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Acne and Bacteria
Although acne is not contagious, some bacteria play a central role in the progression of the skin disease. Find out which bacteria cause acne and how to treat bacterial acne.
Acne vulgaris is a common skin disease that first appears during puberty and then disappears later with treatment. Some people, however, still experience acne long into adulthood.
Acne is differentiated from other skin diseases by the lesions that appear on the skin.
These lesions include comedones such as whiteheads and blackheads; pustules and papules; nodules and cysts. Acne also causes seborrhea which refers to the red, scaly appearance of the skin as well as scars especially in its severe forms.
Acne affects the areas of the skin with the highest concentration of sebaceous follicles. Therefore, it mostly affects the face, neck, upper chest and back. However, severe acne can also spread to other parts of the body such as upper arms, thighs and buttocks.
There are different causes of acne including genetics, stress, diets, drugs and diseases but these causes are presentations of two interconnected root causes:
Both causes are interwoven and anti-acne medications treat either or both causes.
Acne vulgaris is not an infectious disease even though it can be caused by some bacteria.
The types of microbes that can cause acne are those that can colonize and multiply in the follicular ducts. There are only a few microorganisms capable of this feat.
Melassezia can be excluded from this discussion for 2 reasons. First, it is not a bacteria species but a fungi species. Secondly, acne does not respond to anti-fungal therapy, therefore, this fungus must not play an important role in the formation and progression of acne.
Both staphylococcus and peptostreptococcus bacteria are difficult to treat because they develop resistance to antibiotics very quickly (usually within the first week of antibiotic therapy).
However, one of the 3 most important acne-causing bacteria, Staphylococcus epidermis, belongs in this family.
Propionibacterium bacteria are the most studied microbes in acne research. The two prime examples of this bacteria family are P. acnes and P. granulosum.
The population of acne-causing bacteria increases sharply following the production of excess sebum. This is because sebum is the ideal growth environment for these bacteria.
While some of the excess sebum pushed towards the skin surface is trapped inside skin pores, this give rise to comedones such as whiteheads and blackheads. However, some acne-causing bacteria colonizing the follicular ducts are also trapped alongside.
The bacteria trapped along with sebum in comedones produce enzymes that break down fat.
By producing proinflammatory lipids from sebum, these bacteria not only sustain the growth of acne comedones but also cause the deep tissue damage in the dermis that leads to the appearance of inflammatory acne bodies such as papules, pustules, nodules and cysts.
In a self-sustaining cycle involving acne-causing bacteria and excess sebum production, acne vulgaris progresses rapidly.
These bacteria cause an endless wave of inflammation through multiple means. For example, they not only produce inflammatory lipids but also antigens that trigger inflammatory immune reactions.
Bacteria also increase the rate of keratinization. This means that they cause the damage of keratinocytes and accelerate the breakdown of keratin. Therefore, there is a massive increase in the production of dead skin cells.
Propionibacterium acnes is the most important of all the acne-causing bacteria.
It is a non-motile, rod-shaped, anaerobic gram-positive bacterium that is known to break down sugar into propionic acid. P. acnes is the chief bacteria colonizing the parts of the skin with high concentrations of sebaceous glands.
P. acnes is not newly introduced at the beginning of acne breakouts. Rather, it is a natural resident of the skin and it remains on the skin from birth to death.
It is still not clear whether a mutated strain of P. acnes causes acne and is introduced to the skin later, or whether some of the harmless bacteria become virulent under the conditions created by the changing skin nature associated with adolescence.
However, once the acne-causing strain of P. acnes colonizes the skin, it dominates and contributes to perpetuating the production of excess sebum and all other conditions necessary for its growth.
Acne is not even the only disease associated with P. acnes.
The bacterium is implicated in other skin diseases such as cellulitis, folliculitis, sarcoidosis and Kawasaki disease. It has also been found to contribute to SAPHO and the related musculoskeletal diseases such as osteomyelitis and arthritis.
P. acnes also contributes to endopthalmitis, conjunctivitis, endocarditis, meningitis and gingivitis.
There are two mechanisms by which P. acnes causes acne:
For example, the release of lipases by acne-causing bacteria is responsible for the high content of free fatty acids in the sebum found on the skins of acne sufferers. Lipases convert the triglycerides in sebum to free fatty acids.
P. acnes specifically resist phagocytosis. This means it resist being swallowed by specialized cells of the immune system. Even when swallowed, it can stay virulent inside these cells for a long while waiting to be expelled again.
P. acnes is also directly involved in arousing inflammatory response from the immune system.
There are clear evidences that the antigens produced by this bacterium trigger inflammatory hypersensitivity reactions from the immune system. In fact, antibodies specific to this antigens are seen in large numbers in patients with severe acne.
When P. acnes triggers inflammatory responses, lymphocytes are the first immune cells sent to the acne lesions where the bacterium has caused some damage.
Lymphocytes are sent to the skin when P. acnes damages the keratin cells as well as the cells of the sebaceous glands.
Following this, the immune system sends specialized T cells. Different studies have identified CD4+, CD1+ and CD8+ cells present in acne lesions.
Therefore, P. acnes causes the local inflammation that gives rise to inflammatory acne lesions. It is the immune cells sent to these sites of injury that give rise to the pus filling up some acne lesions.
Antibiotics are the most commonly prescribed drugs for treating acne bacteria.
Besides antibiotics, topical antibacterial agents such as benzoyl peroxide and salicylic acid may also be used. They are especially combined with antibiotics to reduce the development of antibiotic resistance and prevent treatment failure.
Some of antibiotics commonly used to kill off acne-causing bacteria are:
Since P. acnes and S. epidermis are the 2 most important bacteria in the development of acne, they are also the ones closely studied for antibiotic resistance.
The emergence of antibiotic resistance to these drugs is well charted. For example, there was no resistance to antibiotics from strains of P. acnes in the early 1970s but later in that decade researchers placed the resistance of P. acnes to clindamycin and erythromycin at 20%.
Over the next 2 decades, resistance to these drugs jumped to 70% and in some countries, resistance was as high as 90%.
S. epidermis even showed greater resistance to erythromycin than P. acnes.
However, newer drugs such as minocycline have lower antibiotic resistance but resistance to that antibiotic is rapidly growing. Currently, multi-drug resistant P. acnes and S. epidermis have been found in acne patients who have never even taken antibiotics for their acne breakouts.
Cross-resistance is also becoming common especially between antibiotics in the same class such as erythromycin and clindamycin.
Antibiotic resistance is also spreading from acne-causing bacteria to non-acne-causing bacteria. For example, there are mounting evidences that S. epidermis is transferring the genetic materials that give it antibiotic resistance to S. aureus.
Fortunately, while S. epidermis can transfer its antibiotic resistance through genetic materials, P. acnes can only mutate to gain the ability to resist antibiotics. This means that it takes P. acnes longer to gain antibiotic resistance while S. epidermis can gain the same ability in one generation.
Besides simple antibiotic resistance, there is also the chance of opportunistic infection following long-term antibiotic therapy.
This occurs when the antibiotic has effectively cleared off gram-positive bacteria such as P. acnes. This then leaves room for gram-negative, drug-resistance bacteria.
This effect is responsible for gram-negative folliculitis, a severe form of acne vulgaris.
As antibiotics resistance increases within the population, physicians are shying away from prescribing antibiotics for acne. Those who still prescribe antibiotics usually combine them with topical antiseptic and antibacterial agents.
When antibiotics fail to control acne, physicians usually move on to prescribing topical retinoids such as adapalene or oral retinoids such as isotretinoin or Accutane.
However, retinoids especially isotretinoin, can have very serious side effects and need to be taken only under the close supervision of the prescribing dermatologist.
Natural acne remedies with antibacterial properties are another option for treating bacteria acne. These natural remedies are not only just as effective, they are safer and there is very little chance of bacteria developing resistance to the antibacterial phytochemicals they contain.
Honey is an especially good example of natural antibacterial acne remedy.
Its antibacterial activity is due to a number of factors including the presence of such antibacterial compounds like methylglyoxal or MGO; its ability to dehydrate bacterial cells; and its generation of hydrogen peroxide on the skin surface.
There are also oral acne supplements such as Actimine that are also used for treating bacterial acne.
Actimine, for example, contains minerals such as zinc (which has an antibacterial property), vitamin A (from which powerful anti-acne drugs such as isotretinoin is made), MSM (methylsulfonyl methane) and gum guggul.
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