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Antimicrob Agents Chemother. 2011 September; 55(9): 4154–4160.
PMCID: PMC3165333

Activity of Ceftaroline and Epidemiologic Trends in Staphylococcus aureus Isolates Collected from 43 Medical Centers in the United States in 2009[down-pointing small open triangle]


A Staphylococcus aureus surveillance program was initiated in the United States to examine the in vitro activity of ceftaroline and epidemiologic trends. Susceptibility testing by Clinical and Laboratory Standards Institute broth microdilution was performed on 4,210 clinically significant isolates collected in 2009 from 43 medical centers. All isolates were screened for mecA by PCR and evaluated by pulsed-field gel electrophoresis. Methicillin-resistant S. aureus (MRSA) were analyzed for Panton-Valentine leukocidin (PVL) genes and the staphylococcal cassette chromosome mec (SCCmec) type. All isolates had ceftaroline MICs of ≤2 μg/ml with an MIC50 of 0.5 and an MIC90 of 1 μg/ml. The overall resistance rates, expressed as the percentages of isolates that were intermediate and resistant (or nonsusceptible), were as follows: ceftaroline, 1.0%; clindamycin, 30.2% (17.4% MIC ≥ 4 μg/ml; 12.8% inducible); daptomycin, 0.2%; erythromycin, 65.5%; levofloxacin, 39.9%; linezolid, 0.02%; oxacillin, 53.4%; tetracycline, 4.4%; tigecycline, 0%; trimethoprim-sulfamethoxazole, 1.6%; vancomycin, 0%; and high-level mupirocin, 2.2%. The mecA PCR was positive for 53.4% of the isolates. The ceftaroline MIC90s were 0.25 μg/ml for methicillin-susceptible S. aureus and 1 μg/ml for MRSA. Among the 2,247 MRSA isolates, 51% were USA300 (96.9% PVL positive, 99.7% SCCmec type IV) and 17% were USA100 (93.4% SCCmec type II). The resistance rates for the 1,137 USA300 MRSA isolates were as follows: erythromycin, 90.9%; levofloxacin, 49.1%; clindamycin, 7.6% (6.2% MIC ≥ 4 μg/ml; 1.4% inducible); tetracycline, 3.3%; trimethoprim-sulfamethoxazole, 0.8%; high-level mupirocin, 2.7%; daptomycin, 0.4%; and ceftaroline and linezolid, 0%. USA300 is the dominant clone causing MRSA infections in the United States. Ceftaroline demonstrated potent in vitro activity against recent S. aureus clinical isolates, including MRSA, daptomycin-nonsusceptible, and linezolid-resistant strains.


Ceftaroline, the active form of the prodrug ceftaroline fosamil, belongs to a new class of cephalosporins with broad-spectrum activity against multidrug resistant Gram-positive organisms including methicillin-resistant Staphylococcus aureus (MRSA), as well as common Gram-negative organisms. Historically β-lactam agents have been considered ineffective against MRSA because of poor affinity for the altered penicillin-binding protein 2a (PBP2a). Ceftaroline has anti-MRSA activity because structural differences allow high binding affinity to the mecA-encoded PBP2a (9, 10, 16). The U.S. Food and Drug Administration (FDA) granted marketing authorization for Teflaro (ceftaroline fosamil) in October 2010 for the treatment of acute bacterial skin and skin structure infections (including those caused by MRSA and methicillin-susceptible S. aureus [MSSA]) and community-acquired bacterial pneumonia (including those caused by MSSA but not those caused by MRSA) (1). Pharmacokinetic/pharmacodynamic (PK/PD) data predicted organisms with a ceftaroline MIC of ≤2 μg/ml could be effectively treated by intravenous infusion of 600 mg every 12 h (23). The FDA-approved susceptibility breakpoint is ≤1 μg/ml for S. aureus skin isolates (Teflaro [ceftaroline fosamil] prescribing information; Forest Laboratories, Inc., St. Louis, MO). Additional clinical trials investigating the efficacy of ceftaroline for treating pneumonia caused by MRSA are under consideration. The primary objective of the present study was to determine the in vitro activity of ceftaroline against a large collection of recent S. aureus isolates collected in 2009 from medical centers across the United States.

The epidemiology of MRSA continues to change. In 2003, the Centers for Disease Control and Prevention (CDC) established a national database to describe major pulsed-field gel electrophoresis (PFGE) types of MRSA in the United States (14). PFGE types USA100, USA200, USA500, USA600, and USA800 were composed of isolates primarily from healthcare-associated infections. USA100 was the most prevalent strain (44% of 667 MRSA isolates) and typically multidrug resistant with carriage of the staphylococcal cassette chromosome mec (SCCmec) type II (14). Two PFGE types associated with community-onset infections, USA300 and USA400, were not multidrug resistant, contained SCCmec IV, and frequently carried the Panton-Valentine leukocidin (PVL) gene (14). By 2005, USA300 was recognized as the most common strain causing community-onset MRSA infections (24). Recently, the USA300 clone has been implicated in healthcare-associated disease (19), and USA300 isolates with resistance to more classes of antimicrobial agents have been reported (6, 13, 24). A second objective of the present study was to evaluate the prevalence of major MRSA clones in the United States. Antimicrobial resistance rates, SCCmec types, PVL production, and the demographic characteristics of MRSA comprising the predominant PFGE types were examined.

(Presented in part at the 50th Interscience Conference on Antimicrobial Agents and Chemotherapy, Boston, MA, 13 September 2010 [abstr. E-820].)


Bacterial isolates.

Medical centers from throughout the United States were asked to submit 100 consecutive, clinically significant S. aureus isolates to the central laboratory at the University of Iowa. Isolates were to be unique (only one isolate per patient) and recovered from specimens submitted to their laboratory during June to December 2009. At least 25% of the isolates from each center were to be from blood cultures. Centers were instructed to not send isolates representing colonization and to remove identifiers that could link the isolate back to a specific patient. Information requested included specimen type and patient demographics (age, gender, inpatient versus outpatient, and whether inpatient specimens were collected within 48 h of admission).

Antimicrobial susceptibility testing.

Susceptibility testing using the Clinical and Laboratory Standards Institute (CLSI) broth microdilution method (3, 4) was performed for 13 antimicrobial agents on the isolates received. The agents tested included ceftaroline, ceftriaxone, clindamycin, daptomycin, erythromycin, levofloxacin, linezolid, mupirocin, oxacillin, tetracycline, tigecycline, trimethoprim-sulfamethoxazole (TMP-SMX), and vancomycin. Inducible clindamycin resistance was determined by the CLSI broth microdilution screening test (4). Linezolid MICs were read at 90% inhibition. FDA breakpoints were applied for agents without CLSI interpretive criteria (ceftaroline and tigecycline). Quality control was performed using S. aureus ATCC 29213, S. aureus ATCC BAA1708 (positive control for high-level mupirocin resistance), and S. aureus ATCC BAA-977 (positive control for inducible clindamycin resistance).

mecA detection.

All isolates were screened for mecA by PCR using modifications of previously described methods (15, 18). Colonies from fresh subcultures on blood agar plates were suspended in 200 μl of distilled water. Amplification was performed with 10× Biolase buffer, 1.5 mM MgCl2, 200 μM deoxynucleoside triphosphate, 800 nM concentrations of the primers MECA P4 and MECA P7, 1.25 U of Biolase Taq polymerase, and 3 μl of cells in a 50-μl final volume. The PCR conditions consisted of denaturation at 94°C (10 min); followed by 30 cycles of 94°C for 30 s, 53°C for 30 s, and 72°C for 1 min; and finally by 72°C for 4 min. The PCR products were separated in a 1.5% SeaKem GTG agarose gel (0.5× Tris-borate-EDTA buffer at 90 V) and stained with ethidium bromide. Testing on isolates with discordant oxacillin MIC and mecA PCR results was repeated as needed to attain a majority consensus result.


All isolates were characterized by PFGE according to published methods (20). Whole chromosomal DNA in agarose was digested with SmaI (Sigma-Aldrich, St. Louis, MO), and the restriction fragments were separated on a CHEF DRII apparatus (Bio-Rad Laboratories, Hercules, CA). After electrophoresis, the gels were stained with ethidium bromide, illuminated under UV light, and photographed. PFGE patterns were analyzed using Bionumerics software (Applied Maths, Kortrijk, Belgium). The unweighted pair group method with arithmetic averages and DICE coefficient (0.5% optimization, 1.0% position tolerance) were used for dendrogram construction. A similarity coefficient of 0.8 was used to define PFGE types. Isolate patterns from the present study were compared to PFGE type strains USA100 to USA800 (14).

SCCmec typing.

All mecA-positive isolates were analyzed for SCCmec types I to IV using previously described PCR methods with some modification (15, 18). Colonies from fresh subcultures on blood agar plates were suspended in 200 μl of distilled water. Amplification was performed with 10× Biolase buffer, 1.5 mM MgCl2, 200 μM deoxynucleoside triphosphate, 800 nM concentrations of the primers DCS F2, DCS R1, MECA P4, and MECA P7, 400 nM concentrations of the primers CIF2 F2, CIF2 R2, MECI P2, MECI P3, RIF5 F10, and RIF5 R13, 200 nM concentrations of the primers KDP F1, KDP R1, RIF4 F3, and RIF4 R9, 1.25 U of Biolase Taq polymerase, and 3 μl of cells in a 50-μl final volume. The PCR conditions consisted of denaturation at 94°C for 10 min; 30 cycles of 94°C for 30 s, 53°C for 30 s, and 72°C for 1 min; and finally 72°C for 4 min. The PCR products were separated in a 1.5% SeaKem GTG agarose gel (0.5× Tris-borate-EDTA buffer at 90 V) and visualized with ethidium bromide stain.

PVL gene detection.

All mecA-positive isolates were analyzed by PCR for genes encoding PVL production (lukS-PV and lukF-PV) using previously published methods (12, 15) with some modification. Organisms were grown overnight at 37°C on blood agar plates. Two or three colonies were taken from the plate and suspended into 200 μl of distilled water. Amplification was performed using 10× Biolase buffer, 200 μM deoxynucleoside triphosphate, 1.5 mM MgCl2, 400 nM luk-PV-1, 400 nM luk-PV-2, 0.04 μM 16S8F, 0.04 μM 16S 1439R, 1.25 U of Biolase Taq polymerase, and 3 μl of cells in a final volume of 50 μl. The PCR conditions were 94°C for 10 min; followed by 30 cycles of 94°C for 30 s, 55°C for 30 s, and 72°C for 1 min; and finally 72°C for 10 min. The PCR products were resolved in a 1.5% SeaKem GTG agarose gel in 0.5× Tris-borate-EDTA buffer at 90 V and stained with ethidium bromide.

Statistical analysis.

The significance of demographic differences between major PFGE types was assessed with the Fisher exact test. The two-tailed P values were calculated.


A total of 4,210 S. aureus isolates were obtained from 43 centers throughout the United States: 20% of isolates were from 9 centers in the Northeast of the United States, 22% were from 9 centers in the Southeast, 23% were from 10 centers in the Midwest, 21% were from 9 centers in the Southwest, and 14% were from 6 centers in the West (see the Acknowledgments for the participating centers in each region). The age distribution of patients with isolates included in the study were as follows: 0 to 5 years (10%), 6 to 20 years (12%), 21 to 64 years (56%), and ≥65 years (22%). A slight majority of isolates were from male patients (56%) and inpatients (54%). Only 14% of the isolates represented nosocomial infections (from inpatient specimen obtained >48 h after admission). The demographic information needed to determine whether an isolate represented a nosocomial infection was provided for 94% of the 4,210 isolates. Isolate sources were as follows: wound/abscess, 48%; blood, 26%; lower respiratory tract, 12%; tissue, 6%; joint fluid, 2%; and other normally sterile body fluids, 5%.

The overall resistance rates for the 4,210 S. aureus isolates, expressed as the percentage of isolates intermediate and resistant (or nonsusceptible), were as follows: ceftaroline, 1.0%; ceftriaxone, 53.5%; clindamycin, 30.2% (17.4% resistant with MICs ≥ 4 μg/ml; 12.8% with inducible resistance); daptomycin, 0.2%; erythromycin, 65.5%; levofloxacin, 39.9%; linezolid, 0.02%; oxacillin, 53.4%; tetracycline, 4.4%; tigecycline, 0% (FDA breakpoint of ≤0.5 μg/ml); TMP-SMX, 1.6%; and vancomycin, 0% (Table 1). High-level mupirocin resistance (MIC > 256 μg/ml) was detected in 93 isolates (2.2%). A comparison of the MICs for MRSA and MSSA isolates is given in Table 2.

Table 1.
MIC frequency distributions for 12 antimicrobial agents tested against 4210 S. aureus isolates
Table 2.
Comparison of MIC distributions for 12 agents against MRSA and MSSA

All isolates had ceftaroline MICs ≤ 2 μg/ml with an MIC50 of 0.5 μg/ml and an MIC90 of 1 μg/ml. MRSA isolates had ceftaroline MICs that ranged from ≤0.12 to 2 μg/ml (MIC50 = 0.5 μg/ml, MIC90 = 1 μg/ml). The ceftaroline MIC range for MSSA isolates was ≤0.12 to 1 μg/ml, with an MIC50 and an MIC90 of 0.25 μg/ml. Ceftaroline activities for isolate subsets are shown in Table 3. Most of the 44 isolates with ceftaroline MICs of 2 μg/ml were from inpatients (77%), and 25% (n = 11) represented nosocomial infections. These ceftaroline nonsusceptible isolates had daptomycin MICs of ≤0.25 μg/ml (66% of the 44 isolates) or 0.5 μg/ml (34%) and linezolid MICs of 2 μg/ml (77%) or 1 μg/ml (23%).

Table 3.
Ceftaroline MIC frequency distributions for subsets of S. aureus isolates

The mecA PCR test was positive for 53.4% of isolates. Four isolates had reproducibly discordant oxacillin MIC and mecA PCR results: two mecA-positive isolates with susceptible oxacillin MICs (≤0.12 μg/ml; 2 μg/ml) and two mecA-negative isolates with oxacillin MICs of 4 μg/ml. The PVL toxin genes were detected in 58.7% of the 2247 mecA-positive isolates tested.

PFGE analysis of the 4,210 S. aureus isolates revealed a diverse population with 452 different PFGE types. Of these, 211 PFGE patterns were each observed in only a single isolate. PFGE types with >20 isolates represented 70% of the population and were assigned capital letters starting with PFGE type A for the group with the largest number of isolates (n = 1,274) through PFGE Z (n = 21 isolates). The remaining PFGE types were assigned lowercase letters based on the number of representative isolates. The number of isolates in PFGE types a to z ranged from 20 to 10 isolates, respectively. The number of isolates in PFGE types assigned two lowercase letters ranged from 9 (PFGE type aa) to only 1 isolate (PFGE types uu1 to uu211).

Seven PFGE types corresponded to a USA clonal strain (Table 4). PFGE type A (n = 1,274) corresponded to USA300, PFGE B (n = 393) corresponded to USA100, PFGE C (n = 209) corresponded to USA200, PFGE d (n = 17) corresponded to USA400, PFGE ss28 (n = 3) corresponded to USA500, PFGE uu147 (n = 1) corresponded to USA800, and PFGE uu170 (n = 1) corresponded to USA600. The USA100 to USA500 PFGE types were composed of MRSA and MSSA isolates. The single USA800 isolate was MSSA. No isolate with a PFGE pattern closely related to USA700 was collected in the present study.

Table 4.
PFGE, SCCmec and PVL gene results for 4210 S. aureus isolates

A total of 186 PFGE types were observed among the 2,247 MRSA isolates, with 51% classified as PFGE A (USA300), 17% classified as PFGE B (USA100), and <1% classified as USA200, USA400, USA500, or USA600 (no USA700 or USA800) PFGE types. The SCCmec and PVL gene test results for the major PFGE types are shown in Table 4. The majority of SCCmec type IV (1,134/1,479) and PVL gene-positive isolates (1,102/1,315) were USA300 strains. Most of the isolates harboring SCCmec type II (367/707) were USA100 strains. Isolates in PFGE type F (2.9% of MRSA) were closely related to PFGE B (USA100; similarity coefficient of 0.77), and 95% carried SCCmec type II.

Demographic and resistance profiles are summarized in Table 5. The 597 isolates (14%) representing nosocomial infections were evenly distributed among the MRSA and MSSA populations. In comparing USA300 and USA100 MRSA isolates, the isolates causing nosocomial infections were observed less often among USA300 strains (8%) than among USA100 strains (23%, P < 0.0001). The USA100 MRSA isolates included more isolates from blood (35%), the lower respiratory tract (22%), and the elderly (age ≥ 65, 43%) than the USA300 MRSA isolates (15, 5, and 11%, respectively; P < 0.0001). Among USA300 strains, there were higher proportions of isolates from wound/abscess (71%) and patients ≤20 years of age (28%) than for USA100 isolates (28 and 9%, respectively; P < 0.0001). The greatest differences in resistance rates were observed for clindamycin (8% of USA300 isolates resistant versus 94% of USA100) and levofloxacin (49% of USA300 isolates resistant versus 95% of USA100).

Table 5.
Comparison of demographics and resistance profiles for USA300 and USA100 MRSA isolates

There was a trend of increasing resistance when we compared USA300 MRSA isolates divided into the following groups: outpatients (n = 615), inpatients within 48 h of admission (n = 385), and inpatients >48 h after admission (n = 88). The rates of levofloxacin resistance for these groups of USA300 MRSA isolates were 47.2% (outpatients), 50.6% (inpatients < 48 h), and 54.5% (nosocomial). A similar trend was observed for resistance to clindamycin (includes inducible phenotype), with rates of 6.3, 8.6, and 12.5%, respectively; tetracycline resistance (2.4, 3.9, and 6.8%, respectively); TMP-SMX resistance (0.5, 1.0, and 2.3%, respectively); erythromycin resistance (90.7, 91.2, and 92.0%, respectively); and daptomycin nonsusceptibility (0, 0.5, and 2.3%, respectively).


Ceftaroline demonstrated potent in vitro activity against the 4,210 S. aureus isolates in this multicenter surveillance study with an overall susceptibility rate of 99% and an MIC90 of 1 μg/ml. For MSSA, the ceftaroline MIC90 of 0.25 μg/ml was identical to earlier studies testing fewer isolates (5, 17, 21). A Japanese study reported a ceftaroline MIC90 value one dilution higher for MSSA (0.5 μg/ml) (7). For MRSA, our ceftaroline MIC90 of 1 μg/ml was also reported by other studies examining isolates from the United States (5, 8), while a higher MIC90 value of 2 μg/ml has been found when testing international MRSA strains (7, 8, 17, 21). The present study demonstrated good ceftaroline activity against isolates that were not susceptible to other anti-MRSA agents. Ten daptomycin-nonsusceptible isolates had ceftaroline MICs ranging from ≤0.12 to 1 μg/ml, and the only linezolid-resistant isolate had a ceftaroline MIC of 1 μg/ml. Of 57 isolates with vancomycin MICs of 2 μg/ml, only 4 had ceftaroline MICs above the FDA breakpoint. All of the USA300 MRSA isolates had ceftaroline MICs of ≤1 μg/ml. In addition to ceftaroline, other agents with high rates of susceptibility in the present study were vancomycin (100%), tigecycline (100%), linezolid (99.9%), daptomycin (99.8%), TMP-SMX (98.4%), and tetracycline (95.6%).

The rate of high-level mupirocin resistance (2.2%) in this collection was similar to the 1.6% detected by disk testing more than a decade ago in a European multicenter study (22). Applying a lower breakpoint of >128 μg/ml (one dilution below the current CLSI criteria), a CDC study detected high-level mupirocin resistance in 2.3% of 1,984 invasive MRSA isolates obtained from 8 states in 2005 and 2006 (11). The 93 high-level mupirocin-resistant isolates in the present study were collected from 36 centers (1 to 7 isolates per site). PFGE characterization of high-level mupirocin-resistant strains revealed a diverse population (37 PFGE types), with the largest fractions represented by the USA300 (37.6%) and USA100 (6.5%) strains. A recent and well-publicized study demonstrated a reduction in surgical site infections by rapid detection of S. aureus carriage at admission and decolonization with a regimen that included mupirocin treatment (2). As mupirocin use increases, it will be important to continue monitoring resistance.

PFGE analysis revealed a diverse S. aureus population (452 different PFGE types), with the predominant PFGE types being closely related to the USA300 (30% of all isolates, 11% MSSA) and USA100 (9% of all isolates, 4% MSSA) clones. The MRSA population was more clonal, with 68% of isolates closely related to USA300 (51%) or USA100 (17%). The present study confirms the predominant role of USA300 in causing MRSA infections within the United States.

USA300 has been recognized as a cause of community-acquired MRSA infections since 2000 when outbreaks began occurring among athletes, prisoners, children in daycare, and military personnel (24). A retrospective study in Alabama revealed sporadic isolation of USA300 exclusively from outpatients from 2000 to 2003, followed by a rapid increase in USA300 isolates in 2004 (70% of the outpatient MRSA isolates and 45% of the inpatient MRSA isolates were USA300) (19). A similar pattern of USA300 recovery from both inpatients and outpatients was evident in our 2009 data: 62% of outpatient MRSA isolates and 41% of inpatient MRSA isolates were USA300 (38% of outpatient MRSA isolates and 23% of inpatient MRSA isolates were USA100). Of the 302 MRSA isolates that met the criteria for nosocomial infections, 29% (n = 88) were USA300 and 28% (n = 85) were USA100.

There are limited multicenter data available regarding the prevalence of MRSA clones in the United States. Active Bacterial Core (ABC) surveillance reported that the predominant MRSA isolates causing invasive disease in 2005 and 2006 were USA300 (31.4%) and USA100 (53.2%) (11). The same prevalence of USA300 (n = 205, 31.4%) was observed among the 652 MRSA isolates recovered from invasive sites in the present study, but there were fewer USA100 strains (n = 159, 24.4%). We confirmed here previously reported trends of USA300 MRSA strains harboring PVL genes (96.9%) and causing disease in a younger population than USA100. The predominant carriage of SCCmec type IV (99.7%) by USA300 and SCCmec type II (93.4%) by USA100 strains in this collection was as expected.

Although USA300 MRSA isolates have acquired resistance to additional drug classes, the overall resistance rates remain lower than for USA100. Clindamycin continues to be effective against USA300, with 92% of isolates susceptible, but the macrolide resistance rate of 91% approaches that of USA100 strains (97%). Levofloxacin is not a reliable agent for either clone, with 49% (USA300) and 95% (USA100) of the isolates now resistant. The ABC surveillance program reported similar rates of resistance for 625 USA300 invasive isolates: erythromycin, 94.4%; levofloxacin, 54.6%, and clindamycin, 9% (11). When USA300 MRSA isolates in the present study were stratified into three groups (outpatient, inpatient ≤48 h, and inpatient >48 h), a trend of increasing resistance was observed with the lowest rates among outpatient isolates and the highest rates in isolates causing nosocomial infections. The study would have been strengthened with review of medical records to categorize isolates not representing nosocomial infection as either healthcare or community associated.

In conclusion, our findings here confirm how successful the USA300 clone has become as both a nosocomial and community-acquired MRSA pathogen in the United States. Since USA300 will likely become more resistant, the availability of a new cephalosporin, ceftaroline, with potent in vitro activity against MRSA is encouraging.


We thank the following individuals, listed by U.S. region, for providing the S. aureus isolates characterized in this study: (i) Joseph Schwartzman, Dartmouth-Hitchcock Medical Center, Lebanon, NH; Andrew Onderdonk, Brigham and Women's Hospital, Boston, MA; Laura Ovittore, Danbury, Hospital, Danbury, CT; Daniel Shapiro, Lahey Clinic, Burlington, MA; Phyllis Della-Latta, Columbia Presbyterian Hospital, New York, NY; Allan Truant, Temple University Hospital, Philadelphia, PA; Deanna Kiska, SUNY Upstate Medical Center, Syracuse, NY; Paul Bourbeau, Danville, PA; Dwight Hardy, University of Rochester Medical Center, Rochester, NY; and Christine Ginocchio, North Shore–LIJ Health System, Lake Success, NY (Northeast); (ii) Betty Forbes, VA Commonwealth University School of Medicine, Richmond, VA; Peter Gilligan, University of North Carolina Hospital, Chapel Hill, NC; Lisa Steed, Medical University of South Carolina, Charleston, SC; Robert Jerris, Children's Healthcare of Atlanta, Atlanta, GA; James Snyder, University of Louisville Hospital, Louisville, KY; Kenneth Rand, Shands Hospital–University of Florida, Gainesville, FL; Diane Halstead, Baptist Medical Center, Jacksonville, FL; Teresa Barnett, University of South Alabama, Mobile, AL; and Yi-Wei Tang, Vanderbilt University Medical Center, Nashville, TN (Southeast); (iii) Gerri Hall, Cleveland Clinic, Cleveland, OH; Wanita Howard, University of Iowa Health Care, Iowa City, IA; Mary Beth Perri, Henry Ford Hospital, Detroit, MI; Gerald Denys, Clarian Pathology Laboratory, Indianapolis, IN; Mary Hayden, Rush University Medical Center, Chicago, IL; Richard Thomson, Jr., Evanston Northwestern Healthcare, Evanston, IL; Joan Hoppe-Bauer, Barnes Jewish Hospital, St. Louis, MO; Rebecca Horvath, University of Kansas Medical Center, Kansas City, KS; Steven Cavalieri, Creighton University, Omaha, NE; and Glenn Hansen, Hennepin County Hospital, Minneapolis, MN (Midwest); (iv) James Versalovic, Houston, TX; Paul Southern, Jr., Dallas, TX; James Jorgenson, San Antonio, TX; Sara Hobbie, Tulsa, OK; Michael Wilson, Denver, CO; Ann Croft, Salt Lake City, UT; and Michael Saubolle, Phoenix, AZ (Southwest); and (v) Ann Robinson, Pathology Associates Medical Lab, Spokane, WA; Janet Hindler, UCLA Medical Center, Los Angeles, CA; Rohan Nadarajah, UCSF Medical Center, San Francisco, CA; Susan Sharp, Northwest Kaiser Permanente, Portland, OR; Brad Cookson, University of Washington Medical Center, Seattle, WA; and Matt Bankowski, Diagnostic Laboratory Services, Inc., Honolulu, HI (West).

G.V.D. received research funding from Abbott Laboratories, Schering-Plough, Bayer Pharmaceutical, Merck, Shionogi, Cubist, and Astra-Zeneca and has been on the speakers' bureaus of Abbott Laboratories, Aventis, Astra-Zeneca, Pfizer, Astellas, and Schering-Plough. D.J.D. has received research funding from Merck, Pfizer, Schering-Plough, Astellas, and bioMérieux. S.S.R. has received research funding from Abbott Laboratories, BD Diagnostics, Forest Laboratories, and Schering-Plough. D.B. and I.A.C. are employees of Cerexa, Inc., a subsidiary of Forest Laboratories, Inc. (New York, NY), which developed ceftaroline.

Financial support for this project was provided by Forest Laboratories, Inc. (New York, NY). Scientific Therapeutics Information, Inc. (Springfield, NJ), provided editorial assistance funded by Forest Laboratories.


[down-pointing small open triangle]Published ahead of print on 27 June 2011.


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