Atopic dermatitis is one of the most common dermatoses presenting to pediatric dermatologists. In addition to
the management of xerosis, pruritus and recurrent flares of dermatitis, there are numerous complications to recognize
and manage. These include sleep deprivation, negative social and emotional sequelae and pigmentary changes or scars. The focus of this article is on the infectious complications of atopic dermatitis.
Case Presentation
Baby R.G. is a 10-month-old baby with atopic dermatitis since the age of
3 months. She has been treated with 1% hydrocortisone on the face and 0.05% betamethasone valerate ointment on her body. She recently developed a worsening of her atopic dermatitis, and her mother describes more open sores than usual
(see photo). She has had no fevers and is systemically well. There are no known infectious contacts. On exam she has multiple well-demarcated erosions on her face — many with hemorrhagic crust. She is afebrile, alert and well hydrated.
Eczema Herpeticum
Kaposi’s varicelliform eruption was first described by Austrian dermatologist Moritz Kaposi in 1887 and referred to the cutaneous infection with herpes simplex virus 1 or 2 (HSV1 or HSV2), vaccinia or coxsackie virus in a patient with an underlying dermatosis.1 Recently, the name eczema herpeticum (EH) has become more accepted for HSV superimposed on eczema or another pre-existing skin disease.
The incidence of EH has been thought to be highest in children younger than 3 years of age, with an equal male-to-female ratio.2 Approxi-mately 3% of children younger than 5 years with atopic dermatitis are at risk of developing EH.2 Although predominance in childhood has always been considered, one study of 75 patients with EH revealed that 80% of patients were older than 15.3
Eczema herpeticum presents in patients with underlying abnormal skin as a disseminated, distinctly monomorphic eruption of dome-shaped vesicles or circular erosions that is often found in a setting of fever, malaise and lymphadenopathy. The head, neck and trunk are more widely affected. Although EH starts in the area affected by the dermatosis, lesions often are reported to spread to the entire body in 7 to 10 days, affecting otherwise normal skin.1 Localized forms may also exist.
The vesicles found at the beginning develop into eroded lesions with crusts and heal, often without scarring, in a 2- to 6-week period (average of 16 days).1,4 Some of these vesicles may become pustular or hemorrhagic, and it is not unusual for them to coalesce leading to larger, painful bleeding erosions that can become superinfected with bacteria and yeast. The most common organisms causing bacterial superinfection are Staphylococcus aureus, Streptococcus pyogenes and Pseudomonas aeruginosa.5
Predisposition to EH
It is unknown whether a deficient immune reaction in the host or decrease in the normal skin barrier function is what predisposes patients with underlying dermatoses to have HSV infections. Some authors mention that the levels of plasmacytoid dendritic cells, which play a role in defense against viruses, are decreased in patients with atopic dermatitis and this may be a possible cause of this infection.4
Another hypothesis postulated has been that decreased numbers of circulating NK cells and the decrease in IL-2 receptors at the time of eczema herpeticum play a part in the susceptibility of children with atopic eczema to cutaneous HSV infections.6
Finally, immunosuppression secondary to medications has been mentioned as a cause.7 EH has been described in many other skin conditions like psoriasis,1 ichthyosis vulgaris,4 contact dermatitis,8 mycosis fungoides,9 Hailey-Hailey disease,10 Sézary syndrome11 and burns,5 among others. This could support the theory that a disruption in the stratum corneum or alteration in the skin’s barrier function can predispose to infection.
HSV1 and HSV2 can be acquired by auto-inoculation or by contact with an infected person. Although direct spread from herpetic lesions to other sites seems to be the likely route of infection, two routes of indirect transmission of this virus have been proposed: manual scratching of herpetic lesions or via contaminated bath towel or clothing.12 HSV may be shed in saliva of 2% to 6% of patients without clinical herpes labialis suggesting a potential source of transmission.5 However, this source of infection was studied and no onset of eczema herpeticum was observed in patients with facial AD in whom HSV DNA was detected.13 Observation of relatives and close friends of patients showed that 68% of them had had HSV infection before the onset of the patient’s EH.4
Predisposing factors for EH have been studied and narrowed to early onset of atopic dermatitis and high total serum IgE level.4 Although topical steroids do not seem to predispose to EH, topical calcineurin inhibitors might increase its incidence.14
Diagnosing EH
Differential diagnoses of EH include other herpes virus (varicella), impetigo, contact dermatitis, exacerbation of the underlying disease and other bullous disorders. Living in an era of possible biological warfare, smallpox would be a remote possibility.
Complications of this condition have to be kept in mind. Bacterial superinfection is one of the common complications. When there is eye involvement, keratoconjunctivitis can occur. Viremia with multiple organ involvement, including meningitis and encephalitis, is possible. Visceral dissemination of HSV1 and subsequent mortality have been estimated at 1% to 9%.15
The diagnosis can be confirmed by polymerase chain reaction (PCR) for viral DNA in blister fluid. Electron microscopy can also detect the herpes group virus from vesicle fluid. Commercial immunofluorescense test can be used to identify HSV infected cells.
The diagnosis can be supported by a positive Tzanck test that shows large multinucleated cells with conventional light microscopy. Viral culture can be performed, but it is time consuming, less sensitive and could be negative if lesions are crusted. Serologic tests are less specific and of little diagnostic value.
Treating EH
Therapy should always be systemic as topical antivirals are not adequate to treat EH. Acyclovir (Zovirax), a nucleoside analogue, interferes with the viral DNA replication shortening the disease course. Depending on the severity, either oral or IV acyclovir can be used.
Patients with severe disease, significant systemic symptoms and in patients younger than 1 year old, we usually recommend IV treatment. One intravenous dosing suggestion is 15 to 30 mg/kg/day IV divided every 8 hours.16 The potential risk of toxicity of IV acyclovir is due to its precipitation as crystals in the kidneys, and can be prevented with good hydration.
Since oral acyclovir has lower bioavailability (15% to 30%) than IV, it should be restricted to mild cases. One suggested dosing for oral acyclovir is 200 mg four times per day, usually for 10 days.16 Acyclovir resistance is 4.7% to 17% and is usually seen in patients with HIV and is rare in EH.17
Valacyclovir (Valtrex) is converted to acyclovir during the first pass metabolism in the liver. It has better bioavailability than acyclovir, but no studies have been performed in EH.
Antibiotics should also be considered in patients in whom superinfection is suspected. Topical compresses help dry vesicles and are a useful adjunct. Although there is no convincing evidence regarding topical and systemic steroid use in the acute phase, many prefer to avoid it. Calcineurin inhibitors are contraindicated in the acute phase.17
In the future, vaccines as preventive measures have been proposed. Meanwhile, it is important to recognize and treat EH since its course without proper treatment carries severe morbidity and could even be fatal.
Impetiginized Eczema
It is well-recognized that patients with atopic dermatitis are commonly colonized with S. aureus. Colonization rates in patients with atopic dermatitis ranges from 64%18 to 90%.19 It is unclear the exact role S. aureus plays in the pathogenesis of atopic dermatitis. It may act through a superantigen mechanism. It may also relate to the ability of the immune system to clear S. aureus.20
Sometimes treatment of the eczema patches alone with antihistamines and topical cortisones can eliminate S. aureus through clearing the dermatitis even in the absence of antimicrobials.20 This may suggest that the dermatitis enables S. aureus binding or hinders staph clearance. Even after treatment patients can be easily re-colonized. Gilani suggests potential sources of recolonization: antibiotic resistance, nasal carriage of S. aureus and contamination of treatment products.21
The clinical relevance for dermatologists is to consider that S. arueus may be contributing to exacerbations of atopic dermatitis. Also, patches of atopic dermatitis have been recognized as portals of entry of bacteria leading to serious systemic staphylococcal infections.22
Two scenarios can be commonly associated with S. aureus in patients with atopic dermatitis. The first is the obviously infected child who develops crust, oozing, increased tenderness, increased redness and possibly systemic symptoms such as fever (see photos ). These rarely present a diagnostic challenge for dermatologists but on occasion may be referred as a perceived “worsening” of eczema.
Usually, for localized lesions, topical antibiotic preparations with activity against S. aureus are useful in conjunction with usual atopic dermatitis management (e.g., emollients, cortisones etc). For severe localized infections or widespread infection, oral antibiotics are the treatment of choice. Children are usually excluded from school, daycare or camp until treatment has been imitated.
The second scenario in which S. aureus may play a role is in patients with resistant patches of eczema. If someone is failing to respond to the “usual” routines of emollients, hydration, cortisones or calcineurin inhibitors and antihistamines, consider a subclinical S. aureus infection even in the absence of obvious clinical signs. A swab may help confirm the role of S. aureus and help with sensitivities to antibiotics. These patients may benefit from a short course of topical or oral antibiotics in addition to standard atopic dermatitis control.
It’s tempting to consider, based on the above discussion, the use of long-term antibiotics to prevent flares of atopic dermatitis or to control chronic dermatitis. However, there are not strong enough data to support this practice.23.
Back to Our Case
A clinical diagnosis of eczema herpeticum was made in the case of R.G. Viral and bacterial cultures were taken as well as viral swabs for PCR, and she was admitted to the hospital to start IV acyclovir and cefazolin (Ancef). Viral culture and PCR were positive for HSV1 and bacterial culture was negative. Given the young age of the baby and the crusting on exam, it is often prudent to cover for bacteria while awaiting cultures.
After 5 days of IV therapy, the baby was discharged home on oral acyclovir to complete a 10-day course. Antibiotics were discontinued after negative cultures. The baby’s regular atopic skincare routine was maintained in hospital in addition to saline compresses to the crusted lesions. She completely recovered without scarring.
Screening for Complications
When consulting on or following patients with atopic dermatitis, it’s important to screen for infectious complications. These infections may present with obvious signs and symptoms such as fever, pus or erosions or may simply present as “worsening” of the eczema.
The history should include inquiring about contacts with HSV, impetigo and failure of the usual therapy to keep eczema under control. On exam, look for evidence of vesicles, pustules, round erosions, thick yellow scale and oozing. Any suspicious lesions should be tested for virus (see above for tests available) and bacterial culture. Finally, treatment selection should be based on age of the child, extent of cutaneous infection and degree of systemic symptoms.
Dermatologists can play a key role in diagnosing and treating these infections that may not be recognized by primary care physicians.
Atopic dermatitis is one of the most common dermatoses presenting to pediatric dermatologists. In addition to
the management of xerosis, pruritus and recurrent flares of dermatitis, there are numerous complications to recognize
and manage. These include sleep deprivation, negative social and emotional sequelae and pigmentary changes or scars. The focus of this article is on the infectious complications of atopic dermatitis.
Case Presentation
Baby R.G. is a 10-month-old baby with atopic dermatitis since the age of
3 months. She has been treated with 1% hydrocortisone on the face and 0.05% betamethasone valerate ointment on her body. She recently developed a worsening of her atopic dermatitis, and her mother describes more open sores than usual
(see photo). She has had no fevers and is systemically well. There are no known infectious contacts. On exam she has multiple well-demarcated erosions on her face — many with hemorrhagic crust. She is afebrile, alert and well hydrated.
Eczema Herpeticum
Kaposi’s varicelliform eruption was first described by Austrian dermatologist Moritz Kaposi in 1887 and referred to the cutaneous infection with herpes simplex virus 1 or 2 (HSV1 or HSV2), vaccinia or coxsackie virus in a patient with an underlying dermatosis.1 Recently, the name eczema herpeticum (EH) has become more accepted for HSV superimposed on eczema or another pre-existing skin disease.
The incidence of EH has been thought to be highest in children younger than 3 years of age, with an equal male-to-female ratio.2 Approxi-mately 3% of children younger than 5 years with atopic dermatitis are at risk of developing EH.2 Although predominance in childhood has always been considered, one study of 75 patients with EH revealed that 80% of patients were older than 15.3
Eczema herpeticum presents in patients with underlying abnormal skin as a disseminated, distinctly monomorphic eruption of dome-shaped vesicles or circular erosions that is often found in a setting of fever, malaise and lymphadenopathy. The head, neck and trunk are more widely affected. Although EH starts in the area affected by the dermatosis, lesions often are reported to spread to the entire body in 7 to 10 days, affecting otherwise normal skin.1 Localized forms may also exist.
The vesicles found at the beginning develop into eroded lesions with crusts and heal, often without scarring, in a 2- to 6-week period (average of 16 days).1,4 Some of these vesicles may become pustular or hemorrhagic, and it is not unusual for them to coalesce leading to larger, painful bleeding erosions that can become superinfected with bacteria and yeast. The most common organisms causing bacterial superinfection are Staphylococcus aureus, Streptococcus pyogenes and Pseudomonas aeruginosa.5
Predisposition to EH
It is unknown whether a deficient immune reaction in the host or decrease in the normal skin barrier function is what predisposes patients with underlying dermatoses to have HSV infections. Some authors mention that the levels of plasmacytoid dendritic cells, which play a role in defense against viruses, are decreased in patients with atopic dermatitis and this may be a possible cause of this infection.4
Another hypothesis postulated has been that decreased numbers of circulating NK cells and the decrease in IL-2 receptors at the time of eczema herpeticum play a part in the susceptibility of children with atopic eczema to cutaneous HSV infections.6
Finally, immunosuppression secondary to medications has been mentioned as a cause.7 EH has been described in many other skin conditions like psoriasis,1 ichthyosis vulgaris,4 contact dermatitis,8 mycosis fungoides,9 Hailey-Hailey disease,10 Sézary syndrome11 and burns,5 among others. This could support the theory that a disruption in the stratum corneum or alteration in the skin’s barrier function can predispose to infection.
HSV1 and HSV2 can be acquired by auto-inoculation or by contact with an infected person. Although direct spread from herpetic lesions to other sites seems to be the likely route of infection, two routes of indirect transmission of this virus have been proposed: manual scratching of herpetic lesions or via contaminated bath towel or clothing.12 HSV may be shed in saliva of 2% to 6% of patients without clinical herpes labialis suggesting a potential source of transmission.5 However, this source of infection was studied and no onset of eczema herpeticum was observed in patients with facial AD in whom HSV DNA was detected.13 Observation of relatives and close friends of patients showed that 68% of them had had HSV infection before the onset of the patient’s EH.4
Predisposing factors for EH have been studied and narrowed to early onset of atopic dermatitis and high total serum IgE level.4 Although topical steroids do not seem to predispose to EH, topical calcineurin inhibitors might increase its incidence.14
Diagnosing EH
Differential diagnoses of EH include other herpes virus (varicella), impetigo, contact dermatitis, exacerbation of the underlying disease and other bullous disorders. Living in an era of possible biological warfare, smallpox would be a remote possibility.
Complications of this condition have to be kept in mind. Bacterial superinfection is one of the common complications. When there is eye involvement, keratoconjunctivitis can occur. Viremia with multiple organ involvement, including meningitis and encephalitis, is possible. Visceral dissemination of HSV1 and subsequent mortality have been estimated at 1% to 9%.15
The diagnosis can be confirmed by polymerase chain reaction (PCR) for viral DNA in blister fluid. Electron microscopy can also detect the herpes group virus from vesicle fluid. Commercial immunofluorescense test can be used to identify HSV infected cells.
The diagnosis can be supported by a positive Tzanck test that shows large multinucleated cells with conventional light microscopy. Viral culture can be performed, but it is time consuming, less sensitive and could be negative if lesions are crusted. Serologic tests are less specific and of little diagnostic value.
Treating EH
Therapy should always be systemic as topical antivirals are not adequate to treat EH. Acyclovir (Zovirax), a nucleoside analogue, interferes with the viral DNA replication shortening the disease course. Depending on the severity, either oral or IV acyclovir can be used.
Patients with severe disease, significant systemic symptoms and in patients younger than 1 year old, we usually recommend IV treatment. One intravenous dosing suggestion is 15 to 30 mg/kg/day IV divided every 8 hours.16 The potential risk of toxicity of IV acyclovir is due to its precipitation as crystals in the kidneys, and can be prevented with good hydration.
Since oral acyclovir has lower bioavailability (15% to 30%) than IV, it should be restricted to mild cases. One suggested dosing for oral acyclovir is 200 mg four times per day, usually for 10 days.16 Acyclovir resistance is 4.7% to 17% and is usually seen in patients with HIV and is rare in EH.17
Valacyclovir (Valtrex) is converted to acyclovir during the first pass metabolism in the liver. It has better bioavailability than acyclovir, but no studies have been performed in EH.
Antibiotics should also be considered in patients in whom superinfection is suspected. Topical compresses help dry vesicles and are a useful adjunct. Although there is no convincing evidence regarding topical and systemic steroid use in the acute phase, many prefer to avoid it. Calcineurin inhibitors are contraindicated in the acute phase.17
In the future, vaccines as preventive measures have been proposed. Meanwhile, it is important to recognize and treat EH since its course without proper treatment carries severe morbidity and could even be fatal.
Impetiginized Eczema
It is well-recognized that patients with atopic dermatitis are commonly colonized with S. aureus. Colonization rates in patients with atopic dermatitis ranges from 64%18 to 90%.19 It is unclear the exact role S. aureus plays in the pathogenesis of atopic dermatitis. It may act through a superantigen mechanism. It may also relate to the ability of the immune system to clear S. aureus.20
Sometimes treatment of the eczema patches alone with antihistamines and topical cortisones can eliminate S. aureus through clearing the dermatitis even in the absence of antimicrobials.20 This may suggest that the dermatitis enables S. aureus binding or hinders staph clearance. Even after treatment patients can be easily re-colonized. Gilani suggests potential sources of recolonization: antibiotic resistance, nasal carriage of S. aureus and contamination of treatment products.21
The clinical relevance for dermatologists is to consider that S. arueus may be contributing to exacerbations of atopic dermatitis. Also, patches of atopic dermatitis have been recognized as portals of entry of bacteria leading to serious systemic staphylococcal infections.22
Two scenarios can be commonly associated with S. aureus in patients with atopic dermatitis. The first is the obviously infected child who develops crust, oozing, increased tenderness, increased redness and possibly systemic symptoms such as fever (see photos ). These rarely present a diagnostic challenge for dermatologists but on occasion may be referred as a perceived “worsening” of eczema.
Usually, for localized lesions, topical antibiotic preparations with activity against S. aureus are useful in conjunction with usual atopic dermatitis management (e.g., emollients, cortisones etc). For severe localized infections or widespread infection, oral antibiotics are the treatment of choice. Children are usually excluded from school, daycare or camp until treatment has been imitated.
The second scenario in which S. aureus may play a role is in patients with resistant patches of eczema. If someone is failing to respond to the “usual” routines of emollients, hydration, cortisones or calcineurin inhibitors and antihistamines, consider a subclinical S. aureus infection even in the absence of obvious clinical signs. A swab may help confirm the role of S. aureus and help with sensitivities to antibiotics. These patients may benefit from a short course of topical or oral antibiotics in addition to standard atopic dermatitis control.
It’s tempting to consider, based on the above discussion, the use of long-term antibiotics to prevent flares of atopic dermatitis or to control chronic dermatitis. However, there are not strong enough data to support this practice.23.
Back to Our Case
A clinical diagnosis of eczema herpeticum was made in the case of R.G. Viral and bacterial cultures were taken as well as viral swabs for PCR, and she was admitted to the hospital to start IV acyclovir and cefazolin (Ancef). Viral culture and PCR were positive for HSV1 and bacterial culture was negative. Given the young age of the baby and the crusting on exam, it is often prudent to cover for bacteria while awaiting cultures.
After 5 days of IV therapy, the baby was discharged home on oral acyclovir to complete a 10-day course. Antibiotics were discontinued after negative cultures. The baby’s regular atopic skincare routine was maintained in hospital in addition to saline compresses to the crusted lesions. She completely recovered without scarring.
Screening for Complications
When consulting on or following patients with atopic dermatitis, it’s important to screen for infectious complications. These infections may present with obvious signs and symptoms such as fever, pus or erosions or may simply present as “worsening” of the eczema.
The history should include inquiring about contacts with HSV, impetigo and failure of the usual therapy to keep eczema under control. On exam, look for evidence of vesicles, pustules, round erosions, thick yellow scale and oozing. Any suspicious lesions should be tested for virus (see above for tests available) and bacterial culture. Finally, treatment selection should be based on age of the child, extent of cutaneous infection and degree of systemic symptoms.
Dermatologists can play a key role in diagnosing and treating these infections that may not be recognized by primary care physicians.
Atopic dermatitis is one of the most common dermatoses presenting to pediatric dermatologists. In addition to
the management of xerosis, pruritus and recurrent flares of dermatitis, there are numerous complications to recognize
and manage. These include sleep deprivation, negative social and emotional sequelae and pigmentary changes or scars. The focus of this article is on the infectious complications of atopic dermatitis.
Case Presentation
Baby R.G. is a 10-month-old baby with atopic dermatitis since the age of
3 months. She has been treated with 1% hydrocortisone on the face and 0.05% betamethasone valerate ointment on her body. She recently developed a worsening of her atopic dermatitis, and her mother describes more open sores than usual
(see photo). She has had no fevers and is systemically well. There are no known infectious contacts. On exam she has multiple well-demarcated erosions on her face — many with hemorrhagic crust. She is afebrile, alert and well hydrated.
Eczema Herpeticum
Kaposi’s varicelliform eruption was first described by Austrian dermatologist Moritz Kaposi in 1887 and referred to the cutaneous infection with herpes simplex virus 1 or 2 (HSV1 or HSV2), vaccinia or coxsackie virus in a patient with an underlying dermatosis.1 Recently, the name eczema herpeticum (EH) has become more accepted for HSV superimposed on eczema or another pre-existing skin disease.
The incidence of EH has been thought to be highest in children younger than 3 years of age, with an equal male-to-female ratio.2 Approxi-mately 3% of children younger than 5 years with atopic dermatitis are at risk of developing EH.2 Although predominance in childhood has always been considered, one study of 75 patients with EH revealed that 80% of patients were older than 15.3
Eczema herpeticum presents in patients with underlying abnormal skin as a disseminated, distinctly monomorphic eruption of dome-shaped vesicles or circular erosions that is often found in a setting of fever, malaise and lymphadenopathy. The head, neck and trunk are more widely affected. Although EH starts in the area affected by the dermatosis, lesions often are reported to spread to the entire body in 7 to 10 days, affecting otherwise normal skin.1 Localized forms may also exist.
The vesicles found at the beginning develop into eroded lesions with crusts and heal, often without scarring, in a 2- to 6-week period (average of 16 days).1,4 Some of these vesicles may become pustular or hemorrhagic, and it is not unusual for them to coalesce leading to larger, painful bleeding erosions that can become superinfected with bacteria and yeast. The most common organisms causing bacterial superinfection are Staphylococcus aureus, Streptococcus pyogenes and Pseudomonas aeruginosa.5
Predisposition to EH
It is unknown whether a deficient immune reaction in the host or decrease in the normal skin barrier function is what predisposes patients with underlying dermatoses to have HSV infections. Some authors mention that the levels of plasmacytoid dendritic cells, which play a role in defense against viruses, are decreased in patients with atopic dermatitis and this may be a possible cause of this infection.4
Another hypothesis postulated has been that decreased numbers of circulating NK cells and the decrease in IL-2 receptors at the time of eczema herpeticum play a part in the susceptibility of children with atopic eczema to cutaneous HSV infections.6
Finally, immunosuppression secondary to medications has been mentioned as a cause.7 EH has been described in many other skin conditions like psoriasis,1 ichthyosis vulgaris,4 contact dermatitis,8 mycosis fungoides,9 Hailey-Hailey disease,10 Sézary syndrome11 and burns,5 among others. This could support the theory that a disruption in the stratum corneum or alteration in the skin’s barrier function can predispose to infection.
HSV1 and HSV2 can be acquired by auto-inoculation or by contact with an infected person. Although direct spread from herpetic lesions to other sites seems to be the likely route of infection, two routes of indirect transmission of this virus have been proposed: manual scratching of herpetic lesions or via contaminated bath towel or clothing.12 HSV may be shed in saliva of 2% to 6% of patients without clinical herpes labialis suggesting a potential source of transmission.5 However, this source of infection was studied and no onset of eczema herpeticum was observed in patients with facial AD in whom HSV DNA was detected.13 Observation of relatives and close friends of patients showed that 68% of them had had HSV infection before the onset of the patient’s EH.4
Predisposing factors for EH have been studied and narrowed to early onset of atopic dermatitis and high total serum IgE level.4 Although topical steroids do not seem to predispose to EH, topical calcineurin inhibitors might increase its incidence.14
Diagnosing EH
Differential diagnoses of EH include other herpes virus (varicella), impetigo, contact dermatitis, exacerbation of the underlying disease and other bullous disorders. Living in an era of possible biological warfare, smallpox would be a remote possibility.
Complications of this condition have to be kept in mind. Bacterial superinfection is one of the common complications. When there is eye involvement, keratoconjunctivitis can occur. Viremia with multiple organ involvement, including meningitis and encephalitis, is possible. Visceral dissemination of HSV1 and subsequent mortality have been estimated at 1% to 9%.15
The diagnosis can be confirmed by polymerase chain reaction (PCR) for viral DNA in blister fluid. Electron microscopy can also detect the herpes group virus from vesicle fluid. Commercial immunofluorescense test can be used to identify HSV infected cells.
The diagnosis can be supported by a positive Tzanck test that shows large multinucleated cells with conventional light microscopy. Viral culture can be performed, but it is time consuming, less sensitive and could be negative if lesions are crusted. Serologic tests are less specific and of little diagnostic value.
Treating EH
Therapy should always be systemic as topical antivirals are not adequate to treat EH. Acyclovir (Zovirax), a nucleoside analogue, interferes with the viral DNA replication shortening the disease course. Depending on the severity, either oral or IV acyclovir can be used.
Patients with severe disease, significant systemic symptoms and in patients younger than 1 year old, we usually recommend IV treatment. One intravenous dosing suggestion is 15 to 30 mg/kg/day IV divided every 8 hours.16 The potential risk of toxicity of IV acyclovir is due to its precipitation as crystals in the kidneys, and can be prevented with good hydration.
Since oral acyclovir has lower bioavailability (15% to 30%) than IV, it should be restricted to mild cases. One suggested dosing for oral acyclovir is 200 mg four times per day, usually for 10 days.16 Acyclovir resistance is 4.7% to 17% and is usually seen in patients with HIV and is rare in EH.17
Valacyclovir (Valtrex) is converted to acyclovir during the first pass metabolism in the liver. It has better bioavailability than acyclovir, but no studies have been performed in EH.
Antibiotics should also be considered in patients in whom superinfection is suspected. Topical compresses help dry vesicles and are a useful adjunct. Although there is no convincing evidence regarding topical and systemic steroid use in the acute phase, many prefer to avoid it. Calcineurin inhibitors are contraindicated in the acute phase.17
In the future, vaccines as preventive measures have been proposed. Meanwhile, it is important to recognize and treat EH since its course without proper treatment carries severe morbidity and could even be fatal.
Impetiginized Eczema
It is well-recognized that patients with atopic dermatitis are commonly colonized with S. aureus. Colonization rates in patients with atopic dermatitis ranges from 64%18 to 90%.19 It is unclear the exact role S. aureus plays in the pathogenesis of atopic dermatitis. It may act through a superantigen mechanism. It may also relate to the ability of the immune system to clear S. aureus.20
Sometimes treatment of the eczema patches alone with antihistamines and topical cortisones can eliminate S. aureus through clearing the dermatitis even in the absence of antimicrobials.20 This may suggest that the dermatitis enables S. aureus binding or hinders staph clearance. Even after treatment patients can be easily re-colonized. Gilani suggests potential sources of recolonization: antibiotic resistance, nasal carriage of S. aureus and contamination of treatment products.21
The clinical relevance for dermatologists is to consider that S. arueus may be contributing to exacerbations of atopic dermatitis. Also, patches of atopic dermatitis have been recognized as portals of entry of bacteria leading to serious systemic staphylococcal infections.22
Two scenarios can be commonly associated with S. aureus in patients with atopic dermatitis. The first is the obviously infected child who develops crust, oozing, increased tenderness, increased redness and possibly systemic symptoms such as fever (see photos ). These rarely present a diagnostic challenge for dermatologists but on occasion may be referred as a perceived “worsening” of eczema.
Usually, for localized lesions, topical antibiotic preparations with activity against S. aureus are useful in conjunction with usual atopic dermatitis management (e.g., emollients, cortisones etc). For severe localized infections or widespread infection, oral antibiotics are the treatment of choice. Children are usually excluded from school, daycare or camp until treatment has been imitated.
The second scenario in which S. aureus may play a role is in patients with resistant patches of eczema. If someone is failing to respond to the “usual” routines of emollients, hydration, cortisones or calcineurin inhibitors and antihistamines, consider a subclinical S. aureus infection even in the absence of obvious clinical signs. A swab may help confirm the role of S. aureus and help with sensitivities to antibiotics. These patients may benefit from a short course of topical or oral antibiotics in addition to standard atopic dermatitis control.
It’s tempting to consider, based on the above discussion, the use of long-term antibiotics to prevent flares of atopic dermatitis or to control chronic dermatitis. However, there are not strong enough data to support this practice.23.
Back to Our Case
A clinical diagnosis of eczema herpeticum was made in the case of R.G. Viral and bacterial cultures were taken as well as viral swabs for PCR, and she was admitted to the hospital to start IV acyclovir and cefazolin (Ancef). Viral culture and PCR were positive for HSV1 and bacterial culture was negative. Given the young age of the baby and the crusting on exam, it is often prudent to cover for bacteria while awaiting cultures.
After 5 days of IV therapy, the baby was discharged home on oral acyclovir to complete a 10-day course. Antibiotics were discontinued after negative cultures. The baby’s regular atopic skincare routine was maintained in hospital in addition to saline compresses to the crusted lesions. She completely recovered without scarring.
Screening for Complications
When consulting on or following patients with atopic dermatitis, it’s important to screen for infectious complications. These infections may present with obvious signs and symptoms such as fever, pus or erosions or may simply present as “worsening” of the eczema.
The history should include inquiring about contacts with HSV, impetigo and failure of the usual therapy to keep eczema under control. On exam, look for evidence of vesicles, pustules, round erosions, thick yellow scale and oozing. Any suspicious lesions should be tested for virus (see above for tests available) and bacterial culture. Finally, treatment selection should be based on age of the child, extent of cutaneous infection and degree of systemic symptoms.
Dermatologists can play a key role in diagnosing and treating these infections that may not be recognized by primary care physicians.
