Introduction:

Staphylococcus Epidermidis is a gram positive, nonmotile, cocci [ 6 ] which is one of the most commonly found bacteria in the human skin microbiome. Once thought to be more or less benign, S. Epidermidis has been found to be a major risk for minor infections (sometimes chronic) and especially in playing a supporting role for other bacterial infections such as with S. Aureus. S. Epidermidis can be aptly describe as "aggressively passive" It typically does not seek to infect the host, but rather seeks to maintain it's ability to inhabit a human's skin. This is seen in the fact that S. Epidermidis does not secrete toxins that would be aggressive towards humans as it doesn't seek to harm it's host. However, it has several ways to avoid immune response [ 4 ] and has a large catalog of antibiotic resistances [ 5 ]. To add to it's hardiness, S. Epidermidis often forms biofilms which helps to further protect the bacteria from immune response and antibiotics, as well as helping ensure it's overall survival via dispersion and nutrient absorption.  However, this is one of the main problems with S. Epidermidis, it is the most common form of nosocomial infection such as from implanted devices like catheters due to the device at some point coming in contact with the individuals skin, allowing S. Epidermidis to attach and form a hard to sterilize biofilm [ 2 ]. While S. Epidermidis doesn't secrete aggressive toxins, it does still pose a problem as it secretes pro-inflammatory peptides which can cause complications in the infected host [ 3 ]. S. Epidermidis also makes mild endotoxins which are capable of at the very least making the infected host uncomfortable and in some rare situations lead to chronic illness [ 6 ].

Interaction With S. Aureus:


While S. Epidermidis itself having antibiotic resistance may not be much of a problem, how it synergizes with S. Aureus poses a serious threat. Unlike Epidermidis, Aureus is capable of making aggressive toxins and can lead to serious infections by itself. However, S. Epidermidis can worsen these infections by transferring antibiotic resistant genes to Aureus via plasmids [ 1 ] making them much more difficult to treat. Aureus secretes exoproteins such as toxic shock syndrome toxin-1, alpha toxin, and tissue degrading enzyme [ 1 ] which makes them a dangerous pathogen in their own right, but when combined with antibiotic resistances the patient's risks of toxic shock or tissue damage are greatly increased. Additionally, the pro-inflammatory peptides and exopolymers secreted by S. Epidermidis helps both bacteria evade the immune system of the host, presenting another dangerous variable into the infection.


Biofilm:

S. Epidermidis is one of the most notorious biofilm forming bacteria, being the bane of every medical institution. It is commonly found on implanted devices such as catheters or other medical machinery such as ventilators. This ability to form a sturdy biofilm on medical devices causes S. Epidermidis to become a serious medical risk, as it can easily infect the patient's blood or cause further illness from it's endotoxins. Additionally, the biofilm formation itself gives S. Epidermidis further resistances to antibiotics and the hosts immune response. Part of how the formation gives resistance is actually the genomic adaptations necessary to encourage biofilm formation. In S. Epidermidis several of these adaptations can be seen such as the down regulation of basic cell processes such as nucleic acid, protein and cell wall biosyntheses [ 4 ]. This down regulation inherently limits the activity of antibiotics. Additionally, the slimy coating of the biofilm as well as the fact that cells are hidden behind other cells helps to protect the bacteria from anything that may harm it.


figure1
Figure 1: [ 4 ] Biofilm formation process of S. Epidermidis.


References:

 [ 1 ] O'GARA, J., & HUMPHREYS, H. (2001). Staphylococcus epidermidis biofilms: importance and implications. J. Med. Microbiol (50). 582-587. DOI[ 2 ] Uçkay, I., Pittet, D., Vaudaux, P., Sax, H., Lew, D., & Waldvogel, F. (2009). Foreign body infections due to Staphylococcus epidermidis. Annals of Medicine (41). 109-119. DOI:10.1080/07853890802337045

[ 3 ] Otto, M. (2012). Molecular basis of Staphylococcus epidermidis infections. Seminars in Immunopathology (34). 201-214. DOI:10.1007/s00281-011-0296-2

[ 4 ] Otto, M. (2009). Staphylococcus epidermidis — the 'accidental' pathogen. Nature Reviews Microbiology (7). 555-567. DOI:10.1038/nrmicro2182

[ 5 ] Raad, I., Alrahwan, A., and Rolston, K. (1998). Staphylococcus epidermidis: Emerging Resistance and Need for Alternative Agents. Clinical Infectious Diseases (26). 1182-1187. DOI:10.1086/520285

[ 6 ] Namvar, A. E., Bastarahang, S., Abbasi, N., et al. (2014). Clinical characteristics of Staphylococcus epidermidis: a systematic review. GMS Hyg Infect Control 9(3). DOI:10.3205/dgkh000243

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7 commentaires

  1. Erika Doroshenko dit :

    This is very interesting Collen! What really spiked my interest was the section regarding the relationship between S. epidermidis and S. aureus. How common is the transfer of antibiotic resistance from S. epidermidis to S. aureus actually observed in nature? Is it something that is of concern and should be looked into finding a way to prevent in the future?

    1. Collen Cole dit :

      Hey Erika, the relationship between the two is a fairly large threat (in humans at least). S. aureas and epidermidis are both common bacteria found in the microbiome of the skin, so if aureus infects an individual then there's a good chance epidermidis is nearby to assist it. It's actually one of the main concerns of epidermidis, Its ability to form biofilms is certainly dangerous but its enhancement of aureus is even more dangerous (albeit, slightly less common, but still far from rare). It's also very difficult to get into either bacteria to experiment (trying to get them to uptake/integrate different DNA) as they have an "impenetrable restriction barrier" that prevents uptake of unknown foreign DNA.

  2. Mary-Anne Courtney dit :

    Nice look at an organism and the biofilms it can develop.

  3. Josephine Bensa dit :

    It is interesting to see how S. epidermidis utilizes its traits and characteristics to impact the body. You mentioned that though it does not secrete aggressive toxins, it does secrete pro-inflammatory peptides which can cause complications in the infected host and I was wondering if you could explain what kinds of complications are normally caused and how the body's immune system responds to that


    1. Collen Cole dit :

      S. epidermidis is notorious for causing urinary tract infections which is the inflammation of the ureters due to it commonly growing on catheters. This is directly caused by the pro-inflammatory peptides and is one of the main risks of an S. epidermidis infection. However, it also is commonly seen to cause inflammation of the eyes or other exposed areas on the body (such as cuts, it can seep in and cause a blood infection). As for how the body handles these, that's a bit beyond me. That's going more into immunology which I have never taken. It would seem that the body tries to kill it via fevers and other commonly used mechanisms, but as for in depth actions the body may take, not a clue.

  4. Dayton Seidel dit :

    The bacteria I did, K. pneumoniae, is also a bacteria that is commonly found to be the cause of nosocomial infections. It's crazy to think about how many different infectious bacteria can be found on hospital equipment if it isn't sterilized correctly. I just want to ask, what are some ways it avoids causing an immune response?

    1. Collen Cole dit :

      As stated in the wiki, the biofilm formation itself as well as the genes necessary to form it are major contributors in its ability to avoid the immune system. The biofilm formation hides cells from the natural killer cells/other immune cells and the genes necessary for biofilm formation down regulates expression in epidermidis making it even more difficult for the immune system to recognize it/ have a substantial effect.