Case Letter

Crusted Demodicosis in an Immunocompetent Patient

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Practice Points

  • The Demodex mite, believed to be a commensal species in humans, has the ability to shift to a pathologic form in immunocompromised patients.
  • Demodicosis can manifest in a variety of forms including pityriasis folliculorum, rosacealike demodicosis, and demodicosis gravis.


 

References

To the Editor:

Demodicosis is an infection of humans caused by species of the genus of saprophytic mites Demodex (most commonly Demodex brevis and Demodex folliculorum) that feed on the pilosebaceous unit.1Demodex mites are believed to be a commensal species in humans; an increase in mite concentration or mite penetration of the dermis, however, can cause a shift from a commensal to a pathologic form.2 Demodicosis manifests in a variety of forms, including pityriasis folliculorum, rosacealike demodicosis, and demodicosis gravis. The likelihood of colonization increases with age; the mite rarely is observed in children but is found at a rate approaching 100% in the elderly population.3 It is hypothesized that manifestation of disease might be due to a decrease in immune function or an inherited HLA antigen that causes local immunosuppression.4

A 51-year-old man who was otherwise healthy presented to our clinic with a crusting rash on the face of 9 weeks’ duration. The rash began a few days after he demolished a rotting wooden shed in his backyard. Lesions began as pustules on the left cheek, which then developed notable crusting over the next 5 to 7 days and spread to involve the forehead, nose, and right cheek (Figure 1A).

Figure 1. Crusted demodicosis. A, Pink to erythematous papules and pustules with crusting on the forehead, nose, and cheeks bilaterally, with greater involvement of the left side. B, Resolution of crusted papules and pustules after 6 weeks of therapy with oral ivermectin and ivermectin cream 1%. There was mild recurrence of pink papules on the forehead, as the patient had been without topical treatment.

The patient had no underlying immunosuppressive disease; a human immunodeficiency virus screen, complete blood cell count, and tests of hepatic function were all unremarkable. He denied a history of frequent or recurrent sinopulmonary infections, skin infections, or infectious diarrheal illnesses. He had been seen by his primary care physician who had treated him for herpes zoster without improvement.

At our initial evaluation, biopsy was performed; specimens were sent for histopathologic analysis and culture. Findings included a dermal neutrophilic inflammation, a dense perivascular and perifollicular lymphoplasmacytic infiltrate with foci of neutrophilic pustules within the follicles (Figure 2), numerous intrafollicular Demodex mites (Figure 3), perifollicular vague noncaseating granuloma, and mild sebaceous hyperplasia. Grocott methenamine-silver stain and acid-fast bacilli stain were negative.

Figure 2. A dense dermal perivascular and perifollicular lymphoplasmacytic infiltrate with foci of neutrophilic pustules within the follicles (H&E, original magnification ×20).

Figure 3. Numerous intrafollicular Demodex mites (H&E, original magnification ×100).

Review of clinical and pathological data yielded a final diagnosis of crusted demodicosis with a background of rosacea. The patient was ultimately treated with a single dose of oral ivermectin 15 mg with a second dose 7 days later in addition to daily application of ivermectin cream 1% to affected areas of his rash. He had notable improvement with this regimen, with complete resolution within 6 weeks (Figure 1B). The patient noted mild recurrence 14 to 21 days after discontinuing topical ivermectin.

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