John and Harvin Table 1 Coagulase-negative staphylococci reported to cause infections in humans1 Species Common site/type of infection S. capitis Urinary tract, skin, blood, CSF shunt S. caprae Urinary tract, blood, access sites, prosthetic joints S. cohnii Wounds, joints, meninges S. epidermidis Widespread sites; wounds, access devices S. haemolyticus Native valve, wound, bone, and joint S. hominis Blood, lung, breast S. lugdunensis Endothelium, heart valves S. pasteurii Orthopedic implants S. saprophiticus Urinary tract S. scheiferi Nosocomial infections, CSF shunts, pacemakers S. warneri Widespread sites; neonatal intensive care units S. xylosus Blood 1Derived from Tristan et al (2006) and Koksal et al (2007). turanose, melezitose, xylose, mannose, trehalose, mannitol, xylitol, and maltose; and phosphatase nitrate reduction and use of arginine. With character types deﬁned through major and minor biochemical routes, a simpliﬁed scheme emerged for speciating staphylococci of human origin (Kloos and Schleifer 1975). Other early speciation methods included antimicrobial susceptibility proﬁle typing, multilocus enzyme electropho- resis, and cellular fatty acid analysis (Birnbaum et al 1991). Due to the intensive labor involved in all of these early typing schemes and because of the assumption of the low virulence of this group of organisms, most isolates with morphology of Gram-positive cocci in clusters and positive for catalase production without coagulase production were described simply as CNS. Clinical debate continued about the clinical or therapeutic utility of speciating CNS; nevertheless, evidence emerged suggesting that particular species of CNS may be associated with speciﬁc diseases, readdressing the question of a need for speciation (Kloos and Bannerman 1994). In the US, bacteremia due to unspeciated CNS have increased from 9% to 27% from 1980 to 1989 (Schaberg et al 1991). Over the last decade, the numbers of CNS species have grown to total 32, with half of these species isolated from human tissue and blood samples (von Eiff et al 2002). Consequently, development of commercial automated sys- tems such as the Microscan Pos ID, Rapid Pos ID (Baxter Diagnostic Inc., MicroScan Division, West Sacramento, CA, USA), and VITEK (bioMérieux Vitek Inc., Hazelwood, MO, USA) have facilitated more rapid testing of staphylococci by 1144 using computer software to analyze combined biochemical and antibiotic susceptibility proﬁles (Kloos and George 1991; Hussain et al 1998; Caierão et al 2006). These robotic sys- tems scan incubated trays using ﬂuorimetric and photometric readings to record ﬂouresence, turbidity, and colormetric signals which indicate relative growth in each well (Ligozzi et al 2002). Each automated system uses a unique set of biochemical tests and species parameters. Small differences in identiﬁca- tion methods, however, have the potential to cause inconsis- tencies in results when comparing one system’s speciation of a microbial isolate to another (Perl et al 1994). Moreover, automated systems can cause outright misidentiﬁcation even at the genus level. In one report, results from an automated typing system were compared to those of a 16s rRNA specia- tion for 19 clinical bacterial isolates (Ben-Ami et al 2005). The automated system identiﬁed all of the isolates as Kocuria, while the 16s rRNA sequence subsequently identiﬁed all 19 isolates as CNS, 18 S. epidermidis and 1 S. hamolyticus; nev- ertheless, the automated identiﬁcation of CNS at the levels of species and subspecies presents potential value for clinical correlation and therapeutic intervention (Rupp and Archer 1994). Other work recently presented suggests S. epidermidis isolates may be misidentiﬁed even as S. auricularis, so it is clear that erroneous typing could delay appropriate and necessary therapeutic intervention (John et al 2006). Regardless of species specificity, treatment of CNS infection has become increasingly difﬁcult due to the high prevalence of antibiotic-resistant strains. Widely used anti- biotics including penicillins, particularly semi-synthetic penicillins, cephalosporins, macrolides, aminoglycosides, and tetracyclines, have proven to be ineffective in inhibit- ing several prevalent species of CNS, thus, augmenting the need for new and effective antimicrobials (Cerca et al 2005; Gaudioso de Allori et al 2006; Arciola et al 2006). To add to the resistance problem, multi resistance in CNS, as in S. aureus, is carried out on a staphylococcal chromosome cassette (SCC) which almost always includes the mecA gene for resistance to semi-synthetic penicillins (SCCmec) (Hanssen et al 2004). SCCmec resides in the chromosome as several cassette variants I-V. CNS are ubiquitous in nature, residing on skin and mucous membranes (Costa et al 2004). When exposed to medical devices, the CNS anchor themselves to a polymer surface via van der Waal’s forces, hydrophobic interactions, and polarity, ultimately forming a thick bioﬁlm (Vuong et al 2003; Mack et al 2006). Production of bioﬁlm reduces the organism’s susceptibility to speciﬁc antimicrobials which Therapeutics and Clinical Risk Management 2007:3(6)