Human Demodicosis: Revisit and a Proposed Classification

W. Chen; G. Plewig

Disclosures

The British Journal of Dermatology. 2014;170(6):1219-1225. 

In This Article

Treatment

Treatment of human demodicosis is so far based on single case reports and is weakly evidence based, due mainly to the following intertwined reasons: (i) lack of ideal in vitro or ex vivo culture systems on which to test the effectiveness of the drugs and their minimal inhibitory concentrations; (ii) clinical confusion of infestation (primary demodicosis) and inflammatory disease (rosacea with or without secondary demodicosis); and (iii) the dual effects, both anti-inflammatory and antimicrobial, of many agents. Ivermectin is purely acaricidal and has proven to be the treatment of choice for canine and human demodicosis.[57–59] However, the dose of oral ivermectin recommended for the treatment of canine generalized demodicosis is much higher (0·3–0·6 mg kg−1 daily for 10–33 weeks) than that used in humans (0·2 mg kg−1 single dose).[60] Although topical use of other acaricides, such as permethrin 5%, benzyl benzoate 10–25%, crotamiton 10%, lindane 1% or malathion 0·5%, has been approved for the treatment of scabies,[61] current evidence for the efficacy of these acaricides in the treatment of demodicosis is very limited. The superiority of topical benzyl benzoate 10% in killing Demodex mites was demonstrated only in a small number of patients.[6] It is unclear whether treatment of rosacea with systemic low-dose tetracycline or macrolide antibiotics, topical azelaic acid 15–20% or topical metronidazole 0·75–2% is due mainly to anti-inflammatory or also partially acaricidal effects. The hypothesis that the tetracycline drugs can influence the proliferation of Demodex mites by targeting the endosymbiotic B. oleronius remains to be confirmed.[62] Failure of such treatments is not uncommonly encountered in genuine primary demodicosis.[57–59] The optimal dose of systemic metronidazole in treating demodicosis remains to be determined and should be compared with that of ivermectin. It would be interesting to see whether moxidectin, approved for treatment of generalized canine demodicosis and currently under development for the treatment of human onchocerciasis, can be used topically to treat human demodicosis.[63] Development of arachnicidal resistance has never been discussed, while the method of the repopulation of the Demodex mites after arachnicidal killing remains elusive.

In conclusion, human Demodex mites are the most prevalent human parasites, enjoying a lifelong symbiotic residence in human beings. The physiological role of human Demodex mites in healthy skin remains enigmatic, and the way in which they evade immune surveillance, especially the innate immune system, can be crucial for the understanding of human–parasite interactions. The typical clinical manifestations and specific therapeutic response to pure acaricides, such as ivermectin, suggest that primary human demodicosis is a disease sui generis. Induction of inflammation is the essential step in the pathogenesis. The proliferation of Demodex mites, activation of unknown virulence factors and the pathogenic role of endosymbionts in the mites are core issues that warrant intensive investigation. Clinical distinction from other mimicking inflammatory dermatoses, such as papulopustular rosacea or perioral dermatitis, is important. Effective acaricidal drugs and their optimal dosage in killing Demodex mites remain to be determined and standardized. Advancement in this field is hampered by the lack of appropriate in vitro or in vivo models for experimental studies. Recognition of human demodicosis as a primary disease will promote further development of novel therapeutic strategies.

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