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LETTER TO THE EDITOR
Year : 2015  |  Volume : 6  |  Issue : 7  |  Page : 60-63  

Dermatophyte infection encircling vitiligo


Department of Dermatology, SVS Medical College, Mahbubnagar, Telangana, India

Date of Web Publication4-Dec-2015

Correspondence Address:
Angoori Gnaneshwar Rao
Department of Dermatology, SVS Medical College, Yenugonda, Mahbubnagar, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2229-5178.171056

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How to cite this article:
Rao AG. Dermatophyte infection encircling vitiligo. Indian Dermatol Online J 2015;6, Suppl S1:60-3

How to cite this URL:
Rao AG. Dermatophyte infection encircling vitiligo. Indian Dermatol Online J [serial online] 2015 [cited 2019 Dec 12];6, Suppl S1:60-3. Available from: http://www.idoj.in/text.asp?2015/6/7/60/171056

Sir,

Tinea corporis is a superficial fungal infection of glabrous skin caused by various species of dermatophytes; epidermophyton, trichophyton, and microsporon. Vitiligo is an autoimmune disease. The occurrence of tinea bordering vitiligo patch is unique and literature search could yield only one case report.

A 30-year-old woman presented with annular itchy, scaly patch on right lower back of one week duration. She was a known case of vitiligo on combination therapy (PUVA and tacrolimus 0.1%) for the last two months and was responding satisfactorily. There was no history of diabetes mellitus or hypertension and she was not on any other medication including immnosuppressives. Family history was negative for similar skin ailments. Cutaneous examination revealed multiple depigmented patches distributed on upper and lower limbs and trunk varying between 2 and 5 cm in size, most of them showing follicular pigmentation. An oval depigmented patch on the right lower back measuring 5 × 3 cm, was encircled by papules, pustules, and scaling [Figure 1], suggestive of dermatophyte infection. Other vitiligo patches did not show any clinical evidence of dermatophyte infection. Hair, nails, and mucous membranes were normal. There was no clinical evidence of dermatophyte infection over other parts of the body. A clinical diagnosis of tinea encircling vitiligo was offered. Her routine blood chemistry including renal function test (RFT) and liver function test (LFT) was unremarkable and serology for human immune deficiency virus (HIV) and VDRL was nonreactive. Scrapings from the margin of the plaque revealed fungal elements on potassium hydroxide 10% mount [Figure 2] and culture on Sabouraud's dextrose agar showed raised creamish-white downy colonies and reverse showed yellow-brown pigmentation, characteristic of Trichophyton rubrum species, thus confirming the diagnosis of tinea corporis [Figure 3]. Biopsy from the depigmented patch with Fontana–Masson stain revealed absence of melanocytes [Figure 4], confirming the diagnosis of vitiligo and presence of fungal elements on periodic acid Schiff stain [Figure 5]. She was diagnosed as dermatophyte infection encircling vitiligo. She was advised topical ketoconazole 2% cream twice a day application with which she responded satisfactorily.
Figure 1: (Original) Vitiligo patch on right lower back surrounded by papules, pustules, and scaling

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Figure 2: (Original) KOH mount of scrapings revealing mycelia

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Figure 3: (Original) Culture on Sabouraud's dextrose agar showing raised creamish-white downy colonies. Reverse showed yellow-brown pigmentation

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Figure 4: (Original) Microphotograph showing absence of melanocytes in the basal cell layer (Fontana–Masson stain ×400)

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Figure 5: (Original) Microphotograph showing fungal hyphae in the hair follicle (PAS stain ×400)

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Dermatophyte infection bordering a vitiligo patch is a rare occurrence and the exact mechanism for such association has not been elucidated. Histologically, in vitiligo there is loss of melanocytes with subsequent replacement by Langerhans cells.[1] These being antigen presenting cells for dermatophytic infection are known to play a pivotal role in inducing T-lymphocyte response to trichophytin in dermatophytosis, ultimately responsible for the elimination of dermatophytic infection.[2] Furthermore, the increased number of Langerhans cells in vitiligo patches may lead to early and rapid elimination of fungus from vitiligo area, only to remain at the border of the patch. Additionally, there is also keratinocyte damage in normal looking skin adjacent to vitiligo patch, which is either absent or decreased in the stable vitiligo lesion.[3] Sharma, while reporting dermatophyte infection bordering vitiligo in a young lady, hypothesized that there may be alteration in the antigenicity of dermatophyte-infected (damaged) keratinocytes surrounding but not within vitiligo lesions, which is recognized by trichophytin-specific T-cells responsible for peripheral localization of dermatophyte infection in the vitiligo lesion.[4]

The other possible mechanism proposed is the actinic theory in which actinic radiation induces recruitment of inflammatory cells (neutrophils and monocytes) into the vitiligenous area and not the normally pigmented skin, leading to death of dermatophytic conidia.[5],[6] This probably explains sparing of the vitiliginous area and involvement of border of the vitiligo patch. However, the actinic radiation might not be responsible for this phenomenon in our case as both vitiligo and the dermatophytosis lesions involved a relatively sun-protected area (the patient wears a saree that covers the involved area).

Okuwa and Horio, while investigating the role of PUVA on dermatophytosis in guinea pigs, found that it has a suppressive effect on the immunity of dermatophytosis and also delayed spontaneous resolution, which was attributed to depletion of ATPase-positive Langerhans cells.[7] In concert with this, it may be speculated that PUVA treatment in our case might have suppressed the immunity against dermatophytosis and delayed spontaneous resolution leading to persistence of infection.

Furthermore, tacrolimus, being an immunosuppressive agent is known to predispose not only to superficial dermatophytosis but also deep dermatomycosis involving the hair follicle. Yamamoto and Nishioka have reported a patient of psoriasis involving the face treated with topical tacrolimus 0.1% who developed deep dermatomycosis over the lesion.[8] It is possible that the independent immunosuppressive actions of PUVA and tacrolimus together might have made our patient vulnerable to fungal infection. However, it is an enigma why dermatophyte infection involved a single patch of vitiligo leaving other vitiligo patches unaffected.

Additionally, it might be reasonable to consider the morphology of dermatophyte infection bordering vitiligo in the index case as an expression of Wolf's isotopic response as the fungal infection occurred on a vitiligo patch.[9]

In conclusion, the mechanisms involved in the peculiar occurrence of dermatophyte infection encircling vitiligo remain cryptic. Various hypotheses have been put forward in an effort to elucidate the same. Establishing the underlying mechanism for such an occurrence might help in understanding co-localization of various dermatological conditions.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Birbeck MS, Breathnach AS, Everall JD. An electron microscope study of basal melanocytes and high-level clear cells (Langerhans cells) in vitiligo. J Invest Dermatol 1961;37:51-64.  Back to cited text no. 1
    
2.
Braathen LR, Kaaman T. Human epidermal Langerhan cells induce cellular immune response to trichophytin in dermatophytosis. Br J Dermatol 1983;109:295-300.  Back to cited text no. 2
[PUBMED]    
3.
Moeffmann G, Klein-Angerer S, Scollay DA, Nordlund JJ, Lerner AB. Extracellular granular material and degeneration of keratinocytes in normally pigmented epidermis of patients with vitiligo. J Invest Dermatol 1982;79:321-30.  Back to cited text no. 3
    
4.
Sharma AK. Tinea bordering vitiligo. Indian J Dermatol 1998;43:132-4.  Back to cited text no. 4
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5.
Lavker RM, Kligman AM. Chronic heliodermatitis: A morphologic evaluation of chronic actinic dermal damage with emphasis on the role of mast cells. J Invest Dermatol 1988;90:325-30.  Back to cited text no. 5
    
6.
Caldron RA, Hay RJ. Fungicidal activity of human neutrophils and monocytes on dermatophyte fungi, Trichophyton quinckeanum and Trichophyton rubrum. Immunology 1986;61:289-95.  Back to cited text no. 6
    
7.
Okuwa T, Horio T. The inhibitory effect of PUVA on the immunity of experimental dermatophytosis in guinea pigs. Arch Dermatol Res 1986;278:320-3.  Back to cited text no. 7
[PUBMED]    
8.
Yamamoto T, Nishioka K. Deep dermatophytosis during topical tacrolimus therapy for psoriasis. Acta Derm Venereol 2003;83:291-2.  Back to cited text no. 8
[PUBMED]    
9.
Wolf R, Wolf D. Tinea in a site of healed herpes zoster (isoloci response?). Int J Dermatol 1985;24:539.  Back to cited text no. 9
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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