scholarly journals Small Molecules Produced by Commensal Staphylococcus epidermidis Disrupt Formation of Biofilms by Staphylococcus aureus

2019 ◽  
Vol 86 (5) ◽  
Author(s):  
Thaís Glatthardt ◽  
Juliana Curityba de Mello Campos ◽  
Raiane Cardoso Chamon ◽  
Thiago Freitas de Sá Coimbra ◽  
Giulia de Almeida Rocha ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Proteinase K ◽  
Antibiofilm Activity ◽  
Skin Microbiome ◽  
Chronic Infections ◽  
Content Type ◽  
Treatment And Prevention

ABSTRACT The microbiota influences host health through several mechanisms, including protecting it from pathogen colonization. Staphylococcus epidermidis is one of the most frequently found species in the skin microbiota, and its presence can limit the development of pathogens such as Staphylococcus aureus. S. aureus causes diverse types of infections ranging from skin abscesses to bloodstream infections. Given the increasing prevalence of S. aureus drug-resistant strains, it is imperative to search for new strategies for treatment and prevention. Thus, we investigated the activity of molecules produced by a commensal S. epidermidis isolate against S. aureus biofilms. We showed that molecules present in S. epidermidis cell-free conditioned media (CFCM) caused a significant reduction in biofilm formation in most S. aureus clinical isolates, including all 4 agr types and agr-defective strains, without any impact on growth. S. epidermidis molecules also disrupted established S. aureus biofilms and reduced the antibiotic concentration required to eliminate them. Preliminary characterization of the active compound showed that its activity is resistant to heat, protease inhibitors, trypsin, proteinase K, and sodium periodate treatments, suggesting that it is not proteinaceous. RNA sequencing revealed that S. epidermidis-secreted molecules modulate the expression of hundreds of S. aureus genes, some of which are associated with biofilm production. Biofilm formation is one of the main virulence factors of S. aureus and has been associated with chronic infections and antimicrobial resistance. Therefore, molecules that can counteract this virulence factor may be promising alternatives as novel therapeutic agents to control S. aureus infections. IMPORTANCE S. aureus is a leading agent of infections worldwide, and its main virulence characteristic is the ability to produce biofilms on surfaces such as medical devices. Biofilms are known to confer increased resistance to antimicrobials and to the host immune responses, requiring aggressive antibiotic treatment and removal of the infected surface. Here, we investigated a new source of antibiofilm compounds, the skin microbiome. Specifically, we found that a commensal strain of S. epidermidis produces molecules with antibiofilm activity, leading to a significant decrease of S. aureus biofilm formation and to a reduction of previously established biofilms. The molecules potentiated the activity of antibiotics and affected the expression of hundreds of S. aureus genes, including those associated with biofilm formation. Our research highlights the search for compounds that can aid us in the fight against S. aureus infections.

scholarly journals Lucilia sericata Chymotrypsin Disrupts Protein Adhesin-Mediated Staphylococcal Biofilm Formation

2012 ◽  
Vol 79 (4) ◽  
pp. 1393-1395 ◽  
Author(s):  
Llinos G. Harris ◽  
Yamni Nigam ◽  
James Sawyer ◽  
Dietrich Mack ◽  
David I. Pritchard
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Lucilia Sericata ◽  
Bacterial Biofilm ◽  
Bacterial Biofilms ◽  
Formation Mechanisms ◽  
Chronic Infections ◽  
Content Type ◽  
Effective Activity

ABSTRACTStaphylococcus aureusandStaphylococcus epidermidisbiofilms cause chronic infections due to their ability to form biofilms. The excretions/secretions ofLucilia sericatalarvae (maggots) have effective activity for debridement and disruption of bacterial biofilms. In this paper, we demonstrate how chymotrypsin derived from maggot excretions/secretions disrupts protein-dependent bacterial biofilm formation mechanisms.

Impact of pH on growth of Staphylococcus epidermidis and Staphylococcus aureus in vitro

2021 ◽  
Vol 70 (9) ◽  
Author(s):  
Vidula Iyer ◽  
Janhavi Raut ◽  
Anindya Dasgupta
Keyword(s):  
Staphylococcus Aureus ◽  
Growth Kinetics ◽  
Staphylococcus Epidermidis ◽  
Type Species ◽  
Ph Dependence ◽  
Skin Microbiome ◽  
Content Type ◽  
Link Type ◽  
Kinetics Of

The pH of skin is critical for skin health and resilience and plays a key role in controlling the skin microbiome. It has been well reported that under dysbiotic conditions such as atopic dermatitis (AD), eczema, etc. there are significant aberrations of skin pH, along with a higher level of Staphylococcus aureus compared to the commensal Staphylococcus epidermidis on skin. To understand the effect of pH on the relative growth of S. epidermidis and S. aureus , we carried out simple in vitro growth kinetic studies of the individual microbes under varying pH conditions. We demonstrated that the growth kinetics of S. epidermidis is relatively insensitive to pH within the range of 5–7, while S. aureus shows a stronger pH dependence in that range. Gompertz’s model was used to fit the pH dependence of the growth kinetics of the two bacteria and showed that the equilibrium bacterial count of S. aureus was the more sensitive parameter. The switch in growth rate happens at a pH of 6.5–7. Our studies are in line with the general hypothesis that keeping the skin pH within an acidic range is advantageous in terms of keeping the skin microbiome in balance and maintaining healthy skin.

Detection and partial characterization of extracellular inducers of persistence in Staphylococcus epidermidis and Staphylococcus aureus

2021 ◽  
Vol 70 (6) ◽  
Author(s):  
Elyse C. Curry ◽  
Ryan G. Hart ◽  
Danni Y. Habtu ◽  
Neal R. Chamberlain
Keyword(s):  
Molecular Weight ◽  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Type Species ◽  
Proteinase K ◽  
Partial Characterization ◽  
Content Type ◽  
Link Type ◽  
Inducing Factors

Introduction. This study describes the identification and partial characterization of persistence-inducing factors (PIFs) from staphylococci. Hypothesis/Gap Statement. Increases in persisters during mid-log phase growth indicate that quorum-sensing factors might be produced by staphylococci. Aim. To identify and partially characterize PIFs from Staphylococcus epidermidis RP62A and Staphylococcus aureus SH1000. Methodology. Others have demonstrated a significant increase in persister numbers during mid-log phase. Inducers of this mid-log increase have yet to be identified in staphylococci. Optical density at 600 nm (OD600) was used instead of time to determine when persister numbers increased during logarithmic growth. Concentrated culture filtrates (CCFs) from S. epidermidis and S. aureus were obtained at various OD600s and following incubation at 16 h. The CCFs were used to develop a PIF assay. The PIF assay was used to partially characterize PIF from S. epidermidis and S. aureus for sizing of PIF activity, temperature and protease sensitivity and inter-species communications. Results. The optimal OD600s for S. epidermidis and S. aureus PIF assays were 2.0 and 0.5, respectively. The highest PIF activity for both species was from CCF following incubation overnight (16 h). S. epidermidis ’ PIF activity was decreased by storage at 4 oC but not at 20 oC (16 h), 37 oC (1 h) or 100 oC (15 min). S. aureus ’ PIF activity was decreased following storage at 4 oC (2 weeks) and after boiling at 100 oC for 5 min but not after incubation at 37 oC (1 h). PIF activity from both species went through a 3000 molecular weight cutoff ultrafilter. Proteinase K treatment of S. aureus PIF decreased activity but did not decrease the PIF activity of S. epidermidis . PIF from S. epidermidis did not increase persisters when used to treat S. aureus cells and nor did PIF from S. aureus increase persisters when used to treat S. epidermidis cells. Conclusions. Attempts to discover PIFs for staphylococci were unsuccessful due to the time-based means used to identify mid-log. Both staphylococcal species produce extracellular, low-molecular-weight inducers of persistence when assayed using an OD600 -based PIF assay.

scholarly journals Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm FormationIn Vivo

2014 ◽  
Vol 58 (12) ◽  
pp. 7606-7610 ◽  
Author(s):  
Kaat De Cremer ◽  
Nicolas Delattin ◽  
Katrijn De Brucker ◽  
Annelies Peeters ◽  
Soña Kucharíková ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Candida Albicans ◽  
Broad Spectrum ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Candida Krusei ◽  
Content Type ◽  
And Staphylococcus Aureus

ABSTRACTWe here report on thein vitroactivity of toremifene to inhibit biofilm formation of different fungal and bacterial pathogens, includingCandida albicans,Candida glabrata,Candida dubliniensis,Candida krusei,Pseudomonas aeruginosa,Staphylococcus aureus, andStaphylococcus epidermidis. We validated thein vivoefficacy of orally administered toremifene againstC. albicans and S. aureusbiofilm formation in a rat subcutaneous catheter model. Combined, our results demonstrate the potential of toremifene as a broad-spectrum oral antibiofilm compound.

scholarly journals Antibacterial Effects of Phage Lysin LysGH15 on Planktonic Cells and Biofilms of Diverse Staphylococci

2018 ◽  
Vol 84 (15) ◽  
Author(s):  
Yufeng Zhang ◽  
Mengjun Cheng ◽  
Hao Zhang ◽  
Jiaxin Dai ◽  
Zhimin Guo ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Multidrug Resistant ◽  
Planktonic Cells ◽  
Content Type ◽  
Resistant Strains ◽  
Staphylococcus Hominis ◽  
Phage Lysin

ABSTRACT Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we observed the ability of the phage lysin LysGH15 to eliminate staphylococcal planktonic cells and biofilms formed by Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus, and Staphylococcus hominis. All these strains were sensitive to LysGH15, showing reductions in bacterial counts of approximately 4 log units within 30 min after treatment with 20 μg/ml of LysGH15, and the MICs ranged from 8 μg/ml to 32 μg/ml. LysGH15 efficiently prevented biofilm formation by the four staphylococcal species at a dose of 50 μg/ml. At a higher dose (100 μg/ml), LysGH15 also showed notable disrupting activity against 24-h and 72-h biofilms formed by S. aureus and coagulase-negative species. In the in vivo experiments, a single intraperitoneal injection of LysGH15 (20 μg/mouse) administered 1 h after the injection of S. epidermidis at double the minimum lethal dose was sufficient to protect the mice. The S. epidermidis cell counts were 4 log units lower in the blood and 3 log units lower in the organs of mice 24 h after treatment with LysGH15 than in the untreated control mice. LysGH15 reduced cytokine levels in the blood and improved pathological changes in the organs. The broad antistaphylococcal activity exerted by LysGH15 on planktonic cells and biofilms makes LysGH15 a valuable treatment option for biofilm-related or non-biofilm-related staphylococcal infections. IMPORTANCE Most staphylococcal species are major causes of health care- and community-associated infections. In particular, Staphylococcus aureus is a common and dangerous pathogen, and Staphylococcus epidermidis is a ubiquitous skin commensal and opportunistic pathogen. Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we found that all tested S. aureus, S. epidermidis, Staphylococcus haemolyticus, and Staphylococcus hominis strains were sensitive to the phage lysin LysGH15 (MICs ranging from 8 to 32 μg/ml). More importantly, LysGH15 not only prevented biofilm formation by these staphylococci but also disrupted 24-h and 72-h biofilms. Furthermore, the in vivo efficacy of LysGH15 was demonstrated in a mouse model of S. epidermidis bacteremia. Thus, LysGH15 exhibits therapeutic potential for treating biofilm-related or non-biofilm-related infections caused by diverse staphylococci.

scholarly journals Tannic Acid Inhibits Staphylococcus aureus Surface Colonization in an IsaA-Dependent Manner

2012 ◽  
Vol 81 (2) ◽  
pp. 496-504 ◽  
Author(s):  
David E. Payne ◽  
Nicholas R. Martin ◽  
Katherine R. Parzych ◽  
Alex H. Rickard ◽  
Adam Underwood ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Tannic Acid ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Host Immune System ◽  
Dependent Manner ◽  
Content Type ◽  
Surface Colonization ◽  
Biofilm Development ◽  
Insight Into

ABSTRACTStaphylococcus aureusis a human commensal and pathogen that is capable of forming biofilms on a variety of host tissues and implanted medical devices. Biofilm-associated infections resist antimicrobial chemotherapy and attack from the host immune system, making these infections particularly difficult to treat. In order to gain insight into environmental conditions that influenceS. aureusbiofilm development, we screened a library of small molecules for the ability to inhibitS. aureusbiofilm formation. This led to the finding that the polyphenolic compound tannic acid inhibitsS. aureusbiofilm formation in multiple biofilm models without inhibiting bacterial growth. We present evidence that tannic acid inhibitsS. aureusbiofilm formation via a mechanism dependent upon the putative transglycosylase IsaA. Tannic acid did not inhibit biofilm formation of anisaAmutant. Overexpression of wild-type IsaA inhibited biofilm formation, whereas overexpression of a catalytically dead IsaA had no effect. Tannin-containing drinks like tea have been found to reduce methicillin-resistantS. aureusnasal colonization. We found that black tea inhibitedS. aureusbiofilm development and that anisaAmutant resisted this inhibition. Antibiofilm activity was eliminated from tea when milk was added to precipitate the tannic acid. Finally, we developed a rodent model forS. aureusthroat colonization and found that tea consumption reducedS. aureusthroat colonization via anisaA-dependent mechanism. These findings provide insight into a molecular mechanism by which commonly consumed polyphenolic compounds, such as tannins, influenceS. aureussurface colonization.

scholarly journals In VitroAnalyses of Ethanol Activity against Candida albicans Biofilms

2012 ◽  
Vol 56 (8) ◽  
pp. 4487-4489 ◽  
Author(s):  
Hallie S. Rane ◽  
Stella M. Bernardo ◽  
Carla J. Walraven ◽  
Samuel A. Lee
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Optimal Dose ◽  
Limited Data ◽  
Common Cause ◽  
Content Type ◽  
Treatment And Prevention ◽  
Lock Therapy ◽  
Candida Albicans Biofilms

ABSTRACTCandida albicansis a common cause of catheter-related bloodstream infections (CR-BSI). Ethanol (EtOH) lock therapy has been attempted despite limited data on optimal dose and duration. Concentrations of 35% EtOH or higher for a minimum of 4 h demonstrated a >99% reduction in matureC. albicansbiofilm metabolic activity and prevented regrowth. Concentrations of 10% EtOH or higher reducedC. albicansbiofilm formation by >99%. Further investigation of EtOH lock therapy for treatment and prevention ofC. albicansCR-BSI is warranted.

scholarly journals The Toxin-Antitoxin MazEF Drives Staphylococcus aureus Biofilm Formation, Antibiotic Tolerance, and Chronic Infection

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Dongzhu Ma ◽  
Jonathan B. Mandell ◽  
Niles P. Donegan ◽  
Ambrose L. Cheung ◽  
Wanyan Ma ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Chronic Infection ◽  
Critical Role ◽  
Antimicrobial Treatment ◽  
Antibiotic Tolerance ◽  
Chronic Infections ◽  
Content Type ◽  
Increased Risk

ABSTRACT Staphylococcus aureus is the major organism responsible for surgical implant infections. Antimicrobial treatment of these infections often fails, leading to expensive surgical intervention and increased risk of mortality to the patient. The challenge in treating these infections is associated with the high tolerance of S. aureus biofilm to antibiotics. MazEF, a toxin-antitoxin system, is thought to be an important regulator of this phenotype, but its physiological function in S. aureus is controversial. Here, we examined the role of MazEF in developing chronic infections by comparing growth and antibiotic tolerance phenotypes in three S. aureus strains to their corresponding strains with disruption of mazF expression. Strains lacking mazF production showed increased biofilm growth and decreased biofilm antibiotic tolerance. Deletion of icaADBC in the mazF::Tn background suppressed the growth phenotype observed with mazF-disrupted strains, suggesting the phenotype was ica dependent. We confirmed these phenotypes in our murine animal model. Loss of mazF resulted in increased bacterial burden and decreased survival rate of mice compared to its wild-type strain demonstrating that loss of the mazF gene caused an increase in S. aureus virulence. Although lack of mazF gene expression increased S. aureus virulence, it was more susceptible to antibiotics in vivo. Combined, the ability of mazF to inhibit biofilm formation and promote biofilm antibiotic tolerance plays a critical role in transitioning from an acute to chronic infection that is difficult to eradicate with antibiotics alone. IMPORTANCE Surgical infections are one of the most common types of infections encountered in a hospital. Staphylococcus aureus is the most common pathogen associated with this infection. These infections are resilient and difficult to eradicate, as the bacteria form biofilm, a community of bacteria held together by an extracellular matrix. Compared to bacteria that are planktonic, bacteria in a biofilm are more resistant to antibiotics. The mechanism behind how bacteria develop this resistance and establish a chronic infection is unknown. We demonstrate that mazEF, a toxin-antitoxin gene, inhibits biofilm formation and promotes biofilm antibiotic tolerance which allows S. aureus to transition from an acute to chronic infection that cannot be eradicated with antibiotics but is less virulent. This gene not only makes the bacteria more tolerant to antibiotics but makes the bacteria more tolerant to the host.

scholarly journals Inhibition of Biofilm Formation by Esomeprazole in Pseudomonas aeruginosa and Staphylococcus aureus

2012 ◽  
Vol 56 (8) ◽  
pp. 4360-4364 ◽  
Author(s):  
Vandana Singh ◽  
Vaneet Arora ◽  
M. Jahangir Alam ◽  
Kevin W. Garey
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Bacterial Growth ◽  
Biofilm Formation ◽  
Antimicrobial Properties ◽  
Antibiofilm Activity ◽  
Biofilm Growth ◽  
Content Type ◽  
Conventional Antibiotics ◽  
And Staphylococcus Aureus

ABSTRACTStaphylococcus aureusandPseudomonas aeruginosaare common nosocomial pathogens responsible for biofilm-associated infections. Proton pump inhibitors (PPI), such as esomeprazole, may have novel antimicrobial properties. The objective of this study was to assess whether esomeprazole prevents sessile bacterial growth and biofilm formation and whether it may have synergistic killing effects with standard antibiotics. The antibiofilm activity of esomeprazole at 0.25 mM was tested against two strains each ofS. aureusandP. aeruginosa. Bacterial biofilms were prepared using a commercially available 96-peg-plate Calgary biofilm device. Sessile bacterial CFU counts and biomass were assessed during 72 hours of esomeprazole exposure. The killing activities after an additional 24 hours of vancomycin (againstS. aureus) and meropenem (againstP. aeruginosa) treatment with or without preexposure to esomeprazole were also assessed by CFU and biomass analyses.P. aeruginosaandS. aureusstrains exposed to esomeprazole displayed decreased sessile bacterial growth and biomass (P< 0.001, each parameter). After 72 h of exposure, there was a 1-log10decrease in the CFU/ml of esomeprazole-exposedP. aeruginosaandS. aureusstrains compared to controls (P< 0.001). After 72 h of exposure, measured absorbance was 100% greater inP. aeruginosacontrol strains than in esomeprazole-exposed strains (P< 0.001). Increased killing and decreased biomass were observed for esomeprazole-treated bacteria compared to untreated controls exposed to conventional antibiotics (P< 0.001, each parameter). Reduced biofilm growth after 24 h was visibly apparent by light micrographs forP. aeruginosaandS. aureusisolates exposed to esomeprazole compared to untreated controls. In conclusion, esomeprazole demonstrated an antibiofilm effect against biofilm-producingS. aureusandP. aeruginosa.

scholarly journals Involvement of the Iron-Regulated Loci hts and fhuC in Biofilm Formation and Survival of Staphylococcus epidermidis within the Host

2022 ◽  
Author(s):  
Fernando Oliveira ◽  
Tânia Lima ◽  
Alexandra Correia ◽  
Ana Margarida Silva ◽  
Cristina Soares ◽  
...  
Keyword(s):  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Central Line ◽  
Nosocomial Pathogens ◽  
Content Type ◽  
Iron Restriction

Staphylococcus epidermidis is one of the most important nosocomial pathogens and a major cause of central line-associated bloodstream infections. Once in the bloodstream, this bacterium must surpass severe iron restriction in order to survive and establish infection.

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