Skin diseases

Moderator –Dr. Teshome

Impetigo
Impetigo is a contagious superficial bacterial infection observed most
frequently in children.
It may be classified as primary impetigo (direct bacterial invasion of
previously normal skin) or secondary impetigo (infection at sites of
minor skin trauma such as abrasions, minor trauma, and insect bites, or
underlying conditions such as eczema)
-there are 2 classic forms of impetigo.
A. Non bullous impetigo
B. Bullous impetigo
Clinically manifestation
Non bullous impetigo
- Lesions typically begin on the skin of the face or on extremities that
have been traumatized like insect bites,abbrasions and lacerations.
- A tiny vesicle or pustule forms initially and rapidly develops into a
honey-colored crusted plaque that is generally <2 cm in diameter.
- Lesions are associated with little to no pain or surrounding erythema,
and constitutional symptoms are generally absent.
Bullous impetigo

• mainly an infection of infants and young children.

• Flaccid, transparent bullae develop most commonly on skin of the
face, buttocks, trunk, perineum, and extremities.
• Neonatal bullous impetigo can begin in the diaper area.
Treatment of impetigo

• Topical therapy with mupirocin 2%, and retapamulin 1% 2-3

times a day for 10-14 days for localized disease by staph.aureus.
• Systemic therapy with oral antibiotics should be prescribed for
patients with streptococcal or widespread involvement of
staphylococcal infection cellulitis, furunculosis, abscess formation,
or suppurative lymphadenitis. Cephalexin, 25-50 mg/kg/day in 3-
4 divided doses for 7-10 days.
complications
• osteomyelitis, septic arthritis, pneumonia, and septicemia
• PSGN
Scabies

• caused by burrowing and release of toxic or antigenic substances

by the female mite Sarcoptes scabiei

• The most important factor that determines the spread of scabies is

the extent and duration of physical contact with an affected
individual and so children and sexual partners are the most
affected.
Ethiology and pathogenesis
• 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 deposits 10-25 oval eggs and numerous brown fecal pellets
(scybala) daily for 4-5 weeks and 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 manifestation

• Scabies is heralded by intense pruritis, 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
• Thread like burrows are the classic lesion in scabies.
• In infants, bullae and pustules are relatively common. The eruption
may also include wheals, papules,vesicles, and a superimposed
eczematous dermatitis .
• The palms, soles, and scalp are often affected.
 older children and adolescents -the clinical pattern is similar to that in
adults

interdigital spaces, wrist flexors, anterior axillary folds,

ankles, buttocks, umbilicus and belt line, groin, genitals
in men, and areolas in women
Crusted scabies- seen in immunocompromised, mental retardation and
sensory loss
Differential diagnosis
• Depends on the type of lesion present.
• Papulovesicular lessions may confuse with papular urticaria,
chickenpox, viral exanthems, drug eruptions, dermatitis herpetiformis,
and folliculitis.
• Eczematous lesions may mimic atopic dermatitis and seborrheic
dermatitis, and the less common bullous disorders of childhood
Diagnosis
• Diagnosis of scabies can often be made clinically but is confirmed by
microscopic identification of mites, ova and scybala in epithelial
debris.
• Scrapings most often test positive when obtained from burrows or
fresh papules.
Treatment -The entire family should be treated
-Clothing, bed linens, and towels should be washed in hot water and
dried using high heat
Tinea capitis
-Dermatophyte infection of the scalp most often caused by
Trichophyton tonsurans, occasionally by Microsporum canis.

-In microsporum and some trychophyton infections, the spores are

distributed in a sheath like fashion around the hair shaft (Ectotrix)
-Trichophyton tonsurans produce infection within the hair shaft
(Endothrix)
1.Scaly patches with alopecia (gray patches) – Single or multiple scaly
patches with hair loss are a common presentation of ectothrix infections
2.Patches of alopecia with black dots- Broken-off hairs near surface give
appearance of “dots”. Tends to be diffuse and poorly circumscribed. Resembles
seborrheic dermatitis
3.Kerion-Characterized by boggy, purulent, inflamed nodules and plaques
extremely painful; drains pus from multiple openings, like honeycomb
4.Favus- Thick yellow adherent crusts (scutula) composed of skin debris and
hyphae that are pierced by remaining hair shafts. Caused by T. schoenleinii
uniquely.
Differential diagnosis
• Tinea capitis can be confused with seborrheic dermatitis,
psoriasis,alopecia areata.
• In adolescents, the patchy, moth-eaten type of alopecia associated
with secondary syphilis may resemble tinea capitis.
• If scarring occurs, discoid lupus erythematosus and lichen planopilaris
must also be considered in the differential diagnosis.
Investigation
• Wood lamp examination of infected hair
• Microscopic examination of a KOH preparation of infected hair from
active border of lesion.
• Culture obtained by planting broken off infected hairs on Sabouraud
medium with reagents to inhibit growth of other organisms. Such
identification.
• may require 2 wk or more
Treatment
• Treatment is with griseofulvin 20 to 25mg/kg/d at least for 8-12
weeks
• Better absorption with fatty food, and given at night.
• Adverse reaction is rare but includes nausea, vomiting, blood
dyscariasis, phototoxicity and hepatotoxicity.
• Terbinafine is also effective at a dosage of 3-6 mg/kg/24 hr for 4-6 wk
or possibly in pulse therapy, although it has limited activity against M.
canis
• All contacts and family members should be examined and treated
• Chronic untreated kerion and favus, can result in permanent scarring
alopecia
• Topical antifungals are not effective alone, but it may be an important
adjunct because it may decrease the shedding of spores, and should
be recommended in all patients.
• Topical antifungals like -2.5% selenium sulfide
. - ketoconazole shampoo
-zinc pyrithione
Atopic dermatitis
• Atopic dermatitis (ie, eczema) is a chronic pruritic skin condition due to
hereditary predisposition to react for sensitizers usually beginning in
infancy.
• is the most common chronic relapsing skin disease seen in infancy and
childhood.
• Occurs in 10-30% children worldwide.
• Occurs with other atopic diseases like asthma, allergic rhinitis and food
allergy
• Atopic march- Infants with AD are predisposed to development of
allergic rhinitis and/or asthma later in childhood.
Clinical manifestation
• Intense pruritus, especially at night, and cutaneous reactivity are the
cardinal features of AD.
• Skin reaction pattern and distribution vary with the patient’s age and
disease activity.
• In Infancy involves the face, scalp, and extensor surfaces of the
extremities. The diaper area is usually spared.
• Older children and children with chronic AD have lichenification and
localization of the rash to the flexural folds of the extremities.
Diagnosis
• AD is diagnosed on the basis of 3 major features:
• pruritus
• An eczematous dermatitis that fits into a typical presentation,
• and a chronic or chronically relapsing course.
• Associated features, such as a family history of asthma, hay fever,
elevated IgE, and immediate skin test reactivity, are variably present.
Treatment
• The treatment of AD requires a systematic, multifaceted approach
that incorporates -skin hydration
• -topical anti-inflammatory therapy
• -identification and elimination of flare factors
• -systemic therapy
Cutaneous hydration

• Moisturizers are first-line therapy. Lukewarm soaking baths for 15-20

min followed by the application of an occlusive emollient to retain
moisture provide symptomatic relief.
• This is because patients with AD have impaired skin barrier function
from reduced lipid levels, they present with diffuse, abnormally dry
skin, or xerosis
Topical corticosteroids

• The cornerstone of antiinflammatory treatment for acute

exacerbations of AD
• There are 7 classes of topical glucocorticoids, ranked according to
their potency as determined by vasoconstrictor assay. Class 4-7 are
considered lower potency.
• ultrahigh-potency glucocorticoids should not be used on the face or
intertriginous areas and should be used only for very short periods on
the trunk and extremities
• Mid-potency glucocorticoids can be used for longer periods to treat
chronic AD involving the trunk and extremities.
• Table 145-5 Selected Topical Corticosteroid
• Preparations*
•GROUP 1
•Clobetasol propionate (Temovate) 0.05% ointment/cream
•Betamethasone dipropionate (Diprolene) 0.05% ointment/lotion/gel
•Fluocinonide (Vanos) 0.1% cream
•GROUP 2
•Mometasone furoate (Elocon) 0.1% ointment
•Halcinonide (Halog) 0.1% cream
•Fluocinonide (Lidex) 0.05% ointment/cream
•Desoximetasone (Topicort) 0.25% ointment/cream
•Betamethasone dipropionate (Diprolene) 0.05% cream
•GROUP 3
•Fluticasone propionate (Cutivate) 0.005% ointment
•Halcinonide (Halog) 0.1% ointment
•Betamethasone valerate (Valisone) 0.1% ointment
• GROUP 4
• Mometasone furoate (Elocon) 0.1% cream
• Triamcinolone acetonide (Kenalog) 0.1% ointment/cream
• Fluocinolone acetonide (Synalar) 0.025% ointment
• GROUP 5
• Fluocinolone acetonide (Synalar) 0.025% cream
• Hydrocortisone valerate (Westcort) 0.2% ointment
• GROUP 6
• Desonide (DesOwen) 05% ointment/cream/lotion
• Alclometasone dipropionate (Aclovate) 0.05% ointment/cream
• GROUP 7
• Hydrocortisone (Hytone) 2.5% , 1%, 0.5% ointment/cream/lotion
Systemic glucocorticoids

• Systemic corticosteroids are rarely indicated in the treatment of

chronicAD.
• The dramatic clinical improvement that may occur with systemic
corticosteroids is frequently associated with a severe rebound flare of
AD after therapy discontinuation.
Seborrheic dermatitis
• Seborrheic dermatitis is a self-limiting eruption consisting of
erythematous plaques with greasy-looking, yellowish scales
distributed on areas rich in sebaceous glands such as the scalp, the
external ear, the center of the face, and the intertriginous areas.
• Pathogenesis is not known, but the associated factors are
• Individual susceptibility
• Sebume and
• Malassezia spp
Clinical manifestation
• The most common manifestation of seborrheic dermatitis in
newborns and infants is "cradle cap," an asymptomatic and non-
inflammatory accumulation of yellowish, greasy scales on the scalp
• The infant is generally well; feeding and sleep are not disturbed. The
pruritus is mild in most cases. The clinical manifestations fluctuate,
but most cases eventually resolve spontaneously within weeks to a
few months.
• The mildest and most common form of scalp seborrheic dermatitis is
dandruff
Differential diagnosis
• Atopic dermatitis-The erythematous, scaly, and crusted lesions of
atopic dermatitis are generally poorly demarcated, and commonly
involve the cheeks, scalp, and extensor surfaces of the limb
• Psoriasis- is uncommon in infancy, psoriatic plaques are sharply
defined, shiny and bright red in color, with the typical large, silvery
scales of psoriasis usually seen in nonintertriginous areas
• Tinea capitis- may present as a scaly scalp dermatitis with moderate
or minimal inflammation . Hair loss generally is present but is not
always easy to detect. KOH examination of the hair shaft and fungal
cultures will confirm the diagnosis.
References
• Nelson 20th edition
• Uptodate 2018
Thank you
prepared by – Dawit Yohannes