Erythrasma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Erythrasma is a dermatological disease caused by Corynebacterium minutissimum. Erythrasma was first officially identified by Burchardt in 1859. Corynebacterium minitissium was first isolated and discovered to be the cause of Erythrasma in 1961. Erythrasma usually presents with erythematous lesions, maceration, and reddish-brown scales indicative of hyperkeratosis. The lesions are usually found in skin folds, and also commonly present in the interdigital regions in hands and feet. Symptoms include reddish-brown scaly patches, itching, pain if irritated, skin shedding, blisters, softening and whitening of the skin, foul odor, and thickening and yellowing of the toenails. Erythrasma develops when Corynebacterium minitissium infiltrates the stratum corneum and proliferate. Hyperkeratosis leads to the formation of reddish-brown lesions characteristic of erythrasma. Microscopic pathology of erythrasmas includes thickening of stratum corneum, decreased electron density around intracellular bacteria and those in direct contact with the cell wall, and widening of intracelluar space, allowing bacterial invasion, and separation of the horny cells. Erythrasma is most commonly found in women over 40 years old, in individuals living in humid and tropical/subtropical climates, and in military personnel. Risk factors for erythrasma include individual and environmental conditions predisposing bacterial infection and proliferation. This includes overweight and obesity, diabetes, immunocompromise, and hyperhidrosis. Erythrasma must be differentiated from other dermatological conditions that present with reddish-brown scales and itching, as well as other diseases resulting from corynebacteria infection. Diagnostic laboratory tests performed for suspected Erythrasma include those that confirm a Corynebacterium minitissimum infection. The most common laboratory test is a Wood’s lamp examination; coral-red fluorescence is indicative of Corynebacterium minitissimum. The mainstay of erythrasma medical therapy is topical and systemic antibiotic therapy. The primary antibiotics used for local and widespread infection include fusidic acid, clindamycin, clarithromycin, and erythromycin, respectively. Additionally, there are studies that display efficacy of systemic administration of tetracycline and chloramphenicol. There is evidence that fusidic acid therapy is more effective than topical clarithromycin and systemic erythromycin, but may be indicated less due to poorer efficiency and patient compliance. Administration of chloramphenicol is limited due to its suppression of bone marrow and heightening risk of developing neutropenia, agranulocytosis and aplastic anaemia. Effective measures of preventing erythrasma are preventative of Corynebacterium minutissimum infection and proliferation. Secondary prevention of erythrasma involves prophylactic use of antibacterial soap on the previously affected region.

Erythrasma was first officially identified by Burchardt in 1859. Corynebacterium minitissium was first isolated and discovered to be the cause of Erythrasma in 1961.

There is no classification system established for erythrasma.

Erythrasma develops when Corynebacterium minitissium infiltrates the stratum corneum and proliferates. Hyperkeratosis leads to the formation of reddish-brown lesions characteristic of erythrasma. Microscopic pathology of erythrasma includes thickening of stratum corneum, decreased electron density around intracellular bacteria and those in direct contact with the cell wall, and widening of intracelluar space, allowing bacterial invasion, and separation of the horny cells. Erythrasma is associated with dermatological conditions, including additional corynebacterium pathologies.

Erythrasma is caused by Corynebacterium minutissimum.

Erythrasma must be differentiated from other dermatological conditions that present with reddish-brown scales and itching, as well as other diseases resulting from corynebacteria infection.

Global epidemiological and demographical information for erythrasma is not well documented. Among diagnosis of dermatomycoses, the incidence of erythrasma was approximated as 4,500 per 100,000 individuals in 1951. Studies on erythrasma prevalence have found high rates in military populations. Erythrasma is most common in individuals over 40 years old. Women are more commonly affected by erythrasma than men. There is no known racial predisposition to erythrasma. Erythrasma of the groin is more commonly found in humid, tropical or subtropical regions; interdigital erythrasma does not have a geographic predisposition.

Risk factors for erythrasma include individual and environmental conditions predisposing bacterial infection and proliferation.^[1]

There is no diagnostic screening procedure for erythrasma.

Upon Corynebacterium minitissium infection, the affected region of the epidermis becomes erythematous and present with pruritus. As hyperkeratosis and keratolysis occurs, the red-pink lesions becomes reddish-brown and begins to scale and shed. Without treatment, the lesions usually remain and spreading occurs concurrent with the spread of bacterial infection. Complications of erythrasma result from persistence of symptoms or spread of infection. Without treatment, the prognosis for erythrasma varies based on the emergence and presence of complications. With treatment, the prognosis for erythrasma is good; complete resolution of symptoms and recovery is expected.

Erythrasma usually presents with reddish-brown scaly patches, itching pain if irritated, skin shedding, blisters, softening and whitening of the skin, foul odor, and thickening and yellowing of the toenails. Erythrasma patients should be examined for history of overweight or obesity, diabetes, and hyperhidrosis.

Erythrasma presents with erythematous lesions, maceration, and reddish-brown scales indicative of hyperkeratosis. The lesions are usually found in skin folds, and also commonly present in the interdigital regions in hands and feet. Erythrasma patients are usually well-appearing, barring complications.

Laboratory tests performed for suspected erythrasma include those that confirm a Corynebacterium minitissimum infection. The most common laboratory test is a Wood’s lamp examination; coral-red fluorescence is indicative of Corynebacterium minitissimum. A culture may be performed to specify the pathogen; Corynebacterium minutissimum will present as non-hemolytic smooth colonies that are 1-1.5mm in size. Gram stain analysis of Corynebacterium minitissimum may reveal slightly curved bacterial rods that display violet or blue coloration, indicative of gram positive.

There are no diagnostic electrocardiogram findings for erythrasma.

There are no diagnostic x ray findings for erythrasma.

There are no diagnostic CT findings for erythrasma.

There are no diagnostic MRI findings for erythrasma.

There are no diagnostic echocardiography or ultrasound findings for erythrasma.

A Wood Lamp examination is commonly performed on patients with suspected Erythrasma to determine a Corynebacterium minitissimum infection. Coral-red fluorescence is indicative of Corynebacterium minitissimum, as a result of produced coproporphyrin III.^[2][3]

The mainstay of erythrasma medical therapy is topical and systemic antibiotic therapy. The primary antibiotics used for local and widespread infection include fusidic acid, clindamycin, clarithromycin, and erythromycin, respectively. Additionally, there are studies that display efficacy of systemic administration of tetracycline and chloramphenicol. There is evidence that fusidic acid therapy is more effective than topical clarithromycin and systemic erythromycin, but may be indicated less due to poorer efficiency and patient compliance. Administration of chloramphenicol is limited due to its suppression of bone marrow and heightening risk of developing neutropenia, agranulocytosis and aplastic anaemia.

Surgical intervention is not recommended for the management of erythrasma.

Effective measures of preventing erythrasma are prevention of Corynebacterium minutissimum infection and proliferation.

Secondary prevention of erythrasma involves prophylactic use of antibacterial soap on the previously affected region.^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Erythrasma was first discovered by Burchardt in 1859. Corynebacterium minitissium was first isolated and discovered to be the cause of Erythrasma in 1961.

• Erythrasma was first discovered by Burchardt in 1859.^[1]
• Corynebacterium minitissium was first isolated and discovered to be the cause of erythrasma in 1961.^[2][3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

There is no classification system established for erythrasma.

There is no classification system established for erythrasma.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Erythrasma develops when Corynebacterium minitissium infiltrates the stratum corneum and proliferates. Hyperkeratosis leads to the formation of reddish-brown lesions characteristic of erythrasma. Microscopic pathology of erythrasma includes thickening of stratum corneum, decreased electron density around intracellular bacteria and those in direct contact with the cell wall, and widening of intracelluar space, allowing bacterial invasion, and separation of the horny cells. Erythrasma is associated with dermatological conditions, including additional corynebacterium pathologies.

• Erythrasma develops when Corynebacterium minitissium infiltrates the stratum corneum and proliferates.^[1]
  • The bacteria proliferates on the epidermis and develops at the intracellular level of the stratum corneum.
  • Penetration of the skin occurs when the horny cells of the plasma membranes rupture.
  • Keratolysis occurs due to the removal of keratin fibrils from the bacteria.
    • The exact cause, chemical or systemic, of the keratolysis is unknown.^[2]
• Hyperkeratosis leads to the formation of reddish-brown lesions characteristic of erythrasma.^[3]

• Erythrasma presents with the following microscopic findings:^[1]
  • Thickening of stratum corneum without signs of parakeratosis
  • Largest concentration of Corynebacterium minitissium in the upper third of the stratum corneum
  • Widening of intracelluar space, allowing bacterial invasion, and separation of the horny cells
  • Disappearance of plasma cell membranes at the sites of Corynebacterium minitissium infiltration.
  • Decreased electron density around intracellular bacteria and those in direct contact with the cell wall

Erythrasma is associated with the following dermatological conditions:

• Other cornyebacterium-infection pathologies:^[4]
  • Pitted keratolysis
  • Trichobacteriosis
• Tinea pedis
• Tinea versicolor^[5]
• Intertrigo^[6]
• Psoriasis^[7]
• Dermatophytosis
• Candidiasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Cornyebacterium is a gram positive, facultatively anaerobic, non motile, rod shaped actinobateria. Infection by diphtheroids tend to occur in elderly, neutropenic, or immunocompromised patients, and those who have indwelling prosthetic devices such as heart valves, neurologic shunts, or catheters. Some nondiphtheria species of Corynebacterium produce disease in specific animal species, and some of these are also human pathogens. Some species attack healthy hosts, and others attack immunosuppressed hosts. Some of their effects include granulomatous lymphadenitis, pneumonitis, pharyngitis, skin infections, and endocarditis. Endocarditis caused by Corynebacterium spp. is particularly seen in patients with indwelling intravascular devices.

• Corynebacterium is a genus of Gram-positive, facultatively anaerobic, non-motile, rod-shaped actinobacteria. Most do not cause disease, but are part of normal human skin flora.
• Some nondiphtheria species of Corynebacterium produce disease in specific animal species, and some of these are also human pathogens. Some species attack healthy hosts, and others attack immunosuppressed hosts. Some of their effects include granulomatous lymphadenitis, pneumonitis, pharyngitis, skin infections, and endocarditis. Endocarditis caused by Corynebacterium spp. is particularly seen in patients with indwelling intravascular devices.
• Infection by diphtheroids tend to occur in elderly, neutropenic, or immunocompromised patients, and those who have indwelling prosthetic devices such as heart valves, neurologic shunts, or catheters.
• Some species of Corynebacterium have sequenced genomes that range in size from 2.5 – 3 Mbp. They can be found in many environments including soil, trees and skin. The non-diptheiroid Corynebecterium can also be found in human mucous membranes. They grow slowly, even on enriched media, and undergo “Chinese Letter” division. Species of Corynebacterium have been used in the mass production of various amino acids including L-Glutamic Acid, a popular food additive that is made at a rate of 1.5 million tons/ year by Corynebacterium. The metabolic pathways of Corynebacterium have been further manipulated to produce L-Lysine and L-Threonine.

• Corynebacterium diphtheriae, the cause of diphtheria in humans.

• Corynebacterium amycolatum
• Corynebacterium aquaticum
• Corynebacterium bovis
• Corynebacterium equi
• Corynebacterium flavescens
• Corynebacterium glutamicum
• Corynebacterium haemolyticum
• Corynebacterium jeikeiun (corynebacteria of group JK)
• Corynebacterium minutissimum
• Corynebacterium parvum (also called Propionibacterium acnes)
• Corynebacterium pseudodiptheriticum (also called Corynebacterium hofmannii)
• Corynebacterium pseudotuberculosis (also called Corynebacterium ovis)
• Corynebacterium pyogenes
• Corynebacterium urealyticum (corynebacteria of group D2)
• Corynebacterium renale
• Corynebacterium striatum, (Axillary odor [2])
• Corynebacterium tenuis (Trichomycosis palmellina, Trichomycosis axillaris) [3]
• Corynebacterium ulcerans
• Corynebacterium xerosis

• Corynebacterium jeikeium^[1]

• Preferred regimen : Vancomycin 1 gm IV q12h
• Alternative regimen : Penicillin G AND Anti pseudomonal aminoglycosides like Tobramycin, Gentamicin, Amikacin

• Corynebacterium urealyticum^[2]

• 1. Post renal transplant obstructive uropathy

• Preferred regimen (1): Vancomycin 1 gm IV q12h
• Preferred regimen (2): Teicoplanin 6 mg/kg/day IV q24h

Template:Wikispecies

• Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.CS1 maint: Extra text: authors list (link) CS1 maint: Extra text (link)
• Database of Corynebacterial Transcription Factors and Regulatory Networks
• Rollins, David M. University of Maryland: Pathogentic Microbiology: Corynebacterium [4]

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Erythrasma must be differentiated from other dermatological conditions that present with reddish-brown scales and itching, as well as other diseases resulting from corynebacteria infection.

Erythrasma must be differentiated from other dermatological conditions that present with reddish-brown scales and itching, as well as other diseases resulting from corynebacteria infection. These include:

Disease	Findings
Psoriasis	Presents with erythema and formation of silvery scales on the epidermis, resulting in itching and pain.[1] Differentiates from erythrasma in that it is usually located throughout the entire body; erythrasma usually manifests in skin folds of the armpit, groin, and perianal regions.[2] Psoriasis is an autoimmune disorder and is not caused by Corynebacteria; therapeutic options include topical corticosteroids, systemic anti-inflammatory therapies (such as methotrexate and cyclosporine), and UVA/UVB phototherapy.[2] Psoriasis is a chronic, recurrent condition; erythrasma will usually resolve with sufficient treatment.
Dermatophytosis	Presents with lesions that vary based on the location of the mycosis, but usually displays in a circular shape with erythema, scaling, and itching at the point of infiltration.[3] Differentiated by its mycotic cause. Visually distinct from Erythrasma by consistently forming circular-shaped “ring” lesions. Treatment involves topical antifungal medication, including miconazole, clotrimazole, ketoconazole, terbinafine, naftifine, and butenafine.[4]
Skin candidiasis	Presents with rash that displays erythema and itching, as well as folliculitis.[5] Differentiated from erythrasma in that it is caused by Candida fungal infection. While erythrasma usually manifests in moist locations, such as skin folds, skin candidiasis is usually found in wet or dry regions of the body. Treatment includes antifungal therapy, including fluconazole, caspofungin, micafungin, anidulafungin, and additional topical and systemic options.[6]
Intertrigo	An inflammatory condition of the epidermis caused by repeated friction between adjacent skin folds.[7] Presents with erythema, itching, and scaling in primarily moist regions of the body. Differentiates from erythrasma in that it can progress to discharge and pain if untreated.[8] May be caused by bacterial or mycotic infection, as well as a non-infectious inflammatory response to moisture and friction. Treatment varies based on the cause; it is important to differentiate erythrasma from intertrigo due to the former’s singular cause as Corynebacterium minitissium to determine appropriate therapy.
Contact dermatitis	An inflammatory condition of the epidermis resulting from direct contact with an allergen or irritant. Contact dermatitis is similar to erythrasma due to the usual presentation of erythema and itching. It differentiates from erythrasma by manifesting with blisters, pain, and discharge. Differentiated from erythrasma by its cause: an allergic response by contact to a specific surface or entity. There is no indication of bacterial infection. Common causes include chemicals from cosmetic and hygienic products, fabrics, metals, and animal hair or skin. Therapy involves avoiding the original cause and application of topical or oral corticosteroids and analgesics.[9]
Seborrheic dermatitis	Presents with erythema and white-yellow scaling skin that sheds, accompanied by pruritus and flaking. Is primarily found in the face, upper chest, and retro-auricular area. Similarly to erythrasma, it can affect skin folds, including the axillae and the genitals.[10] It is differentiated from erythrasma by its varied causes; seborrheic dermatitis causes are not fully known and are speculated to be autoimmunal, neurological, or from nutrition deficiency.[11] Therapy focuses on treating the inflammation, including corticosteroids, or topical antifungal medication if a mycotic causes is determined.[12]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Global epidemiological and demographical information for erythrasma is not well documented. Among diagnosis of dermatomycoses, the incidence of erythrasma was approximated as 4,500 per 100,000 individuals in 1951. Studies on erythrasma prevalence have found high rates in military populations. Erythrasma is most common in individuals over 40 years old. Women are more commonly affected by erythrasma than men. There is no known racial predisposition to erythrasma. Erythrasma of the groin is more commonly found in humid, tropical or subtropical regions; interdigital erythrasma does not have a geographic predisposition.

• Among diagnosis of dermatomycoses, the incidence of erythrasma was approximated as 4,500 per 100,000 individuals in 1951.^[1]
  • Erythrasma of the groin was approximated as 3,000 per 100,000 individuals.

• Studies on erythrasma prevalence have found high rates in military populations.
  • The prevalence of erythrasma is approximately 77.1% in Danish military recruits.^[2]
  • The prevalence of erythrasma is approximately 41.7% in South Korean soldiers.^[3]

• Erythrasma is most common in individuals over 40 years old.^[4][5]

• Women are more commonly affected by erythrasma than men.^[4][5]

There is no racial predisposition to erythrasma.

• Erythrasma of the groin is most commonly found in humid tropical and sub-tropical climates.^[1]
  • Interdigital erythrasma does not have a geographic predisposition.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Risk factors for erythrasma include individual and environmental conditions predisposing bacterial infection and proliferation.

Risk factors for erythrasma include individual and environmental conditions predisposing bacterial infection and proliferation, such as:^[1]

• Obesity or overweight
• Diabetes
• Immunocompromised persons
• Hyperhidrosis^[2]
• Living in a humid, tropical climate^[3]
  • Interdigital erythrasma does not have a geographic predisposition
• Inpatient residence at a psychiatric hospital^[4]
• Participating in the military^[5][6]
• Being age 40 years or older^[7][8]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

There is no diagnostic screening procedure for erythrasma.

There is no diagnostic screening procedure for erythrasma.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Upon Corynebacterium minitissium infection, the affected region of the epidermis becomes erythematous and present with pruritus. As hyperkeratosis and keratolysis occurs, the red-pink lesions becomes reddish-brown and begins to scale and shed. Without treatment, the lesions usually remain and spreading occurs concurrent with the spread of bacterial infection. Complications of erythrasma result from persistence of symptoms or spread of infection. Without treatment, the prognosis for erythrasma varies based on the emergence and presence of complications. With treatment, the prognosis for erythrasma is good; complete resolution of symptoms and recovery is expected.

• Upon Corynebacterium minitissium infection, the affected region of the epidermis becomes erythematous and present with pruritus.^[1]
• As hyperkeratosis and keratolysis occurs, the red-pink lesions becomes reddish-brown and begins to scale and shed.
• Without treatment, the lesions usually remain and spreading occurs concurrent with the spread of bacterial infection.

Complications of erythrasma result from persistence of symptoms or spread of infection:^[2]

• Septicemia
• Contact dermatitis
• Lichenification if lesions are persistently scratched
• Pigmentation scarring and disfiguration
• Dermatophytosis and bacterial co-infections

• Without treatment, the prognosis for erythrasma varies.^[2]
  • The condition is usually chronic and recurrent if the Corynebacterium minitissium infection is not treated.
  • Potential complications of infection, such as septicemia, can lead to poor prognosis.
• With treatment, the prognosis for erythrasma is good; complete resolution of symptoms and recovery is expected.