Bacteria of the Skin
With a market flooded with antibacterial products, humans and bacteria seem to be a part of a never ending fight. It is well understood that antibacterial products often do more harm than good if a person has a basic understanding of Darwin's natural selection theory of survival of the fittest. So, what are bacteria and how do they influence skin health?
Bacteria are single celled organisms that lack a nucleus, differentiating them from eukaryotes. They also lack the organelles or compartmentalized inner structures of the eukaryotic cell but do contain genetic material in the form of a single loop of DNA (Deoxyribonucleic Acid). Some bacteria are specialized and contain one or more loops of DNA known as plasmids. In Physiology, students are taught the hierarchy of an organism's level of organization, beginning with atoms to whole organisms. Students therefore understand that human cells take on a variety of shapes and forms to create a tissue. This can be related to bacterial forms and shapes. Bacteria come in a variety of shapes from spherical (i.e. Staphylococci), rods (Lactobacillus), to corkscrew (spirochaetes). 20
Bacteria make their homes on specific human tissues because of tissue tropism. Tissue tropism is the preference of bacteria for certain tissues due to the nutrients and growth factors that exist on the tissue. Another reason for a bacterium's specificity for a tissue is due to the interaction of the proteins on the bacterium's surface to the receptors on the host's cell membrane. The different adhesion molecules on the surface of a bacterium will prevent or allow a bacterium to attach to mucosal surfaces, such as the lungs, intestines, or the conjunctiva of the eye.
As previously mentioned, skin is an ideal location for microbes to thrive. Christensen and Brggemann state that the most abundant bacterial species found on the human skin include various species belonging to four genera. The most prevalent bacteria found on the skin are: Actinobacteria (51.8%), Firmicutes (24.4%), Proteobacteria (16.5%) and Bacteriodetes (6.3%). 21 This finding was possible because of the development of DNA sequencing techniques that could decipher genetic differences between bacteria, without having to grow them in the laboratory.
Host – Bacteria Interactions
It is well known that the human body is teeming with microbes and yet people are still surprised when they learn that the vast majority of bacteria that exist on our skin's surface is actually beneficial and function to prevent the proliferation of pathogenic bacteria. The normal or "indigenous micro-biota" are the results of thousands of years of mutations, evolution, infections, survival, and resistance to other microbes. The remaining microbes are those best adapted to their current host. Humans and indigenous bacteria have, for the most part, a commensal relationship, where neither party is harmed or benefits from the presence of the other. Of the three types of interactions between hosts and microbes, the most infrequently found relationship is that of commensalism. In this unit both commensalistic and parasitic interactions will be discussed in a sample bacterium.
Staphylococcus epidermidis
One example of well-studied host-bacterium commensalism is the role of gram negative Staphylococcus epidermidis interacting with humans. S. epidermidis is a commonly found aerobic bacterium of human microbiota. Typically the bacteria are found in the head, neck, and armpit skin regions. There are several reasons for the bacterium's success on the skin. Michael Otto in Nature Reviews Microbiology describes S. epidermis's ability to exist on the surface of the skin because it can sustain extreme salt concentrations and osmotic pressure. This is due to the high number of Na+ exchanger channels on its cellular membrane. 22
Additionally, S. epidermidis provides host defense mechanisms by a complementary system of barriers that prevent other organisms from proliferating in the tissues of its host. Cogen et al. summarize these complimentary systems by stating that S. epidermidis helps its host establish a physical barrier and a hostile surface pH. Furthermore, S. epidermidis actively synthesizes genes that produce host defense molecules like natural antibiotics against other microbes. 23 Their review specifically states S. epidermidis produces lantibiotics or bacteriocides which are toxic against other bacteria, thus reducing competitive bacteria from proliferating. Surprisingly, studies have shown that one lantibiotic produced by S. epidermidis inhibits methicllin-resistant S. aureus, showing a competitive superiority of one species over the other. Incredibly, the hosts' immune system actually allows for the bacterium to proliferate on the skin in order to prevent pathogens from dwelling and developing in the same cutaneous tissue where S. epidermidis lies. The immune system does this by increasing the proliferation of keratinocytes which increases the skin's ability to shed the top most layers and thereby trapping potentially pathogenic bacteria. 24 Schommer and Gallo also show that the immune system's T-cells are modulated by the bacteria to control inflammatory responses, supporting the idea that S. epidermidis and its human host interact with one another in a commensalist manner. 25 Finally, Wang, in his articles on the probiotic potential of S. epidermis, states that S. epidermis colonies prevent growth of Propionibacterium acnes, the microbe responsible for some acne problems. 26 Imagine, instead of using Clearasil or Neutrogena, teenagers may one day wipe S. epidermis colonies on their face each night before they sleep!
However, if S. epidermidis accidentally becomes pathogenic it is because the host is immune-comprised, or became compromised because they are drug abusers, were born as premature babies, or were implanted with a medical device like a catheter. In-dwelling implants increase the chance for S. epidermidis infections. While relatively innate on the human skin, in-dwelling medical devices must be carefully monitored because of the bacteria's potential for proliferation on the device's surface. 27 Typically, S. epidermidis creates a biofilm that shields the bacteria from the immune systems of its hosts. S. epidermidis fools its hosts using a variety of mechanisms including intercellular adhesion to proliferate, and production of immune evasion chemicals that hide its presence to the hosts' immune cells. If the host is unable to break through the biofilm that coats the growing infectious bacteria, the host may develop sepsis which is a severe inflammatory infection due to the spread of the bacteria into the bloodstream. Thus far, it is unclear how to distinguish between S. epidermidis strains that are a part of our normal biomes from those causing severe infections. However, Christensen and Brggemann state that S. epidermidis is less problematic than S. aureus in terms of the amount of toxins and degradative enzymes produced by the bacterium. 28 Though S. epidermidis is generally harmless and infections are treatable, if the bacterium infects the lower layers of the skin then it can be difficult to treat with penicillin and methicillin. 29 This presents a concern because of the rise of methicillin-resistant bacteria, which prevent physicians from being able to treat these seemingly innocuous bacteria.
Propionibacterium acnes
The bane of adolescent and teenage life is the dreaded A word – Acne. Beyond the social stigma that develops and self confidence that reduces when a teenager develops signs of acne, acne is problematic because so many factors contribute to its development. Propionibacterium acnes is the bacterium that causes acne. Cogen et al. describes the bacterium as aero-tolerant gram positive anaerobe that thrives in the sebaceous glands of the skin. It is responsible for the irritation of the sebaceous duct, the clogging of its pore, and local folliculitis. If the bacteria were to spread to tissues beyond the dermal layer they may lead to systemic infections include endocarditis. 30
An example of dysbiosis is the proliferation of P. acnes in the human hair follicle and pore, its mechanism of pathogenesis will be discussed though this disease is not completely understood. 31 Due to increased levels of androgen induced sebum levels, altered keratinization, inflammation, and changes to facial skin bacterial colonies, P. acnes tend to create the well known symptoms, of red, inflamed, raised, and irritated pilosebaceous (hair and oil) pores. Essentially, P. acnes is able to create clogged sebaceous pores by the production of free-fatty acids which irritate the hair follicles' wall, causing inflammation. 80% of adult skin infections are due to P. acnes proliferation. Current microbial studies into P. acne have shown that acne was not due to an increased proliferation of the bacteria but rather the development of different strains of the bacteria. 32 Another study points to acne development due to an increased stimulation of the production of bacteriocins, preventing the sebaceous duct from other harmful, more pathogenic bacteria since bacteriocins act like natural antibacterial chemicals. 33
As commonplace as acne infections are to the general public, some people are never affected by acne. People living in Papua New Guinea and Paraguay do not show signs of acne. Schommer and Gallo present the reason for this as the diet consumed in those regions. Papua New Guineans and Paraguayans do not eat foods with high glycemic loads thereby reducing the androgen induced trigger for acne. Treatments for Acne Vulgaris include a host of commonly known antibiotic products, benzoyl peroxide, and sulfur based ointments. Most common treatments included antibiotics. Tetracycline, erythromycin, and clindamycin were readily prescribed but have contributed to P. acnes growing resistance against some antimicrobial treatments. 34
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