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Infectious Diseases in Clinical Practice:
doi: 10.1097/IPC.0b013e31816b5ce7
Editorial Comment

Staphylococcus lugdunensis: A Lion Among Coagulase-Negative Staphylococci?

Johnson, Leonard B. MD

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Division of Infectious Diseases, St John Hospital and Medical Center; and School of Medicine, Wayne State University, Detroit, MI.

Address correspondence and reprint requests to Leonard B. Johnson, MD, 19251 Mack Avenue, Suite 340, Grosse Pointe Woods, MI 48236. E-mail:

Financial support: Speakers Bureau for Pfizer.

Staphylococcus lugdunensis was first identified as a unique coagulase-negative Staphylococcus species in Lyon, France (the modern version of the Roman city, Lugdunum), in 1988.1 Since its first description, it has been associated with a wide range of infections including soft tissue infections, osteomyelitis, and endovascular infections including endocarditis and pacemaker infections. The pathogenicity of the organism was confirmed in a review of 229 S. lugdunensis isolates collected over 5 years.2 Among all isolates, 84.6% were determined to be clinically significant isolates with soft tissue (55.4%) and blood and vascular catheter infections (17.4%), the most common infections identified. The relative virulence of the organism compared with other species of coagulase-negative staphylococci has been confirmed both in animal models and among clinical isolates.3,4 In addition, cases of septic shock and toxic shock syndrome have been attributed to the organism.5,6

Although published cases of S. lugdunensis endocarditis (including pacemaker infections) have been recently been summarized,7 there has been no systematic review of bone and joint infections due to this pathogen. In the accompanying article by Karnani and Myers,8 58 episodes of septic arthritis, osteomyelitis, and infected joint prostheses are summarized. As the authors acknowledge, the true number of cases of these infections greatly exceeds this due to underreporting and the fact that not all clinical laboratories speciate isolates of coagulase-negative staphylococci. The primary infections identified were prosthetic joint infections (25), native joint infections (11), and vertebral osteomyelitis and discitis (11). As with most reports of S. lugdunensis susceptibility, the vast majority of organisms remained susceptible to β-lactam antibiotics. An unexpected finding was a high male to female proportion of cases (3:1). No male predominance was noted among 69 cases of endovascular S. lugdunensis infections.7 The high proportion of bone and joint cases may reflect higher rates of orthopedic surgeries and complications among males. Although a large number of patients (8/18) for whom information was available were receiving immunosuppressant therapy, the lack of information on most cases makes it difficult to generalize host features.

The principal finding that the authors emphasize is the aggressive nature of the infections relative to those from other coagulase-negative staphylococci, mimicking infections due to S. aureus. This conclusion is based on the rapid onset of infections as well as the need to remove prostheses and perform surgical debridement in a large cases to eradicate infection. Although this may indeed be true, the study (as well as the review of endovascular infections by Anguera et al) lacks comparative data to similar cases that could potentially confirm this observation. In particular, a large case-control study comparing cases of S. lugdunensis, S. epidermidis, and S. aureus infections treated at a single center (to avoid biases created by different surgical and antibiotic practices) would be useful to evaluate severity of illness at presentation, frequency of surgical therapy, and outcomes. Unfortunately, it is unlikely that a single institution could generate a sufficient number of cases to provide meaningful statistical analysis of these outcomes. For now, we will have to rely on the clinical judgment of the authors on the Lionesque stature of this species of coagulase-negative Staphylococcus.

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1. Freney J, Brun Y, Bes M, et al. Staphylococcus lugdunensis sp. nov. and Staphylococcus schleiferi sp. nov., two species from human clinical specimens. Int J Syst Bact. 1988;38:168-172.

2. Herchline TE, Ayers LW. Occurrence of Staphylococcus lugdunensis in consecutive clinical cultures and relationship of isolation to infection. J Clin Microbiol. 1991;29:419-421.

3. Ferguson KP, Lambe DW Jr, Keplinger JL, et al. Comparison of the pathogenicity of three species of coagulase-negative Staphylococcus in a mouse model with and without a foreign body. Can J Microbiol. 1991;37:722-724.

4. Tan TY, Ng SY, Ng WX. Clinical significance of coagulase-negative Staphylococci recovered from nonsterile sites. J Clin Microbiol. 2006;44:3413-3414.

5. Pareja J, Gupta K, Koziel H. The toxic shock syndrome and Staphylococcus lugdunensis bacteremia. Ann Intern Med. 1998;128:603-604.

6. Castro JG, Dowdy L. Septic shock caused by Staphylococcus lugdunensis. Clin Infect Dis. 1999;28:681-682.

7. Anguera I, Del Rio A, Miro JM, et al. Staphylococcus lugdunensis infective endocarditis: description of 10 cases and analysis of native valve, prosthetic valve, and pacemaker lead endocarditis clinical profiles. Heart. 2005;91:e10.

8. Karnani R, Myers JP. Bone and joint infections caused by Staphylococcus lugdunensis: report of two cases and review of the literature. Infect Dis Clin Pract. 2008;16(2):94-99.

© 2008 Lippincott Williams & Wilkins, Inc.

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