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useful antimicrobials, and the other was resistant to vancomycin. Only 1 strain of E gallinarum was isolated from cerebrospinal fluid, with sensitivity to penicillin and intermediate resistance to vancomycin. Whether or not the Enterococcus spp were acquired at the hospital was not established. There was only one coincidental isolation date of 2 VRE strains, and these strains demonstrated different antibiotic susceptibility. Our findings are similar to other reports of multidrug-resistant bacteria in nosocomial infections from countries with a very low prevalence of enterococcal infection.7,8 The identification of E faecium vancomycin-resistant strains with van A or van B phenotype resistance is of epidemiologic interest for our institution and signals the need for ongoing epidemiologic surveillance and strict implementation of preventive actions established by Mexican health authorities, as well as other future protective strategies.9,10 To the best of our knowledge, this is the first report of the presence of E faecium vancomycin-resistant strains in Queretaro, Mexico.
5. Official Gazette of the Federation for the Official Mexican Standard, NOM-045-SSA2-2005. For the epidemiological surveillance, prevention and control of nosocomial infections. Mexico, DF; 2009:62-90 (in Spanish). 6. Nakasone I, Kinjo T, Yamane N, Kisanuki K, Shiohira CM. Laboratorybased evaluation of the colorimetric VITEK-2 Compact System for species identification and of the Advanced Expert System for detection of antimicrobial resistances: VITEK-2 Compact system identification and antimicrobial susceptibility testing. Diagn Microbiol Infect Dis 2007;58:191-8. 7. Ofner-Agostini M, Johnston L, Simor AE, Embil J, Matlow A, Mulvey M, et al. Vancomycin-resistant enterococci in Canada: results from the Canadian Nosocomial Infection Surveillance Program, 1999‒2005. Infect Control Hosp Epidemiol 2008;29:271-4. 8. Chowdhury SA, Arias CA, Nallapareddy SR, Reyes J, Willems RJL, Murray BE. A trilocus sequence typing scheme for hospital epidemiology and subspecies differentiation of an important nosocomial pathogen, Enterococcus faecalis. J Clin Microbiol 2009;47:2713-9. 9. Zirakzadeh A, Patel AR. Vancomycin-resistant enterococci: colonization, infection, detection, and treatment. Mayo Clin Proc 2006;81:529-36. 10. Centers for Disease Control and Prevention. Vancomycin-resistant enterococci (VRE) and the clinical laboratory. Available from: www .cdc.gov/ncidod/hip/Lab/FactSheet/vre.htm. Accessed August 27, 2002. doi:10.1016/j.ajic.2010.12.022
We would like to thank F. Padilla, G. Cacho, D. Diaz, and A. Vazquez Mellado for their invaluable assistance in the accomplishment of this work.
Conflicts of interest: None to report.
Guillermo Enrique Leo-Amador, MD, PhD General Regional Hospital 1, Mexican Social Security Institute, Queretaro, Mexico Armando Borbolla-Ramos Javier Alberto Morales-Lara Hugo Alonso P erez-Gonz alez Department of Clinical Infectious Diseases, School of Medicine, Autonomous University of Queretaro, Queretaro, Mexico Hebert L. Hernandez-Montiel, MD, PhD Juan C. Solis-S, MD, PhD Department of Biomedical Research, School of Medicine, Autonomous University of Queretaro, Queretaro, Mexico Address correspondence to Guillermo Enrique LeoAmador, MD, PhD, Facultad de Medicina, Universidad Aut onoma de Queretaro, Clavel 200, Col Prados de la Capilla, Santiago de Queretaro, Queretaro, CP 76170, M exico. E-mail:
[email protected]
References 1. Werner G, Coque TM, Hammerum AM, Hope R, Hryniewics W, Johnson A, et al. Emergence and spread of vancomycin resistance among enterococci in Europe. Eurosurveillance 2008;13:9-11. 2. Luke FC, Chopra T, Kaye KS. Pathogens resistant to antibacterial agents. Infect Dis Clin North Am 2009;23:817-45. 3. Cuellar-Rodrıguez J, Galindo-Fraga A, Guevara V, Perez-Jimenez C, Espinosa-Aguilar L, Rol on AL, et al. Vancomycin-resistant enterococci, Mexico City. Emerg Infect Dis 2007;13: 798-9. 4. Dıaz Ramos R. Main microorganisms related to nosocomial infections. Latin American Journal of Microbiology 2006;48:106-8 (in Spanish).
How many bacteria live on the keyboard of your computer? To the Editor: The ever-increasing use of computers in all fields of health care has led to several recent studies on the role of keyboard contamination as a vehicle to transmit hospital infections. Fewer studies have been conducted in nonhospital environments,1-4 where the use of computers is widespread and the same keyboard may be used by several people, thereby becoming a possible vehicle for infection transmission. The fact that many people eat at their workstation also must be considered;3,5 crumbs remaining on the keyboard may form a medium favoring the growth of microbes. Keyboard contamination may be viewed as a direct index of hygiene, especially of community hand hygiene, that can be used to plan strategies to promote and improve protection of workers’ health. We conducted a study to assess keyboard contamination by common microbes, moulds and yeasts, comparing the results from shared keyboards and nonshared keyboards, and to assess any differences in the entities and types of contamination between keyboards of users who eat at their desks and keyboards of users who do not eat at their desks. We analyzed swabs obtained from the keyboards of 30 computers in use at the University of Siena, 15 not shared and 15 located in computer laboratories used by various students. Swabs of keys were taken. For each key, we tested for a different bacterium among the common bacteria found
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outside of hospital environments using selective culture medium. Typical colonies were counted and typed using the appropriate API galleries. The results were expressed as colony-forming units (CFU) per key. The MannWhitney test was used to compare the CFU/key on shared keyboards and nonshared keyboards, and then the CFU/key in users who ate at their desks and those who did not. Microbes were recovered at 368C from all keyboards, with counts ranging from 6 CFU/key to 430 CFU/key. At 228C, mould was not found on 8 keyboards, but was detected on all other keyboards up to a maximum of 120 CFU/key. Yeast was found on 17 keyboards up to a maximum of 420 CFU/key. Staphylococci were found on all keyboards but one at counts up to 120 CFU/key. Typing using API galleries revealed Staphylococcus aureus, S epidermidis, and Micrococcus spp. Enterococcus was found on only 7 keys, including 6 shared keyboards, and was typed as E avium (1-31 CFU/key). Pseudomonas was not detected on any keyboard. S aureus was significantly more common on shared keyboards than on nonshared keyboards (P 5 .03). Key contamination was significantly greater on the keyboards of users who usually ate at their desks compared with the keyboards of those who did not, and was significant for total microbe load (TML) at 368C (P 5 .06) and Enterococcus (P 5 .037). Bacteria were consistently present on keyboards, but CFU loads on shared keyboards were higher only for Enterococcus. Our results are in partial disagreement with those of an Australian study that showed greater contamination of shared keyboards than nonshared keyboards, especially by staphylococci.2 These discrepant results may be related to the fact that the Australian study examined a smaller percentage of nonshared keyboards (14% vs our 50%) or to differences in hygiene habits between Australians and Italians. The enterococcus that we found was E avium. This might be due to the fact that there are many pigeons on the balconies and in the courtyards of our universities, where students and employees congregate during breaks. Thus, the type of bacteria found on working equipment provides information about the external environment. This must be borne in mind, especially during ‘‘epidemics.’’ Our findings also demonstrate that keyboard contamination can be an indicator of the user’s lifestyle. Indeed, we found greater growth of Staphylococcus and TML on keyboards of users who ate at their desks, probably because crumbs and food residues create an excellent breeding ground for these bacteria.4 If confirmed, this finding suggests that avoiding eating at
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the workstation or cleaning the desk after eating would be good practice. Sources of bacterial contamination can include poor hand hygiene and droplets of saliva6 that inevitably fall on the keyboard during talking, sneezing, and coughing. Thus, to reduce the resident population of microbes with pathogenic potential, it is advisable to observe the general rules of hygiene and to clean keys frequently.7 To prevent transfer of bacteria to and from keyboards via users’ hands, thorough handwashing before and after keyboard contact is recommended. Handwashing is often considered laborious and is subject to low compliance, as demonstrated by some studies.8,9 Another strategy is to regularly disinfect equipment. Several studies have shown that good hygiene reduces keyboard contamination.1,10 Special reminders have been created to promote regular cleaning of keyboards; this measure promoted 87% compliance in one program.8 Gabriele Messina, MD Cecilia Quercioli, MD, PhD Sandra Burgassi, BS Francesca Nistic o, MD Angelo Lupoli, MD Nicola Nante, MD Department of Public Health, University of Siena, Siena, Italy Address correspondence to Nicola Nante, MD, Department of Public Health, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy. E-mail:
[email protected]
References 1. Dogan M, Feyzioglu B, Ozdemir M, Baysal B. Investigation of microbial colonization of computer keyboards used inside and outside hospital environments. Mikrobiyol Bul 2008;42:331-6 (in Turkish). 2. Anderson G, Palombo EA. Microbial contamination of computer keyboards in a university setting. Am J Infect Control 2009;37: 507-9. 3. Hirsch S. Germs are working overtime at the office. Los Angeles Times, February 28, 2005. Available at: http://www.latimes.com/ 2005/feb/28/health/he-germs28. Accessed December 29, 2010. 4. Reynolds KA, Watt PM, Boone SA, Gerba CP. Occurrence of bacteria and biochemical markers on public surfaces. Int J Environ Health Res 2005;15:225-34. 5. Collins J. Letter from the editor: fighting germs in the workplace. Semin Roentgenol 2007;42:1-2. 6. Marinelli P, Montemarano A, Liguori G, D’Amora M. Hygiene, preventive medicine and public health. Padova: Piccin Nuova Libraria; 2002 (in Italian). 7. Schultz M, Gill J, Zubairi S, Huber R, Gordin F. Bacterial contamination of computer keyboards in a teaching hospital. Infect Control Hosp Epidemiol 2003;24:302-3. 8. Wilson AP, Ostro P, Magnussen M, Cooper B. Laboratory and in-use assessment of methicillin-resistant Staphylococcus aureus contamination of ergonomic computer keyboards for ward use. Am J Infect Control 2008;36:e19-25. 9. Boyce JM, Pittet D. Guideline for hand hygiene in health care settings. Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand
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Hygiene Task Force, Society for Healthcare Epidemiology of America/ Association for Professionals in Infection Control/Infectious Diseases Society of America. MMWR Recomm Rep 2002;51(RR-16):1-45. 10. Lu PL, Siu LK, Chen TC, Ma L, Chiang WG, Chen YH, et al. Methicillinresistant Staphylococcus aureus and Acinetobacter baumannii on computer interface surfaces of hospital wards and association with clinical isolates. BMC Infect Dis 2009;9:164. doi:10.1016/j.ajic.2010.12.023
An unusual cause of continuous ambulatory peritoneal dialysis– associated outpatient peritonitis: Stenotrophomonas maltophilia To the Editor: Stenotrophomonas maltophilia (SM) is a nonfermentative aerobic, gram-negative bacillus formerly known as Pseudomonas maltophilia or Xanthomonas maltophilia.1 Because of its low virulence, SM rarely infects healthy people. Infections caused by SM are mostly hospital-acquired; SM peritonitis is a rare complication of chronic peritoneal dialysis that sometimes results in mortality or loss of the dialysis catheter.2,3 A 57-year-old female who had been receiving continuous ambulatory peritoneal dialysis (CAPD) therapy for almost 3 years presented at our outpatient clinic with fever, mild abdominal pain, diffuse abdominal tenderness, and cloudy peritoneal effluent. Diabetic nephropathy was identified as the cause of end-stage renal disease. The patient’s previous medical history did not include peritonitis, exit site tunnel infection, or use of broadspectrum antibiotics. Her peritoneal fluid examination revealed CAPD-associated peritonitis with a leukocyte count of 2,100/mm3 (90% neutrophils). Empirical antibiotic treatment was initiated with intraperitoneal ceftazidime and vancomycin. On the third day of treatment, Stenotrophomonas maltophilia was isolated in peritoneal fluid culture with antibiogram susceptibility to levofloxacine and trimethoprim-sulfamethoxazole. The treatment was switched to ceftazidime and levofloxacine. Even in the face of possible resistance to ceftazidime due to clinical improvement, ceftazidime therapy was continued. The patient was discharged 15 days after admission and recovered completely without the need for catheter removal. SM is more frequently isolated in nosocomial settings.4 Predisposing factors for SM infection include previous antibiotic therapy with broad-spectrum b-lactam agents, prolonged hospitalization,5 malignant lesions,6 central venous catheterization,5,7 and immunosuppressive therapy.8 Diabetes mellitus has been identified as a significant predisposing factor for SM infections.9
Despite its association with higher mortality and catheter loss, appropriate antimicrobial therapy promotes successful recovery from SM peritonitis. Among the known risk factors, including previous antibiotic therapy with broad-spectrum b-lactams, malignancies, central venous catheterization, immunosuppressive treatment, and prolonged hospitalization, diabetes mellitus might have been the predisposing factor in our patient. Almost one-third of the patients receiving CAPD have diabetes. SM infections are rare even in outpatients with diabetes receiving CAPD, but should be considered in these patients. Conflict of interest: None to report.
Alper Azak, MD G€ ulay Kocak, MD B€ ulent Huddam, MD G€ okce I_s¸can, MD Murat Duranay, MD Departments of Nephrology and Internal Medicine, Ankara Education and Research Hospital, Ankara, Turkey Address correspondence to Alper Azak, MD, Sehit Cengiz Karaca Mah 1047, Cad 13/15 Dikmen, Ankara, Turkey. E-mail:
[email protected]
References 1. Nesme X, Vaneechoutte M, Orso S, Hoste B, Swings J. Diversity and genetic relatedness within genera Xanthomonas and Stenotrophomonas using restriction endonuclease site differences of PCR-amplified 16S rRNA gene. Syst Appl Microbiol 1995;18:127-35. 2. Villarino ME, Stevens LE, Schable B, Mayers G, Miller JM, Burke JP, et al. Risk factors for epidemic Xanthomonas maltophilia infection/colonization in intensive care unit patients. Infect Control Hosp Epidemiol 1992;13:201-6. 3. Szeto CC, Li PK, Leung CB, Yu AW, Lui SF, Lai KN. Xanthomonas maltophilia peritonitis in uremic patients receiving continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1997;29:91-5. 4. Laing FP, Ramotar K, Read RR, Alfieri N, Kureishi A, Henderson EA, et al. Molecular epidemiology of Xanthomonas maltophilia colonization and infection in the hospital environment. J Clin Microbiol 1995;33:513-8. 5. Elting LS, Khardori N, Bodey GP, Fainstein V. Nosocomial infection caused by Xanthomonas maltophilia: a case-control study of predisposing factors. Infect Control Hosp Epidemiol 1990;11:134-8. 6. Muder RR, Harris AP, Muller S, Edmond M, Chow JW, Papadakis K, et al. Bacteremia due to Stenotrophomonas (Xanthomonas) maltophilia: a prospective multi-center study of 91 episodes. Clin Infect Dis 1996; 22:508-12. 7. Elting LS, Bodey GP. Septicaemia due to Xanthomonas species and nonaeruginosa Pseudomonas species: increasing incidence of catheter-related infections. Medicine 1990;69:296-306. 8. Szeto CC, Li PK, Leung CB, Yu AW, Lui SF, Lai KN. Xanthomonas maltophilia peritonitis in uremic patients receiving continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1997;29:91-5. 9. Baek JE, Jung EY, Kim HJ, Lee GW, Hahm JR, Kang KR, et al. Stenotrophomonas maltophilia infection in patients receiving continuous ambulatory peritoneal dialysis. Korean J Intern Med 2004;19:104-8. doi:10.1016/j.ajic.2011.01.004