ERYTHRASMABackgroundErythrasma is a chronic superficial infection of the intertriginous areas of the skin. The incriminated organism is Corynebacterium minutissimum, which usually is present as a normal human skin inhabitant. In 1996, Corynebacterium afermentans was reported in one case.[1]

PathophysiologyCorynebacteria invade the upper third of the stratum corneum; under favorable conditions such as heat and humidity, these organisms proliferate. The stratum corneum is thickened. The organisms that cause erythrasma are seen in the intercellular spaces as well as within cells, dissolving keratin fibrils. The coral-red fluorescence of scales seen under Wood light is secondary to the production of porphyrin by these diphtheroids.

EpidemiologyFrequency

InternationalThe incidence of erythrasma is reported to be around 4%. This infection is observed all over the world; the widespread form is found more frequently in the subtropical and tropical areas than in other parts of the world.[2]

In a recent study conducted in Turkey, the rate of erythrasma was found to be 46.7% among 122 patients with interdigital foot lesions.[3]

Mortality/Morbidity

Erythrasma is usually a benign condition. However, it may become widespread and invasive in predisposed and immunocompromised individuals; this is very rare in immunocompetent hosts. In such individuals, this organism has caused infections other than erythrasma. These include abscess formation (3 cases),[4]intravascular catheter–related infections (2 cases),[5] primary bacteremia (3 cases), peritoneal catheter–related infections (2 cases),[5, 6] endocarditis (2 cases),[7, 8] pyelonephritis (2 cases),[9, 10] cellulitis (1 case),[11] endophthalmitis (1 case),[12] arteriovenous fistula infection (1 case), cutaneous granuloma (1 case),[13] and meningitis (1 case).[14]

Race

The incidence of erythrasma is higher in black patients.Sex

Both sexes are equally affected by erythrasma; however, the crural form of erythrasma is more common in men. A 2008 study found that interdigital erythrasma was more common in women (83% of 24 patients).[15]

Age

The incidence of erythrasma increases with age, but no age group is immune to the disease. The youngest patient reported to have erythrasma is a 1-year-old infant.

HistoryDark discoloration associated with erythrasma is usually limited to body folds that are naturally moist and occluded. Infection commonly is asymptomatic, but it can be pruritic. The duration of erythrasma ranges from months to years. Widespread involvement of trunk and limbs is possible.Immunosuppressed patients with erythrasma and the risk of complications are of special concern. Evaluate and treat possible concomitant infection. Suspect diabetes in recurrent erythrasma. Address and modify risk factors for successful treatment

PhysicalThe typical appearance of erythrasma is well-demarcated, brown-red macular patches. The skin has a wrinkled appearance with fine scales (see the image below).

Lichenification and hyperpigmentation are common. The skin occasionally has a wrinkled appearance with scales. KOH test results are negative. Courtesy of Michael Bryan, MD.Infection commonly is located on the inner thighs, crural region, scrotum, and toe webs. The axillae, submammary area, periumbilical region, and intergluteal folds are less commonly involved in erythrasma. Toe web lesions appear as maceration, with the fourth interdigital space most frequently affected.[15]

Due to the association of erythrasma with other corynebacterial skin infections such as pitted keratolysis and trichomycosis axillaris, all body folds and feet should be screened.

CausesC minutissimum, a member of the normal skin flora, is the causative agent of erythrasma. The bacterium is a lipophilic, gram-positive, non–spore-forming, aerobic, and catalase-positive diphtheroid. C minutissimum ferments glucose, dextrose, sucrose, maltose, and mannitol.Predisposing factors for erythrasma include the following:

Excessive sweating/hyperhidrosis Delicate cutaneous barrier Obesity Diabetes mellitus Warm climate Poor hygiene Advanced age Other immunocompromised states

Differential Diagnoses Acanthosis Nigricans Candidiasis, Cutaneous Contact Dermatitis, Allergic Contact Dermatitis, Irritant Intertrigo Psoriasis, Plaque Seborrheic Dermatitis Tinea Corporis Tinea Cruris Tinea Pedis

Laboratory Studies Wood light examination of erythrasma lesions reveals coral-red fluorescence of lesions. Results may be

negative if the patient bathed prior to presentation.[22]Note the image below. The cause of this color fluorescence has been attributed to excess coproporphyrin III synthesis by these organisms, which accumulates in cutaneous tissue and emits a coral-red fluorescence when exposed to a Wood light.[23, 23]

Under Wood lamp examination, the porphyrins produced by the bacteria fluoresce with a coral pink color. A small focus is visible on this photo. If the patient recently has bathed, the pigment may be washed away. In suspicious cases, a repeat examination the following day may be necessary. Courtesy of Michael Bryan, MD.

Gram staining reveals of erythrasma lesions gram-positive filamentous rods. In culture media composed of 20% fetal bovine serum, 2% agar, 78% tissue culture medium #199, and 0.05% tris, the organisms grow as nonhemolytic, 1- to 1.5-mm smooth colonies. Methylene blue stain may be used to highlight both the fungal spores of pityriasis versicolor and the curved or club-shaped bacterial rods of C minutissimum, the causative agent of erythrasma, in case both organisms coexist.[17]

Next Section: Histologic Findings

Histologic FindingsThe diphtheroid bacteria that cause erythrasma are present in the horny layer as rods and filaments.[24]

Medical CarePhotodynamic therapy using red light (broadband, peak at 635 nm) has been reported to clear erythrasma in 23% of 13 patients and to improve erythrasma in the remaining patients.[25]

Medication SummaryThe goals of pharmacotherapy for erythrasma are to reduce morbidity, eradicate the infection, and prevent complications.

Anti-infectivesClass Summary

Antibacterial and/or antifungal agents are used to eradicate C minutissimum and possible concomitant infection. Erythromycin is the DOC. Infection may be treated with topical and/or oral agents. Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting. C minutissimum is generally susceptible to penicillins, first-generation cephalosporins, erythromycin, clindamycin, ciprofloxacin, tetracycline, and vancomycin. However, multiresistant strains have been isolated.[26, 27, 28, 29]

In a recent susceptibility study of 40 patients, several antibiotics were tested, including penicillin G, ampicillin, cefaclor, amoxicillin-clavulanate, ampicillin-sulbactam, tetracycline, erythromycin, ofloxacin, fusidic acid, levofloxacin, and azithromycin. The study revealed statistically significant resistance to erythromycin, azithromycin, penicillin, and ampicillin. Significant susceptibility was statistically found to amoxicillin-clavulanate, cefaclor, and fusidic acid.[30]

In a large double-blind, placebo-controlled, randomized trial, 151 patients older than 18 years were randomized into 5 groups and were given either erythromycin, single-dose clarithromycin, topical fusidic acid, placebo cream, or placebo tablets. Fusidic acid cream was significantly more effective than other therapies. Additionally, the group who received clarithromycin did better at 48 hours than did the group that received erythromycin. However, there was no statistical difference on day 7 and day 14.[31]

Because culture and antibiogram are not performed routinely in daily clinical practice, the recommended initial topical treatment is fusidic acid cream. If this drug is not available, then topical erythromycin solution may be an alternative. In cases of topical treatment failure, erythromycin, single-dose clarithromycin, or amoxicillin-clavulanate should be chosen for the systemic treatment.[30]

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Erythromycin (E.E.S., E-Mycin, Ery-Tab) 

DOC that inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.

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Clarithromycin (Biaxin) 

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.Fusidic acid (Zeta) 

Topical antibacterial that inhibits bacterial protein synthesis, causing bacterial death.Use 2% cream.

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Miconazole topical (Femazole, Lotrimin, Monistat) 

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out and resulting in fungal cell death.Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.Use 2% cream.Benzoic acid 6%, salicylic acid 3% (Whitfield's ointment) 

Treats infection and inflammation associated with erythrasma.Clindamycin (Cleocin) 

Has a bacteriostatic effect; interferes with bacterial protein synthesis similarly to erythromycin and chloramphenicol by binding to 50S subunit of bacterial ribosome.

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Tetracycline (Achromycin) 

Inhibits cell growth by inhibiting mRNA translation. Binds to 16S part of 30S ribosomal subunit and prevents amino-acyl tRNA from binding to A site of ribosome. Binding is reversible in nature.

ComplicationsNote the following possible complications:

Fatal septicemia in immunocompromised patients with erythrasma Infective endocarditis in valvular heart disease patients with erythrasma Postsurgical wound infection in erythrasma patients

PrognosisThe prognosis for erythrasma is excellent; however, the condition tends to recur if the predisposing factors are not eliminated.

Patient EducationPatients with erythrasma should be instructed to keep the area dry.

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