scholarly journals Functional Identification of Serine Hydroxymethyltransferase as a Key Gene Involved in Lysostaphin Resistance and Virulence Potential of Staphylococcus aureus Strains

2020 ◽  
Vol 21 (23) ◽  
pp. 9135
Author(s):  
Nayab Batool ◽  
Kwan Soo Ko ◽  
Akhilesh Kumar Chaurasia ◽  
Kyeong Kyu Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Serine Hydroxymethyltransferase ◽  
Multiple Drug ◽  
Host Immune System ◽  
Functional Identification ◽  
Resistance Development ◽  
Mammalian Cell Lines ◽  
Virulence Potential

Gaining an insight into the mechanism underlying antimicrobial-resistance development in Staphylococcus aureus is crucial for identifying effective antimicrobials. We isolated S. aureus sequence type 72 from a patient in whom the S. aureus infection was highly resistant to various antibiotics and lysostaphin, but no known resistance mechanisms could explain the mechanism of lysostaphin resistance. Genome-sequencing followed by subtractive and functional genomics revealed that serine hydroxymethyltransferase (glyA or shmT gene) plays a key role in lysostaphin resistance. Serine hydroxymethyltransferase (SHMT) is indispensable for the one-carbon metabolism of serine/glycine interconversion and is linked to folate metabolism. Functional studies revealed the involvement of SHMT in lysostaphin resistance, as ΔshmT was susceptible to the lysostaphin, while complementation of the knockout expressing shmT restored resistance against lysostaphin. In addition, the ΔshmT showed reduced virulence under in vitro (mammalian cell lines infection) and in vivo (wax-worm infection) models. The SHMT inhibitor, serine hydroxymethyltransferase inhibitor 1 (SHIN1), protected the 50% of the wax-worm infected with wild type S. aureus. These results suggest SHMT is relevant to the extreme susceptibility to lysostaphin and the host immune system. Thus, the current study established that SHMT plays a key role in lysostaphin resistance development and in determining the virulence potential of multiple drug-resistant S. aureus.

scholarly journals Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa

2020 ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background: The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.Results: Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. Conclusion: Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa

2020 ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background: The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.Results: Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. Conclusion: Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa

2020 ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background: The host-microbial commensalism can shapes the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.Results: Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, OVA-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. Conclusion: Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa

2020 ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background: The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.Results: Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. Conclusion: Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals Rapid resistance development to three antistaphylococcal therapies in antibiotic-tolerant staphylococcus aureus bacteremia

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258592
Author(s):  
Christopher R. Miller ◽  
Jonathan M. Monk ◽  
Richard Szubin ◽  
Andrew D. Berti
Keyword(s):  
Staphylococcus Aureus ◽  
Subsequent Development ◽  
Multidrug Resistant ◽  
Blood Cultures ◽  
Therapeutic Interventions ◽  
Prevention Measures ◽  
Beta Lactam ◽  
Resistance Development

Understating how antibiotic tolerance impacts subsequent resistance development in the clinical setting is important to identifying effective therapeutic interventions and prevention measures. This study describes a patient case of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia which rapidly developed resistance to three primary MRSA therapies and identifies genetic and metabolic changes selected in vivo that are associated with rapid resistance evolution. Index blood cultures displayed susceptibility to all (non-beta-lactam) antibiotics with the exception of trimethoprim/ sulfamethoxazole. One month after initial presentation, during the same encounter, blood cultures were again positive for MRSA, now displaying intermediate resistance to vancomycin and ceftaroline and resistance to daptomycin. Two weeks later, blood cultures were positive for a third time, still intermediate resistant to vancomycin and ceftaroline and resistant to daptomycin. Mutations in mprF and vraT were common to all multidrug resistant isolates whereas mutations in tagH, agrB and saeR and secondary mprF mutation emerged sequentially and transiently resulting in distinct in vitro phenotypes. The baseline mutation rate of the patient isolates was unremarkable ruling out the hypermutator phenotype as a contributor to the rapid emergence of resistance. However, the index isolate demonstrated pronounced tolerance to the antibiotic daptomycin, a phenotype that facilitates the subsequent development of resistance during antibiotic exposure. This study exemplifies the capacity of antibiotic-tolerant pathogens to rapidly develop both stable and transient genetic and phenotypic changes, over the course of a single patient encounter.

SC5005 dissipates the membrane potential to kill Staphylococcus aureus persisters without detectable resistance

2021 ◽  
Author(s):  
Chieh-Hsien Lu ◽  
Chung-Wai Shiau ◽  
Yung-Chi Chang ◽  
Hsiu-Ni Kung ◽  
Jui-Ching Wu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mode Of Action ◽  
Cytoplasmic Membrane ◽  
Resistance Development ◽  
Antibiotic Resistant ◽  
Atp Production ◽  
The Past ◽  
Ht 29

Abstract Objectives In the past few decades, multiple-antibiotic-resistant Staphylococcus aureus has emerged and quickly spread in hospitals and communities worldwide. Additionally, the formation of antibiotic-tolerant persisters and biofilms further reduces treatment efficacy. Previously, we identified a sorafenib derivative, SC5005, with bactericidal activity against MRSA in vitro and in vivo. Here, we sought to elucidate the resistance status, mode of action and anti-persister activity of this compound. Methods The propensity of S. aureus to develop SC5005 resistance was evaluated by assessment of spontaneous resistance and by multi-passage selection. The mode of action of SC5005 was investigated using macromolecular synthesis, LIVE/DEAD and ATPlite assays and DiOC2(3) staining. The effect of SC5005 on the mammalian cytoplasmic membrane was measured using haemolytic and lactate dehydrogenase (LDH) assays and flow cytometry. Results SC5005 depolarized and permeabilized the bacterial cytoplasmic membrane, leading to reduced ATP production. Because of this mode of action, no resistance of S. aureus to SC5005 was observed after constant exposure to sub-lethal concentrations for 200 passages. The membrane-perturbing activity of SC5005 was specific to bacteria, as no significant haemolysis or release of LDH from human HT-29 cells was detected. Additionally, compared with other bactericidal antibiotics, SC5005 exhibited superior activity in eradicating both planktonic and biofilm-embedded S. aureus persisters. Conclusions Because of its low propensity for resistance development and potent persister-eradicating activity, SC5005 is a promising lead compound for developing new therapies for biofilm-related infections caused by S. aureus.

scholarly journals Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models. Results Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. Conclusion Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals In vivo activity of anprocide alone, and in vitro activity in combination with conventional antibiotics against Staphylococcus aureus and Staphylococcus epidermidis biofilms

2009 ◽  
Vol 58 (9) ◽  
pp. 1203-1206 ◽  
Author(s):  
Robin K. Pettit ◽  
Christine A. Weber ◽  
Stacey B. Lawrence ◽  
George R. Pettit ◽  
Melissa J. Kean ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Drug Resistance ◽  
Murine Model ◽  
Staphylococcus Epidermidis ◽  
Multiple Drug Resistance ◽  
Multiple Drug ◽  
In Vitro Activity ◽  
Conventional Antibiotics

The alarming spread of multiple drug resistance in Staphylococcus aureus, combined with the frequent occurrence of S. aureus and Staphylococcus epidermidis in biofilm-type infections, indicates a growing need for new therapies. The experimental steroidal amide anprocide [3β-acetoxy-17β-(l-prolyl)amino-5α-androstane] significantly reduced c.f.u. ml−1 per suture (P <0.0001) in a murine model of topical S. aureus infection. In chequerboard assays with planktonic-grown S. aureus and S. epidermidis, anprocide was synergistic with bacitracin, oxacillin, clindamycin or ceftriaxone. Anprocide was also synergistic in combination with bacitracin or oxacillin against some isolates of biofilm-grown S. aureus and S. epidermidis.

scholarly journals Symbiotic Microbiome Staphylococcus Aureus from Human Nasal Mucus Modulates IL-33-Mediated Type 2 Immune Responses in Allergic Nasal Mucosa

2020 ◽  
Author(s):  
Yung Jin Jeon ◽  
Chan Hee Gil ◽  
Jina Won ◽  
Ara Jo ◽  
Hyun Jik Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Allergic Inflammation ◽  
Host Immune System ◽  
Protein Levels ◽  
Nasal Mucus ◽  
Ar Models

Abstract Background The host-microbial commensalism can shapes the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.Results Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, OVA-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice.Conclusion Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

scholarly journals 1539. Dalbavancin, Vancomycin, and Daptomycin Alone and in Combination with Cefazolin Against Vancomycin Intermediate-Resistant (VISA) and Daptomycin Non-Susceptible (DNS) Staphylococcus aureus

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S561-S562
Author(s):  
Jacinda Abdul-Mutakabbir ◽  
Razieh Kebriaei ◽  
Kyle Stamper ◽  
Philip Maassen ◽  
Michael J Rybak
Keyword(s):  
Staphylococcus Aureus ◽  
Drug Therapy ◽  
Bactericidal Activity ◽  
Growth Control ◽  
Aureus Strain ◽  
Multiple Drug ◽  
Log Reduction ◽  
Mrsa Strains

Abstract Background Glycopeptides and lipopeptides, more specifically vancomycin (VAN) and daptomycin (DAP) have been principally utilized in treating MRSA infections. Due to continued use, MRSA strains have developed resistance to these antibiotics including vancomycin intermediate susceptible Staphylococcus aureus (VISA) and daptomycin non-susceptible strains (DNS). Lipoglycopeptides; notably dalbavancin (DAL), have been employed due to their ease of administration and enhanced activity against highly resistant S. aureus. As previously demonstrated, the use of β-lactams, specifically cefazolin (CFZ) in combination with anti-MRSA drug therapy has been effective in eradicating S. aureus complicated by increased resistance. The objective of this study was to evaluate the activity of DAL, VAN, and DAP, alone and in combination with CFZ in a pharmacokinetic/pharmacodynamic (PK/PD) model. Methods The well-characterized DNS-VISA strain, D712, was evaluated in eight different regimens in duplicate via a one-compartment 7-day PK/PD model. The experimental regimens were as follows: D712 growth control, DAL 1500 mg given on day 1, VAN 2 g given every 12 hours, DAP 10 mg/kg once-daily, CFZ 2 g given every 8 hours and DAL, DAP, and VAN in combination with CFZ. Results The combinations of DAL+CFZ, VAN+CFZ, and DAP+CFZ demonstrated a significant log10 CFU/mL reduction (more than 5 log 10 CFU/mL and up to detection limit), compared with each drug used as monotherapy (P < 0.001). Neither DAP nor VAN demonstrated sustained bactericidal activity, (represented by a >3-log10 CFU/mL reduction from baseline) and resulted in significant regrowth, when administered alone. However, the DAP +CFZ, and VAN+CFZ combination models demonstrated bactericidal activity at 4 hours and 24 hours, respectively. While DAL alone did demonstrate bactericidal activity, the DAL+CFZ combination was more rapidly bactericidal, achieving a > 3-log reduction from baseline in 8 hours vs. 48 hours (P < 0.05). Conclusion The combination of DAL, VAN, or DAP with CFZ demonstrated significantly improved activity against this multiple drug-resistant S. aureus strain. Further research is warranted, both in vivo and in vitro, to explore the synergistic capabilities of anti-MRSA drug therapy in combination with β-lactams. Disclosures All authors: No reported disclosures.

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