Staphylococcus epidermidis is a
Gram-positive bacterium, and one of over 40
species belonging to the genus Staphylococcus.[1] It is part of the
normal human microbiota, typically the
skin microbiota, and less commonly the mucosal microbiota and also found in marine sponges.[2][3] It is a facultative
anaerobic bacteria. Although S. epidermidis is not usually
pathogenic, patients with compromised
immune systems are at risk of developing infection. These infections are generally
hospital-acquired.[4]S. epidermidis is a particular concern for people with
catheters or other surgical implants because it is known to form
biofilms that grow on these devices.[5] Being part of the normal skin microbiota, S. epidermidis is a frequent contaminant of specimens sent to the diagnostic laboratory.[6]
'Staphylococcus' - bunch of grape-like berries, 'epidermidis' - of the epidermis.[7]
Discovery
Friedrich Julius Rosenbach distinguished S. epidermidis from S. aureus in 1884, initially naming S. epidermidis as S. albus.[8] 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.[5] It is a
catalase-positive,[9]coagulase-negative,
facultative anaerobe that can grow by
aerobic respiration or by
fermentation. Some strains may not ferment.[3][10]
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.[11][12] It is sensitive to
novobiocin, providing an important test to distinguish it from Staphylococcus saprophyticus, which is coagulase-negative, as well, but novobiocin-resistant.[4]
Similar to those of S. aureus, the cell walls of S. epidermidis have a transferrin-binding protein that helps the organism obtain iron from
transferrin. The tetramers of a surface exposed protein, glyceraldehyde-3-phosphate dehydrogenase, are believed to bind to transferrin and remove its iron. Subsequent steps include iron being transferred to surface lipoproteins, then to transport proteins which carry the iron into the cell.[5]
Biochemical characteristics
Colony, morphological, physiological, and biochemical characteristics of marine S. epidermidis are shown in the table below.[3]
The normal practice of detecting S. epidermidis is by using appearance of colonies on selective media, bacterial morphology by light microscopy, catalase and slide coagulase testing. Zobell agar is useful for the isolation of Staphylococcus epidermidis from marine organisms.[3] On the
Baird-Parker agar with
egg yolk supplement, colonies appear small and black. Increasingly, techniques such as
quantitative PCR are being employed for the rapid detection and identification of Staphylococcus strains.[13][14] 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.[15] In this case, the production of acid from
trehalose by S. hominis can be used to tell the two species apart.[citation needed]
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.[16] S. epidermidis thrives in warm, moist environments and is a common bacteria of the
human microbiome;[17] 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.[17]
Role in disease
Virulence factors
Biofilm formation
S. epidermidis causes biofilms to grow on plastic devices placed within the body.[18] This occurs most commonly on intravenous
catheters and on medical
prostheses.[19] 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. [citation needed]
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.[5]
Antibiotics are largely ineffective in clearing biofilms. The most common treatment for these infections is to remove or replace the infected implant, though in all cases, prevention is ideal. The drug of choice is often
vancomycin, to which
rifampin or an
aminoglycoside can be added.[citation needed] Hand washing has been shown to reduce the spread of infection.
Preliminary research also indicates S. epidermidis is universally found inside affected
acne vulgaris pores, where Cutibacterium acnes is normally the sole resident.[20]
Staphylococcus epidermidis in the normal skin is nonpathogenic. But in abnormal lesions, it becomes pathogenic, likely in
acne vulgaris. Staphylococcus epidermidis enters the sebaceous gland (colonized by Propionibacterium 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.[21]
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.[22]
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.[23]
^Hedin, G (1993). "Staphylococcus epidermidis--hospital epidemiology and the detection of methicillin resistance". Scandinavian Journal of Infectious Diseases. Supplementum. 90: 1–59.
PMID8303217.