Facial demodicosis

ARTICLE

Auteur(s) : Kamiar ZOMORODIAN¹, Mohsen GERAMISHOAR¹, Farshid SAADAT², Bita TARAZOIE¹, Mehdi NOROUZI², Sassan REZAIE¹

¹ Div. of Molecular Biology, Dept. of Medical Mycology &Parasitology, 
² Div. of Immunology, Dept. of Pathobiology, School of Public Health and Institute of Public Health Research, Tehran University of Medical Sciences, P.O. Box 14155-64410 Tehran, Iran

Article accepted: 01/12/2003

Demodicosis is one of the rare infections of the human skin especially in the facial area, which is characterized by erythemato-macular pruriginous lesions. Its causative agents are Demodex mites which belong to the family Demodicidae of the class Arachnida in the order Acarina [1]. The mite Demodex spp., lives around hair follicles or in the secretory ducts of sebaceous glands connected to the hair follicles of humans [1-3]. The incidence of demodicosis steadily increases with the individual’s age. Only two specious of Demodex (D. follicullorum and D. brevis) have been identified in humans [1]. They have been implicated in at least three facial conditions: Pityriasis follicullorum, Rosacea-like demodicosis and so called demodicosis gravis [1, 4-6].

Case

A 24-year-old man presented with rosacea-like papulovesicular lesions on his forehead and cheeks (Fig. 1). He had received several treatments for rosacea for about 4 years. After unsuccessful treatment for a long time, he was referred to the mycology department with suspicion of cutaneous fungal infection. Following scraping of the lesions, wet mount preparation was made by KOH 20%. Several mites were observed with sizes varies from 0.1 mm to 0.4 mm in direct examination of clarified scales and Demodex was finally identified as the causative agent (Fig. 2). Disappearance of facial mites and complete recovery was achieved by topical treatment with 5% permethrin cream for 6 weeks.

Discussion

Demodex folliculorum is a saprophytic mite of the human pilosebaceous unit. The preferred sites are facial skin, forehead, cheeks, eyelashes and external ear channels [2]. Infestation with them may frequently be free of symptoms. However, suppurative or granulomatous reactions and inflammation may occur in acute and chronic demodicosis in humans [2, 5, 7].
The highest incidence of demodicosis is seen in the age-range 20-30. This is concomitant with increasing sebum excretion rate, which reaches its maximum level between the ages of 16 and 40 years [3].
The participation of Demodex in the pathogenesis of skin lesions has long been a matter of debate. Although Demodex is usually considered as a non-pathogenic parasite in parasitological textbooks, recent research has proved that Demodex is associated with many pathogenic kinds of skin conditions [4, 8, 9]. Our case tentatively illustrates the pathogenic potential of Demodex, inasmuch as it does not explain how such a common parasite is able to produce such a rare disease.
Some papers deal with the density of the mite population, assuming that increased density is correlated with the amplification of its irritating action and in turn can provoke a perifollicular inflammation and clinical manifestation [4, 6, 10, 11]. Proper diagnosis rests on the demonstration of large numbers of mites in the skin. Undoubtedly, infestation with D. folliculorum, particularly in large numbers, causes rosacea-like demodicosis [12, 13]. There is also some evidence of tissue damage in association with Demodex mites. Moreover, granulomatous reactions and inflammation may be considered, at least, as a secondary complicating factor in the pathogenesis of the lesions [2, 10, 12].
Research has also shown that people or animals with weak immune systems are more prone to be infested with the mite [14-17]. However, our case had no prior history of immune system disorders.
The clinical pictures of demodicosis, rosacea and some mycotic infections (i.e. Tinea) are so overlapping that they sometimes lead to inappropriate treatment [18]. Administration of corticosteroids as an alleviative treatment of rosacea-like papulovesicular lesions is not only unable to cure demodicosis but also promotes exacerbation of symptoms due an increase in the Demodex burden [13]. Considering the differences in the treatment of rosacea and demodicosis, laboratory examinations are thus imperative for precise diagnosis prior to treatment. Otherwise, as in our case, if the infection is not diagnosed properly, it may last for many months or years.
In conclusion, many criteria may be involved in the alteration of these saprophytic mites to the pathogenic form, including increased mite density and its metabolites, immunodeficiency disorders, HIV infection and corticosteroid administration.
Therefore, these triggering factors should be considered in the management of facial skin disorders to avoid the complication of lesions and inflammatory reactions due to an increased number of demodex mites. n

References

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18. Piewing G. Imitators of rosacea. J Euro Acad Derm Venero 1995; 5:S40.