Correspondence
Nasal Carriage of Staphylococcus aureus
N Engl J Med 2001; 344:1399-1401May 3, 2001
- Article
To the Editor:
The study conducted by von Eiff and colleagues (Jan. 4 issue)1 might give readers the impression that a bacterial nose swab was merely a blind sample from the vestibulum nasi. The authors do not provide a precise description of the method used to obtain bacterial swabs from the nose. A colleague and I found that the bacterial spectrum differs considerably between the vestibulum nasi and the cavitas nasi; for example, Staphylococcus aureus was present in the cavitas nasi but not in the vestibulum nasi in 22 percent of 412 patients (P=0.001).2 This finding indicates that disinfection of the vestibule alone may not prevent colonization of the nasal cavity by S. aureus. The fact that the bacterial populations differ is not surprising, because the linings of the vestibule and cavity differ and constitute dissimilar microenvironments. There is also evidence of a genetically determined affinity between the nasal mucosa cells and certain bacteria such as S. aureus. 3 From our experience, nasal swabs should always be obtained through a nasal speculum with the help of a head mirror so as to obtain representative microbial samples from both the vestibule and the cavity.
3 ReferencesUlrich Glück, M.D.
Schweizerische Unfallversicherungsanstalt, 6002 Lucerne, Switzerland1
von Eiff C ,Becker K ,Machka K ,Stammer H ,Peters G . Nasal carriage as a source of Staphylococcus aureus bacteremia. N Engl J Med 2001;344:11-16
Full Text | Web of Science | Medline2
Gluck U ,Gebbers J-O . The nose as bacterial reservoir: important differences between the vestibule and cavity. Laryngoscope 2000;110:426-428
CrossRef | Web of Science | Medline3
Kinsman OS ,McKenna R ,Noble WC . Association between histocompatability antigens (HLA) and nasal carriage of Staphylococcus aureus. J Med Microbiol 1983;16:215-220
CrossRef | Web of Science | Medline
To the Editor:
Von Eiff et al. reported that the origin of a substantial proportion of cases of S. aureus bacteremia is endogenous — from the nares. We suggest that in some cases nasal colonization with S. aureus may be secondary to chronic ischemic skin lesions.
In response to a marked increase in the frequency of methicillin-resistant S. aureus, we increased hygienic measures and studied patients with arterial or venous leg ulcers or diabetic foot lesions. We monitored patients prospectively and determined the incidence of methicillin-resistant S. aureus infections in skin lesions and in the usual sites of colonization, such as the nose and armpits. From January 1997 to March 1998, all inpatients with ischemic skin lesions were enrolled. Bacteriologic swabs for methicillin-resistant S. aureus were obtained from skin lesions, the anterior nares, and the armpits of patients at admission and at discharge. A total of 160 consecutive patients were enrolled, including 18 with diabetic foot infections, 45 with venous leg ulcers, 65 with arterial leg ulcers, and 32 with other causes of skin necrosis. Methicillin-resistant S. aureus was isolated from skin lesions in the case of 64 patients (40 percent) and from swabs of the nose or armpits in the case of only 18 patients (11 percent), including 11 patients with methicillin-resistant S. aureus isolated from skin lesions; 55 percent of the patients with infections had no evidence of colonization. At discharge, nine new infections with methicillin-resistant S. aureus and two instances of colonization were observed.
Our data show that the prevalence of methicillin-resistant S. aureus was very high in these high-risk patients. However, when preventive measures were undertaken, the rate of acquisition was low during hospitalization. The swabs of skin lesions provided the best indicator of the presence of methicillin-resistant S. aureus. The rate of colonization with methicillin-resistant S. aureus in patients with ischemic lesions was different from that reported by von Eiff et al. or the rate among patients in the intensive care unit.1 Although screening of these high-risk patients is essential, attempts to eliminate nasal carriage of S. aureus should be considered only after skin lesions have completely healed.
1 ReferencesFrédéric Lecomte, M.D.
Michèle Nouvellon, M.D.
Hervé Lévesque, M.D., Ph.D.
Centre Hospitalier Universitaire, 76031 Rouen CEDEX, France1
Revised guidelines for the control of methicillin-resistant Staphylococcus aureus infection in hospitals. J Hosp Infect 1998;39:253-290[Erratum, J Hosp Infect 1999;42:83.]
CrossRef | Web of Science | Medline
To the Editor:
The report by von Eiff et al. of the relation of nasal colonization with S. aureus to bacteremia does not reveal the proportion of patients with S. aureus bacteremia who had negative nasal cultures for S. aureus. Consequently, the proportion of episodes of S. aureus bacteremia that were caused by the patient's own nasal S. aureus strain cannot be determined from the data presented, in contrast to the assertion of von Eiff et al. and the authors of the accompanying editorial1 that the results show this proportion to be greater than 50 percent. Yet, these data are needed to clarify the true proportion of episodes of S. aureus bacteremia that could be prevented by an effective program to eliminate nasal colonization.
The report also does not reveal the total number of patients who were prospectively screened to identify the 1278 patients who had nasal colonization with S. aureus. This denominator is needed to clarify the cost–benefit ratio for the comprehensive screening of all patients admitted to the hospital that the editorialists propose. The cost per colonized patient identified should vary inversely with the prevalence of colonization in the screened population.
1 ReferencesJames R. Johnson, M.D.
Veterans Affairs Medical Center, Minneapolis, MN 554171
Archer GL ,Climo MW . Staphylococcus aureus bacteremia -- consider the source. N Engl J Med 2001;344:55-56
Full Text | Web of Science | Medline
To the Editor:
It was in treating victims of the devastating Cocoanut Grove fire in Boston in November 1942 that penicillin made its first large and highly acclaimed clinical appearance in the United States.1 The success of penicillin bred its overuse. An increasing prevalence of penicillin resistance among gram-positive cocci has led to a progressive narrowing of the spectrum of indications for this remarkable, but narrow-spectrum agent. To add insult to injury, a severe shortage of penicillin G in the United States, which began in 1999, has made it very difficult for physicians to obtain this drug to treat susceptible microorganisms for which penicillin G is still the treatment of choice.2 This drug shortage has led to a paradoxical scenario. Half a century after its introduction as a “priceless miracle drug,” penicillin G now must be imported from Austria, and the costs of a 10-day treatment course have increased to almost $200. These costs are even higher than those for an equivalent course of broad-spectrum antibiotics such as levofloxacin or ampicillin–sulbactam.
2 ReferencesStephan Harbarth, M.D.
Children's Hospital, Boston, MA 02115Adi V. Gundlapalli, M.D., Ph.D.
Matthew H. Samore, M.D.
University of Utah School of Medicine, Salt Lake City, UT 841321
Cope O . Care of the victims of the Cocoanut Grove fire at the Massachusetts General Hospital. N Engl J Med 1943;229:138-147
Full Text | Web of Science2
Harbarth S . Antibiotic policy and penicillin-G shortage. Lancet 2000;355:1650-1650
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Author/Editor Response
The authors reply:
To the Editor: The nasal swabs were obtained from the anterior nares according to what was considered the state-of-the-art method to identify patients as carriers of S. aureus.1-3 Although other sites may be involved, carriage of S. aureus is most common in the anterior nares. The swab cultures in the single-center part of our study were obtained as part of routine surveillance cultures. Although the study by Glück and Gebbers is interesting 4 and we agree that nasal swabs obtained through a nose speculum with the help of a head mirror may yield additional information regarding colonization, this approach has not been a routine technique for surveillance cultures.
We agree with Lecomte et al. that in some cases nasal colonization with S. aureus may be secondary to chronic ischemic skin lesions. Skin damage caused by minor lesions, eczema, psoriasis, or the insertion of foreign bodies increases the risk of nasal carriage.5 Also, S. aureus adheres better to nasal epithelial cells obtained from carriers or from patients with eczema than to nasal epithelial cells obtained from other persons. However, the reservoir for chronic staphylococcal carriage has been shown to be the anterior nares. In our study, we found that for most of the strains, the isolates from the blood were identical to those from the anterior nares of a patient as well as from areas other than the nares.
Previous studies were not large and did not use modern molecular methods to determine the clonal relation of the organisms. Therefore, the purpose of our study was to correlate strains colonizing the anterior nares with strains derived from the blood in patients with S. aureus bacteremia, using an established molecular-typing method. Analyzing the results of both approaches (the rates of clonal identity between S. aureus strains isolated from blood and those isolated from the anterior nares before and after the detection of bacteremia were 85.7 percent and 82.2 percent, respectively), we concluded that a substantial proportion of cases of S. aureus bacteremia appear to be of endogenous origin. We agree with Johnson that additional data, such as the proportion of patients with S. aureus bacteremia who had negative nasal cultures for S. aureus, would be helpful to define the risk of bacteremia in carriers of S. aureus. In future clinical trials, an assessment of the relative risk may permit an evaluation of screening and preventive strategies.
5 ReferencesChristof von Eiff, M.D.
Karsten Becker, M.D.
Georg Peters, M.D.
Westfälische Wilhelms-Universität Münster, 48149 Münster, Germany1
Tenover FC, Gaynes R. The epidemiology of Staphylococcus infections. In: Fischetti VA, Novick RP, Ferretti JJ, Portnoy DA, Rood JI, eds. Gram-positive pathogens. Washington, D.C.: ASM Press, 2000:414-21.
2
VandenBergh MF ,Yzerman EP ,van Belkum A ,Boelens HA ,Sijmons M ,Verbrugh HA . Follow-up of Staphylococcus aureus nasal carriage after 8 years: redefining the persistent carrier state. J Clin Microbiol 1999;37:3133-3140
Web of Science | Medline3
Pujol M ,Pena C ,Pallares R , et al. Nosocomial Staphylococcus aureus bacteremia among nasal carriers of methicillin-resistant and methicillin-susceptible strains. Am J Med 1996;100:509-516
CrossRef | Web of Science | Medline4
Gluck U ,Gebbers J-O . The nose as bacterial reservoir: important differences between the vestibule and cavity. Laryngoscope 2000;110:426-428
CrossRef | Web of Science | Medline5
Casewell MW . The nose: an underestimated source of Staphylococcus aureus causing wound infection. J Hosp Infect 1998;40:Suppl B:S3-S11
CrossRef | Web of Science | Medline
- Citing Articles (3)
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Sara Elena Satorres, Lucía Esther Alcaráz, Ethelina Cargnelutti, Maria Silvia Di Genaro. (2009) IFN-γ plays a detrimental role in murine defense against nasal colonization of Staphylococcus aureus. Immunology Letters 123:2, 185-188
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Lefa E Alksne. (2002) Virulence as a target for antimicrobial chemotherapy. Expert Opinion on Investigational Drugs 11:8, 1149-1159
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