Control and treatment of methicillin-resistant Staphylococcus aureus in Canadian paediatric healthcare institutions

Infectious Diseases and Immunization Committee, Canadian Paediatric Society (CPS) 

Abstract published in Paediatrics & Child Health 2006; 11(3): 163-165
Reference No. ID06-01

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Contents

EPIDEMIOLOGY

In the United States and in Europe, the presence of methicillin-resistant Staphylococcus aureus (MRSA) in hospitalized patients is no longer a sporadic occurrence, and MRSA has become endemic in many institutions (1,2). MRSA is found sporadically in many health care facilities in Canada , but has become endemic in a number of institutions and outbreaks occur. A recent report from the 38 acute care hospitals participating in the Canadian Nosocomial Infection Surveillance Program (CNISP) noted an increase in the rate of patients colonized or infected with MRSA from 0.46 patients per 1000 admissions in 1995 to 5.10 per 1000 admissions in 2003. The proportion of S. aureus isolates that were methicillin-resistant increased from 0.95% to 10.39% (3). These 10 fold increases indicate that many hospitals have not been successful in controlling transmission of MRSA.  

Of the patients identified as having MRSA in these 38 hospitals, only 2.4% were children (4). Given the relatively low number of cases in children, prevention of MRSA transmission to paediatric patients hospitalized in Canada should be an achievable goal if appropriate measures are taken.  

MRSA is no longer an exclusively nosocomial pathogen. Community acquisition of MRSA in children without risk factors has emerged in many countries in recent years (5-10) and has been reported in Canada, especially in the Aboriginal population (3,11,12). In the Canadian CNISP hospitals, 6% of all patients where source of MRSA was identified had acquired it in the community, but 24% of the children had community-acquired MRSA (4). Although MRSA strains of hospital origin may be transmitted in the community (1,10), the increasing prevalence of community acquisition of MRSA is not explained by the spread of hospital strains. Community strains are frequently distinct from hospital strains and appear to have arisen outside the health care setting as a result of antibiotic pressure (13-15). Transmission has been documented in child care centres, (16,17) between siblings (7,17) and in athletic teams (18). Strains acquired in the community are usually more susceptible to non beta-lactam antibiotics (clindamycin, trimethoprim-sulfamethoxazole, tetracycline, ciprofloxacin) than are hospital strains and often have different genotypes (10,15).  

Community strains are often characterized by a specific type IV methicillin resistance gene cassette and Panton –Valentine leukocidin (PVL) genes (19,20). Strains carrying the PVL gene have been identified worldwide (10,15,20). These strains appear to occur more frequently in young children than in adults (15). In the Canadian CNISP hospitals 39% of the isolates from children but only 10% of those from adults expressed type IV resistance (4). 

There are conflicting data on the virulence of MRSA. In some instances morbidity and mortality attributable to S aureus appear to be similar for methicillin-susceptible and MRSA (21). In others, introduction of MRSA has resulted in increased infection and case fatality rates (22,23). Differences in strains may explain these discrepancies. The PVL gene has been associated with increased virulence manifested by severe necrotizing pneumonia and complicated musculoskeletal infections (20,24-25).  

Community MRSA strains have been introduced into hospitals and transmitted there (26-30). Transmission in newborn nurseries is of increasing concern (28-30). A study in Houston indicated that community MRSA strains in a neonatal intensive care nursery were due to multiple introductions and not nosocomial spread (31).  

IDENTIFICATION OF MRSA

Standard microbiology laboratory methods to detect MRSA include an oxacillin screen plate. Rapid tests which detect the mecA gene of MRSA by polymerase chain reaction or the mecA gene product PLP2A by immune agglutination are also used (32,33). PCR may be performed directly on specimens, thus shortening the time to obtain test results. However, cultures are still essential to guide antibiotic therapy. Strains apparently susceptible to clindamycin should be tested for inducible clindamycin resistance (34,35).  

Typing of MRSA isolates may be needed to identify potential sources of MRSA and to differentiate between endemic and epidemic strains. The antimicrobial profile is readily available in clinical laboratories but provides limited information for strain differentiation. Molecular typing techniques may be indicated in an epidemiological investigation (36).  

TREATMENT OF DOCUMENTED OR SUSPECTED MRSA INFECTIONS

If there is an increased prevalence of MRSA in the community and S. aureus infection is suspected, efforts should be made to obtain specimens for microbiology culture in order to determine antimicrobial sensitivity (10,15). It has been suggested that when more than 10% of community S aureus isolates are resistant to methicillin, empiric therapy for suspected S aureus infections should include treatment for MRSA (35,37). Likewise, decisions on empiric therapy for suspected nosocomial S aureus infection should take into consideration the possibility of exposure to MRSA. Where prevalence of community MRSA is low and exposure to MRSA unlikely, beta-lactam antibiotics remain the drugs of choice for empiric therapy.  

Serious suspected or documented MRSA infection should be treated with vancomycin. As methicillin sensitive S aureus infections respond more rapidly to beta-lactam antibiotics than to vancomycin, empiric therapy for severe infection should include a beta-lactam as well, pending microbiology results. For life threatening infections, gentamicin and/or rifampin should be added. Abscesses should be drained promptly. Clindamycin may be an option for therapy of selected serious MRSA infections once sensitivity results are available and inducible clindamycin resistance has been excluded. As it is bacteriostatic, it should not be used if a bactericidal antibiotic is required. For selected patients, linezolid, which is also bacteriostatic, may be warranted. The bactericidal agent quinupristin-dalfopristin is a further option, but experience in paediatrics is quite limited at present (9,10,15,35,37,38).  

For less serious infections, such as localized skin or soft tissue infections, options for empiric therapy of suspected MRSA infection of community origin include oral clindamycin, trimethoprim-sulfamethoxazole, tetracycline, a macrolide or a quinolone. Local sensitivity patterns should be considered. Clindamycin is the drug of choice if group A streptococcus may also be involved. Tetracyclines should be avoided in children less than 8 years of age unless benefit outweighs risk of toxicity. For minor superficial infections, incision and drainage may suffice(7,8,10,15.35,37).  

TRANSMISSION

MRSA is most commonly introduced into an institution by an infected or colonized patient who serves as a reservoir. The principal mode of transmission is transfer from patient to patient on the hands of hospital personnel. Contaminated equipment may also be involved. Less commonly a colonized or infected health care worker may disseminate the organism. Environmental contamination is uncommon, but may be an important route of transmission in a burn unit, and droplet transmission may occur during the care of a patient with MRSA pneumonia (1,39).

Colonization

Approximately 30-50% of healthy children and adults are nasal carriers of S aureus (40). Examples of populations with an increased frequency of S aureus carriage are newborns, hospital workers, hemodialysis patients and those with desquamating skin disorders such as eczema. The most frequently colonized site is the anterior nares, but other potential sites include the skin, especially with dermatitis, burns, wounds or other skin lesions, the rectum, the respiratory tract and ostomy sites. The nares have been found to be the most useful site with a sensitivity of 93% and negative predictive value 95% (41). Factors associated with MRSA colonization are prolonged hospitalization, intensive care admission, burns and treatment with multiple antibiotics (1,2,39). MRSA may be carried for an extremely long period. A study of known carriers indicated a carriage half-life of about 40 months (41).  

Eradication of the carrier state

Eradicating carriage of MRSA is very difficult and should not been attempted routinely. It should be considered for specific situations, such as the health care worker who has been epidemiologically linked to an outbreak, a patient for whom MRSA colonization poses a particular risk of infection or of transmission to others, and for a limited period of time in attempts to control an outbreak.  

Eradication rates of 30-90% have been reported but relapse or reinfection is common. Most reports are based on uncontrolled studies with short follow-up periods. Decolonization is more likely to be successful when colonization is limited to the nose, and is unlikely to be successful if colonization involves devices such as foley catheters, endotracheal or tracheostomy tubes, or ostomy sites (1,38).   

Although many agents are active in vitro, few agents reach sufficient concentrations in colonized sites to be clinically useful. Topical agents can deliver higher concentrations to the colonized site, especially the nares where oral agents achieve lower concentrations. Treatment with any antibiotic may lead to the emergence of resistance, especially if used for large numbers of patients or repeatedly on the same patient (1,38).  

Topical agents that have been used include mupirocin, bacitracin, povidone-iodine, and chlorhexidine or hexachloraphene soap for bathing. Oral therapies used include trimethoprim /sulfamethoxazole (TMP/SMX), ciprofloxacin and minocycline, usually used in combination with rifampin. No regimen has been shown to be clearly superior (42). A 90% eradication rate was reported using a combination of chlorhexidine baths, mupirocin ointment application to the nares, and oral rifampin combined with TMP/SMX or doxycycline, although follow-up time was short (43). Until more conclusive studies are performed, it is reasonable to use a combination of topical and oral therapy for the eradication of nasal carriage in specific situations where it is considered warranted. A combination of antiseptic bathing, a topical agent applied to the nares, and at least two oral antibiotics to which the colonizing strain is known to be susceptible, should be considered.

Judicious use of antibiotics

A large proportion of hospitalized patients receive antibiotic therapy, sometimes unnecessarily. Widespread use of antibiotics in general and fluoroquinolones in particular increase the risk of MRSA colonization in the individual and MRSA transmission in institutions. Excessive or inappropriate antibiotic therapy and prophylaxis should be avoided (1,2).  

PREVENTION OF TRANSMISSION IN INSTITUTIONS - INFECTION CONTROL MEASURES

Aggressive infection control measures including surveillance cultures of at risk patients, contact precautions, and reduction of overcrowding have been shown to decrease MRSA transmission in hospitals, including paediatric settings (1,2, 44-46).  

Current policies for MRSA screening identify patients with known risk factors. The increasing prevalence of community acquisition of MRSA is a reminder that it is impossible to identify all patients colonized with multi-resistant organisms without implementing universal screening, which would entail high costs. Therefore it is imperative that appropriate routine practices be observed for all patients, to minimize risk of transmission from unidentified carriers. These include handwashing before and after contact with a patient, wearing gloves when anticipating direct hand contact with blood, body fluids, secretions or excretions, or items contaminated with these substances, or with mucous membranes or non-intact skin; wearing a surgical mask and eye protection (goggles or face shield) during procedures which may result in splashing of blood, body fluids, secretions or excretions into the face, and wearing a gown to protect uncovered skin and clothing during procedures likely to generate splashes of blood, body fluids, secretions, or excretions. The need for additional precautions should be based on the child’s clinical presentation – eg, contact precautions for all children with draining wounds or skin infections, and contact-droplet precautions for those with respiratory tract infections (47). Implementation of these measures should go a long way to prevent transmission of MRSA from children without risk factors and not known to be colonized on admission.  

The Canadian Paediatric Society recommends that the measures detailed in the following table be implemented to interrupt MRSA transmission and prevent MRSA from becoming endemic in paediatric health care facilities (1, 40, 47-49).

TABLE:  Summary of recommendations to control methicillin-resistant Staphylococcus aureus (MRSA) transmission in health care facilities  
1.  Routione practices and
     additional precautions
  • Reinforce Routine Practices for care of all patients
  • Implement Additional Precautions based on clinical presentation, regardless of MRSA status. This includes contact precautions for children with draining wounds or skin lesions that cannot be kept covered, and droplet precautions for those with respiratory infections  
2.  Identification of cases  
     Selective screening of
     patients
  • Screen patients if:
    • hospitalized outside of Canada within the past year
    • transferred from a centre with endemic MRSA or a current or recent outbreak of MRSA
    • known contact with a person colonized with MRSA, in hospital or other institution, or a colonized family member
    • known previously colonized or infected with MRSA
    Sporadic cases
  •  Sporadic cases identified by isolation of MRSA from clinical specimens:
    • arrange for microbiology laboratories to promptly inform the infection control practitioner and attending physician so that appropriate measures may be undertaken
    Previously known cases
  • Identify by a flagging system
    Screening procedure
  • Culture both anterior nares (one swab)
  • Culture wounds, skin lesions, ostomy sites; endotracheal aspirate if intubated; urine if indwelling catheter in place
  • Culture umbilicus of neonate
3.  Patient placement  

    Inpatients                 
– known MRSA

 
  • Place in a single room if possible 
  • If not, prioritize single rooms for patients more likely to transmit (with infected wounds, uncovered skin lesions, stomas, respiratory tract infections, young children with inadequate hygiene who cannot be confined to their bed or bedspace)
  • In shared rooms, maintain strict physical separation of at least a metre between patients and choose roommates who are at low risk of MRSA acquisition or of adverse outcome if infection should occur
  •  Patients colonized with MRSA strains with similar antibiograms may be cohorted
  • Do not cohort a patient with a community strain (which may be more virulent) with a patient with a hospital strain (which may be more resistant)

    Outpatients
 – known MRSA

 
  • Separate a child with risk factors for transmission (colonized wounds, skin lesions or stomas, respiratory tract infection) from other patients and place in an exam room as soon as possible; consider scheduling clinic visits for the end of the day
    Patients exposed to
    MRSA, awaiting results
  • Place in single room if possible. Otherwise prioritize as above
  • Maintain strict physical separation between patients and choose roommates carefully
4. Barrier precautions  
    Inpatients
  • Wear gloves to enter the patient’s room or bedspace
  • Wear a surgical/procedure mask and eye protection as for Routine Practices (during suctioning of patient and for procedures which may result in splashing of secretions, excretions, blood or other body fluids into the face)
  • Wear a surgical/procedure mask if within a metre of patient with respiratory tract infection
  • Wear a gown if it is anticipated that the forearms or clothing will have direct contact with the patient or potentially contaminated items in the patient’s environment
  • Remove gown and gloves before leaving the room
    Outpatients
  • Use gloves, gowns and masks and eye protection as per routine practices
  • If patient has risk factors for transmission (infected wounds, uncovered skin lesions, stomas or respiratory tract infection), use gloves and gowns as for inpatients
5.  Hand hygiene
  • Wash hands using an antiseptic soap or handrinse after patient contact, after touching contaminated equipment or surfaces, and when leaving the patients room or bedspace
  • Wash hands after removing gloves
6.  Patient bathing
  • Use antiseptic skin cleanser for patient bathing (chlorhexidine, triclosan, hexachlorophene)
7.  Environment
  • Reserve equipment for use with the patient or disinfect before use with another patient
8.  Eradication of MRSA

     Consider in selective
     situations only
  • May be indicated for
    • outbreak control
    • for patients to be transferred to a facility where isolation is not feasible
    • healthcare workers implicated in transmission
    • selected high risk patients, to reduce their risk of MRSA infection
  • Use a combination of daily antiseptic bathing (e.g. chlorhexidine), topical therapy (eg, mupirocin 2% ointment to nares three times a day) and oral therapy based on antimicrobial sensitivity of the colonizing strain (e.g. trimethoprim/sulfamethoxazole 4/20 mg TMP/SMX/kg/dose bid (maximum dose 160/800 mg bid) plus rifampin 10 mg/kg/dose bid (maximum dose 300 mg bid) for 7 days
9.  Duration of  precautions  
      Known MRSA carrier
  • Continue for the entire duration of hospitalization, unless long stay  
  • Long stay patients (e.g. over 2 months): discontinue after three sets of cultures taken at intervals of at least one week, and when patient has not received antibiotic therapy for at least a week, are negative for MRSA. Culture nares and any other potentially positive sites
     If re-admitted
  • Screen for MRSA; continue precautions until three consecutive sets of cultures, taken as above, are negative
  • Screening should also be performed on follow-up clinic visits
     MRSA contact
  • Discontinue if screening tests are negative
10.  Management of
        contacts		  
        If one case
  • If patient with MRSA identified and precautions had not been taken, screen likely patient contacts. May be indicated for roommates only, a patient care unit, or special care area (e.g. hemodialysis), depending on the index patient’s activities
       If one nosocomial case
  • Further screening may be warranted to identify the potential source
       If an outbreak
  • Outbreak defined as increase in incidence or prevalence of MRSA over background rates 
    • if MRSA endemic, knowledge of background rate important to permit detection of outbreak
    • if no previous cases, two cases documented concurrently or in close proximity should be investigated
  • Seek the advice of an expert for outbreak management
11.  Education
  • Educate all staff about infection control policies 
  • Provide information for patient and family (reasons for precautions, implications for the patient, what to do at home and if returning a health care facility)
12.  Transfer to another
        facility
  • Inform the facility in advance
13.  Judicious antibiotic
        use
  • Use antibiotics wisely; avoid excessive or inappropriate use. Limit use of fluroquinolones


REFERENCES

  1. Muto CA, Jernigan JA, Ostrowsky BE, Richet HM, Jarvis WR, Boyce JM, Farr BM. SHEA Guideline for preventing nosocomial transmission of multidrug-resistant strains of Staphylococcus aureus and Enterococcus. Infect Control Hosp Epidemiol 2003;24:362-86.
  2. Boyce JM, Havill NL, Kohan C, Dumigan DG, Ligi CE. Do infection control measures work for methicillin-resistant Staphylococcus aureus? Infect Control Hosp Epidemiol 2004;25:395-401.  
  3. Simor AE, Ofner-Agostini M, Gravel D, et al.; and members of the Canadian Hospital Epidemiology Committee and Canadian Nosocomial Infection Surveillance Program, Health Canada. Surveillance for methicillin-resistant Staphylococcus aureus in Canadian hospitals – A report update from the Canadian Nosocomial Infection Surveillance Program. CCDR 2005;31:33-40.
  4. Vanderkooi OG, Bryce E, McGeer A, et al. Epidemiology of methicillin-resistant Staphylococcus aureus in Canadian children from 1995 to 2002. (abstract). AMMI Canada–CACMID 2005 Annual Conference, Ottawa, Ontario, April 14-17, 2005; Can J Infect Dis Med Micro 2005;16:123 (P1.11).
  5. Hussain FM, Boyle-Vavra S, Bethel CD, Daum RS. Current trends in community-acquired methicillin-resistant Staphylococcus aureus at a tertiary care pediatric facility. Pediatr Infect Dis J 2000;19:1163-6.  
  6. Baggett HC, Hennessy TW, Rudolph K, et al. Community-onset methicillin-resistant Staphylococcus aureus associated with antibiotic use and the cytotoxin Panton-Valentine leukocidin during a furunculosis outbreak in rural Alaska. J Infect Dis. 2004;189:1565-73.
  7. Dietrich DW, Auld DB, Mermel LA. Community-acquired methicillin-resistant Staphylococcus aureus in southern New England children. Pediatrics. 2004;113:e347-52.
  8. Lee MC, Rios AM, Aten MF, et al. Management and outcome of children with skin and soft tissue abscesses caused by community-acquired methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. 2004;23:123-7.
  9.  Kaplan S, Hulten K, Gonzalez B, et al. Three-year surveillance of community-acquired Staphylococcus aureus infections in children. Clin Infect Dis 2005;40:1785-91.  
  10. Zetola N, Francis SF, Nuermberger EL, Bishai WR. Community-acquired methicillin-resistant Staphylococcus aureus: an emerging threat. Lancet Infect Dis 2005;5:275-86.  
  11. Embil J, Ramotar K, Romance L, et al. Methicillin- resistant Staphylococcus aureus in tertiary care institutions on the Canadian prairies 1990-1992. Infect Control Hosp Epidemiol 1994;15:646-51.
  12. Canadian Paediatric Society, First Nations and Inuit Health Committee. Methicillin-resistant Staphylococcus aureus in First Nations communities. Paediatr Child Health 2005;10(9):557-9.  
  13. Buckingham SC, McDougal LK, Cathey LD, et al. Emergence of community-associated methicillin-resistant Staphylococcus aureus at a Memphis, Tennessee Children's Hospital. Pediatr Infect Dis J. 2004;23:619-24.
  14. Sattler CA, Mason EO Jr, Kaplan SL. Prospective comparison of risk factors and demographic and clinical characteristics of community-acquired, methicillin-resistant versus methicillin-susceptible Staphylococcus aureus infection in children Pediatr Infect Dis J 2002;21:910-7.  
  15. Fridkin SK , Hageman JC, Morrison M, et al.; Active Bacterial Core Surveillance Program of the Emerging Infections Program Network. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med 2005;352:1436-44.  
  16. Adcock PM, Pastor P, Medley F, Patterson JE, Murphy TV. Methicillin-resistant Staphylococcus aureus in two child care centers. J Infect Dis 1998;178:577-80.
  17. Shahin R, Johnson IL, Jamieson F, McGeer A, Tolkin J, Ford-Jones EL. Methicillin-resistant Staphylococcus aureus carriage in a child care center following a case of disease. Toronto Child Care Center study Group. Arch Pediatr Adolesc Med 1999;153:864-8.
  18. Lindenmeyer JM, Schoenfeld S, O’Grady R, Carney JK. Methicillin-resistant Staphylococcus aureus in a high school wrestling team and the surrounding community. Arch Intern Med 1998;158:895-9.
  19. Daum RS, Ito T, Hiramatsu K, et al. A novel methicillin-resistance cassette in community-acquired methicillin-resistant Staphylococcus aureus isolates of diverse genetic backgrounds. J Infect Dis 2002;186:344-7.  
  20. Chambers HF. Community-associated MRSA-resistance and virulence converge. N Engl J Med 2005;352:1485-7.  
  21. Hershow RC, Khayr WF, Smith NL. A comparison of clinical virulence of nosocomially acquired methicillin-resistant and methicillin-sensitive Staphylococcus aureus infections in a university hospital. Infect Control Hosp Epidemiol 1992;13:587-93.
  22. Jernigan JA, Clemence MA, Stott GA, et al. Control of methicillin-resistant Staphylococcus aureus at a university hospital: one decade later. Infect Control Hosp Epidemiol 1995;16:686-96.  
  23. Cosgrove SE, Sakoulas G, Perencevich EN, Schwaber MJ, Karchmer AW, Carmeli Y. Comparison of mortality associated with methicillin-resistant and methicillin-susceptible Staphylococcus aureus bacteremia: a meta-analysis. Clin Infect Dis 2003;36:53-9.  
  24. Gillet Y, Issartel B, Vanhems P, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet 2002;359:753-9.
  25. Martinez-Aguilar G, Avalos-Mishaan A, Hulten K, Hammerman W, Mason EO Jr, Kaplan SL. Community-acquired, methicillin-resistant and methicillin-susceptible Staphylococcus aureus musculoskeletal infections in children. Pediatr Infect Dis J 2004;23:701-6.
  26. O’Brien FG, Pearman JW, Gracey M, Riley TV, Grubb WB. Community strain of methicillin-resistant Staphylococcus aureus involved in a hospital outbreak. J Clin Microbiol 1999;37:2858-62.  
  27. Saiman L, O’Keefe M, Graham PL 3rd, et al. Hospital transmission of community-acquired methicillin-resistant Staphylococcus aureus among postpartum women. Clin Infect Dis 2003;37:1313–9.  
  28. Eckhardt C, Halvosa JS, Ray SM, Blumberg HM. Transmission of methicillin-resistant Staphylococcus aureus in the neonatal intensive care unit from a patient with community-acquired disease. Infect Control Hosp Epidemiol 2003;24:460-1.  
  29. Bratu S, Eramo A, Kopec R, et al. Community-associated methicillin-resistant Staphylococcus aureus in hospital nursery and maternity units. Emerg Infect Dis 2005;11:808-13.  
  30. Regev-Yochay G, Rubinstein E, Barzilai A, et al. Methicillin-resistant Staphylococcus aureus in neonatal intensive care unit. Emerg Infect Dis 2005;11:453-6.  
  31. Healy CM, Hulten KG, Palazzi DL, Campbell JR, Baker CJ. Emergence of new strains of methicillin-resistant Staphylococcus aureus in a neonatal intensive care unit. Clin Infect Dis 2004;39:1460-6.
  32. Unal S, Werner K, DeGirolami P, Barsanti F, Eliopoulos G. Comparison of tests for detection of methicillin-resistant Staphylococcus aureus in a clinical microbiology laboratory. Antimicrob Agents Chemother 1994;38:345-7.
  33. Louie L, Matsumura SO, Choi E, Louie M, Simor AE. Evaluation of three rapid methods for detection of methicillin resistance in Staphylococcus aureus. J Clin Microbiol 2000;38:2170-3.  
  34. Lewis JS 2nd, Jorgensen JH. Inducible clindamycin resistance in Staphylococci: should clinicians and microbiologists be concerned? Clin Infect Dis 2005;40:280-5.  
  35. Kaplan SL. Treatment of community-associated methicillin-resistant Staphylococcus aureus infections. Pediatr Infect Dis J 2005;24:457-8.
  36. Mulvey MR, Chui L, Ismail J, et al; Canadian Committee for the Standardization of Molecular Methods. Development of a Canadian standardized protocol for subtyping methicillin-resistant Staphylococcus aureus using pulsed-field gel electrophoresis. J Clin Microbiol 2001;39:3481-5.  
  37. Baker CJ, Frenck RW. Change in management of skin/soft tissue infections needed. AAP news 2004;25:105.  
  38. Simor AE, Loeb M; and the CIDS/CAMM Guidelines Committee. The management of infection and colonization due to methicillin-resistant Staphylococcus aureus: A CIDS/CAMM position paper. Can J Infect Dis Med Micro 2004; 15:39 -48.
  39. 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.
  40. American Academy of Pediatrics. Summaries of infectious diseases. Staphylococcal infections. In: Pickering LK, ed. 2003 Red Book: Report of the Committee on Infectious Diseases, 26th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2003: pp 561-573.
  41. Sanford MD, Widmer AF, Bale MJ, Jones RN, Wenzel RP. Efficient detection and long term persistence of the carriage of methicillin-resistant Staphylococcus aureus. Clin Infect Dis 1994;19:1123-8.
  42. Loeb M, Main C, Walker-Dilks C, Eady A. Antimicrobial drugs for treating methicillin-resistant Staphylococcus aureus colonization. Cochrane Database Syst Rev 2003;(4):CD003340.  
  43. Fung SK, Louie M, Simor AE. Combined topical and oral antimicrobial therapy for the eradication of methicillin-resistant Staphylococcus aureus (MRSA) colonization in hospitalized patients. Can J Infect Dis 2002;13:287-92.
  44. Haley RW, Cushion NB, Tenover FC, et al. Eradication of endemic methicillin‑resistant Staphylcoccus aureus infections from a neonatal intensive care unit. J Infect Dis 1995;171:614-24.  
  45. Jernigan JA, Titus MG, Gröschel DHM, Getchell-White SI, Farr BM. Effectiveness of contact isolation during a hospital outbreak of methicillin‑resistant Stapylococcus aureus. Am J Epidemiol 1996:143;496-504.  
  46. Cosseron-Zerbib M, Roque Afonso AM, Naas T, et al. A control programme for MRSA (methicillin-resistant Staphylococcus aureus) containment in a paediatric intensive care unit: evaluation and impact on infections caused by other micro-organisms. J Hosp Infect 1998;40:225-35.  
  47. Health Canada, Steering Committee on Infection Control Guidelines. Infection control guidelines. Routine practices and additional precautions for preventing the transmission of infection in health care. Can Commun Dis Rep 1999;25S4:1-142.
  48. Revised guidelines for the control of methicillin-resistant Staphylococcus aureus infection in hospitals. British Society for Antimicrobial Chemotherapy, Hospital Infection Society and the Infection Control Nurses Association. J Hosp Infect 1998;39:253-90.
  49. Arnold MS, Dempsey JM, Fishman M, McAuley PJ, Tibert C, Vallande NC. The best hospital practices for controlling methicillin-resistant Staphylococcus aureus: on the cutting edge. Infect Control Hosp Epidemiol 2002;23:69-76.


INFECTIOUS DISEASES AND IMMUNIZATION COMMITTEE (2005-06)

Members: Drs Simon Richard Dobson, BC’s Children’s Hospital, Vancouver, British Columbia; Joanne Embree, The University of Manitoba, Winnipeg, Manitoba (chair); Joanne Langley, IWK Health Centre, Halifax, Nova Scotia; Dorothy Moore, The Montreal Children’s Hospital, Montreal, Quebec; Gary Pekeles, The Montreal Children’s Hospital, Montreal, Quebec (board representative); Élisabeth Rousseau-Harsany, Hôpital Sainte-Justine, Montreal, Quebec (board representative); Lindy Samson, Children’s Hospital of Eastern Ontario, Ottawa, Ontario
Consultant: Dr Noni MacDonald, Department of Pediatrics, IWK Health Centre, Halifax, Nova Scotia
Liaisons: Drs Upton Allen, The Hospital for Sick Children, Toronto, Ontario (Canadian Pediatric AIDS Research Group); Scott Halperin, IWK Health Centre, Halifax, Nova Scotia (IMPACT); Monica Naus, BC Centre for Disease Control, Vancouver, British Columbia (Health Canada, National Advisory Committee on Immunization); Larry Pickering, Centers for Disease Control and Prevention, Atlanta, Georgia, USA (American Academy of Pediatrics, Committee on Infectious Diseases)
Principal author: Dr Dorothy Moore, The Montreal Children’s Hospital, Montreal, Quebec

Posted March 2006
Disclaimer: The recommendations in this position statement do not indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate. Internet addresses are current at time of publication.