AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Majocchi granuloma (MG) can be defined as a deep folliculitis due to a cutaneous dermatophyte infection.¹ MG is most commonly due to Trichophyton rubrum infection. MG commonly occurs in young women who frequently shave their legs. MG also commonly occurs as a result of the use of potent topical steroids on unsuspected tinea. MG is also known as granuloma trichophyticum.

Many species of dermatophytes can cause MG. Today, MG is usually due to T rubrum; however, Trichophyton violaceum was the most common organism identified historically. Other causes of MG include Trichophyton mentagrophytes and Epidermophyton floccosum.

In 1883, Professor Domenico Majocchi (1849-1929) first described this disorder, he called granuloma tricofitico.² He is also credited with describing a type of chronic pigmented purpura: purpura annularis telangiectodes, which is commonly known as Majocchi disease. Majocchi, an important figure in Italian academic dermatology, was a professor of dermatology first at the University of Parma and later at the University of Bologna.

eMedicine's Tinea Corporis article may be helpful.

Pathophysiology

The pathophysiology of the fungal infection and defense mechanisms against superficial dermatomycosis has been studied.³ Two series of experimental infections of T mentagrophytes were made on the forearm of a male volunteer with topical steroid ointment and vehicle alone. Steroid ointment suppressed the immune reactions locally to produce little inflammatory reaction with abundant fungal elements (so-called atypical tinea) and a mixed cell granuloma.

While inflammatory tinea capitis or kerion is the result of a hypersensitivity reaction to a dermatophytic infection, MG usually begins as a suppurative folliculitis and may culminate in a granulomatous reaction.⁴ Nineteen cases of kerion of the scalp in children were evaluated. Histopathological findings demonstrated a spectrum from suppurative folliculitis to dense granulomatous infiltrates without a clear relationship with the clinical features.

Widespread trichophytic granulomas may occur in patients receiving immunosuppressive therapy for leukemia or lymphoma, autoimmune diseases, and post–organ transplantation. However, these dermatophyte infections may also occur in patients with atopic dermatitis, probably because of their immunological susceptibility.⁵

Frequency

United States

To the authors' knowledge, no specific data on the incidence and prevalence of MG exist.

International

To the authors' knowledge, no specific data on the incidence and prevalence of MG exist.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Patients may complain of nonpruritic solitary or multiple persistent papulopustules or plaques.
• • The legs are common sites for MG in young women who frequently shave.
  • Patients may also complain of onychomycosis or tinea pedis.
• Two clinical forms of MG exist.
• • The follicular type is secondary to trauma or topical corticosteroid use. It commonly occurs in young women who repeatedly shave their legs. Long-standing immunosuppression with steroids certainly predisposes individuals to widespread dermatophytosis, a component of which may be follicular papules consistent with MG.
  • The subcutaneous nodular type occurs in immunocompromised hosts such as persons with graft versus host disease, those who undergo bone marrow and organ transplantation, and those receiving long-term immunosuppressive medication for lymphoma, leukemia, and autoimmune diseases. Whether trichophytic abscesses in neutropenic bone marrow transplant recipients are MGs is debatable because these patients lack specific cellular immunity. These granulomas may be widespread.⁵
• Antibiotic use does not result in MG because MG is an atypical course of a fungal disease that may result from a modified local and/or systemic immune response or a damaged skin barrier.
• The use of potent topical steroids, especially under occlusion or on preexistent tinea, may predispose the patient to MG.

Physical

• MG or granuloma trichophyticum may develop on any hair-bearing area, but most often, the scalp, face, forearms, hands, and legs are involved. A superficial perifollicular form of MG on the scrotum, caused by T rubrum, has been described.²⁶ 
• MG may begin as solitary or multiple well-circumscribed oval patches or as indistinct scaling ones. MG evolves into perifollicular papulopustules and nodules with or without background erythema and scaling.
• A plaque may demonstrate keloidal features, but these findings are unusual.
• Nodules are often clustered, but they can be solitary as well.
• Pressure does not result in pus exudation.
• Unlike a kerion, granuloma trichophyticum does not become clinically suppurative until late in its course, unless secondarily impetigo develops.
• If the cutaneous features of MG are associated with the use of topical steroids, they may be affected by the complications of topical steroid therapy, including poikiloderma with atrophy and telangiectasia, papular rosacea, or a hypopigmented patch suggestive of indeterminate leprosy.
• MG may rarely resemble Kaposi sarcoma, as it does in patients with AIDS or lymphocytoma cutis. In such cases, MGs are painful and appear as blue-red papules and nodules on an erythematous base.²⁷

Causes

• MG is a foreign body granuloma most commonly caused by T rubrum. T violaceum was the most common organism identified historically.
• Other causes of MG include T mentagrophytes and E floccosum.⁶
• The fungal infections may be due to or linked with a widespread contiguous dermatophytosis, immunosuppression, and/or the use of topical steroids.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Tinea incognito
Bacterial folliculitis
Herpetic folliculitis
Pseudofolliculitis barbae
Nodular scabies
Follicular mucinosis
Poikiloderma with atrophy
Telangiectasia without scaling
Papular rosacea
Indeterminate leprosy
Kerion

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• A potassium hydroxide (KOH) preparation of scales and pustules usually reveals no hyphal elements.
• Samples from a contiguous dermatophyte infection, if present, may stain positive.

Other Tests

• Gram stains, calcofluor stains, scale cultures, and exudate or tissue biopsy samples may reveal hyphae when the KOH test result is negative.
• In general, tissue homogenate cultures are more sensitive than special stains.

Histologic Findings

MG is essentially a deep suppurative and granulomatous folliculitis. The earliest sign is hyphal invasion in the cornified keratinocytes of the hair follicle, which produces a suppurative folliculitis with the rupture of the hair follicle and the spillage of its contents into the dermis. This rupture causes a granulomatous dermal response. Such nodules may heal with fibrosis. Periodic acid-Schiff or Gomori methenamine-silver stains may reveal fungal hyphae in the tissue, surrounded by a foreign body granulomatous reaction.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Systemic antifungal treatment is preferred in both patients who are immunocompetent and in those who are immunocompromised.

• Treatment should last at least 4-6 weeks. For example, the administration of systemic terbinafine for 6 weeks is the best treatment option in a patient with a transplanted kidney and MG.
• Oral antifungals are usually necessary because topical agents alone are not effective. For example, systemic antifungal medication is the best option for patients who are immunocompromised.
• Physicians should avoid the use of compound products containing a potent topical steroid (see Medical/Legal Pitfalls).
• To the authors' knowledge, no specific data about treating immunocompromised patients with MG exist.
• The treatment of secondary bacterial infections and the removal of any exacerbating factors (eg, topical steroid use, occlusion) are indicated.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The 2 classes of antifungal medications most commonly used to treat dermatophyte infections are the azoles and the allylamines. Azoles inhibit lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, an important component of the fungal cell wall. Membrane damage leads to permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, an enzyme that converts squalene to ergosterol, leading to the accumulation of toxic levels of squalene in the cell and cell death. Examples of both classes of antifungal antibiotics are available for topical and systemic administration.

To achieve the best results, particularly with follicular or extensive disease, the authors often recommend a combination of topical and systemic therapy.

Drug Category: Antifungal agents

The mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.

Drug Name	Butenafine (Mentax)
Description	Potent antifungal related to the allylamines. Damages fungal cell membranes, arresting fungal cell growth. Available in cream form only. Use 1% cream.
Adult Dose	Apply to affected area qd
Pediatric Dose	<12 years: Not established >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Use topically; not for use in eyes, vagina, or other internal routes

Drug Name	Clotrimazole (Lotrimin, Mycelex)
Description	Broad-spectrum agent that inhibits fungal growth by altering cell membrane permeability, causing fungal cell death. Reevaluate diagnosis if no clinical improvement seen after 4 wk. Often a first-line topical drug. Prescription only. Cream, solution/spray, and lotion forms available. Use 1%.
Adult Dose	Apply to affected area bid
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Not for treatment of systemic fungal infections; avoid contact with eyes; discontinue use and initiate appropriate therapy if irritation or sensitivity develops

Drug Name	Itraconazole (Sporanox)
Description	Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. Absorption improved with food and in presence of normal gastric acidity. Patients should be cautioned against ingesting grapefruit juice while on itraconazole therapy (decreased oral bioavailability of itraconazole). Discontinue if sensitivity or chemical irritation occurs; for external use only; avoid contact with eyes.
Adult Dose	200 mg PO qd for 4-6 wk; not to exceed 400 mg/d; increase in 100-mg increments if no improvement (administer >200 mg/d in divided doses)
Pediatric Dose	5 mg/kg/d PO for 4-6 wk
Contraindications	Documented hypersensitivity; congestive heart failure or history of congestive heart failure (itraconazole cap for treatment of superficial fungal infections), concurrent administration with cisapride, midazolam, triazolam, lovastatin, dofetilide, pimozide, levacetylmethadol (levomethadyl), quinidine, lovastatin, simvastatin, ergot alkaloids metabolized by CYP3A4, such as dihydroergotamine, ergometrine (ergonovine), ergotamine, and methylergometrine (methylergonovine); women contemplating pregnancy
Interactions	As CYP3A4 inhibitor (P450 metabolism), many drugs have interactions when coadministered with itraconazole; avoid alcohol use because disulfiramlike reaction may occur; antacids may reduce absorption; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; high doses may increase tacrolimus and cyclosporine plasma concentrations; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (eg, lovastatin, simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death; may increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce levels (phenytoin metabolism may be altered) Reduced itraconazole plasma concentrations reported with concurrent use of H2 antagonist and aluminum-, calcium-, or magnesium-containing products (administer aluminum-, calcium-, or magnesium-containing products at least 1 h before or 2 h after itraconazole cap); enhances anticoagulant effects of coumarinlike drugs
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Caution in hepatic insufficiencies; adverse effects include headache, nausea, vomiting, reversible elevation of liver enzyme levels, hepatotoxicity, hallucinations, hypokalemia, heart failure, edema, congestive heart failure, and neutropenic disorder; oral solution and oral capsules not to be used interchangeably; injection not for use in patients with CrCl <30 mL/min, and use with caution in patients with CrCl of 30-80 mL/min

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• The best objective measure is to observe the patient clinically.
• Culture and KOH specimens may be useful, but relapse occurs if the use of occlusion and topical steroids continues or is reinitiated.

Deterrence/Prevention

• The avoidance of occlusion, topical steroids use, and leg shaving may prevent this eruption.

Complications

• Uncommonly, scarring and alopecia may result.
• Widespread cutaneous disease and/or fungal septicemia are potential complications in patients who are immunocompromised.

Prognosis

• Cure is expected with appropriate systemic antifungal therapy.
• To the authors' knowledge, no data about relapse rates or the complications of not treating MG exist.

Patient Education

• Patients should be educated about the cause of MG, as well as the predisposing and exacerbating factors.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Physicians should not use potent topical steroids to treat possible dermatophytic infections.
• Combination products such as betamethasone dipropionate with clotrimazole 1% cream should be used with care or not at all.
• • The authors do not favor the use of such products in children younger than 12 years.
  • If such medications are used in adolescents, the authors suggest doing so for only 2 weeks.
• Similarly, physicians should apply topical steroids with occlusion only when they are confident that the eruption is not a dermatophytosis, because this treatment may predispose the patient to MG.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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24. Sequeira M, Burdick AE, Elgart GW, Berman B. New-onset Majocchi's granuloma in two kidney transplant recipients under tacrolimus treatment. J Am Acad Dermatol. Mar 1998;38(3):486-8. [Medline].
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Article Last Updated: May 12, 2008