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Infectious Disease and Microbiology – Acne Vulgaris
Acne vulgaris (common acne) is a chronic inflammatory disorder of the pilosebaceous unit, particularly the sebaceous follicles. It is characterized by comedones, papules, pustules, nodules, and in more severe cases, scarring. The condition primarily affects areas rich in sebaceous glands, including the face, neck, chest, upper back, and upper arms.
Acne is one of the most common skin diseases, affecting more than 85% of individuals at some point between adolescence and early adulthood, with a mean age of approximately 24 years. It accounts for up to 2 million office visits annually among adolescents aged 15–19 years. A major risk factor is increased responsiveness of sebaceous glands and keratinocytes to androgenic hormones, particularly during puberty. Elevated androgen levels such as testosterone, dehydroepiandrosterone sulfate (DHEAS), or androstenedione may worsen acne severity, especially in women.
The pathophysiology involves inflammatory changes within sebaceous follicles, leading to accumulation of lipid-rich sebum and proliferation of Cutibacterium acnes (formerly Propionibacterium acnes), a Gram-positive anaerobic bacterium that normally exists in low numbers on the skin. Overgrowth of this organism within the follicle triggers inflammation, follicular rupture, and extension of inflammation into the surrounding dermis. This process results in the formation of papules, pustules, and nodules.
Clinically, patients present with open comedones (blackheads) or closed comedones (whiteheads). As inflammation progresses, lesions may become painful and form pustules or nodules. Scarring suggests more aggressive disease. Acne is classified as mild when primarily noninflammatory comedones are present, moderate when inflammatory papules and pustules affect larger skin areas, and severe when large painful nodules with potential scarring are present.
Treatment depends on severity. Mild to moderate acne often responds to topical therapy, including retinoids, benzoyl peroxide, and topical antimicrobials. Retinoids reduce sebaceous gland activity and normalize follicular keratinization. Benzoyl peroxide acts as a bactericidal agent and is often combined with topical antibiotics to reduce resistance. More severe cases may require oral antibiotics such as doxycycline, minocycline, tetracycline, trimethoprim-sulfamethoxazole, erythromycin, or clindamycin, although resistance has become increasingly common.
For severe nodulocystic acne or cases associated with scarring, oral isotretinoin is indicated. It reduces sebaceous gland size and sebum production, inhibits bacterial growth, and has anti-inflammatory properties. However, isotretinoin is highly teratogenic and may cause hypertriglyceridemia. Women of childbearing age must use two forms of contraception during treatment. Reports have also suggested possible associations with mood changes.
Additional therapies may include spironolactone or oral contraceptives in patients with hyperandrogenism. Intralesional corticosteroids can be used for severe inflammatory nodules. With appropriate treatment and adherence, most patients experience significant improvement, and early management helps reduce the risk of permanent scarring.
Acne vulgaris (common acne) is a chronic inflammatory disorder of the pilosebaceous unit, particularly the sebaceous follicles. It is characterized by comedones, papules, pustules, nodules, and in more severe cases, scarring. The condition primarily affects areas rich in sebaceous glands, including the face, neck, chest, upper back, and upper arms.
Acne is one of the most common skin diseases, affecting more than 85% of individuals at some point between adolescence and early adulthood, with a mean age of approximately 24 years. It accounts for up to 2 million office visits annually among adolescents aged 15–19 years. A major risk factor is increased responsiveness of sebaceous glands and keratinocytes to androgenic hormones, particularly during puberty. Elevated androgen levels such as testosterone, dehydroepiandrosterone sulfate (DHEAS), or androstenedione may worsen acne severity, especially in women.
The pathophysiology involves inflammatory changes within sebaceous follicles, leading to accumulation of lipid-rich sebum and proliferation of Cutibacterium acnes (formerly Propionibacterium acnes), a Gram-positive anaerobic bacterium that normally exists in low numbers on the skin. Overgrowth of this organism within the follicle triggers inflammation, follicular rupture, and extension of inflammation into the surrounding dermis. This process results in the formation of papules, pustules, and nodules.
Clinically, patients present with open comedones (blackheads) or closed comedones (whiteheads). As inflammation progresses, lesions may become painful and form pustules or nodules. Scarring suggests more aggressive disease. Acne is classified as mild when primarily noninflammatory comedones are present, moderate when inflammatory papules and pustules affect larger skin areas, and severe when large painful nodules with potential scarring are present.
Treatment depends on severity. Mild to moderate acne often responds to topical therapy, including retinoids, benzoyl peroxide, and topical antimicrobials. Retinoids reduce sebaceous gland activity and normalize follicular keratinization. Benzoyl peroxide acts as a bactericidal agent and is often combined with topical antibiotics to reduce resistance. More severe cases may require oral antibiotics such as doxycycline, minocycline, tetracycline, trimethoprim-sulfamethoxazole, erythromycin, or clindamycin, although resistance has become increasingly common.
For severe nodulocystic acne or cases associated with scarring, oral isotretinoin is indicated. It reduces sebaceous gland size and sebum production, inhibits bacterial growth, and has anti-inflammatory properties. However, isotretinoin is highly teratogenic and may cause hypertriglyceridemia. Women of childbearing age must use two forms of contraception during treatment. Reports have also suggested possible associations with mood changes.
Additional therapies may include spironolactone or oral contraceptives in patients with hyperandrogenism. Intralesional corticosteroids can be used for severe inflammatory nodules. With appropriate treatment and adherence, most patients experience significant improvement, and early management helps reduce the risk of permanent scarring.
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