This bacterium is largely commensal and part of the skin flora present on most healthy adult humans' skin. It is usually just barely detectable on the skin of healthy preadolescents. It lives primarily on, among other things, fatty acids in sebum secreted by sebaceous glands in the follicles. It may also be found throughout the gastrointestinal tract in humans and many other animals.
P. acnes bacteria live deep within follicles and pores, away from the surface of the skin. In these follicles, P. acnes bacteria use sebum, cellular debris and metabolic byproducts from the surrounding skin tissue as their primary sources of energy and nutrients. Elevated production of sebum by hyperactive sebaceous glands (sebaceous hyperplasia) or blockage of the follicle can cause P. acnes bacteria to grow and multiply.
P. acnes bacteria secrete many proteins, including several digestive enzymes. These enzymes are involved in the digestion of sebum and the acquisition of other nutrients. They can also destabilize the layers of cells that form the walls of the follicle. The cellular damage, metabolic byproducts and bacterial debris produced by the rapid growth of P. acnes in follicles can trigger inflammation. This inflammation can lead to the symptoms associated with some common skin disorders, such as folliculitis and acne vulgaris.
The damage caused by P. acnes and the associated inflammation make the affected tissue more susceptible to colonization by opportunistic bacteria, such as Staphylococcus aureus. Preliminary research shows healthy pores are only colonized by P. acnes, while unhealthy ones universally include the nonpore-resident Staphylococcus epidermidis, amongst other bacterial contaminants. Whether this is a root causality, just opportunistic and a side effect, or a more complex pathological duality between P. acnes and this particular Staphylococcus species is not known.
P. acnes has been found in herniated discs. The propionic acid which it secretes creates micro-fractures of the surrounding bone. These micro-fractures are sensitive and it has been found that antibiotics have been helpful in resolving this type of low back pain.
P. acnes can be found in bronchoalveolar lavage of approximately 70% of patients with sarcoidosis and is associated with disease activity, but it can be also found in 23% of controls. The subspecies of P. acnes that cause these infections of otherwise sterile tissues (prior to medical procedures), however, are the same subspecies found on the skin of individuals who do not have acne-prone skin, so are likely local contaminants. Moderate to severe acne vulgaris appears to be more often associated with virulent strains.
P. acnes bacteria are susceptible to a wide range of antimicrobial molecules, from both pharmaceutical and natural sources. Antibiotics are commonly used to treat infections caused by P. acnes. Acne vulgaris is the disease most commonly associated with P. acnes infection. The antibiotics most frequently used to treat acne vulgaris are: erythromycin, clindamycin, doxycycline and minocycline. Several other families of antibiotics are also active against P. acnes bacteria, including quinolones, cephalosporins, pleuromutilins, penicillins and sulfonamides.
The emergence of antibiotic-resistant P. acnes bacteria represents a growing problem worldwide. The problem is especially pronounced in North America and Europe. The antibiotic families that P. acnes are most likely to acquire resistance to are the macrolides (e.g. erythromycin and azithromycin), lincosamides (e.g. clindamycin) and tetracyclines (e.g. doxycycline and minocycline).
The elements silver,sulfur, and copper have also been demonstrated to be toxic towards many bacteria, including P. acnes. Natural honey has also been shown to have some antibacterial properties that may be active against P. acnes.
P. acnes glows orange when exposed to Wood's light, possibly due to the presence of endogenous porphyrins. The bacterium is killed by ultraviolet light. P. acnes is also especially sensitive to light in the 405–420 nanometer (near the ultraviolet) range due to an endogenic porphyrin–coporphyrin III. A total irradiance of 320 J/cm² is found to inactivate this bacterium in vitro. This fact is used in phototherapy. Its photosensitivity can be enhanced by pretreatment with aminolevulinic acid, which boosts production of this chemical, although this causes significant side effects in humans, and in practice was not significantly better than the light treatment alone.
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