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The Pathology of Acne Report

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Updated: Mar 29th, 2020

The Enemy – Microbes

Acne vulgaris is a widespread skin condition that affects a significant fraction of adolescents as well as some adults (Cordain et al. 2002). The condition is caused by the overgrowth of the Gram-positive anaerobic bacteria known as Propionibacterium acnes. Propionibacterium acnes are normal microflora that reside on the surface of the skin. High sebum levels in the skin contain provide favourable conditions for the growth of this bacteria hence leading to the development of the skin condition. Acne vulgaris, therefore, is not categorized under infectious diseases.

The War – Infection and Transmission of Disease

Several factors affect the pilosebaceous unit. For instance, the adolescent period leads to elevated production of androgens that cause the pilosebaceous gland to increase. Consequently, the amount of sebum secreted increases. Increased growth and development of the follicular epithelium leading to the obstruction of the pilosebaceous duct (Krautheim & Gollnick 2004). As a result, a microcomedo, which is the first acne lesion, forms. Propionibacterium acnes then inhabit the pilosebaceous gland multiply. The bacteria alongside ductal corneocytes and proinflammatory agents stimulate inflammatory reactions leading to swellings and redness.

The Defence – Host Disease

The innate immune response takes effect during the pathogenesis of acne vulgaris (Koreck et al. 2003).The pilosebaceous unit, which comprises keratinocytes and sebocytes, is an immunocompetent organ. These cells can recognize pathogens and aberrant lipid organization thereby triggering the innate immune response. Chemotactic materials produced by P. acnes draw immune cells, for example, lymphocytes, neutrophils and monocytes. The bacteria can also initiate the complement system releasing C5a, a strong chemoattractant that magnifies the immune response. Consequently, proinflammatory cytokines such as interleukin-8 and tumour necrosis factor are produced leading to inflammatory acne lesions.

The Casualty – Clinical Manifestations

Inflammatory or noninflammatory acne lesions are formed depending on the production of proinflammatory agents during the immune response. Noninflammatory acne is characterized by the formation of comedones and microcomedones while inflammatory acne is marked by papules, pustules and nodules (Tanghetti 2013). These lesions are confined to areas with numerous sebaceous glands such as the nose, cheeks, forehead, back and chest.

The Victory – Diagnosis, Treatment and Control

Acne is diagnosed by physical examination, laboratory tests and patient history. Systemic (oral) and topical treatments are available for acne treatment. Topical treatments include ointments and chemicals such as benzoyl peroxide that mitigate inflammation and kill bacteria. Antibiotics such as erythromycin, clindamycin and metronidazole can be administered orally and topically. Hormonal therapy is also used to regulate the production of androgens particularly in women. A low-fat diet is also encouraged.

Exam Question and Answer

John Pimple is a 14-year-old high school student who has seen an increase in acne on his jaw line and forehead over the last 6 months and decides to see his local GP about it.

  1. Provide one recommendation for treatment and one recommendation for lifestyle change to reduce symptoms.
    John Pimple should apply a topical antibiotic such as benzoyl peroxide and wash his face gently with warm water and soap twice a day.
  2. Provide a key factor in the innate defence that causes the inflammatory response associated with the symptoms of the disease.
    Bacteria trigger the complement system that promotes secretion of proinflammatory cytokines that cause inflammation and pustules.
  3. Choose the most correct answer from the below:
    1. The acne is a result of the contagious H. Pylori invading the epithelial layers and eliciting an inflammatory response
    2. Acne is the result of latent viral particle which presents when the hosts immune system is vulnerable
    3. Baceria propionibacteria acnes increase in concentration in sebaceous glands after a build up of sebum.
    4. Hormones in post adolescence build up in epithelial cell gland and cause inflammation


Cordain, L., Lindeberg, S., Hurtado, M., Hill, K., Eaton, B., & Brand-Miller, J., 2002, “Acne vulgaris: a disease of western civilization,” Archives of Dermatology, vol. 138 no. 2002, pp. 1584-1590.

Koreck, A., Pivarcsi, A., Dobozy, A., & Kemény, L., 2003, “The role of innate immunity in the pathogenesis of acne,” Dermatology, vol.206 no. 2003, pp. 96-105.

Krautheim, A., & Gollnick, P. M. H, 2004, “Acne: topical treatment,” Clinics in Dermatology, vol. 22 no.5, pp.398-407.

Tanghetti, E. A., 2013, “The role of inflammation in the pathology of acne,” Journal of Clinical Aesthetic Dermatology, vol.6 no.9, pp. 27-35.

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