Case Summary

AJ, a 9-year-old female from Bacacay, Albay, was admitted to the hospital due to itchy and painful lesions. One week before admission, rashes
appeared on the child's face, particularly around the mouth, as clusters of small, pus-filled or fluid-filled blisters. A few days later, the rashes spread
rapidly to her neck, trunk, and upper and lower extremities. New lesions have continued to emerge, and some existing blisters have ruptured. Aside
from painful oozing ulcers, the child has developed a fever with temperatures spiking up to 38.9°C, and Dolan, an Ibuprofen has afforded relief. She
also appears very fatigued and has lost her appetite. The pruritic lesions have also caused the child to have difficulty sleeping. She was given Allerkid
and Dermovate cream but it has provided no relief. Due to the worsening discomfort, the child was brought to the Emergency Room.

Aside from being breastfed, the birth history of the patient was uneventful. The patient is already fully vaccinated.

Past medical history revealed that the patient has had atopic dermatitis since 2 months old, and had the most recent flare up just a month ago.
Allerkid which is an Antihistamine, and Dermovate ointment which is a Corticosteroid, were given to manage the flare-ups. However, with the patient’s
present lesions, the same medications were deemed ineffective. Antibiotics and paracetamol were also given whenever skin infections and fever
arose due to frequent skin breakage and scratching.

The patient was also diagnosed with bronchial asthma at 2 years old, with the last asthma exacerbation two months ago which was treated at
home with a nebulization and oral prednisone. Family history revealed that both parents have bronchial asthma. In addition, the father has also HPN
and Diabetes, while the mother has also allergic rhinitis. The patient’s aunt was also mentioned to have celiac disease. All of which may have
contributed to the patient’s immunocompromised status.

Nothing amiss was found with the child’s review of the system. Physical examination, however, showed that the patient is presently having a slight
fever. The skin lesions almost cover the whole body and are now characterized as dewdrop-like, crusted, and oozing vesicles and pustules. Some
lesions have ruptured leaving behind shallow, painful-to-touch, eroded areas (punch-out), and the surrounding skin is erythematous. shallow and
painful vesicles and ulcers are also observed in the buccal mucosa and gums, although there is no nasal nor aural discharge.
 Salient Features
Subjective
AJ, 9 yr old
Female child
From Bacacay, Albay
“Itchy and painful lesions”
Fatigue
Loss of appetite
Dropped energy levels
Constant itching resulting to
sleep disturbance
Worsening discomfort
Objective
Rashes on the face (around the mouth)
Clusters of small fluid-filled blisters and some are pus-filled
Spread of rashes to the neck, trunk, and both upper and lower extremities
Emergence of new lesions
Existing blisters have ruptured
Fever (38.9°C; low-grade fever)
Medications taken
Dolan 200 mg every 6 hours
Allerkid syrup 5 ml once a day
Dermovate cream
Past History of Atopic Dermatitis; wheezing in infancy; bronchial asthma; skin infections
Appears ill and distressed
No cardiorespiratory distress
BP: 90/70- normal
Shallow and painful vesicles and ulcers on the buccal mucosa and gums
Crusted and oozing vesicles and pustules (dewdrop-like) around the mouth, on the face,
with lesion near the eyes neck, trunk, upper and lower extremities
Some lesions are ruptured vesicles leaving behind shallow, painful to touch, eroded
areas (punch-out)
Surrounding skin are erythematous.
Elevated WBC (neutrophils)
Decreased Lymphocytes
Multinucleated giant cells seen on Tzanck smear
 Initial Impression
Infectious Immunologic
Chickenpox Food/drug allergy - less likely
Crops of vesicles on erythematous base (“dewdrops No allergies specified
on rose petal”) Symptom onset: min–2 hr of urticaria, angioedema,
Associated with fever cough, wheeze, dyspnea, etc.

Hand, foot & mouth disease - Urticaria - less likely

less likely
Characterized by vesicular lesions on the mouth and
an exanthem on the hands and feet
Impetigo
Secondary impetigo w/ S. aureus is the most
common secondary skin infection found in atopic
dermatitis
Characterized by recurrent, pruritic, wheals with pale,
central swelling and surrounding epidermal erythema
which can appear over any part of the body
Cutaneous lupus erythematosus
- less likely
CLE patients display well-defined skin lesions (ie. malar
rash), often in sun-exposed areas.

Scabies - less likely Atopic dermatitis

Papules are distributed in the axillae, umbilicus, groin, Characterized by xerosis, pruritus, and characteristic
penis, wrist, instep of the foot, and interdigital spaces skin findings (erythematous papules or plaques with ill-
defined borders)
Eczema herpeticum (HSV)
Grouped vesicles on erythematous base
One of the potentially serious infectious
complications in atopic dermatitis
 CHICKEN POX (VARICELLA-ZOSTER VIRUS)
Caused by varicella-zoster virus (VZV), an enveloped,
icosahedral, double-stranded DNA virus that is a member of the
herpesvirus family.
Humans are the only natural host. VZV infects susceptible
individuals via the conjunctivae or respiratory tract and replicates in
the nasopharynx and upper respiratory tract.
It disseminates by a primary viremia and infects regional lymph
nodes, the liver, the spleen, and other organs. A secondary
Definition/ viremia follows, resulting in a cutaneous infection with the typical
vesicular rash. After resolution of chickenpox, the virus persists in
Etiology
latent infection in the dorsal root ganglia cells.
Chickenpox (varicella) is the manifestation of primary infection.
Chickenpox is highly communicable in susceptible individuals, with a
secondary attack rate of more than 90%. The period of
communicability ranges from 2 days before to 7 days after the
onset of the rash, when all lesions are crusted.
Zoster (shingles) is the manifestation of reactivated latent infection
of endogenous VZV.
Primarily occurs in children (mostly by age of 10)
Before vaccines were widely introduced, ∼ 90% of all children
had been infected by the age of 15.
More severe in young infants, adults, and
immunocompromised individuals, leading to more
complications and deaths.
Epidemiology Transmission within households is high, but casual contact,
like in school classrooms, results in lower infection rates.
Contagious before the rash appears, primarily spread by
aerosolization from cutaneous lesions.
Exposure to varicella reduces the likelihood of herpes
zoster by boosting the immune response to VZV.
1. Primary Infection (Varicella)
• Begins with the introduction of the virus to the upper respiratory tract and tonsillar lymphoid tissue.
• An incubation period of 10-21 days follows.
• Virus replicates in local lymphoid tissue and spreads to T lymphocytes, causing viremia.
• The virus eventually reaches the skin where innate immunity initially controls VZV replication.
• Widespread cutaneous lesions appear at the end of the incubation period.
• Adaptive host immune responses, particularly cellular immunity, limit viral replication and lead to recovery from
infection.
2. Latent Infection:
• VZV establishes latent infection during or after the incubation period.
Pathogenesis • Virus travels in a retrograde manner through sensory axons to dorsal root ganglia in the spinal cord and
cranial nerve ganglia.
• Latency can also develop in autonomic ganglia, such as those in the enteric nervous system.
• Latency only occurs in ganglionic neurons.
3. Reactivation:
• Reactivation of latent VZV leads to herpes zoster (shingles), typically resulting in a unilateral vesicular rash
following a dermatomal distribution.
• Reactivation may also occur without a rash, leading to conditions like zoster sine herpete, aseptic meningitis,
and enteric zoster.
• Herpes zoster can cause necrotic changes in neurons and satellite cells in associated ganglia.
Incubation period: 14–16 days
Prodromal symptoms: Fever, malaise, anorexia
Characteristic rash:
Small red papules that progress to nonumbilicated, oval, teardrop-
like vesicles on an erythematous base.
Clinical Fluid progresses from clear to cloudy.
manifestations Vesicles ulcerate, crust, and heal.
New crops appear for 3–4 days.
Begins from the trunk followed by the head, the face, and, less commonly,
the extremities
Pruritus is universal and marked.
Lesions generally are unilateral and may be present on mucous membranes.
CHICKEN POX (VARICELLA-ZOSTER)
ECZEMA HERPETICUM SECONDARY TO ATOPIC DERMATITIS
Atopic dermatitis (AD) AD = impaired skin barrier, especially a filaggrin and claudin
Complex genetic disorder deficit as well as increased Nectin-1 accessibility.
Defective skin barrier
Reduced skin innate immune response An abnormal immune response is found and includes
Polarized adaptive immune responses to environmental allergens overexpression of type 2 cytokines such as interleukin (IL)-4 and IL-
and microbes 13 and other inflammatory mediators such as IL-25, IL-22, and TSLP.
Cutaneous infection
Eczema Herpeticum (EH) These cytokines lead to lower induction of antimicrobial peptides
cutaneous superinfection with herpes simplex virus (HSV), HSV-1 than in other inflammatory skin diseases and exacerbate skin
reactivation of HSV is more common barrier defects.
Patients with AD are more likely to acquire recurrent bacterial and
During the development of EH in AD patients (ADEH+ patients),
Etiology viral skin infections
Risk factors associated with EH development: Pathogenesis immune cells are also affected with a lack of plasmacytoid
Severe atopic skin disease dendritic cells (pDCs), defective natural killer cells (NK), expansion
decreased epidermal expression of filaggrin
decreased production of cathelicidin and other antimicrobial of regulatory T cells (Treg), and overexpression of IDO1 by DCs
peptides altering the production of interferon (IFN), an important antiviral
Exhibits biomarkers associated with Th2 cell responses cytokine.
eosinophil
Finally, the lesional skin microbiota of AD patients is unbalanced
IgE
Food and environmental allergies, asthma, early onset of AD, and with sizable colonization of S. aureus producing toxins such α-
history of S. aureus and M. contagious infection toxin. All these modifications interact with each other, promoting
Expression of IL-10 & IL-25 entry or reactivation and replication of HSV and, finally, the
development of EH

HSV infection is ubiquitous

Skin trauma with macro or micro abrasions and exposure to Intense pruritus specially at night
infectious secretions
No seasonal variations
Acute: Intensely pruritic papules
ONLY natural host is HUMAN Subacute: erythematous excoriated scaling papules
Epidemiology Severe or life threatening to patients with EH Clinical
Chronic: lichenification and fibrotic papule
Direct contact between mucocutaneous surfaces manifestations
HSV-1 and HSV-2 are EQUALLY capable to cause initial infection Most patients dry skin
Highest in developed countries and lower socioeconomic groups Involves scalp, face and extensor surface of extremeties
HSV-1 is more common during childhood and adolescence
also occurs in flexural folds
ECZEMA HERPETICUM SECONDARY TO ATOPIC DERMATITIS

Impetigo is a common superficial bacterial
infection of skin caused most often by
Staphylococcus aureus and in some cases by
group A β-hemolytic streptococci
Streptococcal lesions are most common among
Etiology and
young children 2–5 years of age
Epidemology
Impetigo tends to occur during warmer
months, and is more common in semitropical
or tropical climates than in cooler regions.
Infection is more common among children living
under conditions of poor hygiene
Bacteremia with subsequent osteomyelitis,
septic arthritis, pneumonia, and septicemia
Cellulitis (10% of px with localized lesions)
Complications
Lymphangitis, suppurative lymphadenitis,
guttate psoriasis, and scarlet fever occasionally
follow streptococcal disease.
IMPETIGO
There are 2 classic forms of impetigo: nonbullous and bullous.
Staphylococcus aureus is the predominant organism of nonbullous
impetigo in the United States
Group A β-hemolytic streptococci (GABHS) are implicated in the
development of some lesions.
Staphylococci from the nose--> skin
Pathogenesis The skin becomes colonized with GABHS an average of 10 days before
development of impetigo
Bullous impetigo is always caused by S. aureus strains that produce
exfoliative toxins.
Staphylococcal exfoliative toxins--> hydrolyzation of human
desmoglein 1
blistering of the superficial epidermis--> subcorneal vesicle
Demarcated erythematous patches with blisters or honey-yellow crusting;
NON BULLOUS IMPETIGO
appears first as discreet papulovesicular lesion surrounded by a localized
area of redness
vesicles become purulent and covered with thick, confluent, amber-
colored crust
Clinical most common on the face and extremities.
manifestations regional lymphadenitis is common
generally not accompanied by fever
BULLOUS IMPETIGO
flaccid, transparent bullae (usually < 3 cm in diameter) on previously
untraumatized skin
usually on face, buttocks, trunks, and perineum
 DIAGNOSTICS
Complete Blood Count Tzanck Smear
WBC 15,000
5,000 – 10,000 High WBC is indicative
cells/mcL
of infection.
Hb 12 11 – 13 g/dL Consequently, a high
Hct 35 32 – 40% neutrophil indicates a
150,000 – bacterial infection.
Pl 170,000 450,000
cells/mcL
However, use of
glucocorticoids may
Neutro 80 40-70%
also elevate the Presence of multi-nucleated giant cells,
Lympho 15 20-40%
neutrophil count. along with ballooning degeneration of
Eo 2 1-4% Low lymphocyte count epithelial cells
4 – 5.5 Million is consistent in However, the sensitivity of this method is
RBC 4.5
cells/mcL low (~60%). Test is generally not
indicating infections
considered specific enough to
MCV 85 80-96 fL
distinguish between HSV and Varicella
AST 35 30-40 U/L (Both belong to the herpesvirus family)
ALT 40 7-56 U/L PCR technology for the detection of
viral DNA in vesicular fluid isthe
CREATININE 0.9 0.2-1.00 mg/dL
diagnostic method of choice
 Final Diagnosis
Eczema Herpeticum Secondary to Atopic
Dermatitis

Disseminated cutaneous infection with herpes simplex virus that develops in

a patient with atopic dermatitis.
Sudden onset eruption of monomorphic vesicles and "punched-out" erosions
with hemorrhagic crusts over eczematous areas
Lesions are superimposed on areas of pre-existing atopic dermatitis, most
commonly on the face, neck, and upper trunk.
The lesions are pruritic, painful, and may spread to involve normal skin over
seven to 10 days.
Systemic symptoms such as fever, lymphadenopathy, or malaise
Treatment /Management
Extensive eczema herpeticum has resolved promptly with the
1 administration of IV acyclovir.

Mild cases can be treated with oral acyclovir or valacyclovir for 7-21
2 days or until all lesions are crusted over.

Severe cases or immunocompromised patients should be

3 hospitalized for intravenous acyclovir 5-10 mg/kg every 8 hours.

Critically ill patients may need intravenous fluids, electrolyte

4 repletion, wound care, pain control, and nutritional support.
Treatment /Management
 Prognosis

Potentially life-threatening disease with mortality risk due

to complications of systemic viremia, bacteremia,
and fungal infection leading to multi-organ failure.
Step 1 Step 2 Step 3
Prior to the use of acyclovir, mortality rates in EH
patients were reportedly 10% to 50%
Since the widespread implementation of systemic
antiviral treatment, mortality rates have decreased
significantly (0.1%, with 98.1% of patients classified as
minor mortality risk.)