Answer: Propionibacterium acnes is a bacteria that can colonize the the skin and hair follicles. This bacteria is the primary pathogenic agent responsible for acne vulgaris.
Propionibacterium acnes bacteria
Propionibacterium acnes (P. acnes) is a bacteria that grows deep inside of pores, where it feeds on the sebum that is produced by the sebaceous glands that surround the base of the hair shaft. In most cases, P. acnes bacteria are partially responsible for acne symptoms. Several studies have indicated that specific strains of P. acnes bacteria are more commonly associated with acne vulgaris. However, other bacteria (e.g. Staphylococcus and Corynebacterium) can also reside in the follicle and on the surface of the skin.
Propionibacteria are members of the “gram-positive” classification of bacteria, which includes many other species of infectious bacteria. Gram positive bacteria have thick cell walls that are rich in peptidoglycans and lippolysacharides, (sugar molecules attached to proteins and fatty acids).
P. acnes is an oxygen tolerant, anaerobic bacteria that prefers to grow in low oxygen environments (like deep within a plugged follicle). P. acnes uses sebum as an energy source. In a plugged follicle, the low oxygen levels and accumulating sebum create a prime environment for the growth of P. acnes bacteria.
P. acnes bacteria can form sticky clumps of bacteria known as biofilms that help to anchor and protect the bacteria at the site of infection. In many cases, bacterial biofilms have been shown to contribute to long term infections, and may play a role in the persistence of P. acnes infection in some individuals.
The Relationship Between Sebum and Propionibacterium acnes
Propionibacterium acnes growing in pores produces a fluorescent orange glow when illuminated by ultraviolet light
P. acnes bacteria use sebum, which is produced in follicles, as a primary source of food. P. acnes bacteria use specialized enzymes that digest the fatty acids and triglycerides that are abundant in sebum. In an anaerobic environment, P. acnes ferments the fatty acids and triglycerides, and releases short chain fatty acids and propionic acid as metabolic byproducts (that’s why it’s called Propionibacterium).
P. acnes has several complementary metabolic pathways as well, designed to harvest energy from additional sources. Research indicates that the digestion of sebum by the bacterial enzymes can create comedogenic byproducts, a potential contributing factor to the severity of acne symptoms.
There is also some evidence that sebum production may be stimulated by the presence of P. acnes bacteria. If this is true, it is possible that the bacteria has adapted to the environment of the follicle, and part of this adaptation includes a mechanism to get more food (sebum) from the surrounding tissue.
Propionibacterium acnes, Inflammation and Acne vulgaris
White Blood Cells Mediate Inflammation
Propionibacterium does not directly cause significant damage to the skin. Instead, most of the damage caused by acne is due to the inflammatory process of the immune system.
For most people who suffer from inflammatory acne, the immune system over-reacts to the bacteria and sends in lots of white blood cells. The immune system of some people may be more sensitive to P. acnes bacteria and may respond strongly, which can lead to symptoms of inlammatory acne vulgaris (eg. Types 2,3 and 4).
Many of the individual components that make up the bacteria are easily recognized by the immune system as “enemy” molecules. This material includes components of the bacterial cell wall, like peptidoglycans, lipopolysacharides and proteins. Even the DNA from P. acnesbacteria is recognized as foreign by the immune system.
The bacteria doesn’t even have to be alive to trigger a powerful immune response, dead bacteria can also set off alarms with the immune system.
Dysfunctional Immune Responses and Acne vulgaris
Inflamed follicle full of white blood cells (blue)
In some people who suffer from acne (especially severe acne), the root of the problem can be traced back to a faulty immune response. There are two main types of immune failure that can lead to acne symptoms.
The first is known as a hyper-sensitive response. In this situation an individual’s immune system reacts over-aggressively to the presence of the bacteria and produces large amounts of inflammatory cytokines. These inflammatory cytokines induce white blood cells to release destructive enzymes and free radicals into the site of infection and that causes unnecessary collateral damage to the surrounding tissue. This damage often stimulates the production of more inflammatory cytokines and this can become a vicious cycle. In some cases, this damage can actually make it easier for the bacteria to proliferate.
The other main type of dysfunctional immune response occurs when an individual’s white blood cells do not effectively destroy and process the bacteria that they encounter. In an ideal situation, white blood cells engulf (phagocytose) all of the bacteria that they come in contact with. Once engulfed, the white blood cell isolates the bactiera into an intracellular compartment called a phagosome, and pumps toxic molecules and enzymes into this compartment. These molecules and enzymes kill the bacteria and digest it into small pieces. These pieces are then presented to the immune system, which uses them to design specific antibodies (and several other things) that specifically target the bacteria. In people who suffer from chronic, inflammatory infections (like acne vulgaris), they often have white blood cells that have a defect in this processing pathway. In these individuals, their white blood cells ingest bacteria normally, but their cells have an unusually difficult time killing the bacteria after eating them. If this happens, the white blood cell will often continue to secrete lots of inflammatory cytokines till it exhausts itself and dies in a process called apoptosis. After the cell dies, the bacteria isn’t necessarily dead, and can sometimes escape and keep proliferating.
Both of the above examples of immune system dysfunction are usually genetic in origin. The susceptibility to acne vulgaris is likely hereditary. Individuals whose parents experienced difficulty with acne vulgaris are at an increased risk of encountering acne symptoms.
Extensive screening has been done to test the susceptibility of P. acnes bacteria to different classes of antibiotics. In general, what researchers have found is that P. acnes is moderately susceptible, when directly exposed, to many classes of antibiotics.
Researchers have also found that P. acnes bacteria is becoming increasingly resistant to some of the common antibiotics used to treat acne, like erythromycin and tetracycline family drugs (tetracycline, doxycycline and minocycline). Interestingly, numerous studies have shown that P. acnes bacteria is extremely sensitive to Penicillin G, which was one of the first antibiotics ever developed.
It is important to keep in mind that these tests are primarily done on a petri dish in a laboratory. When asking whether an antibiotic is effective when treating a clinical acne infection there are additional factors that need to be considered. The biggest question is whether the antibiotic makes it to the site of infection. Many antibiotics may be effective at killing P. acnes bacteria on a petri dish, but they do not accumulate in sufficient concentration in the follicle and sebaceous glands to be effective at treating active acne infections.
Several Over-The-Counter medications, like benzoyl peroxide and triclosan, are also directly toxic to P. acnes bacteria. However, these topically applied medications have difficulty penetrating to the base of the hair follicle, which is where the P. acnes bacteria are causing problems.
P. acnes bacteria use the fatty acids and triglycerides found in sebum as its primary food source. Limiting the amount of sebum production can suppress the growth of P. acnes bacteria by reducing its food supply.
Treatment with retinoids can decrease the production of sebum in the skin. This is true for both oral retinoids (isotretinoin, accutane) and topical retinoids (retin-A, Adapalene). Hormonal treatments (like androgen inhibitors (Spironolactone, Cyproterone) and birth control) may also decrease sebum production. Certain light and laser therapies (diode lasers) can also decrease the production of sebum.
These light-based therapies work by exciting a particular molecule called a porphyrin, which is produced in large quantities by P. acnes bacteria. Excitation of porphyrins with blue light causes them to release free radicals into the bacteria and killing them.
P. acnes growing in pores on the human face produce a red fluorescence when illuminated by an ultraviolet (UV) light source.
There are several naturopathic treatments that may also be helpful in inhibiting or killing P. acnes bacteria.
Many essential oils are toxic to P. acnes bacteria, such as Tea Tree Oil and Thyme Essential Oil.
Other natural compounds, like aloe vera gel and natural honey, have also been shown to have antibacterial properties against P. acnes.
Certain metals (eg. silver and copper) and other elements (sulfur) are also toxic to bacteria in pure form.
References and Sources
Habif, et al. 2011. Skin Disease: Diagnosis and Treatment, 3rd Edition
Bauman. 2011. Microbiology with Diseases by Body System, 3rd Edition
PDR Staff. 2011. Physicians’ Desk Reference, 66th Edition
Pizzorno, et al. 2007. The Clinician’s Handbook of Natural Medicine, 2nd Edition
Gladwin, et al. 2011. Clinical Microbiology Made Ridiculously Simple
Brüggemann, et al. 2004.The Complete Genome Sequence of Propionibacterium Acnes, a Commensal of Human Skin.
Kurokawa, et al. 2009. New developments in our understanding of acne pathogenesis and treatment.
Bayston, et al. 2006. Biofilm formation by Propionibacterium acnes on biomaterials in vitro and in vivo: impact on diagnosis and treatment.
Holmberg, et al. 2009. Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates.
Burkhart, et al. 2007. Expanding the microcomedone theory and acne therapeutics: Propionibacterium acnes biofilm produces biological glue that holds corneocytes together to form plug.
Zouboulis. 2009. Propionibacterium acnes and Sebaceous Lipogenesis: A Love–Hate Relationship?
Ashkenazi, et al. 2002. Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light.
Seo, et al. 2000. Fluorescence spectroscopy for endogenous porphyrins in human facial skin.
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Patients and its Modulation by Acne Treatment.