The bacterium Propionibacterium acnes, recently reclassified as Cutibacterium acnes (C. acnes), is a common resident of human skin. While C. acnes is a normal component of the skin’s microbial landscape for most people, its presence does not automatically result in acne. The development of acne lesions is determined by factors within an individual’s skin environment that allow the bacterium to proliferate.
Contagiousness Between Individuals
A frequent question is whether acne can be transmitted between people. Since C. acnes is a standard inhabitant of the skin for most individuals, acne is not considered a contagious condition. You cannot “catch” acne through casual contact like sharing towels or hugging. The development of acne is caused by an individual’s specific skin conditions, such as hormonal activity and oil production, not by the transmission of the bacterium.
Proliferation Within the Hair Follicle
The “spread” of C. acnes primarily refers to its multiplication within an individual’s hair follicles, also known as pilosebaceous units. This overgrowth is triggered by specific conditions within the pore. The bacterium is anaerobic, meaning it thrives in low-oxygen environments. A primary factor in this process is an increase in sebum, the oil produced by the skin’s sebaceous glands. Hormonal fluctuations can signal these glands to produce excess sebum, which serves as a food source for C. acnes. The bacteria produce enzymes, such as lipases, to break down the lipids in sebum for energy.
This environment is further altered by hyperkeratinization, where dead skin cells in the follicle lining do not shed properly. These cells mix with the excess sebum to form a dense plug, or microcomedone, that blocks the pore. This blockage creates the oxygen-deprived conditions ideal for C. acnes to proliferate rapidly, setting the stage for an inflammatory response.
Mechanical Transfer Across the Skin
While the main spread is proliferation within a pore, C. acnes can also be physically transferred from one area of the skin to another. This mechanical transfer can introduce the bacterium to unaffected follicles, seeding new acne lesions. Actions such as touching, picking, or popping pimples can contribute to this transfer. When a pimple is squeezed, the follicle wall can rupture, releasing its contents—bacteria, sebum, and dead cells—onto the skin or deeper into surrounding tissue.
Contaminated objects are another vehicle for transfer. Items that frequently contact the face, such as smartphones, pillowcases, and unwashed hands, can harbor the bacteria. When these objects touch the skin, they can deposit bacteria onto new areas. Maintaining hygiene for these items can help reduce this type of transfer.
The Inflammatory Response to Bacterial Growth
The visible signs of acne are not caused by the bacteria directly damaging the skin, but by the body’s immune system responding to the bacterial overgrowth. As C. acnes multiplies, it produces metabolic byproducts and proteins that act as irritants. The immune system recognizes the high concentration of C. acnes as a threat and launches an inflammatory cascade, sending immune cells to the follicle.
This immune reaction causes the characteristics of inflammatory acne lesions, such as:
- Redness
- Swelling
- Pain
- Pus
The resulting blemish is a consequence of the body’s defense mechanisms. The severity of this inflammatory response can vary among individuals, contributing to the different types of acne lesions seen.