Diffusely Scattered Linear Folliculopapular Eruption

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Diffusely Scattered Linear Folliculopapular Eruption

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

CT117002009_e-Fig1_AB
FIGURES 1. A and B, Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis. A mild superficial perivascular infiltrate also was present. The surrounding skin was largely normal without notable papillomatosis, acanthosis, or hyperkeratosis (H&E, original magnification ×40 and ×100).

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund1 in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.2 Recurrent remission and exacerbation occurs in many patients.3

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

CT117002009_e-Fig2_ABC
FIGURE 2. A-C, Bilateral monomorphic eruption consisting of numerous 1- to 2-mm, follicular round papules affecting the neck, back, chest, and proximal upper extremities.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.3

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.5 Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.6 Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.7 Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.8-10

References
  1. Hitch JM, Lund HZ. Disseminate and recurrent infundibulo-folliculitis: report of a case. Arch Dermatol. 1968;97:432-435.
  2. Ma BC, Sahni VN, Sahni DR, et al. Disseminate and recurrent infundibulofolliculitis: an under-recognized yet treatable entity. J Drugs Dermatol. 2021;20:1353-1354. doi:10.36849/jdd.6173
  3. Nair SP, Gomathy M, Kumar GN. Disseminate and recurrent infundibulo- folliculitis in an Indian patient: a case report with review of literature. Indian Dermatol Online J. 2017;8:39-41. doi:10.4103/2229- 5178.198775
  4. Rekha S, Kumar V, Rao P, et al. Disseminate and recurrent infundibulofolliculitis. Indian J Dermatol. 2019;64:404-406. doi:10.4103/ijd.IJD_77_18
  5. Jones AL, Koerner RJ, Natarajan S, et al. Dietzia papillomatosis sp. nov., a novel actinomycete isolated from the skin of an immunocompetent patient with confluent and reticulated papillomatosis. Int J Syst Evol Microbiol. 2008;58(pt 1):68-72. doi:10.1099/ijs.0.65178-0
  6. Cohen PR. Follicular contact dermatitis revisited: a review emphasizing neomycin-associated follicular contact dermatitis. World J Clin Cases. 2014;2:815-821. doi:10.12998/wjcc.v2.i12.815
  7. Butterworth T, Johnson WC. Justa-clavicular beaded lines. Arch Dermatol. 1974;110:891-893.
  8. Calka O, Metin A, Ozen S. A case of disseminated and recurrent infundibulo-folliculitis responsive to treatment with isotretinoin. J Dermatol. 2002;29:431-434.
  9. Goihman-Yahr M. Disseminate and recurrent infundibulofolliculitis: response to psoralen plus UVA therapy. Int J Dermatol. 1999;38:75-76.
  10. Hinds GA, Heald PW. A case of disseminate and recurrent infundibulofolliculitis responsive to treatment with topical steroids. Dermatol Online J. 2008;14:11.
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The authors have no relevant financial disclosures to report.

Correspondence: Michael Land, DO (michael.f.land.mil@health.mil).

Cutis. 2026 February;117(2):E9-E11. doi:10.12788/cutis.1363

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The authors have no relevant financial disclosures to report.

Correspondence: Michael Land, DO (michael.f.land.mil@health.mil).

Cutis. 2026 February;117(2):E9-E11. doi:10.12788/cutis.1363

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Dr. Land is from A.T. Still University Osteopathic Medical School, Kirksville, Missouri. Drs. Kowtoniuk, Maxon, Edens, and Bandino are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Joint Base San Antonio, Texas.

The authors have no relevant financial disclosures to report.

Correspondence: Michael Land, DO (michael.f.land.mil@health.mil).

Cutis. 2026 February;117(2):E9-E11. doi:10.12788/cutis.1363

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THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

CT117002009_e-Fig1_AB
FIGURES 1. A and B, Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis. A mild superficial perivascular infiltrate also was present. The surrounding skin was largely normal without notable papillomatosis, acanthosis, or hyperkeratosis (H&E, original magnification ×40 and ×100).

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund1 in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.2 Recurrent remission and exacerbation occurs in many patients.3

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

CT117002009_e-Fig2_ABC
FIGURE 2. A-C, Bilateral monomorphic eruption consisting of numerous 1- to 2-mm, follicular round papules affecting the neck, back, chest, and proximal upper extremities.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.3

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.5 Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.6 Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.7 Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.8-10

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

CT117002009_e-Fig1_AB
FIGURES 1. A and B, Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis. A mild superficial perivascular infiltrate also was present. The surrounding skin was largely normal without notable papillomatosis, acanthosis, or hyperkeratosis (H&E, original magnification ×40 and ×100).

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund1 in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.2 Recurrent remission and exacerbation occurs in many patients.3

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

CT117002009_e-Fig2_ABC
FIGURE 2. A-C, Bilateral monomorphic eruption consisting of numerous 1- to 2-mm, follicular round papules affecting the neck, back, chest, and proximal upper extremities.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.3

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.5 Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.6 Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.7 Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.8-10

References
  1. Hitch JM, Lund HZ. Disseminate and recurrent infundibulo-folliculitis: report of a case. Arch Dermatol. 1968;97:432-435.
  2. Ma BC, Sahni VN, Sahni DR, et al. Disseminate and recurrent infundibulofolliculitis: an under-recognized yet treatable entity. J Drugs Dermatol. 2021;20:1353-1354. doi:10.36849/jdd.6173
  3. Nair SP, Gomathy M, Kumar GN. Disseminate and recurrent infundibulo- folliculitis in an Indian patient: a case report with review of literature. Indian Dermatol Online J. 2017;8:39-41. doi:10.4103/2229- 5178.198775
  4. Rekha S, Kumar V, Rao P, et al. Disseminate and recurrent infundibulofolliculitis. Indian J Dermatol. 2019;64:404-406. doi:10.4103/ijd.IJD_77_18
  5. Jones AL, Koerner RJ, Natarajan S, et al. Dietzia papillomatosis sp. nov., a novel actinomycete isolated from the skin of an immunocompetent patient with confluent and reticulated papillomatosis. Int J Syst Evol Microbiol. 2008;58(pt 1):68-72. doi:10.1099/ijs.0.65178-0
  6. Cohen PR. Follicular contact dermatitis revisited: a review emphasizing neomycin-associated follicular contact dermatitis. World J Clin Cases. 2014;2:815-821. doi:10.12998/wjcc.v2.i12.815
  7. Butterworth T, Johnson WC. Justa-clavicular beaded lines. Arch Dermatol. 1974;110:891-893.
  8. Calka O, Metin A, Ozen S. A case of disseminated and recurrent infundibulo-folliculitis responsive to treatment with isotretinoin. J Dermatol. 2002;29:431-434.
  9. Goihman-Yahr M. Disseminate and recurrent infundibulofolliculitis: response to psoralen plus UVA therapy. Int J Dermatol. 1999;38:75-76.
  10. Hinds GA, Heald PW. A case of disseminate and recurrent infundibulofolliculitis responsive to treatment with topical steroids. Dermatol Online J. 2008;14:11.
References
  1. Hitch JM, Lund HZ. Disseminate and recurrent infundibulo-folliculitis: report of a case. Arch Dermatol. 1968;97:432-435.
  2. Ma BC, Sahni VN, Sahni DR, et al. Disseminate and recurrent infundibulofolliculitis: an under-recognized yet treatable entity. J Drugs Dermatol. 2021;20:1353-1354. doi:10.36849/jdd.6173
  3. Nair SP, Gomathy M, Kumar GN. Disseminate and recurrent infundibulo- folliculitis in an Indian patient: a case report with review of literature. Indian Dermatol Online J. 2017;8:39-41. doi:10.4103/2229- 5178.198775
  4. Rekha S, Kumar V, Rao P, et al. Disseminate and recurrent infundibulofolliculitis. Indian J Dermatol. 2019;64:404-406. doi:10.4103/ijd.IJD_77_18
  5. Jones AL, Koerner RJ, Natarajan S, et al. Dietzia papillomatosis sp. nov., a novel actinomycete isolated from the skin of an immunocompetent patient with confluent and reticulated papillomatosis. Int J Syst Evol Microbiol. 2008;58(pt 1):68-72. doi:10.1099/ijs.0.65178-0
  6. Cohen PR. Follicular contact dermatitis revisited: a review emphasizing neomycin-associated follicular contact dermatitis. World J Clin Cases. 2014;2:815-821. doi:10.12998/wjcc.v2.i12.815
  7. Butterworth T, Johnson WC. Justa-clavicular beaded lines. Arch Dermatol. 1974;110:891-893.
  8. Calka O, Metin A, Ozen S. A case of disseminated and recurrent infundibulo-folliculitis responsive to treatment with isotretinoin. J Dermatol. 2002;29:431-434.
  9. Goihman-Yahr M. Disseminate and recurrent infundibulofolliculitis: response to psoralen plus UVA therapy. Int J Dermatol. 1999;38:75-76.
  10. Hinds GA, Heald PW. A case of disseminate and recurrent infundibulofolliculitis responsive to treatment with topical steroids. Dermatol Online J. 2008;14:11.
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Diffusely Scattered Linear Folliculopapular Eruption

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A 31-year-old man with a darker skin tone and a history of childhood eczema presented with papules on the trunk and upper arms of several years’ duration. The papules were persistent and were generally asymptomatic but occasionally pruritic. The patient previously had self-treated with over-the counter lotions and topical hydrocortisone with no appreciable changes. On physical examination, a hyperpigmented patch with follicular monomorphic papules was noted across the upper back along with confluent papules and plaques predominantly on the trunk and upper arms. Additionally, the patient had several monomorphic papules in a linear distribution on the neck. Review of systems and examination of the remaining skin were unremarkable. A biopsy from a representative papule on the left upper back was performed.

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Erythematous Annular Scaly Plaques on the Upper Chest

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Erythematous Annular Scaly Plaques on the Upper Chest

THE DIAGNOSIS: Tinea Corporis

Due to the scaly and acute nature of the rash, a potassium hydroxide (KOH) preparation was performed, and hyphal elements were floridly present. After further questioning, the patient reported finding a stray kitten a few weeks before the onset of the eruption and shared a picture of it lying on her chest in the area corresponding with the main distribution of the rash (Figure). Based on the patient’s personal history and the positive KOH preparation, a diagnosis of tinea corporis was made. She was immediately started on fluconazole 300 mg once weekly for 4 weeks and naftifine gel 1%, which she used for 6 to 8 weeks with complete resolution of the eruption.

FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.
FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.

Tinea corporis is a dermatophyte infection that typically affects exposed areas of the skin such as the chest, arms, and legs. Spread via human-to-human contact, Trichophyton rubrum is the most common cause worldwide. The second most common is Trichophyton mentagrophytes, which is spread through animal-to-human contact.1,2

Symptoms of tinea corporis usually appear 1 to 3 weeks after exposure and manifest as itchy scaly papules that spread outward, forming annular, circinate, and petaloid erythematous plaques with central clearing. The condition most commonly is diagnosed through the examination of scale from the affected area using a KOH preparation, which will reveal hyphae when positive.2-4 Cultures are the gold standard for identifying dermatophyte species,5 but results can take several weeks. Biopsy also can confirm the diagnosis by showing the presence of hyphae in the stratum corneum, which can be highlighted using periodic acid–Schiff or silver stains.3

Topical antifungals are the first-line treatment for cutaneous dermatophyte infections.3-5 The most effective topical therapies are allylamines and azoles, which work by inhibiting the growth of the fungus. Allylamines are more effective than azoles due to their fungicidal properties and ability to penetrate the skin more effectively.6,7 Topical medications should be applied at least 2 cm beyond the infected area for 2 to 4 weeks or until the infection has cleared.3 Systemic antifungals may be necessary in more complicated cases.

It is important to consider a broad differential and take into consideration the distribution of the plaques, the patient’s history, and other clinical features when differentiating tinea corporis from other conditions. Erythema annulare centrifugum more often presents as nonpruritic annular plaques with a trailing scale instead of a leading scale seen in tinea corporis. Biopsy exhibits a dense, perivascular, lymphocytic infiltrate in superficial vessels, resembling a coat sleeve.3,8 Pemphigus foliaceous can manifest with painful crusted scaly plaques and vesicles in a seborrheic distribution. Biopsy reveals subcorneal acantholytic vesicles and can be confirmed on direct immunofluorescence.3,8 Subacute cutaneous lupus erythematosus presents with annular plaques that often are symmetric and most prominent in sun-exposed areas, sparing the face.3,9,10 It can be associated with other autoimmune conditions as well as medications such as thiazides, terbinafine, and calcium channel blockers. Additionally, 76% to 90% of patients are Ro/SSA antibody positive.3 Biopsy often demonstrates follicular plugging, perivascular and periadnexal lymphocytic infiltrates, and mucin.3,10 Lastly, pityriasis rosea typically begins with a herald patch, followed by a widespread rash that often appears in a Christmas tree distribution.3

References
  1. Havlickova B, Czaika VA, Friedrich M. Epidemiological trends in skin mycoses worldwide. Mycoses. 2008;51 (suppl 4):2-15. doi: 10.1111 /j.1439-0507.2008.01606.x
  2. Yee G, Al Aboud AM. Tinea corporis. 2022 Aug 8. In: StatPearls [Internet]. StatPearls Publishing; 2023
  3. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 4th ed. Elsevier; 2018.
  4. Diseases resulting from fungal and yeast. In: James WD, Berger TG, Elston DM, et al, eds. Andrews’ Diseases of The Skin: Clinical Dermatology. 12th ed. Elsevier; 2016: 289-290.
  5. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6 . doi:10.7573/dic.2020-5-6
  6. El-Gohary M, van Zuuren EJ, Fedorowicz Z, et al. Topical antifungal treatments for tinea cruris and tinea corporis. Cochrane Database Syst Rev. 2014;2014:CD009992. doi:10.1002/14651858 .CD009992.pub2
  7. Wolverton SE. Comprehensive Dermatologic Drug Therapy. 4th ed. Elsevier; 2018.
  8. Burgdorf W. Erythema annulare centrifugum and other figurate erythemas. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. McGraw-Hill; 2008: 366-368.
  9. Modi GM, Maender JL, Coleman N, et al. Tinea corporis masquerading as subacute cutaneous lupus erythematosus. Dermatol Online J. 2008;14:8.
  10. Stavropoulos PG, Goules AV, Avgerinou G, et al. Pathogenesis of subacute cutaneous lupus erythematosus. J Eur Acad Dermatol Venereol. 2008;22:1281.
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The authors have no relevant financial disclosures to report.

Correspondence: Aeja Weiss, MD, Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, 111 Probandt St #302, San Antonio, TX 78204 (aeja89@gmail.com).

Cutis. 2025 March;115(3):E17-E18. doi:10.12788/cutis.1185

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Correspondence: Aeja Weiss, MD, Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, 111 Probandt St #302, San Antonio, TX 78204 (aeja89@gmail.com).

Cutis. 2025 March;115(3):E17-E18. doi:10.12788/cutis.1185

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The authors have no relevant financial disclosures to report.

Correspondence: Aeja Weiss, MD, Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, 111 Probandt St #302, San Antonio, TX 78204 (aeja89@gmail.com).

Cutis. 2025 March;115(3):E17-E18. doi:10.12788/cutis.1185

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THE DIAGNOSIS: Tinea Corporis

Due to the scaly and acute nature of the rash, a potassium hydroxide (KOH) preparation was performed, and hyphal elements were floridly present. After further questioning, the patient reported finding a stray kitten a few weeks before the onset of the eruption and shared a picture of it lying on her chest in the area corresponding with the main distribution of the rash (Figure). Based on the patient’s personal history and the positive KOH preparation, a diagnosis of tinea corporis was made. She was immediately started on fluconazole 300 mg once weekly for 4 weeks and naftifine gel 1%, which she used for 6 to 8 weeks with complete resolution of the eruption.

FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.
FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.

Tinea corporis is a dermatophyte infection that typically affects exposed areas of the skin such as the chest, arms, and legs. Spread via human-to-human contact, Trichophyton rubrum is the most common cause worldwide. The second most common is Trichophyton mentagrophytes, which is spread through animal-to-human contact.1,2

Symptoms of tinea corporis usually appear 1 to 3 weeks after exposure and manifest as itchy scaly papules that spread outward, forming annular, circinate, and petaloid erythematous plaques with central clearing. The condition most commonly is diagnosed through the examination of scale from the affected area using a KOH preparation, which will reveal hyphae when positive.2-4 Cultures are the gold standard for identifying dermatophyte species,5 but results can take several weeks. Biopsy also can confirm the diagnosis by showing the presence of hyphae in the stratum corneum, which can be highlighted using periodic acid–Schiff or silver stains.3

Topical antifungals are the first-line treatment for cutaneous dermatophyte infections.3-5 The most effective topical therapies are allylamines and azoles, which work by inhibiting the growth of the fungus. Allylamines are more effective than azoles due to their fungicidal properties and ability to penetrate the skin more effectively.6,7 Topical medications should be applied at least 2 cm beyond the infected area for 2 to 4 weeks or until the infection has cleared.3 Systemic antifungals may be necessary in more complicated cases.

It is important to consider a broad differential and take into consideration the distribution of the plaques, the patient’s history, and other clinical features when differentiating tinea corporis from other conditions. Erythema annulare centrifugum more often presents as nonpruritic annular plaques with a trailing scale instead of a leading scale seen in tinea corporis. Biopsy exhibits a dense, perivascular, lymphocytic infiltrate in superficial vessels, resembling a coat sleeve.3,8 Pemphigus foliaceous can manifest with painful crusted scaly plaques and vesicles in a seborrheic distribution. Biopsy reveals subcorneal acantholytic vesicles and can be confirmed on direct immunofluorescence.3,8 Subacute cutaneous lupus erythematosus presents with annular plaques that often are symmetric and most prominent in sun-exposed areas, sparing the face.3,9,10 It can be associated with other autoimmune conditions as well as medications such as thiazides, terbinafine, and calcium channel blockers. Additionally, 76% to 90% of patients are Ro/SSA antibody positive.3 Biopsy often demonstrates follicular plugging, perivascular and periadnexal lymphocytic infiltrates, and mucin.3,10 Lastly, pityriasis rosea typically begins with a herald patch, followed by a widespread rash that often appears in a Christmas tree distribution.3

THE DIAGNOSIS: Tinea Corporis

Due to the scaly and acute nature of the rash, a potassium hydroxide (KOH) preparation was performed, and hyphal elements were floridly present. After further questioning, the patient reported finding a stray kitten a few weeks before the onset of the eruption and shared a picture of it lying on her chest in the area corresponding with the main distribution of the rash (Figure). Based on the patient’s personal history and the positive KOH preparation, a diagnosis of tinea corporis was made. She was immediately started on fluconazole 300 mg once weekly for 4 weeks and naftifine gel 1%, which she used for 6 to 8 weeks with complete resolution of the eruption.

FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.
FIGURE. Patient with a kitten sleeping on the upper chest in the area of the main distribution of the rash diagnosed as tinea corporis.

Tinea corporis is a dermatophyte infection that typically affects exposed areas of the skin such as the chest, arms, and legs. Spread via human-to-human contact, Trichophyton rubrum is the most common cause worldwide. The second most common is Trichophyton mentagrophytes, which is spread through animal-to-human contact.1,2

Symptoms of tinea corporis usually appear 1 to 3 weeks after exposure and manifest as itchy scaly papules that spread outward, forming annular, circinate, and petaloid erythematous plaques with central clearing. The condition most commonly is diagnosed through the examination of scale from the affected area using a KOH preparation, which will reveal hyphae when positive.2-4 Cultures are the gold standard for identifying dermatophyte species,5 but results can take several weeks. Biopsy also can confirm the diagnosis by showing the presence of hyphae in the stratum corneum, which can be highlighted using periodic acid–Schiff or silver stains.3

Topical antifungals are the first-line treatment for cutaneous dermatophyte infections.3-5 The most effective topical therapies are allylamines and azoles, which work by inhibiting the growth of the fungus. Allylamines are more effective than azoles due to their fungicidal properties and ability to penetrate the skin more effectively.6,7 Topical medications should be applied at least 2 cm beyond the infected area for 2 to 4 weeks or until the infection has cleared.3 Systemic antifungals may be necessary in more complicated cases.

It is important to consider a broad differential and take into consideration the distribution of the plaques, the patient’s history, and other clinical features when differentiating tinea corporis from other conditions. Erythema annulare centrifugum more often presents as nonpruritic annular plaques with a trailing scale instead of a leading scale seen in tinea corporis. Biopsy exhibits a dense, perivascular, lymphocytic infiltrate in superficial vessels, resembling a coat sleeve.3,8 Pemphigus foliaceous can manifest with painful crusted scaly plaques and vesicles in a seborrheic distribution. Biopsy reveals subcorneal acantholytic vesicles and can be confirmed on direct immunofluorescence.3,8 Subacute cutaneous lupus erythematosus presents with annular plaques that often are symmetric and most prominent in sun-exposed areas, sparing the face.3,9,10 It can be associated with other autoimmune conditions as well as medications such as thiazides, terbinafine, and calcium channel blockers. Additionally, 76% to 90% of patients are Ro/SSA antibody positive.3 Biopsy often demonstrates follicular plugging, perivascular and periadnexal lymphocytic infiltrates, and mucin.3,10 Lastly, pityriasis rosea typically begins with a herald patch, followed by a widespread rash that often appears in a Christmas tree distribution.3

References
  1. Havlickova B, Czaika VA, Friedrich M. Epidemiological trends in skin mycoses worldwide. Mycoses. 2008;51 (suppl 4):2-15. doi: 10.1111 /j.1439-0507.2008.01606.x
  2. Yee G, Al Aboud AM. Tinea corporis. 2022 Aug 8. In: StatPearls [Internet]. StatPearls Publishing; 2023
  3. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 4th ed. Elsevier; 2018.
  4. Diseases resulting from fungal and yeast. In: James WD, Berger TG, Elston DM, et al, eds. Andrews’ Diseases of The Skin: Clinical Dermatology. 12th ed. Elsevier; 2016: 289-290.
  5. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6 . doi:10.7573/dic.2020-5-6
  6. El-Gohary M, van Zuuren EJ, Fedorowicz Z, et al. Topical antifungal treatments for tinea cruris and tinea corporis. Cochrane Database Syst Rev. 2014;2014:CD009992. doi:10.1002/14651858 .CD009992.pub2
  7. Wolverton SE. Comprehensive Dermatologic Drug Therapy. 4th ed. Elsevier; 2018.
  8. Burgdorf W. Erythema annulare centrifugum and other figurate erythemas. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. McGraw-Hill; 2008: 366-368.
  9. Modi GM, Maender JL, Coleman N, et al. Tinea corporis masquerading as subacute cutaneous lupus erythematosus. Dermatol Online J. 2008;14:8.
  10. Stavropoulos PG, Goules AV, Avgerinou G, et al. Pathogenesis of subacute cutaneous lupus erythematosus. J Eur Acad Dermatol Venereol. 2008;22:1281.
References
  1. Havlickova B, Czaika VA, Friedrich M. Epidemiological trends in skin mycoses worldwide. Mycoses. 2008;51 (suppl 4):2-15. doi: 10.1111 /j.1439-0507.2008.01606.x
  2. Yee G, Al Aboud AM. Tinea corporis. 2022 Aug 8. In: StatPearls [Internet]. StatPearls Publishing; 2023
  3. Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 4th ed. Elsevier; 2018.
  4. Diseases resulting from fungal and yeast. In: James WD, Berger TG, Elston DM, et al, eds. Andrews’ Diseases of The Skin: Clinical Dermatology. 12th ed. Elsevier; 2016: 289-290.
  5. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6 . doi:10.7573/dic.2020-5-6
  6. El-Gohary M, van Zuuren EJ, Fedorowicz Z, et al. Topical antifungal treatments for tinea cruris and tinea corporis. Cochrane Database Syst Rev. 2014;2014:CD009992. doi:10.1002/14651858 .CD009992.pub2
  7. Wolverton SE. Comprehensive Dermatologic Drug Therapy. 4th ed. Elsevier; 2018.
  8. Burgdorf W. Erythema annulare centrifugum and other figurate erythemas. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. McGraw-Hill; 2008: 366-368.
  9. Modi GM, Maender JL, Coleman N, et al. Tinea corporis masquerading as subacute cutaneous lupus erythematosus. Dermatol Online J. 2008;14:8.
  10. Stavropoulos PG, Goules AV, Avgerinou G, et al. Pathogenesis of subacute cutaneous lupus erythematosus. J Eur Acad Dermatol Venereol. 2008;22:1281.
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Erythematous Annular Scaly Plaques on the Upper Chest

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Erythematous Annular Scaly Plaques on the Upper Chest

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A 60-year-old woman with a history of keratinocyte carcinomas, hypertension, diabetes mellitus, and anxiety presented to the dermatology department with a widespread rash of more than 2 weeks’ duration. The patient had tried 1 to 2 days of self-treatment with triamcinolone cream that she had previously been prescribed for an unknown dermatitis and zinc oxide cream, which caused considerable inflammation of the rash and prompted her to discontinue use. She could not recall any recent use of new personal care products or medications or eating any new foods. She also denied any recent yard work, known arthropod bites, illnesses, prolonged sun exposure, or constitutional symptoms. Her medications included metformin, hydrochlorothiazide, losartan, and sertraline. She also reported taking daily supplements of vitamins D, K, and C as well as acetaminophen and ibuprofen as needed. Physical examination revealed several 2- to 4-cm, erythematous, annular, circinate, petaloid plaques with scale mostly on photodistributed areas of the central anterior chest, neck, lower cheeks, and chin as well as a few scattered lesions with similar morphology on the arms, lower abdomen, left buttock, and back.

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