Erythrasma

Etiology

In 1961, Sarkay et al examined scrapings from erythrasma lesions using microscopy and identified gram-positive rods corresponding to C minutissimum.[4] The bacterium can cause severe disease in immunocompromised patients, including cutaneous fistulas, granulomatous lesions, and subcutaneous abscesses. Corynebacterium species normally exist as commensal skin bacteria.[5][6] Owing in part to the potential for serious complications in immunocompromised hosts, the genome of C minutissimum has been sequenced by organizations within the Centers for Disease Control and Prevention in Atlanta, Georgia.[7] Additional environmental and host factors that increase erythrasma risk include residence in humid climates, excessive sweating, diabetes mellitus, inadequate hygiene, advanced age, coexisting skin disorders, and obesity.[8][9]

Epidemiology

Most erythrasma cases occur in healthy adults. The infection is less common in children. Prevalence increases in hot, humid climates.[10] Institutional living is an additional risk factor, particularly in settings such as college dormitories, military barracks, and nursing facilities.[11] Incidence may rise with age. The condition occurs worldwide and appears more frequent in men. Epidemiologic data suggest erythrasma is most common among African Americans.

Pathophysiology

C minutissimum colonizes the upper stratum corneum under moist, occluded conditions. The organism produces coproporphyrin III, resulting in coral-red fluorescence on Wood lamp examination.[12]

Histopathology

A biopsy is rarely required for erythrasma diagnosis. Microscopic examination of affected skin reveals rod-like organisms in the stratum corneum, although these bacteria may be missed. Coccoid forms may also be present. Histopathology demonstrates hyperkeratosis with a mild lymphohistiocytic perivascular infiltrate in the upper dermis.

Gram staining shows gram-positive rods. Prolonged culture of C minutissimum may result in gram-negative staining and variable morphologies. The organism is not acid-fast. C minutissimum produces acid from dextrose, sucrose, and maltose, but not lactose. In vitro studies demonstrate sensitivity to erythromycin and resistance to penicillin. Visualization is challenging on hematoxylin and eosin–stained slides, but periodic acid-Schiff and Giemsa stains may enhance detection.

History and Physical

Erythrasma is most commonly observed in the toe webs, followed by the groin crease. The condition is less frequently found in the axilla. Affected individuals may report mildly pruritic skin discoloration in these areas. Scaling may also be present. Lesions are typically dark red and moist. Pruritus intensity varies. Lesions present as well-demarcated macular patches. The affected skin often exhibits a wrinkled appearance.

Interdigital Presentation

C minutissimum is the most common cause of bacterial infection in the interdigital spaces of the feet. Infection produces maceration and scaling. The fourth and fifth toes are most often affected. Lesions are usually asymptomatic but may be pruritic. Coinfection with dermatophytes or Candida species occasionally occurs. Potassium hydroxide preparation may be required to assess for coexisting infection.[13]

Intertriginous Variant

Lesions may be mildly pruritic or asymptomatic. The condition presents as patches or plaques in intertriginous areas, producing a "cigarette paper" appearance. Fine scaling may be present (see Image. Axillary Erythrasma).[14]

Disciform Pattern

Disciform erythrasma is a rare variant that may involve any body region. This form occurs more frequently in Black women in tropical climates. Lesions are well-defined, scaly plaques on the trunk and proximal limbs and exhibit coral-red fluorescence under Wood lamp examination.

Evaluation

Wood lamp examination aids in the diagnosis of erythrasma. However, empiric treatment based on clinical evaluation is reasonable in the absence of a lamp. Coral-red fluorescence results from coproporphyrin III produced by C minutissimum (see Image. Erythrasma Under Wood Lamp). Biopsy of suspected erythrasma may reveal rod-like organisms.[15] Visualization is often difficult, and Giemsa or periodic acid-Schiff staining may be required. These limitations render biopsy impractical for routine diagnosis.

Treatment / Management

Erythrasma responds to topical and oral therapies, although recurrence is common. Topical treatments include fusidic acid, clindamycin, and erythromycin. Fusidic acid, an antibiotic unavailable in the United States, inhibits aminoacyl–tRNA transfer during protein synthesis in susceptible bacteria. Researchers at University Hospital in Izmir, Turkey, conducted a randomized, double-blind, placebo-controlled trial involving 151 patients aged 18 years or older. Participants received 1 of 5 regimens: a single 1-g clarithromycin tablet; erythromycin 1 g orally daily for 14 days; a matching oral placebo for 14 days; fusidic acid 2% cream applied twice daily for 14 days; or a matching placebo cream twice daily for 14 days. Fusidic acid cream demonstrated superior reduction in Wood lamp scores compared with oral clarithromycin and erythromycin. Scores were based on coral-red fluorescence intensity, reflecting removal of coproporphyrin III from the stratum corneum. Complete clinical response was achieved in 96% of patients treated with fusidic acid, compared with 66% with clarithromycin and 53% with erythromycin.[16][17][18][19] Extensive erythrasma requires oral therapy. Oral options include a single 1-g dose of clarithromycin or 1 g of erythromycin daily, administered in divided doses for 14 days.(B2)

Clarithromycin offers advantages over erythromycin because it can be administered as a single dose. Clarithromycin is a macrolide that inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit. Hydroxy-to-O-methyl substitution at position 6 of the lactone ring enhances bioavailability relative to erythromycin. Clarithromycin may be more effective for groin erythrasma. Few comparative studies between erythromycin and clarithromycin have been conducted. Adverse effects of both oral therapies include nausea, abdominal pain, metallic taste, hearing loss, ventricular arrhythmias, cholestatic jaundice, and toxic epidermal necrolysis.

Differential Diagnosis

The differential diagnosis for erythrasma includes seborrheic dermatitis, inverse psoriasis, candidiasis, dermatophytosis, tinea versicolor, parapsoriasis, and pityriasis rotunda. Seborrheic dermatitis typically presents with greasy, erythematous lesions along the scalp and nasolabial folds, while inverse psoriasis exhibits shiny plaques. Coral-red fluorescence under Wood lamp examination facilitates distinction of erythrasma from both seborrheic dermatitis and inverse psoriasis. Potassium hydroxide preparation may be required to differentiate erythrasma from dermatophytosis affecting the toe webs. Erythrasma involving the groin is readily distinguished from tinea cruris by the presence of a scaling border in tinea cruris.

Prognosis

Outcomes for most patients with erythrasma are excellent. Recurrence is possible if predisposing factors are not addressed; the infection does not produce residual sequelae in immunocompetent individuals. In contrast, C minutissimum can spread rapidly in immunocompromised patients.

Complications

Complications of erythrasma occur primarily in immunocompromised individuals and include endocarditis, abscess formation, intravascular catheter–associated infection, cellulitis, and pyelonephritis. Prompt recognition and appropriate antimicrobial therapy reduce the risk of systemic spread.