Disruption of the Orthologue in the Locus Variable Region of Enterococcus faecalis Causes Cell Surface Changes and Suppresses an -Dependent Lysozyme Resistance Phenotype.

The disease-producing capacity of the opportunistic pathogen Enterococcus faecalis is enhanced by the ability of the bacterium to evade killing by antimicrobial agents. Survival of E. faecalis in the presence of the human antimicrobial enzyme lysozyme is mediated in part by the site 2 metalloprotease Eep; however, a complete model of enterococcal lysozyme resistance has not been elucidated.

Diverse Enterococcus faecalis strains show heterogeneity in biofilm properties.

Biofilm formation is important for Enterococcus faecalis to cause healthcare-associated infections. It is unclear how E. faecalis biofilms vary in parameters such as development and composition.

The Cationic Antimicrobial Peptide Activity of Lysozyme Reduces Viable Cells in Biofilms.

Enterococcus faecalis, a leading cause of health care-associated infections, forms biofilms and is resistant to many antimicrobial agents. Planktonic-phase E. faecalis is resistant to high concentrations of the enzyme lysozyme, which catalyzes the hydrolysis of -acetylmuramic acid and -acetylglucosamine linkages in peptidoglycan and is also a cationic antimicrobial peptide (CAMP).

colonizes and forms persistent biofilm microcolonies on undamaged endothelial surfaces in a rabbit endovascular infection model.

Infectious endocarditis (IE) is an uncommon disease with significant morbidity and mortality. The pathogenesis of IE has historically been described as a cascade of host-specific events beginning with endothelial damage and thrombus formation and followed by bacterial colonization of the nascent thrombus. is a Gram-positive commensal bacterial member of the gastrointestinal tract microbiota in most terrestrial animals and a leading cause of opportunistic biofilm-associated infections, including endocarditis.

Enterococcal Endocarditis: Hiding in Plain Sight.

is a major opportunistic bacterial pathogen of increasing clinical relevance. A substantial body of experimental evidence suggests that early biofilm formation plays a critical role in these infections, as well as in colonization and persistence in the GI tract as a commensal member of the microbiome in most terrestrial animals. Animal models of experimental endocarditis generally involve inducing mechanical valve damage by cardiac catheterization prior to infection, and it has long been presumed that endocarditis vegetation formation resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage.

Utilizing glycoside hydrolases to improve the quantitation and visualization of biofilm bacteria.

The complexity of microbial biofilms offers several challenges to the use of traditional means of microbial research. In particular, it can be difficult to calculate accurate numbers of biofilm bacteria, because even after thorough homogenization or sonication, small pieces of the biofilm remain, which contain numerous bacterial cells and result in inaccurately low colony forming units (CFU). In addition, imaging of infected tissue often results in a disparity between the CFU and the number of bacterial cells observed under the microscope.

Manganese acquisition is essential for virulence of Enterococcus faecalis.

Manganese (Mn) is an essential micronutrient that is not readily available to pathogens during infection due to an active host defense mechanism known as nutritional immunity. To overcome this nutrient restriction, bacteria utilize high-affinity transporters that allow them to compete with host metal-binding proteins. Despite the established role of Mn in bacterial pathogenesis, little is known about the relevance of Mn in the pathophysiology of E.

Basal levels of (p)ppGpp differentially affect the pathogenesis of infective endocarditis in Enterococcus faecalis.

The alarmone (p)ppGpp mediates the stringent response and has a recognized role in bacterial virulence. We previously reported a stringent response-like state in Enterococcus faecalis isolated from a rabbit foreign body abscess model and showed that E. faecalis mutants with varying levels of cellular (p)ppGpp [Δrel, ΔrelQ and the (p)ppGpp ΔrelΔrelQ] had differential abilities to persist within abscesses.

PrgU: a suppressor of sex pheromone toxicity in Enterococcus faecalis.

Upon sensing of the peptide pheromone cCF10, Enterococcus faecalis cells carrying pCF10 produce three surface adhesins (PrgA, PrgB or Aggregation Substance, PrgC) and the Prg/Pcf type IV secretion system and, in turn, conjugatively transfer the plasmid at high frequencies to recipient cells. Here, we report that cCF10 induction is highly toxic to cells sustaining a deletion of prgU, a small orf located immediately downstream of prgB on pCF10. Upon pheromone exposure, these cells overproduce the Prg adhesins and display impaired envelope integrity, as evidenced by antibiotic susceptibility, misplaced division septa and cell lysis.

Antagonistic Donor Density Effect Conserved in Multiple Enterococcal Conjugative Plasmids.

Unlabelled: Enterococcus faecalis, a common causative agent of hospital-acquired infections, is resistant to many known antibiotics. Its ability to acquire and transfer resistance genes and virulence determinants through conjugative plasmids poses a serious concern for public health. In some cases, induction of transfer of E.

Evaluation of the Enterococcus faecalis Biofilm-Associated Virulence Factors AhrC and Eep in Rat Foreign Body Osteomyelitis and In Vitro Biofilm-Associated Antimicrobial Resistance.

Enterococcus faecalis can cause healthcare-associated biofilm infections, including those of orthopedic devices. Treatment of enterococcal prosthetic joint infection is difficult, in part, due to biofilm-associated antimicrobial resistance. We previously showed that the E.

Transcriptome analysis of Enterococcus faecalis during mammalian infection shows cells undergo adaptation and exist in a stringent response state.

As both a commensal and a major cause of healthcare-associated infections in humans, Enterococcus faecalis is a remarkably adaptable organism. We investigated how E. faecalis adapts in a mammalian host as a pathogen by characterizing changes in the transcriptome during infection in a rabbit model of subdermal abscess formation using transcriptional microarrays.

Enterococcus faecalis pCF10-encoded surface proteins PrgA, PrgB (aggregation substance) and PrgC contribute to plasmid transfer, biofilm formation and virulence.

Enterococcus faecalis pCF10 transfers at high frequencies upon pheromone induction of the prgQ transfer operon. This operon codes for three cell wall-anchored proteins - PrgA, PrgB (aggregation substance) and PrgC - and a type IV secretion system through which the plasmid is delivered to recipient cells. Here, we defined the contributions of the Prg surface proteins to plasmid transfer, biofilm formation and virulence using the Caenorhabditis elegans infection model.

Enterococcus faecalis 6-phosphogluconolactonase is required for both commensal and pathogenic interactions with Manduca sexta.

Enterococcus faecalis is a commensal and pathogen of humans and insects. In Manduca sexta, E. faecalis is an infrequent member of the commensal gut community, but its translocation to the hemocoel results in a commensal-to-pathogen switch.

AhrC and Eep are biofilm infection-associated virulence factors in Enterococcus faecalis.

Enterococcus faecalis is part of the human intestinal microbiome and is a prominent cause of health care-associated infections. The pathogenesis of many E. faecalis infections, including endocarditis and catheter-associated urinary tract infection (CAUTI), is related to the ability of clinical isolates to form biofilms.

Comparison of Staphylococcus aureus strains for ability to cause infective endocarditis and lethal sepsis in rabbits.

Staphylococcus aureus is a major cause of infective endocarditis (IE) and sepsis. Both methicillin-resistant (MRSA) and methicillin-sensitive (MSSA) strains cause these illnesses. Common S.

Ecto-5'-nucleotidase: a candidate virulence factor in Streptococcus sanguinis experimental endocarditis.

Streptococcus sanguinis is the most common cause of infective endocarditis (IE). Since the molecular basis of virulence of this oral commensal bacterium remains unclear, we searched the genome of S. sanguinis for previously unidentified virulence factors.

Use of recombinase-based in vivo expression technology to characterize Enterococcus faecalis gene expression during infection identifies in vivo-expressed antisense RNAs and implicates the protease Eep in pathogenesis.

Enterococcus faecalis is a member of the mammalian gastrointestinal microflora that has become a leading cause of nosocomial infections over the past several decades. E. faecalis must be able to adapt its physiology based on its surroundings in order to thrive in a mammalian host as both a commensal and a pathogen.

From clinical microbiology to infection pathogenesis: how daring to be different works for Staphylococcus lugdunensis.

Staphylococcus lugdunensis has gained recognition as an atypically virulent pathogen with a unique microbiological and clinical profile. S. lugdunensis is coagulase negative due to the lack of production of secreted coagulase, but a membrane-bound form of the enzyme present in some isolates can result in misidentification of the organism as Staphylococcus aureus in the clinical microbiology laboratory.

Intravenously administered pharmaceuticals impact biofilm formation and detachment of Staphylococcus lugdunensis and other staphylococci.

Coagulase-negative staphylococci and Staphylococcus aureus are major causes of catheter-related infections because of their ability to form biofilms on indwelling polymeric devices. Staphylococcus lugdunensis is a particularly virulent coagulase-negative species responsible for several types of biofilm-related infections, but factors that influence biofilm formation by this species remain undetermined. Heparin and catecholamine inotropes are common intravenously administered drugs reported to stimulate biofilm formation of some staphylococci.

Poly-N-acetylglucosamine is not a major component of the extracellular matrix in biofilms formed by icaADBC-positive Staphylococcus lugdunensis isolates.

Staphylococcus lugdunensis is a pathogen of heightened virulence that causes infections resembling those caused by Staphylococcus aureus rather than those caused by its coagulase-negative staphylococcal counterparts. Many types of S. lugdunensis infection, including native valve endocarditis, prosthetic joint infection, and intravascular catheter-related infection, are associated with biofilm etiology.

Activity of sodium metabisulfite against planktonic and biofilm Staphylococcus species.

Biofilm-forming staphylococci cause a majority of intravascular catheter-related infections. We evaluated the effect of sodium metabisulfite, a preservative commonly added to intravenously administered pharmaceuticals as an antioxidant and previously used as a catheter lock solution, on planktonic and biofilm staphylococci at clinically encountered concentrations. Sodium metabisulfite exhibited bactericidal activity against planktonic Staphylococcus aureus, Staphylococcus lugdunensis, and Staphylococcus epidermidis at concentrations of 512, 512, and 1024 microg/mL, respectively.

Searching historical herbal texts for potential new drugs.

Historical herbal texts provide a window for resurrecting lost knowledge, and “mining” of these texts can lead to the identification of new drugs

In vitro effects of antimicrobial agents on planktonic and biofilm forms of Staphylococcus lugdunensis clinical isolates.

Staphylococcus lugdunensis is an atypically virulent coagulase-negative staphylococcal species associated with acute and destructive infections that often resemble Staphylococcus aureus infections. Several types of infection caused by S. lugdunensis (e.