Anti-Biofilm Perspectives of Propolis against Staphylococcus epidermidis Infections.

Staphylococcus epidermis has emerged as the main causative agent of medical device-related infections. Their major pathogenicity factor lies in its ability to adhere to surfaces and proliferate into biofilms, which increase their resistance to antibiotics. The main objective of this study was to evaluate the use and the mechanism of action of an ethanolic extract of Spanish propolis (EESP) as a potential alternative for preventing biofilm-related infections caused by S. epidermidis. The chemical composition of propolis is reported and its antibacterial activity against several strains of S. epidermidis with different biofilm-forming capacities evaluated. The influence of sub-inhibitory concentrations (sub-MICs) of EESP on their growth, physicochemical surface properties, adherence, and biofilm formation were studied. EESP interferes with planktonic cells, homogenizing their physicochemical surface properties and introducing a significant delay in their growth. The adherence and biofilms at the EESP concentrations investigated were decreased up to 90.5% among the strains. Microscopic analysis indicated that the planktonic cells that survived the treatment were the ones that adhere and proliferate on the surfaces. The results obtained suggest that the EESP has a high potential to be used as an inhibitor of both the adhesion and biofilm formation of S. epidermidis.

Control of Staphylococcus epidermidis biofilm by surfactins of an endophytic bacterium Bacillus sp. 15 F.

The present paper deals with the preparation and annotation of a surfactin(s) derived from a culture of the endophytic bacterium Bacillus 15 F. The LC-MS analysis of the acetonitrile fraction confirmed the presence of surfactins Leu/Ile7 C15, Leu/Ile7 C14 and Leu/Ile7 C13 with [M+H]+ at m/z 1036.6895, 1022.6741 and 1008.6581, respectively. Various concentrations of the surfactin(s) (hereafter referred to as surfactin-15 F) were used to reduce the adhesion of Staphylococcus epidermidis S61, which served as a model for studying antibiofilm activity on polystyrene surfaces. Incubation of Staphylococcus epidermidis S61 with 62.5 µg/ml of surfactin-15 F resulted in almost complete inhibition of biofilm formation (90.3 ± 3.33 %), and a significant reduction of cell viability (resazurin-based fluorescence was more than 200 times lower). The antiadhesive effect of surfactin-15 F was confirmed by scanning electron microscopy. Surfactin-15 F demonstrated an eradication effect against preformed biofilm, causing severe disruption of Staphylococcus epidermidis S61 biofilm structure and reducing viability. The results suggest that surfactins produced by endophytic bacteria could be an alternative to synthetic products. Surfactin-15 F, used in wound dressings, demonstrated an efficient treatment of the preformed Staphylococcus epidermidis S61 biofilm, and thus having a great potential in medical applications.

Unveiling the mechanism of essential oil action against skin pathogens: from ancient wisdom to modern science.

Essential oils are among the most well-known phyto-compounds, and since ancient times, they have been utilized in medicine. Over 100 essential oils have been identified and utilized as therapies for various skin infections and related ailments. While numerous commercial medicines are available in different dosage forms to treat skin diseases, the persisting issues include their side effects, toxicity, and low efficacy. As a result, researchers are seeking novel classes of compounds as substitutes for synthetic drugs, aiming for minimal side effects, no toxicity, and high efficacy. Essential oils have shown promising antimicrobial activity against skin-associated pathogens. This review presents essential knowledge and scientific information regarding essential oil's antimicrobial capabilities against microorganisms that cause skin infections. Essential oils mechanisms against different pathogens have also been explored. Many essential oils exhibit promising activity against various microbes, which has been qualitatively assessed using the agar disc diffusion experiment, followed by determining the minimum inhibitory concentration for quantitative evaluation. It has been observed that Staphylococcus aureus and Candida albicans have been extensively researched in the context of skin-related infections and their antimicrobial activity, including established modes of action. In contrast, other skin pathogens such as Staphylococcus epidermidis, Streptococcus pyogens, Propionibacterium acnes, and Malassezia furfur have received less attention or neglected. This review report provides an updated understanding of the mechanisms of action of various essential oils with antimicrobial properties. This review explores the anti-infectious activity and mode of action of essential against distinct skin pathogens. Such knowledge can be valuable in treating skin infections and related ailments.

Eosinophilic pleural effusion due to Staphylococcus epidermidis infection: A case report.

Eosinophilic pleural effusion is rare, and the cause is often obscure. A 73-year-old man with no relevant medical history presented with exertional dyspnea. Chest imaging revealed left-sided pleural effusion, and pleural fluid examination revealed eosinophilic pleural effusion. Blood tests revealed an increased peripheral blood eosinophil count and elevated Immunoglobulin E levels. Staphylococcus epidermidis was detected in pleural specimens collected via thoracoscopy. Antimicrobial therapy targeting Staphylococcus epidermidis resolved the eosinophilic pleural effusion and elevated peripheral blood eosinophil count. Staphylococcus epidermidis infection may be considered as a cause of eosinophilic pleural effusion when the diagnosis is difficult.

Catalase-positive Staphylococcus epidermidis based cryo-millineedle platform facilitates the photo-immunotherapy against colorectal cancer via hypoxia improvement.

The synergistic anti-tumor impact of phototherapy and a cascading immune response are profoundly limited by hypoxia and a weakened immune response. Intravenous and intratumoral injection of therapeutic drugs also cause pain, rapid drug clearance and low utilization rates. Here, a novel cryo-millineedle platform for intratumoral delivery of a phototherapy system, S.epi@IR820, is developed in this work, combining the properties of Staphylococcus epidermidis (S. epidermidis) and IR820 for photo-immunotherapy of colorectal cancer. In this cryo-millineedle platform, S. epidermidis enhances the near-infrared absorption and light stability of IR820 and catalyzes the decomposition of H2O2 into O2 via an endogenous catalase to relieve tumor hypoxia, improve phototherapy and enhance immunogenic cell death (ICD). More interestingly, the native immunogenicity of S. epidermidis and ICD elicited by phototherapy achieved a potent anti-tumor immune response. To the best of our knowledge, this is the first study to utilize native S. epidermidis to relieve hypoxia and facilitate phototherapy. Both in vitro and in vivo experiments showed that the millineedle based phototherapy system can efficiently catalyse the decomposition of H2O2 into O2, facilitate phototherapeutic killing of CT26 tumor cells by S.epi@IR820 and enhance ICD, thus successfully activated the immune response and achieved the photo-immunotherapy against colorectal cancer. In conclusion, this study provides a novel strategy for enhanced anti-tumor efficiency of photo-immunotherapy, and develops an effective method for orthotopic administration of tumors.

C1q is elevated during chronic Staphylococcus epidermidis central nervous system catheter infection.

Introduction: Significant neurologic morbidity is caused by pediatric cerebrospinal fluid (CSF) shunt infections. The underlying mechanisms leading to impaired school performance and increased risk of seizures are unknown, however, a better understanding of these mechanisms may allow us to temper their consequences. Recent evidence has demonstrated important roles for complement proteins in neurodevelopment and neuroinflammation. Methods: We examined complement activation throughout Staphylococcus epidermidis (S. epidermidis) central nervous system (CNS) catheter infection. In addition, based on accumulating evidence that C3 plays a role in synaptic pruning in other neuroinflammatory states we determined if C3 and downstream C5 led to alterations in synaptic protein levels. Using our murine model of S. epidermidis catheter infection we quantified levels of the complement components C1q, Factor B, MASP2, C3, and C5 over the course of infection along with bacterial burdens. Results: We found that MASP2 predominated early in catheter infection, but that Factor B was elevated at intermediate time points. Unexpectedly C1q was elevated at late timepoints when bacterial burdens were low or undetectable. Based on these findings and the wealth of information regarding the emerging roles of C1q in the CNS, this suggests functions beyond pathogen elimination during S. epidermidis CNS catheter infection. To identify if C3 impacted synaptic protein levels we performed synaptosome isolation and quantified levels of VGLUT1 and PSD95 as well as pre-, post- and total synaptic puncta in cortical layer V of C3 knockout (KO) and wild type mice. We also used C5 KO and wild type mice to determine if there was any difference in pre-, post- and total synaptic puncta. Discussion: Neither C3 nor C5 impacted synaptic protein abundance. These findings suggest that chronic elevations in C1q in the brain that persist once CNS catheter infection has resolved may be modulating disease sequalae.

The extracellular serine protease from Staphylococcus epidermidis elicits a type 2-biased immune response in atopic dermatitis patients.

Background: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease with skin barrier defects and a misdirected type 2 immune response against harmless antigens. The skin microbiome in AD is characterized by a reduction in microbial diversity with a dominance of staphylococci, including Staphylococcus epidermidis (S. epidermidis). Objective: To assess whether S. epidermidis antigens play a role in AD, we screened for candidate allergens and studied the T cell and humoral immune response against the extracellular serine protease (Esp). Methods: To identify candidate allergens, we analyzed the binding of human serum IgG4, as a surrogate of IgE, to S. epidermidis extracellular proteins using 2-dimensional immunoblotting and mass spectrometry. We then measured serum IgE and IgG1 binding to recombinant Esp by ELISA in healthy and AD individuals. We also stimulated T cells from AD patients and control subjects with Esp and measured the secreted cytokines. Finally, we analyzed the proteolytic activity of Esp against IL-33 and determined the cleavage sites by mass spectrometry. Results: We identified Esp as the dominant candidate allergen of S. epidermidis. Esp-specific IgE was present in human serum; AD patients had higher concentrations than controls. T cells reacting to Esp were detectable in both AD patients and healthy controls. The T cell response in healthy adults was characterized by IL-17, IL-22, IFN-γ, and IL-10, whereas the AD patients' T cells lacked IL-17 production and released only low amounts of IL-22, IFN-γ, and IL-10. In contrast, Th2 cytokine release was higher in T cells from AD patients than from healthy controls. Mature Esp cleaved and activated the alarmin IL-33. Conclusion: The extracellular serine protease Esp of S. epidermidis can activate IL-33. As an antigen, Esp elicits a type 2-biased antibody and T cell response in AD patients. This suggests that S. epidermidis can aggravate AD through the allergenic properties of Esp.

Diclofenac sodium effectively inhibits the biofilm formation of Staphylococcus epidermidis.

Staphylococcus epidermidis is an opportunistic pathogen commonly implicated in medical device-related infections. Its propensity to form biofilms not only leads to chronic infections but also exacerbates the issue of antibiotic resistance, necessitating high-dose antimicrobial treatments. In this study, we explored the use of diclofenac sodium, a non-steroidal anti-inflammatory drug, as an anti-biofilm agent against S. epidermidis. In this study, crystal violet staining and confocal laser scanning microscope analysis showed that diclofenac sodium, at subinhibitory concentration (0.4 mM), significantly inhibited biofilm formation in both methicillin-susceptible and methicillin-resistant S. epidermidis isolates. MTT assays demonstrated that 0.4 mM diclofenac sodium reduced the metabolic activity of biofilms by 25.21-49.01% compared to untreated controls. Additionally, the treatment of diclofenac sodium resulted in a significant decrease (56.01-65.67%) in initial bacterial adhesion, a crucial early phase of biofilm development. Notably, diclofenac sodium decreased the production of polysaccharide intercellular adhesin (PIA), a key component of the S. epidermidis biofilm matrix, in a dose-dependent manner. Real-time quantitative PCR analysis revealed that diclofenac sodium treatment downregulated biofilm-associated genes icaA, fnbA, and sigB and upregulated negative regulatory genes icaR and luxS, providing potential mechanistic insights. These findings indicate that diclofenac sodium inhibits S. epidermidis biofilm formation by affecting initial bacterial adhesion and the PIA synthesis. This underscores the potential of diclofenac sodium as a supplementary antimicrobial agent in combating staphylococcal biofilm-associated infections.

Impact of Perioperative Dexamethasone Administration on Infection and Implant Osseointegration in a Preclinical Model of Orthopedic Device-Related Infection.

Glucocorticoids may be given prior to major orthopedic surgery to decrease postoperative nausea, vomiting, and pain. Additionally, many orthopedic patients may be on chronic glucocorticoid therapy. The aim of our study was to investigate whether glucocorticoid administration influences Orthopedic-Device-Related Infection (ODRI) in a rat model. Screws colonized with Staphylococcus epidermidis were implanted in the tibia of skeletally mature female Wistar rats. The treated groups received either a single shot of dexamethasone in a short-term risk study, or a daily dose of dexamethasone in a longer-term interference study. In both phases, bone changes in the vicinity of the implant were monitored with microCT. There were no statistically significant differences in bacteriological outcome with or without dexamethasone. In the interference study, new bone formation was statistically higher in the dexamethasone-treated group (p = 0.0005) as revealed by CT and histopathological analysis, although with relatively low direct osseointegration of the implant. In conclusion, dexamethasone does not increase the risk of developing periprosthetic osteolysis or infection in a pre-clinical model of ODRI. Long-term administration of dexamethasone seemed to offer a benefit in terms of new bone formation around the implant, but with low osseointegration.

The pathogenicity and virulence of the opportunistic pathogen Staphylococcus epidermidis.

The pervasive presence of Staphylococcus epidermidis and other coagulase-negative staphylococci on the skin and mucous membranes has long underpinned a casual disregard for the infection risk that these organisms pose to vulnerable patients in healthcare settings. Prior to the recognition of biofilm as an important virulence determinant in S. epidermidis, isolation of this microorganism in diagnostic specimens was often overlooked as clinically insignificant with potential delays in diagnosis and onset of appropriate treatment, contributing to the establishment of chronic infection and increased morbidity or mortality. While impressive progress has been made in our understanding of biofilm mechanisms in this important opportunistic pathogen, research into other virulence determinants has lagged S. aureus. In this review, the broader virulence potential of S. epidermidis including biofilm, toxins, proteases, immune evasion strategies and antibiotic resistance mechanisms is surveyed, together with current and future approaches for improved therapeutic interventions.

Completed genome and emergence scenario of the multidrug-resistant nosocomial pathogen Staphylococcus epidermidis ST215.

BACKGROUND: A multidrug-resistant lineage of Staphylococcus epidermidis named ST215 is a common cause of prosthetic joint infections and other deep surgical site infections in Northern Europe, but is not present elsewhere. The increasing resistance among S. epidermidis strains is a global concern. We used whole-genome sequencing to characterize ST215 from healthcare settings. RESULTS: We completed the genome of a ST215 isolate from a Swedish hospital using short and long reads, resulting in a circular 2,676,787 bp chromosome and a 2,326 bp plasmid. The new ST215 genome was placed in phylogenetic context using 1,361 finished public S. epidermidis reference genomes. We generated 10 additional short-read ST215 genomes and 11 short-read genomes of ST2, which is another common multidrug-resistant lineage at the same hospital. We studied recombination's role in the evolution of ST2 and ST215, and found multiple recombination events averaging 30-50 kb. By comparing the results of antimicrobial susceptibility testing for 31 antimicrobial drugs with the genome content encoding antimicrobial resistance in the ST215 and ST2 isolates, we found highly similar resistance traits between the isolates, with 22 resistance genes being shared between all the ST215 and ST2 genomes. The ST215 genome contained 29 genes that were historically identified as virulence genes of S. epidermidis ST2. We established that in the nucleotide sequence stretches identified as recombination events, virulence genes were overrepresented in ST215, while antibiotic resistance genes were overrepresented in ST2. CONCLUSIONS: This study features the extensive antibiotic resistance and virulence gene content in ST215 genomes. ST215 and ST2 lineages have similarly evolved, acquiring resistance and virulence through genomic recombination. The results highlight the threat of new multidrug-resistant S. epidermidis lineages emerging in healthcare settings.

Increased Involvement of Staphylococcus epidermidis in the Rise of Polymicrobial Periprosthetic Joint Infections.

BACKGROUND: In this study, we aimed to analyze the temporal distribution of polymicrobial periprosthetic joint infections (PJIs), while also evaluating the patient risk factors associated with these infections following total joint arthroplasty at our institution across 2 distinct periods. METHOD: This retrospective cross-sectional study evaluated 259 patients who had knee or hip PJI from 2001 to 2006 and 2018 to 2022. A PJI was diagnosed using the 2018 International Consensus Meeting criteria. We utilized the Polymicrobial Pathogens' Co-occurrence Network Analysis, a novel approach that leverages network theory to map and quantify the complex interplay of organisms in PJIs. RESULTS: Of the 259 patients who had polymicrobial PJI, 58.7% were men, with mean age 67 years (range, 24 to 90). Of the 579 identified pathogens, Staphylococcus epidermidis was the most common (22.1%), followed by Staphylococcus aureus (9.0%) and Cutibacterium acnes (7.8%). The co-occurrence analysis indicated that Staphylococcus epidermidis frequently coexisted with Cutibacterium acnes (26 cultures) and Staphylococcus capitis (22 cultures). A notable increase in body mass index from 27.7 ± 4.4 in 2001 to 2006 to 29.7 ± 6.2 in 2018 to 2022 was observed (P = .001). Moreover, infections from Staphylococcus epidermidis, Cutibacterium acnes, and Staphylococcus capitis saw a significant uptick (P < .001). CONCLUSIONS: The study shows that from 2001 to 2022, there was a significant change in the pathogens responsible for polymicrobial PJIs, particularly an increase in Staphylococcus epidermidis, Cutibacterium acnes, and Staphylococcus capitis. Alongside these microbial changes, there was a rise in body mass index and shifts in comorbid conditions, such as more renal disease and fewer cases of congestive heart failure. These changes highlight the dynamic interplay between host and microbial factors in the pathogenesis of polymicrobial PJIs, necessitating adaptive strategies in both surgical and postoperative care to mitigate the rising tide of these complex infections.

Comparative virulome analysis of four Staphylococcus epidermidis strains from human skin and platelet concentrates using whole genome sequencing.

Staphylococcus epidermidis is one of the predominant bacterial contaminants in platelet concentrates (PCs), a blood component used to treat bleeding disorders. PCs are a unique niche that triggers biofilm formation, the main pathomechanism of S. epidermidis infections. We performed whole genome sequencing of four S. epidermidis strains isolated from skin of healthy human volunteers (AZ22 and AZ39) and contaminated PCs (ST10002 and ST11003) to unravel phylogenetic relationships and decipher virulence mechanisms compared to 24 complete S. epidermidis genomes in GenBank. AZ39 and ST11003 formed a separate unique lineage with strains 14.1 .R1 and SE95, while AZ22 formed a cluster with 1457 and ST10002 closely grouped with FDAAGOS_161. The four isolates were assigned to sequence types ST1175, ST1174, ST73 and ST16, respectively. All four genomes exhibited biofilm-associated genes ebh, ebp, sdrG, sdrH and atl. Additionally, AZ22 had sdrF and aap, whereas ST10002 had aap and icaABCDR. Notably, AZ39 possesses truncated ebh and sdrG and harbours a toxin-encoding gene. All isolates carry multiple antibiotic resistance genes conferring resistance to fosfomycin (fosB), ß-lactams (blaZ) and fluoroquinolones (norA). This study reveales a unique lineage for S. epidermidis and provides insight into the genetic basis of virulence and antibiotic resistance in transfusion-associated S. epidermidis strains.

Combined metagenomic- and culture-based approaches to investigate bacterial strain-level associations with medication-controlled mild-moderate atopic dermatitis.

Background: The skin microbiome is disrupted in atopic dermatitis (AD). Existing research focuses on moderate to severe, unmedicated disease. Objective: We sought to investigate metagenomic- and culture-based bacterial strain-level differences in mild, medicated AD and the effects these have on human keratinocytes (HKs). Methods: Skin swabs from anterior forearms were collected from 20 pediatric participants (11 participants with AD sampled at lesional and nonlesional sites and 9 age- and sex-matched controls). Participants had primarily mild to moderate AD and maintained medication use. Samples were processed for microbial metagenomic sequencing and bacterial isolation. Isolates identified as Staphylococcus aureus were tested for enterotoxin production. HK cultures were treated with cell-free conditioned media from representative Staphylococcus species to measure barrier effects. Results: Metagenomic sequencing identified significant differences in microbiome composition between AD and control groups. Differences were seen at the species and strain levels for Staphylococci, with S aureus found only in participants with AD and differences in Staphylococcus epidermidis strains between control and AD swabs. These strains showed differences in toxin gene presence, which was confirmed in vitro for S aureus enterotoxins. The strain from the participant with the most severe AD produced enterotoxin B levels more than 100-fold higher than the other strains (P < .001). Strains also displayed differential effects on HK metabolism and barrier function. Conclusions: Strain-level differences in toxin genes from Staphylococcus strains may explain varying effects on HK, with S aureus and non-aureus strains negatively affecting viability and barrier function. These differences are likely important in AD pathogenesis.

The Emergence of Linezolid-Resistant Staphylococcus Epidermidis in the COVID-19 Hospitalized Intubated Patients in North Khorasan, Iran.

The present study aimed to investigate secondary bacterial infections among patients infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Coagulase-negative Staphylococci can infect immunocompromised patients. Linezolid resistance among Staphylococcus epidermidis is one of the most critical issues. In 2019, 185 SARS-CoV-2-positive patients who were admitted to North Khorasan Province Hospital (Bojnurd, Iran), were investigated. Patients having positive SARS-CoV-2 reverse transcriptase real-time polymerase chain reaction (RT-PCR) test results, who had a history of intubation, mechanical ventilation, and were hospitalized for more than 48 hours were included. After microbiological evaluation of pulmonary samples, taken from intubated patients with clinical manifestation of pneumonia, co-infections were found in 11/185 patients (5.94%) with S. epidermidis, Staphylococcus aureus, and Acinetobacter baumani, respectively. Remarkably, seven out of nine S. epidermidis isolates were linezolid resistant. Selected isolates were characterized using antimicrobial resistance patterns and molecular methods, such as Staphylococcal cassette chromosome mec (SCCmec) typing, and gene detection for ica, methicillin resistance (mecA), vancomycin resistance (vanA), and chloramphenicol-florfenicol resistance (cfr) genes. All of the isolates were resistant to methicillin, and seven isolates were resistant to linezolid. Nine out of 11 isolated belonged to the SCCmec I, while two belonged to the SCCmec IV. It should be noted that all patients had the underlying disease, and six patients had already passed away. The increasing linezolid resistance in bacterial strains becomes a real threat to patients, and monitoring such infections, in conjunction with surveillance and infection prevention programs, is very critical for reducing the number of linezolid-resistant Staphylococcal strains. A preprint of this study was published at https://europepmc.org/article/ppr/ppr417742.

Antibiofilm activity of carotenoid crocetin against Staphylococcal strains.

Staphylococcus aureus and Staphylococcus epidermidis stand as notorious threats to human beings owing to the myriad of infections they cause. The bacteria readily form biofilms that help in withstanding the effects of antibiotics and the immune system. Intending to combat the biofilm formation and reduce the virulence of the pathogens, we investigated the effects of carotenoids, crocetin, and crocin, on four Staphylococcal strains. Crocetin was found to be the most effective as it diminished the biofilm formation of S. aureus ATCC 6538 significantly at 50 µg/mL without exhibiting bactericidal effect (MIC >800 µg/mL) and also inhibited the formation of biofilm by MSSA 25923 and S. epidermidis at a concentration as low as 2 µg/mL, and that by methicillin-resistant S. aureus MW2 at 100 µg/mL. It displayed minimal to no antibiofilm efficacy on the Gram-negative strains Escherichia coli O157:H7 and Pseudomonas aeruginosa as well as a fungal strain of Candida albicans. It could also curb the formation of fibrils, which partly contributes to the biofilm formation in S. epidermidis. Additionally, the ADME analysis of crocetin proclaims how relatively non-toxic the chemical is. Also, crocetin displayed synergistic antibiofilm characteristics in combination with tobramycin. The presence of a polyene chain with carboxylic acid groups at its ends is hypothesized to contribute to the strong antibiofilm characteristics of crocetin. These findings suggest that using apocarotenoids, particularly crocetin might help curb the biofilm formation by S. aureus and S. epidermidis.

Predisposing Factors and Clinical-Microbiological Profile of Neonatal Corneal Ulcer: A Systematic Review and Analysis.

OBJECTIVE: To provide a comprehensive overview of predisposing factors and clinical-microbiological profile of neonatal corneal ulcer. METHODS: The literature search was undertaken in PubMed, SCOPUS, Embase, Web of Science, and Google Scholar databases on published papers from inception to May 31, 2023. The included articles were independently assessed for methodological quality using a Joanna Briggs Institute checklist. Weighted analysis was utilized, assigning a weight of one to each case report and a weight equivalent to the sample size for the case series/original studies. RESULT: We included 34 relevant case reports/series and one original study. Seventy-four neonates were enrolled with a boy-to-girl ratio of 1.3:1 and a median age of 17 days (1-27 days). Prematurity and neonatal intensive care unit (NICU) care (21.6%), congenital horizontal tarsal kink (13.5%), neonatal herpes infection (13.5%), congenital entropion (5.4%), and jaundice (5.4%) were the most common potential risk factors and coexisting conditions. Microbiology evaluation showed positive results in 53.8% (21/39 cases). Viral and bacterial infections were the most common cause, followed by fungal infections. Herpes virus (18.9%), Pseudomonas aeruginosa (18.9%%) and Staphylococcus epidermidis (6.7%) were the most prevalent causative agents. Negative microbiology was significantly more common in neonates with structural abnormalities (14.9%) compared to others (6.8%) (p = 0.01). CONCLUSION: Based on the findings of reported studies, this systematic review has increased awareness of the risk factors and etiologies that lead to developing corneal ulcers in neonates.

Comprehensive genomic landscape of antibiotic resistance in Staphylococcus epidermidis.

Staphylococcus epidermidis, a common commensal bacterium found on human skin, can cause infections in clinical settings, and the presence of antibiotic resistance genes (ARGs) impedes the treatment of S. epidermidis infections. However, studies characterizing the ARGs in S. epidermidis with regard to genomic and ecological diversities are limited. Thus, we performed a comprehensive and comparative analysis of 405 high-quality S. epidermidis genomes, including those of 35 environmental isolates from the Han River, to investigate the genomic diversity of antibiotic resistance in this pathogen. Comparative genomic analysis revealed the prevalence of ARGs in S. epidermidis genomes associated with multi-locus sequence types. The genes encoding dihydrofolate reductase (dfrC) and multidrug efflux pump (norA) were genome-wide core ARGs. ß-Lactam class ARGs were also highly prevalent in the S. epidermidis genomes, which was consistent with the resistance phenotype observed in river isolates. Furthermore, we identified chloramphenicol acetyltransferase genes (cat) in the plasmid-like sequences of the six river isolates, which have not been reported previously in S. epidermidis genomes. These genes were identical to those harbored by the Enterococcus faecium plasmids and associated with the insertion sequence 6 family transposases, homologous to those found in Staphylococcus aureus plasmids, suggesting the possibility of horizontal gene transfer between these Gram-positive pathogens. Comparison of the ARG and virulence factor profiles between S. epidermidis and S. aureus genomes revealed that these two species were clearly distinguished, suggesting genomic demarcation despite ecological overlap. Our findings provide a comprehensive understanding of the genomic diversity of antibiotic resistance in S. epidermidis. IMPORTANCE: A comprehensive understanding of the antibiotic resistance gene (ARG) profiles of the skin commensal bacterium and opportunistic pathogen Staphylococcus epidermidis needs to be documented from a genomic point of view. Our study encompasses a comparative analysis of entire S. epidermidis genomes from various habitats, including those of 35 environmental isolates from the Han River sequenced in this study. Our results shed light on the distribution and diversity of ARGs within different S. epidermidis multi-locus sequence types, providing valuable insights into the ecological and genetic factors associated with antibiotic resistance. A comparison between S. epidermidis and Staphylococcus aureus revealed marked differences in ARG and virulence factor profiles, despite their overlapping ecological niches.

Dual-function antimicrobial-antibiofilm peptide hybrid to tackle biofilm-forming Staphylococcus epidermidis.

BACKGROUND: Due to their resistance and difficulty in treatment, biofilm-associated infections are problematic among hospitalized patients globally and account for 60% of all bacterial infections in humans. Antibiofilm peptides have recently emerged as an alternative treatment since they can be effectively designed and exert a different mode of biofilm inhibition and eradication. METHODS: A novel antibiofilm peptide, BiF, was designed from the conserved sequence of 18 α-helical antibiofilm peptides by template-assisted technique and its activity was improved by hybridization with a lipid binding motif (KILRR). Novel antibiofilm peptide derivatives were modified by substituting hydrophobic amino acids at positions 5 or 7, and both, with positively charged lysines (L5K, L7K). These peptide derivatives were tested for antibiofilm and antimicrobial activities against biofilm-forming Staphylococcus epidermidis and multiple other microbes using crystal violet and broth microdilution assays, respectively. To assess their impact on mammalian cells, the toxicity of peptides was determined through hemolysis and cytotoxicity assays. The stability of candidate peptide, BiF2_5K7K, was assessed in human serum and its secondary structure in bacterial membrane-like environments was analyzed using circular dichroism. The action of BiF2_5K7K on planktonic S. epidermidis and its effect on biofilm cell viability were assessed via viable counting assays. Its biofilm inhibition mechanism was investigated through confocal laser scanning microscopy and transcription analysis. Additionally, its ability to eradicate mature biofilms was examined using colony counting. Finally, a preliminary evaluation involved coating a catheter with BiF2_5K7K to assess its preventive efficacy against S. epidermidis biofilm formation on the catheter and its surrounding area. RESULTS: BiF2_5K7K, the modified antibiofilm peptide, exhibited dose-dependent antibiofilm activity against S. epidermidis. It inhibited biofilm formation at subinhibitory concentrations by altering S. epidermidis extracellular polysaccharide production and quorum-sensing gene expression. Additionally, it exhibited broad-spectrum antimicrobial activity and no significant hemolysis or toxicity against mammalian cell lines was observed. Its activity is retained when exposed to human serum. In bacterial membrane-like environments, this peptide formed an α-helix amphipathic structure. Within 4 h, a reduction in the number of S. epidermidis colonies was observed, demonstrating the fast action of this peptide. As a preliminary test, a BiF2_5K7K-coated catheter was able to prevent the development of S. epidermidis biofilm both on the catheter surface and in its surrounding area. CONCLUSIONS: Due to the safety and effectiveness of BiF2_5K7K, we suggest that this peptide be further developed to combat biofilm infections, particularly those of biofilm-forming S. epidermidis.