Enterococcus faecalis readily colonizes the entire gastrointestinal tract and forms biofilms in a germ-free mouse model.

The mammalian gastrointestinal (GI) tract is a complex organ system with a twist-a significant portion of its composition is a community of microbial symbionts. The microbiota plays an increasingly appreciated role in many clinically-relevant conditions. It is important to understand the details of biofilm development in the GI tract since bacteria in this state not only use biofilms to improve colonization, biofilm bacteria often exhibit high levels of resistance to common, clinically relevant antibacterial drugs.

The Natural Surfactant Glycerol Monolaurate Significantly Reduces Development of Staphylococcus aureus and Enterococcus faecalis Biofilms.

Background: Bacterial biofilms are involved in a large proportion of clinical infections, including device-related infections. Unfortunately, biofilm-associated bacteria are typically less susceptible to antibiotics, and infected devices must often be removed. On the basis of a recent observation that lipid-rich biofilm matrix material is present in early biofilm formation and may protect a population of bacteria from interacting with ordinarily diffusible small molecules, we hypothesized that surfactants may be useful in preventing biofilm development.

Antibacterial synergy of glycerol monolaurate and aminoglycosides in Staphylococcus aureus biofilms.

Glycerol monolaurate (GML) is a natural surfactant with antimicrobial properties. At ∼0.3 mM, both GML and its component lauric acid were bactericidal for antibiotic-resistant Staphylococcus aureus biofilms.

Aminoglycoside inhibition of Staphylococcus aureus biofilm formation is nutrient dependent.

Biofilms represent microbial communities, encased in a self-produced matrix or extracellular polymeric substance. Microbial biofilms are likely responsible for a large proportion of clinically significant infections and the multicellular nature of biofilm existence has been repeatedly associated with antibiotic resistance. Classical in vitro antibiotic-susceptibility testing utilizes artificial growth media and planktonic microbes, but this method may not account for the variability inherent in environments subject to biofilm growth in vivo.

Anoxia inhibits biofilm development and modulates antibiotic activity.

Background: Many infections involve bacterial biofilms that are notoriously antibiotic resistant. Unfortunately, the mechanism for this resistance is unclear. We tested the effect of oxygen concentration on development of Staphylococcus aureus biofilms, and on the ability of gentamicin and vancomycin to inhibit biofilm development.

Enterococcus faecalis produces abundant extracellular structures containing DNA in the absence of cell lysis during early biofilm formation.

Unlabelled: Enterococcus faecalis is a common Gram-positive commensal bacterium of the metazoan gastrointestinal tract capable of biofilm formation and an opportunistic pathogen of increasing clinical concern. Dogma has held that biofilms are slow-growing structures, often taking days to form mature microcolonies. Here we report that extracellular DNA (eDNA) is an integral structural component of early E.

Ultrastructure of a novel bacterial form located in Staphylococcus aureus in vitro and in vivo catheter-associated biofilms.

Bacterial biofilms are ubiquitous in nature, industry, and medicine, and understanding their development and cellular structure is critical in controlling the unwanted consequences of biofilm growth. Here, we report the ultrastructure of a novel bacterial form observed by scanning electron microscopy in the luminal vegetations of catheters from patients with active Staphylococcus aureus bacteremia. This novel structure had the general appearance of a normal staphylococcal cell but up to 10 to 15 times as large.

Interplay of antibiotics and bacterial inoculum on suture-associated biofilms.

Background: Biofilms are often antibiotic resistant, and it is unclear if prophylactic antibiotics can effectively prevent biofilm formation. Experiments were designed to test the ability of high (bactericidal) concentrations of ampicillin (AMP), vancomycin (VAN), and oxacillin (OXA) to prevent formation of suture-associated biofilms initiated with low (10(4)) and high (10(7)) numbers of Staphylococcus aureus.

Materials And Methods: S.

Relation between antibiotic susceptibility and ultrastructure of Staphylococcus aureus biofilms on surgical suture.

Background: Infectious biofilms are recalcitrant to antimicrobial therapy, but the mechanism(s) responsible for the greater resistance are unclear. Experiments were designed to clarify the association between antibiotic resistance and biofilm ultrastructure.

Methods: Staphylococcus aureus was cultivated for 24 h on silk suture, where robust biofilms formed.

Gentamicin promotes Staphylococcus aureus biofilms on silk suture.

Background: Communities of bacteria, termed biofilms, develop on biotic and abiotic surfaces, including medical devices and surgical suture. Biofilm-associated bacteria are typically recalcitrant to antibiotic therapy, and the effects of antibiotics on microbial biofilms are not clearly understood. There is emerging evidence that under specific conditions, aminoglycosides may actually promote biofilm development.

Role of Staphylococcus aureus protein A in adherence to silastic catheters.

Background: Communities of bacteria, termed biofilms, frequently develop on central venous catheters, and bacterial contamination of central venous catheters is the most common cause of nosocomial bloodstream infections. Little is known about the initial events in bacterial adherence to the catheter surface, and experiments were designed to clarify the role of staphylococcal protein A, serum, and immunoglobulin in adherence of Staphylococcus aureus to silastic catheters. We hypothesized that S.

Acceleration of Enterococcus faecalis biofilm formation by aggregation substance expression in an ex vivo model of cardiac valve colonization.

Infectious endocarditis involves formation of a microbial biofilm in vivo. Enterococcus faecalis Aggregation Substance (Asc10) protein enhances the severity of experimental endocarditis, where it has been implicated in formation of large vegetations and in microbial persistence during infection. In the current study, we developed an ex vivo porcine heart valve adherence model to study the initial interactions between Asc10(+) and Asc10(-)E.

Bacterial contamination of surgical suture resembles a biofilm.

Background: Although much attention is currently directed to studying microbial biofilms on a variety of surfaces, few studies are designed to study bacterial growth on surgical suture. The purpose of this study was to compare the kinetic development of Staphylococcus aureus and Enterococcus faecalis on five surgical suture materials and to clarify factors that might influence this growth.

Methods: Pure cultures of S.

Selected factors affecting Staphylococcus aureus within silastic catheters.

Background: Catheter-related infections are frequent complications in hospitalized patients, and Staphylococcus aureus is a frequent etiologic agent. Little is known about factors that contribute to the growth and viability of S. aureus within contaminated catheters.

Escherichia coli and TNF-alpha modulate macrophage phagocytosis of Candida glabrata.

Background: The incidence of systemic nonalbicans Candida (especially C. glabrata) infections is increasing dramatically in intensive care units, but relatively little is known about the pathogenesis or host defenses associated with these life threatening infections.

Materials And Methods: The course of systemic C.

Multiple functional domains of Enterococcus faecalis aggregation substance Asc10 contribute to endocarditis virulence.

Aggregation substance proteins encoded by sex pheromone plasmids increase the virulence of Enterococcus faecalis in experimental pathogenesis models, including infectious endocarditis models. These large surface proteins may contain multiple functional domains involved in various interactions with other bacterial cells and with the mammalian host. Aggregation substance Asc10, encoded by plasmid pCF10, is induced during growth in the mammalian bloodstream, and pCF10 carriage gives E.

Polyethylene glycol influences microbial interactions with intestinal epithelium.

There is emerging evidence that polyethylene glycol (PEG), widely used as a bowel preparation before surgery, may protect the intestinal epithelium from microbial invasion. Experiments were designed to study the effects of both low-molecular-weight (LMW; 3.35 kd) and high-molecular-weight (HMW; 15-20 kd) PEG on interactions of Escherichia coli, Candida albicans, and Candida glabrata with intestinal epithelium (these three intestinal microbes are frequently involved in systemic infection in shock and trauma patients.

Candida glabrata colonizes but does not often disseminate from the mouse caecum.

Candida glabrata is the second or third most frequent cause of candidaemia. The gastrointestinal tract is considered to be a major portal of entry for systemic candidiasis, but relatively few studies have investigated the pathogenesis of C. glabrata.

A eukaryotic-type Ser/Thr kinase in Enterococcus faecalis mediates antimicrobial resistance and intestinal persistence.

Antibiotic-resistant enterococci are major causes of hospital-acquired infections. The emergence of Enterococcus faecalis as a significant nosocomial pathogen is a consequence of its inherent resistance to certain antibiotics and of its ability to survive and proliferate in the intestinal tract. Genetic determinants of E.

Synergistic effect of tumor necrosis factor-alpha and interferon-gamma on enterocyte shedding of syndecan-1 and associated decreases in internalization of Listeria monocytogenes and Staphylococcus aureus.

Syndecan-1 is a heparan sulfate proteoglycan expressed on epithelia, and its ectodomain can be shed into the extracellular milieu, affecting a variety of cellular functions. Using two bacteria known to react with heparan sulfate, Listeria monocytogenes and Staphylococcus aureus, experiments were designed to clarify the effect of syndecan-1 shedding on bacterial internalization by human HT-29 enterocytes. Mature enterocytes were incubated with tumor necrosis factor (TNF)-alpha and/or interferon (IFN)-gamma for 16h prior to addition of bacteria.

Heparan sulfate proteoglycans mediate Staphylococcus aureus interactions with intestinal epithelium.

Staphylococcus aureus can be internalized by non-professional phagocytes, and may colonize the intestine in normal and antibiotic-treated individuals. Intestinal colonization may depend on the interactions of S. aureus with the intestinal epithelium.

Ability of the heparan sulfate proteoglycan syndecan-1 to participate in bacterial translocation across the intestinal epithelial barrier.

Although hundreds of microbial species reside in the human intestinal tract, comparatively few (e.g., Escherichia coli and other enterobacteria, Enterococcus faecalis, etc.

Escherichia coli modulates extraintestinal spread of Staphylococcus aureus.

Staphylococcus aureus remains one of the most frequent causes of life-threatening systemic infection in surgical and trauma patients. It is understood that S. aureus colonization predisposes to complicating infection, but extraintestinal dissemination of S.

Impact of the indigenous flora in animal models of shock and sepsis.

Septicemia is currently the 10th leading cause of death in the United States, and shock and trauma patients are the source of much of the morbidity and mortality associated with septicemia. There is substantial evidence that the composition of the indigenous flora plays an important role in modulating outcome variables in animal models of shock and sepsis. Germ-free animals that lack an indigenous flora are not as susceptible to shock as their conventionally reared counterparts.