JEADV
DOI: 10.1111/jdv.12715
REVIEW ARTICLE
Infectious eczematoid dermatitis: a comprehensive review T. Yamany, R.A. Schwartz* Dermatology and Pathology, Rutgers University New Jersey Medical School, Newark, NJ, USA *Correspondence: R. A. Schwartz. E-mail: [email protected]
Abstract Infectious eczematoid dermatitis (IED) is characterized by an acute eczematous eruption triggered by purulent discharge from a primary infected site. Alcohol consumption, cigarette smoking and occupations with higher incidences of contact dermatitis portend increased risk for IED. Staphylococcus aureus is the most commonly cultured microbe from affected skin, with Streptococcus species the second most. Patients are first evident with peripherally spreading vesicles and pustules radiating from an infected site. Older areas of involvement become crusty, scaly and erythematous. Diagnosis is clinical. Other eczematous rashes, including autoeczemitization and contact dermatitis, should be on the differential diagnosis list. The treatment centres on topical antibiotics and soaks. Prognosis has improved since the advent of antibiotics. However, cases with multiple relapses and poor response to therapy are still observed. Received: 30 April 2014; Accepted: 28 July 2014
Conflicts of interest None declared.
Funding sources None.
Introduction
Epidemiology
Infectious eczematoid dermatitis (IED) is a condition seldom mentioned in the literature. It is characterized by an acute eczematous eruption brought on by a primary infected exudative site. Engman,1 in 1902, was the first to describe the entity and gave it the name ‘Staphylogenetic eczematoid dermatitis’. In 1920, Sutton2 described a diffuse eczematous reaction occurring days after the development of IED and delineated new treatment regimens for both. Several authors confirmed the efficacy of antibiotic treatments for IED in the late 19300 s, the same time antibiotics began to gain popularity.3–9 In 1953, Kennedy et al.4 lamented that little was known about the aetiology of the disease, but that, thanks to antibiotics, much progress had been made in its management. In 1992, Karvonen et al.10 detailed risk factors for IED development. A recent survey11 noted the rate of IED among patients admitted to a specialized dermatology inpatient service to be 2.9%, identical to the percentage found by Engman in 1902. Remarkably, despite its apparently stable and non-trivial incidence, IED has garnered little attention in the literature. This paper is meant to revive awareness of this entity by providing a comprehensive review.
The first estimation of incidence came in 1902 with Engman’s1 initial description of IED. Engman1 stated that, out of 1200 new cases seen in Hardaway’s dermatologic outpatient clinic, 35, or 2.9%, matched the description of IED. The timeframe over which the 1200 new cases were seen was not specified. Nearly a century later, similar results were obtained, but in an inpatient setting, in a study performed at the Mayo Clinic. From 2000 to 2010, Storan et al.11 looked at reasons for admission to the adult dermatology inpatient service at the Mayo Clinic. They found that 2.9% of 2216 admissions were attributed to IED. In 1950, in a case series of 30 patients with IED, the baseline skin type was classified as dry, oily or neither.7 It was found that 17 patients had dry skin, two had oily skin and 11 had neither. Occupation was found to be a risk factor for development of IED in situations where the initial insult was an irritant contact dermatitis. Vitamin deficiencies and endocrine abnormalities were not reported to be significant risk factors, but how such states were measured was not explained. Additionally, 11 out of 30 patients had a family history of allergy, with nine of those 11 suffering the diffuse eczematous reaction that Sutton2 had described 30 years earlier. In a case-control study performed in Finland in 1992, Karvonen et al.10 found alcohol consumption and cigarette smoking to be risk factors for the development of IED among men aged 19–50. For alcohol consumption of 50 grams per day vs. no
Definition IED is an acute, eczematous eruption resulting from autosensitization to purulent drainage. It originates near a primary infection and spreads peripherally.
JEADV 2015, 29, 203–208
© 2014 European Academy of Dermatology and Venereology
Yamany and Schwartz
204
(a)
(b)
Figure 1 Infectious eczematoid dermatitis. Note the oozing, crusting and vesicles surrounding a draining otitis media (a, b).
intake, the odds ratio of developing IED was 1.7 (95% CI of 1.03–2.70). For cigarette smoking of 20 cigarettes a day vs. no smoking, the odds ratio of developing IED was 2.1 (95% CI of 1.20–3.70). They also found that coffee consumption, age and marital status were not risk factors for the development of IED.
Aetiology The aetiology of IED is unclear. We adhere to the current prevailing belief that it is an acute eruption around an infected exudative site. The infected site is often a draining otitis media or externa, mastitis, boil, blepharitis or ulcer.12–15 Studies have shown that in the majority of cases, Staphylococcus is responsible. In 1948, Slatkin9 cultured the wounds of IED patients and found 50% to be purely coagulase positive Staphylococcus, 12% to be a mix of coagulase positive Staphylococcus and beta-haemolytic Streptococcus, and 38% to be a mixed culture of Staphylococcus, Streptococcus and other organisms. In 1950, McDaniel et al.7 cultured the wounds of 30 patients and found 24 grew Staphylococcus aureus and 11 grew Streptococcus. In 1952, Kile et al.5 cultured the wounds of patients with IED. Of those cultures that did not come back sterile or contaminated, 31 grew Staphylococcus aureus, one grew haemolytic Streptococcus, and two grew both. An alternative aetiology implicating psychosomatic factors was proposed but never gained traction.4 That theory’s support, at the time, was an earlier study on the relationship between atopic dermatitis and emotional lability.16,17
is similar to that of Templeton and associates: a purulent drainage causes a secondary infection or an autosensitization with the Staphylococcal products acting as haptens.15,20,21 Infectivity from person-to-person that Engman described is no longer believed to be a viable way to contract the disease.12 Autoinoculation, on the other hand, does appear to be the primary mechanism.12 However, in an experiment by McDaniel et al.7, 22 out of 30 patients with IED had normal and abraded skin of the upper back inoculated with exudate from a lesion. The inoculated sites were covered with a patch and re-examined 24 and 48 hours later. In all cases, the only reaction seen was faint erythema along the lines of abrasion – undermining confidence in the autoinoculation theory.
Clinical manifestations IED begins as a circumscribed plaque with overlying vesicles and pustules, spreading peripherally from a central source of infection. As the lesion spreads peripherally, older areas of involvement become characterized by erythema, oozing, crusting and scaling (Fig. 1).4,12 Lichenification, weeping or exudation may also be seen.14,20,21 In an alternate presentation, the peripherally spreading plaque lacks the initial vesicles and pustules and instead has the same appearance as the older areas of involvement: oozing, crusted and scaly in nature.1 This disorder can manifest anywhere on the body. However, in children, the ears, nares and face are predominately affected, while in adults, the legs and feet are the most involved.7 No central clearing, as seen in dermatophyte infections, is
Pathogenesis Engman1 believed that an exudative discharge or existing eczematoid surface, present on oneself or another, could inoculate healthy skin and bring about the changes seen in IED. In 1944, Hopkins et al.18 showed that hypersensitivity can develop to a combination of tissues and bacterial toxins. They suggested that Staphylococcal aureus toxin could somehow alter keratin from a patient’s skin. Five years later, Templeton et al.19 extended this theory to explain the mechanism behind IED. The current belief
JEADV 2015, 29, 203–208
Table 1 Proposed diagnostic criteria Major criteria (2 of 2 must be present) Primary infected lesion with purulent drainage Eruption spreading peripherally from primary lesion Minor criteria (1 of 2 must be present) Peripheral vesicles and pustules with central oozing, crusting and scaling Oozing, crusting and scaling throughout entirety of eruption
© 2014 European Academy of Dermatology and Venereology
Medium-high potency topical corticosteroids Emollients Avoidance of allergen/irritant Topical corticosteroids Systemic steroids if severe
Epidermis: mild spongiosis, acanthosis, scale, crust Dermis: perivascular inflammatory infiltrate Allergic: Epidermis: spongiosis Dermis: infiltrate (lymphocytes, histiocytes, eosinophils) Irritant: Epidermis: focal spongiosis, necrosis of keratinocytes Dermis: perivascular infiltrate with lymphocytes
Extremities Trunk
Allergic: distal lower extremity Irritant: hands
Vesicles Papules
JEADV 2015, 29, 203–208 Mild scaling In severe form: criss-cross pattern of superficial cracks and fissures resembling dried river bed Brown hyperpigmentation Dull erythema Petechiae Thickened, scaling skin Excoriations, 1–3 cm discoid, lichenified, hyperkeratotic patches Patches or plaques with angular corners, geometric outlines, sharp margins
Prevalent in elderly
Prevalent in elderly History of venous stasis
–
Allergic: history of contact with metals, plants, medicines, cosmetics Irritant: history of contact with acids, alkalis, solvents, detergents
Middle-aged men of Jewish origin
Asteatotic eczema (xerotic eczema)
Stasis dermatitis
Nummular dermatitis
Contact dermatitis
Oid-oid disease (SulzbergerGarbe disease)27
Excoriations, 1–3 cm discoid, lichenified, hyperkeratotic patches
Epidermis: mild focal spongiosis, parakeratosis, scale and crust Dermis: neovascularization, hemosiderin deposition, fibrosis
Distal lower extremity
Epidermis: spongiosis, parakeratosis Dermis: endothelium swelling, perivascular infiltrate
Epidermis: Mild focal spongiosis, parakeratosis, compact and slightly irregular stratum corneum Dermis: lymphocytic infiltrate with neutrophils
Distal lower extremity Posterior axillary line
Extremities Trunk
Spongiosis Perivascular infiltrate
Hands/Feet Generalized
Oral corticosteroids
Topical corticosteroids Emollients Compression stockings Elevation
Topical corticosteroids Emollients
Topical steroids
Topical corticosteroids Emollients
History of contact dermatitis superimposed on stasis dermatitis
Epidermis: spongiosis, thickened hyperkeratosis Dermis: perivascular inflammation
Autoeczematization26
Infants: papules, vesicles, oozing, crusting Adults: lichenified, scaling
Infants: head, diaper area, extensor surfaces Adults: antecubical / popliteal fossa
More prevalent in children than adults Personal / family history of asthma / allergic rhinitis
Topical corticosteroids Emollients Soaks Topical antibiotics
Epidermis: spongiosis, crusting, lymphocytic infiltrate, clumps of cocci in corneum
Spreading peripherally from primary infected site Children: ears, nares, face Adults: distal extremity, feet
Atopic Dermatitis17
Plaque with vesicles and pustules and central erythema, crusting, scaling
History of primary purulent infection
IED
Treatment
Histopathology
Distribution
Patient Population
Disease
Morphology
Table 2 A comparison of patient characteristics, morphology, distribution, pathology and treatment of IED and other entities on the differential diagnosis
IED: a comprehensive review 205
© 2014 European Academy of Dermatology and Venereology
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Children History of minor skin trauma
Impetigo
–
Non-bullous Epidermis; subcorneal neutrophils, serum and parakeratotic foci Dermis: inflammatory infiltrate Bullous Epidermis: subcorneal bulla, acantholysis, neutrophils, Gram-positive cocci Dermis: inflammatory infiltrate
Scalp Axillae Groin Ears Paranasal skin Eyelid margins Neck Face and extremities
Exudative, crusty patches
Non-bullous: erosion with ‘honey-colored’ crust and extension of infection to surrounding skin Bullous: flaccid, transparent bullae with collarette of scale after rupture
Topical antibiotics Systemic antibiotics
Oral antibiotics Topical antibiotics Topical steroids Bleach bath
Infected with HTLV-1 Residence in Caribbean, Japan, Brazil, subSaharan Africa History of IV drug use
Infective dermatitis29
Shampoo (zinc pyrithione, selenium sulphide, ketoconazole) Topical steroids Calcineurin inhibitors
Epidermis: spongiosis, scale, crust, neutrophils
History of sebum overproduction
Seborrhoeic dermatitis28 Scalp Nasolabial folds Face Central chest
Eczema herpeticum: acyclovir Impetiginization: mupirocin
–
Eczema herpiticum: any site but with predilection for head, neck, trunk
Eczema herpeticum: numerous monomorphic, punched-out erosions with haemorrhagic crusting Impetiginization: weeping, pustules, honey-coloured crusting
History of atopic dermatitis with exposure to viral or bacterial pathogen
Superinfected (atopic) dermatitis -Eczema Herpiticum (herpes simplex virus) -Impetiginization (S. aureus, S. pyogens) ill-defined to sharply demarcated patches with bran-like scale
Treatment
Histopathology
Distribution
Morphology
Patient Population
Disease
Table 2 Continued
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© 2014 European Academy of Dermatology and Venereology
IED: a comprehensive review
evident.1,12 Associated pruritus is evident in most cases.1,12 When the process occurs near the eye, keratitis or conjunctivitis can be seen.20
Histopathology The histopathology of IED shows surface crusting, spongiosis and a migration of leucocytes and lymphocytes through the epidermis.22 Clumps of cocci in the stratum corneum may also be evident. The changes are similar to seborrhoeic dermatitis, but with a greater discharge of serum and amount of crusting. Cocci in the stratum corneum, if present, also serve to distinguish IED from seborrhoeic dermatitis.
Diagnosis Diagnosis is typically made by history and physical exam. Biopsy is usually not necessary. If methicillin-resistant Staphylococcus aureus infection is suspected, bacterial culture and antibiotic sensitivity of the affected skin should be performed.14 Our proposed diagnostic criteria are outlined in Table 1.
207
of care for that class of infection. Gauze soaked in Burrow’s solution should be applied to affected skin for 20 min, three times a day. Accumulated debris should be removed after the wet packs are taken off.15 Antibiotics, such as bacitracin or mupirocin ointment, and corticosteroid cream, such as triamcinolone 0.1%, should be applied three times a day after the wet packs are removed.12 We also recommend the application of emollients to affected areas.14 If there is a diffuse involvement, hospitalization, daily mild soap baths, oral antibiotics and systemic corticosteroid, therapy should be considered.12 When the primary infection is ophthalmologic in nature, topical antibiotic ointment such as erythromycin or bacitracin can be given twice a day for 10 days. Topical corticosteroids can be added to the treatment regimen to control skin eruptions. Antimicrobial-steroid combinations such as sulphacetamide-prednisolone are particularly effective. If the infection is severe, systemic antibiotics such as erythromycin or dicloxicillin four times daily may be necessary.13,20
Prognosis Differential diagnosis The differential diagnosis for IED is extensive and should include the other eczematous rashes (Table 2). There is a critical distinction to be made between IED and autoeczematization (id reaction). IED is a local process, occurring in proximity to the primary infected lesion. Sensitization to purulent discharge is responsible. Autoeczematization occurs at a site distant to a primary dermatitis and is often generalized; circulating activated memory T cells and decreased irritancy threshold of skin due to inflammatory processes have been implicated.23–25 Another entity on the differential warranting further discussion is contact dermatitis. Nosologically, the argument can be made that IED is a type of allergic contact dermatitis. It has not been proven in IED, but both may represent type IV hypersensitivities of the skin. However, in IED the reaction is to a self-generated antigen, namely purulent discharge, and there is a peripherally spreading eruption in areas not in direct contact with the irritant, which in our opinion, justifies a unique classification. Furthermore, the morphologic and histological differences between the two entities further argue for IED as a unique entity.
Management The management of IED has evolved significantly since its description in 1902. Therapies such as menthol ointment, sulphur paste, and calamine lotion dominated the early part of the century.1,2 Attempts at using roentgen ray doses and injections of staphylococcus toxin followed.7,18 By the midpoint of the century, antibiotic therapy was ubiquitous. Treatment with penicillin, sulphonamides, bacitracin, neomycin and chloramphenicol has been described.3–9 Modern day treatment methods are similar. The primary source of infection should be treated according to the standard
JEADV 2015, 29, 203–208
Historically, prognosis was linked to the availability of antibiotics.4 However, today, with their widespread availability, the primary determinant of prognosis is the extent of the initial eruption. Additionally, chronic cases tend to respond poorly to therapy; recurrences are common even after the primary infection has healed.12 Autoeczematization can be seen as a sequelae of IED in up to 25% of cases.7,12 Eczematous patches at a site distant to the primary dermatitis will develop a few days after the initial IED eruption.7 This is probably the diffuse reaction initially described by Sutton.2
Search strategy & selection criteria References for this review were identified through searches of PubMed using the terms ‘infectious eczematoid dermatitis’, ‘infectious eczematous dermatitis’, ‘eczematoid dermatitis’ and ‘autosensitization’. Articles resulting from these searches and relevant references cited in those articles were reviewed. Books were identified through the authors’ personal collections and a search of MD Consult and OVID for the same terms as above. All articles and books found were in English. No filter was applied on the basis of language.
References 1 Engman MF. An infectious form of an eczematoid dermatitis. St Louis Courier of Medicine 1902; 27: 401–414. 2 Sutton RL. Infectious eczematoid dermatitis. J Am Med Assoc 1920; 75: 976–979. 3 Cohen TM, Pfaff RO. Penicillin in dermatologic therapy: report of results in one hundred cases. Arch Dermatol 1945; 51: 172–177. 4 Kennedy CB, Henington VM, Garvin WH. The present day status of infectious eczematoid dermatitis. South Med J 1953; 46: 707–711. 5 Kile RL, Rockwell EM, Schwarz J. Use of neomycin in dermatology. J Am Med Assoc 1952; 148: 339–343.
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6 Kile RL, Welsh AL, McAfee GD. Topical use of neomycin: preliminary Report. Arch Dermatol 1950; 62: 911. 7 McDaniel WE, Tamura J. Autosensitization in infectious eczematoid dermatitis. Arch Dermatol 1950; 62: 703. 8 Newman BA, Feldman FF. Treatment of pyogenic dermatoses with topical chloramphenicol. Arch Dermatol 1951; 64: 212–214. 9 Slatkin MH. Local use of bacitracin. J Invest Dermatol 1948; 10: 179–188. 10 Karvonen J, Poikolainen K, Reunala T, Juvakoski T. Alcohol and smoking: risk factors for infectious eczematoid dermatitis. Acta Derm Venereol 1992; 72: 208. 11 Storan E, McEvoy M, Wetter D et al. Experience with the dermatology inpatient hospital service for adults: Mayo Clinic, 2000–2010. J Eur Acad Dermatol Venereol 2013; 27: 1360–1365. 12 Hall JC. Dermatologic bacteriology. In: Hall BJ, Hall JC, eds. Sauer’s manual of skin diseases, 10th edn. Lippincott Williams & Wilkins, Philadelphia, 2010: 211–212. 13 Langston DP. Cornea and external disease. In Langston DP, ed. Manual of ocular diagnosis and therapy, 5th edn. Lippincott Williams & Wilkins, Philadelphia, 2002: 79. 14 Whitmore SE. Dermatitis and psoriasis. In Fiebach NH, Barker LR, Zieve PD, Burton JR, eds. Barker, Burton and Zieve’s Principles of Ambulatory Medicine, 7th edn. Lippincott Williams & Wilkins, Philadelphia, 2007: 1906–1914. 15 Lindstrom CJ, Lucente FE. Infections of the external ear. In Bailey BJ, Johnson JT, Newlands SD, eds. Head & Neck Surgery-Otolaryngology, 4th edn. Lippincott Williams & Wilkins, Philadelphia, 2006: 1988– 2001. 16 Wittkower E, Edgell PG. Eczema: a psychosomatic study. Arch Dermatol 1951; 63: 207. 17 Turner JD, Schwartz RA. Atopic dermatitis A clinical challenge. Acta Dermatovenerol Alp Panonica Adriat 2006; 15: 59–68.
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18 Hopkins H, Burky E. Cutaneous autosensitization: role of staphylococci in chronic eczema of the hands. Arch Dermatol 1944; 49: 124. 19 Templeton H, Lunsford C, Allington H. Autosensitization dermatitis: report of five cases and protocol of an experiment. Arch Dermatol 1949; 59: 68. 20 Hussein N, Scwab IR. Blepharitis and inflammation of the eyelids. In Tasman W, Jaeger EA, Duane TD, eds. Duane’s Ophthalmology, Rev. ed. Lippincott Williams & Wilkins, Philadelphia, 2013. 4. 21 Haddad J. External otitis (otitis externa). In Kliegman R, Nelson WE, eds. Nelson Textbook of Pediatrics, 19th edn. Elsevier Saunders, Philadelphia, 2011: 2196–2199. 22 Montgomery H. Dermatopathology. Harper & Row, New York, 1967: 201–202. 23 Cockayne SE, Gawkrodger DJ. Angry back syndrome is often due to marginal irritants: a study of 17 cases seen over 4 years. Contact Derm 2000; 43: 280–282. 24 Memon AA, Friedmann PS. Angry back syndrome: a non-reproducible phenomenon. Br J Dermatol 1996; 135: 924–930. 25 Roper SS, Jones HE. An animal model for altering the irritability threshold of normal skin. Contact Derm 1985; 13: 91–97. 26 Ilkit M, Durdu M, Karakas M. Cutaneous id reactions: a comprehensive review of clinical manifestations, epidemiology, etiology, and management. Crit Rev Microbiol 2012; 38: 191–202. 27 Tabara K, Noweta M, Bienias W, Kaszuba-Bartkowiak K, Kaszuba A. A 6year-old boy with Sulzberger and Garbe dermatosis: a case report and literature review. Postepy Dermatol Alergol 2013; 30: 403–408. 28 Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: an overview. Am Fam Physician 2006; 74: 125–130. 29 Lee R, Schwartz RA. Human T-lymphotrophic virus type 1-associated infective dermatitis: a comprehensive review. J Am Acad Dermatol 2011; 64: 152–160.
© 2014 European Academy of Dermatology and Venereology
DOI: 10.1111/jdv.12715
REVIEW ARTICLE
Infectious eczematoid dermatitis: a comprehensive review T. Yamany, R.A. Schwartz* Dermatology and Pathology, Rutgers University New Jersey Medical School, Newark, NJ, USA *Correspondence: R. A. Schwartz. E-mail: [email protected]
Abstract Infectious eczematoid dermatitis (IED) is characterized by an acute eczematous eruption triggered by purulent discharge from a primary infected site. Alcohol consumption, cigarette smoking and occupations with higher incidences of contact dermatitis portend increased risk for IED. Staphylococcus aureus is the most commonly cultured microbe from affected skin, with Streptococcus species the second most. Patients are first evident with peripherally spreading vesicles and pustules radiating from an infected site. Older areas of involvement become crusty, scaly and erythematous. Diagnosis is clinical. Other eczematous rashes, including autoeczemitization and contact dermatitis, should be on the differential diagnosis list. The treatment centres on topical antibiotics and soaks. Prognosis has improved since the advent of antibiotics. However, cases with multiple relapses and poor response to therapy are still observed. Received: 30 April 2014; Accepted: 28 July 2014
Conflicts of interest None declared.
Funding sources None.
Introduction
Epidemiology
Infectious eczematoid dermatitis (IED) is a condition seldom mentioned in the literature. It is characterized by an acute eczematous eruption brought on by a primary infected exudative site. Engman,1 in 1902, was the first to describe the entity and gave it the name ‘Staphylogenetic eczematoid dermatitis’. In 1920, Sutton2 described a diffuse eczematous reaction occurring days after the development of IED and delineated new treatment regimens for both. Several authors confirmed the efficacy of antibiotic treatments for IED in the late 19300 s, the same time antibiotics began to gain popularity.3–9 In 1953, Kennedy et al.4 lamented that little was known about the aetiology of the disease, but that, thanks to antibiotics, much progress had been made in its management. In 1992, Karvonen et al.10 detailed risk factors for IED development. A recent survey11 noted the rate of IED among patients admitted to a specialized dermatology inpatient service to be 2.9%, identical to the percentage found by Engman in 1902. Remarkably, despite its apparently stable and non-trivial incidence, IED has garnered little attention in the literature. This paper is meant to revive awareness of this entity by providing a comprehensive review.
The first estimation of incidence came in 1902 with Engman’s1 initial description of IED. Engman1 stated that, out of 1200 new cases seen in Hardaway’s dermatologic outpatient clinic, 35, or 2.9%, matched the description of IED. The timeframe over which the 1200 new cases were seen was not specified. Nearly a century later, similar results were obtained, but in an inpatient setting, in a study performed at the Mayo Clinic. From 2000 to 2010, Storan et al.11 looked at reasons for admission to the adult dermatology inpatient service at the Mayo Clinic. They found that 2.9% of 2216 admissions were attributed to IED. In 1950, in a case series of 30 patients with IED, the baseline skin type was classified as dry, oily or neither.7 It was found that 17 patients had dry skin, two had oily skin and 11 had neither. Occupation was found to be a risk factor for development of IED in situations where the initial insult was an irritant contact dermatitis. Vitamin deficiencies and endocrine abnormalities were not reported to be significant risk factors, but how such states were measured was not explained. Additionally, 11 out of 30 patients had a family history of allergy, with nine of those 11 suffering the diffuse eczematous reaction that Sutton2 had described 30 years earlier. In a case-control study performed in Finland in 1992, Karvonen et al.10 found alcohol consumption and cigarette smoking to be risk factors for the development of IED among men aged 19–50. For alcohol consumption of 50 grams per day vs. no
Definition IED is an acute, eczematous eruption resulting from autosensitization to purulent drainage. It originates near a primary infection and spreads peripherally.
JEADV 2015, 29, 203–208
© 2014 European Academy of Dermatology and Venereology
Yamany and Schwartz
204
(a)
(b)
Figure 1 Infectious eczematoid dermatitis. Note the oozing, crusting and vesicles surrounding a draining otitis media (a, b).
intake, the odds ratio of developing IED was 1.7 (95% CI of 1.03–2.70). For cigarette smoking of 20 cigarettes a day vs. no smoking, the odds ratio of developing IED was 2.1 (95% CI of 1.20–3.70). They also found that coffee consumption, age and marital status were not risk factors for the development of IED.
Aetiology The aetiology of IED is unclear. We adhere to the current prevailing belief that it is an acute eruption around an infected exudative site. The infected site is often a draining otitis media or externa, mastitis, boil, blepharitis or ulcer.12–15 Studies have shown that in the majority of cases, Staphylococcus is responsible. In 1948, Slatkin9 cultured the wounds of IED patients and found 50% to be purely coagulase positive Staphylococcus, 12% to be a mix of coagulase positive Staphylococcus and beta-haemolytic Streptococcus, and 38% to be a mixed culture of Staphylococcus, Streptococcus and other organisms. In 1950, McDaniel et al.7 cultured the wounds of 30 patients and found 24 grew Staphylococcus aureus and 11 grew Streptococcus. In 1952, Kile et al.5 cultured the wounds of patients with IED. Of those cultures that did not come back sterile or contaminated, 31 grew Staphylococcus aureus, one grew haemolytic Streptococcus, and two grew both. An alternative aetiology implicating psychosomatic factors was proposed but never gained traction.4 That theory’s support, at the time, was an earlier study on the relationship between atopic dermatitis and emotional lability.16,17
is similar to that of Templeton and associates: a purulent drainage causes a secondary infection or an autosensitization with the Staphylococcal products acting as haptens.15,20,21 Infectivity from person-to-person that Engman described is no longer believed to be a viable way to contract the disease.12 Autoinoculation, on the other hand, does appear to be the primary mechanism.12 However, in an experiment by McDaniel et al.7, 22 out of 30 patients with IED had normal and abraded skin of the upper back inoculated with exudate from a lesion. The inoculated sites were covered with a patch and re-examined 24 and 48 hours later. In all cases, the only reaction seen was faint erythema along the lines of abrasion – undermining confidence in the autoinoculation theory.
Clinical manifestations IED begins as a circumscribed plaque with overlying vesicles and pustules, spreading peripherally from a central source of infection. As the lesion spreads peripherally, older areas of involvement become characterized by erythema, oozing, crusting and scaling (Fig. 1).4,12 Lichenification, weeping or exudation may also be seen.14,20,21 In an alternate presentation, the peripherally spreading plaque lacks the initial vesicles and pustules and instead has the same appearance as the older areas of involvement: oozing, crusted and scaly in nature.1 This disorder can manifest anywhere on the body. However, in children, the ears, nares and face are predominately affected, while in adults, the legs and feet are the most involved.7 No central clearing, as seen in dermatophyte infections, is
Pathogenesis Engman1 believed that an exudative discharge or existing eczematoid surface, present on oneself or another, could inoculate healthy skin and bring about the changes seen in IED. In 1944, Hopkins et al.18 showed that hypersensitivity can develop to a combination of tissues and bacterial toxins. They suggested that Staphylococcal aureus toxin could somehow alter keratin from a patient’s skin. Five years later, Templeton et al.19 extended this theory to explain the mechanism behind IED. The current belief
JEADV 2015, 29, 203–208
Table 1 Proposed diagnostic criteria Major criteria (2 of 2 must be present) Primary infected lesion with purulent drainage Eruption spreading peripherally from primary lesion Minor criteria (1 of 2 must be present) Peripheral vesicles and pustules with central oozing, crusting and scaling Oozing, crusting and scaling throughout entirety of eruption
© 2014 European Academy of Dermatology and Venereology
Medium-high potency topical corticosteroids Emollients Avoidance of allergen/irritant Topical corticosteroids Systemic steroids if severe
Epidermis: mild spongiosis, acanthosis, scale, crust Dermis: perivascular inflammatory infiltrate Allergic: Epidermis: spongiosis Dermis: infiltrate (lymphocytes, histiocytes, eosinophils) Irritant: Epidermis: focal spongiosis, necrosis of keratinocytes Dermis: perivascular infiltrate with lymphocytes
Extremities Trunk
Allergic: distal lower extremity Irritant: hands
Vesicles Papules
JEADV 2015, 29, 203–208 Mild scaling In severe form: criss-cross pattern of superficial cracks and fissures resembling dried river bed Brown hyperpigmentation Dull erythema Petechiae Thickened, scaling skin Excoriations, 1–3 cm discoid, lichenified, hyperkeratotic patches Patches or plaques with angular corners, geometric outlines, sharp margins
Prevalent in elderly
Prevalent in elderly History of venous stasis
–
Allergic: history of contact with metals, plants, medicines, cosmetics Irritant: history of contact with acids, alkalis, solvents, detergents
Middle-aged men of Jewish origin
Asteatotic eczema (xerotic eczema)
Stasis dermatitis
Nummular dermatitis
Contact dermatitis
Oid-oid disease (SulzbergerGarbe disease)27
Excoriations, 1–3 cm discoid, lichenified, hyperkeratotic patches
Epidermis: mild focal spongiosis, parakeratosis, scale and crust Dermis: neovascularization, hemosiderin deposition, fibrosis
Distal lower extremity
Epidermis: spongiosis, parakeratosis Dermis: endothelium swelling, perivascular infiltrate
Epidermis: Mild focal spongiosis, parakeratosis, compact and slightly irregular stratum corneum Dermis: lymphocytic infiltrate with neutrophils
Distal lower extremity Posterior axillary line
Extremities Trunk
Spongiosis Perivascular infiltrate
Hands/Feet Generalized
Oral corticosteroids
Topical corticosteroids Emollients Compression stockings Elevation
Topical corticosteroids Emollients
Topical steroids
Topical corticosteroids Emollients
History of contact dermatitis superimposed on stasis dermatitis
Epidermis: spongiosis, thickened hyperkeratosis Dermis: perivascular inflammation
Autoeczematization26
Infants: papules, vesicles, oozing, crusting Adults: lichenified, scaling
Infants: head, diaper area, extensor surfaces Adults: antecubical / popliteal fossa
More prevalent in children than adults Personal / family history of asthma / allergic rhinitis
Topical corticosteroids Emollients Soaks Topical antibiotics
Epidermis: spongiosis, crusting, lymphocytic infiltrate, clumps of cocci in corneum
Spreading peripherally from primary infected site Children: ears, nares, face Adults: distal extremity, feet
Atopic Dermatitis17
Plaque with vesicles and pustules and central erythema, crusting, scaling
History of primary purulent infection
IED
Treatment
Histopathology
Distribution
Patient Population
Disease
Morphology
Table 2 A comparison of patient characteristics, morphology, distribution, pathology and treatment of IED and other entities on the differential diagnosis
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Children History of minor skin trauma
Impetigo
–
Non-bullous Epidermis; subcorneal neutrophils, serum and parakeratotic foci Dermis: inflammatory infiltrate Bullous Epidermis: subcorneal bulla, acantholysis, neutrophils, Gram-positive cocci Dermis: inflammatory infiltrate
Scalp Axillae Groin Ears Paranasal skin Eyelid margins Neck Face and extremities
Exudative, crusty patches
Non-bullous: erosion with ‘honey-colored’ crust and extension of infection to surrounding skin Bullous: flaccid, transparent bullae with collarette of scale after rupture
Topical antibiotics Systemic antibiotics
Oral antibiotics Topical antibiotics Topical steroids Bleach bath
Infected with HTLV-1 Residence in Caribbean, Japan, Brazil, subSaharan Africa History of IV drug use
Infective dermatitis29
Shampoo (zinc pyrithione, selenium sulphide, ketoconazole) Topical steroids Calcineurin inhibitors
Epidermis: spongiosis, scale, crust, neutrophils
History of sebum overproduction
Seborrhoeic dermatitis28 Scalp Nasolabial folds Face Central chest
Eczema herpeticum: acyclovir Impetiginization: mupirocin
–
Eczema herpiticum: any site but with predilection for head, neck, trunk
Eczema herpeticum: numerous monomorphic, punched-out erosions with haemorrhagic crusting Impetiginization: weeping, pustules, honey-coloured crusting
History of atopic dermatitis with exposure to viral or bacterial pathogen
Superinfected (atopic) dermatitis -Eczema Herpiticum (herpes simplex virus) -Impetiginization (S. aureus, S. pyogens) ill-defined to sharply demarcated patches with bran-like scale
Treatment
Histopathology
Distribution
Morphology
Patient Population
Disease
Table 2 Continued
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IED: a comprehensive review
evident.1,12 Associated pruritus is evident in most cases.1,12 When the process occurs near the eye, keratitis or conjunctivitis can be seen.20
Histopathology The histopathology of IED shows surface crusting, spongiosis and a migration of leucocytes and lymphocytes through the epidermis.22 Clumps of cocci in the stratum corneum may also be evident. The changes are similar to seborrhoeic dermatitis, but with a greater discharge of serum and amount of crusting. Cocci in the stratum corneum, if present, also serve to distinguish IED from seborrhoeic dermatitis.
Diagnosis Diagnosis is typically made by history and physical exam. Biopsy is usually not necessary. If methicillin-resistant Staphylococcus aureus infection is suspected, bacterial culture and antibiotic sensitivity of the affected skin should be performed.14 Our proposed diagnostic criteria are outlined in Table 1.
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of care for that class of infection. Gauze soaked in Burrow’s solution should be applied to affected skin for 20 min, three times a day. Accumulated debris should be removed after the wet packs are taken off.15 Antibiotics, such as bacitracin or mupirocin ointment, and corticosteroid cream, such as triamcinolone 0.1%, should be applied three times a day after the wet packs are removed.12 We also recommend the application of emollients to affected areas.14 If there is a diffuse involvement, hospitalization, daily mild soap baths, oral antibiotics and systemic corticosteroid, therapy should be considered.12 When the primary infection is ophthalmologic in nature, topical antibiotic ointment such as erythromycin or bacitracin can be given twice a day for 10 days. Topical corticosteroids can be added to the treatment regimen to control skin eruptions. Antimicrobial-steroid combinations such as sulphacetamide-prednisolone are particularly effective. If the infection is severe, systemic antibiotics such as erythromycin or dicloxicillin four times daily may be necessary.13,20
Prognosis Differential diagnosis The differential diagnosis for IED is extensive and should include the other eczematous rashes (Table 2). There is a critical distinction to be made between IED and autoeczematization (id reaction). IED is a local process, occurring in proximity to the primary infected lesion. Sensitization to purulent discharge is responsible. Autoeczematization occurs at a site distant to a primary dermatitis and is often generalized; circulating activated memory T cells and decreased irritancy threshold of skin due to inflammatory processes have been implicated.23–25 Another entity on the differential warranting further discussion is contact dermatitis. Nosologically, the argument can be made that IED is a type of allergic contact dermatitis. It has not been proven in IED, but both may represent type IV hypersensitivities of the skin. However, in IED the reaction is to a self-generated antigen, namely purulent discharge, and there is a peripherally spreading eruption in areas not in direct contact with the irritant, which in our opinion, justifies a unique classification. Furthermore, the morphologic and histological differences between the two entities further argue for IED as a unique entity.
Management The management of IED has evolved significantly since its description in 1902. Therapies such as menthol ointment, sulphur paste, and calamine lotion dominated the early part of the century.1,2 Attempts at using roentgen ray doses and injections of staphylococcus toxin followed.7,18 By the midpoint of the century, antibiotic therapy was ubiquitous. Treatment with penicillin, sulphonamides, bacitracin, neomycin and chloramphenicol has been described.3–9 Modern day treatment methods are similar. The primary source of infection should be treated according to the standard
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Historically, prognosis was linked to the availability of antibiotics.4 However, today, with their widespread availability, the primary determinant of prognosis is the extent of the initial eruption. Additionally, chronic cases tend to respond poorly to therapy; recurrences are common even after the primary infection has healed.12 Autoeczematization can be seen as a sequelae of IED in up to 25% of cases.7,12 Eczematous patches at a site distant to the primary dermatitis will develop a few days after the initial IED eruption.7 This is probably the diffuse reaction initially described by Sutton.2
Search strategy & selection criteria References for this review were identified through searches of PubMed using the terms ‘infectious eczematoid dermatitis’, ‘infectious eczematous dermatitis’, ‘eczematoid dermatitis’ and ‘autosensitization’. Articles resulting from these searches and relevant references cited in those articles were reviewed. Books were identified through the authors’ personal collections and a search of MD Consult and OVID for the same terms as above. All articles and books found were in English. No filter was applied on the basis of language.
References 1 Engman MF. An infectious form of an eczematoid dermatitis. St Louis Courier of Medicine 1902; 27: 401–414. 2 Sutton RL. Infectious eczematoid dermatitis. J Am Med Assoc 1920; 75: 976–979. 3 Cohen TM, Pfaff RO. Penicillin in dermatologic therapy: report of results in one hundred cases. Arch Dermatol 1945; 51: 172–177. 4 Kennedy CB, Henington VM, Garvin WH. The present day status of infectious eczematoid dermatitis. South Med J 1953; 46: 707–711. 5 Kile RL, Rockwell EM, Schwarz J. Use of neomycin in dermatology. J Am Med Assoc 1952; 148: 339–343.
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6 Kile RL, Welsh AL, McAfee GD. Topical use of neomycin: preliminary Report. Arch Dermatol 1950; 62: 911. 7 McDaniel WE, Tamura J. Autosensitization in infectious eczematoid dermatitis. Arch Dermatol 1950; 62: 703. 8 Newman BA, Feldman FF. Treatment of pyogenic dermatoses with topical chloramphenicol. Arch Dermatol 1951; 64: 212–214. 9 Slatkin MH. Local use of bacitracin. J Invest Dermatol 1948; 10: 179–188. 10 Karvonen J, Poikolainen K, Reunala T, Juvakoski T. Alcohol and smoking: risk factors for infectious eczematoid dermatitis. Acta Derm Venereol 1992; 72: 208. 11 Storan E, McEvoy M, Wetter D et al. Experience with the dermatology inpatient hospital service for adults: Mayo Clinic, 2000–2010. J Eur Acad Dermatol Venereol 2013; 27: 1360–1365. 12 Hall JC. Dermatologic bacteriology. In: Hall BJ, Hall JC, eds. Sauer’s manual of skin diseases, 10th edn. Lippincott Williams & Wilkins, Philadelphia, 2010: 211–212. 13 Langston DP. Cornea and external disease. In Langston DP, ed. Manual of ocular diagnosis and therapy, 5th edn. Lippincott Williams & Wilkins, Philadelphia, 2002: 79. 14 Whitmore SE. Dermatitis and psoriasis. In Fiebach NH, Barker LR, Zieve PD, Burton JR, eds. Barker, Burton and Zieve’s Principles of Ambulatory Medicine, 7th edn. Lippincott Williams & Wilkins, Philadelphia, 2007: 1906–1914. 15 Lindstrom CJ, Lucente FE. Infections of the external ear. In Bailey BJ, Johnson JT, Newlands SD, eds. Head & Neck Surgery-Otolaryngology, 4th edn. Lippincott Williams & Wilkins, Philadelphia, 2006: 1988– 2001. 16 Wittkower E, Edgell PG. Eczema: a psychosomatic study. Arch Dermatol 1951; 63: 207. 17 Turner JD, Schwartz RA. Atopic dermatitis A clinical challenge. Acta Dermatovenerol Alp Panonica Adriat 2006; 15: 59–68.
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18 Hopkins H, Burky E. Cutaneous autosensitization: role of staphylococci in chronic eczema of the hands. Arch Dermatol 1944; 49: 124. 19 Templeton H, Lunsford C, Allington H. Autosensitization dermatitis: report of five cases and protocol of an experiment. Arch Dermatol 1949; 59: 68. 20 Hussein N, Scwab IR. Blepharitis and inflammation of the eyelids. In Tasman W, Jaeger EA, Duane TD, eds. Duane’s Ophthalmology, Rev. ed. Lippincott Williams & Wilkins, Philadelphia, 2013. 4. 21 Haddad J. External otitis (otitis externa). In Kliegman R, Nelson WE, eds. Nelson Textbook of Pediatrics, 19th edn. Elsevier Saunders, Philadelphia, 2011: 2196–2199. 22 Montgomery H. Dermatopathology. Harper & Row, New York, 1967: 201–202. 23 Cockayne SE, Gawkrodger DJ. Angry back syndrome is often due to marginal irritants: a study of 17 cases seen over 4 years. Contact Derm 2000; 43: 280–282. 24 Memon AA, Friedmann PS. Angry back syndrome: a non-reproducible phenomenon. Br J Dermatol 1996; 135: 924–930. 25 Roper SS, Jones HE. An animal model for altering the irritability threshold of normal skin. Contact Derm 1985; 13: 91–97. 26 Ilkit M, Durdu M, Karakas M. Cutaneous id reactions: a comprehensive review of clinical manifestations, epidemiology, etiology, and management. Crit Rev Microbiol 2012; 38: 191–202. 27 Tabara K, Noweta M, Bienias W, Kaszuba-Bartkowiak K, Kaszuba A. A 6year-old boy with Sulzberger and Garbe dermatosis: a case report and literature review. Postepy Dermatol Alergol 2013; 30: 403–408. 28 Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: an overview. Am Fam Physician 2006; 74: 125–130. 29 Lee R, Schwartz RA. Human T-lymphotrophic virus type 1-associated infective dermatitis: a comprehensive review. J Am Acad Dermatol 2011; 64: 152–160.
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