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While of infections in AD and features common to both can make it difficult to make a clinical diagnosis of infections.
Addressing this issue, the International Eczema Council Skin Infection Group reviewed the most current evidence on the clinical features of bacterial infections and the interaction between host and bacterial factors that affect severity and morbidity in people with atopic dermatitis (AD). Recurrent skin infections, especially from Staphylococcus aureus and occasionally from beta-hemolytic streptococci, are more common in people with AD than those who do not have AD for a variety of reasons, Helen Alexander, MD, from the unit for population-based dermatology research at St. John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust and King’s College London, and associates wrote in the review article published in the British Journal of Dermatology.
“The reduced skin barrier, cutaneous innate and adaptive immune abnormalities and trauma from scratching all contribute to the increased risk of skin infection,” they wrote. “However, the wide variability in clinical presentation of bacterial infection in AD and the inherent features of AD – cutaneous erythema and warmth, oozing associated with edema, and regional lymphadenopathy – overlap with those of infection, making clinical diagnosis challenging.”
The clinical appearance of AD may also mask signs of the bacterial infection, they added, and providers cannot rely on positive skin swab culture from the possibly infected area since S. aureus is so common in AD. An added challenge can occur in patients of different ethnicities, in whom both AD and bacterial infection may manifest differently. For example, perifollicular accentuation often occurs with AD in dark-skinned patients with violet-colored, often muted erythema.
An estimated 70% of lesional and 39% of nonlesional AD skin is colonized with S. aureus, the authors noted, but it’s not clear how best to recognize and manage asymptomatic S. aureus colonization. Among the factors that can increase susceptibility to S. aureus colonization and infection are impaired skin barriers, type 2 inflammation and lower levels of microbial diversity in the skin microbiome.
Specific clinical features of S. aureus in patients with AD include “weeping, honey-colored crusts and pustules, both interfollicular and follicular based,” and the pustules, though not common, can involve pain and itching. By comparison, signs of beta-hemolytic streptococcal infection may include “well-defined, bright red erythema, thick-walled pustules and heavy crusting,” the authors wrote.
Fever and lymphadenopathy may occur in severe cases, as well as abscesses, particularly with methicillin-resistant S. aureus (MRSA) infection. It’s unclear whether MRSA occurs more often in people with AD since its incidence varies so widely geographically, they noted.
In the differential diagnosis, providers should consider the possibility that a patient has a concomitant viral or fungal infection. Eczema herpeticum from herpes simplex virus is a common viral infection with risk factors that include “moderate to severe AD, filaggrin loss-of-function mutation, a history of S. aureus skin infection, greater allergen sensitization and type 2 immunity,” the authors wrote.
The yeast Malassezia is implicated in inflammation in patients with dermatitis that affects the head, neck, upper chest, back, and other areas high in sebaceous glands. Some patients have greater sensitivity to Malassezia, and “cross-reactivity between Malassezia-specific IgE and Candida albicans” has occurred as well, they wrote. Current evidence favors benefit from antifungal drugs, though not conclusively.
“Although we have some understanding of how S. aureus colonizes the skin and causes inflammation in AD, many questions related to this complex relationship remain unanswered,” the authors concluded. They added that better understanding the mechanisms of S. aureus and downstream host immune mediators of inflammatory pathways involving S. aureus could potentially lead to new therapeutic targets for infection in AD patients.
The statement was funded in part by the senior author’s fellowships from the National Institutes of Health Research, and the International Eczema Council received sponsorship from AbbVie, Amgen, Asana Biosciences, Celgene, Chugai, Dermavant, Dermira, Eli Lilly, Galderma, Incyte, LEO Pharma, Kyowa Kirin, Novartis, Pierre Fabre, Pfizer, Sanofi Genzyme, Regeneron Pharmaceuticals, Sienna and Valeant. Of the 16 authors, 13 disclosed financial ties to a wide range of pharmaceutical companies, including those listed above.
SOURCE: Alexander H et al. Br J Dermatol. 2019 Nov 1. doi: 10.1111/bjd.1864319.
While of infections in AD and features common to both can make it difficult to make a clinical diagnosis of infections.
Addressing this issue, the International Eczema Council Skin Infection Group reviewed the most current evidence on the clinical features of bacterial infections and the interaction between host and bacterial factors that affect severity and morbidity in people with atopic dermatitis (AD). Recurrent skin infections, especially from Staphylococcus aureus and occasionally from beta-hemolytic streptococci, are more common in people with AD than those who do not have AD for a variety of reasons, Helen Alexander, MD, from the unit for population-based dermatology research at St. John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust and King’s College London, and associates wrote in the review article published in the British Journal of Dermatology.
“The reduced skin barrier, cutaneous innate and adaptive immune abnormalities and trauma from scratching all contribute to the increased risk of skin infection,” they wrote. “However, the wide variability in clinical presentation of bacterial infection in AD and the inherent features of AD – cutaneous erythema and warmth, oozing associated with edema, and regional lymphadenopathy – overlap with those of infection, making clinical diagnosis challenging.”
The clinical appearance of AD may also mask signs of the bacterial infection, they added, and providers cannot rely on positive skin swab culture from the possibly infected area since S. aureus is so common in AD. An added challenge can occur in patients of different ethnicities, in whom both AD and bacterial infection may manifest differently. For example, perifollicular accentuation often occurs with AD in dark-skinned patients with violet-colored, often muted erythema.
An estimated 70% of lesional and 39% of nonlesional AD skin is colonized with S. aureus, the authors noted, but it’s not clear how best to recognize and manage asymptomatic S. aureus colonization. Among the factors that can increase susceptibility to S. aureus colonization and infection are impaired skin barriers, type 2 inflammation and lower levels of microbial diversity in the skin microbiome.
Specific clinical features of S. aureus in patients with AD include “weeping, honey-colored crusts and pustules, both interfollicular and follicular based,” and the pustules, though not common, can involve pain and itching. By comparison, signs of beta-hemolytic streptococcal infection may include “well-defined, bright red erythema, thick-walled pustules and heavy crusting,” the authors wrote.
Fever and lymphadenopathy may occur in severe cases, as well as abscesses, particularly with methicillin-resistant S. aureus (MRSA) infection. It’s unclear whether MRSA occurs more often in people with AD since its incidence varies so widely geographically, they noted.
In the differential diagnosis, providers should consider the possibility that a patient has a concomitant viral or fungal infection. Eczema herpeticum from herpes simplex virus is a common viral infection with risk factors that include “moderate to severe AD, filaggrin loss-of-function mutation, a history of S. aureus skin infection, greater allergen sensitization and type 2 immunity,” the authors wrote.
The yeast Malassezia is implicated in inflammation in patients with dermatitis that affects the head, neck, upper chest, back, and other areas high in sebaceous glands. Some patients have greater sensitivity to Malassezia, and “cross-reactivity between Malassezia-specific IgE and Candida albicans” has occurred as well, they wrote. Current evidence favors benefit from antifungal drugs, though not conclusively.
“Although we have some understanding of how S. aureus colonizes the skin and causes inflammation in AD, many questions related to this complex relationship remain unanswered,” the authors concluded. They added that better understanding the mechanisms of S. aureus and downstream host immune mediators of inflammatory pathways involving S. aureus could potentially lead to new therapeutic targets for infection in AD patients.
The statement was funded in part by the senior author’s fellowships from the National Institutes of Health Research, and the International Eczema Council received sponsorship from AbbVie, Amgen, Asana Biosciences, Celgene, Chugai, Dermavant, Dermira, Eli Lilly, Galderma, Incyte, LEO Pharma, Kyowa Kirin, Novartis, Pierre Fabre, Pfizer, Sanofi Genzyme, Regeneron Pharmaceuticals, Sienna and Valeant. Of the 16 authors, 13 disclosed financial ties to a wide range of pharmaceutical companies, including those listed above.
SOURCE: Alexander H et al. Br J Dermatol. 2019 Nov 1. doi: 10.1111/bjd.1864319.
While of infections in AD and features common to both can make it difficult to make a clinical diagnosis of infections.
Addressing this issue, the International Eczema Council Skin Infection Group reviewed the most current evidence on the clinical features of bacterial infections and the interaction between host and bacterial factors that affect severity and morbidity in people with atopic dermatitis (AD). Recurrent skin infections, especially from Staphylococcus aureus and occasionally from beta-hemolytic streptococci, are more common in people with AD than those who do not have AD for a variety of reasons, Helen Alexander, MD, from the unit for population-based dermatology research at St. John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust and King’s College London, and associates wrote in the review article published in the British Journal of Dermatology.
“The reduced skin barrier, cutaneous innate and adaptive immune abnormalities and trauma from scratching all contribute to the increased risk of skin infection,” they wrote. “However, the wide variability in clinical presentation of bacterial infection in AD and the inherent features of AD – cutaneous erythema and warmth, oozing associated with edema, and regional lymphadenopathy – overlap with those of infection, making clinical diagnosis challenging.”
The clinical appearance of AD may also mask signs of the bacterial infection, they added, and providers cannot rely on positive skin swab culture from the possibly infected area since S. aureus is so common in AD. An added challenge can occur in patients of different ethnicities, in whom both AD and bacterial infection may manifest differently. For example, perifollicular accentuation often occurs with AD in dark-skinned patients with violet-colored, often muted erythema.
An estimated 70% of lesional and 39% of nonlesional AD skin is colonized with S. aureus, the authors noted, but it’s not clear how best to recognize and manage asymptomatic S. aureus colonization. Among the factors that can increase susceptibility to S. aureus colonization and infection are impaired skin barriers, type 2 inflammation and lower levels of microbial diversity in the skin microbiome.
Specific clinical features of S. aureus in patients with AD include “weeping, honey-colored crusts and pustules, both interfollicular and follicular based,” and the pustules, though not common, can involve pain and itching. By comparison, signs of beta-hemolytic streptococcal infection may include “well-defined, bright red erythema, thick-walled pustules and heavy crusting,” the authors wrote.
Fever and lymphadenopathy may occur in severe cases, as well as abscesses, particularly with methicillin-resistant S. aureus (MRSA) infection. It’s unclear whether MRSA occurs more often in people with AD since its incidence varies so widely geographically, they noted.
In the differential diagnosis, providers should consider the possibility that a patient has a concomitant viral or fungal infection. Eczema herpeticum from herpes simplex virus is a common viral infection with risk factors that include “moderate to severe AD, filaggrin loss-of-function mutation, a history of S. aureus skin infection, greater allergen sensitization and type 2 immunity,” the authors wrote.
The yeast Malassezia is implicated in inflammation in patients with dermatitis that affects the head, neck, upper chest, back, and other areas high in sebaceous glands. Some patients have greater sensitivity to Malassezia, and “cross-reactivity between Malassezia-specific IgE and Candida albicans” has occurred as well, they wrote. Current evidence favors benefit from antifungal drugs, though not conclusively.
“Although we have some understanding of how S. aureus colonizes the skin and causes inflammation in AD, many questions related to this complex relationship remain unanswered,” the authors concluded. They added that better understanding the mechanisms of S. aureus and downstream host immune mediators of inflammatory pathways involving S. aureus could potentially lead to new therapeutic targets for infection in AD patients.
The statement was funded in part by the senior author’s fellowships from the National Institutes of Health Research, and the International Eczema Council received sponsorship from AbbVie, Amgen, Asana Biosciences, Celgene, Chugai, Dermavant, Dermira, Eli Lilly, Galderma, Incyte, LEO Pharma, Kyowa Kirin, Novartis, Pierre Fabre, Pfizer, Sanofi Genzyme, Regeneron Pharmaceuticals, Sienna and Valeant. Of the 16 authors, 13 disclosed financial ties to a wide range of pharmaceutical companies, including those listed above.
SOURCE: Alexander H et al. Br J Dermatol. 2019 Nov 1. doi: 10.1111/bjd.1864319.
FROM THE BRITISH JOURNAL OF DERMATOLOGY