonization in infant rabbits, R2-V10 resistance mutants can be expected to have compromised virulence. Thus we demonstrate the principle that R-type pyocins targeting virulence factors forces resistant mutants to have a virulence-compromised phenotype. 1. Ho TD, Waldor MK. Enterohemorrhagic Escherichia coli O157:H7 gal mutants are sensitive to bacteriophage P1 and defective in intestinal colonization. Infect Immun. 2007;75(4): Scholl D, Martin DW Jr. Antibacterial efficacy of R-type pyocins towards Pseudomonas aeruginosa in a murine peritonitis model. Antimicrob Agents Chemother Mar 10; [Epub ahead of print].

52 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P16 Differences in Outpatient Antibiotic Treatment Perception Among Health Care Providers K. C. Lindfield, L. A. Scoppettuolo, W. J. Martone, D. E. Katz Clinical Development/Medical Affairs, Cubist Pharmaceuticals, Lexington, MA Objective: To discuss factors that may influence outpatient antibiotic treatment (OPAT) usage patterns. Background: OPAT use has grown rapidly in recent years. In the US, OPAT is provided to 1 in 1,000 Americans each year. The adoption of OPAT has many benefits including reduced costs and better quality of life for patient and caregivers. Although recent guidelines have been established for OPAT 1, information is needed regarding practice patterns and infrastructure required to support OPAT use. Methods: A questionnaire was administered to 54 healthcare professionals attending an investigator s meeting for a clinical study. Respondents were asked to use a 5-point scale to rate the importance of ten aspects of the IDSA practice guidelines for OPAT therapy 1. Data were summarized according to type of caregiver (doctor, nurse or pharmacist) and whether the caregiver was a key decision maker for OPAT treatment. Results: 51.9% of respondents were key decision makers; 53.7% pharmacists; 25.9% medical doctors. 41.5% worked in inpatient settings, 18.9% in outpatient settings, and 39.6% in both settings. Key decision makers gave higher ratings than others to having a rapid communication system in place between patients and team members (p = 0.03), and 24-hr availability of case manager and billing staff (p = 0.03). Both doctors and nurses stressed the importance of patient willingness to participate and having a doctor available 24 hours per day (p = 0.04 and 0.003, respectively). Conclusion: The perceived importance of aspects of OPAT practice differed depending on professional category. Primary caregivers placed higher emphasis on patient input and 24- hour availability of medical professionals. Reference: 1. Tice AD, Rehm SJ, Dalovisio JR et al. Practice guidelines for outpatient parenteral antimicrobial therapy. Clin Infect Dis. 2004;38(12): P17 Antibacterial Properties of a Novel Polymer Hydrogel-Decon Gel H. Tang 1, S. Shors 1, S. Rogelj 1, G. Edgington 2, M. O Neill 2 1Biology Department, New Mexico Institute of Mining and Technology, Socorro, NM, 2 Cellular Bioengineering, Inc., Honolulu, HI Background: DG is a polymer hydrogel that dries to a thin layer of film for peel-off removal or can be used as an anti-bacterial solution on contaminated surfaces. The dried film can be re-hydrated for bio-agent identification. Objective: Evaluation of DG s antibacterial activity on Gram-positive and negative, non-pathogenic and pathogenic bacteria, either on planktonic growth or on biofilm formation. Methods: DG was either dried on bacteriacontaining plastic surface and the film peeled off, or added directly in solution to bacterial growth medium. Planktonic growth was tracked by OD measurements and viability counts, while biofilm accumulation was assessed by crystal violet staining. MTT assays were used to determine mammalian cytotoxicity. Results: When 10 7 CFU of E. coli, S. epidermidis, S. aureus (MRSA), B. cepacia, E. coli O157:H7, P. aeruginosa, A. baumannii, and group A Streptococcus were covered by 0.2ml of 10-50% DG (~ 0.8mm thickness before drying) and air-dried at room temperature, bacteria in all DG-treated samples were completely killed and sterile surfaces were left behind. Though the minimal inhibitory concentration was species dependent, all of these species were also killed when DG was present in the growth medium at concentrations well below 10%. DG also inhibited S. epidermidis and P. aeruginosa biofilm formation, and killed the pre-formed biofilms. DG is about 100 times less toxic to HeLa cells in culture than chlorhexidine gluconate. Summary: Numerous pathogenic bacteria are susceptible to effective inactivation by Decon Gel treatment in solution and upon drying. Applications are wide ranging and include mitigation/identification of potential bioterrorism events. Reference: 1. Flemming HC, Neu TR, Wozniak DJ. The EPS matrix: the house of biofilm cells. J Bacteriol. 2007;189(22): Gilbert P, Moore LE. Cationic antiseptics: diversity of action under a common epithet. J Appl Microbiol. 2005;99(4): P18 Impact of an Antimicrobial Stewardship Program on Antimicrobial Use and Resistance in Intensive Care Units (ICU) A. R. Sarwari 1, K. O. Petros 2, R. B. Sager 2, A. Wilson 3, H. V. Dedhia 4, C. J. Mullett 5, J. Thomas 6, P. Miller-Canfield 6, D. Slain 7, K. Moffett 5, H. C. Palmer, Jr. 8 1Infectious Diseases, West Virginia University, Morgantown, WV, 2Pharmacy, West Virginia University Hospitals, Morgantown, WV, 3Surgery, West Virginia University, Morgantown, WV, 4 Pulmonary Critical Care Medicine, West Virginia University, Morgantown, WV, 5Pediatrics, West Virginia University, Morgantown, WV, 6 Clinical Microbiology, West Virginia University, Morgantown, WV, 7 School of Pharmacy, West Virginia University, Morgantown, WV, 8 Internal Medicine, West Virginia University, Morgantown, WV Background: Intensive care units (ICU s) have the highest density of antimicrobial use and the worst problems with resistance. General institution wide and specific unit based interventions are needed to control antimicrobial use and resistance in ICU s. Methods: Between 2003 and 2007, the Antimicrobial Stewardship Program at a tertiary care university teaching hospital implemented the systematic semi-annual monitoring of antimicrobial use (in defined daily doses/1000 patient days) and antimicrobial resistance (by monitoring select bug/drug combinations) along with an institutionwide discouragement of antimicrobials with higher potential to promote resistance (e.g., quinolones, ceftazidime) for those with a lower potential (e.g., aminoglycosides, cefepime). In 2005, a ventilator associated pneumonia protocol centered on antimicrobial cycling and de-escalation (imipenem to ertapenem, cefepime to ceftriaxone, and piperacillin-tazobactam to ampicillinsulbactam) was implemented. Results: The ICU use of intravenous ciprofloxacin and ceftazidime declined from 180 and 115 DDD/1000 patient days to 39 and 26 respectively. Tobramycin and cefepime use increased from 2 and 0 DDD/1000 patient days to 49 and 73 respectively. The number and proportion of ICU microorganisms resistant to select antimicrobials and the total patient days is shown in the table. Conclusions: While our current strategies appear to have been successful in curtailing antimicrobial resistance among ICU Klebsiella, Pseudomonas and Acinetobacter isolates, the increasing resistance to ciprofloxacin among E. coli isolates suggests their limitations in affecting imported resistance. Reference: 1. Dellit TH, Owens RC, McGowan JE, et al. Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship. Clin Infect Dis. 2007;44(2):

53 SCIENCE PREVENTION CONTROL 53 ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P19 The Phenotypic Expression of Multidrug Resistant Escherichia coli Recovered from Spontaneous Diseased Dogs and Cats B. W. Shaheen, D. M. Boothe, T. Smaha Anatomy, Physiology and Pharmacology, Auburn University, Auburn, AL Previously we reported the high incidence of multidrug resistant E. coli recovered from the spontaneously diseased companion animals (2007 Annual Conference on Antimicrobial Resistance). The purpose of this study was to phenotypically describe a sample population of E. coli associated with spontaneous disease in dogs and cats, with a focus on single drug resistance (SDR) versus multiple drug resistance (MDR). Isolates were phenotyped to 7 drugs using E-test following CLSI based guidelines: amoxicillin (A), amoxicillin-clavulanic acid (X), cefpodoxime (P), doxycycline, enrofloxacin, gentamicin, trimethoprim-sulfamethoxazole. 194/377 isolates expressed resistance, 85 as SDR. SDR to beta-lactams (any combination of A, X or P) was most common (83%; n=71/85 [30% A, 28% X, and 24% AXP] and to E least (3.5%; 3/85). The remaining 109 isolates expressed MDR, with resistance to all 7 drugs (Z) representing the largest proportion (18.3%; 20/109). Drugs most commonly involved in MDR were A (96.3 %), X (85%) and E (61 %). The MIC 90 (mcg/ml) for isolates expressing MDR generally indicated high level resistance to all drugs. For example, A: MIC 90 > 256 in 92% of MDR isolates versus 32% SDR isolates and MIC 90 for E was > 32 in 82% of MDR isolates versus only < 1 mcg/ml in 2/3 isolates expressing SDR. In this study, MDR most commonly involved all 5 drug classes, and was associated with high level resistance. Further, it was not unusual for SDR to be expressed towards beta lactams, but was unusual for SDR to be expressed toward enrofloxacin. Finally, MDR most commonly involved amoxicillin with or without clavulanic acid, and enrofloxacin. 1. Guardabassi L, Schwarz S, Lloyd DH. Pet animals as reservoirs of antimicrobial resistant bacteria. J Antimicrob Chemother. 2004;54(2): Cooke CL, Singer RS, Jang SS, et al. Enrofloxacin resistance in Escherichia coli isolated from dogs with urinary tract infections. J Am Vet Med Assoc. 2002;220(2): P20 Antimicrobial Resistance and Class 1 Integrons in Resistant Escherichia coli Recovered from Spontaneous Diseased Dogs and Cats B. W. Shaheen 1, D. M. Boothe 1, O. A. Oyarzabal 2, T. Smaha 1 1Anatomy, Physiology and Pharmacology, Auburn University, Auburn, AL, 2 Poultry Science, Auburn University, Auburn, AL Integrons associated with plasmids may carry genes conferring multidrug resistance (MDR). We previously reported the emergence of MDR in canine and feline E. coli isolates (n=240/377) collected in dogs and cats with spontaneous disease (2007 Annual Conference on Antimicrobial Resistance). The purpose of this study was to describe the role of Class I integrons in the emergence of MDR in these isolates. A total of 32 isolates were randomly selected. Susceptibility to 7 drugs was determined by E-test following CLSIbased guidelines: amoxicillin, amoxicillin-clavulanic acid, cefpodoxime, doxycycline, enrofloxacin, gentamicin, trimethoprim-sulfamethoxazole. A total of 32 isolates were characterized by 7 phenotypes: no resistance (n=10), resistance to one drug (SDR; n=8) or resistance to more than one drug class (MDR; n=14, with n=12 for all 7 drugs). Isolates were subjected to DNA extraction. Class I integrons were detected by PCR and sequencing. A total of 19/32 isolates contained a Class I intergons. Plasmids were then extracted from all isolates and tested for the presence of Class I integrons. Integrons revealed that 59.4% (19/32) of the isolates contained class 1 integrons. MIC 90 for integron-positive isolates were more than four fold higher than the break point for all drugs tested. Integron-positive isolates were more likely to be multi-resistant 73.7% (14/19); only 1 of the MDR isolates did not have a class I integrons. The majority 94.7% (18/19) of classes 1 integrons was detected in the plasmids of the same integron-positive isolates; one isolate had an integron not associated with a plasmid. This association suggests that integrons may confer high MIC level, multidrug resistance in E. coli isolates associated with spontaneous disease in dogs and cats. Further, the integrons may confer MDR. 1. Sanchez S, McCrackin Stevenson MA, et al. Characterization of multidrugresistant Escherichia coli isolates associated with nosocomial infections in dogs. J Clin Microbiol. 2002;40(10): Rowe-Magnus DA, Mazel D. The role of integrons in antibiotic resistance gene capture. Int J Med Microbiol. 2002;292(2): P21 Antibiotic Resistance among Uropathogenic E.coli (UPEC) in a College Population in Michigan C. Barbosa-Cesnik, M. Buxton, J. Debusscher, M. LaFontaine, L. Zhang, B. Foxman University of Michigan, Ann Arbor, MI Background: About 90% of all urinary tract infections (UTI), a common bacterial infection, are caused by Escherichia coli 1. UTI are usually treated empirically without culture; therefore, ongoing monitoring of local antibiotic resistance patterns is crucial for prescribing appropriate therapy. Methods: E. coli isolates were collected between September 2005 and June 2007 from women with uncomplicated cystitis participating in a clinical trial. All unique isolates collected from an individual were tested for antibiotic susceptibility testing using a Vitek 2 (biomerieux, Inc., NC), automated system. Results: 63 isolates were tested in Year1 and 139 in year2. 37% of isolates were resistant to >1, 27% to > 2, and 17% to > 3 of the 18 antimicrobial drugs investigated. Resistance was most common to ampicillin (32%), tetracycline (19%), trimethoprim/ sulfamethoxazole (TMP-SMX) (17%), and piperacillin (11%). 3% of E. coli isolates were resistant to cefazolin and ciprofloxacin, and 2% were resistant to gentamicin, levofloxacin and amoxicillin-clavulanic acid. Resistance patterns were similar in and , but TMP-SMX was higher in year one than in year two (22% vs14%). Conclusion: TMP-SMX resistance in the same study population has changed little since 1999 when it was 15.8%; but resistance to ciprofloxacin has doubled. The slow rate of increase in TMP-SMX resistance among urinary isolates in the same geographic area over a 6 year period is reassuring; however, the long-term utility of TMP-SMX as a first line UTI treatment is in doubt. Reference: 1. Johnson JR, Stamm WE. Urinary tract infections in women: diagnosis and treatment. Ann Intern Med. 1989;111(11):

54 Conference on Antimicrobial Resistance ABSTRACTS OF SUBMITTED POSTER PRESENTATIONS P22 Pyrosequencing for Rapid Detection of Fluoroquinolone Resistance Among Mycobacterium Tuberculosis Isolates from the Philippines L. C. Bravo 1, M. Tuohy 2, C. Ang 3, N. Shrestha 1 1Infectious Disease, Cleveland Clinic Foundation, Cleveland, OH, 2Pathology and Lab Medicine, Cleveland Clinic Foundation, Cleveland, OH, 3 Philippine General Hospital, University of the Philippines Manila, Philippines Objective: Discuss pyrosequencing as a novel method to rapidly detect fluoroquinolone resistance among M. tuberculosis (MTB) isolates. Background: The importance of testing MTB for fluoroquinolone susceptibility has become even greater with the emergence of extensively-drug resistant (XDR) TB. Mutations in the quinolone resistance determining region (QRDR) of the gyra gene have been found in 50 to 80% of fluoroquinolone resistant MTB isolates 1. Pyrosequencing is a rapid method of DNA sequencing by synthesis used previously in MTB resistance testing for rifampin and isoniazid. This is the first study to apply pyrosequencing in fluoroquinolone resistance testing. Methods: 76 crude mycobacterial lysates from a TB laboratory in the Philippines were tested for phenotypic susceptibilities to ciprofloxacin and ofloxacin using the agar proportion method. Amplification was done by real-time PCR with the 2X Sensimix DNA Kit (Quantace) on the Rotor-Gene 3000 (Corbett Research). The QRDR of the gyra gene was then sequenced by pyrosequencing (Biotage) as previously described 2. Genotypic testing results were then compared to those of phenotypic testing. Results: 19 (25%) isolates were resistant to ciprofloxacin only. Of these, 9 were resistant to ofloxacin also. The pyrosequencing assay yielded good quality sequences up to 30 base pairs. Mutations in the QRDR were found in 6 of the 9 (67%) isolates that were resistant to both ciprofloxacin and ofloxacin, a proportion consistent with current published data. All susceptible isolates had wild type sequences. Conclusion: Pyrosequencing is a rapid and specific assay that can accurately detect ofloxacin resistance in the majority of M. tuberculosis. Genotypic resistance testing based on gyra gene QRDR sequencing correlates better with ofloxacin than with ciprofloxacin phenotypic resistance testing. 1. Sulochana S, Narayanan S, Paramsivan CN, Suganthi C, Narayanan PR. Analysis of fluoroquinolone resistance in clinical isolates of Mycobacterium tuberculosis from India. J Chemother. 2007;19(2): Zhao JR, Bai YJ, Wang Y, Zhang QH, Luo M, Yan XJ. Development of a pyrosequencing approach for rapid screening of rifampin, isoniazid and ethambutol-resistant Mycobacterium tuberculosis. Int J Tuberc Lung Dis. 2005;9(3):

55 SCIENCE PREVENTION CONTROL 55 AUTHOR INDEX Numbers beginning with I are invited speakers, those beginning with P are poster presentations, and those beginning with S are submitted oral presentations. Author Abstract Number Author Abstract Number Author Abstract Number Adams, Jennifer S4 Adams-Haduch, Jennifer M....S3 Ahmed, Sabeena S2 Aiello, Allison E S5 Ang, Concepcion P22 Angulo, Frederick I19 Aron, David S4 Ashcraft, Deborah S P8 Barbosa-Cesnik, Cibele......P21 Barzilay, Ezra P4, P7 Bennish, Michael L S2 Bonomo, Robert A S4 Boothe, Dawn M P19, P20 Bowen, Anna P4 Bravo, Lulette Tricia C P22 Buxton, Miatta P21 Carson, Robyn S5 Chen, Michaeline P6 Cho, Yong Kyun P12 Cohen, Morris P5 Cohen, Stuart H I2 Cook, Heather S7 Cosgrove, Sara E I15 Cynamon, Michael P6 Debusscher, Joan P21 Dedhia, Harakh V P18, S10 Doi, Yohei S3 Donskey, Curtis S4 Doyle, Michael P I21 Drlica, Karl I16 Duquaine, Damon S7 Ecker, David J S4 Edgington, Garry P17 Eliopoulos, George M I6 Essa, Zakiya P2 Essack, Sabiha Y P2, P3 Fitzgerald, Collette P7 Folster, Jason P4 Fox, Barry S9 Foxman, Betsy P12, P21 Fraser, Thomas G S6 Gebhart, Dana P14 Gray, Barry P11 Griffin, Dale W I23 Hall, Geraldine S S6 Hearn, Michael P6 Howie, Rebecca L P4 Hujer, Andrea M. S4 Hujer, Krisitine M S4 Hulten, Edward A S4 Ip, Dawn S7 Jacobs, Micah A S6 Jimenez, Humberto R P1 Johann-Liang, Rosemary....I18 John, Alice S7 Joyce, Kevin P4, P7 Kahn, Rehana P1 Kapell, Deborah S7 Katz, David E P16 Kerndt, Peter S8 Khan, Wasif A S2 Kim, Jin Yong P12 Kohner, Peggy C S1 Kornblum, John S7 Kotarski, Susan F I11 Kreiswirth, Barry S7 Krieger, Daniel S7 Krueger, Amy L P10 LaFontaine, Marisol P21 Lamp, Kenneth P9 Larson, Elaine L S5 Lazzar, Megan S8 Levy, Stuart B S5 Lindfield, Kimberly C P16 Livermore, David M I1

56 Conference on Antimicrobial Resistance AUTHOR INDEX Author Abstract Number Author Abstract Number Author Abstract Number Lue, Yvonne S7 Mankin, Peggy P11 Marshall, Bonnie S5 Martin, David P14, P15 Martone, William J P16 Marx, Melissa A S7 McDonald, L. Clifford I5 Medalla, Felicita P7 Mediavilla, Jose S7 Miller-Canfield, Patricia.P18, S10 Moffett, Kathryn P18, S10 Mongkolrattanothai, Kanoporn P11 Mullett, Charles J P18, S10 Murillo, Jeremias L P5 O Brien, Thomas F I10 O Neill, Michael P17 Oyarzabal, Omar A P20 Palmer, Hugh C P18, S10 Pankey, George A P8 Park, Yoon Soo P12 Pasculle, Anthony W S3 Patel, Kinjal P1 Patel, Robin S1 Paterson, David L S3, S4 Perez, Federico S4 Petros, Karen O P18, S10 Potoski, Brian A S3 Powers, John H I12, I17 Pruckler, Jan P7 Raju, Venkedesh P11 Rehana, Zeenath S7 Rieder, Ronald P13 Robberts, Frans J. L S1 Rogelj, Snezna P17 Rudy, Ellen S8 Safdar, Nasia S9 Sager, Renee B P18, S10 Saiman, Lisa I8 Salam, Mohammad A S2 Sanchez, Pablo J I14 Sarwari, Arif R P18, S10 Schlemme, Claire P6 Scholl, Dean P14, P15 Scoppettuolo, Lisa A P16 Shaheen, Bashar W.....P19, P20 Shors, Scott P17 Shrestha, Nabin P22 Shrestha, Nabin K S6 Sidjabat, Hanna E S3 Singer, Randall I24 Slain, Douglas P18, S10 Slim, Jihad P1 Smaha, Timothy P19, P20 Smith, Jacinta P7 Songer, J. Glenn I4 Stuart, Andrew P7 Svenson, Jim E S9 Tang, Hong P17 Tauxe, Robert V I20 Thomas, John P18, S10 Thweatt, Katherine S4 Tuohy, Marion P22 Wang ondu, Ruth P6 Weese, J. Scott I3 Weiss, Don S7 Whichard, Jean P4, P7 White, David G I9 Wigton, Robert S9 Williams, Steve P14 Wilson, Alison P18, S10 Wilson, Deborah A S6 Wortmann, Glenn I7 Wright, Gerry I22 Xavier, Ylone P5 Yeung, Alice S7 Yu, Victor L I13 Zavizion, Boris P13 Zhang, Lixin P12, P21

57 Thank you for attending the Annual Conference on Antimicrobial Resistance Please join us for the next Annual Conference on Antimicrobial Resistance February 1-3, 2010 Hyatt Regency Bethesda Bethesda, Maryland 6 Visit our website for more information about the National Foundation for Infectious Diseases.

58

11/22/2016. Antimicrobial Stewardship Update Disclosures. Outline. No conflicts of interest to disclose

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