Community-acquired methicillin-resistant ... - Hindawi
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Can J Infect Dis Med Microbiol Vol 16 No 6 November/December 2005 323 Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba Correspondence: Dr LE Nicolle, Department of Internal Medicine, University of Manitoba, Health Sciences Centre, GG443 – 820 Sherbrook Street, Winnipeg, Manitoba R3A 1R9. Telephone 204-787-7029, fax 204-787-4826, e-mail [email protected] T here are three sure things in life: death, taxes and antimi- crobial resistance appearing on the heels of the introduc- tion and widespread use of an antimicrobial agent. Staphylococcus aureus has always been a poster child for the emergence of antimicrobial resistance (1). Penicillin-resistant strains of S aureus surfaced immediately following the intro- duction of penicillin in the late 1940s; within a few years, most hospital strains were penicillin resistant. There was also the rapid emergence of methicillin-resistant S aureus (MRSA) following the introduction of methicillin in the 1960s. While the replacement of nosocomial methicillin-susceptible S aureus by MRSA has proceeded at different rates in different regions, the overall global progression has been relentless. MRSA became common in Canadian health care facilities later than in the United States; however, since the early 1990s, nosocomial MRSA in Canada has steadily and irrevo- cably increased (2). The current chapter in this story is the progressive dissem- ination of community-acquired MRSA (CAMRSA), mirror- ing the experience with penicillin-resistant S aureus 50 years ago (1). In fact, CAMRSA has been common in some Canadian communities for almost 20 years (3). Northern Aboriginal communities in the prairies have been primarily affected, although there have been rare reports of outbreaks and community spread elsewhere (4). Now, Canadian CAMRSA has appeared in populations at risk identified else- where in North America and Europe. These populations include incarcerated people, as described in this issue of the Journal (pages 343-348), as well as parenteral drug users, homeless people and other marginalized groups. Even in com- munities with long-standing experiences with CAMRSA, more severe S aureus infections may now be recognized. The specific strains identified in Canada are the same as those reported outside our borders and are usually characterized by the presence of Panton-Valentine leukocidin (5). The pvl gene is associated with more serious infections, particularly skin and soft tissue infections and pneumonia. A relatively unique feature of CAMRSA in Canada is that a high proportion of strains are mupirocin resistant (5). Mupirocin resistance is principally a characteristic of the strains isolated from northern Aboriginal communities in the prairies, where CAMRSA has been present since the 1980s (3). Subsequent widespread use of mupirocin in these communities has, predictably, been followed by the emergence of mupirocin resistance (5). Fortunately, Canadian CAMRSA strains, as elsewhere, generally remain susceptible to several oral antimi- crobials, such as trimethoprim/sulfamethoxazole, doxycycline and clindamycin. The medical and public health response to a previously unappreciated virulent organism with potential unique attrib- utes is to consider it to be a ‘new’ organism – ‘emerging’ in the current parlance. Generally, this response entails characteriz- ing the epidemiology, morbidity and mortality, managing cases, and controlling transmission. This idea of ‘uniqueness’ of MRSA has been the paradigm within which the response to nosocomial MRSA has developed. However, genetic rearrangement in microorganisms is ceaseless, and countless genetic variants of an organism are the norm. Acquisition of resistance genes, pvl genes or other virulence genes is simply a manifestation of this diversity. CAMRSA is not exceptional. The paradigm of CAMRSA as ‘extraordinary’ also suggests humans and the microbiological environment are distinct entities – us and them. But we do not stand apart from micro- organisms. Human beings and microorganisms are part of the same environment and, often, are interdependent. S aureus is part of the normal flora of the anterior nares of humans. No amount of isolation, restriction or handwashing alters the real- ity that approximately 20% of adults are permanent nasal car- riers of S aureus, and that another 60% are intermittent nasal carriers. And the more ill people are, the more likely they are to be colonized. Separation, barriers and intense handwashing have some role in health care settings to delay or prevent transmission of microorganisms, including S aureus. The goal is to prevent acquisition by patients at increased risk of serious infection because of interventions or immune impairment sec- ondary to disease and treatment. But outside of the health care setting, effectively eliminating the transmission of commensal bacteria between humans cannot, and arguably should not, be prevented. The apocalyptic vision of untreatable strains of common community pathogens is repeatedly raised and may ultimately prove true, but we are not there yet. In addition to the antimi- crobials already mentioned, linezolid, rifampin, fusidic acid, quinupristin-dalfopristin, tigecycline and vancomycin, ©2005 Pulsus Group Inc. All rights reserved EDITORIAL Community-acquired methicillin-resistant Staphylococcus aureus: Getting over it LE Nicolle MD FRCP, Editor-in-Chief
Transcript of Community-acquired methicillin-resistant ... - Hindawi
Can J Infect Dis Med Microbiol Vol 16 No 6 November/December 2005 323
Department of Internal Medicine, University of Manitoba, Winnipeg, ManitobaCorrespondence: Dr LE Nicolle, Department of Internal Medicine, University of Manitoba, Health Sciences Centre, GG443 – 820 Sherbrook
Street, Winnipeg, Manitoba R3A 1R9. Telephone 204-787-7029, fax 204-787-4826, e-mail [email protected]
There are three sure things in life: death, taxes and antimi-crobial resistance appearing on the heels of the introduc-
tion and widespread use of an antimicrobial agent.Staphylococcus aureus has always been a poster child for theemergence of antimicrobial resistance (1). Penicillin-resistantstrains of S aureus surfaced immediately following the intro-duction of penicillin in the late 1940s; within a few years,most hospital strains were penicillin resistant. There was alsothe rapid emergence of methicillin-resistant S aureus (MRSA)following the introduction of methicillin in the 1960s. Whilethe replacement of nosocomial methicillin-susceptibleS aureus by MRSA has proceeded at different rates in differentregions, the overall global progression has been relentless.MRSA became common in Canadian health care facilitieslater than in the United States; however, since the early1990s, nosocomial MRSA in Canada has steadily and irrevo-cably increased (2).
The current chapter in this story is the progressive dissem-ination of community-acquired MRSA (CAMRSA), mirror-ing the experience with penicillin-resistant S aureus 50 yearsago (1). In fact, CAMRSA has been common in someCanadian communities for almost 20 years (3). NorthernAboriginal communities in the prairies have been primarilyaffected, although there have been rare reports of outbreaksand community spread elsewhere (4). Now, Canadian CAMRSA has appeared in populations at risk identified else-where in North America and Europe. These populationsinclude incarcerated people, as described in this issue of theJournal (pages 343-348), as well as parenteral drug users,homeless people and other marginalized groups. Even in com-munities with long-standing experiences with CAMRSA,more severe S aureus infections may now be recognized. Thespecific strains identified in Canada are the same as thosereported outside our borders and are usually characterized bythe presence of Panton-Valentine leukocidin (5). The pvlgene is associated with more serious infections, particularlyskin and soft tissue infections and pneumonia.
A relatively unique feature of CAMRSA in Canada is that ahigh proportion of strains are mupirocin resistant (5).Mupirocin resistance is principally a characteristic of the strainsisolated from northern Aboriginal communities in the prairies,where CAMRSA has been present since the 1980s (3).
Subsequent widespread use of mupirocin in these communitieshas, predictably, been followed by the emergence of mupirocinresistance (5). Fortunately, Canadian CAMRSA strains, aselsewhere, generally remain susceptible to several oral antimi-crobials, such as trimethoprim/sulfamethoxazole, doxycyclineand clindamycin.
The medical and public health response to a previouslyunappreciated virulent organism with potential unique attrib-utes is to consider it to be a ‘new’ organism – ‘emerging’ in thecurrent parlance. Generally, this response entails characteriz-ing the epidemiology, morbidity and mortality, managing cases,and controlling transmission. This idea of ‘uniqueness’ ofMRSA has been the paradigm within which the response tonosocomial MRSA has developed. However, geneticrearrangement in microorganisms is ceaseless, and countlessgenetic variants of an organism are the norm. Acquisition ofresistance genes, pvl genes or other virulence genes is simply amanifestation of this diversity. CAMRSA is not exceptional.
The paradigm of CAMRSA as ‘extraordinary’ also suggestshumans and the microbiological environment are distinctentities – us and them. But we do not stand apart from micro-organisms. Human beings and microorganisms are part of thesame environment and, often, are interdependent. S aureus ispart of the normal flora of the anterior nares of humans. Noamount of isolation, restriction or handwashing alters the real-ity that approximately 20% of adults are permanent nasal car-riers of S aureus, and that another 60% are intermittent nasalcarriers. And the more ill people are, the more likely they areto be colonized. Separation, barriers and intense handwashinghave some role in health care settings to delay or preventtransmission of microorganisms, including S aureus. The goal isto prevent acquisition by patients at increased risk of seriousinfection because of interventions or immune impairment sec-ondary to disease and treatment. But outside of the health caresetting, effectively eliminating the transmission of commensalbacteria between humans cannot, and arguably should not, beprevented.
The apocalyptic vision of untreatable strains of commoncommunity pathogens is repeatedly raised and may ultimatelyprove true, but we are not there yet. In addition to the antimi-crobials already mentioned, linezolid, rifampin, fusidic acid,quinupristin-dalfopristin, tigecycline and vancomycin,
©2005 Pulsus Group Inc. All rights reserved
EDITORIAL
Community-acquired methicillin-resistantStaphylococcus aureus: Getting over it
LE Nicolle MD FRCP, Editor-in-Chief
nicolle_9165.qxd 11/21/2005 9:46 AM Page 323
together or in combination, provide treatment options forMRSA. The need to support and prioritize discovery anddevelopment of new antimicrobial agents is also repeatedlyhighlighted. The systematic clinical evaluation of antimicro-bials already available would, however, be of more immediatevalue, including clarifying when not to use antimicrobials.The political and scientific agenda in Canada (as in otherdeveloped countries), however, favours the discovery agendarather than expanding the knowledge base for optimal use ofavailable antimicrobials. A better understanding of how bestto use, or not use, existing agents would resolve many thera-peutic questions for CAMRSA.
Where should we go with CAMRSA? The sky is not falling;this is the anticipated evolution of a ubiquitous human colo-nizer and pathogen. It is simply another skirmish at theantimicrobial-microorganism interface. Morbidity and mortal-ity in the general population attributable to the introductionand spread of a more virulent strain of S aureus that is alsomethicillin resistant do need to be characterized. Practical,effective strategies to limit morbidity should be identified,implemented and evaluated. The same can be said for anyS aureus strain, irrespective of susceptibility. With respect toCAMRSA, practitioners must have access to timely informa-tion describing the regional spectrum of resistance to facilitateappropriate antimicrobial therapy. Pursuing all strains of thisubiquitous human commensal through widespread or nonse-lective screening for colonization or decolonization of carriersshould be discouraged. These approaches are unlikely to limittransmission or morbidity, and antimicrobial-based interven-tions for patients who are not infected will have the oppositeeffect: increased resistance. Canada has already harvested the
fruits of widespread mupirocin use, with substantial resistanceto the only current agent recommended for decolonization.
The approach to the management of S aureus infection inthe community is one of basic hygiene – washing, cleaningand laundering – together with appropriate care of woundsand management of active infections. Optimal approaches tothe management of infections – both antimicrobial andnonantimicrobial – need to be promoted and refined. Vaccinestrategies are always relevant, but such an approach remainsspeculative for S aureus. There are also many research oppor-tunities: the predictors of organism virulence and transmis-sion, the efficacy of therapy, and the outcomes in thecommunity for persons colonized by specific S aureus strainsare just a few of the outstanding issues. But framing all of ourapproaches must be an acknowledgement and continuingappreciation that human beings and their commensal organ-isms are inseparable.
Editorial
Can J Infect Dis Med Microbiol Vol 16 No 6 November/December 2005324
REFERENCES
1. Chambers HF. The changing epidemiology of Staphylococcus aureus?Emerg Infect Dis 2001;7:178-82.
2. Simor AE, Ofner-Agostini M, Bryce E, et al. The evolution ofmethicillin-resistant Staphylococcus aureus in Canadian hospitals: 5 years of national surveillance. CMAJ 2001;165:21-6.
3. Embil J, Ramotar K, Romance L, et al. Methicillin-resistantStaphylococcus aureus in tertiary care institutions on the Canadianprairies 1990-1992. Infect Control Hosp Epidemiol 1994;15:646-51.
4. Kurbis CA, Wyler JL. Community-based cluster of methicillin-resistant Staphylococcus aureus in Manitoba. Can J Infect Dis2001;12:149-52
5. 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.
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