Impetigo: An acute contagious superficial pyogenic skin infection that occurs most
commonly in children especially those who live in a hot humid climate
Aetiology
Aetiologically impetigo is grouped into two types
• Non-bullous impetigo caused by Staphylococcus aureus, group A streptococcus
(Streptococcus pyogenes) or both
• Bullous impetigo caused by Staphylococcus aureus, group II type 71 which produce
exfoliatin toxin
Clinical Features
• Impetigo often develops at the site of minor trauma or scratched skin where it is a portal
of entry.
• Non bullous impetigo affects mostly ages 2 - 5 years.
• Bullous impetigo affects mostly newborns and old infants.
• Lesions usually present after days or weeks rather than months.
• The lesions are usually painless although other patients may report burning and pruritis.
• Constitutional symptoms are usually absent.
Non Bullous Impetigo
• Lesion begins as thin walled vesicles or pustules on an erythematous base.
• The lesions promptly rupture releasing their serum which dries and form a light brown
honey-coloured crust.
• Multiple lesions generally occur at the same site often coalescing.
• The affected areas of the skin may enlarge as the infection spread peripherally.
• Skin on any part of the body can be involved but the face and extremities are affected
most common.
• Pruritis of infected area may result into excoriation from scratching.
• As the lesions resolve either spontaneously or after antibiotic treatment, the crusts slough
from affected areas and heal without scarring.
• If the course of disease is prolonged and patients do not seek treatment as many as 90%
will develop regional lymphadenopathy.
Bullous Impetigo
• Lesions may form on grossly normal or previously traumatized skin
• The vesicles do not rupture as easily or quickly as in non bullous lesions but they do
enlarge into bullae that are usually 1-2 cm
• Initially the bullae contain clear yellow fluid that subsequently turns cloudy and dark
yellow
• After 1 to 3 days the lesions rupture to leave a thin light brown vanish like crust
• Central healing results in circinate lesions
Investigations, Treatment and Complications of Impetigo
Investigations
• Impetigo can usually be diagnosed from the clinical picture, but laboratory is supportive
and mainly for treatment purposes.
• Culture of the fluid and involved skin confirms the diagnosis and definite causation
organisms for choosing appropriate antibiotic therapy.
Treatment
• Medical care
Topical therapy
First remove the infected crusts with soap and water
Topical mupirocin may be the only necessary therapy
Studies show that topical antibiotics are as effective as oral antibiotics e.g.
erythromycin
Disadvantage of topical treatment is the inability to eradicate organisms from the
blood
• Systemic Therapy
When infection is moderate to severe accompanied by lymphadenopathy systemic
therapy is indicated
Streptococci pyogenes are sensitive to penicillin
Substitute penicillin with clindamycin in patients allergic to penicillin
In erythromycin resistant Staphylococcus aureus, substitute with cephalosporin
(cephalexin and clidamycin)
Phenoxymethylpenicillin (penicillin V)500mg/qid PO for 10days (adult dosing)
Cephalexin 500mg PO every 6 hours for 10 days (adult dosing)
Clindamycin 300mg PO every 6 hours for 10 days (adult dosing)
Complications
• Acute post streptococcal glomerulonephitis
• Rheumatic carditis
• Erysipelas
• Erthema muliforme
• Urticaria
Definition, Clinical Features and Treatment of Different Viral Skin
Infections
• Viral skin infection is inflammation of the skin caused by various types of virus such as
Herpes virus
Varicella zoster
Human papilloma virus
Herpes Zoster (Shingles)
• Herpes zoster (shingles) is an infection with herpes zoster virus result from reactivation of
the varricella zoster virus.
Clinical Features
• Shingles never occurs as primary infection but results from reactivation of latent
varicella zoster virus from dorsal root and/or cranial nerve ganglia
• Reactivation may be preceded by a prodromal phase of tingling or pain that is followed
by eruption of painful and tender blistering in a dermatomal distribution
• Blisters tend to occur in crops and may become pustules which later crust over
• The rash lasts for 2-4 weeks and is usually more severe in the elderly
• It is very rare for more than one dermatome to be involved
• There can be ongoing pain in the area of the shingles lesions long after the blisters have
resolved, this is called post-herpetic neuralgia.
Treatment
• Herpes zoster requires analgesic
• Antibiotics are only given if there is secondary bacterial infection
• Antiviral drugs used for 7 days help to shortage the attack if given early stage of illness.
These drugs include
Acyclovir 800mg 5 times daily or
Valacyclovir 1g three times daily or
Famciclovir 500mg 3 times daily
• If ocular involvement (VI dermatome), this should prompt referral to eye specialist for
appropriate management
Complications
• Complications of herpes zoster include
Severe persistent pain (post-herpetic neuralgia)
Ocular disease that can necessitate removal of the eyeball (evisceration)
Rarely motor neuropathy
Herpes Simplex Virus (HSV)
• This is infection of human being caused by a virus called herpes simplex virus (HSV)
occurring in two genomic subtypes (type I and II).
• HSV type I is transmitted through direct contact and droplet infection.
• HSV type II infection occurs after puberty and usually transmitted through sexual
intercourse.
Epidemiology of Herpes Simplex Virus (HSV)
• HSV I is the major cause herpetic stomatitis, herpes labialis (cold acne),
Keratoconjuctivitis and encephalitis.
• HSV-2 causes genital herpes and may be responsible for systemic infection in immune
compromised host.
• Transmission for HSV I is usually via mouth or occasionally the skin.
• Primary lesion can go unnoticed or can undergo severe inflammatory reaction with
vesicle formation leading to painful ulcers (gingivostomatitis).
• The virus then remain latent most commonly in trigeminal ganglia but may be activated
by stress, trauma, febrile illness and irradiation produce the recurrent form of the disease
as herpes labialis (cold sore).
• Approximately 70% of population is affected with HSV I and recurrent infection occur in
1/3 of individuals.
• Reactivation produces localized paraesthesias in the lip before the appearance of cold sore
• Transmission for HSV 2-infection through genitalia is usually more severe and
recurrences are common.
• The viruses remains latent in sacral ganglia and during recurrence can produce a
radiculomyelopathy with pain in the groin, buttocks and upper thighs.
• Primary anorectal herpes infection is common in male homosexuals.
• In patients with AIDS or receiving intensive cancer treatment may develop disseminated
HSV infected involving viscera.
• In severe cases death may result from hepatitis and encephalitis.
• Neonates may develop primary HSV infection following vagina delivery in the active
genital HSV infected mother.
• The disease in babies varies from localized skin lesions to widespread visceral diseases
with encephalitis.
Clinical Features
• Most people are affected in early childhood and are usually subclinical
• Occasionally it can cause pyrexia as primary illness, with either cluster of painful blister
on the face or gingivostomalitis.
• It can inoculate into site of trauma and present as painful blister/pustules at the fingers
(herpetic Withlow)
• Other complications of HSV infection include
Corneal ulceration
Eczema herpeticum
Chronic perineal ulceration in AIDS patients
Treatment
• Oral valacyclovir (500 mg twice daily for 3-5 days) or Acyclovir (400 mg 3 times a day
for 5 days) for primary HSV and painful genital HSV
• Recurrent cold sore treated with acyclovir cream
• Intravenous Acyclovir may be used in severe lesions such as in immune suppressed
Patients
Types of Various Viral Skin Infections
‘Slapped Cheek ‘Syndrome (Erythema Infectiosum Fifths Disease)
• This affects children and is caused by parvovirus
• It is mild viral disease which is followed by an intense erythema on the check (slapped
check) and to proximal limb
• Adults can be infected with parvovirus as well and it typically presents as fatigue and
reactive arthritis. Anemia may also be present
Treatment
• Treatment for parvovirus is symptomatic. No antivirals are needed
Varicella Zoster Virus
• Varicella zoster virus (VZV) is the cause of chicken pox as well as the reactivation of
chicken pox known as shingles
•
• The primary infection is chickenpox. It usually occurs in childhood
• Mode of transmission is by airborne virus entering through mucosa of respiratory tract
also by direct contract from fresh skin lesion.
Clinical Features
• Incubation period is 14-21 days
• Followed by a period of fever, headache, malaise and eruption of macules then vesicles
to pustules within several hours
• The lesions occur on the face, scalp and trunk and to lesser extent in the extremities
• It is characteristic to see skin lesion at all stages of development on the same area of skin
Fever subsides as soon as new lesions cease to appear
• Eventually the pustules crust and heal without scarring
Complications
• Pneumonia
• Skin eruption
• Bacteria super infection of skin lesions
• Immunocomprised people are susceptible to disseminated infection with multiorgan
involvement
Treatment
• Usually require no treatment with antiviral therapy
• After recovery a patient develops a lifelong immunity
• Human Papilloma Virus (HPV)
• Is infection responsible of the common cutaneous warts
• There are more than 70 subtypes as detected by DNA hybridization
• All can cause overgrowth of differentiated squamous epithelium
Types of Warts
• There are popular lesions with a coarse roughened surface often seen on hands and feet
but also on can be seen on other sites, namely
Plantar Warts (verrucal)
Filiform Warts
Plan Warts
Anogenital Warts
• Children and adolescents are usually affected.
• The transmission is by direct contact and is also associated within trauma.
Plantar Warts (verrucal)
• These are lesions on soles of feet
They often appear flat (inward growing) although they have the same papillomatous
surface change and black dots are often revealed if the skin is pared down
Warts may be painful or tender if they are over pressure points or around nail folds.
Filiform Warts
• These occur on the face, at the nasal vestibule or around the mouth
• They are elongated with a honey cap
Plane Warts
• These are much less common and caused by certain HPV subtypes.
• They are clinically different and appear as very small, flesh coloured or pigmented, flat
topped lesions (best seen with side-on lighting) with little in the way of surface change
and no black dots within them.
• They are usually multiple and are frequently found on the face or back of hands.
Anogenital Warts
• There are usually seen in adults and are normally transmitted by sexual contact
• They are rare in childhood and when seen sexual abuse should be considered
• HPV subtypes 16 and 18 are potentially oncogenic and are associated with cervical and
anal carcinomos
Treatments
• Warts are difficult to treat effectively but they almost always resolve spontaneously after
months to years
• Regular use of topical kerotolytic agents (e.g. 2-10% salicylic acid) over many months
• A course of cryotherapy (freezing) can help
• Cautery surgery
• Carbon dioxide laser
• Alpha-interfection injection
• Bleomycin injection (rarely used)
• Genital warts are usually treated with either
Cryotherapy
Trichloroacetic acid
Imiquimod cream or
Topical podophyllin
• Screening of other sexual transmitted diseases should be done especially syphilis
Other Skin Conditions
Folliculitis
• Is defined histologically as the presence of inflammatory cells within the wall and ostia of
the hair follicle, creating a follicular base pustule.
The actual type of inflammatory cells can vary and may be dependent on the aetiology
of the folliculitis, the stage at which the biopsy specimen was obtained or both.
Folliculitis is a primary inflammation of the hair follicle that occurs as a result of
various infections, or it can be secondary to follicular trauma or occlusion.
Eosinophilic folliculitis differs with ordinary folliculitis in that it is thought to occur
as a result of an autoimmune process directed against the sebocytes or some
component of the sebum. It is also common in severely immunecompromised persons
(e.g. HIV).
Aetiology
• Papulopustular eruption is secondary to epidermal growth factor receptor (EGF – R)
inhibitor is unknown
• It is hypothesized to occur secondariy to abnormal epidermal differentiation that leads to
follicular obstruction and subsequent inflammation
Clinical Picture
• Acne represents a noninfectious form of folliculitis.
• There is superficial and deep folliculitis.
• Folliculitis occurs in persons of any race but pseudofolliculitis occurs commonly in
African American.
• The patient typically reports an acute onset of papules and pustules associated with
pruritus or mild discomfort.
• Patient with deep folliculitis usually experience more pain and may suppurate and if
develops persistent drainage or recurrent lesion, may result in scarring and permanent hair
loss.
• Patient with papulopustular eruption secondary to EGC-R inhibitors typically occurs
within the first 2 weeks of the initiation of therapy and can be associated with pruritis and
desquamation.
• Superficial folliculitis presents with multiple small papules and pustules on erythematous
base that are pierced by a central hair
• In deep lesions it is manifested as erythematous often fluctuant, sometimes patterned
folliculitis
• One superficial form of infectious folliculitis is known as impetigo and is caused by
Staphylococcus aureus or Streptococcus pyogenes
• When involvement of the follicle is more extensive or follicular centered, a dermal
abscess results
Investigation
• In order to reach to diagnosis the following investigations is formed to confirm as
diagnosis is usually made based on history and physical examination findings alone.
Gram stain and bacterial culture are performed.
Gram stain and bacterial culture are performed
Nasal culture of family members to look for Staphylococcus aureus (usually reserved
for recurrent severe cases)
Potassium hydroxide (KOH) inspection, fungal culture or both can be used for
diagnosing dermatophytes infection
Viral culture or biopsy assets in identification of folliculitis caused by herpes simples
virus
Small punch biopsy (3-4mm) of an active lesion should be performed in atypical
cases or in patients resistant to standard treatments
Treatments
Recurrent Uncomplicated Superficial Folliculitis
• Use antibacterial soaps for hand washing
• If systemic antibiotics are indicated coverage should include S. aureus as is the most
common pathogen
• Pseudomonus folliculitis is usually self limited and does not require treatment. If the
patient is immunocompromised or the lesions are persistent then ciprofloxacin is the drug
of choice
• Eosinophilic pustular folliculitis does not respond to systemic antibiotic, but may respond
to isotretinoin
Eczema
• Eczema or dermatitis is a superficial skin inflammation characterised by epidermal edema
and clinically with red, patches or vesicles that typically are pruritic
• Primary lesions may include
Papules
Erythematous macules and vesicles, which can coalesce to form patches and plaques.
In severe eczema, secondary lesions form infection or excoriation, marked by
weeping and crusting
Long-standing dermatitis is often dry and is characterized by thickened, scaling skin
(lichenification)
Common Types of Eczema
• Atopic dermatitis
• Contact dermatitis
• Nummular dermatitis
• Lichen Simplex Chronicus
• Asteatotic eczema
• Seborrheic dermatitis
Atopic Dermatitis
• This is the cutaneous expression of the atopic state characterized by a family history of
asthma. Hay fever or dermatitis in up to 70% of patients.
Aetiology
• There is a clear genetic predisposition.
• When both parents are affected by atopic dermatitis over 80% of their children manifest
the disease.
• When only one parent is affected, the prevalence drops to slightly over 50%.
• A number of genes have been tentatively linked to atopic dermatitis including
Genes coding for IgE
High affinity IgE receptor
Mast cell tryptase and
Interleukin 4
• Patients with atopic dermatits may display a variety of immunoregulatory abnormalities
including increased IgE synthesis.
Clinical Presentation
• Often varies with age
• Half of patients with atopic dermatitis present within the first year of life and 80% present
by 5 years of age.
• Some 80% ultimately coexpress allergic rhinitis or asthma later in life.
• The infantile pattern is characterized by weeping inflammatory patches and crusted
plaques that occur on the face, neck, extensor surfaces, and groin.
• The childhood and adolescent pattern is marked by dermatitis of flexural skin particularly
in the antecubital and popliteal fossae.
• Atopic dermatitis may resolve spontaneously in adults, but the dermatitis will persist into
adult life in over half of individuals affected as children.
• The distribution of lesions may be similar to those seen in childhood
• Adults affected with atopic dermatitis frequently have localized disease manifesting as
hand eczema or lichen simplex chronicus
• Pruritus is a prominent characteristic of atopic dermatitis and many of the cutaneous
findings in affected patients are secondary to rubbing and scratching
• Other cutaneous stigmata of atopic dermatitis are
Perioral pallor
An extra fold of skin beneath the lower eyelid (dennie's line)
Increased palmar markings and
Increased incidence of cutaneous infections particularly with staphylococcus aureus
• Atopic individuals often have dry itchy skin, abnormalities in cutaneous vascular
responses
Treatment of Atopic Dermatitis
• Therapy of atopic dermatitis should be based on
Avoidance of cutaneous irritants
Adequate cutaneous hydration
Judicious use of low or mid-potency topical steroids to affected areas
Prompt treatment of secondarily infected skin lesions
Patients should be instructed to bathe using warm, but not hot, water and to limit their
use of soap.
Immediately after bathing while the skin is still moist, the skin should be lubricated
using a more oil based lotion
Potent fluorinated topical steroids should not be used on the face or intertriginous
areas
(It takes a minimum of 30 g of glucocorticoid ointment to cover the entire body
surface of an average adult)
Crusted and weeping skin lesions should be treated with systemic antibiotics with
activity against S. aureus and S. pyogenes since secondary infection often exacerbates
eczema
o Control of pruritus is essential for treatment since atopic dermatitis often represents
‘an itch that rashes’.
Antihistamines are useful to control the pruritus.
Treatment with systemic steroids should be limited to severe exacerbations
unresponsive to conservative topical therapy.
In the patient with chronic atopic dermatitis therapy with systemic steroids will
generally clear the skin only briefly but cessation of the systemic therapy will
invariably be accompanied by return, if not worsening, of the dermatitis.
Contact Dermatitis
• Is an inflammatory process in skin caused by an exogenous agent or agents that directly
or indirectly injure the skin.
• Common sensitizers include preservatives in topical preparations, nickel sulfate,
potassium dichromate, thimerosal in ocular preparations, neomycin sulfate, fragrances,
formaldehyde and rubber-curing agents.
• This injury may be caused by an inherent characteristic of a compound irritant contact
dermatitis.
• An example of irritant contact dermatitis would be dermatitis induced by a concentrated
acid or base.
• Agents that cause allergic contact dermatitis induce an antigen-specific immune response.
• The clinical lesions of contact dermatitis may be acute (wet and oedematous) or chronic
(dry, thickened, and scaly) depending on the persistence of the insult.
• The most common presentation of contact dermatitis is hand eczema and it is frequently
related to occupational exposures.
• Occupation related contact dermatitis represents a significant proportion of occupation
induced injury.
• Irritant contact dermatitis is generally strictly demarcated and often localized to areas of
thin skin (eyelids, intertriginous areas) or to areas where the irritant was occluded.
• Lesions may range from
Minimal skin erythema to areas of marked edema
Vesicles and ulcers
• Chronic low-grade irritant dermatitis is the most common type of irritant contact
dermatitis and the most common area of involvement is the hands.
• The most common irritants encountered are
Chronic wet work
Soaps
Detergents
• Treatment should be directed to avoidance of irritants and use of protective gloves or
clothing.
• Allergic contact dermatitis is a manifestation of delayed type hypersensitivity mediated
by memory T lymphocytes in the skin.
• The most common cause of allergic contact dermatitis is exposure to plants.
• Poison ivy, poison oak, and poison sumac from plants cause allergic reaction marked by
erythema, vesiculation, and severe pruritus.
• The eruption is often linear, corresponding to areas where plants have touched the skin.
• These irritants may adhere to skin, clothing, tools, pets and cause dermatitis.
Treatment of Contact Dermatitis
• If allergic contact dermatitis is suspected and an offending agent is identified and
removed the eruption will resolve.
• High potency fluorinated topical steroids are enough to relieve symptoms while the
allergic contact dermatitis runs its course.
• For those patients who require systemic therapy a tapering course over 2 to 3 weeks given
as single morning doses is the preferred method.
• They should be questioned carefully regarding occupational exposures, topical
medicaments and oral medications.
• For those patients who require systemic therapy a tapering course over 2 to 3 weeks given
as single morning doses is the preferred method.
• They should be questioned carefully regarding occupational exposures, topical
medicaments and oral medications.
Lichen Simplex Chronicus
• Is chronicus may represent the end stage of a variety of pruritic and eczematous disorders.
• It consists of a well-circumscribed plaque or plaques with lichenified or thickened skin
due to chronic scratching or rubbing.
• Common areas involved include the posterior nuchal region, dorsum of the feet, or ankles
• Treatment of lichen simplex chronicus is centered around breaking the cycle of chronic
itching and scratching which often occur during sleep
• High potency topical steroids are helpful in alleviating pruritus in most cases but in
recalcitrant cases application of topical steroids under occlusion or intralesional injection
of steroids may be required.
• Patients need to be counseled regarding driving or operating heavy equipment after taking
these medications due to their potentially potent sedative activity.
Seborrheic Dermatitis
• Seborrheic dermatitis is a common chronic disorder characterized by greasy scales
overlying erythematous patches or plaques.
• The most common location is in the scalp where it may be recognized as severe dandruff
• On the face seborrheic dermatitis affects the
Eyebrows
Eyelids
Glabella
Nasolabial fold, or ears
• Scaling within the external ear is often mistaken for a chronic fungal infection
(otomycosis), and postauricular dermatitis often becomes macerated and tender.
• Additionally seborrheic dermatitis may develop in the central chest, axilla, groin,
submammary folds and gluteal cleft.
• Rarely may cause a widespread generalized dermatitis.
• Seborrheic dermatitis is usually symptomatic with patients complaining of itching or
burning.
• Seborrheic dermatitis may be evident within the first few weeks of life and tends to occur
in the scalp (‘cradle cap’), face or groin.
• It is rarely seen in children beyond infancy but becomes evident again during adult life.
• Although it is frequently seen in patients with parkinson's disease in those who have had
cerebrovascular accidents and in those with human immunodeficiency virus (HIV)
infection the overwhelming majority of individuals with seborrheic dermatitis have no
underlying disorder.
Treatment of Seborrheic Dermatitis
• Treatment with low potency topical steroids in conjunction with shampoos containing
coal tar and/or salicylic acid is generally sufficient to control this disorder.
• High potency topical steroids solutions (betamethasone or fluocinonide) are effective for
control of scalp involvement if severe
• Fluorinated topical steroids should not be used on the face since this is often associated
with the development of rebound worsening and steroid induced rosacea or atrophy.
         
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