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Methods

Surveillance for MRSA has been conducted by 38 hospitals participating in the CNISP since January 1995. Surveillance methods have been described elsewhere.⁶ When a new case of MRSA infection or colonization in an inpatient was identified, the infection control practitioner used a standardized data collection form to abstract demographic and clinical information from the medical records. Aboriginal ethnicity was defined by federal registration as status or nonstatus Indian, Metis, or Inuit, or by self‐identification of individuals as “First Nations People” or “aboriginal.” The presence of infection caused by MRSA was defined according to standard definitions.⁷ MRSA colonization was defined as the presence of MRSA without clinical signs or symptoms of infection. For MRSA to be considered to have been acquired in a hospital or healthcare facility there had to be no evidence that the organism was present at the time of admission, or there had to be evidence that it was likely acquired during a previous hospitalization. The organism was assumed to have been community‐acquired or community‐associated if there was no evidence of acquisition in a hospital or a long‐term care or other healthcare facility.

MRSA isolates were typed with pulsed‐field gel electrophoresis (PFGE) after extraction of DNA and digestion of the extract with SmaI, as described elsewhere.⁸ Electrophoretically generated DNA profiles were digitized and analyzed using GelCompar software, version 4.1 (Applied Maths). Isolates with certain specific DNA profiles were grouped into 1 of 6 Canadian epidemic strains of MRSA (designated “CMRSA‐1, CMRSA‐2,” etc),⁸ and compared with MRSA clones described in the United States.⁹ For SCCmec typing, PCR was done using 9 primer pairs targeting loci of the 4 different SCCmec cassettes.¹⁰ Detection of the Panton‐Valentine leukocidin (PVL) gene locus was done with PCR as described elsewhere.¹¹

Data were analyzed using SAS software, version 6.12 (SAS Institute). Categorical variables were compared using the Fisher exact test or the χ² test, as appropriate. Continuous variables were compared using Student’s t test. All P values were 2‐tailed, and a P value of .05 or less was considered to be statistically significant. Variables found to be significant in univariate analysis were included in a backward logistic regression model. Effect modification between factors was searched for by testing appropriate interaction terms for statistical significance.

Results

In the years 1995‐2002, a total of 279 aboriginals in whom MRSA was detected were hospitalized in CNISP hospitals, representing 2.2% of all detected persons with MRSA who were identified in the surveillance, and 3.5% of those for whom ethnicity was reported. Although the incidence of MRSA colonization or infection in these hospitals increased from 0.5 cases per 1,000 admissions in 1995 to 4.5 cases per 1,000 admissions in 2002 ( ), the proportion of cases in aboriginals did not vary over time.

Demographic and clinical characteristics of patients with MRSA isolated are summarized in Table 1. In the logistic regression analysis, variables that were found to be independently associated with isolation of MRSA from aboriginals included the following: age of less than 18 years (odds ratio [OR], 11.0; 95% confidence interval [CI], 7.5‐16.0; P < .0001), female sex (OR, 1.7; 95% CI, 1.3‐2.2; ), hospitalization in western Canadian provinces (OR, 11.4; 95% CI, 4.7‐27.8; ), MRSA infection at any anatomical site (OR, 3.8; 95% CI, 2.1‐7.2; ), and MRSA infection or colonization involving skin and soft tissues (OR, 4.1; 95% CI, 1.7‐9.9; ).

Table 1.  Demographic and Clinical Characteristics of Patients Infected With Methicillin‐Resistant Staphylococcus aureus (MRSA) in Canadian Hospitals, 1995‐2002

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A total of 148 MRSA isolates from aboriginals and 3,589 isolates from nonaboriginals were available for antimicrobial susceptibility testing and molecular typing by PFGE. Isolates from aboriginals were less likely to be resistant to erythromycin or clindamycin, compared with MRSA isolates from nonaboriginals (72% vs 94% of isolates; ), as well as to trimethoprim‐sulfamethoxazole (22% vs 49%; P < .0001) and ciprofloxacin (46% vs 90%; ). However, MRSA isolates from aboriginals were more likely to be resistant to mupirocin than were isolates from nonaboriginals (10% vs. 4%; ). Resistance to glycopeptides was not detected in any MRSA isolates. Only 64% of the isolates from aboriginals could be grouped into 1 of 6 previously described Canadian epidemic clones, compared with 92% of the strains from nonaboriginals ( ) (Table 2).⁸ More than half (59%) of the MRSA isolates from aboriginals were SCCmec type IV. Fifteen (10%) of 149 isolates from aboriginals contained the PVL gene locus.

Table 2.  Strains of Methicillin‐Resistant Staphylococcus aureus (MRSA) Isolates Recovered From Aboriginals and From Nonaboriginals in Canada, 1995‐2002

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Discussion

In the past decade, the dissemination of MRSA in native aboriginal populations has been reported in parts of the United States, Australia, New Zealand, and islands of the south Pacific.^1‐4 Infections caused by MRSA have also been reported among First Nations People in Canada, most often from the prairie provinces.^5,12,13 Aboriginal Canadians comprise approximately 3% of the Canadian population and are known to have higher rates of many respiratory, enteric, and bloodborne infectious diseases.¹⁴ To our knowledge, this is the first study in Canada to determine the clinical and epidemiologic features of MRSA colonization and infection in hospitalized aboriginals, using data obtained from national surveillance.⁶

In this study, aboriginals in whom MRSA was detected were almost twice as likely to be infected (61%) than were nonaboriginals (33%) ( ). This may not be surprising, given that the majority of cultures that yielded MRSA for aboriginals were performed to confirm suspected infection, rather than for screening or surveillance. This could bias the results, if criteria for MRSA screening were applied differently to hospitalized aboriginals and nonaboriginals, although we do not believe this was likely to have occurred. Most of these infections involved skin and soft tissues, as reported elsewhere.^2,4,15

In previous studies, it was assumed that the majority of MRSA isolates from aboriginal patients were community associated.^1‐5^,12,15 In several of these studies, transmission of a single clone of MRSA was thought to have occurred in the community.^1,2,15 In the present study, we used stringent criteria to define community acquisition, and we considered that most MRSA isolates from hospitalized aboriginals were associated with a hospital or healthcare facility. Nevertheless, Canadian aboriginals were 6 times more likely to have had community‐associated MRSA isolated than were nonaboriginals (26% vs. 4%; ). A lower rate of healthcare‐associated MRSA colonization and infection among Canadian aboriginals may be explained, in part, by reduced access to healthcare facilities. Further evidence of community acquisition of at least a subset of MRSA strains isolated from aboriginals may also be provided by laboratory characterization of these isolates. MRSA isolates from Canadian aboriginals tended to be more susceptible to antimicrobial agents and to possess the SCCmec type IV locus and the PVL gene locus. These findings are typical of community‐acquired MRSA strains internationally, even when strains are of diverse genetic backgrounds.^16‐19

The results of this study are similar to those of previous reports from Canadian prairie provinces,^5,12,13 indicating that MRSA is being transmitted within native communities. These observations may be explained, in part, by socioeconomic and demographic factors. Several markers for poorer health status among First Nations People in Canada have been identified, including lower life expectancy, higher infant mortality, and higher hospitalization rates.^14,20 Overcrowded housing on native reserves has been a recognized problem for many years; in 1999, nineteen percent of dwellings had more than 1 person per room, and only 57% of the housing units were considered to be adequate.²⁰ Overcrowding, as reflected by large household size, was recently found to be associated with MRSA carriage in a rural American Indian population in Washington state.²¹

The results of this study indicate that the epidemiology and clinical characteristics of MRSA infection in Canadian aboriginals is similar to that reported in other native or aboriginal populations around the world. However, they are distinct from those of the general patient population with MRSA infection in Canadian hospitals. The genetic background of the MRSA isolates from aboriginals also varies from that of non‐aboriginal strains. Further investigations are required to determine the incidence of MRSA infection in aboriginals in Canada and to define risk factors associated with the acquisition of this organism in native communities.

Members of the Canadian Nosocomial Infection Surveillance Program (CNISP)

Dr. Elizabeth Bryce, Vancouver General Hospital, Vancouver, British Columbia; Dr. John Conly, Foothills Medical Centre, Calgary, Alberta; Dr. John Embil, Health Sciences Centre, Winnipeg, Manitoba; Dr. Joanne Embree, Health Sciences Centre, Winnipeg, Manitoba; Dr. Michael Gardam, University Health Network, Toronto, Ontario; Ms. Denise Gravel, Centre for Infectious Disease Prevention and Control, Health Canada; Dr. Elizabeth Henderson, Peter Lougheed Centre, Calgary, Alberta; Dr. James Hutchinson, Health Sciences Centre, St. John’s, Newfoundland.; Dr. Michael John, London Health Sciences Centre, London, Ontario; Dr. Lynn Johnston, Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia; Dr. Pamela Kibsey, Victoria General Hospital, Victoria, British Columbia; Dr. Joanne Langley, I. W. K. Grace Health Science Centre, Halifax, Nova Scotia; Dr. Mark Loeb, Hamilton Health Sciences Corporation, Hamilton, Ontario; Dr. Anne Matlow, Hospital for Sick Children, Toronto, Ontario; Dr. Allison McGeer, Mount Sinai Hospital, Toronto, Ontario; Dr. Sophie Michaud, CHUS‐Hôpital Fleurimont, Sherbrooke, Quebec; Dr. Mark Miller, SMBD‐Jewish General Hospital, Montreal, Quebec; Dr. Dorothy Moore, Montreal Children’s Hospital, Montreal, Quebec; Dr. Michael Mulvey, Canadian Science Centre for Human and Animal Health, Health Canada; Ms. Marianna Ofner‐Agostini, Centre for Infectious Disease Prevention and Control, Health Canada; Ms. Shirley Paton, Centre for Infectious Disease Prevention and Control, Health Canada; Dr. Virginia Roth, The Ottawa Hospital, Ottawa, Ontario; Dr. Andrew Simor, Sunnybrook and Women’s College Health Sciences Centre, Toronto, Ontario; Dr. Geoffrey Taylor, University of Alberta Hospital, Edmonton, Alberta; Dr. Mary Vearncombe, Sunnybrook and Women’s College Health Sciences Centre, Toronto, Ontario; Dr. Alice Wong, Royal University Hospital, Saskatoon, Saskatchewan; Dr. Dick Zoutman, Kingston General Hospital, Kingston, Ontario.