Demodex
DEMODECTIC ERUPTIONS: MORE THAN YOU MITE HAVE IMAGINED
By Warren R. Heymann, MD, FAAD
April 26, 2023
Vol. 5, No. 17
The pathophysiology of Demodex mites is eloquently discussed by Aktaş Karabay and Aksu Çerman: "D. folliculorum and D. brevis, the two Demodex species, are ubiquitously found on the normal skin of adult humans, particularly in the pilosebaceous units of the face. D. folliculorum resides within the hair follicle, whereas D. brevis is found predominantly in the sebaceous and meibomian glands. Demodex mites penetrate into skin cells (particularly the keratinocytes that line pilosebaceous follicles) and ingest their contents. Demodex mites feed on the sebum and cellular proteins that are obtained by protease containing the salivary enzymes of the mites. The lipase enzymes of Demodex are also thought to play a role in digesting bacteria or other microorganisms in addition to the digestion of lipid material. The enzymatic process leads to degradation of the follicular epithelium, which may result in perifollicular inflammation. Demodex mites may also cause mechanical blockage of the follicle opening. Moreover, it is thought that extrafollicular mites may induce a granulomatous foreign body reaction through their chitinous exoskeleton. Dying mites are thought to trigger an immune response in the host by releasing their internal contents and the chitinous exoskeletons of degrading, dying mites, followed by inflammatory changes. Demodex mites may also suppress the innate immune response of the hosts that provide for their survival. It has been shown that the Tn antigen, which is a carbohydrate coating providing protection for cancer cells and parasites from immunity, is expressed by Demodex mites. Demodex mites are also shown to affect the secretion of inflammatory cytokines, such as IL-8 and TNF-alpha and TLR expression, through the interaction with cells of the pilosebaceous unit." (1) Factors that influence the proliferation of D. folliculorum and D. brevis include age, marked immunosuppression, sebaceous gland hyperplasia, and hypervascularization-related factors. (2)
The role of immunosuppression (or immunodysregulation) in demodectic eruptions (demodicidosis) cannot be overemphasized. Recent examples include:
What makes demodectic eruptions so intriguing is their element of surprise in disorders where you were not expecting it. Consider the following examples:
Location. I was not familiar with demodicidosis of the nipple until a colleague sent in a dermatopathology specimen to rule out Paget disease of the breast. Demodex infestation of the nipple may present with pruritus alone (6,7), although histologically perifollicular inflammation accompanies the intrafollicular mites. (6) Vulvar demodicidosis may cause suppurative granulomatous disease on the vaginal labia where Fordyce spots are infiltrated by the mites. These lesions may become tender and drain; in the case reported by Hedberg et al, there was a good therapeutic response to oral ivermectin and topical metronidazole. (8)
Demodex-induced follicular mucinosis (FM) mimicking folliculotropic mycosis fungoides.Trager et al present four cases of FM due to Demodex, two of whom demonstrated clonal T-cell receptor gene rearrangements. Cases responded to mite-targeted therapy, which mycosis fungoides would not. Aside from the pathophysiology of Demodex infestations previously discussed, the authors report that "a bacterium, Bacillus oleronius, has been isolated from Demodex. Release of Bacillus proteins leads to increased neutrophil signaling, activation, chemotaxis, and pro-inflammatory cytokine release, possibly contributing to the development of FM." (10)
What has escaped me (until now) is considering the possibility that demodicidosis may cause facial hyperpigmentation. The usual differential diagnosis includes melasma, post-inflammatory hyperpigmentation, drug-induced hyperpigmentation, lichen planus actinicus, or lupus. Ayres and Ayres encountered 12 patients with "blotchy, brownish pigmentation of the face in association with the characteristic dryness and follicular scaling" attributed to Demodex infestation. (In their treatise, they also discuss similar cases by Dubreuilh from 1919!) (11) Neema et al detail 7 cases of facial frictional melanosis. Demodex was suspected on dermoscopy and confirmed histologically. Patients were treated with oral ivermectin and topical metronidazole. Within a month, facial pruritus resolved in all cases and pigmentation improved significantly in 3 patients. (12) Feuerman et al studied demodicidosis-associated hyperpigmentation in 19 patients (13 male) aged 42-76 years, all with Fitzpatrick skin type 3-4. All presented with mostly asymptomatic dusky, brown-gray, facial pigmentation, localized or diffuse with background erythema in 36.8% of cases, and skin roughness in 26.3%. Dermoscopy demonstrated characteristic findings of white gelatinous or opaque protrusions from hair follicles or infiltration of follicular openings with an amorphic material. A specific finding was perifollicular and reticulated pigmentation of the affected areas. Findings were confirmed on microscopic (n = 7) and histopathologic (n = 5) studies. Anti-demodectic treatment (with 12 patients using 1% ivermectin cream) led to complete (73.6%) or partial (23.4%) resolution of pigmentation within 2 years. The authors propose the term "pigmented demodicidosis" that should be considered in the differential diagnosis of facial hyperpigmentation noted above. (13)
In conclusion, although dermatologists are familiar with "classical" disorders such as rosacea where Demodex might (yes, I meant might) play a role, there are other conditions where the mite might be mighty important.
Point to Remember: Although the precise role of Demodex mites remains to be defined in disorders such as rosacea, these mites could play a role in other diseases, the most under-recognized possibly being so-called pigmented demodicidosis.
Our expert's viewpoint
Lorraine L. Rosamilia, MD, FAAD
Geisinger Health System – State College, PA
One of my favorite moments of residency was when my co-resident recorded a live video of a Demodex mite wriggling through the oil immersion under the microscope and then set the video to music for one of our conferences. The organism is a quandary; so dynamic and ubiquitous but largely underappreciated and poorly understood in its true role (or bystander role) in many inflammatory conditions. For example, one of my patients was taking 'horse ivermectin' (from his farm supply to ward off COVID-19) and stated that his seborrheic keratoses also melted away. Who knows?! One thing is for sure: these mites are everywhere, they are here to stay, and they know how to party. (See the Twitter video from @ScienceChannel for proof!)
Rina Segal, MD
Dermatology department, Rabin Medical Center, Israel
The Demodex mite plays a role in disease pathogenicity of various facial and extra-facial dermatoses, including the many variants of rosacea, but the extent of its contribution to disease pathogenicity is still under debate. While some think Demodex is a key player, others argue it is just an innocent bystander. As a medical dermatologist who successfully treats patients with skin manifestations of demodicidosis using anti-demodectic therapies and studies Demodex pathogenicity in skin diseases for more than 20 years, I belong to the first group; Demodex is a key player in a spectrum of dermatoses given the clinical picture, the demonstration of the Demodex mites in affected skin and the beneficial response to anti-demodectic therapy. Diseases like spinulosis of face, pityriasis folliculorum, demodex dermatitis, perioral dermatitis, acneiform eruptions, facial pustulosis, and the many variants of rosacea are all grouped under the causative agent: demodex.
Recently, we described facial hyperpigmentation associated with Demodex infestation and proposed the name "pigmented demodicidosis." It is noteworthy that the very first descriptions of Demodex infestation in human were forms of pigmented demodicidosis: "Demodex folliculorum e ipercromia cutanea" described in 1898 by De Amicis and "Pigmentation cutanee par le Demodex folliculorum" (described by Dubreuilh in 1901). In our cohort, all patients had darkly pigmented skin (Fitzpatrick 3-4), some with mild erythema, and dermoscopic evidence of Demodex infestation. Histopathological evaluation showed melanophages and multiple Demodex mites in hair follicles. Thus, the hyperpigmentation probably represents post-inflammatory hyperpigmentation and the Demodex is involved in inflammation. The prompt and beneficial response to anti-demodectic treatment furthermore confirmed this mite as the causative agent.
By acknowledging Demodex as a key player in different clinical manifestations, and with the aid of dermatoscope, it becomes an easy task to diagnose and relief various, mostly facial, annoying dermatoses including rosacea. There are many anti-demodectic agents, and the most potentin my experience is topical ivermectin. Yet, starting with anti-demodectic agent application on inflamed skin infested with Demodex frequently causes disease worsening, (perhaps due to sort of a Herxheimer reaction). Therefore, we recommend starting with a mild steroid cream for few days, followed by miticidal cream for a long period of time. The gratitude of your patients will soon arrive.
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posted by dermatica at
May 02, 2023
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