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Clinical and Diagnostic Laboratory Immunology, November 2001, p. 1064-1069, Vol. 8, No. 6
1071-412X/01/$04.00+0   DOI: 10.1128/CDLI.8.6.1064-1069.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Determinants of Staphylococcus aureus Nasal Carriage

Alexander M. Cole, Samuel Tahk, Ami Oren, Dawn Yoshioka, Yong-Hwan Kim, Albert Park, and Tomas Ganz*

Departments of Medicine and Pathology and Will Rogers Institute for Pulmonary Research, UCLA School of Medicine, Los Angeles, California

Received 16 May 2001/Returned for modification 23 July 2001/Accepted 31 July 2001

Nasal carriage of Staphylococcus aureus has been identified as a risk factor for community-acquired and nosocomial infections. We screened 230 donors of diverse ethnic and socioeconomic backgrounds and identified 62 (27%) whose nasal secretions were colonized by S. aureus. In 18 donors in whom the various regions of the nasal luminal surface were separately sampled, the predominant region of S. aureus colonization was the moist squamous epithelium on the septum adjacent to the nasal ostium. Nasal fluid from carriers was defective in killing endogenous S. aureus and nasal carrier isolates of S. aureus but not a laboratory S. aureus strain. Transmission electron microscopy revealed that S. aureus isolates incubated in nasal fluid from carriers for 2 h at 37°C were less damaged than those incubated in noncarrier fluid and were coated with an electron-dense layer. Compared with that from healthy donors and patients with acute rhinitis, nasal fluid from carriers contained elevated concentrations of the neutrophil-derived defensins human neutrophil peptides 1 to 3 (47- and 4-fold increases, respectively), indicative of a neutrophil-mediated inflammatory host response to S. aureus colonization. The concentration of the inducible epithelial antimicrobial peptide human beta -defensin 2 was also highly elevated compared to that in healthy donors, in whom the level was below the detection limit, or patients with acute rhinitis (sixfold increase). Thus, nasal carriage of S. aureus takes hold in nasal fluid that is permissive for colonization and induces a local inflammatory response that fails to clear the colonizing bacteria.

* Corresponding author. Mailing address: Department of Medicine, Division of Pulmonary and Critical Care, UCLA School of Medicine, CHS 37-055, 10833 Le Conte Ave., Los Angeles, CA 90095-1690. Phone: (310) 825-7499. Fax: (310) 206-8766. E-mail: tganz{at}mednet.ucla.edu.

Clinical and Diagnostic Laboratory Immunology, November 2001, p. 1064-1069, Vol. 8, No. 6
1071-412X/01/$04.00+0   DOI: 10.1128/CDLI.8.6.1064-1069.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.