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MARCH 2007
Main Article:
Methicillin-Resistant Staphylococcus Aureus in the Correctional Setting
Joseph Bick, M.D. Chief Medical Officer California Medical Facility California Department of Corrections Assistant Clinical Professor Division of Infectious Diseases University of California, Davis Disclosures: None Introduction The crowded conditions that exist in many of this nation's jails and prisons create an ideal environment for the transmission of infectious diseases. Congregate living environments, insufficient availability of soap, water, and clean laundry, and barriers to prompt access to health care increase the probability that microorganisms will be transmitted from one person to another. Furthermore, inmates are frequently moved from one location to another with little, if any, advance notice, complicating the diagnosis of infection, recognition of an outbreak, interruption of transmission, and control of disease. Further complicating the appropriate management of contagious illnesses in the correctional setting is the high prevalence of comorbidities such as mental illness and ongoing substance abuse. Many inmates are distrustful of authority and reluctant to cooperate with health care providers. In addition, some jails and prisons have been slow to ask for assistance from outside agencies when faced with outbreak situations, and published guidelines for the diagnosis and treatment of communicable diseases are not always readily applicable to the correctional setting. Over the past several years, infections due to methicillin-resistant Staphylococcus aureus (MRSA) have been increasingly recognized as a major problem in many jails and prisons. This article will review the epidemiology of S. aureus (SA) and MRSA infections, provide recommendations for MRSA diagnosis and treatment, discuss education and prevention measures, and propose new correctional-specific standard and transmission based (contact) precautions for MRSA. Bacteriology and Epidemiology SA is a bacterium commonly found colonizing the skin or in the anterior nares of healthy individuals. Up to 50% of those in the general population are colonized with SA, and asymptomatic colonization is much more common than symptomatic infection and disease.1 The prevalence of SA colonization is increased among injection drug users, health care workers (HCWs), diabetics, the incarcerated, and those who have chronic skin conditions or indwelling urinary or vascular catheters.1,2,3 In addition to the anterior nares, common colonization sites include the axillae, perineum, rectum, and pharynx. Although SA often colonizes humans without causing disease, it can be responsible for both minor skin infections and life threatening infections of the skin, bone, joints, blood, heart valves, and lungs. SA is easily spread from person to person by contact with the skin of someone who is infected or colonized with the bacteria. Until World War II, SA was almost universally susceptible to penicillin. Within a few years of the first clinical use of penicillin in the 1940s, penicillin resistance was identified, predominantly in the hospital setting. Penicillin resistance in SA is often due to the production of beta lactamases, enzymes that break down penicillin's beta lactam ring and render the drug inactive. To date, over 200 penicillinases have been identified. Another common resistance mechanism is the production of altered penicillin binding proteins. In an effort to combat penicillin resistance among SA, semi-synthetic penicillins that were less susceptible to bacterial penicillinases were developed. The first such agent was methicillin, and for this reason SA that is resistant to semi-synthetic penicillins is referred to as MRSA. Within a year of the introduction of the beta-lactamase stable penicillin methicillin in 1960, MRSA strains were identified. By the 1970s, MRSA was increasingly recognized as an important pathogen in hospitals, nursing homes, and other long term care facilities in the United States. Currently, more than half of all health care associated SA infections in hospitals in this country are due to MRSA (HA MRSA).4,5 The prevalence of MRSA colonization is less than that of SA, but is rising. MRSA colonization can be transient or persist for many years.6 Risk factors for colonization with MRSA include those associated with SA colonization, as well as current or recent hospitalization, residence in a long-term care facility (nursing home, skilled nursing facility, hospice), end stage renal disease (ESRD), dialysis, surgery, a prior history of MRSA disease or colonization, recent or frequent antibiotic therapy, recurrent skin disease, close contact with a person who is infected or colonized with MRSA, overcrowded living conditions such as those encountered in military service and correctional settings, skin or soft tissue infections that respond poorly to beta lactam antibiotics, and participation in athletic activities that involve abrasions, skin to skin contact, and/or sharing of equipment. Although MRSA colonization increases the risk for infection, most of those who are colonized with MRSA do not develop infection and many of those who do develop infection were not previously colonized. Initially, MRSA infections were predominantly found among residents of hospitals, nursing homes, and other health care facilities and most community-acquired SA infections were not MRSA. Over the past two decades, community-acquired MRSA (CA MRSA) have become increasingly common causes of skin and soft tissue infections (SSTI) outside of the health care setting. Outbreaks have been described in the military, in jails and prisons, in day care settings, among MSM, and in those participating in athletic events.7,8,9,10, 11,12,13 Risk factors identified in jail and prison MRSA outbreaks have included prolonged incarceration, the presence of skin lacerations and abrasions, previous antibiotic use, inadequate skin hygiene, draining one's own abscesses or performing one's own wound dressing changes, washing one's own clothing by hand, sharing razors, clothing, linen, or soap, restricted access to medical care, and requiring co-payments to see a clinician.11,12,13 New risk factors for MRSA infection continue to be identified. In one recent report, sexual contact with an infected partner was found to be the likely etiology of MRSA transmission in three households in Manhattan.14 Most recently, an increasing number of community-acquired SSTIs due to MRSA have been seen in persons with no identifiable risk factors. In one recent study of 280 consecutive patients who were hospitalized with SA infection, clinical and epidemiologic risk factors did not reliably distinguish between MRSA and methicillin-sensitive SA (MSSA).15 There is ample evidence documenting the role of HCWs in the spread of MRSA from patient to patient and from HCWs to their families. MRSA has been cultured from computer keyboards used by clinicians in hospitals, stethoscopes, blood pressure cuffs, otoscopes, and pagers.16,17,18,19,20,21,22 Some HCWs erroneously believe that they do not need to adhere to contact precautions when they enter the rooms of MRSA-infected patients as long as they avoid contact with the MRSA infected person. However, MRSA can be readily cultured from the gloves and the gowns or uniforms of HCWs who have been in the room of MRSA infected patients, regardless of whether they were involved in direct patient care or were performing other non-patient care activities.23 Clinicians who examine MRSA infected patients while wearing gloves but not gowns frequently acquire MRSA on their clothing and later transfer MRSA to their hands.24 In addition, MRSA can be cultured from environmental surfaces in most hospital rooms housing MRSA infected or colonized patients. SA can survive for months on environmental surfaces, creating a potential reservoir for later transmission.24,25 HA MRSA has historically been distinguished from CA MRSA based upon antibiotic susceptibility profiles, genetic features, and the presence or absence of toxins such as bacteriocin, enterotoxins, and the Panton-Valentine leukocidin. Over time, some of these distinctions between CA and HA MRSA have begun to fade, and some CA MRSA now have susceptibility profiles that are more similar to those traditionally found in HA MRSA. Often, microorganisms that develop resistance pay a competitive price and are less virulent. However, HA MRSA appears to be even more virulent than MSSA, leading to longer hospitalizations, higher mortality, and increased costs.26,27,28 Contrary to the experience with HA MRSA, the outcomes among patients who have required admission to the hospital with CA MRSA have been found to be quite similar to those with CA MSSA.29 In both the correctional setting and the free community, SSTIs have often been mistakenly attributed to spider bites. This may be due to the sudden appearance of painful lesions, and the common finding of arachnids in correctional settings. In reality, spiders infrequently bite people and most spider bites are benign. The misinterpretation of MRSA skin lesions as spider bites has led to delays in appropriate treatment and misguided vector control measures. HCWs in the correctional setting should be advised to consider "spider bites" as infections due to MRSA until proven otherwise. Treatment The first step in adequately treating infections due to MRSA is to ensure rapid access to health care for all inmates who have SSTIs. Access to medical care can be improved by eliminating co-payment requirement for contagious conditions, employing an adequate number of clinical staff, and maintaining a 24/7 clinical operation for urgent medical conditions. One intervention that may be particularly useful in high risk correctional settings is the establishment of wound evaluation and treatment clinics. Utilizing specially trained dedicated health care teams to provide active surveillance for SSTI, promptly initiate treatment, and attend to wound dressings may lead to more rapid diagnosis, treatment, and resolution of skin lesions and less opportunity for transmission to others. When evaluating SSTIs and other infections in which SA is common, clinicians must maintain a high degree of suspicion for MRSA. When possible, all significant SSTIs should be cultured. Cultures are especially valuable for establishing the local epidemiology and resistance pattern for SSTI. Once MRSA is identified within a facility as an endemic organism causing SSTI, empiric antibiotic selection should include an agent that has activity against this organism. The ongoing collection of cultures helps guide infection control decisions and assists in definitive antibiotic selection for infections that are rapidly progressing, severe and/or life threatening, or poorly responsive to empiric therapy. Cultures can be collected by either swabbing purulent material obtained at the time of incision and drainage or by aspiration of lesions with a syringe. Surface swabs of open lesions are generally less useful as they often reflect colonization rather than causative infection. In many cases, incision and drainage of the accumulated purulent material is all that is needed to resolve minor MRSA SSTI infections, and antibiotics are unnecessary. With early lesions that have not yet suppurated, moist heat can be applied with a hot washcloth to promote drainage. Antibiotics should be utilized when sepsis, large facial lesions, periorbital lesions, and/or significant cellulitis are present. Antibiotics should also be strongly considered as part of the treatment for patients who have SSTIs in the setting of immune compromise due to neutropenia, ESRD, diabetes, or HIV infection. Table 1 provides detailed information regarding antimicrobial agents useful in the treatment of MRSA. The indiscriminate use of antibiotics can lead to increased drug resistance and should be discouraged. MRSA are resistant to all beta lactam antibiotics, including: penicillin, the semi-synthetic penicillins methicillin, nafcillin, oxacillin, dicloxacillin, and cloxacillin, all cephalosporins (including cephalexin, cephalothin, ceftriaxone, cefuroxime, ceftazidime, and cefazolin), and penicillins that are co-formulated with clavulinic acid or sulbactam (for example augmentin, timentin, unasyn). In addition, MRSA strains often carry plasmids that lead to resistance to other non-beta lactam antibiotics, such as aminoglycosides, fluoroquinolones, macrolides, and chloramphenicol. Many MRSA strains are susceptible to trimethoprim-sulfamethoxazole, clindamycin, the longer acting tetracyclines minocycline or doxycycline, and rifampin. Rifampin should never be used as a single agent for the treatment of MRSA, as resistance will rapidly evolve.30,31 Clinicians should bear in mind that skin lesions are commonly caused by bacteria other than SA. Group A streptococci (GAS) can cause impetigo and erysipelas, and are commonly resistant to antibiotics that may be used for MRSA such as trimethoprim-sulfamethoxazole and the tetracyclines. If GAS is suspected, it may be prudent to include a second agent with activity against GAS in the initial empiric therapy. Alternatively, clindamycin has the added benefit of being effective against most MRSA as well as GAS, and also has excellent bone penetration. It is important to note that most MRSA resistant to erythromycin have inducible resistance to clindamycin. This resistance may not be recognized and reported to the clinician unless the laboratory performs additional testing. This test, referred to as a d-zone test or d-test, should be routinely performed upon all SA isolates that are found to be resistant to erythromycin. Unless a d-zone test has demonstrated susceptibility to clindamycin, this agent should not be used for SA that is erythromycin resistant. For more serious infections, vancomycin, linezolid, daptomycin, tigacycline or quinupristin-dalfopristin may be used (Table 1 and Spotlight). Vancomycin has been used for many years for the treatment of SA and MRSA, and virtually all SA are fully susceptible to vancomycin. However, occasional clinical isolates of SA with reduced susceptibility to vancomycin have been reported for over a decade.30,31,32,33 The first documented case of infection caused by vancomycin-resistant S. aureus (VRSA) (vancomycin MIC >32 µg/mL) in a patient in the United States was reported in 2002.34,35 Other concerns about vancomycin include hypersensitivity reactions, a histamine release syndrome (also known as red man syndrome) related to rapid intravenous infusion, the lack of an oral formulation that can be used for the treatment of systemic infection, and the possibility of vancomycin use contributing to the development of vancomycin resistant enterococcus (VRE). Preventive and Infection Control Strategies In 2003, the Society for Health Care Epidemiology of America (SHEA) released guidelines for preventing the nosocomial transmission of MRSA within hospitals.36 These guidelines included three main points:
Most recently, state governments have waded into the debate. At least two states (Illinois and Maryland) have proposed legislation that would mandate active screening of all hospitalized patients for MRSA. SHEA and the Association of Practitioners in Infection Control (APIC) have come out in opposition to legislative mandates for active surveillance.37 It should be noted that there are limited data to support these intensified screening and isolation strategies. In the United States the most compelling data for routine surveillance come from experiences in the control of hospital outbreaks and high risk settings such as intensive care units and hemodialysis units. Proponents of more widespread screening in the hospital setting often cite the experience in Denmark and Holland. These countries have maintained a very aggressive practice of isolating all newly admitted patients, screening them for MRSA, and attempting environmental eradication measures. In some hospitals in Denmark and Holland, MRSA represents only a few percent of all SA isolated. It is significant, however, that the prevalence of MRSA in the community in these countries is significantly lower than that seen in most parts of the United States. The high prevalence of CA MRSA in this country may overwhelm efforts to actively screen and isolate all those admitted to hospitals. Health care and correctional facilities considering a more intensive approach to screening for MRSA and isolation must consider a number of potential negative consequences. The workload involved in collecting and processing specimens is formidable. Facilities must have a physical plant that will allow for single cell contact isolation or cohorting of those who are found to be infected or colonized. Tracking all involved patients and cultures will require a functioning information technology system, and the financial costs associated with routine culturing could be significant. Studies have demonstrated that hospitalized patients who are placed in isolation experience twice as many adverse events, are less likely to have vital signs performed, have more days without a doctor's progress note, have longer lengths of stay, and are more likely to file a formal complaint as compared to those who are not isolated.38 Evidence-based experience with MRSA control measures in the correctional setting is quite limited. Suggested interventions include wide spread screening for skin disease, implementation of standardized antimicrobial treatment recommendations, improvements in laundry practices, inmate education, the use of chlorhexidine containing soaps, and the use of alcohol-based hand rubs. In 2003, the Federal Bureau of Prisons issued recommendations that include reporting and tracking of patients with MRSA, draining abscesses, culturing skin lesions, and selecting antibiotics known to be effective against MRSA.39 Clearly, more research is needed to define best practices within jails and prisons for MRSA prevention, diagnosis, and treatment. Can MRSA be Eradicated? In general, routine eradication of MRSA colonization has not been shown to be practical or efficacious. In some cases in which the same person develops repeated episodes of infection, clearance of the organism from the nose can be beneficial in preventing additional infections. Mupirocin calcium 2% ointment (Bactroban) applied to both anterior nares twice daily for 5-7 days is commonly used for this purpose. One recent encouraging study utilized a triple approach with an oral regimen of rifampin and doxycycline, intranasal 2% mupirocin ointment, and 2% chlorhexidine gluconate for washing.40 In this study, 112 hospitalized patients who were colonized with MRSA were randomized to receive this decolonization therapy for seven days or no treatment. Of those treated, 74% had negative MRSA cultures at 3 months, while only 32% of those who were not treated were culture-negative at follow-up. Eight months later, 54% of those who were treated remained culture-negative. This same study found that patients who were colonized with mupirocin-resistant MRSA at baseline were more than nine times likely to fail treatment. Although worthy of further study, widespread utilization of this approach within the correctional setting cannot be recommended at this time. Education: Inmates All inmates should be educated about the importance of seeking prompt evaluation and treatment for all potentially contagious conditions. Specific educational points concerning MRSA include: Education: Employees
In addition to standard precautions, the CDC has published transmission-based precautions to be used based upon the mechanism of transmission of specific organisms. Transmission-based precautions fall into three main categories: airborne, droplet, and contact. Airborne precautions are to be used for organisms that are transmitted via the respiratory route by small particle aerosols, such as Mycobacterium tuberculosis and Varicella zoster virus. Droplet precautions are used for organisms that are transmitted by larger droplets either through the air for short distances or by contaminated surfaces, such as influenza virus. Contact precautions are to be used for organisms that are transmitted by contact with the skin of an infected or colonized person or with contaminated surfaces. Examples include most diarrheal pathogens, lice, scabies, and MRSA. All correctional employees should be familiar with transmission based (contact) precautions that are appropriate for the correctional setting (See Standard Precautions 101). The importance of infection control measures cannot be overemphasized, as even many healthcare professionals neglect hand washing. In an effort to improve hand hygiene, the use of alcohol-containing antiseptic scrubs is increasingly being encouraged. However, security concerns may lead to these particular disinfectants not being universally embraced in the correctional setting. Environmental surfaces that are used by multiple people should be routinely decontaminated. Inmates commonly wash their own clothes using soap and tap water. This process may remove soil and odors, but does little to kill pathogenic organisms. Inmates should be educated that the only way to reliably remove organisms that can cause disease is to use the institutional laundry. A laundry temperature of at least 71 degrees Celsius (160 degrees F) for a minimum of 25 minutes has commonly been recommended to effectively kill microorganisms.42 Lower temperature washing at 22-50 degrees Celsius can effectively reduce microorganism concentrations when adequate amounts of chlorine bleach are utilized.43,44 The high temperatures achieved during drying and ironing are also microbicidal. The involvement of experts in infection control and infectious diseases can be useful in both managing individual patients and establishing protocols specific to the unique needs of each facility. Correctional facilities experiencing outbreaks of MRSA should seek assistance from their local and state health departments. MRSA outbreaks can be reported to CDC through state departments of corrections and state health departments (telephone: 800.893.0485). Preventing MRSA infections among inmates might be an important measure for preventing MRSA in the community outside the correctional facility. Additional information about MRSA is available at the CDC website (www.cdc.gov).45 Conclusions Infections due to MRSA have become an increasingly common cause of morbidity and mortality in this country. Outbreaks have been recognized within health care settings, long-term care facilities, and in a variety of community settings. Congregate living environments such as jails and prisons have been particularly impacted by this pathogen. A variety of measures can be implemented that can improve the prevention, early diagnosis, and treatment of disease attributable to MRSA. Research on best practices in jails and prisons is urgently needed to help guide correctional professionals in best addressing this problematic pathogen. References: 1 Kluytmans J, Van Belkum A, Verbrugh H. Nasal Carriage of Staphylococcus Aureus: Epidemiology, Underlying Mechanisms, and Associated Risks. Clin Microbiol Rev 1997;10:505-20 2 Tuazon CV, Sheagren JN. Increased Rate of Carriage of Staphylococcus Aureus Among Narcotic Addicts. J Infect Dis 1974;129:275 3 Kirmani N, Tuazon CV, Murray HW et al. Staphylococcus Aureus Carriage Rate of Patients Receiving Long term Hemodialysis. Arch Intern Med 1978; 138: 165-167 Tuazon CV, Perez A, Kishaba T et al. Staphylococcus Aureus Among Insulin Injecting Diabetic Patients: An Increased Carriage Rate. JAMA 1975;231:1272 4 Chambers HF. The Changing Epidemiology of Staphylococcus Aureus? Emerg Infect Dis. 2001; 7:178-82. 5 National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) System report, data summary from January 1992 through June 2003, issued August 2003. Am J Infect Control. 2003;31:481-98 6Sanford MD, Widmer AF, Bale MJ, et al. Efficient Detection and Long-Term Persistence of the Carriage of Methicillin-Resistant Staphylococcus Aureus. Clin Infect Dis. 1994; 19:1123-1128 7 Zinderman CE, Conner B, Malakooti, MA et al. Community-Acquired Methicillin-Resistant Staphylococcus Aureus Among Military Recruits. Emerging Infect Dis. May 2004;10(5):941-44 8 Kazakova SV, Hageman JC, Matava M et al. A Clone of Methicillin-Resistant Staphylococcus Aureus Among Professional Football Players. N Engl J Med. Feb 2005;352(5):468-75 9 Adcock PM, Pastor P, Medley F. Methicillin Resistant Staphylococcus Aureus in Two Day Care Centers. J Infect. Dis. Aug 1998;178(2):577-80 10 Methicillin-Resistant Staphylococcus Aureus Infections Among Competitive Sports Participants-Colorado, Indiana, Pennsylvania, and Los Angeles County, 2000-2003. MMWR 2003;52:793-95 11 Methicillin-Resistant Staphylococcus Aureus Skin or Soft Tissue Infections in a State Prison-Mississippi, 2000. MMWR 2001;50:919-22 12 Outbreaks of Community-Associated Methicillin-Resistant Staphylococcus Aureus Skin Infections-Los Angeles County, California, 2002-2003. MMWR 2003;52:88 13 Methicillin-Resistant Staphylococcus Aureus Infections in Correctional Facilities-Georgia, California, and Texas, 2001-2003. MMWR 2003;52:992-96 ONTR 14 Cook, H, Fuquay E, Vasquez G et al. Heterosexual Transmission of Community-Associated Methicillin-Resistant Staphylococcus Aureus. CID 2007;44:410-13 15 Miller L, Perdreau-Remington F, Bayer A, et al. Clinical and Epidemiologic Characteristics Cannot Distinguish Community-Associated Methicillin-Resistant Staphylococcus Aureus Infection from Methicillin-Susceptible S. Aureus Infection: A Prospective Investigation. CID 2007;44:471-482 16 Eveillard M, Martin Y, Hidri N, et al. Carriage of Methicillin Resistant Staphylococcus Aureus Among Hospital Employees: Prevalence, Duration, and Transmission to Households. Infect Control Hosp Epidemiol. 2004;25:114-20 17 Devine J, Cooke RP, Wright EP. Is Methicillin-Resistant Staphylococcus aureus (MRSA) Contamination of Ward-Based Computer Terminals a Surrogate Marker for Nosocomial MRSA Transmission and Handwashing Compliance. J Hosp Infect 2001;48:72-75. 18 Bernard L, Kereveur A, Durand D, et al. Bacterial Contamination of Hospital Physicians' Stethoscopes. Infect Control Hosp Epidemiol 1999;20:626-28. 19 Breathnach AS, Jenkins DR, Pedler SJ. Stethoscopes as Possible Vectors of Infection by Staphylococci. BMJ 1992;305:1573-74. 20 Smith MA, Mathewson JJ, Ulert IA, et al. Contaminated Stethoscopes Revisited. Arch Intern Med 1996; 156: 82-84. 21 Cohen HA, Amir J, Matalon A, et al. Stethoscopes and Otoscopes: A Potential Vector of Infection? Fam Pract 1997;14:446-49. 22 Singh D, Kaur H, Gardner WG, et al. Bacterial Contamination of Hospital Pagers. Infect Control Hosp Epidemiol 2002;23:274-76. 23 Boyce JM, Chenevert C. Isolation Gowns Prevent Health Care Workers From Contaminating Their Clothing, and Possibly Their Hands, With Methicillin-Resistant Staphylococcus Aureus and Resistant Enterococci. 8th Annual Meeting of the Society for Healthcare Epidemiology of America; April 1998; Abstract S74:52. 24 Boyce JM, Potter-Bynoe G, Chenevert C, et al. Environmental Contamination Due to Methicillin-Resistant Staphylococcus Aureus: Possible Infection Control Implications. Infect Control Hosp Epidemiol 1997;18:622-27. 25 Neely AN, Maley MP. Survival of Enterococci and Staphylococci On Hospital Fabrics and Plastics. J Clin Microbiol 2000;38:724-26. 26 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;36:592-98 27 Cosgrove SE, Qi Y, Kaye S, et al. The Impact of Methicillin Resistance in Staphylococcus Aureus Bacteremia on Patient Outcomes: Mortality, length of Stay, and Hospital Charges. Infect Control Hosp Epidemiol 2005;26:166-74 28 Cosgrove SE, Sakoulas G, Perencevich EN, et al. Comparison of Mortality Associated with Methicillin-Resistant and Methicillin-Susceptible Staphylococcus Aureus Bacteremia: a Meta-Analysis. Clin Infect Dis 2003;36:53-59 29 Miller L, Quan C, Shay A et al. A Prospective Investigation of Outcomes After Hospital Discharge for Endemic, Community Acquired Methicillin -Resistant and Susceptible Staphylococcus Aureus Skin Infection. CID 2007;44:483-92 30 Schmitz FJ, Fluit AC, Hafner D, et al. Development of Resistance to Ciprofloxacin, Rifampin, and Mupirocin in Methicillin-Susceptible and Resistant Staphylococcus Aureus Isolates. Antimicrob Agents Chemother 2000;44:3229-31. 31 O'Neill AJ, Cove JH, Chopra I. Mutation Frequencies for Resistance to Fusidic Acid and Rifampin in Staphylococcus Aureus. J Antimicrob Chemother 2001;47:647-50. 32 Hiramatsu K, Hanaki H, Ino T, et al. Methicillin-Resistant Staphylococcus Aureus Clinical Strain with Reduced Vancomycin Susceptibility. J Antimicrob Chemother 1997;40:135-36 33 Fridkin SK, Hageman J, McDougal LK, et al, Vancomycin-Intermediate Staphylococcus Aureus Epidemiology Study Group. Epidemiological and Microbiological Characterization of Infections Caused by Staphylococcus Aureus with Reduced Susceptibility to Vancomycin, United States, 1997-2001. Clin Infect Dis. 2003;36:429-39 34 Staphylococcus Aureus Resistant to Vancomycin- United States, 2002. MMWR 2002;51(26): 565-67 35 Liu C, Chambers HF. Staphylococcus Aureus with Heterogeneous Resistance to Vancomycin: Epidemiology, Clinical Significance, and Critical Assessment of Diagnostic Methods. Antimicrob Agents Chemother. 2003;47:3040-45 36 Muto CA, Jernigan JA, Ostrowsky BE et al. SHEA Guidelines for Preventing Nosocomial Transmission of Multidrug Resistant Strains of Staphylococcus Aureus and Enterococcus. Infect Control Hosp Epidem 2003;24:362-86 37 Weber S, Huang S, Oriola, S. Legislative Mandates for the Use of Active Surveillance Cultures to Screen for Methicillin Resistant Staphylocccus Aureus and Vancomycin Resistant Enterococci. Position Statement from the Joint SHEA and APIC Task Force. 2007. 38 Stelfox HT, Bates DW, Redelmeier DA. Safety of Patients Isolated for Infection Control. JAMA 2003;290:1890-1905. 39 Federal Bureau of Prisons. Clinical Practice Guidelines for the Management of Methicillin-Resistant Staphylococcus Aureus (MRSA) Infections (October 2003). http://www.nicic.org/Resources/BOPMedicalGuidelines.aspx) 40 Simor A, Phillips E, McGeer A, et al. Randomized Controlled Trial of Chlorhexidine Gluconate for Washing, Intranasal Mupirocin, and Rifampin and Doxycycline Versus No Treatment for the Eradication of Methicillin-Resistant Staphylococcus Aureus Colonization. Clin Infect Dis 2007;44: 178-85. 41 Garner JS. Guideline for Isolation Precautions in Hospitals. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol 1996;17:53-80 42 Walter WG, Schillinger JE. Bacterial Survival in Laundered Fabrics. Appl Microbiol 1975;29: 368-73 43 Christian RR, Manchester JT, Mellor MT. Bacteriological Quality of Fabrics Washed at Lower- Than-Standard Temperatures in a Hospital Laundry Facility. Appl Env Microbiol 1983;45:591-97. 44 Blaser MJ, Smith PF, Cody HJ, Wang WL, LaForce FM. Killing of Fabric-Associated Bacteria in Hospital Laundry by Low Temperature Washing. J Infect Dis 1984;149:48-57. 45 http://www.cdc.gov/ncidod/dhqp/ar_mrsa.html |
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