Si va a consultar bibliografía la mejor opción es la vancomicina intravenosa pero como se imaginará necesita administración intrahospitalaria, del resto de opciones la nitrofurantoína se puede usar puesto que el embarazo no está a término.
Le dejo la información actualizada a Enero de 2011 en base a la revisión de toda la evidencia científica en el tratamiento de los estafilococos coagulasa negativos (primero le dejo las conclusiones y luego el resto del documento, está en inglés pero no creo que tenga problema).
TREATMENT — The agent of choice for empiric treatment of infections due to coagulase-negative staphylococci is vancomycin. In the setting of infection due to CoNS that is known to be methicillin susceptible, the preferred agent is nafcillin or oxacillin.
Newer agents include quinupristin-dalfopristin, linezolid, daptomycin, tigecycline, and telavancin; these have largely been developed for and evaluated in the setting of MRSA infection. Quinupristin-dalfopristin has in vitro activity against multiple-resistant CoNS, although it does not have FDA approval for treatment of these organisms [43-45]. Linezolid has significant bacteriostatic activity versus methicillin-resistant CoNS in vitro and has been successfully used in infected patients, although it does not have FDA approval for treatment of methicillin-resistant CoNS infections [46-48].
Published clinical experience with daptomycin for the treatment of CoNS infections is limited; it appears to have high in vitro activity against clinical isolates, including bloodstream isolates obtained from bone marrow transplant patients with symptomatic bacteremia. Tigecycline has demonstrated in vitro activity against CoNS; there are little clinical data on its efficacy [49-51]. Telavancin is a new glycopeptide with excellent in vitro activity against staphylococci; there is limited clinical experience with its clinical efficacy . Further discussion of efficacy and adverse effects of these agents is outlined in detail separately. (See "Treatment of invasive methicillin-resistant Staphylococcus aureus infections in adults".)
Alternative agents with possible efficacy include teicoplanin (a glycopeptide antibiotic), clindamycin, and the macrolides.
Investigational agents for treatment of MRSA may also prove effective against CoNS. (See "Treatment of invasive methicillin-resistant Staphylococcus aureus infections in adults", section on 'Investigational agents'.)
Combinations of antimicrobial agents are frequently used to treat CoNS prosthetic device infections (eg, prosthetic valve endocarditis) . This approach is primarily based on clinical experience rather than clinical trials.
ast literature review version 19.1: January 2011 | This topic last updated: May 7, 2010 (More)
INTRODUCTION — Coagulase-negative staphylococci (CoNS) are common colonizers of the human skin and the most frequent constituent of the normal flora at this site . Once considered relatively avirulent and usually a contaminant when isolated from a clinical specimen, these organisms have become increasingly recognized as agents of clinically significant nosocomial bloodstream infections.
Patients at risk include those with prosthetic devices, intravascular catheters, or other foreign bodies in place, and immunocompromised hosts. These infections are inherently difficult to treat given the frequent presence of foreign material and the often multiple drug resistant nature of the organisms.
Issues related to antimicrobial resistance in CoNS will be reviewed here. The microbiology, pathogenesis, epidemiology of CoNS and the clinical features, diagnosis, and treatment of specific infections caused by these organisms are discussed separately. (See "Microbiology, pathogenesis, and epidemiology of coagulase-negative staphylococci".)
Epidemiology — More than 80 percent of coagulase-negative staphylococcal isolates are resistant to methicillin and semisynthetic penicillins .
Although detailed epidemiologic studies describing the acquisition and spread of these resistant organisms are generally lacking, such studies have been performed in patients undergoing cardiac surgery. A common finding in each of these studies was that acquisition of resistant skin flora did not occur in the absence of antibiotic prophylaxis [3-7].
Preoperatively, cardiac surgery patients generally have skin isolates of CoNS that are susceptible to methicillin . However, one study that utilized techniques to amplify the number of bacteria recovered was able to detect rare methicillin-resistant coagulase-negative staphylococci preoperatively from at least one site in almost three-quarters of patients . After surgery, 17 of the 28 sites with preoperative low-level colonization contained high levels of methicillin-resistant staphylococci. Antibiograms and plasmid profile patterns suggested that these resistant organisms were derived from the small number of preoperative resistant organisms. This observation is consistent with the hypothesis that resistant clones emerged with the selective pressure of perioperative antibiotic prophylaxis.
Other studies have confirmed that patients who have undergone cardiac surgery have a postoperative skin flora composed primarily of methicillin-resistant CoNS. In one report, 91 percent of patients were colonized with organisms resistant to both methicillin and gentamicin by 10 days after surgery, a resistance pattern that was not present preoperatively [5,6]. However, plasmid pattern analysis revealed that pre- and postoperative isolates were distinct. Some of the nurses in the cardiothoracic intensive care unit were colonized with CoNS resistant to methicillin and gentamicin of the matching plasmid type .
Methicillin resistance — According to the NNIS survey, the incidence of methicillin resistance among CoNS rose from 20 to 60 percent between 1980 and 1989 . Such isolates are often resistant to multiple classes of antibiotics in addition to beta-lactams. Because CoNS are commensal skin flora, they are frequently exposed to antibiotics used to treat infections at other sites. As a result, they may become antibiotic resistant and persist on the skin. The genes responsible for this resistance are often found on plasmids facilitating the horizontal exchange of resistance genes among strains.
The mecA gene encoding a low-affinity penicillin-binding protein (PBP 2a) is responsible for mediating methicillin or oxacillin resistance in coagulase-negative staphylococci as it is in S. aureus . This resistance is heterotypic in both coagulase-negative and -positive strains, since only a minority of the bacterial population (as few as one in 10(3) or 10(6) organisms) expresses the resistant phenotype, making detection of resistance especially challenging . (See "Microbiology of methicillin-resistant Staphylococcus aureus".)
Reliable detection of methicillin resistance is critical to permit the initiation of appropriate antimicrobial therapy and to prevent the overuse of glycopeptides for the treatment of CoNS infections. Because many laboratories were detecting isolates that were mecA positive but testing susceptible to oxacillin by MIC or disk diffusion, breakpoints for determining the susceptibility of CoNS to oxacillin were revised by the Clinical and Laboratory Standards Institute (CLSI) [11,12].
The MIC breakpoints for CoNS (except S. lugdunensis) are ≤0.25 mcg/mL for susceptibility to oxacillin and ≥0.5 mcg/mL for resistance. This is in contrast to S. aureus (and S. lugdunensis), for which the oxacillin MIC breakpoints are ≤2 mcg/mL for susceptibility and ≥4 mcg/mL for resistance . For disk susceptibility testing, the cefoxitin disk is the preferred method to detect CoNS oxacillin susceptibility .
Accurate detection of resistance in the clinical laboratory requires the use of measures to enhance expression of this phenotype, including :
Incubation at a lower temperature (30 to 35ºC)Incubation for a prolonged period of time (24 to 48 hours)Medium with an increased sodium chloride content (2 percent NaCl)
If the results remain in doubt, one can pursue detection of the mecA gene using DNA hybridization or polymerase chain reaction techniques [15-17]. In addition, a latex agglutination test developed for detection of PBP 2a of methicillin-resistant S. aureus (MRSA-Screen, Denka Seiken Co., Niigata, Japan) has been investigated for its applicability in identifying methicillin resistance in a variety of species of CoNS [18-21]. This rapid assay has shown 98 percent sensitivity and high specificity in the hands of some investigators for S. epidermidis , although non-S. epidermidis strains occasionally yielded false-positive results.
An isolate determined to be methicillin-resistant should, regardless of the in vitro susceptibility results, be considered resistant to all beta-lactam antibiotics, including beta-lactamase inhibitor combinations, cephalosporins, and carbapenems .
Intermediate resistance to vancomycin — The emergence of S. aureus with intermediate resistance to vancomycin has received much attention. (See "Vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus infections".)
Similarly, there have been several case reports of coagulase-negative staphylococci (CoNS) with reduced susceptibility to vancomycin: two in patients on continuous ambulatory peritoneal dialysis (CAPD) and one during empiric therapy for febrile neutropenia [23-25]. The minimum inhibitory concentrations (MICs) were 8 to 16 mg/L in these patients. One of these reports documented the emergence of relative vancomycin resistance (with a stepwise increase in the MIC from 2 to 8 mg/L) in a CAPD patient who was treated with vancomycin for S. haemolyticus peritonitis . MIC cutoffs for CoNS vancomycin testing are: susceptible if ≤4 mg/L, intermediate if 8 to 16 mg/L, and resistant if ≥32 mg/L . The vancomycin MIC breakpoints for S. aureus were modified by the CLSI in 2006 and differ from those of coagulase-negative staphylococci.
Because glycopeptide resistance, like methicillin resistance, appears to be due to heteroresistant subpopulations of staphylococci, its accurate detection in the laboratory can be problematic. As an example, one group reported the isolation of vancomycin-intermediate S. epidermidis (VISE) from peritoneal fluid specimens of a patient undergoing CAPD who developed peritonitis . The primary isolate yielded a vancomycin MIC of 12 to 16 mcg/mL. However, upon subculture and testing by a variety of methods, the strains appeared to be susceptible to vancomycin. (See "Overview of antibacterial susceptibility testing", section on 'Heteroresistance'.)
The authors proposed that the phenotype of intermediate vancomycin resistance may have been expressed by only a small subpopulation of organisms in the original specimen, which may have been lost or diluted upon subculture, perhaps due to loss of selective pressure of the antibiotic. Some investigators have used induction methods, including an aztreonam disk placed on vancomycin-salt agar to demonstrate growth of satellite colonies, in order to screen for potential vancomycin resistance in CoNS .
The mechanism of glycopeptide resistance among staphylococci appears to be associated with alterations in cell wall metabolism, including cell wall thickening [28-31]. Increased cell wall thickness has also been observed in various CoNS clinical strains that demonstrate heterogeneous resistance to vancomycin . (See "Vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus infections".)
Resistance to other antibiotics — Vancomycin has been the mainstay of treatment for methicillin-resistant coagulase-negative staphylococcal infections. Gentamicin or rifampin may be added for the treatment of some deep-seated infections, such as prosthetic valve endocarditis and central nervous system shunt infections.
Although gentamicin is rapidly bactericidal for CoNS, resistance to gentamicin has increased to 60 to 70 percent of isolates in some studies, limiting the clinical utility of this agent [33,34]. More than 90 percent of CoNS remain susceptible to rifampin , but this drug must be used in combination with another antibiotic since resistance develops rapidly if rifampin is used as a single agent [3,35].
Trimethoprim-sulfamethoxazole has been used to treat a variety of serious staphylococcal infections, including prosthetic joint infections, endocarditis, meningitis, and CSF shunt infections [36-39]. Unfortunately, approximately half of methicillin-resistant CoNS in the United States are also resistant to trimethoprim .
The widespread use of ciprofloxacin has resulted in an increase in fluoroquinolone resistance among CoNS, perhaps due to selective pressure on skin flora since the drug is excreted into sweat . Some of the newer fluoroquinolones have greater activity than ciprofloxacin against staphylococci, but ciprofloxacin-resistant strains have reduced susceptibility to these other quinolones as well .
An outbreak of colonization with linezolid-resistant coagulase-negative staphylococci was reported among 16 ICU patients over a six month period. Such resistance is extremely rare. The resistant strains were isolated from several sites and contained the G2576T mutation conferring linezolid resistance. Nasal screening among ICU staff was negative. Institution and reinforcement of infection control procedures and restrictions on linezolid prescribing were successful in controlling the outbreak 
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