Diverse clinical presentations of demodicosis: A clinicodermoscopic study

INTRODUCTION

Demodicosis is caused by the overpopulation of Demodex mites, primarily Demodex folliculorum and Demodex brevis, which are part of the normal human microbiome. These mites inhabit hair follicles and sebaceous glands, especially in the facial region. While Demodex mites are typically asymptomatic in small numbers, their proliferation can lead to inflammatory skin diseases.^[1] The skin manifestations thus caused are included under the umbrella term “demodicosis.” Clinically, the condition may present as facial erythema, scaling, papules, and pustules, mimicking other dermatoses such as rosacea, seborrheic dermatitis, and perioral dermatitis. Clinical manifestations of demodicosis appear to be spectral, with pityriasis folliculorum having a profuse number of mites but a low host immune reaction at one pole and papulopustular rosacea with an exaggerated immune response against mite at the other pole.^[2] Several factors contribute to Demodex overgrowth, including local immune dysregulation, sebaceous gland hyperactivity, and external triggers like prolonged use of topical corticosteroids.^[3,4] Corticosteroid use, in particular, has been associated with local immunosuppression of the skin, promoting an imbalance between Demodex and other microorganisms. Secondary demodicosis may occur in individuals with underlying skin diseases like rosacea and acne or in those with immunosuppressive conditions, whereas primary demodicosis typically occurs in otherwise healthy individuals.^[5]

Diagnosis of demodicosis can be confirmed by standardized skin surface biopsy (SSSB), which quantifies the number of mites per square centimeter. A mite density exceeding five per square centimeter is considered diagnostic.^[6] The present study detailed 11 patients diagnosed with demodicosis over a 1-year period, focusing on clinical presentations, the potential role of corticosteroid misuse, and the effectiveness of acaricidal treatments. Through this study, we aimed to broaden the understanding of demodicosis, especially in clinical scenarios where it mimics other dermatological conditions.

MATERIALS AND METHODS

The study was a retrospective, record-based analysis conducted after obtaining clearance from the Institutional Ethics Committee (letter No. HIMS/RC/2024/243). The inclusion criteria included all patients clinically suspected of demodicosis with more than five Demodex mites visualized in a square centimeter area on SSSB, seen from January 2023 to December 2023. Detailed information regarding age, gender, disease duration, and morphology of lesions was noted from their case records. Information regarding comorbidities and history of topical corticosteroid abuse was also recorded. Their dermoscopic images were retrieved from the database and were analyzed (DermLite DL4, iPhone 14 Pro). Cases lacking good-quality dermoscopic images were excluded from the study. Patients were categorized as having primary demodicosis in the absence of any underlying skin or systemic disease and secondary demodicosis if a preexisting dermatosis, such as rosacea, perioral dermatitis, or topical steroid abuse, was present.

SSSB was done as a routine in the department of dermatology in patients suspected to have primary demodicosis without pre-existing or concurrent inflammatory disease presenting with pityriasis folliculorum (yellow-white fine scales at the base of hair follicles giving a sandpaper feel), papulopustular or nodular demodicosis, and periorbital or perioral demodicosis. Furthermore, the cases of suspected secondary demodicosis that failed to respond to adequate treatment of the primary disease, notably rosacea, acne, perioral dermatitis, and seborrheic dermatitis, as per the clinical judgment of the treating dermatologists, were subjected to SSSB. In addition, SSSB was also done in patients having sensitive skin, defined as the occurrence of unpleasant sensations of stinging, burning, pain, and tingling in response to innocuous stimuli as per the departmental protocol.^[7]

RESULTS

During the study duration of 1 year, 25 patients suspected to have either primary or secondary demodicosis or sensitive skin were subjected to SSSB; however, in only 11 patients, it was positive [Figure 1]. These comprised four men and seven women with a mean age of 27.4 ± 10.8 years. Clinical presentations varied from patients presenting with only sensitive skin (2), pityriasis folliculorum (3), perioral/orbital demodicosis (3), papulopustular demodicosis (2), and nodulocystic demodicosis (1) [Figure 2 and 3]. Six patients had a history of topical corticosteroid abuse for a variable time duration ranging from 1 to 2 months [Table 1], and one patient had uncontrolled diabetes mellitus. In two patients, the lesions were distributed asymmetrically, leading to a suspected diagnosis of demodicosis. Predominant dermoscopy findings noted were the presence of Demodex tails (63.6%), Demodex follicular opening (72.7%), short linear/arborizing vessels (45.5%), and pustules (36.3%) [Figure 4]. All patients with primary demodicosis showed a significant improvement with topical 1% ivermectin monotherapy. Those with underlying dermatoses or topical corticosteroid abuse were additionally administered oral doxycycline (100 mg/day) for 4–6 weeks with good response.

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Figure 1:

Demodex mites seen on standardized skin surface biopsy (a): 10× and (b): 40×.

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Figure 2

(a): Diffuse erythema, sand paper-like texture, and white scales at the base of the hair follicles (pityriasis folliculorum-like demodicosis). (b): Dermoscopy showing Demodex follicles (arrow) (Dermlite DL4, polarized light, 10×).

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Figure 3

(a): Multiple perioral papules (perioral dermatitis like demodicosis; (b): Dermoscopy showing Demodex tails (circle), (Dermlite DL4, polarized light, 10×).

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Figure 4

(a): Asymmetrical nodulocystic lesions (nodulocystic demodicosis); (b): Dermoscopy showing Demodex tails (circles), demodex follicles (square) and pustules (arrow), (Dermlite DL4, polarized light, 10×).

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DISCUSSION

The present study highlights the important clinical aspects of demodicosis, with findings that are in line with and expand upon existing literature. As in other reports, the patients in this series presented with diverse symptoms ranging from papulopustular lesions to more generalized erythema and scaling, which frequently overlapped with other skin conditions like rosacea. Zhao et al. and Forton similarly described this challenge, noting that Demodex mite overgrowth can lead to diagnostic confusion, especially in cases that closely resemble rosacea or seborrheic dermatitis.^[2,8] Chen and Plewig identified two types of demodicosis: primary, which occurs in the absence of other inflammatory skin diseases and improves with acaricidal treatment, and secondary, where Demodex overpopulation is associated with existing skin or systemic conditions. The lesions in primary demodicosis are usually asymmetrically distributed, follicle-centric, mildly pruritic, and lack typical rosacea features such as erythema, flushing, or telangiectasia. Secondary demodicosis can involve the trunk, present with more diffuse and symmetrical inflammation, and is often associated with underlying conditions like perioral dermatitis or rosacea, or immunosuppression (local/systemic) [Table 2].^[9] In the current study, five patients were labeled as primary demodicosis, and the remaining seven as secondary demodicosis. Three patients each had pityriasis folliculorum and perioral/orbital dermatitis, two had papulopustular lesions, and one had nodulocystic lesions. The remaining two patients presented with sensitive skin without overt cutaneous lesions. Literature detailing cutaneous presentation in demodicosis is limited. Hsu et al., in their series of 15 patients, described skin lesions in the form of acne-rosacea-like, perioral dermatitis-like, granulomatous rosacea-like like and pityriasis folliculorum.^[10]

The widely prevalent terminologies add confusion to the existing difficulty in classifying demodicosis in primary and secondary forms. Common entities include pityriasis folliculorum, rosacea-like demodicosis, Demodex facial dermatitis, perioral/periorbital dermatitis-like demodicosis, and abscess-like conglomerates. To streamline this difficulty in classification, a new nomenclature has been proposed. Pityriasis folliculorum presenting with scaly and spiky sebaceous hair follicles should be renamed as spinulate demodicosis. Demodex folliculitis resulting from inflammation of follicles due to Demodex mite should encompass papulopustular, nodulocystic, and conglobate patterns.^[9] The differentiation between primary and secondary demodicosis often seems more academic than practical in a clinical setting, as patients usually present after using various topical treatments for differing durations. It is challenging to determine whether erythema and telangiectasia are de novo or treatment-induced.^[11] A retrospective assumption of primary demodicosis could be made if symptoms improve with acaricide monotherapy. However, in practice, it may be more pragmatic to treat the cases as secondary demodicosis to provide faster relief to the patient.

Sensitive skin being characterized by unpleasant sensations like stinging, burning, pain, itching, and tingling in response to normally non-irritating stimuli, can be another manifestation of demodicosis. Previous studies have reported higher Demodex mite density in association with increased skin sensitivity.^[12] Two patients in the current study reported with sensitive skin without overt cutaneous lesions. Thus, Demodex density in patients with sensitive skin should be investigated to improve management through targeted treatments and preventive strategies.

Dermoscopy as a diagnostic aid has been used in demodicosis. In a study of 55 confirmed cases of demodicosis, characteristic dermoscopy findings were Demodex tails and Demodex follicular openings. Demodex tails appear as 1-3 mm long whitish creamy/gelatinous threads protruding through the follicular openings, representing Demodex mite tails, and are seen more frequently in pityriasis folliculorum.^[13] In the present study, 63.6% of patients had identifiable Demodex tails. These should be distinguished from skin scales and white beard hair.^[14] The second main dermoscopy finding predominantly observed in inflammatory variants of demodicosis is Demodex follicular openings visible as dilated follicles containing gray-brown plugs surrounded by an erythematous halo. 72.7% of patients in the current study had these follicles in a variable number. Open comedones that pose a diagnostic challenge can be differentiated by being randomly distributed, brown in color, and surrounded by the ring of hyperpigmentation. Other reported dermoscopy findings include reticular red dilated vessels and lakes of pus.^[13] In secondary demodicosis, dermoscopy changes of coexisting dermatoses may predominate, sometimes obscuring identification of Demodex tails and Demodex follicular openings.

The significant role of topical corticosteroid abuse was observed in 6 of the 11 cases, supporting the findings from previous studies that have identified corticosteroids as a contributing factor to Demodex proliferation. Corticosteroid-induced immunosuppression allows Demodex to multiply unchecked.^[9] This underscores the importance of proper guidance in the use of corticosteroids, particularly on sensitive facial skin, where the potential for adverse effects, including demodicosis, is higher.

The treatment goals for demodicosis are to inhibit parasite reproduction, eliminate mites, and prevent recurrence. Key strategies include maintaining proper hygiene with the regular use of soaps, shampoos, and wipes for daily care of the face and eye area, along with frequent washing of linens, especially at high temperatures. Ivermectin, through its neurotoxic effects on Demodex mites, continues to be one of the most reliable treatments for demodicosis. All five patients labeled as primary demodicosis in this series responded well to topical ivermectin monotherapy. Oral doxycycline was added to the treatment regimen of the remaining patients. Oral metronidazole, when added to oral ivermectin therapy, has been found to be more effective than ivermectin alone. Topical metronidazole has shown improvement in reducing erythema, papules, and pustules compared to placebo. Daily or twice-daily application of permethrin significantly reduces Demodex density with minimal irritation. In addition, benzyl benzoate and crotamiton, when applied twice daily, have also been found to be effective treatment options [Table 3].^[15,16]

CONCLUSION

Demodex mite resides as a normal commensal flora on facial skin; however, an increase in its number results in variable clinical manifestations. In addition, there can be a secondary increase in rosacea, acne, and perioral dermatitis. Primary demodicosis, by definition, should lack an underlying disease and must respond to acaricidal monotherapy. Although suspected in 25 cases, diagnostic confirmation with standardized skin surface biopsy could be done in eleven patients only. Topical corticosteroid abuse appears to be a significant predisposing factor. A thorough knowledge of demodicosis and its manifestations is essential for appropriate management.