eMedicine Specialties > Dermatology > Fungal Infections
Majocchi Granuloma
Updated: Nov 20, 2009
Introduction
Background
Majocchi granuloma can be defined as a deep folliculitis due to a cutaneous dermatophyte infection.1 Majocchi granuloma is most commonly due to Trichophyton rubrum infection. Majocchi granuloma tends to occur in young women who frequently shave their legs, although Majocchi granuloma also is seen in men.2 Majocchi granuloma also commonly occurs as a result of the use of potent topical steroids on unsuspected tinea. Majocchi granuloma is also known as granuloma trichophyticum.
Many species of dermatophytes can cause Majocchi granuloma. Today, Majocchi granuloma is usually due to T rubrum; however, Trichophyton violaceum was the most common organism identified historically. Other causes of Majocchi granuloma include Trichophyton mentagrophytes and Epidermophyton floccosum.
In 1883, Professor Domenico Majocchi (1849-1929) first described this disorder, he called granuloma tricofitico.3 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.
Also see the eMedicine article Tinea Corporis.
Pathophysiology
The pathophysiology of the fungal infection and defense mechanisms against superficial dermatomycosis has been studied.4 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, Majocchi granuloma usually begins as a suppurative folliculitis and may culminate in a granulomatous reaction.5 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.6
Frequency
United States
To the authors' knowledge, no specific data on the incidence and prevalence of Majocchi granuloma exist.
International
To the authors' knowledge, no specific data on the incidence and prevalence of Majocchi granuloma exist. A patient was recently described in Brazil.2
Clinical
History
- Patients may complain of nonpruritic solitary or multiple persistent papulopustules or plaques.
- The legs are common sites for Majocchi granuloma in young women who frequently shave.
- Patients may also complain of onychomycosis or tinea pedis.
- Two clinical forms of Majocchi granuloma 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 Majocchi granuloma.
- 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 Majocchi granulomas is debatable because these patients lack specific cellular immunity. These granulomas may be widespread.6
- Antibiotic use does not result in Majocchi granuloma because Majocchi granuloma 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 Majocchi granuloma.
Physical
- Majocchi granuloma 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 Majocchi granuloma on the scrotum, caused by T rubrum, has been described.7
- Majocchi granuloma may begin as solitary or multiple well-circumscribed oval patches or as indistinct scaling ones. Majocchi granuloma 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 Majocchi granuloma 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.
- Majocchi granuloma may rarely resemble Kaposi sarcoma, as it does in patients with AIDS or lymphocytoma cutis. In such cases, Majocchi granulomas are painful and appear as blue-red papules and nodules on an erythematous base.8
Causes
- Majocchi granuloma is a foreign body granuloma most commonly caused by T rubrum. T violaceum was the most common organism identified historically.
- Other causes of Majocchi granuloma include T mentagrophytes and E floccosum.9
- The fungal infections may be due to or linked with a widespread contiguous dermatophytosis, immunosuppression, and/or the use of topical steroids.
Differential Diagnoses
| Acne Keloidalis Nuchae | Lymphocytoma Cutis |
| Eosinophilic Pustular Folliculitis | Scabies |
| Erythema Induratum (Nodular Vasculitis) | |
| Folliculitis | |
| Kaposi Sarcoma |
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
Laboratory 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
Majocchi granuloma 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
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 Majocchi granuloma.
- 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 Majocchi granuloma exist.
- The treatment of secondary bacterial infections and the removal of any exacerbating factors (eg, topical steroid use, occlusion) are indicated.
Medication
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.
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.
Terbinafine (Lamisil)
Allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. This inhibition results in a deficiency in ergosterol within the fungal cell wall that causes fungal cell death. Terbinafine is available by prescription only. Some clinicians reserve the use of this drug for more widespread and/or resistant infections because of its broad coverage and cost. This medication is effective and well tolerated in children.
Dosing
Adult
Topical: Apply to affected area qd
Oral: 250 mg/d PO for 4-6 wk; not to exceed 12 wk
Pediatric
Topical: Administer as in adults
Weight-based dosing:
12-20 kg: 62.5 mg/d PO for 4-6 wk
20-40 kg: 125 mg/d PO for 4-6 wk
>40 kg: Administer as in adults
Interactions
Possible interactions with drugs metabolized by the CYP-450 (P-450) 2D6 enzyme (eg, TCAs, propranolol, theophylline); may decrease cyclosporin levels; rifampin increases clearance; cimetidine may increase toxicity
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Reduce oral dose in renal insufficiency; discontinue if hepatobiliary dysfunction, neutropenia, Stevens-Johnson syndrome, or changes in ocular lens or retina develop; discontinue topical use if chemical irritation develops; monitor patient response and adjust caffeine dosage during combined treatment with terbinafine; observe for signs of caffeine toxicity (headache, agitation, insomnia, diuresis, fever)
Butenafine (Mentax)
Potent antifungal related to the allylamines. Damages fungal cell membranes, arresting fungal cell growth. Available in cream form only. Use 1% cream.
Dosing
Adult
Apply to affected area qd
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
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
Clotrimazole (Lotrimin, Mycelex)
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%.
Dosing
Adult
Apply to affected area bid
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
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
Itraconazole (Sporanox)
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.
Dosing
Adult
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
5 mg/kg/d PO for 4-6 wk
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
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
Precautions
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
Further Outpatient Care
- The best objective measure in Majocchi granuloma 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 Majocchi granuloma.
Complications
- Uncommonly, scarring and alopecia may result from Majocchi granuloma.
- Widespread cutaneous disease and/or fungal septicemia are potential complications in patients who are immunocompromised.
Prognosis
- Majocchi granuloma cure is expected with appropriate systemic antifungal therapy.
- To the authors' knowledge, no data about relapse rates or the complications of not treating Majocchi granuloma exist.
Patient Education
- Patients should be educated about the cause of Majocchi granuloma, as well as the predisposing and exacerbating factors.
Miscellaneous
Medicolegal 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 Majocchi granuloma.
References
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Keywords
Majocchi granuloma, MG, granuloma trichophyticum, granuloma tricofitico, dermatophytes
Contributor Information and Disclosures
Author
Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.
Coauthor(s)
Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, New Jersey Medical School
Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Medical Editor
David P Fivenson, MD, Associate Director, St Joseph Mercy Hospital Dermatology Program, Ann Arbor, Michigan
David P Fivenson, MD is a member of the following medical societies: American Academy of Dermatology, Medical Dermatology Society, Michigan Dermatological Society, Michigan State Medical Society, Photomedicine Society, Society for Investigative Dermatology, and Wound Healing Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Managing Editor
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.
CME Editor
Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.