Use of Infection Control Procedures in an Out-Patient Clinic for Leg Ulcers and the Rate of Contamination with Methicillin-Res

  • Thu, 9/4/08 - 11:52am
  • 0 Comments
  • 3549 reads
Author(s): 
Avi Shai, MD;[1] Natalya Bilenko, MD;[2] Rina Ben-Zeev, RN;[2] Sima Halevy, MD[2]

Introduction

During the last 20 years, methicillin-resistant Staphylococcus aureus (MRSA) has become a major nosocomial worldwide pathogen.[1–5] The acquired resistance of S. aureus strains is not limited to methicillin. S. aureus strains, including MRSA, acquire resistance against other antibiotics, such as gentamicin, ciprofloxacin, fusidic acid, mupirocin, and vancomycin.[6–14] Subsequently, infections that until recently could be dealt with by using traditional antibiotics have become uncontrolled and unresponsive to conventional therapeutic regimens.

The selection of resistant organisms has certain unique aspects when dealing with cutaneous ulcers due to the following causes: 1) Wound beds serve as an optimal breeding ground for pathogenic bacteria; 2) Secretions from these ulcers further increase the risk of environmental spread; and 3) Administration of antibiotics is relatively frequent among patients with cutaneous ulcers, which subsequently leads to the selection of resistant strains.

The presence of cutaneous ulcers is indeed a well-established risk factor for colonization and a prolonged carriage of MRSA.[15–18] Significant risk factors associated with MRSA colonization are hospitalization, admission to intensive care units, antibiotic treatment, and nursing home residence. Additional risk factors for MRSA colonization are old age, male gender, significant disability or immobilization, steroid therapy, immunosuppression or immunosuppressive therapy, diabetes, presence of catheters/tubes, extensive skin disease, surgery, and malnutrition.[15–23]

In general, it is somewhat complicated to compare the prevalence of MRSA in patients with leg ulcers between different clinics/medical centers, since the data are subject to many variables. The prevalence depends on whether the patients are embulatory or hospitalized; whether they are enrolled from a general dermatology clinic or a clinic that specially focuses on treating leg ulcers; and the underlying causes of the ulcers (e.g., percentage of diabetic or pressure ulcers). Thus, the reported range is wide. Trividic, et al.,[15] reported positive isolation of MRSA in 53 of 4,579 (1.1%) patients who were hospitalized in a dermatolgy department during 1997 to 1998; 34 of the 53 patients presented with cutaneous ulcers. In 2001, Roghmann, et al.,[18] reported positive isolation of MRSA in 166 of 545 (30%) patients hospitalized between 1990 to 1995 with chronic ulcers consisting mainly of pressure ulcers. The prevalence of MRSA also depends on the overall prevalence of Staphylococcus strains and their subtypes in certain geographical areas. The use of infection-control procedures may also affect the prevalence, as discussed in the present article.

In June of 1999, strict implementation of infection-control guidelines (detailed below) were carried out in the Out-Patient Clinic for Cutaneous Ulcers at the Soroka University Medical Center in Beer-Sheba, Israel. Up to that point, the infection control policy had been rather inconsistent. The objective was to evaluate the efficacy of accepted infection-control procedures in our clinic.

Methods

Study design. The study was designed as a program evaluation, comparing two patient groups enrolled before and after implementing infection-control procedures.

Main outcome measure. The main outcome measure was the presence of MRSA. The presence of MRSA reflects the transmission rate of bacteria between patients. Patients were regarded as contaminated by MRSA if the organism was isolated at least once at our clinic as of the second visit (see exclusion criteria).

Colonization vs. infection. Identifying an ulcer as infected was based on the currently accepted definition,[24,25] i.e., the presence of erysipelas or cellulitis manifested by systemic signs (fever) and/or local signs (warmth, redness, swelling), or the presence of purulent secretions on the ulcer bed.

References: 

References

1. Ayliffe GA. The progressive intercontinental spread of methicillin-resistant Staphylococcus aureus. Clin Infect Dis 1997;24 (Suppl 1):S74–S79.
2. Mulligan ME, Murray-Leisure KA, Ribner BS, et al. Methicillin-resistant Staphylococcus aureus: A consensus review of the microbiology, pathogenesis, and epidemiology with implications for prevention and management. Am J Med 1993;94:313–28.
3. The Hopital Propre II Study Group. Methicillin-resistant Staphylococcus aureus in French hospitals: A 2-month survey in 43 hospitals. Infect Control Hosp Epidemiol 1999;20:478–86.
4. Vincent JL, Bihari DJ, Suter PM, et al. The prevalence of nosocomial infection in intensive care units in Europe. Results of the European Prevalence of Infection in Intensive Care (EPIC) Study. JAMA 1995;274:639–44.
5. National Nosocomial Infections Surveillance (NNIS) system report: data summary from January, 1992 to April, 2000, issued June, 2000. Am J Infect Control 2000;28:429–48.
6. Price MF, McBride ME, Wolf JE jr. Prevalence of methicillin-resistant Staphylococcus aureus in a dermatology outpatient population. South Med J 1998;91:369–71.
7. Nishijima S, Kurokawa I. Antimicrobial resistance of Staphylococcus aureus isolated from skin infections. Int J Antimicrob Agents 2002;19:241–3.
8. Piddock LJ, Jin YF, Webber MA, et al. Novel ciprofloxacin-resistant, nalidixic-susceptible mutant of Staphylococcus aureus. Antimicrob Agents Chemother 2002;46:2276–8.
9. Hershow RC, Khayr WF, Schreckenberger PC. Ciprofloxacin resistance in methicillin-resistant Staphylococcus aureus: Associated factors and resistance to other antibiotics. Am J Ther 1998;5:213–20.
10. Ravenscroft JC, Layton A, Barnham M. Observations on high levels of fusidic acid resistant Staphylococcus aureus in Harrogate, North Yorkshire, UK. Clin Exp Dermatol 2000;25:327-30.
11. Jones PG, Sura T, Harris M, et al. Mupirocin resistance in clinical isolates of Staphylococcus aureus. Infect Control Hosp Epidemiol 2003;24:300–1.
12. Walker ES, Vasquez JE, Dula R, et al. Mupirocin-resistant, methicillin-resistant Staphylococcus aureus does mupirocin remain effective? Infect Control Hosp Epidemiol 2003;24:342–6.
13. Staphylococcus aureus resistant to vancomycin—United States, 2002. Morb Mortal Wkly Rep 2002;51: 565–7.
14. Vancomycin-resistant Staphylococcus aureus—Pennsylvania, 2002. Morb Mortal Wkly Rep 2002;51: 902.
15. Trividic M, Gauthier ML, Sparsa A, et al. Methicillin-resistant Staphylococcus aureus in dermatological practice: Origin, risk factors and outcome. Ann Dermatol Venereol 2002;129:27–9.
16. Beaujean DJ, Weersink AJ, Blok HE, et al. Determining risk factors for methicillin-resistant Staphylococcus aureus carriage after discharge from hospital. J Hosp Infect 1999;42:213–8.
17. Bradley SF, Terpenning MS, Ramsey MA, et al. Methicillin-resistant Staphylococcus aureus: Colonization and infection in a long-term care facility. Ann Intern Med 1991;115:417–22.
18. Roghmann MC, Siddiqui A, Plaisance K, et al. MRSA colonization and the risk of MRSA bacteraemia in hospitalized patients with chronic ulcers. J Hosp Infect 2001;47:98–103.
19. Merrer J, Santoli F, Appere De Vecchi C, et al. “Colonization pressure” and risk of acquisition of methicillin-resistant Staphylococcus aureus in a medical intensive care unit. Infect Control Hosp Epidemiol 2000;21:718–23.
20. Lucet JC, Chevret S, Durand-Zaleski I, et al. Prevalence and risk factors for carriage of methicillin-resistant Staphylococcus aureus at admission to the intensive care unit: Results of a multicenter study. Arch Intern Med 2003;163:181–8.
21. Graffunder EM, Venezia RA. Risk factors associated with nosocomial methicillin-resistant Staphylococcus aureus (MRSA) infection including previous use of antimicrobials. J Antimicrob Chemother 2002;49:999–1005.
22. Warshawsky B, Hussain Z, Gregson DB, et al. Hospital- and community-based surveillance of methicillin-resistant Staphylococcus aureus: Previous hospitalization is the major risk factor. Infect Control Hosp Epidemiol 2000;21:724–7.
23. Hori S, Sunley R, Tami A, et al. The Nottingham Staphylococcus aureus population study: Prevalence of MRSA among the elderly in a university hospital. J Hosp Infect 2002;50:25–9.
24. Browne A, Dow G, Sibbald RG. Infected wounds: Definitions and controversies. In: Falanga V (ed). Cutaneous Wound Healing. London: Martin Unitz, 2001:203–19.
25. Lipsky BA, Berendt AR. Principles and practice of antibiotic therapy of diabetic foot infections. Diabet Met Res Rev 2000;16(Suppl):S42–S46.
26. Perspectives in disease prevention and health promotion update: Universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other bloodborne pathogens in health-care settings. Morb Mortal Wkly Rep 1988;37(No. 24):377–88.
27. Bolyard EA, Tablan OC, Williams WW, et al. Guideline for infection control in health care personnel. Am J Infect Control 1998;26:289–354.
28. Larson E. APIC guideline for handwashing and hand antisepsis in health care settings. Am J Infect Control 1995;23:251–69.
29. Edmond MB, Wenzel RP. Isolation. In: Mandell GL, Bennett JE, Dolin R (eds). Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases, Fourth Edition. New York: Churchill Livingstone, 1995:2575–9.
30. Rutala WA. Selection and use of disinfectants in health care. In: Mayhall CG (ed). Hospital Epidemiology and Infection Control. Baltimore: Williams & Wilkins, 1996:913–36.
31. Rotter ML. Hand washing and hand disinfection. In: Mayhall CG (ed). Hospital Epidemiology and Infection Control. Baltimore, MD: Williams & Wilkins, 1996:1052–68.
32. Hugonnet S, Pittet D. Hand hygiene revisited: Lessons from the past and present. Curr Infect Dis Rep 2000;2:484–9.
33. Teare L, Cookson B, Stone S. Hand hygiene. Use alcohol hand rubs between patients: They reduce the transmission of infection. Br Med J 2001;323:411–2.
34. Smith PW, Roccaforte JS. Epidemiology and prevention of infections in home health care. In: Mayhall CG (ed). Hospital Epidemiology and Infection Control. Baltimore,MD: Williams & Wilkins, 1996:1171–6.
35. Boyce JM, Pittet D. Guideline for hand hygiene in health-care settings. Morb Mortal Wkly Rep 2002;51(No. RR-16):1–45.
36. Doebbeling BN, Stanley GL, Sheetz CT, et al. Comparative efficacy of alternative hand-washing agents in reducing nosocomial infections in intensive care units. N Engl J Med 1992;327:88–93.
37. Pittet D, Hugonnet S, Harbarth S, et al. Effectiveness of a hospital-wide programme to improve compliance with hand hygiene. Infection Control Programme. Lancet 2000;356:1307–12.
38. Maki DG. The use of antiseptics for handwashing by medical personnel. J Chemother 1989;1 (Suppl 1):3–11.
39. Larson EL, Early E, Cloonan P, et al. An organizational climate intervention associated with increased handwashing and decreased nosocomial infections. Behav Med 2000;26:14–22.

image description image description