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Acne and Propionibacterium Acnes
Propionibacterium acnes is the most important acne-causing bacteria. Find out how a harmless, commensal bacterium colonizes the skin and turns harmful and also how it is wiped out in acne treatment.
Acne vulgaris is the most common skin disease. It usually starts off mild during puberty and if left untreated, it will quickly worsen. When treated acne clears off when teenagers become young adults.
However, acne may persist long into adulthood in some people.
The parts of the body affected by acne are the areas of the skin with the highest concentration of sebaceous follicles. These are areas with high population of sebaceous glands and follicles which are easily colonized by acne-causing bacteria.
Such areas include the face, neck, upper parts of the chest, upper arm and the back as well as the thighs and buttocks in severe cases of acne.
Acne can produce superficial and deep lesions. These lesions can also be inflammatory or non-inflammatory.
Acne lesions include comedones such as whiteheads and blackheads; pustules and papules; nodules and cysts. Seborrhea is another presentation of acne. It is responsible for the red, scaly appearance of the skin during acne breakouts.
A number of factors can cause acne. These include stress, diet, genetics, bacterial infection and hormones. All factors causing acne involve hormones such as androgens and acne-causing bacteria such as Propionibacterium acnes.
Propionibacterium acnes is a rod-shaped, anaerobic, gram-positive bacterium.
It was formerly known as Bacillus acnes and Corynebacterium acnes. P. acnes is a commensal that lives naturally on the skin and in the mouth, urinary tract and parts of the gastrointestinal tract.
Although P. acnes is found on the skin of neonates, it soon disappears and only returns a few years before puberty. Then its population increases 10,000 folds especially on the face, neck and upper part of the chest.
On the skin, P. acnes grows in hair follicles ducts. Although it is primarily an anaerobic bacterium, P. acnes can also grow in microaerobic environments such as the lipid-rich nooks of hair follicles.
However, the population and activity of P. acnes depends on the availability of nutrient, pH of the skin and oxygen supply to the skin.
This growth environment is shared by other bacteria such as the acne-causing bacteria, P. granulosum (which is found at one hundredth of P. acnes population) and Staphylococcus epidermis. Other bacteria found in the same environment are S. aureus and Pityrosporum ovale.
Because P. acnes is found on the skin with or without acne present, experts are not quite sure whether a virulent strain of the bacterium is transferred to the skin or whether it is the harmless, commensal strain that later mutates into the acne-causing strain.
However, studies have shown that acne is not contagious. Therefore, the more likely theory is that the nature of P. acnes changes under the right conditions.
What is clear is that somewhere during early puberty, the increased production of sebum not only increases the population of P. acnes on the skin but also its activity.
Sebum is the ideal growth environment for P. acnes.
Excess sebum is produced in response to the constant stimulation of the sebaceous glands by hormones such as androgens. Since male sex hormones are produced in increasing amounts during adolescence in order to fuel sexual maturity and rapid growth, they reach the skin in increasing amounts.
The androgens of interest in this regard are testosterone and dihydrotestosterone or DHT. These hormones bind to the androgen receptors in the cells of the skin especially the sebocytes. They cause increased production of new sebocytes, and therefore, the enlargement of sebaceous glands.
This effect directly translates to increased sebum production.
While the excess sebum is being pushed to the skin surface, some of it gets trapped, alongside acne-causing bacteria and dead skin cells, inside the skin pores and give rise to acne comedones such as whiteheads and blackheads.
However, the closed environment of the blocked pores is the ideal anaerobic or microaerobic environment for the growth and spread of P. acnes.
Therefore, P. acnes thrives in the excess sebum produced. It breaks down the walls of the dermal cells; it attracts inflammatory factors from the immune system; and it causes the deep tissue damage that leads to severe acne.
P. acnes secretes certain enzymes that break down the lipids and proteins on the skin while changing the skin pH too.
On the other hand, P. acnes also aggravates the cells of the immune system.
For example, it resists being swallowed up by phagocytes and even when it is taken up, P. acnes can last a long while inside the immune cells and still remain virulent when discharged.
But more importantly, P. acnes causes local inflammation because the immune system sends specialized cells to contain the damage the bacterium causes to the dermis.
Unfortunately, these immune cells are also proinflammatory. At first, lymphocytes are sent to repair the damage done by P. acnes.
However, T-cells such as CD4+, CD8+ and CD1+ have also been found in acne lesions.
P. acnes attracts these immune cells by the byproducts of its metabolism (the breakdown products of the enzymes it secretes) and also by the antigen it releases. The body synthesizes specific antibodies to these antigens especially during severe acne breakouts.
The presence of P. acnes has also been positively correlated with increased production of proinflammatory lipids such as free fatty acids and such specialized inflammatory factors like TNF-alpha (tissue necrosis factor-alpha) and IL-1 alpha (interleukin-1 alpha).
Beyond playing an important role in the swift progression of mild acne to different forms of severe acne, P. acnes is also implicated in a number of medical conditions including other skin diseases, brain damage and musculoskeletal disorders.
P. acnes has been cultured from skins affected by Kawasaki disease, sarcoidosis, folliculitis and cellulitis.
When it colonizes the tissues of the eye, it causes infectious keratitis, conjunctivitis and endopthalmitis. It also causes dental infections, brain abscesses, endocarditis and peritonitis.
However, one of the most remarkable diseases caused or aggravated by P. acnes is the musculoskeletal disease complex called SAPHO.
SAPHO refers to a number of interrelated bone and joint diseases that may or may not include skin diseases. Acne is the most common skin disease experienced with SAPHO syndrome (the A in SAPHO stands for acne). Therefore, both the skin disease and musculoskeletal disease share a common factor: P. acnes.
P. acnes has been isolated from joints and bone foci. It causes bone lesions and it is believed to the responsible for the fever accompanying acne fulminans, a severe form of acne vulgaris.
P. acnes can cause some forms of arthritis and osteomyelitis although in rare cases. It is commonly introduced into joints and bones by injections and prosthetics.
Antibiotics have historically served as the first-line treatment for acne caused by P. acnes.
Both topical and oral antibiotics can be used. Topical antibiotics used for treating P. acnes include clindamycin and erythromycin. Oral erythromycin is also used for this purpose but the tetracycline antibiotics are more commonly used against P. acnes.
Tetracycline antibiotics include tetracycline, minocycline, doxycycline, oxytetracycline and lymecycline. These are broad spectrum antibiotics and, when effective, they are fast-acting.
However, antibiotic resistance has rapidly developed towards all the antibiotics used in the treatment of acne caused by P. acnes. Currently, some of these antibiotics are all but useless against this bacterium.
In order to improve the efficacy of antibiotic therapy and reduce the risks of antibiotic resistance developing, these antibiotics, but especially erythromycin and clindamycin, are combined with other anti-acne agents such as tretinoin and benzoyl peroxide.
The rising incidence of antibiotic resistance is making most prescribers forego antibiotics altogether for the treatment of acne caused by P. acnes.
Instead of directly killing off P. acnes, these other drugs try to starve it by cutting off the factors promoting its colonization of the skin.
Retinoids are the new acne drugs to prescribe for stubborn acne like the one perpetrated by antibiotic-resistant P. acnes. These drugs can either be topical or oral.
Oral retinoids usually come with serious side effects and should never be used without prescriptions.
There are 3 generations of retinoids and each successive generation is safer than the last.
First generation retinoids include isotretinoin (commonly known under the Accutane brand) and topical tretinoin. The second generation retinoids are not commonly used for treating acne but psoriasis.
Third generation retinoids include adapalene and tazarotene.
Retinoids generally reduce inflammation and remove acne comedones. They also normalized the rate of breakdown of keratin but more importantly, they reduce sebum production by killing off some sebocytes.
When its cover of dead skin cells, its nutrient of sebum and its anaerobic environment of comedones are all removed, the population of P. acnes on the skin is rapidly reduced.
Oral contraceptives containing estrogens and progestins are also effective for treat acne caused by P. acnes and so are anti-androgens such as spironolactone.
These drugs work by reducing the production of androgens, especially testosterone, in women.
These oral contraceptives also have anti-acne properties. They specifically block the effect of androgens on the sebaceous glands.
Spironolactone competes with androgens by preventing them from binding to the receptors they need. Besides reducing the activity of testosterone and its metabolites, spironolactone also reduces the serum levels of free testosterone.
The overall effect of these drugs is to reduce the production of sebum. Without its supply of excess sebum to thrive on, the population of P. acnes quickly drops off.
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