Tietz, Andreas

Trampuz, Andrej

Widmer, Andreas F.

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CORRESPONDENCE • CID 2005:40 (1 March) • 7671 M A R C HCorrespondenceEffect of Colonizationwith Methicillin-ResistantStaphylococcus aureuson Subsequent InfectionSir—We are indebted to Davis et al. [1]for their valuable study, which strengthensthe role of active surveillance. The follow-up period of 12 months is laudable, be-cause infections detected after a patient’sdischarge from the hospital could also beobserved.One important and very alarming find-ing in the study [1] is that 2.7%–4.4% ofpatients in the studied population wereinfected with methicillin-resistant Staph-ylococcus aureus (MRSA) during their hos-pitalization, regardless of their coloniza-tion status. Also alarming is the higher riskof MRSA infection for noncolonized pa-tients, compared with colonized patients,in the intensive care units of surgical andtrauma departments. Only one-third ofMRSA infections occurred in patients whowere previously colonized with MRSA.Two-thirds of MRSA infections are ap-parently acquired via transmission. This isa strong argument for the roles of activesurveillance, contact isolation precautions,and hand hygiene (the utility of the latterhas recently and repeatedly been ques-tioned). A systematic review has shownmoderate evidence for a preventive effectof isolation precautions [2], but we pos-tulate that concerted use of these precau-tions could have prevented, at leastpartially, the morbidity and mortality as-sociated with 19 MRSA infections re-ported in Davis et al. [1]. We would liketo obtain more information on the use ofbarrier precautions and hand hygiene inthe institution discussed in Davis et al. [1].There are 4 additional comments thatwe wish to make. First, the rate of MRSAprevalence is generally defined in the lit-erature as the proportion of all S. aureusisolates that are methicillin resistant. Thus,the actual rate of MRSA in the study pop-ulation would be 15.9% of isolates (26MRSA isolates out of 163 S. aureus iso-lates), rather than the 3.4% of isolates re-ported by Davis et al. [1].Second, the question of whether MRSAis more virulent than methicillin-suscep-tible S. aureus (MSSA) cannot be answeredby comparing the incidence rates of MRSAinfection in patients who are colonizedwith either MSSA or MRSA. Ideally, therate of MSSA infection in patients who arecolonized with MSSA would have beencompared with the rate of MRSA infectionin those who are colonized with MRSA.The latter figure is reported as 19%, buthow many patients with MSSA coloniza-tion acquire MSSA infection? Wertheim etal. [3] have recently reported a relative riskof 3.0 for MSSA bacteremia in MSSA car-riers. A case-case-control study design, asshown by Kaye et al. [4], would answerthis question, because risk factors for in-fection might be different in the 3 groups(MSSA, MRSA, or no colonization).Third, the use of susceptibility patternsto determine whether MRSA strains are no-socomial or community-acquired strainsseems somewhat outdated. Modern mo-lecular techniques for making this deter-mination are available, including PFGE forstrain typing and epidemiological analysis[5] and PCR for determination of the mecAgenetic element and virulence factors as-sociated with community-acquired strains[6]. It is not clear whether the infections innoncolonized patients originate from pa-tients with MRSA colonization or from an-other source.Finally, Davis et al. [1] used only swabsof the nares to determine colonizationstatus. Adding cultures of the throat, asis common in epidemiological studies,would have increased the sensitivity oftesting [7] and thus changed the statisticalsignificance of the findings.In conclusion, the findings of Davis etal. [1] are plausible and valuable from apathogenetic and epidemiologic point ofview. Colonization with MRSA clearlyleads to infection, but not only in patientswho are colonized. Reduction of trans-mission is the key, and intervention stud-ies are needed. As stated by Cooper et al.[2] in their systematic review evaluatingthe evidence for barrier precautions: “lackof evidence … should not be mistaken forevidence of lack of effect” [2, p. 538].AcknowledgmentsPotential conflicts of interest. All authors: noconflicts.Andreas Tietz, Andrej Trampuz,and Andreas F. WidmerDivision of Infection Control and HospitalEpidemiology, University Hospital Basel, SwitzerlandReferences1. Davis KA, Stewart JJ, Crouch HK, Florez CE,Hospenthal DR. Methicillin-resistant Staphy-lococcus aureus (MRSA) nares colonization athospital admission and its effect on subsequentMRSA infection. Clin Infect Dis 2004; 39:776–82.2. Cooper BS, Stone SP, Kibbler CC, et al. Iso-lation measures in the hospital managementof methicillin-resistant Staphylococcus aureus(MRSA): systematic review of the literature.BMJ 2004; 329:533–40.3. Wertheim HFL, Vos MC, Ott A, et al. Risk andoutcome of nosocomial Staphylococcus aureusbacteraemia in nasal carriers versus noncarriers.Lancet 2004; 364:703–5.4. Kaye KS, Engemann JJ, Mozaffari E, CarmeliY. Reference group choice and antibiotic resis-tance outcomes. Emerg Infect Dis 2004; 10:1125–8.5. Tenover FC, Arbeit RD, Goering RV. How toselect and interpret molecular strain typingmethods for epidemiological studies of bacterialinfections: a review for healthcare epidemiol-ogists. Molecular Typing Working Group of theSociety for Healthcare Epidemiology of Amer-768 • CID 2005:40 (1 March) • CORRESPONDENCEica. Infect Control Hosp Epidemiol 1997; 18:426–39.6. Francois F, Renzi G, Pittet D, et al. A novelmultiplex real-time PCR assay for rapid typingof major staphylococcal cassette chromosomemec elements. J Clin Microbiol 2004; 42:3309–12.7. Uemura E, Kakinohana S, Higa N, Toma C,Nakasone N. Comparative chracterization ofStaphylococcus aureus isolates from throats andnoses of healthy volunteers. Jpn J Infect Dis2004; 57:21–4.Reprints or correspondence: Dr. Andreas Tietz, Div. of InfectionControl and Hospital Epidemiology, University Hospital Basel,Petersgraben 4, CH-4031 Basel, Switzerland (atietz@uhbs.ch).Clinical Infectious Diseases 2005; 40:767–8 2005 by the Infectious Diseases Society of America. Allrights reserved. 1058-4838/2005/4005-0023$15.00Reply to Tietz et al.Sir—We appreciate the comments onour recent article [1] by Tietz et al. [2]and would like to address some of theissues they raise. In accordance with themost recently published guidelines by theSociety for Healthcare Epidemiology ofAmerica (SHEA) for the prevention ofnosocomial transmission of multidrug-resistant Staphylococcus aureus [3], pa-tients admitted to our facility who arecolonized or infected with methicillin-resistant S. aureus (MRSA) are placed incontact isolation, and strict hand hygieneis encouraged of all health care personnelwho have contact with patients. Tietz etal. [2] questioned the utility of includingsamples of the pharynx to increase thesensitivity of testing for MRSA coloniza-tion. The findings of previous studies byour group [4, 5] and others [6, 7], in ad-dition to the previously mentioned SHEAguidelines, support the sampling of onlythe nares to assess for MRSA colonization.On this basis, we are confident that veryfew subjects who were colonized withMRSA were not identified during our in-vestigation, and we doubt that obtainingsamples from multiple sites would haveyielded significantly different results.Tietz et al. [2] point out that two-thirdsof the absolute number of MRSA infec-tions occurred in patients who were notcolonized with MRSA. Although this iscorrect, the appropriate evaluation of thedata, as we reported [1], is the discordancein the rates of MRSA infection among thedifferent patient populations studied. Theincidence of MRSA infection was signifi-cantly higher among patients who werecolonized with MRSA (19% of colonizedpatients) than among patients who werenot colonized with MRSA (1.9% of non-colonized patients). Furthermore, patientswho were found to be colonized withMRSA at admission were more likely todevelop infection during the hospitaliza-tion in which MRSA colonization wasidentified than during a future hospitali-zation. The patients who developed MRSAinfection but who were not colonized withMRSA at admission were more likely todevelop infection during a future hospi-talization. Although our study [1] did notspecifically address the question of in-creased virulence of MRSA compared withthat of methicillin-susceptible S. aureus(MSSA), there is increasing evidence thatcommunity-acquired MRSA may be morevirulent. Another recent report by ourgroup [8] demonstrated a higher rate ofsoft-tissue infection in subjects colonizedwith community-acquired MRSA, com-pared with subjects colonized with MSSAor not colonized with S. aureus. The find-ings of that study [8] and others [9] addto the growing evidence that most com-munity-acquired MRSA isolates now ex-press a specific exotoxin, encoded by thePanton-Valentine leukocidin gene, thatis likely to be responsible for increasedvirulence.The role of MRSA eradication in re-ducing the rates of subsequent MRSA in-fection of MRSA-colonized patients andin decreasing the transmission of MRSAin health care facilities needs to be ade-quately addressed. We are currently pur-suing these questions with a randomized,double-blind, placebo-controlled study todetermine the effect of topical mupirocinwhen used to eradicate MRSA coloniza-tion of nares identified at admission to theintensive care unit. Our hypothesis is thatMRSA eradication will decrease the rateof subsequent MRSA infection in these pa-tients. If true, this would significantly de-crease the negative impact that MRSA in-fection has on hospitalized patients.AcknowledgmentsPotential conflicts of interest. All authors: noconflicts.Kepler A. Davis and Duane R. HospenthalInfectious Disease Service,Brooke Army Medical Center,Fort Sam Houston, TexasReferences1. Davis KA, Stewart JJ, Crouch HK, Florez CE,Hospenthal DR. Methicillin-resistant Staphy-lococcus aureus (MRSA) nares colonization athospital admission and its effect on subsequentMRSA infection. Clin Infect Dis 2004; 39:776–82.2. Tietz A, Trampuz A, Widmer AF. Effect of col-onization with methicillin–resistant Staphylo-cocus aureus on subsequent infection. Clin In-fect Dis 2005; 40:767–8 (in this issue).3. Muto CA, Jernigan JA, Ostroswsky BE, et al.SHEA guideline for preventing nosocomialtransmission of multidrug-resistant strains ofStaphylococcus aureus and enterococcus. InfectControl Hosp Epidemiol 2003; 24:362–86.4. Kenner J, O’Connor T, Piantanida N, et al.Rates of carriage of methicillin-resistant andmethicillin-susceptible Staphylococcus aureus inan outpatient population. Infect Control HospEpidemiol 2003; 24:439–44.5. Fishbain JT, Lee JC, Nguyen HD, et al. Noso-comial transmission of methicillin-resistantStaphylococcus aureus: a blinded study to es-tablish baseline acquisition rates. Infect ControlHosp Epidemiol 2003; 24:415–21.6. Sanford MD, Widmer AF, Bale MJ, Jones RN,Wenzel RP. Efficient detection and long-termpersistence of the carriage of methicillin-resis-tant Staphylococcus aureus. Clin Infect Dis1994; 19:1123–8.7. Papia G, Louie M, Tralla A, Johnson C, Col-lins V, Simor AE. Screening high-risk pa-tients for methicillin-resistant Staphylococcusaureus on admission to the hospital: is it costeffective? Infect Control Hosp Epidemiol1999; 20:473–7.8. Ellis MW, Hospenthal DR, Dooley DP, Gray PJ,Murray CK. Natural history of community-acquired methicillin-resistant Staphylococcusaureus colonization and infection in soldiers.Clin Infect Dis 2004; 39:971–9.9. Boubaker K, Diebold P, Blanc DS, et al. Panton-Valentine leukocidin and staphylococcal skininfections in schoolchildren. Emerg Infect Dis2004; 10:121–4.The views expressed herein are those of the authors and donot reflect the official policy or position of the Departmentof the Army, Department of Defense, or the US Government.

Effect of Colonization with Methicillin-Resistant Staphylococcus aureus on Subsequent Infection

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