The patient is a 44-year-old woman who presents with a 2-month history of a pruritic rash on her arm. The patient states that she noticed the rash when her arm began to itch. On examination, the rash appears to be an annular, erythematous plaque with overlying scale. Over the past 2 months, the rash has grown in size and become more pruritic. She has tried over-the-counter lotions with no relief. The patient has a past medical history of type 2 diabetes. The patient has no relevant family or social history.
The patient is a 33-year-old healthy man who presents with a quickly spreading rash on his right thigh. The patient says the rash is asymptomatic but is cosmetically troublesome. He states that he has had similar rashes in the past that resolved on their own. He is worried because his rash recurs. On examination, the patient has an erythematous, figurate plaque with a trailing scale. The patient is otherwise healthy and has no medical problems, or relevant family or social history.
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Tinea corporis is a cutaneous fungal infection colloquially called ringworm; it is especially common in warm, humid climates, and shows no predilection for any sex or age group. After acne, tinea infections are the most frequently reported skin disease.1-3 Tinea corporis occurs on the trunk and limbs, and is distinguished from other tinea infections based on location. Other specific varieties are tinea capitis (scalp), tinea cruris (groin), onychomycosis (nails), tinea manuum (hands), tinea pedis (feet), and tinea barbae (beard).2 Although tinea infections occur in all demographics, tinea corporis and tinea capitis are more common in prepubescent children, whereas tinea cruris, onychomycosis, and tinea pedis are more common in adolescents and adults.4 Wrestlers are particularly susceptible to ringworm; it is called tinea corporis gladiatorum in these cases.2,5 Tinea corporis is seen in healthy individuals, but is more prevalent in people with chronic conditions such as diabetes, immunodeficiency, and leukemia.2
The causative organisms are aerobic fungi from the Trichophyton, Microsporum, or Epidermophyton genera, which are collectively called dermatophytes.6 Every species in these genera is a pathogen and is anthropophilic, zoophilic, or geophilic; Trichophyton rubrum, T mentagrophytes, and Microsporum canis are the most common agents responsible for cases worldwide; other species, such as T violaceum, are more common in India and Africa.1,3,7,8 Cases result from direct contact with infected individuals, as well as from contaminated soil, animals, spores known as arthroconidia, or other fomites; carriers are often asymptomatic.3,7 Dermatophytes are capable of producing enzymes such as keratinase that allow them to survive in the stratum corneum of the epidermis, nails, and hair. Hair follicles can act as reservoirs, making the infection more resistant to treatment.4,8 The incubation period for a new infection is approximately 1 to 3 weeks, and targets exposed skin; the degree of inflammation is determined by the host’s immune response and the specific pathogen (zoophilic species stimulate more inflammation).3,8
Tinea corporis is characterized by annular, scaly, erythematous patches and plaques that occur in cyclical patterns due to the pathogen’s hyphae extending centrifugally once in the host.9 The peripheral border of the lesion is more pronounced and sometimes pustular. The annular border usually surrounds a pale, erythematous resolving center.8,9 Multiple lesions can coalesce together to create intricate, polycyclic designs with papular borders; the lesions are distributed asymetrically.1,6 The lesions are commonly pruritic and can cause a burning sensation; however, they can also be asymptomatic.6,8 Individual lesions are approximately 1 to 5 cm.4 It should be noted that topical corticosteroids can alter the appearance of tinea corporis by reducing scale and allowing expansion of the lesions.1,2,8
The majority of tinea corporis cases are diagnosed clinically.10 If clinicians want to diagnose tinea corporis in the office, they may perform a potassium hydroxide (KOH) preparation to look for fungal hyphae. This is performed by scraping the active border of the lesion, then treating the scrapings with 10% KOH and observing them under a light microscope. In many cases of tinea corporis, translucent fungal hyphae are visible under light microscopy.2,6 Alternatively, clinicians may perform a biopsy (for routine histologic examination) or fungal culture of the lesion to confirm the diagnosis.7 The differential diagnosis for tinea corporis often includes erythema annulare centrifugum (EAC), eczema, seborrheic dermatitis, psoriasis, granuloma annulare, impetigo, and pityriasis.7
Most localized tinea corporis infections respond well to topical antifungal agents such as butenafine and terbinafine; these are preferred over older medications such as miconazole and clotrimazole.4,7 The topical cream should be applied to the entire lesion, and 2 cm around the active border; treatment should be continued for at least 2 weeks, or until the lesions have completely resolved.1,7 If the lesions are widespread or severe, oral antifungal treatment with medications such as terbinafine can be used (usually a 30-day course for cutaneous involvement). If the patient has nail involvement (onychomycosis), he or she may require up to 3 months of terbinafine daily. Common side effects of oral terbinafine include liver enzyme elevations and interactions with β-blockers. Thus, clinicians should confirm that patients do not have a history of elevated liver function enzymes and are not taking β-blockers before prescribing oral terbinafine. Some recommendations also suggest checking liver function enzymes at 6 weeks in patients taking a 3-month course of terbinafine for onychomycosis.
In this case, due to the localized nature of the patient’s rash, the patient was treated with topical butenafine. The patient applied topical butenafine twice daily for 1 month, which led to the resolution of the rash.
EAC (also known as palpable migrating erythema or erythema perstans) is characterized by red, annular patches or plaques that can grow 2 to 3 mm per day, and can reach 6 cm in diameter in less than 2 weeks. Individual lesions can reach approximately 10 cm in diameter, with areas of pale, central clearance and slightly raised, scaling edges.8,11-13 These lesions originate as pinkish, firm papules and occur primarily on the trunk and limbs/extremities (especially the thighs and hips). Although they are typically asymptomatic, some lesions can develop pruritis.11,8 One of the main distinguishing features of EAC is the presence of a “trailing scale.” The term refers to the fact that the scaling border of EAC is located on the interior edge of the erythematous ring, as opposed to the exterior edge of the lesion.8,11 The surface of the lesions do not typically have crusts or vesicles. EAC is more prevalent in adults.8 Individual lesions can last from a few days to several months, and often disappear and reappear in monthly or yearly cycles (in a cyclical fashion).8,11,14
Diagnosis of EAC can be difficult because of the vagueness of symptoms and the wide variety of associated risk factors; therefore, histologic examination (hematoxylin and eosin stain) can be helpful for diagnosis. The three major histologic characteristics of EAC are parakeratosis, spongiosis, and a distinctive arrangement of lymphocytes around cutaneous vasculature (colloquially referred to as a “coat sleeve”).8,11,13 Due to the vagueness of EAC’s characteristics, the differential diagnosis includes many other cutaneous, annular ailments, including tinea infections, granuloma annulare, Hansen disease, annular urticaria, and secondary syphilis.11
Most cases are idiopathic and spontaneously resolve .11 The majority of patients with EAC do not have an underlying condition; however, EAC is has been associated with underlying infection, neoplasms, pregnancy, pharmaceutical use, and specific foods.8 Some clinicians consider EAC to be a hypersensitivity reaction to a number of different antigens.8,15 If a patient’s EAC is secondary to an underlying condition, treating the underlying condition results in the resolution of the rash.8 EAC is commonly associated with cutaneous infections; 48% of these are caused by dermatophytes (the fungal organisms responsible for tinea infections).16 However, it should be noted that underlying infection occurs in a separate location than the associated EAC. Other specific pathogens associated with EAC include Epstein-Barr virus, human immunodeficiency virus, and chronic viral hepatitis.14,16 Less frequently, EAC has been associated with benign or malignant hematologic or solid neoplasms.16 Some pharmaceuticals associated with EAC include antimalarial drugs, gold, nonsteroidal anti-inflammatory drugs, and diuretics.8 Two notable foods linked to EAC are tomatoes and bleu cheese; bleu cheese contains a mold organism (Penicillium genus), which may cause this phenomenon.8,11
If EAC is not associated with an underlying condition, the outbreaks are usually self-limited. However, treatment with calcipotriol, topical steroids, topical tacrolimus, and oral metronidazole may be considered for nonspontaneously resolving cases.8,11,14
In this case presentation, the patient had no signs or symptoms indicating a secondary or underlying cause for his EAC. The patient was given topical triamcinolone (a topical steroid), which assisted in the resolution of his rash.
Evan A. Schauer, BS, is a medical student at the Baylor College of Medicine; Arielle Gray, BS, is a medical student at Loyola University Chicago; and Christopher Rizk, MD, is a dermatology resident at the Baylor College of Medicine in Houston.
- Ferri FF. Ferri’s Clinical Advisor 2017. Philadelphia, PA: Elsevier; 2017.
- Paller AS, Mancini AJ. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. 5th ed. Philadelphia, PA: Elsevier, 2016.
- Shy R. Tinea corporis and tinea capitis. Pediatr Rev. 2007;28:164-174.
- Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and management of tinea infections. Am Fam Physician. 2014;90:702-710.
- Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 6th ed. Philadelphia, PA: Elsevier, 2016.
- Frankel DH. Field Guide to Clinical Dermatology. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
- Andrews MD, Burns M. Common tinea infections in children. Am Fam Physician. 2008;77:1415-1420.
- Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.
- Zaidi Z, Lanigan SW. Dermatology in Clinical Practice. New York, NY: Springer-Verlag; 2010.
- Pariser RJ, Pariser DM. Primary care physicians’ errors in handling cutaneous disorders. A prospective survey. J Am Acad Dermatol. 1987;17(2 Pt 1):239-245.
- James WD, Berger TG, Elston DM, Neuhaus IM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia, PA: Elsevier; 2016.
- White JW Jr. Gyrate erythema. Dermatol Clin. 1985;3:129-139.
- Weyers W, Diaz-Cascajo C, Weyers I. Erythema annulare centrifugum: results of a clinicopathologic study of 73 patients. Am J Dermatopathol. 2003;25:451-462.
- Mir A, Terushkin V, Fischer M, Meehan S. Erythema annulare centrifugum. Dermatol Online J. 2012;18:21.
- Ziemer M, Eisendle K, Zelger B. New concepts on erythema annulare centrifugum: a clinical reaction pattern that does not represent a specific clinicopathological entity. Br J Dermatol. 2009;160:119-126.
- Regula CG, Anderson BE. Erythema annulare centrifugum. In: Lebwohl MG, Heymann WR, Berth-Jones J, Coulson I, eds. Treatment of Skin Disease: Comprehensive Therapeutic Strategies. 4th ed. Philadelphia, PA: Elsevier Saunder; 2014:219-221.