Abstract

Demodicosis is the term applied to cutaneous diseases caused by Demodex folliculorum and Demodex brevis. Demodex mites are acquired shortly after birth. They are saprophytic ectoparasites that are found primarily in areas rich in sebaceous glands, like face, scalp, neck. While human demodicosis is a skin disease sui generis, it can mimic many other inflammatory dermatoses. Therefore demodicosis are commonly underdiagnosed, and are masked behind other diagnoses such as papulopustular rosacea, erythemato telangiectasic rosacea, seborrheic dermatitis, perioral dermatitis, contact dermatitis, atopic dermatitis, phyma, seborrhea, etc. Human demodicosis is classified into a primary and secondary form by Chen and Plewig. Absence of pre-existing or concurrent inflammatory dermatosis (acne, rosacea or perioral dermatitis), abnormal increase in mite colonization in active lesions, and remission of the lesions following adequate treatment with topical or systemic acaricides/arachnicides, but not with antibiotics with antiinflammatory effects are diagnostic criteria of primary demodicosis. Secondary demodicosis is defined to skin lesions associated with an abnormal increase of Demodex mites in patients with other known skin or systemic diseases. Clinically, demodicosis has a wide range of variants and may manifest as folliculitis (Pityriasis folliculorum), papulopustular erythema (Rosacea-like demodicosis), blepharoconjunctivitis (demodectic blepharitis), and granulomatous rosacea-like demodicosis (Demodicosis gravis) The pathogenesis of human demodicosis remains largely obscure Here, we discuss the clinical manifestations, pathogenesis of demodicosis, and treatment strategies.

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