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The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

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The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is diagnosed with atopic dermatitis (AD) complicated by skin infection. 

AD is the most common chronic pruritic inflammatory skin disorder that affects both children and adults. In the United States, up to 18% of children and 7% of adults are affected. Atopic dermatitis is associated with diminished quality of life, including disruption in activities of daily living, sleep disturbance, depression, and anxiety. Moreover, patients with AD have an increased risk for infections. A significantly higher prevalence of cutaneous and systemic infections is seen in patients with AD compared with individuals without AD.

Bacterial infections are common in AD and are usually caused by Staphylococcus aureus. Examples include impetigo, which typically presents with oozing serum that dries, resulting in a honey-crusted appearance surrounded by an erythematous base. Fluid-filled blisters (bullous impetigo) may also be present, which can be mistaken for eczema herpeticum (EH).

Nonpurulent skin and soft tissue infections (SSTIs) include erysipelas and cellulitis. In most cases, these infections begin in a focal skin area but spread rapidly across the affected sites such as the arms, legs, trunk, or face. Signs typically include focal erythema, swelling, warmth, and tenderness; fever and bacteremia may also be present. 

Purulent SSTIs present as skin abscesses, involving fluctuant or nonfluctuant nodules or pustules surrounded by an erythematous swelling; the lesions may also be tender and warm. Methicillin-resistant S aureus (MRSA) is a common cause of purulent SSTIs. 

Systemic complications of SSTI in AD may include bacteremia, osteomyelitis, septic arthritis, or bursitis; less often, endocarditis and staphylococcal scalded skin syndrome may occur. Clinicians should maintain a high index of suspicion for these complications in patients who present with an ill-looking appearance, lethargy, focal point tenderness of the bone, joint swelling, heart murmur, and widespread desquamation. Persistent elevated inflammatory markers (eg, C-reactive protein or erythrocyte sedimentation rate) should increase the level of suspicion.

Nonbacterial infections can occur concurrently with bacterial skin infections and the two can be difficult to distinguish. For example, EH results from the local spread of herpes simplex virus, which has a predilection for AD lesions. Early during EH, skin lesions appear as superficial clusters of dome‐shaped vesicles and/or small, round, punched‐out erosions. With progression, the lesions may become superficially infected with S aureus and may develop the characteristic honey-colored scale of impetigo.

Factors that contribute to the increased prevalence of infections in AD include skin barrier defects, suppression of cutaneous innate immunity by type 2 inflammation, S aureus colonization, allergen sensitivity, filaggrin loss-of-function mutation, and cutaneous dysbiosis. 

Daily skin hydration and moisturization is a fundamental component of treatment for any patient with AD, both to treat the AD and prevent infection. Patients with AD should bathe daily, followed by gentle drying and application of a moisturizer or a prescribed topical medication. Standard topical anti-inflammatory medications, including topical corticosteroids and topical calcineurin inhibitors, improve skin barrier functions and have been reported to decrease S aureus colonization in AD lesions. Similarly, the monoclonal antibody dupilumab has been shown to decrease S aureus colonization and increase microbial diversity.
 
In the presence of an uncomplicated, nonpurulent skin infection, a beta-lactam antibiotic that covers both S aureus and beta-hemolytic streptococci (eg, cefazolin or cephalexin) may be sufficient, depending on clinical response or culture and in consideration of local epidemiology and resistance patterns. For patients with AD who present with a skin abscess, history of MRSA colonization, close contacts with a history of skin infections, or recent hospitalization, coverage for MRSA should be considered. Acceptable oral options for MRSA skin infections include clindamycin, doxycycline, trimethoprim-sulfamethoxazole, and linezolid, assuming that the isolate is susceptible in vitro. Topical mupirocin ointment can be used for patients with minor, localized skin infections (eg, impetigo). 

 

William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.

Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

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An 8-year-old girl presents with pruritic lesions on her upper arms. As an infant, the patient was treated for widespread dermatitis with topical steroids and emollients; recently, after a long symptom-free period, she has had multiple bouts of dermatitis on her face, knees, ankles, and elbows. According to the patient's mother, the patient bathes every 2-3 days to not dry out her skin. At the current visit, physical examination reveals scaly patches and plaques with a honey-colored crust surrounded by an erythematous base. No other family members are experiencing symptoms. There is a positive family history for atopy and asthma. 

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