Definition

Clinical manifestations
Etiology, epidemiology in children
Clinical criteria
Pathognomonic markers
Rule in
Rule out
Treatment and management

(Questions for history based on Harrisons)

1. Evolution of lesions
a. a.Site of onset
b. b.Manner in which eruption progressed or regressed
c. c.Duration
d. d.Periods of resolution or improvement in chronic eruptions
2. Symptoms associated with the eruption
a. a.Itching, burning, pain, numbness
b. b.What, if anything has relieved the symptoms
c. c.Time of the day when symptoms are most severe
3. Current or recent medications
4. Associated systemic symptoms
a. Does the patient have pre-existing skin diseases or is the patient
immunocompromised (steroids, autoimmune diseases?)
5. Ongoing or previous illness
6. History of allergies
7. Presence of photosensitivity
8. Review of systems
9. Family history (particularly relevant for patients with melanoma, atopy)
a. Does anyone in the family experience the same lesions/symptoms?
b.
10. Social, sexual, travel history
a. Immunization history- measles, chickenpox
b. Did the patient take any medication prior to onset of symptoms- drug
allergies
c. Does the patient have any known allergies
d. Insect bites
e. Living conditions, pet in household
f. Hygiene practices of the family
g. When was the child last breastfed
h. Caretaker of child
 i. Neighborhood condition
j. What is the usual diet of the patient?
(Techniques for Examination based on Bates)
1. Note color
2. Moisture (dryness, sweating, oiliness)
3. Temperature
4. Texture (roughness or smoothness)
5. Lesions
a. Anatomic location (general or localized)
b. Types of skin lesions (find representative lesion that have not been
traumatized by scratching or otherwise altered)
c. Color
d. Patterns and shape

Herpes Simplex Virus

Definition
HSV 1 is a member of the Alphaherpesviridae subfamily. Its structure is composed of linear
dsDNA with a spikey envelope. In general, HSV-1 infection follows a cycle of primary infection of
epithelial cells, latency in neurons, and reactivation.

Clinical manifestations
HSV 1 is responsible for establishing primary and recurrent vesicular eruptions, primarily in
the orolabial and genital mucosa. Most commonly, it is asymptomatic and when manifests, it
presents with “cold sore” or fever blister.
In children symptomatic orolabial HSV-1 infections often present as gingivostomatitis that leads
to pain, halitosis, and dysphagia.
Symptoms of a primary orolabial infection occur between three days and one week after the
exposure. Patients will often experience a viral prodrome consisting of malaise, anorexia,
fevers, tender lymphadenopathy, localized pain, tenderness, burning, or tingling prior to the
onset of mucocutaneous lesions. Primary HSV-1 lesions usually occur on the mouth and lips.
Patients will then demonstrate painful grouped vesicles on an erythematous base. These
vesicles exhibit a characteristic scalloped border. These vesicles may then progress to
pustules, erosions, and ulcerations. Within 2 to 6 weeks, the lesions crust over and symptoms
resolve.
Symptoms of recurrent orolabial infection are typically milder than those of primary infection,
with a 24-hour prodrome of tingling, burning, and itch. Recurrent orolabial HSV-1 infections
classically affect the vermillion border of the lip (as opposed to the mouth and lips as seen in
primary infection).

Etiology
For orolabial herpes, risk factors include any activity that exposes one to an infected person’s
saliva (drinkware, mouth to mouth contact)
Epidemiology
Infection with HSV is one of the most prevalent infections worldwide
Children aged 6-13 (31.1%)
Children aged 6-7 (26.3%)
Children aged 12-13 (36.1%)

Clinical criteria
The gold standard for diagnosing HSV-1 infection is HSV-1 serology (antibody detection via
western blot). The most sensitive and specific mechanism is viral polymerase chain reaction
(PCR)
Viral culture - very specific and relatively rapid compared with serologic tests
Skin biopsies
Crusted, eroded or ulcerative lesions are best diagnosed by viral culture, DFA (direct fluorescent
antibody, histologic methods, or PCR. (Andrews’)

Rule in
Nose and perioral location
Vesiculopapular lesions with an erythematous base
Progress to papules
Pruritic
Eventually crusting

Rule out
Lesion began as erythematous macular rash present in the gluteal area
In children symptomatic orolabial HSV-1 infections often present as gingivostomatitis that leads
to pain, halitosis, and dysphagia.
malaise, anorexia, fevers, tender lymphadenopathy, localized pain, tenderness, burning, or
tingling prior to the onset of mucocutaneous lesions
tingling, burning

Scabies
Definition
- Also known as human itch mite, Sarcoptes scabiei var. hominis, is a common cause of
itching dermatosis, infesting ~300 million persons worldwide at any one time. (Harrison)
 - Scabies is caused by burrowing and release of toxic or antigenic substances by the
female mite Sarcoptes scabiei var. hominis. The most important factor that determines
spread of scabies is the extent and duration of physical contact with an affected
individual. Children and sexual partners of affected individuals are most at risk. Scabies
is transmitted only rarely by fomites because the isolated mite dies within 2-3 days.
(Nelson)
Clinical manifestations (Nelson)
- Itchy superficial burrows and pustules on palms and soles, between fingers, and on
genitalia; might produce secondary eczematous changes (nelson)
- pruritus, particularly at night .
- The first sign of the infestation
- often consists of 1-2 mm red papules, some of which are excoriated, crusted, or
scaling.
- Threadlike burrows- classic lesion of scabies
- may not be seen in infants.
- In infants
- bullae and pustules are relatively common.
- The eruption may also include wheals, papules, vesicles, and a superimposed
eczematous dermatitis
- In older alms, soles, and scalp are often affected.
- palms, soles, and scalp are often affected.
- the clinical pattern is similar to that in adults
Etiology, epidemiology in children (Nelson)
- Scabies is a common condition found worldwide; it affects people of all races and social
classes. Scabies can spread easily under crowded conditions where close body and skin
contact is common. Institutions such as nursing homes, extended-care facilities, and
prisons are often sites of scabies outbreaks. Child care facilities also are a common site
of scabies infestations.

- An adult female mite measures approximately 0.4 mm in length, has 4 sets of legs, and
has a hemispheric body marked by transverse corrugations, brown spines, and bristles
on the dorsal surface. A male mite is approximately half her size and is similar in
configuration. After impregnation on the skin surface, a gravid female exudes a
keratolytic substance and burrows into the stratum corneum, often forming a shallow well
within 30 min. She gradually extends this tract by 0.5-5.0 mm/24 hr along the boundary
with the stratum granulosum.She deposits 10-25 oval eggs and numerous brown fecal
pellets (scybala) daily. When egg laying is completed, in 4-5 wk, she dies within the
burrow. The eggs hatch in 3-5 days, releasing larvae that move to the skin surface to
molt into nymphs. Maturity is achieved in approximately 2-3 wk. Mating occurs, and the
gravid female invades the skin to complete the life cycle.
Clinical criteria
- Microscopic identification of mites, ova and sybala in epithelial debris
- Scrapings most often positive when obtained from burrows or fresh papules. A reliable
method is application of a drop of mineral oil on the selected lesion, scraping it with a
No. 15 blade, and transferring the oil and scrapings to a glass slide.
Pathognomonic markers
- Burrows - pathognomonic for human scabies
Rule in
- Papulovesicular lesions
- Pruritus
- Common in children
Rule out
- No pathognomonic lesion (Burrow)
- palms, soles, and scalp are often affected
- No crusting
Treatment and management
- The treatment of choice for scabies is permethrin 5% cream (Elimite) applied to the
entire body from the neck down, with particular attention intensely involved areas, which
is also standard therapy The medication is left on the skin for 8-12 hr and should be
reapplied in 1 wk for another 8-12 hr period.
- Additional therapies
- sulfur ointment 5–10%,
- crotamiton 10% lotion or cream.
- Lindane 1% lotion or cream
- only be used as an alternative therapy, given risk of systemic toxicity.
IMPETIGO
Reference: Nelson’s Pediatrics
Definition:
● Most common skin infection among children throughout the world. (Nelson’s Pediatrics)
● common superficial bacterial infection of skin caused most often by S. aureus; some
cases by group A β-hemolytic streptococci ( Harrisons)

Non-Bullous (Impetigo Contagiosa) Bullous

S.aureus or GAHBS (cannot be distinguished S.aureus only
clinically; only upon culture)

Develops on non-intact skin (GAHBS) Develops on an intact skin

10 days colonization before development to Produces exofoliative toxins (responsible for

impetigo blisters/subcorneal vesicle)

Skin is the source of acquisition

Clinical manifestations:

Non-Bullous Bullous

Percentage 70% The rest of the percentage

Age commonly affected Children (2-5 years of age) Neonates (4th and tenth day
of life) and younger than 2
years of age

Beginning of the lesions Face and extremities Face, buttocks, trunks,

perineum and extremities

Cause of the lesions Insect bites, abrasions, Manifestation of SSSS and

lacerations, chickenpox, develop on intact skin
scabies, pediculosis and
burns that causes skin
trauma

Formation of the lesion Tiny vesicle or pustule rapidly Flaccid, transparent bulae
 developing into
honey-colored crusted plaque
Rupture of the bulla occurs
easily, leaving a narrow rim of
scale at the edge of shallow,
moist erosion.

Mode of Transmission Fingers, clothing, towels direct/indirect

(direct/indirect)

Pain involvement Little to no pain Present

Erythema Present Absent

Constitutional Symptoms Absent Present

Pruritus Occasionally Present

Regional Lymphadenopathy Present Absent

Leukocytosis Present -

● Because GAS cannot penetrate intact skin, impetigo usually occurs at the site of open
lesions (insect bites, traumatic wounds, burns).
● Fingernails and the perianal region can harbor GAS and play a role in disseminating
impetigo. Multiple cases of impetigo in the same family are common.
● Both impetigo and pharyngitis are more likely to occur among children living in crowded
homes and in poor hygienic circumstances.
● Exfoliatins A and B are serologically distinct proteins that produce localized (bullous
impetigo) or generalized (scalded skin syndrome, staphylococcal scarlet fever)
dermatologic manifestations.
○ Exfoliatins produce skin separation by splitting the desmosome and altering the
intracellular matrix in the stratum granulosum. S. aureus can produce more than
20 distinct ent
(Harrisons)
- a superficial pustule that ruptures and forms a characteristic yellow-brown honey-colored
crust
- lesions on normal skin (primary infection) or in areas already affected by another skin
disease (secondary infection)
- bullous impetigo
o caused by staphylococci
o tense, clear bullae
o less common form of the disease
- Ecthyma
o deep nonbullous variant of impetigo
o punched-out ulcerative lesions
o caused by a primary or secondary infection with Streptococcus pyogenes
o deeper infection than typical impetigo and resolves with scars
Complications
 ● Rare complications of either nonbullous or bullous impetigo:
○ Osteomyelitis
○ Septic arthritis
○ Pneumonia
○ Septicemia
● Cellulitis -more on nonbullous impetigo and rarely follows the bullous form.
● There is no correlation between number of lesions and clinical involvement of the
lymphatics or development of cellulitis in association with streptococcal impetigo.
● Infection with nephritogenic strains of GABHS may result in acute poststreptococcal
glomerulonephritis.
○ The clinical character of impetigo lesions is not predictive of the development of
poststreptococcal glomerulonephritis.
○ The most commonly affected age group is children 3-7 yr of age.
○ The latent period from onset of impetigo to development of poststreptococcal
glomerulonephritis averages 18-21 days.
○ Poststreptococcal glomerulonephritis occurs epidemically after either pharyngeal
or skin infection.
Epidemiology in children (Medscape)
● 10% of skin problems in pediatric clinics
● Most common bacterial skin infection
● More frequent in a warm, humid environment
● British stats:
○ Incidence - 2.8% children aged 4 years and younger
○ Incidence - 1.69% children aged 5-15 years
● Most common secondary bacterial skin infection to scabies
● Children: equal sexes
● Adults: males than females
● Age of onset: 2-5 years of age
● No philippine statistical data
○ Asia: 7.3% prevalence rate
Diagnostic criteria (Medscape)
Diagnosis of impetigo is usually based solely on history and clinical appearance. Bacterial
culture and sensitivity are recommended (1) to identify possible methicillin-resistant
Staphylococcus aureus (MRSA), (2) if an outbreak of impetigo has occurred, or (3) if
poststreptococcal glomerulonephritis is present.
Pathognomonic markers
- A pathognomonic finding is a “collarette” of scale surrounding the blister roof at the
periphery of ruptured lesions (Hartman-Adams et al (2014). Impetigo: Diagnosis and
Treatment. Am Fam Physician. 2014 Aug 15;90(4):229-23)
Rule in
Impetigo was ruled in due to the evolution ofdry into the characteristic honey-colored crust.
Lesions were found in commonly affected areas (face, buttocks and extremities). It is also the
most common skin condition in children worldwide. erythematous macules to vesiculopapular
lesions that ruptured, releasing serous contents that

Treatment and management

 Drug Dose/Interval/Indication

Mupirocin 2% 2-3 times a day for 10-14 days

Retapamulin 1%

Cephalexin For widespread involvement

25-50 mg/kg/day in 3-4 divided doses for

7-10 days

Clindamycin, Doxycycline or MRSA

Sulfamethoxazole-Trimethroprim

Cefuroxime Perianal streptococcal disease

Erythromycin Mild to Moderate Impetigo

Polysporin and Bacitracin Not as effective

● Systemic therapy with oral antibiotics should be prescribed for patients with
streptococcal or widespread involvement of staphylococcal infections; when lesions are
near the mouth, where topical medication may be licked of; or in cases with evidence of
deep involvement, including cellulitis, furunculosis, abscess formation, or suppurative
lymphadenitis.
● The emergence of methicillin-resistant S. aureus (MRSA) dictates that if a satisfactory
clinical response is not achieved within 7 days, a culture should be performed and an
appropriate antibiotic based on drug sensitivity should be given for an additional 7 days.
● Antibiotic therapy for a patient with nonbullous impetigo can prevent local extension of
the lesions, spread to distant infectious foci, and transmission of the infection to others.
● Mass prophylaxis is generally not feasible except to reduce the number of infections
during epidemics of impetigo and to control epidemics of pharyngitis in military
populations and in schools.
○ Because the ability of antimicrobial agents to prevent GAS infections is limited, a
group A streptococcal vaccine offers the possibility of a more effective approach.
● Mupirocin, fusidic acid, and retapamulin are the most effective topical agents currently
available and are as effective as oral erythromycin in treatment of mild to moderate
impetigo. Polysporin and bacitracin are not as effective.

● In areas of high prevalence of MRSA or if cultures are positive for MRSA, clindamycin
or doxycycline are the preferred treatments. Trimethoprim-sulfamethoxazole is effective
against MRSA, but should only be used if group A streptococci are not the causative
agent, or in addition to an anti-streptococcal antibiotic. (NCBI, 2020)

● Children with impetigo should maintain good personal hygiene and avoid other children
during the active outbreak. It is important to wash hands, linens, clothes and affected
 areas that may have come into contact with infected fluids. Sores can be covered with a
bandage to help prevent spread by contact. (NCBI, 2021)

Contact Dermatitis
Definition:.Contact dermatitis is an inflammatory eczematous skin disease. It is caused by
chemicals or metal ions that exert toxic effects without inducing a T-cell response (contact
irritants) or by small reactive chemicals that modify proteins and induce innate and adaptive
immune responses (contact allergens).
This is a T-cell–mediated hypersensitivity reaction that is provoked by application of an
antigen to the skin surface. The antigen penetrates the skin, where it is conjugated with a
cutaneous protein, and the hapten-protein complex is transported to the regional lymph nodes
by antigen-presenting Langerhans cells. -nelsons, 21st
Clinical manifestations:
Acute allergic contact dermatitis is an erythematous, intensely pruritic, eczematous
dermatitis. Acute cases may be edematous and vesiculobullous. The chronic condition has the
features of long-standing eczema: lichenification, scaling, fissuring, and pigmentary change-
nelsons, 21st

Contact dermatitis usually occurs on areas of your body that have been directly exposed
to the reaction-causing substance. The rash usually develops within minutes to hours of
exposure and can last two to four weeks.Signs and symptoms of contact dermatitis include:
● A red rash
● Itching, which may be severe
● Dry, cracked, scaly skin
● Bumps and blisters, sometimes with oozing and crusting
● Swelling, burning or tenderness
-https://www.mayoclinic.org/diseases-conditions/contact-dermatitis/symptoms-caus
es/syc-20352742

Etiology, epidemiology in children:

Allergic contact dermatitis is common in childhood and should be considered in any child
with recalcitrant eczema. Allergic contact dermatitis is underestimated in children with atopic
dermatitis, and it has been reported to affect up to 41–77% of all children in the United
States.-nelsons

Common irritants that can cause contact dermatitis in children include:

● Soaps and detergents
● Spit (saliva)
● Urine in a diaper
 ● Lotions and perfumes

Childhood exposures do result in allergy, and the frequency of allergy in this age group is
increasing. The most common relevant allergens in young children are nickel, cobalt, fragrance,
lanolin, and neomycin.-andrews

Metals. These include nickel, chrome, and mercury. Nickel is found in costume jewelry, belt
buckles, and wristwatches, as well as zippers, snaps, and hooks on clothing. Chrome-plated
items may also contain nickel. Mercury is found in contact lens solutions. It may cause problems
for some children.
Latex. Latex is found in products such as rubber toys, balloons, balls, rubber gloves, bandages,
and pacifiers or nipples.
Clinical criteria:
Patch Test. The patch test is used to detect hypersensitivity to a substance that is in contact
with the skin so that the allergen may be determined and corrective measures taken. The patch
test is confirmatory and diagnostic, but only within the framework of the history and physical
findings; it is rarely helpful if it must stand alone.. The patch test consists of application of
substances suspected to be the cause of the dermatitis to intact uninflamed skin. Patch testing
may be administered by the thin-layer rapid-use epicutaneous (TRUE) test or by individually
prepared patches. T Test substances are applied usually to the upper back, although if only one
or two are applied, the upper outer arm may be used. Each patch should be numbered to avoid
confusion. The patches are removed after 48 hours (or sooner if severe itching or burning
occurs at the site) and read. The patch sites need to be evaluated again at day 4 or 5 because
positive reactions may not appear earlier. Some allergens may take up to day 7 to show a
reaction, and the patient should be advised to return if such a delayed reaction occurs.
Erythematous papules and vesicles with edema are indicative of allergy.
Pathognomonic markers
It causes many symptoms including skin redness, blistering, and itching.

Acute phase: erythema, edema, oozing, crusting, tenderness, vesicles or pustules

Subacute phase: crusts, scales, and hyperpigmentation
Chronic phase: Lichenification

Rule in:
Contact Dermatitis was ruled in due to the skin manifestation of the patient showing
erythematous, macular rashes that are pruritic. Blistering of the lesion can also be seen in
severe contact dermatitis and rashes may also last two to four weeks. Furthermore, the patient
did not experienced fever.
Rule out: Contact Dermatitis was ruled out since it could not explain the recent lesions that
grew in peri-oral lesion, with honey-colored crusts. There was also no mention if the patient is
allergic to any allergens and or irritants.
Treatment and management
 ● Steroid creams or ointments. These topically applied creams or ointments help
soothe the rash of contact dermatitis. A topical steroid may be applied one or two
times a day for two to four weeks.
● Oral medications. In severe cases, your doctor may prescribe oral corticosteroids
to reduce inflammation, antihistamines to relieve itching or antibiotics to fight a
bacterial infection.

VARICELLA -ZOSTER VIRUS

Definition
Varicella-zoster virus (VZV) causes two distinct clinical syndromes: primary infection
manifested as varicella (chickenpox) which establishes a lifelong latent infectin of sensory
ganglionic neurons and reactivation of the latent infection herpes zoster (shingles).
Clinical manifestations
Chickenpox
- low-grade fever
- malaise
- development of prodrome 1-2 days before onset of xanthem.
- maculopapules, vesicles, and scabs
Infectious Complications:
- Bacterial superinfection of S. pyogenes / S. aureus which results from excoriation of
lesions after scratching.
- CNS involvement: cerebellar ataxia and meningeal inflammation that generally appears
21 days after the onset of rash
- Varicella Pneumonia: onset of 3-5 days into illness associated with tachypnea, chest
pain, and hemoptysos

Etiology, epidemiology in children

VZV is a member of the family Herpesviridae an enveloped viruses containing
double-stranded DNA and proteins that targets cellular and humoral immunity. Infects both
sexes and all races equally. the virus becomes epidemic among suesceptible individuals during
seasonal peak- in late winter and early spring in the temperate zone. children ages 5-9 years
old are most commonly affected in 50% of the cases but may also affect children 1-4 and 10-14
years of age. Incubation period of chicken pox ranges from 10-21 dats but is usually 14-17
days. Patients are infectious 48 hrs before the onset of vesicular rash, during the period of
vesicle formation (which generally lasts 4–5 days), and until all vesicles are crusted.
Primary Infection:
● Rash often first sign of disease in children; adults may have 1 to 2 days of fever and
malaise before rash
● In unvaccinated individuals, generalized and pruritic rash progresses rapidly
● Clinical course in healthy children is mild; adults may have more severe disease
 ● Recovery usually results in lifetime immunity
Complications:
● Bacterial infection of the skin, Pneumonia, CNS manifestations, Teye’s syndorme
Congenital VZV:
● Results from maternal infection in the first 20 weeks of gestation
● Associated with newborn link hypoplasia, skin scarring, localized muscular atrophy
● Cortical atrophy
● Chorioenteritis, micrioeaphaly, low birth wiegyht

Diagnostic
Harrisons
- isolation of VZV in susceptible tissue-culture cell lines, the demonstration of either
seroconversion or a fourfold or greater rise in antibody titer between acute-phase and
convalescent-phase serum specimens, or the detection of VZV DNA by PCR.
- Tzanck smear, with scraping of the base of the lesions in an attempt to demonstrate
multinucleated giant cells; however, the sensitivity of this method is low (~60%)
- serologic tools for assesing host response ELISA test and FAMA, appear to be the most
sensitive
Nelsons
- Leukopenia is typical during the first 72 hrs after the onset of rash followed by a relative and
absolute lymphocytosis. Mildly elevated liver function tests.
- Patients with neurologic complications or uncomplicated infections have mild lymphocytic
pleocytosis and a slight to moderate increase in protein content in the CSF with CSF gluc
concecntration that is usually normal.
Pathognomonic markers
Hallmark of infection includes the evolution of lesions from maculopapules to vesciles
over hours to days that appear on the trunk and face and rapidly spreads to involve the other
areas of the body that are samll and have an erythematous base with a diameter of 5-10mm.
Rule in
Varicella Zoster Virus was ruled in due to the patients’ age and skin manifestation of the
patient showing erythematous macular rashes.
Rule out
This was ruled out due to the lack of data suggestive for an outbreak, recent exposure,
signs and symptoms of low grade fever, mild abdominal pain, mild cough and runny nose,
malaise and irritability (CNS involvement) and laboratory criteria such as positive PCR, >in
antibody titre.
Hand-foot and mouth disease

Hand, foot, and mouth disease (HFMD) is a common viral illness usually affecting infants and
children but can affect adults. The infection usually involves the hands, feet, mouth, and
sometimes, even the genitals and buttocks
Clinical manifestations
low-grade fever, reduced appetite, and general malaise
Cutaneous lesions:
● Lesions on the dorsal and palmar surfaces of the hands and feet. The progression is from
flat pink patches to small, elongated greyish blisters, and, within a week, these peel off
leaving no scars.
● Small vesicles and ulcers in and around the mouth, palate, and pharynx. These are
sometimes painful, so the child eats little and frets.
● Red macules and papules on the buttocks and sometimes on the arms. Lesions can also
occur on the genitalia.

Etiology

Hand, foot, and mouth disease is a viral exanthem, and it is most commonly caused by the
coxsackievirus, of the Enterovirus family

Epidemiology

In United States, epidemics of HFMD generally occur in the summer to early fall
months, although cases can occur sporadically all year. It has also become a societal
burden in parts of Asia with pandemic potential.

Diagnostic

The diagnosis of hand, foot, and mouth disease is usually made clinically. The virus can be
detected in the stool for about 6 weeks after infection, however, shedding from oropharynx is
usually less than 4 weeks. Light microscopy of biopsies or scrapings of vesicles will differentiate
hand, foot, and mouth disease from varicella zoster virus and herpes simplex virus

Rule in

The same skin lesions as of the patient in the case, age

Rule out

No history of recent exposure, no low grade fever and other constitutional symptoms, lesions are
not pruritus, no lesions inside the mouth