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Staphylococcus lugdunensis

INTRODUCTION

Staphylococcus lugdunensis is a coagulase-negative staphylococcus (CNS). Like other CNS, S. lugdunensis in humans ranges from a harmless skin commensal to a life-threatening pathogen (as with infective endocarditis). Unlike other CNS, however, S. lugdunensis can cause severe disease reminiscent of the virulent infections frequently attributable to S. aureus [1]. In addition, most S. lugdunensis isolates remain susceptible to a large number of antimicrobial agents.

S. lugdunensis was first described in 1988 and was distinguished from other coagulase-negative staphylococcal species via DNA relatedness studies based on 11 clinical strains. The new species was named after Lyon, the French city where the organism was first isolated (Lugdunum, the Latin name of Lyon) [2]. S. lugdunensis is unique among CNS because of its propensity for causing aggressive native valve infective endocarditis (IE) and its susceptibility to a vast array of antimicrobial agents.

The microbiology, clinical features, and treatment of S. lugdunensis infections will be reviewed here. Other issues related to coagulase-negative staphylococci are discussed in detail separately.

EPIDEMIOLOGY

S. lugdunensis infections in humans range from harmless skin colonization to invasive infection. The majority of infections are related to skin and soft tissue, the bloodstream, and prosthetic devices.

The frequency of S. lugdunensis infection is probably underappreciated, since many clinical laboratories do not routinely speciate coagulase-negative staphylococci [3,4]. Among 494 coagulase-negative staphylococcal isolates from a clinical setting, S. lugdunensis accounted for 3 percent of isolates [3]. Unlike S. epidermidis, in general S. lugdunensis should be presumed to be a true pathogen. Among 229 S. lugdunensis clinical isolates in one series, only 15 percent were considered contaminants or colonizing organisms [5].

                

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Literature review current through: Apr 2013. | This topic last updated: Sep 21, 2012.
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