INTRODUCTION — Coagulase-negative staphylococci (CoNS) are part of normal human skin flora [1]. While the virulence of these organisms is relatively low, they can cause clinically significant infections of the bloodstream and other tissue sites. Risk factors for CoNS infection include the presence of prosthetic material (such as an intravascular catheter) and immune compromise.
Distinguishing true infection from contamination can be difficult; this is discussed separately. (See "Infection due to coagulase-negative staphylococci: Epidemiology, microbiology, and pathogenesis", section on 'Distinguishing infection from contamination'.)
General issues related to antimicrobial resistance and treatment of CoNS infections will be reviewed here. Issues related to treatment of Staphylococcus lugdunensis are discussed separately. (See "Staphylococcus lugdunensis".)
The epidemiology, microbiology, pathogenesis, and clinical manifestations of CoNS are discussed separately. (See "Infection due to coagulase-negative staphylococci: Epidemiology, microbiology, and pathogenesis" and "Infection due to coagulase-negative staphylococci: Clinical manifestations".)
ANTIMICROBIAL RESISTANCE
Methicillin — According to Clinical Laboratory and Standards Institute (CLSI) guidelines, the minimum inhibitory concentration (MIC) breakpoints for CoNS (except S. lugdunensis) are ≤0.5 mcg/mL for oxacillin susceptibility and ≥1 mcg/mL for oxacillin resistance [2-5]. According to European Committee on Antimicrobial Susceptibility Testing (EUCAST) guidelines, the MIC breakpoint for oxacillin resistance is >0.25 mg/L (except S. lugdunensis and S. saprophyticus) [6].
Mechanism of resistance — Resistance to penicillin among CoNS approaches 90 to 95 percent. Resistance to methicillin and semisynthetic penicillins is present in more than 80 percent of clinical CoNS isolates, far higher than is commonly seen in Staphylococcus aureus [7]; these isolates are also often resistant to multiple classes of antibiotics in addition to beta-lactams. Exception include S. saprophyticus (which is usually methicillin susceptible) and S. lugdunensis (which is susceptible to a wide range of antimicrobials). (See "Staphylococcus lugdunensis".)
Methicillin resistance in CoNS is mediated by the mecA gene (as in S. aureus), which encodes a low-affinity penicillin-binding protein (PBP 2a) and is part of a mobile genetic element called SCCmec (staphylococcal cassette chromosome) [8]. This resistance is usually heterotypic, since only a minority of the bacterial population (as few as one in 103 or 106 organisms) expresses the resistant phenotype; this makes detection of resistance especially challenging [9].
Testing approach — Reliable detection of methicillin resistance is important to facilitate selection of appropriate antimicrobial therapy [10]. This is complicated by the heterogeneous expression of resistance, which occurs more commonly among CoNS isolates than S. aureus [11-14].
For infections due to Staphylococcus epidermidis, Staphylococcus pseudintermedius, or Staphylococcus schleiferi with oxacillin MIC ≥0.5 mg/L, beta-lactams should not be used pending additional testing for PBP 2a or mecA gene testing if feasible; this is particularly important in the setting of serious infections such as endocarditis or device-related infections. For infections due to S. epidermidis, laboratory tools that reliably predict mecA-mediated beta-lactam resistance include cefoxitin disk diffusion, oxacillin disk diffusion, and oxacillin broth microdilution (BMD) [5,15,16]. Incubation at 33 to 35°C is recommended, as testing at temperatures above 35°C may not detect methicillin-resistance staphylococci [5,15]. For S. pseudintermedius and S. schleiferi, oxacillin disk diffusion and oxacillin BMD are appropriate for detecting oxacillin resistance; however, cefoxitin disk diffusion does not reliably predict the presence of mecA [5,17,18].
A rapid latex agglutination test developed for detection of PBP 2a of methicillin-resistant S. aureus has been investigated for its applicability in CoNS species [19-22]. Some studies have demonstrated high sensitivity and specificity, although non-S. epidermidis strains occasionally yield false-positive results [19]; others studies have reported poorer correlation of PBP 2a latex agglutination results with other phenotypic and genotypic assays, suggesting that growth conditions may be critical to obtaining accurate results [14].
Detection of resistance with phenotypic assays may be difficult, especially for some of the less common species [21,23]. If the accuracy of phenotypic testing methods are uncertain, mecA gene detection using DNA hybridization or polymerase chain reaction (PCR) techniques can be pursued [24-26]. Detection of resistance with genotypic assays may be falsely positive when the mecA gene is identified but is not fully expressed due to gene mutations.
For circumstances in which laboratory testing yields discrepant results (for example, negative mecA phenotypic testing but positive PCR), further characterization is required to determine whether the discrepancy is due to inability of the phenotypic assay to detect resistance or due to presence of mutations in the mecA gene impacting its function or expression.
Other agents — Antimicrobial resistance among CoNS has also been described for vancomycin and linezolid:
●Vancomycin − According to CLSI guidelines, MIC vancomycin breakpoints for CoNS are susceptible if ≤4 mcg/mL, intermediate if 8 to 16 mcg/mL, and resistant if ≥32 mcg/mL [5,27]. According to EUCAST guidelines, an MIC >4 mg/L indicates vancomycin resistance for CoNS [28,29]. The vancomycin MIC breakpoints for CoNS differ from those of S. aureus. (See "Staphylococcus aureus bacteremia with reduced susceptibility to vancomycin".)
Glycopeptide resistance is emerging among CoNS [30-35]. In England between 1997 and 2002, up to 1 percent of isolates causing hospital-acquired bacteremia were vancomycin resistant [33]. The molecular mechanisms of glycopeptide resistance among staphylococci remain incompletely understood; in S. aureus, resistance appears to be associated with alterations in cell wall metabolism including decreased activity of autolytic enzymes, leading to cell wall thickening [36-40]. Increased cell wall thickness has also been observed in various CoNS clinical strains that demonstrate heteroresistance to vancomycin [41]; heteroresistance refers to the presence of subpopulations of bacteria with variable susceptibility to vancomycin. For S. aureus, these heteroresistant subpopulations may represent precursors to development of vancomycin-intermediate S. aureus and may facilitate persistence by stimulating altered host immune responses [42]. (See "Staphylococcus aureus bacteremia with reduced susceptibility to vancomycin", section on 'Overview of mechanisms' and "Overview of antibacterial susceptibility testing", section on 'Heteroresistance'.)
Because CoNS glycopeptide resistance appears to occur in the form of heteroresistant subpopulations of organisms, accurate detection in the laboratory can be difficult [43]. Due to small inocula and slow growth rates, standard methods for susceptibility testing (such as E-tests) can fail to detect heteroresistance; the optimal testing methods remain uncertain. Alternative methods studied for S. aureus have included vancomycin BMD, modified E-test methods, and use of brain heart infusion agar containing 4 mcg/ml vancomycin and casein [44,45]. The clinical significance of heteroresistance and its effect on treatment outcomes remains uncertain [46].
●Linezolid − There have been an increasing number of reports of linezolid resistance among CoNS [47-50]. In one study including 176 bloodstream isolates of S. epidermidis (including 39 linezolid-resistant strains), most linezolid-resistant strains were grouped into a single subclade based on whole genome sequencing [49]. In some cases, the resistant clones contained a cfr gene encoding a 23S ribosomal RNA methyltransferase associated with linezolid resistance. The authors postulated that exposure to a linezolid-resistant clone and linezolid use (resulting in reduction of competing microflora) led to emergence and dissemination of the resistant strains.
Nosocomial epidemiology — The factors contributing to the spread of drug-resistant CoNS in hospital environments remain to be fully elucidated; in addition to the selective pressure of antibiotic exposure, features of the pathogen (such as its capacity to adhere to foreign materials and to form biofilms) may play roles, as may issues of infection control such as hand hygiene and disinfection of equipment and surfaces [1].
Several studies have described acquisition and spread of resistant organisms among patients undergoing cardiac surgery [51-56]. Preoperatively, cardiac surgery patients generally have CoNS skin isolates that are susceptible to methicillin; resistant clones appear to emerge with selective pressure of perioperative antibiotic prophylaxis [51]. This observation may reflect selection of resistant organisms from the patient's preoperative flora and/or postoperative acquisition from the nosocomial environment [52-54,56].
A number of studies have demonstrated the spread of single clones and molecular clusters of drug-resistant CoNS in neonatal intensive care units and other hospital settings [57-61]. In a study of S. epidermidis colonization in ventricular-assist device recipients at four medical centers, the isolates fit into one of seven clones that were all highly antibiotic resistant, suggesting that these clones may be prevalent in health care settings [62]. In contrast, community-associated isolates of S. epidermidis demonstrate a low level of methicillin resistance and are genetically diverse [63].
FORMS OF INFECTION — Clinical manifestations of CoNS infection are outlined separately. (See "Infection due to coagulase-negative staphylococci: Clinical manifestations".)
Details regarding the management approach for certain manifestations of CoNS infection are discussed separately:
●Intravascular catheter infection (see "Intravascular non-hemodialysis catheter-related infection: Treatment")
●Endocarditis (see "Antimicrobial therapy of left-sided native valve endocarditis" and "Right-sided native valve infective endocarditis" and "Antimicrobial therapy of prosthetic valve endocarditis")
●Cardiac device infection (see "Infections involving cardiac implantable electronic devices: Treatment and prevention")
●Osteomyelitis (see "Nonvertebral osteomyelitis in adults: Treatment")
●Prosthetic joint infection (see "Prosthetic joint infection: Treatment")
●Central nervous system shunt infection (see "Infections of cerebrospinal fluid shunts")
●Breast implant infection (see "Breast implant infections")
●Urinary tract infection (see "Acute simple cystitis in adult and adolescent females" and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents")
DEVICE REMOVAL — For patients with CoNS infection associated with presence of an indwelling device, assessment regarding whether the device warrants removal is an important component of management. Given the importance of biofilm in the pathogenesis of CoNS infection, successful treatment often requires device removal. (See "Infection due to coagulase-negative staphylococci: Epidemiology, microbiology, and pathogenesis", section on 'Biofilm'.)
ANTIBIOTIC SELECTION
Parenteral versus oral therapy — Treatment with parenteral antibiotic therapy is warranted for patients with systemic infection due to CoNS; relevant conditions include bacteremia, endovascular infection (including intravascular catheter infection, endocarditis, cardiac device infection, and vascular graft infection), and bone and joint infections.
In some circumstances, oral antibiotic therapy may be used to complete treatment following an initial course of parenteral therapy. (See 'Oral therapy' below.)
In addition, patients with a urinary tract infection (UTI) due to S. saprophyticus may be treated with oral antibiotic therapy.
General principles related to selection of antibiotic therapy for treatment of CoNS infection are addressed in the following sections. Details regarding the management approach for certain manifestations of CoNS infection are discussed separately. (See 'Forms of infection' above.)
Parenteral therapy
Empiric therapy — The agent of choice for empiric parenteral therapy of CoNS infection is vancomycin (adult dosing summarized in the table (table 1); pediatric dosing: 15 mg/kg/dose every 6 to 8 hours), given the high frequency of methicillin-resistant strains and concerns about heteroresistance. (See "Overview of antibacterial susceptibility testing", section on 'Heteroresistance'.)
If specialized resistance testing (such as a gene probe for the mecA gene) is not available, methicillin resistance should be assumed. (See 'Methicillin-resistant isolates' below.)
Methicillin-resistant isolates — Methicillin-resistant isolates should be considered resistant to all beta-lactam antibiotics, including beta-lactamase inhibitor combinations, cephalosporins, and carbapenems (regardless of in vitro susceptibility results) [11]. Ceftaroline is an exception; it is a cephalosporin that retains activity against methicillin-resistant strains.
For treatment of infection due to methicillin-resistant CoNS strains or in situations where specialized resistance testing is not available, the parenteral agent of choice is vancomycin (adult dosing summarized in the table (table 1); pediatric dosing: 15 mg/kg/dose every 6 to 8 hours). Vancomycin is the agent for which there is the greatest cumulative clinical experience for treatment of systemic staphylococcal infection. This approach is extrapolated from the clinical approach to treatment of infection due to methicillin-resistant S. aureus (MRSA). (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of bacteremia".)
Daptomycin is an acceptable alternative to vancomycin for treatment of methicillin-resistant CoNS bacteremia. It has in vitro bactericidal activity against staphylococci. Clinical efficacy data for its use in the setting of CoNS infection are limited and mostly based on its efficacy for treatment of MRSA infections [64,65]. Successful use of daptomycin for treatment of bacteremia due to methicillin-resistant S. epidermidis has been described in case reports [66,67]. Daptomycin dosing is based on experience with treatment of bacteremia due to MRSA; we are in agreement with guidelines published by the Infectious Diseases Society of America, which recommend dosing daptomycin at 6 mg/kg IV once daily [68]. Some experts recommend higher doses (8 to 10 mg/kg per day), including in the setting of vancomycin treatment failure with persistent bacteremia.
Additional agents with potential activity for treatment of CoNS bacteremia include linezolid, lipoglycopeptides (telavancin, dalbavancin, oritavancin), and ceftaroline. In general, data on the efficacy of these agents against CoNS are limited:
●Linezolid has in vitro bacteriostatic activity against staphylococci, although clinical efficacy data for its use in the setting of CoNS infection are limited. Successful use of linezolid for treatment of bacteremia due to methicillin-resistant S. epidermidis has been described [69-71]. Dosing consists of 600 mg orally or IV twice daily. Linezolid-resistant CoNS have been reported [47].
●Telavancin has potent in vitro activity against CoNS, although clinical efficacy data are limited [72,73]. The US Food and Drug Administration has included boxed warnings regarding nephrotoxicity and decreased efficacy with moderate/severe baseline renal impairment [74]. Oritavancin and dalbavancin are long-acting lipoglycopeptides with anti-staphylococcal activity. Clinical data on their efficacy against CoNS infections are limited; in vitro studies demonstrate excellent activity [75,76].
●Ceftaroline has excellent in vitro activity against MRSA and methicillin-susceptible S. aureus, but clinical data regarding efficacy against CoNS are limited [77,78]. Ceftaroline has been used (both alone and in combination with daptomycin) as salvage therapy for persistent bacteremia, although experience is primarily with S. aureus [79-81].
●Teicoplanin is a glycopeptide with antibacterial activity similar to vancomycin. It has a longer half-life than vancomycin and appears to be better tolerated [82]. It is not available in the United States; in countries where available, it is sometimes used in place of vancomycin.
Methicillin-susceptible isolates — In the setting of infection due to CoNS that is known to be methicillin susceptible (as confirmed by specialized testing such as a gene probe for the mecA gene), treatment consists of nafcillin (2 g IV every 4 hours), oxacillin (2 g IV every 4 hours), or flucloxacillin (2 g IV every 6 hours). Cefazolin (2 g IV every 6 to 8 hours) is an acceptable alternative. If the patient has a history of beta-lactam allergy or there is concern for undetected heterotypic resistance, vancomycin is a reasonable alternative vancomycin (adult dosing summarized in the table (table 1); pediatric dosing: 15 mg/kg/dose every 6 to 8 hours).
This approach is extrapolated from the clinical approach to treatment of infection due to methicillin-susceptible S. aureus; clinical trial data evaluating treatment of methicillin-susceptible CoNS are limited. (See "Clinical approach to Staphylococcus aureus bacteremia in adults", section on 'Methicillin-sensitive S. aureus'.)
Data on the relative efficacy of beta-lactams versus vancomycin are limited. In one observational study including 124 patients with endocarditis due to methicillin-susceptible CoNS (of whom 88 received an anti-staphylococcal beta-lactam and 36 received vancomycin), no difference in 6-month mortality was observed [83].
CoNS are rarely susceptible to penicillin and limited clinical data are available on its use for treatment of infection due to CoNS.
Vancomycin-resistant isolates — The approach to treatment of infection due to CoNS with resistance to vancomycin depends on individual circumstances, including the form of infection and the antimicrobial susceptibility data. Data to guide management in such cases are limited; in general, the approach may be modeled on the approach to treatment of S. aureus with reduced susceptibility to vancomycin. Such cases should be managed in consultation with infectious disease expertise. (See "Staphylococcus aureus bacteremia with reduced susceptibility to vancomycin".)
Oral therapy — In some circumstances, oral antibiotic therapy may be used to complete treatment following an initial course of parenteral therapy; as an example, certain orthopedic infections warrant antibiotic suppression in the setting of retained hardware and/or presence of residual involved bone not amenable to complete debridement (see "Nonvertebral osteomyelitis in adults: Treatment" and "Prosthetic joint infection: Treatment"). In addition, treatment with oral antibiotic therapy is warranted for patients with UTI due to S. saprophyticus (which is almost always methicillin susceptible).
Ideally, antibiotic selection should be based on antibiotic susceptibility testing; if such information is not available, methicillin resistance should be assumed and antibiotic selection should be guided by local surveillance summaries of antibiotic susceptibility.
●Regimens with activity against methicillin-resistant CoNS include trimethoprim-sulfamethoxazole (one double-strength tablet twice daily), tetracyclines such as doxycycline (100 mg orally twice daily) or minocycline (100 mg orally twice daily), clindamycin (300 to 450 mg orally four times daily), and linezolid (600 mg orally twice daily).Prolonged use of linezolid may be limited by toxicity. (See "Linezolid and tedizolid (oxazolidinones): An overview".)
●Regimens with activity against methicillin-susceptible CoNS include oral semisynthetic penicillins (such as dicloxacillin [500 mg orally four times daily] or flucloxacillin [500 mg orally four times daily]) or cephalosporins (such as cephalexin 500 mg orally four times daily). Alternative agents include agents with activity against methicillin-resistant CoNS summarized above. CoNS are rarely susceptible to penicillin and limited clinical data are available on its use for treatment of infection due to CoNS.
Clinical efficacy data for use of these agents in the setting of CoNS infection are limited; the approach is extrapolated from data for S. aureus. (See "Acute cellulitis and erysipelas in adults: Treatment" and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections".)
In general, fluoroquinolone monotherapy is not appropriate for treatment of CoNS infection, due to the relatively high level of resistance to these agents (55 percent in one study) [7] and the emergence of resistance during therapy [84]. Later-generation fluoroquinolones may have greater activity than earlier-generation agents and higher barriers to the development of resistance; however, the potential for emergence of resistance to the newer fluoroquinolone has been demonstrated in in vitro models [85-89]. Fluoroquinolones are excreted in sweat, which may be associated with rapid emergence of resistance among CoNS in skin flora [90,91].
DURATION OF THERAPY
Isolated bacteremia — The duration of therapy for isolated CoNS bacteremia depends on individual clinical circumstances, as discussed in the following sections.
Use of an algorithm to guide management of staphylococcal bacteremia may be useful to optimize duration of antibiotic therapy. In a randomized trial including 385 patients with CoNS bacteremia (260 with simple bacteremia [single positive blood culture], 91 with uncomplicated bacteremia [≥2 blood cultures positive for CoNS drawn ≤24 hours apart], and 34 with complicated bacteremia [≥2 blood cultures positive for CoNS drawn >24 hours apart]), patients received treatment for ≤3 days, 5 days, or 7 to 14 days, respectively [92]. Among patients with uncomplicated CoNS bacteremia, the mean duration of therapy was 5.3 days for algorithm-based therapy versus 8.4 days for usual practice (difference -3.1, 95% CI -4.9 to -1.3); intravenous catheters were removed in all patients with uncomplicated CoNS bacteremia. Clinical success rates were comparable (87 versus 92 percent); there was no significant difference in serious adverse events between the algorithm-based and usual practice groups.
Single positive blood culture — For patients with simple CoNS bacteremia (single positive blood culture; often a contaminant rather than a true bacteremia), a treatment duration of ≤3 days (eg, until follow-up blood culture results are available) is reasonable [92]; criteria include (all of the following must be met):
●Negative follow-up blood culture(s)
●No signs or symptoms of metastatic infection
●No signs or symptoms of local infection at a catheter site
●No indwelling intravascular prosthetic devices
For patients (outside the neonatal age group) with a single positive blood culture for CoNS in the absence of a central line or prosthetic device, antibiotics may be deferred pending follow-up blood culture results.
≥2 positive blood cultures ≤24 hours apart — For patients with uncomplicated CoNS bacteremia (≥2 blood cultures positive for CoNS drawn ≤24 hours apart), a treatment duration of 5 days is reasonable; criteria include (all of the following must be met):
●Negative follow-up blood culture(s)
●No signs or symptoms of metastatic infection
●No indwelling intravascular prosthetic devices
This approach is supported by the study findings described above [92]. (See 'Isolated bacteremia' above.)
For patients with an indwelling vascular catheter and ≥2 positive blood cultures, the clinical approach is discussed separately. (See "Intravascular non-hemodialysis catheter-related infection: Clinical manifestations and diagnosis" and "Intravascular non-hemodialysis catheter-related infection: Treatment".)
≥2 positive blood cultures >24 hours apart — For patients with complicated CoNS bacteremia (≥2 blood cultures positive for CoNS drawn >24 hours apart) and for patients with CoNS bacteremia in the setting of an indwelling intravascular prosthetic device (such as prosthetic cardiac valve), evaluation for endocarditis is warranted. The approach is discussed separately. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Right-sided native valve infective endocarditis" and "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".)
For patients with an indwelling vascular catheter and ≥2 positive blood cultures, the clinical approach is discussed separately. (See "Intravascular non-hemodialysis catheter-related infection: Clinical manifestations and diagnosis" and "Intravascular non-hemodialysis catheter-related infection: Treatment".)
For patients with complicated CoNS bacteremia in the absence of metastatic infection or endocarditis, a treatment duration of 7 to 14 days is reasonable [92].
Other manifestations — For other manifestations of CoNS, the duration of therapy depends on individual clinical circumstances. (See 'Forms of infection' above.)
SUMMARY AND RECOMMENDATIONS
●Microbiology − Coagulase-negative staphylococci (CoNS) are part of the normal flora of human skin. These organisms have relatively low virulence but are increasingly recognized as significant pathogens in the setting of infection involving the bloodstream and other tissue sites.
●Risk factors − These include presence of prosthetic material (such as an intravascular catheter) and immune compromise. (See 'Introduction' above.)
●Antibiotic resistance − Resistance to methicillin and semisynthetic penicillins has been observed in more than 80 percent of clinical CoNS isolates. (See 'Antimicrobial resistance' above.)
●Antibiotic selection − Treatment with parenteral antibiotic therapy is warranted for patients with systemic infection due to CoNS. (See 'Parenteral versus oral therapy' above.)
•Methicillin-resistant pathogens − For treatment of systemic infection due to methicillin-resistant CoNS (or in absence of antimicrobial susceptibility data), we suggest vancomycin over other agents (Grade 2C). Vancomycin is the agent for which there is the greatest cumulative clinical experience for treatment of staphylococcal infection; daptomycin is an acceptable alternative agent. (See 'Empiric therapy' above and 'Methicillin-resistant isolates' above.)
•Methicillin-susceptible pathogens − For treatment of systemic infection due to methicillin-susceptible CoNS, we suggest a beta-lactam antibiotic in preference to vancomycin or daptomycin (Grade 2C). Regimens include nafcillin, oxacillin, or flucloxacillin. A first-generation cephalosporin such as cefazolin is an acceptable alternative in patients with hypersensitivity to the preceding agents. (See 'Methicillin-susceptible isolates' above.)
•Role of oral therapy − In some circumstances, oral antibiotic therapy may be used to complete treatment of CoNS infection following an initial course of parenteral therapy. In addition, patients with a urinary tract infection due to Staphylococcus saprophyticus may be treated with oral antibiotic therapy. Oral antibiotic selection should be guided by antimicrobial susceptibility results. (See 'Oral therapy' above.)
●Duration of treatment − For isolated CoNS bacteremia, duration depends on individual clinical circumstances. (See 'Isolated bacteremia' above.)
•For patients with a single blood culture positive for CoNS (often a contaminant rather than a true bacteremia), a treatment duration of ≤3 days (eg, until follow-up blood culture results are available) is reasonable; criteria are summarized above. (See 'Single positive blood culture' above.)
•For patients with ≥2 blood cultures positive for CoNS drawn ≤24 hours apart, a treatment duration of five days is reasonable; criteria are summarized above. (See '≥2 positive blood cultures ≤24 hours apart' above.)
•For patients with ≥2 blood cultures positive for CoNS drawn >24 hours apart, and for patients with CoNS bacteremia in the setting of an indwelling intravascular prosthetic device (such as prosthetic cardiac valve), evaluation for endocarditis is warranted. In the absence of endocarditis or metastatic infection, a treatment duration of 7 to 14 days is reasonable. (See '≥2 positive blood cultures >24 hours apart' above.)
•For patients with ≥2 positive blood cultures and an indwelling vascular catheter, the clinical approach is discussed separately. (See "Intravascular non-hemodialysis catheter-related infection: Clinical manifestations and diagnosis" and "Intravascular non-hemodialysis catheter-related infection: Treatment".)
•For patients with CoNS infection other than isolated bacteremia, duration depends on individual clinical circumstances. (See 'Forms of infection' above.)
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