Jan 11, 2016 - Diagnosis: Tinea imbricata. Tinea imbricata is usually diagnosed by simple visual in- spection of the characteristic lesions (figures 1 and 2).
ANSWER TO PHOTO QUIZ Philip A. Mackowiak, Section Editor
Chronic Figurate Skin Lesions (See page 532 for Photo Quiz)
Polycyclic cutaneous lesions, neck and shoulder
Diagnosis: Tinea imbricata. Tinea imbricata is usually diagnosed by simple visual inspection of the characteristic lesions (figures 1 and 2). In this case, KOH wet mounting of skin scrapings revealed organisms with septate, branching hyphae in epithelial cells (figure 3). The diagnosis was confirmed by culture in potato agar with chloramphenicol (prepared in-house) and Sabouraud’s dextrose agar with chloramphenicol and cycloheximide. The culture yielded slow-growing, elevated, convoluted, glabrous, creamcolored fungal colonies (figure 4) with a pale yellow reverse. Tinea imbricata is an unusual form of tinea corporis caused by the strictly anthropophilic dermatophyte Trichophyton concentricum [1]. Individual lesions appear on the skin as itchy, noninflammatory, concentric rings that may fuse upon 582 • CID 2004:39 (15 August) • ANSWER TO PHOTO QUIZ
Figure 2.
Scaly cutaneous lesions, right elbow
enlargement to form scaly polycyclic or serpiginous plaques [2]. It is not known to affect hair. In the Sepik region of Papua New Guinea, it is known as “grille,” and it has also been called “beauty ringworm” for its striking filigree patterns in the skin. Despite the distinctive appearance of the lesions, tinea imbricata is most frequently confused with ritual scarification. Tinea imbricata may infect people of any age. Its geographic distribution is thought to be limited to the South Pacific and tropical Americas, where it most commonly affects indigenous populations [3]. Transmission is usually by direct personal contact between family members sharing household items or from parent to child soon after birth. High humidity and warmth are likely environmental factors in the incidence of infection [4]. Autosomal recessive inheritance has been implicated to
Downloaded from http://cid.oxfordjournals.org/ by guest on January 11, 2016
Figure 1.
Figure 4. Trichophyton concentricum colony after 4 weeks on potato dextrose agar.
play a role in the high susceptibility rates in some regions [5]. Though clinical sequelae are minimal, patients may suffer from extreme pruritus. Curative treatment is usually prohibitively expensive or inaccessible for affected populations. Optimal treatment would be oral terbinafine, 250 mg daily for 4 weeks, or griseofulvin, 500 mg twice daily for 4 weeks [6, 7]. Recurrence following treatment is common [8].
et al., eds. Manual of Clinical Microbiology, Vol. 2. 8th ed. Washington, DC: ASM Press, 2003:1798–819. Hay RJ. Tinea imbricata. Curr Top Med Mycol 1988; 2:55–72. DaFonseca O. The endodermophyceae: tinea imbricata (tokelau-chimbereˆ). In: March J, ed. Essays on tropical dermatology. Amsterdam: Excerpta Medica, 1972:339–55. Kwon-Chung KJ, Bennett JE. Dermatophytoses. In: Medical Mycology. Philadelphia: Lea & Febiger, 1992:105–61. Ravine D, Turner KJ, Alpers MP. Genetic inheritance of susceptibility to tinea imbricata. J Med Genet 1980; 17:342–8. 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; 150:119–26. Budimulja U, Kuswadji K, Bramono S, et al. A double-blind, randomized, stratified controlled study of the treatment of tinea imbricata with oral terbinafine or itraconazole. Br J Dermatol 1994; 130(Suppl 43); 43: 29–31. Hay RJ, Reid S, Talwat E, Macnamara K. Endemic tinea imbricata—a study on Goodenough Island, Papua New Guinea. Trans R Soc Trop Med Hyg 1984; 78:246–51.
2. 3.
4. 5. 6.
Acknowledgment Conflict of interest.
All authors: No conflict.
7.
Elissa Meites, Nancy B. McClenny, and Ellen J. Baron Department of Pathology, Stanford University School of Medicine, Stanford, California
References 1. Summerbell RC. Trichophyton, Microsporum, Epidermophyton, and agents of superficial mycoses. In: Murray PR, Baron EJ, Jorgenson JH,
8.
Reprints or correspondence: Ellen J. Baron, Clinical Microbiology/Virology Laboratory, Stanford Hospital, 300 Pasteur Dr., Stanford, CA 94305-5250. Clinical Infectious Diseases 2004; 39:582–3 2004 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2004/3904-0027$15.00
ANSWER TO PHOTO QUIZ • CID 2004:39 (15 August) • 583
Downloaded from http://cid.oxfordjournals.org/ by guest on January 11, 2016
Figure 3. Septate, branching fungal hyphae in KOH mount, with blue dye added for color (original magnification, x400). Epithelial cell outlines are faintly visible.
