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INTRODUCTION

Staphylococci are ubiquitous inhabitants of the skin and mucous membranes of humans and other mammals. They exist in a commensal relationship until a breach in a cutaneous or mucosal barrier permits staphylococci access to deeper tissues and the bloodstream or until a foreign body or medical device provides a foothold. The production of coagulase, an enzyme that clots plasma, distinguishes Staphylococcus aureus from other medically important staphylococci. Those that do not produce coagulase are grouped collectively as coagulase-negative staphylococci (CoNS) and represent the most common resident bacteria of humans. All staphylococci are nonmotile, non–spore-forming, facultative anaerobic bacteria. In gram-stained specimens, they appear as gram-positive cocci in clusters, as well as in pairs and tetrads. Peptidoglycans and lipoteichoic acids form the basic cell wall structures of staphylococci, and most exhibit microcapsule formation. Colony morphology followed by selected biochemical reactions allows identification of pathogenic staphylococci. Typical 24-hour S aureus colonies are larger, yellow pigmented, and surrounded by a small zone of hemolysis. Colonies of Staphylococcus epidermidis are typically small, white or beige, and approximately 1 to 2 mm in diameter after overnight incubation. Small-colony variants of S aureus, important in some persistent infections, may be missed initially because of their pinpoint size. Staphylococcal colonies in general will be catalase-positive, distinguishing them from streptococci.

COAGULASE-NEGATIVE STAPHYLOCOCCUS

PATHOGENESIS AND EPIDEMIOLOGY

Most infections attributed to CoNS are facilitated by the formation of biofilm on host tissue or medical device surfaces. CoNS can attach directly to foreign bodies via hydrophobic interactions mediated by cell wall–anchored proteins, the surface charge of teichoic acids, and van der Waals forces. Host extracellular matrix and plasma proteins including fibrinogen, fibronectin, and collagen can cover foreign bodies and serve as additional attachment sites for CoNS via covalent binding with staphylococcal cell wall–anchored adhesins. Following attachment, the bacteria multiply to form multilayered cell aggregates mediated by polysaccharide intercellular adhesin and proteinaceous adhesins resulting in biofilm formation. Biofilms are key to the pathogenesis of foreign body–associated infections, providing CoNS with a physical barrier to evade both host immune responses and systemic antimicrobial therapy. Staphylococcus saprophyticus is uniquely outfitted as a genitourinary pathogen because of a novel cell wall–anchored protein involved in adherence to uroepithelial cells, redundant urine adaptive transporter systems, and urease. The virulence factors for Staphylococcus lugdunensis are unclear but likely involve its production of extracellular glycocalyx, which assists immune evasion, and enzymes such as esterase, protease, and lipases, which facilitate tissue invasion.

CoNS colonize virtually all normal skin with a predilection for areas of higher humidity, such as the anterior nares, axillae, inguinal and gluteal regions, umbilicus, the antecubital and popliteal spaces, as well as conjunctiva. Because of the commensal nature of the CoNS, they are often recovered in specimens from superficial sites and may be recovered from body fluids and deep sites when inadequate or improper collection techniques have been employed. Recovery of CoNS from a normally sterile ...

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