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Manuscript Number: 7265R1

Title: Tinea Imbricata

Article Type: CME

Corresponding Author: Dr Elizabeth K Satter, MD/MPH

Corresponding Author's Institution: US Navy

First Author: Elizabeth K Satter, MD/MPH

Order of Authors: Elizabeth K Satter, MD/MPH

Abstract: Tinea imbricata (TI) is a chronic superficial mycosis caused exclusively by Trichophyton

concentricum. Characteristically the lesions are composed of multiple concentric annular plaques that have

thick adherent peripheral rims of scale. A brief review of this unique infection is presented in the following

article.

Tinea Imbricata

Elizabeth K. Satter, MD/MPHDepartments of Dermatology and DermatopathologyNaval Medical Center 34520 Bob Wilson Drive Suite 300San Diego, CA 92134-2300619-532-9702Elizabeth.Satter@med.navy.mil

The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

The authors report no conflict of interest.

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Table 1: Clinical Subtype of Tinea Imbricata. Modified from Hay et al5 with permission

1. Classical, multiple adjacent concentric annular plaques 2. Lamellar, a diffuse pattern with juxtaposition of adjacent rings reminiscent of

ichthyosis 3. Classical pattern, but limited to an isolated plaque4. Hypochromatic macules or hyperchromatic macules (rare)5. Seborrhea-like areas affecting the scalp and face without involvement of the hair 6. Annular plaques, with tinea corporis-like pattern7. Lichenified plaques8. Palmoplantar ranging from irregular distributed lines or rings of scale to intense

hyperkeratosis with yaw-like lesions (uncommon)9. Nail dystrophy or distal subungual onychomycosis (rare)

Table (Microsoft Word format only)

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Tinea Imbricata

Abstract

Tinea imbricata (TI) is a chronic superficial mycosis caused exclusively by Trichophyton concentricum. Characteristically the lesions are composed of multiple concentric annular plaques that have thick adherent peripheral rims of scale. A brief review of this unique infection is presented in the following article.

Tinea imbricata (TI) is a chronic superficial mycosis that is known by a multitude of regional names such as Tokelau, chimberé, grillé, and roña. Recognition of this unique infection dates back to 1686 where it is recorded in William Damper’s Travels Around the World.1 It is a geographically restricted mycosis that is rarely seen in more developed countries; however, in certain endemic areas it can affect between 9-18% of the indigenous population 2, 3, 4. It is endemic to several islands in the South Pacific and Oceania (Papua New Guinea, Mindanao, Malaysia, Fiji, Samoa, Borneo, Indonesia, New Zealand and Tokelau), and can bee seen in some areas of South-East Asia (China and India). 1-6 Although more prevalent in the South Pacific, it has also been reported to occur in various regions of Central and South America (Amazon region of Brazil, Colombia, Panama, El Salvador and Guatemala) as well as in Mexico.1, 4-6

The term imbricata is derived from the Latin word imbrex meaning overlapping tiles, which is apropos since characteristically the lesions are composed of multiple concentric annular plaques that have thick adherent peripheral rims of scale. Within each ring of scale there is a circle of hypopigmented skin and inside this is a ring of normally pigmented skin (Figure 1).2 Manson believed that the periodicity of the lesion was due to the intermittent removal of scale along with the fungal organisms, followed by its subsequent regeneration. 2 Although TI is primarily known for its characteristic concentric rings, there are at least nine clinical subtypes with most patients having several different patterns of clinical lesions (Table 1).2-5 The various morphologic appearances of the lesions are dependent upon thickness of the skin in different anatomical regions, as well as, the duration of the infection and whether the lesions have been scratched.2

Tinea imbricata has a predilection for the extensor surfaces and the trunk with relative sparing of the axilla and groin. 1, 2, 4-6 On the face, lips and nipple the delicate scale is easily removed resulting in areas of altered pigmentation.2, 5 Typically there is minimal involvement of heavily keratinized sites such as palms and soles. 1, 2, 4-6 In patients who have involvement of the palms or soles, the lesions slightly differ from tinea manus or pedis in that the scaling is more irregular distributed and often extends along the sides of the digits, rather than being accentuated in the skin creases. 4, 5 If there is a more intense infection of the palms or soles, the normal dermatoglyphic pattern can be obscured and the hyperkeratotic lesions may be indistinguishable from those characteristically seen in yaws.2 The paucity of reported infections involving the soles may simply be due to the fact that the infection is obscured by heavy calluses incurred by the lack of footwear in the native population. 2 Rarely are the nails involved, but when it does occur it typically results in nail dystrophy with involvement of the distal subungual region. 4, 5 Despite the fact that the infection does not involve the hair, the scalp and face

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are often involved resulting in a seborrhea-like picture (Figure 2). 4, 5 Sometimes the truncal lesions can resemble tinea corporis, presenting as an expanding annular plaque with central clearing. 5 One study done in the Maprik area of Papua New Guinea, showedthat up to 49% of patients who had been diagnosed with tinea corporis were actually colonized by T. concentricum and therefore it was determined that these lesions merely represented another clinical variant of TI.3 Often early in the course of the disease there may only be a solitary isolated concentric plaque, most commonly located on buttock; however, over time there is usually more widespread involvement (Figure 3). 3, 6, 7

Although lichenified plaques have been sited as a distinct clinical subtype, 5

lichenification is simply a result of the chronic scratching that occurs from the intense pruritus that is experienced by some people resulting in the destruction of the ornate pattern that is typically seen.

Tinea imbricata is a strictly anthropophilic dermatophyte that primarily is seen in individuals of “pure race” who live in primitive, isolated conditions, and is often associated with poor hygiene. 4 It affects both males and females, but is slightly more common in males during childhood and among females in adulthood. 5 The infection is often acquired in childhood, but there may be some improvement, at least of the scalp infection, at puberty with changes in the sebum composition. 6, 8 Despite prolonged close contact and cohabitation only certain indigenous people are affected by this condition; therefore, a familial component appears to be involved in acquiring this infection. Currently the exact mode of inheritance is unknown; however, the two major hypotheses are that the condition occurs as a result of an autosomal dominant inheritance with incomplete penetrance, or that the condition is inherited in an autosomal recessive fashion. 6, 9-11 Besides the genetic predisposition, specific environmental conditions, the nutritional status of the patient, poor hygiene, and an altered immune system appear to be involved in contracting this infection. 8, 12 One study which examined the indigenous people in Papa New Guinea showed that 52% of affected people had an immediate-type hypersensitivity response to intradermal trichophytin, yet the majority of patients failed to develop a delayed-type hypersensitivity reaction; 12 thereby implying that people who become infected have a decreased cellular immunity. 8, 12

In most incidences the diagnosis is generally made by simple clinical inspection; but if a microscope is available, examination of the scale with the use of potassium hydroxide, reveals abundant closely packed septate hyphae (Figure 4). The gold standardfor diagnosis remains a fungal culture; however, it is often impractical in the isolated geographic locations in which these infections arise.

Originally it was believed that the infection could only be found on tropical islands located at sea-level with year-round hot humid temperatures; however, small subsets of cases are seen in mild to colder climates of Guatemala and Mexico where the altitude is 1000-2500 meters. Moreover it has been reported that some cases have improved when the climate was changed. 4 Therefore, it has been postulated that there areat least two distinct strains of Trichophytum concentricum with one strain that is thermo-sensitive with growth at 28 to 30 degrees centigrade and the other thermo-tolerant growing at 20 to 25 degrees centigrade. 1, 4 On Mycosel or Sabouraud’s glucose agar, Trichophytum concentricum appears as a heaped-up, deeply folded, cerebriform colony that has a slightly brownish center with a white scattered powdery edge and a deep amber color underside. 1, 3 Growth of the colony takes approximately 8-18 days and the majority

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of isolates are stimulated by the addition of thiamine to the culture media. 1, 3, 4

Microscopic evaluation of the colony shows a tangled mass of short branching septate hyphae, with irregular swollen cells and numerous chlamydospores.1, 3

In the past it was speculated that the unique patterns produced by TI were the impetus for tribal tattooing among those not affected; 6 however, as isolated tribes have become infiltrated by people from the outside world, the disease has become a greater social burden and patients may seek treatment .12 The azole antifungal agents have been tried, but there was only minimal improvement and rapid recurrence of lesions with cessation of the medications. 6 The best therapeutic results are obtained with the use of Whitfield’s ointment (benzoic acid and salicylic acid) to manually remove the scale along with oral antifungals. 4, 6 In the past the oral griseofulvin was thought to be the best treatment; however, terbinafine has been shown to be highly effective. 6, 8 Yet even with the appropriate treatment, remission only lasts up to 8 weeks and there is a significantly high relapse rate. 6

In summary, although most dermatologists are familiar with the classical clinical presentation of this unique ornate superficial fungal infection, many will never personally see a patient with TI due to its restricted occurrence in indigenous populations located in geographically isolated communities. However as a caveat to the aforementioned statement, recently reported there were three separate cases of patients native to the United Kingdom who presented with concentric annular lesions similar those seen in TI. These latter lesions differed however, in that they were caused by Trichophyton tonsurans or Trichophyton mentagrophytes, rather than Trichophytum concentricum. 13-15

1. Figuera H, Conant N. The first Case of Tinea Imbricata. Am J Trop Med. 1940; s1-20(2): 287-303.

2. Polunin I. Tinea imbricata in Malaya*. Br J Dermatol. 1952; 64 (10): 378-384.3. Maclennan R, O’Keeffe MF. Superficial fungal infections in an area of lowland

New Guinea. Clinical and mycological observations. Aust J Dermatol. 1966; 8 (3): 157-163.

4. Bonifaz A, Archer-Dubon C, Saul A. Tinea imbricata or Tokelau. Int J Dermatol 2004, 43(7):506-510.

5. Hay RJ, Reid S, Talwat E, Macamara K. Endemic tinea imbricata- a study on Goodenough Island, Papa New Guinea. Trans R Soc Trop Med Hyg 1984;78(2):246-251.

6. Wingfield AB, Fernandez-Obregon AC, Wignall FS, Greer DL. Treatment of tinea imbricata: a randomized clinical trial using griseofulvin, terbinafine, itraconazole and fluconazole. Br J Dermatol 2004;150:119-126.

7. Serjeantson S, Lawrence G. Autosomal recessive inheritance of susceptibility to tinea imbricata. Lancet.1977; 1:13-15.

8. Hay RJ. Tinea Imbricata. The factors affecting persistent dermatophytosis. Int J Dermatol 1985;24 (9):562-564.

9. Hay RJ. Genetic susceptibility to dermatophytosis. Eur J Epidemiol. 1992;8(3):346-349.

10. Ravine D, Turner KJ, Alper MP. Genetic inheritance of susceptibility to tinea imbricata. J Med Genet 1980;17:342-348.

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11. Bonifaz A, Araiza J, Koffman-Alfaro, Paredes-Solis V, Cuevas-Covarrubias S, Rivera MR. Tinea imbricata: autosomal dominate pattern of susceptibility in a polygamous indigenous family of the Nahuatl zone in Mexico. Mycoses 2004;47(7):288-291.

12. Hay RJ, Reid S, Talwat E, Macnamara K. Immune responses of patients with tinea imbricata. Br J Dermatol 1983; 108:581-586.

13. Batta K, Ramlogan D, Smith AG, Garrido MC, Moss C. ‘Tinea indecisiva’ may mimic the concentric ring of tinea imbricata. Br J Dermatol 2002;147: 384.

14. Hoque SR, Holden CA. Trichophyton tonsurans infection mimicking tinea imbricata. Clin and Exper Dermatol 2007;32(3):345-346.

15. Lim SPR and Smith AG. “Tinea pseudoimbricata”: Tinea corporis in a renal transplant recipient mimicking the concentric rings of tinea imbricata. Clin and Exper Dermatol 2003; 28:332-333.

Table 1: Clinical Subtype of Tinea Imbricata. Modified from Hay et al5 with permission

1. Classical, multiple adjacent concentric annular plaques 2. Lamellar, a diffuse pattern with juxtaposition of adjacent rings reminiscent of

ichthyosis 3. Classical pattern, but limited to an isolated plaque4. Hypochromatic macules or hyperchromatic macules (rare)5. Seborrhea-like areas affecting the scalp and face without involvement of the

hair 6. Annular plaques, with tinea corporis-like pattern7. Lichenified plaques8. Palmoplantar ranging from irregular distributed lines or rings of scale to

intense hyperkeratosis with yaw-like lesions (uncommon)9. Nail dystrophy or distal subungual onychomycosis (rare)

Figure Captions:

Figure 1: Classic concentric annular plaques on trunk and extremitiesFigure 2: Seborrhea-like facial lesionsFigure 3: Isolate plaque on buttockFigure 4: KOH showing long branching septate hyphae, 40x

Questions:

1. What organism is responsible for tinea imbricata?a. Trichophyton rubrumb. Microsporum gypseumc. Trichophyton concentricumd. Trichophyton mansonie. Aspergillus tokelau

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2. The organism has been shown to affect all regions except? a. Trunkb. Palmsc. Scalpd. Haire. Nails

3. The most effective treatment for tinea imbricata?a. Salicylic acidb. Brilliant greenc. Ketoconazoled. Nystatin and Triamcinolone Acetonide Creame. Terbinafine

4. In what fashion is tinea imbricata is inherited?a. Autosomal recessiveb. X-linked recessivec. X- linked dominant d. Autosomal dominante. Not inherited

5. What pattern of infection is rarely seen with tinea imbricata?a. Classical

b. Lamellar c. Hypochromatic d. Isolated Plaque e. Onychomycosis

"I certify that any affiliations with or financial involvement in any organization or entity with a direct financial interest in the subject matter or materials discussed in the manuscript (eg, employment, consultancies, stock ownership, honoraria, expert testimony) is disclosed below. Any financial project support of this work is identified in an acknowledgment in the manuscript."

Elizabeth Satter, MD

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* Financial Disclosure

-----Original Message-----From: Rod Hay [mailto:Rod.Hay@lshtm.ac.uk] Sent: Wednesday, November 07, 2007 6:18 AMTo: Satter, Elizabeth K CDRSubject: Re: Article on Tinea imbricata

No problem at all. I hope it is accepted.Rod Hay

>>> "Satter, Elizabeth K CDR" <Elizabeth.Satter@med.navy.mil> 11/06/075:49 PM >>>Dear Dr. Hay,

I am in the US Navy and was on a humanitarian mission in Papua New Guinea (Madang). I am writing a brief article on Tinea Imbricata for Cutis, an American Dermatology Journal. I would like to include a table in the paper, which is a modified version of yours that was printed in: Endemic tinea imbricata- a study on Goodenough island, papa new guinea R.J. HAY, S. REID, E. TALWAT, K. MACNAMARA Trans R Soc Trop Med Hyg 1984;78(2):246-251.

Other references that I used to compose the table were:

Polunin I. Tinea imbricata in Malaya*. Br J Dermatol. 1952; 64 (10):378-384.

Maclennan R, O'Keeffe MF. Superficial fungal infections in an area of lowland New Guinea. Clinical and mycological observations. Aust J Dermatol. 1966; 8 (3): 157-163.

Bonifaz A, Archer-Dubon C, Saul A. Tinea imbricata or Tokelau. Int J Dermatol 2004,43(7):506-510.

This is the Table that I would like to use in my article

1. Classical, multiple adjacent concentric annular plaques 2. Lamellar, a diffuse pattern with juxtaposition of adjacent ringsreminiscent of ichthyosis 3. Classical pattern, but limited to an isolated plaque4. Hypochromatic macules or hyperchromatic macules (rare)5. Seborrhea-like areas affecting the scalp and face withoutinvolvement of the hair 6. Annular plaques, with tinea corporis-like pattern7. Lichenified plaques8. Palmoplantar ranging from irregular distributed lines or ringsof scale to intense hyperkeratosis with yaw-like lesions (uncommon)9. Nail dystrophy or distal subungual onychomycosis (rare)

Could I have your permission to modify the table for my article?

Thank-you for your consideration into this matter

Dr. Elizabeth Satter

Reprint Permission

November 5, 2007

Melissa SteigerEditor, Cutis

(Submitted electronically)

Dear Ms. Steiger:

Enclosed please find a manuscript entitled, “Tinea Imbricata”, which I would like to submit as a CME article for Cutis.

In brief, after visiting Papua New Guinea recently I saw several cases of Tinea imbricata and the submitted article is a review of this unique superficial fungal infection that is rarely clinically seen by most dermatologists.

Thank you for your consideration in this matter. I look forward to hearing from you with possible editorial improvements.

With best regards,

Elizabeth K. Satter, M.D.

(Submitted electronically)

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