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Report in DERMATOLOGY
PUSTULAR DISEASE, VESICULAR DISEASE AND BULLOUS DERMATOSIS
SECTION C
GROUP 5
MANGUBAT, Mary Love Joy
MANSUKHANI, Sujata
MARANION, Maria Cristina
MARAYAG, Eric John
MARCELO, Pamela
MARCIAL, Karmi Margaret
MATEMATICO, Michelle
MATIAS, Evangeline Grace
MAULION, Marienelle
MENDOZA, Trisha
MILIARIA
It is a common disorder of the eccrine sweat glands caused by blockage of the sweat
ducts, which results in the leakage of eccrine sweat into the epidermis or dermis.
Causative agents: Staphylococcus epidermidis and Staphylococcus aureus
Types of Miliaria according to the level of injury to the sweat gland or duct:
1. miliaria crystallina
2. miliaria rubra (when pustules develop it is termed as miliaria pustulosa)
3. miliaria profunda
Predisposing factors
- Immaturity of the eccrine ducts of neonates
- Hot, humid conditions: Tropical climates, febrile illnesses.
- Exertion: Any stimulus to sweat may precipitate or exacerbate miliaria.
MILIARIA CRYSTALLINA (SUDAMINA)
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Ductal obstruction is most superficial, occurring in the stratum corneum
Characterized by small, clear, and very superficial vesicles occurring at stratum
corneum with no inflammatory reaction.
Appears in bedridden patients in whom fever produces increased perspiration or in
situations in which clothing prevents dissipation of heat and moisture, as in bundled
children
Lesions are asymptomatic and their duration is short lived because they tend to
rupture at the slightest trauma
Lesions are self limited
No treatment is required
MILIARIA PUSTULOSA
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It is always preceded by some other dermatitis that has produced injury, destruction,
or blocking of the sweat duct.
Pustules are distinct, superficial and independent of the hair follicle
Pruritic pustules occur most frequently on the intertriginous areas, on the flexure
surfaces of the extremities , on the scrotum, and on the back of bedridden patients.
Associated with contact dermatitis, lichen simplex chronicus, and intertrigo ( it may
occur several weeks after the disease has subsided
Contents of pustules are usually sterile, but may contain nonpathogenic cocci
IMPETIGO
It is a superficial bacterial infection of the epidermis.
Causative agents: Staph and Strep infections
Types:
1. Bullous impetigo
2. Non-Bullous impetigo
Predisposing factors:
 Children with poor hygiene and malnutrition
 Patients with chronic diseases i.e. diabetes
 Climates i.e warm or tropical
Site of predilection: Most commonly involves the face (mouth and nose), extremities, hands,
and neck
Treatment:
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Topical antiseptics or fusidic acid
Systemic antibiotics (penicillinase-resistant
cephalosporins) may speed course of healing.
penicillins
or
first-generation
BULLOUS IMPETIGO
Causative agent: S.aureus
Pathogenesis: Caused by phage types 71 or 55 coagulase-positive S. aureus or a related
group 2 phage type. They produce a toxin, exfoliatin, which is capable of splitting the epidermis
in the stratum granulosum thus, producing large superficial blisters.
Clinical features:
According to age:
 Neonatal: Neonatal bullous impetigo is highly contagious and it usually begins
between the 4th-10th day of life. It starts of with the appearance of bullae which
may appear on any part of the body but the common early sites are the face and
hands.
 Children: History of insect bite at the site of onset of lesions
 Adults: Common sites are the axillae, groins or hands; No scalp lesions
Constitutional Symptoms: will only manifest later during the course of the disease
 Weakness
 Fever or subnormal temperature
 Diarrhea with green stools
 Bacteremia
 Pneumonia
 Meningitis
Lesions: Large, fragile bullae with clear yellow fluid which later becomes darker and more
turbid. When they rupture, they leave circinate, weepy, or crusted, brown lesions which are
called impetigo circinata.
Complications: Death due to rapid development of bacteremia/ pneumonia/ or meningitis.
NON-BULLOUS IMPETIGO
Causative agents: S. aureus and S. pyogenes
Pathogenesis: Bacteria colonizes the skin surface and superficially invade any areas where the
integrity of the skin is compromised.
Clinical features:
 Develops as a small, red, vesiculopustular lesion which will later on break
and leak fluid, leaving a punched-out ulceration with honey-colored crust or
plaque <2cm.
 Regional adenopathy (90%)
Complications:
 Acute Glomerulonephritis (due to Group A-Beta Hemolytic Strep)
 Lymphangitis
Prevalence
Etiology
Site of
Predilection
History
Adenopathy
Speed of spread
Erythema
BULLOUS IMPETIGO
NON-BULLOUS IMPETIGO
Less Common; children <24 More common; children > 24
months of age
months of age
S. aureus
S. aureus and S. pyogenes
Intact Skin
Areas of traumatized skin on the
face or extremities
Flaccid, transparent, roofed bullae Discrete, fragile vesicles surrounded
that rupture spontaneously without by
an
erythematous
border.
a
history
of
localized Vesicles become pustular, rupture
lymhadenopathy or cutaneous and discharge a honey colored fluid
disruption
that quickly forms honey-colored
crusted plaque with rapid spread,
occasional pruritus, and regional
lymphadenopathy may follow a
break in the skin
Absent
Present
Moderate
Rapid
Minimal or none
Marked
ECTHYMA
It is an ulcerative staphylococcal or streptococcal pyoderma of the skin; often referred to
as a deeper form of impetigo as it extends into the dermis
Causative Agents: S. aureus or Group A Streptococcus
Predisposing factors:
- Uncleanliness and Trauma
o Lesion may evolve from other skin lesions i.e. boils or sites of preexisting trauma in diabetic patients
- Malnutrition
- Intravenous drug use
Clinical Features:
Starts out as a solitary lesion – vesicle or vesicopustule, which enlarges (2-3cm in
diameter) within a few days and becomes thickly crusted and as the crust is removed,
there is a superficial saucer-shaped ulcer with a raw base and elevated edges. The
lesions heal after a few weeks, leaving scars. However, they may rarely proceed to
gangrene when resistance is low. Local adenopathy may also be present. They most
commonly appear on the shins or dorsal feet.
Treatment:
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Cleansing with soap and water
Application of Mupirocin or Bacitracin ointment twice a day
Oral Dicloxacillin or first-generation Cephalosporin
Proper hygiene and nutrition
HERPES SIMPLEX
It is an infection caused by Herpes simplex virus and is one of the most prevalent
infections worldwide.
Two forms of HSV:
1. HSV-1
- the most common cause of OROLABIAL HERPES, with 50% infected person
had history of it.
2. HSV-2
- infected persons are asymptomatic (latent infection), 20% have GENITAL
HERPES and 60% have lesions that they do not recognize as gential herpes.
Diagnosis:
 Tzanck smear- most common procedure used; non specific because it can test positive for
both HSV and VZV ( formation of multinucleate epidermal giant cells)
 DFA test- more accurate; identify virus type and results are available in hours
 Viral culture- very accurate and rapid
 PCR- as accurate as viral culture; can be performed on dried or fixed tissue.
 Skin biopsies- detect viropathic changes and with specific HSV antibodies,
immunoperoxidase techniques can accurately diagnose infection.
OROLABIAL HERPES
It is virtually always caused by HSV-1
Clinical features and accompanying symptoms:
 the onset is often accompanied by high fever, regional lymphadenopathy and malaise
lesions in mouth are usually broken vesicles that appear as erosions or ulcers covered
with white membrane.
 erosions may become widespread on the oral mucosa, tongue, and tonsils, and produce
pain, foul breath and dysphagia.
 most common clinical manifestation is the “cold sore” or “fever blister” (grouped blister
on an erythematous base)
 The lips near the vermillion are most frequently involved
 Recurrences maybe seen on the cheeks, eyelid and earlobes
Treatment and Prevention
 use of a sunblock daily on lip and facial skin may reduce recurrence
 tetracaine cream and penciclovir creams has modest effects on reduction of lesion
number, healing time and discomfort.
 Intermittent treatment with valacyclovir 2g twice a day for 1 day starting at the onset of
prodome is a simple and effective oral regimen
GENITAL HERPES
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Genital Herpes infection is usually due to HSV-2 (85% of initial infections and up to 98%
of recurrent lesions)
 It is spread by skin to skin contact, usually during sexual activity, with 5 days incubation
period.
 Most transmission occurs during subclinical or unrecognized outbreaks, or while the
infected person is shedding asymptomatically.
 maybe from totally asymptomatic to severe genital ulcer disease ( erosive vulvovaginitis
to proctitis).
Lesions: classic grouped blisters on a erythematous base
 May appear on the vagina, rectum or on penis with continued development of new
blisters over 7 to 14 days
 bilaterally asymmetrical, often extensive, and the inguinal lymph nodes may enlarge
bilaterally.
 typical recurrent gential herpes begins with a prodrome ofburning, itching, or tingling.
Usually 24h, red papules appear at the site, progress to blisters filled with clear fluid over
24h, form erosions over the next 24 to 36 h and heal in another 2 to 3 days.
Treatment:
 initial episode maybe treated with oral acyclovir, famciclovir , Valacyclovir for 7 to 10
days.
 for recurrent genital herpes may be acyclovir, or famciclovir.
HERPETIC SYCOSIS
It is a recurrent or initial herpes simplex infections affecting primarily the hair follicle.
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Lesions may appear from eroded follicular papules to extensive lesions involving the
whole beard area
Diagnostic clues: tendency for erosions, a self limited course of 2 to 3 weeks, and an
appropriate risk behavior, and confirmed by biopsy.
HERPES GLADIATORUM
A condition caused by HSV-1. It affects individuals who participate in contact sports such
as wrestling. It is also known as wrestler’s herpes.
Clinical features and accompanying symptoms:
 Lesions on the lateral side of the neck, side of the face, and the forearm, all areas in
direct contact with the face of the infected wrestler
 Vesicles appear 4 to 11 days after exposure,
 often preceded by 24h of malaise, sore throat, and fever
Prevention:
 Any wrestler with a confirmed history of orolabial herpes should be on suppressive
antiviral therapy during all periods of training and competition.
HERPETIC WHITLOW
It is a painful infection that typically affects the fingers or thumbs. Occasionally infection
occurs on the toes or on the nail cuticle.
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Lesions begin with tenderness and erythema usually of the lateral nailfold or on the
palm.
Deep-seated blisters develop 24 to 48h after symptoms begin
much less frequent among health care workers since the institution of universal
precautions and glove use during contact with oral mucosa.
HERPETIC KERATOCONJUNCTIVITIS
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Herpes simplex infection of the eye
common cause of blindness.
It occurs as a punctuate or marginal keratitis, or as a dendrite corneal ulcer, which may
cause disciform keratitis and leave scars that impair vision.
Topical corticosteroids in this situation may induce perforation of the ulcer.
Vesicles may appear on the lids and preauricular nodes may be enlarged and tender.
Recurrences are common.
INTRAUTERINE AND NEONATAL HERPES SIMPLEX
Newborn infants can become infected with herpes virus:
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In the uterus (intrauterine herpes -- very rare)
Passing through the birth canal (birth-acquired herpes, the most common method of
infection)
postpartum (through contact with a person with orolabial disease)
The clinical spectrum of perinatally acquired neonatal herpes can be divided into three
forms: 1.) Localized infections of the skin, eyes, and/or mouth;
2.) CNS disease
3.) disseminated disease ( encephalitis, hepatitis, pneumonia and coagulopathy)
Diagnosis:
 viral culture
 DFA staining of material from skin or ocular lesions.
 PCR of CSF
Treatment:
 IV acyclovir 60mg/kg/day for 14 days for SEM disease and 21 days for CNS and
disseminated disease.
ECZEMA HERPETICUM
Infection with herpes virus in patients with atopic dermatitis may result in spread of
herpes simplex throughout the eczematous areas ( Kaposi varicelliform eruption).
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Treatment: IV or oral acyclovir therapy should be given in all cases of Kaposi
varicelliform eruption.
Herpes infection in immunocompromised patients
 primary or recurrent herpes simplex are more severe, more persistent and more
symptomatic.
 Lesions appear as erosions or crusts.
 3 clinical hallmarks of herpes simplex infections: pain, an active vesicular border, and a
scalloped periphery.
HERPES ZOSTER
It is a painful, blistering skin rash due to the reactivation of Varicella-Zoster Virus
Cause:
 immunosuppression and age are the factors involved in reactivation of VZV
 VZV remains dormant in the sensory dorsal root ganglion cells after an infection or
vaccination. At some later time, the virus begins to replicate and travels down the
sensory nerve into the skin.
Clinical features
 cutaneous eruption of the affected area preceded by one to several days of pain
 eruptions are papules and plaques of erythema in the dermatomes; plaques develop
blisters which appear for several days and may become hemorrhagic, necrotic or
bullous.
 Lesions may develop on the mucous membranes within the mouth ( zoster of maxillary
or mandibular division of the facial nerve) or in the vagina (zoster in the S2 or S3
dermatome); may also appear in recent surgical scar
 Zoster Sine Herpete pain with no skin lesions which rarely occurs in a patient
 pain severity depends on the extent of skin lesions; and in the elderly persons, pain is
more severe
 total duration of the eruption depends on 3 factors: age, severity of eruption and
presence of underlying immunosuppression
 younger patients: 2-3 weeks for the lesions to heal while elderly requires >6 weeks
Disseminated Herpes Zoster
 defined as more than 20 lesions outside the affected dermatome
 risk factor: low levels of serum antibody against VZV
 occurs more in the old and debilitated persons, especially in patients with
lymphoreticular malignancy or AIDS.
 lesions are either hemorrhagic or gangrenous and the outlying vesicles or bullae are
usually not grouped.
 visceral dissemination to the lungs and CNS may occur.
Ophthalmic Zoster
 involves the ophthalmic division of the 5th cranial nerve
Hutchinson’s sign
 involvement of the external division of the nasociliary branch with vesicles on the side
and tip of the nose.
Diagnosis:
 Tzanck smear- confirmatory test
 Biopsy- necessary to demonstrate the typical herpes virus cytopathic effects
 Immunoperoxidase stain- can then be used on paraffin-fixed tissue to specifically identify
VZV
Histopathology:
The vesicles in zoster are intraepidermal. Within and at the sides of the vesicles are
balloon cells (large, swollen cells), which are degenerated cells of the spinous layer. Acidophilic
inclusion bodies are present in the nuclei of the cells of the vesicle epithelium. Multinucleated
keratinocytes, nuclear moulding and peripheral condensation of the nucleoplasm are
characteristic and confirmatory of infection of either HSV or VZV.
Treatment and Management:
 Antiviral therapy (Acyclovir) is the cornerstone in the management of herpes zoster.
o The main benefit of therapy is in reduction of duration of zoster-associated pain.
Therapy should be started as soon as diagnosis is confirmed, preferably within 34 days.
 Valcyclovir and famciclovir may be given 3 times a day. They are as safe as acyclovir.
 For the middle-aged and elderly, they are urged to restrict their physical activities or
even stay home in bed for a few days.
 Younger patients may continue their usual activities.
 Bed rest is so important in preventing neuralgia.
 Local applications of heat such as electric heating pad or a hot-water bottle are
recommended.
 Simple local application of gentle pressure with the hand or with an abdominal binder
often gives great relief.
Complications:
 Motor Nerve neuropathy
 Ramsay Hunt syndrome results from the involvement of facial and auditory nerves by
VZV, and the cause of this syndrome is the herpetic inflammation of the geniculate
ganglion. The presenting features include:
 zoster of the external ear or tympanic membrane;
 herpes auricularis with ipsilateral facial paralysis;
 or herpes auricularis facial paralysis, and auditory symptoms (mild to
severe tinnitus, deafness, vertigo, nausea and vomiting and nystagmus).
ZOSTER-ASSOCIATED PAIN (POSTHERPETIC NEURALGIA)
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the most troublesome symptom of Zoster and is very difficult to control
Oral antivirals are recommended in all patients over 50 with pain in whom blisters are
still present, even if they are not given within the first 96 hours of the eruption.
Oral analgesia should be maximized using acetaminophen, NSAIDS and opiate
analgesia as required.
Capsaicin applied topically every few hours may reduce pain.
Local anesthetics may acutely reduce pain.
Botulinum toxin at the site of most significant pain following zoster of the trunk was
associated with complete resolution of the pain.
Systemic corticosteroids reduce the overall severity of acute ZAP, improve quality of life,
and return the patient to full daily activity sooner but they are contraindicated in
immunosuppressed patients.
PYOGENIC PARONYCHIA
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Paronychia is an inflammatory reaction involving the folds of the skin surrounding the
fingernail. The feature of this disease is summarized in the table below.
Character
Cause
Chronic infection
Recurrence
acute or chronic purulent, tender, and painful swellings of the tissue
around the nail
abscess in the nail fold
horizontal ridges appear at the base of the nail
recurrent bouts new ridges appear
Predisposing factor:
 disease is said to be work-related for workers who frequently have their hands wet (eg.
bartenders, food servers, nurses, etc.).
 trauma brought about by moisture-induced maceration of the nailfolds cause the
separation of the eponychium from the nail plate.
Causative agents:
 Bacterial agents are: S. aureus, S. pyogenes, Pseudomonas, Proteus, and anaerobes;
while the yeast infection is caused by Candida albicans.
 Staphylococci cause acute abscess formation, Streptococci cause erythema and
swelling but in chronic swelling Candida is the most frequently recovered organism
Diagnosis:
If an abcess is suspected, pressure is applied with index finger against distal volar
aspect of affected digit. To demonstrate the extent, a well-demarcated blanching is induced. In
addition, smear of purulent material is done to confirm the diagnosis.
Differential diagnosis would include myremecial warts that mimic paronychia. Likewise,
in osteomyelitis in children with atopic dermatitis, there are subungual black macules followed
by edema, pain and swelling. This must also be considered as the causative agents are
similarly S. aureus and S. viridians.
Management:
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Pyogenic paronychia is primarily treated through:
- Protection against trauma
- Keep affected fingernails meticulously dry
- Incision and drainage for acutely inflamed pyogenic abscess
- To open abscess, push nailfold away from the nailplate
For acute suppurative paronychia
- for pyogenic cocci infection- semisynthetic penicillin or a cephalosporin with
excellent staphylococcal activity should be given orally
- for MRSA or mixed anaerobic bacterial infection, Augmentin (Amoxicillin
clavulanate) can be used
- otherwise, appropriate treatment must be based on culture and sensitivity
studies. However, rarely is long-term antibiotic therapy required.
For chronic paronychia caused by Candida
- topical or oral antifungals lead to cure in only ~50% of cases.
- Topical steroids are more reliable (~80% cured in one study), which decrease
inflammation and allow for tissue repair.
- often a liquid antifungal (eg. Miconazole) is combined with a topical corticosteroid
cream or ointment
INTERTRIGINOUS CANDIDIASIS
Intertrigo - superficial inflammatory dermatitis which occur in areas where two skin are in
apposition
-mostly seen during hot and humid whether resulting from friction, heat and moisture
thus the area becomes erythematous, macerated and secondarily infected
Causative agent:
Candida albicans -an opportunistic organism commonly found in the gastrointestinal and
genitourinary tracts and skin acting as a pathogen in persons with impaired immune response or
in areas where conditions favor growth: warm, moist, high skin pH, reduced microbial flora
resulting from antibiotic therapy.
Lesion:
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pruritic pink to red intertriginous moist patches surrounded by a thin collarette
(overhanging fringe of macerated epidermis) scale. Surrounded by pustules which are
closely adjacent to the patches.
Area of predilection:
 Folds of the geitals, groins or armpits, in between buttocks, under large pendulous
breast(inframamary breast area), under overhanging abdominal folds or in the umbilicus.
Treatment:
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Topical Anticandidal Agents:
clotrimazole (Lotrimin, Mycelex), econazole (Spectazole), ketokonazole (Nizoral),
miconazole, oxinazole ( Oxistat), naftifine (Naftine), sulconazole (Exelderm), terconazole,
butenafine (mentax), terbinafine (Lamisil), nystatin, topical amphotericin-B, gentian violet, boric
acid, castellani paint (preferred by patients).
 Note: recurrence is common
 For rapid relief: topical agent + mid-strength corticosteroid
STEVEN JOHNSON SYNDROME
It is an extensive and symptomatic febrile form of Erythema multiforme, which is often
but not exclusively seen in children.
Etiologic agents:
SJS usually represents adverse reactions to medications. Common inciting medications are:
Drug
Incidence
Nevirapine, lamotrigine
1 in 1000 adults; 3 in 1000 children
Carbamazepine
14 in 100,000
Fansidar-R, sulfadoxine plus
10 in 100,000
pyrimethamine
Trimethoprim-sulfamethoxazole
1-3 in 100,000
Antibiotics (long acting sulfa drugs and
penicillins), other anticonvulsants,
antiinflammatories (NSAIDS), & allopurinol
Clinical presentation:
 Fever and influenza-like symptoms often precede the eruption by a few days.
 Skin lesions – initially, macular, followed by desquamation, or may form atypical targets
with pruritic centers that coalesce, form bullae, then slough. They appear on the face
and trunk and rapidly spread to their maximum extent. Typically, erosions and
hemorrhagic crusts involve the lips and oral mucosa, although the conjunctiva, urethra,
and genital and perianal areas may also be affected.
 Other symptoms include photophobia, difficulty swallowing, painful urination, and cough.
Pathogenesis:
 Erythema multiforme has a cytotoxic reaction pattern typified by extensive epithelial cell
degeneration and death.
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Epithelial cells are killed by CD8+ cytotoxic T lymphocytes (CTLs) more prominent in
the epidemis, while helper T cells in the dermis.
Diagnosis:
 Skin biopsy is usually performed to exclude other diseases and to confirm the diagnosis.
 Early lesions show a superficial perivascular, lymphocytic infiltrate associated with
dermal edema and accumulation of lymphocytes along the dermoepidermal junction,
where they are intimately associated with degerating and necrotic keratinocytes. With
time, there is upward migration of lymphocytes into the epidermis.
Management:
 similar to an extensive burn, wherein they suffer fluid and electrolyte imbalances,
bacteremia from loss of the protective skin barrier, hypercatabolism, and sometimes
acute respiratory distress syndrome.
 Nutritional support is also critical.
Treatment:
 Immunosuppressive therapy is used to stop the process of drug eruptions very quickly
and thereby reduce the ultimate amount of skin lost.
 However, once most of the skin loss has occurred, immunosuppressives would only add
to the morbidity and perhaps mortality of the disorder.
 Therefore, if immunosuppressive treatment is considered, it should be used as soon as
possible, given as a short trial to see if the process may be arrested, and then tapered
rapidly to avoid the risk of immunosuppression in a patient with substantial skin loss.
CONTACT DERMATITIS
Is the generic term applied to acute and chronic inflammatory reactions to substances
that come in contact with the skin.
ACUTE DERMATITIS is characterized by pruritus, erythema, and vesiculation
CHRONIC DERMATITIS is characterized by pruritus, xerosis, lichenification, hyperkeratosis,
and/or fissuring
Regional predilection:
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Scalp: hair dyes, hair spray, shampoo or permanent wave solutions
Ear: neomycin, jewelry
Eyelids: nail polish, volatile gases, false-eyelashes adhesive, fragrances, preservatives,
mascara, eyeshadow
Mouth/Gums: flavoring agents, shellac, medicaments, sunscreen in lipstick and lip balms
Neck: Perfume, jewelry, aromatic oils
Trunk/Axilla: dye or finish of clothing, deodorant, brassieres
Arms: jewelry, back of the watches and clasps, leather wristbands
Hands: variety of substances, plants, rubber gloves
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Abdomen/Waistline: Rubber from elastic pants and undergarments, metallic rivets in
jeans, piercings
Groin/Buttocks/Upper Thighs: dyes, poison ivy, condom, suppositories, fragrance/
cleansing materials
Lower Extremities: elastic stockings, rubber or leather shoes
Tests for Sensitivity:
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Patch Test
o detect hypersensitivity to a substance that is in contact with the skin so that the
allergen may be determined and corrective measures taken; confirmatory and
diagnostic with history and physical findings
Method of Administration:
- Application to intact uninflamed skin of suspected substances in low concentration
usually on the upper back or upper outer arm if one or two will be applied
- Administered by thin-layer rapid-use epicutaneous (TRUE) test or individually prepared
aluminum (finn) chambers mounted on a Scanpor Tape;each patch is numbered to
avoid confusion
- Removed after 48 h or sooner if severe itching or burning occur at the site, then Read.
- Erythematous papules and vesicles with edema  indication of allergy
- Excited skin syndrome – state of hyperirritability due to strong patch test reactions that
may cause false positive to negative test
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Provocative Use Test
o Confirms a positive closed patch test reaction to ingredients of a substance; to
test products that are made to stay on the skin once applied
Method of Administration:
- The material is rubbed onto normal skin of the inner aspect of forearm
- Several times a day for 5 days
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Photopatch Test
o To evaluate for contact photoallergy to such substances as sulfonamides,
phenothiazines, PABA, oxybenzone, musk ambrette
Method of Administration:
- Substance is applied for 24 hour
- It is then exposed to 5 to 15 J/m2 of UVA
- Read after another 48 h
- Duplicate non irradiated patch - test for presence of delayed hypersensitivity
Types of Contact Dermatitis:
1. Irritant Contact Dermatitis – caused by a chemical irritant
2. Allergic Contact Dermatitis – caused by an antigen/allergen eliciting Type IV delayed
hypersensitivity reaction (Cell-mediated)
IRRITANT CONTACT DERMATITIS
It is defined as an inflammatory reaction in the skin resulting from exposure to a
substance that causes an eruption in most people who come in contact with it
Etiologic Agents:
 Water, soaps, detergents, bleaches, lye, drain pipe cleaners, toilet bowl and oven
cleansers
 Acids and Alkalis: hydrochloric acid, sulfuric and nitric acid, hydrofluoric acid, Oxalic acid,
Phenol, Acetic acid
 Solvents and Hydrocarbons: crude petroleum, lubricating and cutting oils, creosote, coal
tar solvents, chlorinated hydrocarbons, alcohol solvents, ethylene glycol ether, turpentine,
ethyl ether
 Others: Fiberglass, dust, capsaicin, teargas, metal salts
Predisposing Factors:
 History of atopic dermatitis
 Occupational exposure/ Repeated exposure
 Low temperature/ Low humidity
 Condition of the skin
Pathogenesis:
The irritants cause cell damage if applied for sufficient time and in adequate
concentration. Inflammatory response occurs because of the inability of the skin to defend and
repair its integrity and function from penetrating chemicals.
Clinical Features:
Acute Irritant Contact Dermatitis
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Chronic Irritant Contact Dermatitis
Burning, stinging, painful sensations can  Stinging and itching, pain as fissures
occur immediately within seconds after
develop
exposure or may be delayed up to 24 hour
 LESION
 LESION
Dryness  chapping  erythema 
Erythema with a dull, nonglistening
hyperkeratosis and scaling  fissures
surface  vesiculation (or blister formation)
and crusting
 erosion  crusting  shedding of crusts
- Lichenification, vesicles, pustules, and
and scaling or (in chemical burn) erythema erosions
 necrosis  shedding of necrotic tissue 
ulceration  healing
ALLERGIC CONTACT DERMATITIS
It is an acquired sensitivity, cell-mediated hypersensitivity or immunity, to various
substances that produce inflammatory reactions in those and only those, who have been
previously sensitized to the allergen. This condition continues to get worse as long as allergen
continues to come into contact with the skin.
Etiologic Agents/Allergens:
 Plants: Toxicodendron (Poison Ivy), raw cashew nuts and cashew nutshell oil, mango,
ginkgo biloba, chrysanthemum, prairie crocus, lichens, pollens and seeds, Peruvian lily,
castor bean, latex of fig and rubber trees, daffodil, lilac, magnolia, timber and sawdust,
marine blue-green alga
 Clothing: Fabric finishers, dyes, rubber additives, polyvinyl resins, silk, anti-wrinking and
crease-holding chemicals, polyester and acetate liners, brassieres
 Shoes: rubber accelerators, leathers, and adhesives, foam rubber padding, felt, cork
liners, formaldehyde, asphalt, tar
 Metal/Metal Salts: nickel-containing (earrings, watch, necklace), chromate (paint, gloves,
cellphone, cement), mercury (gelatin waving solution, bentonite gels, amalgams), cobalt
(polyester resin, paints, cement, ceramics, metal alloys, glass), arsenic (ores, wallpaper,
fabric dyes, disinfectants), gold (dental gold, gold jewelry contaminated with radon)
 Cosmetics: Fragrance, cosmetic preservatives, permanent hair dye, Balsam of Peru, acid
permanent wave preparation, gum arabic, sunscreens, mechanical hair removers,
tincture of cinchona, nail lacquers, deodorants
Pathogenesis
Sensitization occurs when the allergen is processed by the Langerhan cells in the
epidermis and presented to a CD4+ T-cell, the allergen is then recognized. Sensitized T-cells go
back to skin carrying the specific antigen, produce and mediate release of cytokine making skin
hypersensitive to the allergen and will react wherever, whenever there is allergen reexposure.
Clinical Features:
Acute allergic contact dermatitis
Chronic allergic contact dermatitis
 Well-demarcated erythema and edema on
which are superimposed closely spaced,
nonumbilicated vesicles, and/or papules
 Plaques of lichenification (thickening of
the epidermis with deepening of the skin
lines in parallel or rhomboidal pattern),
scaling with satellite, small, firm, rounded
or flat-topped papules, excoriations,
erythema, and pigmentation
 LESION:
-Papules scaling lichenification
excoriations
 LESION:
-Erythema
papules
vesicles
erosions crusts scaling.
-Papules occur only in acute allergic
contact dermatitis
Summary Table: Irritant Contact Dermatitis vs. Allergic Contact Dermatitis
Excerpt from Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology 5th edition
Irritant Contact Dermatitis
Allergic Contact Dermatitis
Acute
Stinging, smarting itching
Itching  Pain
Chronic
Itching/Pain
Itching/Pain
Acute
Erythema  vesicles  erosion
 crusting  scaling
Erythema  papules  vesicles
 erosion  crusting  scaling
Chronic
Papules, plaques, fissures,
scaling, crusts
Papules, plaques, scaling, crusts
Acute
Sharp, strictly confined to site of
exposure
Sharp, confined to site of
exposure but spread in the
periphery, usually tiny papules;
may become generalized
Chronic
Ill-defined
Ill-defined, spreads
Acute
Rapid (minutes to few hours
after exposure)
Not so rapid (12 to 72 hours after
exposure
Chronic
Months to years of repeated
exposure
Months or longer, exacerbations
after every reexposure
Causative
agents
Dependent on concentration of
agent and state of skin barrier;
occurs only above threshold
level
Relatively independent of amount
applied, usually very low
concentrations sufficient but
depends on degree of
sensitization
Incidence
May
occur
everyone
Symptoms
Lesion
Margination
and Site
Evolution
in
practically Occur only in the sensitized
Management for Contact Dermatitis
Prevention:
 Avoid exposure to potential allergen
 Avoid repeated and prolonged exposure to irritants
 Wear protective clothing
 Check skin reactions to cosmetics before applying
Treatment for Irritant Contact Dermatitis
 Identify and remove the etiologic agent
 Wet dressings with gauze soaked in Burow's solution, changed every 2 to 3 h
 Larger vesicles may be drained, but tops should not be removed
 Topical class I glucocorticoid preparations
 In severe cases, systemic glucocorticoids: Prednisone, 2-week course, 60 mg initially,
tapering by steps of 10 mg.
Treatment for Allergic Contact Dermatitis
 Identify and remove the etiologic agent.
 Topical glucocorticoid ointments/gels (classes I to III) for early nonbullous lesions
 Larger vesicles may be drained, but tops should not be removed
 Wet dressings with cloths soaked in Burow's solution changed every 2 to 3 h
 Systemic glucocorticoids are indicated for severe and exudative lesions: Prednisone,
initial 70 mg (adults), tapering by 5 to 10 mg/d over a 1- to 2-week period.
VESICULAR TINEA PEDIS
It is a dermatophyte infection of the feet and considered as the most common fungal
disease. It is also known as Athlete’s foot.
Etiologic agents: Dermatophytes:
Trichophyton rubrum (Non-inflammatory dermatophytosis)
 Causes majority of cases
 Characterized by dull erythema and pronounced scaling that may involve the entire sole
and sides of the foot, giving it a moccasin sandal appearance.
 Eruption of lesions is limited to a small patch adjacent to a fungus-infected toe nail or to
a patch between or under the toes
 Lesions are usually bilateral and limited to one hand or both feet.
Trichophyton mentagrophytes (Inflammatory dermatophytosis)
 Acute inflammation presenting as acute vesicular or bullous eruptions
 Vasicles: 2-3mm in diameter, coalesce to form bullae of various sizes with bluish tint and
are firm to touch. They do not rupture spontaneously but dry up as the acute stage
subsides leaving yellowish brown crusts.
 Burning and itching of that accompany the formation of vesicles cause great discomfort
and is relieved by opening the tense vesicles which contain clear tenacious fluid of the
consistency of glycerin.
Predisposing Factor:
Hyperhidrosis - sweat between the toes and on the soles has a high pH and keratin
damp with it is a good culture medium for the fungi.
Clinical Manifestations:



Maceration, scaling and occasional vesiculation and fissures between and under the
toes
3rd toe web - most commonly affected area, inner sole of the foot is involved first, mostly
bilateral but may be limited to one hand, both feet
Hallmark : Moccasin sandal appearance, active borders, central clearing
Diagnosis:
 Demonstration of fungus by microscopic examination of scrapings taken from involved
site
 Culture on Saboraud Dextrose Agar with Chloramphenicol (appear fluffy, granular or
folded and microconidia is found in clusters and singly on hyphae), Mycosel Agar or
DTM (pH indicator changes from yellow to red due to alkaline metabolites)
Treatment/Prophylaxis:
 Dry toes thoroughly after bathing
 Good toe antiseptic powder (Tolnaftate, Zeazorb)
 Fungicides : Azoles, Naftifine, Terbinafine, Butenafine, Griseofulvin
Period of therapy depends on the response of the lesions. Repeated KOH scrapings and
cultures should be negative.