Staphylococcus epidermidis

'Staphylococcus' - bunch of grape-like berries, 'epidermidis' - of the epidermis. ==Discovery==

Friedrich Julius Rosenbach distinguished S. epidermidis from S. aureus in 1884, initially naming S. epidermidis as S. albus. He chose aureus and albus since the bacteria formed yellow and white colonies, respectively. == Microbiology ==

Staphylococcus epidermidis is a very hardy microorganism, consisting of nonmotile, Gram-positive cocci, arranged in grape-like clusters. It forms white, raised, cohesive colonies about 1–2 mm in diameter after overnight incubation, and is not hemolytic on blood agar. coagulase-negative, facultative anaerobe that can grow by aerobic respiration or by fermentation. Some strains may not ferment. Biochemical tests indicate this microorganism also carries out a weakly positive reaction to the nitrate reductase test. It is positive for urease production, is oxidase negative, and can use glucose, sucrose, and lactose to form acid products. In the presence of lactose, it will also produce gas. Nonpathogenic S. epidermidis unlike pathogenic S. aureus does not possess the gelatinase enzyme, so it cannot hydrolyze gelatin. It is sensitive to novobiocin, providing an important test to distinguish it from Staphylococcus saprophyticus, which is coagulase-negative, as well, but novobiocin-resistant. Normally, sensitivity to desferrioxamine can also be used to distinguish it from most other staphylococci, except in the case of Staphylococcus hominis, which is also sensitive. In this case, the production of acid from trehalose by S. hominis can be used to tell the two species apart. Microbial ecology Role in foot odor A common misconception about foot odor and body odor in general is that sweat itself smells and causes people to smell. However, sweat itself is almost entirely odorless. Rather, microbes present on the skin metabolize certain compounds in sweat as a source of nutrients, producing compounds with an unpleasant smell in the process. S. epidermidis thrives in warm, moist environments and is a common bacteria of the human microbiome; it is thus primarily responsible for foot odor as feet have more sweat glands than any other part of the body and thus are often moist, which creates an ideal environment for S. epidermidis to thrive. The bacteria produces enzymes that degrade the leucine present in sweat, producing unpleasant smelling volatile compounds such as isovaleric acid. Feet with stronger odors have a higher density of microorganisms than those with weaker foot odor. == Role in disease ==

Virulence factors Biofilm formation S. epidermidis causes biofilms to grow on plastic devices placed within the body. This occurs most commonly on intravenous catheters and on medical prostheses. Infection can also occur in dialysis patients or anyone with an implanted plastic device that may have been contaminated. It also causes endocarditis, most often in patients with defective heart valves. In some other cases, sepsis can occur in hospital patients. The ability to form biofilms on plastic devices is a major virulence factor for S. epidermidis. One probable cause is surface proteins that bind blood and extracellular matrix proteins. It produces an extracellular material known as polysaccharide intercellular adhesin (PIA), which is made up of sulfated polysaccharides. It allows other bacteria to bind to the already existing biofilm, creating a multilayer biofilm. Such biofilms decrease the metabolic activity of bacteria within them. This decreased metabolism, in combination with impaired diffusion of antibiotics, makes it difficult for antibiotics to effectively clear this type of infection. Staphylococcus epidermidis in the normal skin is nonpathogenic and innocuous. But in abnormal lesions (such as openings or cuts on the skin), it becomes pathogenic, likely in acne vulgaris. Staphylococcus epidermidis enters the sebaceous gland (colonized by Cutibacterium acnes, the main bacterium that causes acne vulgaris) and damages the hair follicles by producing lipolytic enzymes that change the sebum from fraction to dense (thick) form leading to inflammatory effect. Moreover, S. epidermidis biofilm formation by releasing the exopolysaccharide intercellular adhesion (PIA) provides the susceptible anaerobic environment to P. acnes colonisation and protects it from the innate human immunity molecules. Both P. acnes and S. epidermidis can interact to protect the host skin health from pathogens colonisation. But in the case of competition, they use the same carbon source (i.e. glycerol) to produce short chain fatty acids which act as antibacterial agent against each other. Also, S. epidermidis helps in skin homeostasis and reduces the P. acnes pathogenic inflammation by decreasing the TLR2 protein production that induces the skin inflammation. == Role in skin health ==

Skin barrier reinforcement Commensal S. epidermidis also has been shown to contribute to skin barrier homeostasis through the generation of protective ceramides, which helps maintain the integrity of the skin barrier. By modulating the moist, inner lining of some organs and body cavities and their specific immune defense mechanisms, skin commensals interact with infectious agents like pathogens. Sphingomyelin phosphodiesterase is the main driver in the S. epidermidis production of ceramides - a lipid that includes sphingosine and sphingosine-1-phosphate. This lipid, both obtains nutrients essential for bacteria and helps the host in the production of ceramides. Ceramides are important components of the epithelial barrier, and they play a key role in preventing skin from losing moisture; this acts as a protectant and averts against both dehydration and aging of the skin. Salicylic acid is known to reduce the population of S. epidermidis; the mechanism of this is currently unfamiliar, but it is hypothesized that salicylic acid inhibits S. epidermidis' biofilms. Metabolic interaction S. epidermidis plays a key role in metabolic processes that influence skin conditions. The bacterium can affect biochemical pathways within skin cells, which can impact skin health and disease states. Specifically, this is seen in the modulation of the aryl hydrocarbon receptor. Immune response Commensal S. epidermidis also influences the skin's immune response. Through interacting with a host's immune cells, the skin's mucosal immune defense against various pathogens is strengthened. The skin commensal will directly interfere with harmful pathogens. In the case of S. aureus, S. epidermidis may amplify the innate immune response by causing a reaction of keratinocytes toward this pathogen. S. epidermidis produces molecules such as lipoteichoic acid (LTA), cell wall polysaccharides, peptidoglycan and aldehyde dipeptides which are recognized by toll-like receptors (TLRs) as molecules that modulate the immune response. These immunomodulatory molecules create a relationship between bacteria and keratinocytes and have a significant impact in the modulation of the innate immune response, mainly because of their interactions with TLRs. == See also ==