Background

Erythrasma 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]

Pathophysiology
Corynebacteria 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.

Epidemiology
Frequency
International
The 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 catheterrelated infections (2 cases),[5]
primary bacteremia (3 cases), peritoneal catheterrelated 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.

History
Dark 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.

Physical
The 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.

Causes
C minutissimum, a member of the normal skin flora, is the causative agent of erythrasma.
The bacterium is a lipophilic, gram-positive, nonspore-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

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]

Histologic Findings

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

edical Care

Photodynamic 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 Summary
The goals of pharmacotherapy for erythrasma are to reduce morbidity, eradicate the
infection, and prevent complications.

Anti-infectives
Class 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]
View full drug information

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.
View full drug information

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.
View full drug information

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.
View full drug information

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.

Complications
Note 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