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MISCELLANY Acinetobacter Infection: What Was the True Impact during the Vietnam Conflict? Clinton K. Murray,1 Heather C. Yun,2 Matthew E. Griffith,1 Duane R. Hospenthal,1 and Myron J. Tong3 1 Department of Medicine, Infectious Disease Service, Brooke Army Medical Center, Fort Sam Houston, and 2Department of Infectious Disease, Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas; and 3Pfleger Liver Institute, David Geffen School of Medicine at University of California–Los Angeles We read with interest 2 recent articles in Clinical Infectious Diseases highlighting the recognition of Acinetobacter baumannii as one of the more challenging bacteria facing us today [1, 2]. We agree that this bacterium significantly impacts the US military, because the bacterium frequently colonizes and/or infects our casualties returning from overseas deployments in support of the global war on terrorism. Although Acinetobacter species are often reported to have been among the predominant pathogens infecting war wounds in the Vietnam conflict, there are significant questions surrounding this assumption. One of the earliest descriptions of war wound bacteriology was by Fleming [3] in his 1919 report. He described the evolution of war wounds through 3 phases: initial infection involved sporulating anaerobes (such as Clostridium species) and streptococci that transitioned, after ∼7 days, to nonsporulating bacteria of fecal origin (e.g., Escherichia coli and Klebsiella species) and then to pyogenic organisms (including Staphylococcus species and Streptococcus pyogenes) during the third phase. The introduction of aggressive surgical debridement likely led to the essential disappearance of clostridial gas gangrene between World War I and the Korean War. Implementation of penicillin treatment during World War II probably led to the diminution of S. pyogenes infection. The expanded use and broader spectra of antimicrobial agents occurred simultaneously with the appearance of increasingly resistant bacteria [4, 5]. Received 24 March 2006; accepted 24 March 2006; electronically published 15 June 2006. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of Defense or the US government. Reprints or correspondence: Dr. Clinton K. Murray, Infectious Disease (MCHE-MDI), Brooke Army Medical Center, 3851 Roger Brooke Dr., Fort Sam Houston, TX 78234 (Clinton.Murray@ amedd.army.mil). Clinical Infectious Diseases 2006; 43:383–4 2006 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2006/4303-0021$15.00 Identifying the role of Acinetobacter species in war wounds is challenging, because the bacteria’s name has undergone significant evolution [6, 7]. Possibly the first description of Acinetobacter species infection dates back to the Korean War, when Achromobacter (one of the prior Acinetobacter names) species was isolated from blood culture of a casualty [8]. Tong’s [9] 1972 description of 30 Marines with 63 extremity wounds is the most cited description of the role of Acinetobacter infection in the Vietnam conflict. Culture samples included wound and blood obtained at the initial time of presentation and then on dressing change days 3 and 5 after wounding. Initial cultures were performed within 2.5 h after injury. The article states, “The predominant gram-negative bacteria on admission were members of the Mimeae-Herellea-Bacterium-Alcaligenes group” (p. 1044). The other common gram-negative bacteria included Pseudomonas aeruginosa and Enterobacter species (table 1). The Mimeae-Herellea-Bacterium-Alcaligenes group was commonly identified in bacteremic patients, second only to Enterobacter species. There is no further description of the microbiology of the Mimeae-Herellea-Bacterium-Alcaligenes group to enable us to clearly identify the bacteria today, although by 1971, Acinetobacter was clearly identified as a genus [6, 7]. Tong was not able to provide further insight into the correct identification of these bacteria using today’s taxonomy. If this bacterium was the predominant gram-negative bacterium identified from war wounds in Vietnam, it is surprising that this is the only report describing such a fact. Another article from the Vietnam conflict reported findings from 112 initial wound cultures, 2 of which yielded Alcaligenes (possible Acinetobacter species). The other gram-negative pathogens identified included Aerobacter aerogenes and Pseudomonas species, but no Acinetobacter species or Mimeae-Herellea-Bacterium-Alcaligenes group were described [4]. An analysis of 1531 initial wound cultures performed in Japan from US soldiers wounded in Vietnam during 1967 and 1968 revealed that the most common gram negative bacteria were P. aeruginosa, Proteus species, E. coli, Aerobacter aerogenes, and Klebsiella pneumonia [10]. Mimeae-HerelleaBacterium-Alcaligenes group, Acinetobacter, or other names commonly used for Acinetobacter were not described. Among orthopedic war wounds evaluated at Brooke General Hospital (now Brooke Army Medical Center) during the Vietnam conflict, 100 tissue samples revealed that P. aeruginosa, Proteus species, Klebsiella-Enterobacter group, and E. coli were the predominant gram-negative bacteria identified [11]. Acinetobacterlike bacteria were not identified in this patient population either. Overall, it is unclear what role Acinetobacter played during MISCELLANY • CID 2006:43 (1 August) • 383 Table 1. The percentage of bacterial cultures of 63 extremity wound specimens with positive results. Percentage of extremity wounds, by day a Pathogen Pseudomonas aeruginosa Enterobacter species Proteus species Mimeae-Herellea-Bacterium-Alcaligenes group Escherichia coli Day 1 Day 3 Day 5 5 38 3 46 25 25 23 8 22 22 67 41 27 25 19 NOTE. Data are from Tong [9]. a Shown are the 5 most frequently identified gram-negative bacteria. the Vietnam conflict, in contrast to the role described by most articles. Acinetobacter species are associated with war wounds among casualties returning from the global war on terrorism, although the source of the infection/colonization is unclear. Three likely sources have been proposed. The first is that bacteria colonize soldiers, who are inoculated at the time of injury; the second is that bacteria are introduced into the wound from the environment at the time of injury; and the third is that nosocomial infection is responsible, with inoculation occurring during stabilization in theater and/or subsequent evacuation through higher echelons of medical care. To date, no source has been clearly identified; however, active investigations are still underway and tend to support nosocomial transmission. Acinetobacter species remain important pathogens among casualties 384 • CID 2006:43 (1 August) • MISCELLANY because of their multidrug resistant patterns, and we appreciate the emphasis placed on them by the Infectious Diseases Society of American and by other authors. Acknowledgments Potential conflicts of interest. All authors: no conflicts. References 1. Talbot GH, Bradley J, Edward JE, Gilber D, Scheld M, Bartlett JG. Bad bugs need drugs: an update on the development pipeline from the antimicrobial availability task force of the Infectious Disease Society of America. Clin Infect Dis 2006; 42:657–68. 2. Fournier PE, Richet H. The epidemiology and control of Acinetobacter baumannii in health care facilities. Clin Infect Dis 2006; 42:692–9. 3. Fleming A. On the bacteriology of septic wounds. Lancet 1915; 2: 638–43. 4. Kovaric JJ, Matsumoto T, Dobek AS, Hamit HF. Bacterial flora of one hundred and twelve combat wounds. Mil Med 1968; 133:622–4. 5. Klein RS, Berger SA, Yekutiel P. Wound infection during the Yom Kippur War: observations concerning antibiotic prophylaxis and therapy. Ann Surg 1975; 182:15–21. 6. Allen DM, Hartman BJ. Acinetobacter species. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious diseases. 6th ed. Pennsylvania: Elsevier Churchill Livingston, 2005:2632–6. 7. Henriksen SD. Moraxella, Acinetobacter and the Mimeae. Bacteriol Rev 1973; 37:522–61. 8. Lindberg RB, Wetzler TF, Newton A, Howard JM, Davis JH, Strawitz J. The bacterial flora of the blood stream in the Korean battle casualty. Ann Surg 1955; 141:366–8. 9. Tong MJ. Septic complications of war wounds. JAMA 1972; 219:1044–7. 10. Matsumoto T, Wyte SR, Moseley RV, Hawley RJ, Lackey GR. Combat surgery in communication zone I: war wound and bacteriology (preliminary report). Mil Med 1969; 134:655–65. 11. Heggers JP, Barnes ST, Robson MC, Ristroph JS, Omer GE. Microbial flora of orthopedic war wounds. Mil Med 1969; 134:602–3.