Methicillin-resistant Staphylococcus aureus in 
First Nations communities in Canada

First Nations and Inuit Health Committee, Canadian Paediatric Society (CPS)

Paediatr Child Health 2005;10(9):557-9
Reference No. FNIH05-02

Revision in progress February 2009

Index of position statements from the First Nations, Inuit and Métis Health Committee

Contents

• Community-acquired MRSA
• MRSA in First Nations communities in Canada
• Antibiotic sensitivity
• Recommendations
• References

First reported in Canada in 1981 by Low et al (1), methicillin-resistant Staphylococcus aureus (MRSA) has emerged as an important hospital-based bacterial pathogen in Canada (2,3). Hospital surveillance data from nine Canadian provinces have been collected since 1995 (4). Reported from 1995 to 1999, this surveillance documents a steady increase in the incidence of infections caused by MRSA and MRSA colonization. Regional variations in MRSA prevalence are observed. By 1999, just over 5% of S aureus strains isolated from hospitalized patients in Canada were methicillin-resistant (4). The corresponding rate for isolates from American hospitals was 35% (5,6). Prevention of transmission of MRSA in hospitals has focused on infection-control practices and surveillance (6-8).

In 1999, the Canadian Paediatric Society published the statement “Control of methicillin-resistant Staphylococcus aureus in Canadian paediatric institutions is still a worthwhile goal” (8) (Table 1). The present statement describes the development of community-acquired MRSA infections in First Nations communities in Canada.  

Community-acquired MRSA

MRSA emerged as a community-acquired pathogen in children in the 1990s. Paediatric hospital series from Chicago, Illinois (9), and Corpus Christi, Texas (10), identified an increasing incidence of community-acquired MRSA. Four fatal paediatric cases attributed to community-acquired MRSA were reported in Minnesota and North Dakota between 1997 and 1999 (11). Community-acquired MRSA was defined as a culture-positive specimen collected in a community setting or collected within 48 h to 72 h of hospital admission (12).

There have been several reports (13-16) of asymptomatic paediatric MRSA carriage, with published rates in urban Canadian and American communities of 0.2% to 2.2%. Carriage rates for S aureus, sensitivity not specified, have been identified as 30% to 50% for intermittent carriage and 10% to 20% for persistent carriage (7,8). Nares, perineum and skin are principal sites of paediatric colonization (8). A meta-analysis (17) of 10 community surveys of MRSA carriage pooled over 8000 patients on three continents and found an MRSA prevalence of 1.3%. Risk factors for MRSA carriage included hospitalization or recent outpatient attendance, antibiotic use, chronic illness, intravenous drug abuse and close contact with an individual with any of these risk factors.

MRSA in first nations communities in Canada

One of the earliest reports of community carriage of MRSA was in a First Nations community in Alberta (18). Twenty-one of 422 (4.9%) consecutive patients admitted to hospital from that community between 1987 and 1989 were identified as carrying MRSA. Prior hospital care was the only identifying risk factor. A retrospective survey of five teaching hospitals in the Canadian Prairies between 1990 and 1992 identified First Nations patients as accounting for 62% of those who were MRSA-positive on hospital admission (19).

In 1999, a resident in a long-term care facility in northeastern Saskatchewan who had been recently hospitalized was found to have MRSA. By 2002, 180 cases and carriers were reported in the region, with 76% of these community-acquired infections occurring in three First Nations and Métis communities. Children younger than 10 years of age accounted for 39% of the cases and carriers (20). In six First Nations and Métis communities in northern Saskatchewan, community-acquired MRSA was endemic between 2000 and 2002. Approximately 50% of the cases were among children 14 years of age or younger. Most cases had skin infections (J Irvine, personal communication).

Community-acquired MRSA has also been identified as the cause of infection in American Indian communities. Forty-six of 62 (74%) MRSA infections were classified as community-acquired at an Indian Health Service outpatient clinic in a rural midwestern community (21). Community-acquired MRSA has been identified among Australian Aboriginals from remote communities in the Northern Territory (22). In their paper, Maguire et al (22) called for a community-based control program to improve housing and hygiene, control skin sepsis and make appropriate use of antibiotics.

Crowding, lack of quality running water and heavy antibiotic use may be additional reasons for the MRSA observed in First Nations communities in Canada.

Antibiotic sensitivity

The majority of strains of S aureus produce beta-lactamase, capable of inactivating beta-lactam antibiotics including penicillin and ampicillin. MRSA has further adapted the mechanism for cell wall assembly, with modified receptors for binding penicillin. Bacteria with these modified receptors are resistant to all penicillins and cephalosporins (7). Current Canadian hospital data (23) on the reported resistance and sensitivity pattern of MRSA to antibiotics are as follows:

• 93% resistant to erythromycin and clindamycin;
• 87% resistant to ciprofloxacin;
• 46% resistant to trimethoprim/sulfamethoxazole;
• 3% resistant to fusidic acid; and
• 2% resistant to mupirocin

No Canadian isolates of MRSA have been identified as having reduced sensitivity to vancomycin (23,24). Strains of MRSA with reduced sensitivity to vancomycin have been identified in Japan, the United States and Europe (24,25).

Community-acquired strains of MRSA are less likely than hospital-acquired MRSA strains to be resistant to nonbeta-lactam antibiotics (9,10,12,15,26,27). Clindamycin and trimethoprim/sulfamethoxazole sensitivity has been retained for over 90% of community-acquired MRSA isolates from patients in American centres (28,29). Some Canadian clones of MRSA are reported to have developed mupirocin resistance (30).

Recommendations

Awareness

• Practitioners must be aware of the emergence of community-acquired MRSA as a cause of infection in Canada, particularly in First Nations communities.

Prevention

• Use antibiotics appropriately to reduce or minimize antibiotic resistance (31).
• Optimize the water supply in First Nations communities.
• Provide instruction, beginning in early childhood, regarding the method and value of frequent handwashing.

Infection control

• Emphasize the importance of hand hygiene before and after each completed patient contact by all staff.
• Maintain available ‘waterless’ handwashing supplies in locations where sinks and running water are not readily available.

Treatment

• Incision and drainage, with collection of specimens for antimicrobial culture (when possible) before treating potential S aureus infection.
• Antibiotic selection for potential S aureus infection (28,29,32):
  • mild, localized cutaneous infections: washing with antibacterial soap and water.
  • superficial, localized infections: consider topical treatment with fusidic acid in addition to washing with soap and water.
  • mild to moderate, more generalized infections – one of the following:
    • standard therapy: start with cloxacillin, first-generation cephalosporin or amoxicillin/clavulanic acid
    • in MRSA community: trimethoprim/sulfamethoxazole or clindamycin (note that trimethoprim/sulfamethoxazole does not provide coverage for Group A beta-hemolytic streptococcus)
  • severe or life-threatening staphylococcal infection: initial coverage should include vancomycin pending culture and sensitivity.
• In communities in which MRSA is known to occur, general efforts to determine carriage rates among asymptomatic household contacts are not recommended (33).

References

1. Low DE, Garcia M, Callery S, et al. Methicillin-resistant Staphylococcus aureus – Ontario. Can Dis Wkly Rep 1981;7:249-50.
2. Cooper CL, Dyck B, Ormiston D, et al. Bed utilization of patients with methicillin-resistant Staphylococcus in a Canadian tertiary-care centre. Infect Control Hosp Epidemiol 2002;23:483-4.
3. Kim T, Oh PI, Simor AE. The economic impact of methicillin-resistant Staphylococcus aureus in Canadian hospitals. Infect Control Hosp Epidemiol 2001;22:99-104.
4. Simor AE, Ofner-Agostini M, Bryce E, et al. The evolution of methicillin-resistant Staphylococcus aureus in Canadian hospitals: 5 years of national surveillance. CMAJ 2001;165:21-5.
5. 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.
6. Conly J. Antimicrobial resistance in Canada. CMAJ 2002;167:885-91.
7. Lowy FD. Staphylococcus aureus infections. N Engl J Med 1998;339:520-32.
8. Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Control of methicillin-resistant Staphylococcus aureus in Canadian paediatric institutions is still a worthwhile goal. Paediatr Child Health 1999;4:337-41.
9. Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA 1998;279:593-8.
10. Fergie JE, Purcell K. Community-acquired methicillin-resistant Staphylococcus aureus infections in south Texas children. Pediatr Infect Dis J 2001;20:860-3.
11. From the Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus – Minnesota and North Dakota, 1997-1999. JAMA 1999;282:1123-5.
12. Cookson BD. Methicillin-resistant Staphylococcus aureus in the community: New battlefronts, or are the battles lost. Infect Control Hosp Epidemiol 2000;21:398-403.
13. Suggs AH, Maranan MC, Boyle-Vavra S, Daum RS. Methicillin-resistant asymptomatic Staphylococcus aureus colonization in children without identifiable risk factors. Pediatr Infect Dis J 1999;18:410-4.
14. Shahin R, Johnson IL, Jamieson F, et al. 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.
15. 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.
16. Nakamura MM, Rohling KL, Shashaty M, Lu H, Tang YW, Edwards KM. Prevalence of methicillin-resistant Staphylococcus aureus nasal carriage in the community pediatric population. Pediatr Infect Dis J 2002;21:917-22.
17. Salgado CD, Farr BM, Calfee DP. Community-acquired methicillin-resistant Staphylococcus aureus: A meta-analysis of prevalence and risk factors. Clin Infect Dis 2003;36:131-9.
18. Taylor G, Kirkland T, Kowalewska-Grochowska K, Wang Y. A multistrain cluster of methicillin-resistant Staphylococcus aureus based in a native community. Can J Infect Dis 1990;1:121-6.
19. 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.
20. MacDougall L. MRSA outbreak in three Aboriginal communities in northern Saskatchewan. Melfort, Saskatchewan: Field Epidemiology Training Program. Ottawa: Health Canada, 2002.
21. Groom AV, Wolsey DH, Naimi TS, et al. Community-acquired methicillin-resistant Staphylococcus aureus in a rural American Indian community. JAMA 2001;286:1201-5.
22. Maguire GP, Arthur AD, Boustead PJ, Dwyer B, Currie BJ. Clinical experience and outcomes of community-acquired and nosocomial methicillin-resistant Staphylococcus aureus in a northern Australian hospital. J Hosp Infect 1998;38:273-81.
23. Simor AE, Ofner-Agostini M, Bryce E, McGeer A, Paton S, Mulvey MR; Canadian Hospital Epidemiology Committee and Canadian Nosocomial Infection Surveillance Program, Health Canada. Laboratory characterization of methicillin-resistant Staphylococcus aureus in Canadian hospitals: Results of 5 years of National Surveillance, 1995-1999. J Infect Dis 2002;186:652-60.
24. Conly JM, Johnston BL. VISA, hetero-VISA and VSRA: The end of the vancomycin era? Can J Infect Dis 2002;13:282-4.
25. Sieradzki K, Roberts RB, Haber SW, Tomasz A. The development of vancomycin resistance in a patient with methicillin-resistant Staphyloccus aureus infection. N Engl J Med 1999;340:517-23.
26. Okuma K, Iwakawa K, Turnidge JD, et al. Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community.J Clin Microbiol 2002;40:4289-94.
27. Chambers HF. The changing epidemiology of Staphylococcus aureus? Emerg Infect Dis 2001;7:178-86.
28. Martinez-Aguilar G, Hammerman WA, Mason EO Jr, Kaplan SL. Clindamycin treatment of invasive infections caused by community-acquired methicillin-resistant and methicillin-sensitive Staphylococcus aureus in children. Pediatr Infect Dis J 2003;22:593-8.
29. Naimi TS, LeDell KH, Boxrud DJ, et al. Epidemiology and clonality of community-acquired methicillin-resistant Staphylococcus aureus in Minnesota, 1996-1998. Clin Infect Dis 2001;33:990-6.
30. Mulvey MR, MacDougall L, Cholin B, Horsman G, Fidyk M, Woods S; Saskatchewan CA-MRSA Study Group. Community-associated methicillin-resistant Staphylococcus aureus, Canada. Emerg Infect Dis 2005;11:844-50.
31. Baggett HC, Hennessy TW, Leman R, et al. An outbreak of community-onset methicillin-resistant Staphylococcus aureus skin infections in southwestern Alaska. Infect Control Hosp Epidemiol 2003;24:397-402.
32. Paradisi F, Corti G, Messeri D. Antistaphylococcal (MSSA, MRSA, MSSE, MRSE) antibiotics. Med Clin North Am 2001;85:1-17.
33. Simor AE, Loeb M. The management of infection and colonization due to methicillin-resistant Staphylococcus aureus: A CIDS/CAMM position paper. Can J Infect Dis 2004; 15:39 -48.

First Nations and Inuit Health Committee

Members: Drs James Carson, University of Manitoba, Winnipeg, Manitoba (chair, 2000-2005); James Irvine, La Ronge, Saskatchewan; Marie-Claude Lebeau, Stanton Regional Hospital, Yellowknife, Northwest Territories (2002-2005); Heather Onyett, Queen’s University, Kingston, Ontario (board representative); Kent Saylor, Montreal Children’s Hospital, Montreal, Quebec (chair); Leigh Wincott, Thompson General Hospital, Thompson, Manitoba
Liaisons: Dr George Brenneman, Baltimore, Maryland, USA (American Academy of Pediatrics, Committee on Native American Child Health); Ms Debbie Dedam-Montour, Kahnawake, Quebec (National Indian and Inuit Community Health Representatives Organization); Ms Claudette Dumont-Smith, Ottawa, Ontario (Aboriginal Nurses Association of Canada, 2003-2004); Ms Doris Fox, Ottawa, Ontario (Aboriginal Nurses Association of Canada); Ms Carolyn Harrison, Ottawa, Ontario (Health Canada); Ms Margaret Horn, Kahnawake, Quebec (National Indian and Inuit Community Health Representatives Organization,1995-2004); Ms Kathy Langlois, Ottawa, Ontario (First Nations and Inuit Health Branch, Health Canada); Ms Melanie Morningstar, Ottawa, Ontario (Assembly of First Nations); Dr Vincent Tookenay, Ottawa, Ontario (Native Physicians Association of Canada, 1993-2004)
Principal author: Dr James Carson, University of Manitoba,Winnipeg, Manitoba

Posted November 2005