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Infectious Dermatology 1

The document summarizes various dermatological infections and infestations. It discusses superficial bacterial skin infections like impetigo, folliculitis, furuncle, and cellulitis caused by bacteria like Staphylococcus aureus and Streptococcus pyogenes. It also covers mycobacterial infections like leprosy (Hansen's disease) caused by Mycobacterium leprae, describing the different classifications and treatments.

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0% found this document useful (0 votes)
321 views206 pages

Infectious Dermatology 1

The document summarizes various dermatological infections and infestations. It discusses superficial bacterial skin infections like impetigo, folliculitis, furuncle, and cellulitis caused by bacteria like Staphylococcus aureus and Streptococcus pyogenes. It also covers mycobacterial infections like leprosy (Hansen's disease) caused by Mycobacterium leprae, describing the different classifications and treatments.

Uploaded by

markylopez23
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
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Dermatological

Infections & Infestations


Mariecon O. Escuadro, MD
Diplomate, Philippine Dermtological Society
Diplomate, Philippine Society of Venereologists, Inc
Superficial
Bacterial Skin Infections
1. Impetigo Contagiosa
2. Bullous Impetigo
3. Folliculitis
4. Furuncle & Carbuncle
5. Ecthyma
6. Cellulitis
7. Erysipelas
8. Erythrasma
Impetigo Contagiosa
Etiology:

Staphylococcus aureus: 50-70%
Streptococcus pyogenes or mixed
Group A Strep- usual
Group B Strep- newborn
Group C, G Strep-rare

Impetigo Contagiosa
Common sources:
Adults
Barbershops, parlors, meat packing plants,
swimming pools, infected children

Children
Pets, dirty fingernails, daycare, crowded housing
and other infected children

Impetigo Contagiosa
Clinical Presentation
Age group: early childhood most common

Sites: exposed areas (face, hands, neck &
extremities)

Lesions: starts as 2 mm erythematous
macules-thin-walled vesicles or bullae-
pustules, which rupture: seropurulent
discharge-dries up: honey-colored/golden-
yellow crusts.

Impetigo Contagiosa
Complications

Acute Glomerulonephritis (Grp A Beta-hemolytic
Strep)
Incidence: 10-15% with Nephritogenic strains
Prognosis: excellent in children, not as good in
adults
Bullous Impetigo
Etiology

Phage type 71 coagulase positive
Staphylococcus aureus

Group 2 phage type Staphylococcus aureus
Bullous Impetigo
Clinical Presentation
Age groups:
newborn (4
th
&10
th
day)
children
Sites:
Face & hands
Axilla & groin- adults in warm climates
Lesions:
Large fragile bullarupture: circinate, weeping or crusted
lesions with varnish-like crusts (impetigo circinata)

Bullous Impetigo
Constitutional Symptoms:
Fever & weakness develops
Diarrhea

Complications:
Bacteremia
Pneumonia
Meningitis
Folliculitis
Etiology
Staphylococcus aureus
Clinical Presentation
Sites:
Extremities and scalp
Axillae, thighs, pubis & eyelashes
Gluteal & genital maybe STDs
Lesions:
Thin-walled pustule at follicle orifices

Furuncle & Carbuncle
Etiology
Break in the skin (pressure, friction, irritation,
hyperhidrosis, dermatitis, dermatophytosis or
shaving), provides portal of entry of
Staphylococcus aureus
Autoinoculation from a carrier focus (nose or
groin)
Predisposing factors: alcoholism, malnutrition,
blood dycrasias, disorder of neutrophil
function, iatrogenic or immunosuppression
(HIV or Diabetes)
Furuncle & Carbuncle
Clinical Presentation
Sites
Nape, axilla, buttocks
Lesions
Furuncle/boil: acute, round, tender, circumscribed
perifollicular abscess
Carbuncle: 2 or more confluent furuncles with
multiple opening, +/- purulent discharge
Furuncle & Carbuncle
Complications
Cavernous sinus thrombosis, meningitis &
septicemia (upper lip & nose)
Treatment
Warm compress
Systemic Antibiotics
Cloxacillin
1
st
gen Cephalosporin
Surgical: incision (acutely inflamed), incision
& drainage (fluctuant)
Ecthyma
Etiology
Streptococcus
Staphylococcus aureus- IVD users & HIV

Predisposing Factors
Malnutrition
Poor hygiene
Trauma

Ecthyma
Clinical Presentation
Sites: shins or dorsal feet
Lesions: vesicle or vesicopustules- increase
in size-thickly crusted. Removal of crust:
superficial, saucer shaped ulcer w/ elevated
edges & raw base
(+) scarring
(+/-) lymphadenopathy

Cellulitis
Suppurative inflammation of the subcutaneous
tissue
Etiology:
Staphylococcus aureus
Steptococcus pyogenes
Predisposing Factors:
Breaks in the skin
Tinea pedis- most common portal of entry
Others: hematologic malignancy, diabetes
mellitus, IVD abuse, cardiovascular disorder
Cellulitis
Clinical Presentation:
Lesions: mild local erythema & tenderness
associated with malaise & chilly sensation. +/-
fever & chills
Erythema spreadswarmth, swelling &
tenderness, +/- pitting on pressure
Occasionally: vesicles appear, rupture &
discharge purulent material
(+/-) streaks of lymphangitis
Cellulitis
Complications
Gangrene, metastaic abscess & sepsis in
children & immunocompromised

Treatment
Syatemic Antibiotics
Erysipelas
Aka St. Anthonys Fire
Etiology:
Grp A Beta hemolytic Strep-supfl dermal
lymphatics
Strep C or G-occasional
Grp B Strep- newborns, abdominal or perineal
erysipelas in post partum women
Erysipelas
Predisposing Factors
Break in the skin barrier
Operative wounds
Fissures in the nares, auditory meatus, under
the earlobes, on the anus, penis, between or
under the toes (little toe)
Accidental scalp wounds
Chronic leg ulcers
Erysipelas
Clinical Presentation
Sites: face & legs
Prodrome: malaise, chills, high grade fever,
headache, vomiting & joint pains
Lesions: intensely erythematous (scarlet),
warm, swollen, brawny, well-demarcated
plaque w/ characteristic raised indurated
border
+/- vesicles/bullae w/ seropurulent fluid
Spread; peripheral extension
Erysipelas
Lesions, contd
On face: ear may become swollen & distorted; +/-
delirium
Leukocytosis (PMNLs >/= 20,000/mm3)

Complications:
Septicemia
Deep Cellulitis
*** in newborns or surgical operations in the elderly

Erysipelas
Treatment
Systemic: at least 10 days, rapid improvement
in 24-48 hours
Penicillin V
IV Penicillin
Erythromycin
Supportive Measures: cold compresses
Cellulitis & Erysipelas
Cellulitis Erysipelas
Staphylococcus or
Streptococcus
Grp A Streptococcus
Subcutaneous Tissue Superficial Dermal
lymphatics
Poorly demarcated Well-demarcated with
characteristic raised
indurated border
Erythrasma
Etiology
Corynebacterium minutissimum
Extensive: diabetes or debilitating diseases

Clinical Presentation
Sites: intertriginous areas (axilla, genitocrural
crease & the webs between the 4
th
& 5
th
toes>
3
rd
& 4
th
toes; intergluteal cleft, perianal skin,
inframammary area & nails)
Erythrasma
Clinical Presentation, contd
Lesions:
asymptomatic except for groin lesions which may
present with burning & pruritus
Sharply delineated, dry, brown, slightly scaling
patches
(+) Coral Red Fluorescence with Woods light
Due to Porphyrin

Erythrasma
Treatment
Localized
Topical erythromycin/clindamycin
Topical azoles
Topical Benzoyl Peroxide Wash or 5% gel
Widespread
Oral Erythromycin
Mycobacterial Infections
1. Hansens Disease
2. Cutaneous Tuberculosis
Hansens Disease
Mycobacterium leprae
Classification:
1. Indeterminate
2. Tuberculoid (TT)
3. Borderline Tuberculoid (BT)
4. Borderline (BB)
5. Borderline Lepromatous (BL)
6. Lepromatous (LL)
Indeterminate Leprosy
Solitary, ill-defined hypopigmented macule
or patch
Sensory: normal or minimally altered
(earliest: sense of cold & light touch)
Peripheral nerves: not enlarged
If immunity is good: resolves
spontaneously
Tuberculoid Leprosy (TT)
Lesions are solitary, few & asymmetrical
Lesion: large erythematous plaque w/
sharply elevated border & atrophic center
Sensory: anesthetic or hyposthetic &
anhidrotic
Nerve involvement: early, superficial
peripheral nerves are enlarged, tender or
both
Tuberculoid Leprosy (TT)
Contracture of fingers (claw hand), facial
muscle paralysis & foot drop may occur
Interosseous muscles may be atrophied:
wasting of thenar & hypothenar eminences
Slow skin lesions evolution
(+) Lepromin skin test, good cell-mediated
immunity
Tuberculoid Leprosy (TT)
Histopathology
Well defined granuloma with Langhans giant
cells, perineural infiltrates, AFB rare
Borderline Tuberculoid (BT)
Similar to TT but smaller & more
numerous
Borderline Leprosy (BB)
Skin lesions numerous, asymmetrical &
irregularly shaped
Moderate anesthesia
Borderline Lepromatous (BL)
Lesions are numerous, symmetrical &
small
Nerve involvement is symmetrical &
appears later
Lepromatous Leprosy (LL)
Lesions are ill-defined, infiltrated,
numerous & symmetrical
Nerve involvement: symmetrical, develops
slowly and at later stages
Nerve damage: massive bacillary
infiltration w/ compression & fibrosis
+/- hyperesthesia
(-) changes in sweating
Lepromatous Leprosy (LL)
Hair: slow progressive hair loss w/ thinning
of outer thrid of eyebrow
Progressively worsen w/o treatment
(-) lepromin skin test, poor CMI
Lepromatous Leprosy (LL)
Histopathology:
Foamy histiocytes, abundant AFB
Hansens Disease
Diagnosis
Sensory Test- pin-prick or ballpen-point test
Skin biopsy stained with Fite Faraco stain
Skin slit smears: Zieh-Neelsen stain
Bacteriologic Index





Lepromin skin test: immunologic status
6+ >1000 bacilli/f
5+ 100-1000
4+ 10-100
3+ 1-10
2+ 1-10 in 10 OIF
1+ 1-10 in 100 OIF
Hansens Disease
Diagnosis
Lepromin skin test: immunologic status
Fernandez reaction: 24-48 hours
Mitsuda reaction: 4 weeks
Hansens Disease
Treatment
Paucibacillary (Indeterminate & TT)
Multibacillary (BT, BB, BL, LL)

WHO Protocol:
1. Single lesion Paucibacillary
Single dose: Rifampin 600mg, Ofloxacin 400mg &
Minocycline 100mg (ROM)
2. Paucibacillary (Indeterminate, TT)
Rifampin 600mg once a month x 6 months
Dapsone 100mg OD x 6 months
Hansens Disease
WHO Protocol:
3. Multibacillary (BT, BB,BL,LL)
Rifampin 600mg and Clofazimine 300mg once a month
Dapsone 100mg and Clofazimine 50mg OD x 12 months,
or until smear negative
4. Special Cases
For patients who cannot take dapsone & rifampin
Clofazimine 50 mg , Ofloxacin 400mg & Minocycline 100mg OD x 6mos,
Ffd by: Clofazimine 50mg plus Ofloxacin 400mg OD or Minocycline 100
mg OD x 18 months
For patients who refuse Clofazimine
Minocycline 100mg or Ofloxacin 400mg OD x 12 mos or
Rifampin 600mg, Ofloxacin 400mg & Minocycline 100mg once a mo x 24
months (ROM)
Hansens Disease
Treatment
Dapsone
effective, inexpensive & free of side effects at recommended doses
side effects: Methemoglobinemia & anemia (in G6PD deficient);
exfoliative dermatitis, hepatitis, neuropathy & agranulocytosis
Rifampin
highly bactericidal, not used as monotherapy to avoid resistance
side effects: red-orange urine, elevated liver enzymes & flu-like lesions
Clofazimine
bacteriostatic & anti-inflammatory
Side effects: red-brown to grayish blue skin pigmentation

Hansens Disease
Reactional States
Acute episodes characterized by remissions &
relapses for a week to a few months in a
chronic course of infection
Neuritis is the most imptortant consideration
Precipitating factors: infection, surgery,
physical, physiologic & mental stress,
vaccination, pregnancy, Vitamin A, iodides &
bromides
Hansens Disease
Reactional States
1. Type 1 reaction
Cell mediated; in BT, BB, BL
Inflammation (swollen, erythematous & tender) of
existing lesions
No systemic symptoms; mj complication- nerve
damage
a. Reversal- w/ antibiotic tx, shift toward
tuberculoid pole
B. Downgrading- before antibiotic, shift toward
lepromatous pole
Hansens Disease
Reactional States
2. Type 2 reaction/Erythema nodosum
leprosum
Circulating immune complex-mediated dse;In BL,
LL
Painful, erythematous subcutaneous & dermal
nodules
With systemic symptoms: fever, myalgia,
arthralgia, anorexia & iritis
Hansens Disease
Management of Reactions:
Type 1 Reversal Mild
Analgesics
Chloroquine (1-2weeks)
Type 1 Reversal Severe
Prednisone 40-80mg OD x 5-7 days then taper for 2-6
months
Clofazimine 300mg OD x 6 weeks
Type 2/ ENL
Clofazimine 300 mg OD x 6 weeks, 200mg OD x 2-6 mos &
100 mg OD x 1-2 years
Thalidomide 400mg OD, tapered to 50-100 mg OD in 1 week
(teratogenic)
Prednisone 40-80mg OD
Cutaneous Tuberculosis
Cutaneous TB
M. tuberculosis, M. bovis

Classification is based on the mode of
onfection & immunologic state of the host

Diagnosis is based on clinical
manifestations, histopathologic analyisis,
demonstration of relevant mycobacteria in
tissue or in culture & host reaction
Cutaneous TB
1. Primary Inoculation TB/Tuberculous Chancre/
Tuberculous Primary Complex

2. Tuberculous Verrucosa Cutis/Warty TB

3. Lupus Vulgaris

4. Scrofuloderma/TB Colliquativa Cutis

5. Orificial TB/TB Ulcerosa Cutis et mucosae

6. Others: Tuberculous Gumma, Acute Miliary TB of the
skin, Sequelae of BCG inoculation
Tuberculous Chancre
Tuberculous chancre & affected regional LN
Children
Sites: face, conjunctivae & oral cavity; hands &
lower extremities

Pathogenesis (MBPB):
Tubercle bacilli are introduced into the tissue at the site
of minor wounds
Oral lesions caused by bovine bacilli in nonpasteurized
milk & after mucosal trauma or tooth extraction
Tuberculous Chancre
Chancre (small papule, crust or erosion w/
little tendency to heal) appears 2-4 weeks
after inoculation

Painless ulcer: shallow w/ a granular or
hemorrhagic base studded w/ miliary
abscess or covered by necrotic tissue;
undermined ragged edges & reddish blue
huemore indurated w/ thick adherent
crusts
Tuberculous Chancre
Mucosal: painless ulcers or fungating
granulomas

Slowly progressive, regional LAD x 3-8
weeks after infectionweeks or months:
cold abscess that perforate to surface &
form sinuses
Tuberculous Chancre
Histopathology (Fite Stain):
3-6 weeks: tuberculoid appearance & caseation

Diagnosis
Ulcer w/ little or no tendency to heal
Unilateral regional LAD
Bacterial culture

Tuberculous Chancre
Course
Untreated: 12 mos
Hematogenous spread: bones & joints
Calcification of regional LN
Tuberculosis Verrucosa Cutis
Paucibacillary caused by exogenous re
infection (inoculation) in previously sensitized
individuals w/ high immunity
Clinical Manifestations:
Small asymptomatic papule or papulopustule w/ puple
inflammatory halo
Hyperkeratotic
Slow growth & peripheral expansion verrucous
plaque w/ irregular border; solitary
Spontaneous involutionatrophic scar
Tuberculosis Verrucosa Cutis
Histopathology

Pseudoepitheliomatous hyperplasia w/ marked
hyperplasia w/ marked hyperkeratosis, a dense
inflammatory infiltrate & abscess in the supfl
dermis or within the pseudoepitheliomatous
rete pegs

Epitheloid cells & giant cells in upper & middle
dermis
Lupus Vulgaris
Chronic, progressive form
Moderate immunity & a high degree of
tuberculin sensitivity
Females, 2-3x
Pathogenesis: post primary, PB caused by
hematogenous, lymphatic or contguous
spread
Lupus Vulgaris
Clinical Manifestation
Sites: nose, cheek, earlobe or scalp
Initial lesion:
brownish red, soft or friable macule or papule w/ a
smooth or hyperkeratotic surface.
Apple jelly color on diascopy
Progression:
Elevation, deeper brownish color & plaque
Nasal or auricular cartilage: extensive destruction
& disfigurement
Lupus Vulgaris
Clinical Manifestation
Sites: nose, cheek, earlobe or scalp
Initial lesion:
brownish red, soft or friable macule or papule w/ a
smooth or hyperkeratotic surface.
Apple jelly color on diascopy
Progression:
Elevation, deeper brownish color & plaque
Nasal or auricular cartilage: extensive destruction
& disfigurement
Lupus Vulgaris
Diagnosis
Softness of lesion, brownish red color & slow
evolution
Apple jelly nodules
Histopathology
Typical tubercles
Secondary changes: epidermal thinning,
atrophy or acanthosis w/ excessive
hyperkeratosis or psedoepitheliomatous
hyperplasia
Lupus Vulgaris
Course
Long term disorder
Functional impairment & disfigurement
Squamous Cell CA
Pulmonary TB: 4-10x
Scrofulderma
Subcutaneous TB leading to cold abscess
formation breakdown of overlying skin
MB or PB
Represents contiguous involvement of
skin overlying another site of infection (TB
lymphadenitis, bones & joints or
epididymitis)
Children, adolescents & aged
Scrofulderma
Site: parotidal, submandibular &
supraclavicular; bilateral
Lesion: firm, subcutaneous nodule, well
defined, freely movable & asymptomatic
softens, liquefaction w/ perforation
causing ulcers & sinuses
Scrofulderma
Histopathology:
Massive necrosis & abscess formation in center
Course
protracted
Orificial TB
Rare TB of mucous membranes
Autoinoculation
Underlying Disease: far advanced
pulmonary, intestinal or genitourinary TB
Clinical Manifestation:
Small, yellowish or reddish nodules soft
ulcer w/ typical punched-out appearance,
undermined edges & circular or irregular
border
Orificial TB
Clinical Manifestation:
Multiple yellowish tubercles & bleeds easily
Edematous & inflamed
Extremely painful: dysphagia
Sites:
TB of Pharynx & Larynx: tongue (tip & lateral
margins), soft & hard palate; lips (advanced cases)
TB of Genitourinary: vulva
Orificial TB
Histopathology
Massive, non-specific inflammatory infiltrate &
necrosis, but tubercles w/ caseation maybe
found
Mycobacterial Infections
Superficial Fungal
Infections
Dermatophytoses
Infects non-viable keratinized cutaneous
tissues including stratum corneum, nails &
hair
Microsporum
Trichophyton
Epidermophyton
Factors that promote dermatophytoses
Environmental
Immunosuppression
Genetic susceptibility

Dermatophytoses
Diagnostics
KOH smear- septated hyphae
Histopathology- with PAS & methenamine
silver stains exhibiting septated hyphae within
the stratum corneum
Fungal cultures
Woods lamp
Dermatophytoses
Tinea capitis (ringworm of scalp & kerion)
Tinea barbae (beard)
Tinea faciei (face)
Tinea corporis (body)
Tinea manus (hands)
Tinea pedis (feet)
Onychomycosis (nail)



Tinea Capitis
Clinical Manifestations
1. Non Inflammatory Type
a. Black-dot
b. Gray patch

2. Inflammatory Type
a. Kerion
b. Favus

Tinea Capitis
Non-inflammatory Type

A. Black dot- endothrix; infected hairs broken
off at or below the surface of the scalp

B. Gray patch- ectothrix; scaly patches with
areas of stubs of broken hair
Tinea Capitis
Endothrix: arthrospores are formed inside the
hair shaft; no fluorescence
T. tonsurans
T. schoenleinii
T. violaceum
Ectothrix: hair is surrounded w/ sheath of tiny
spores; greenish fluorescence
Microsporum species
T. verrucosum
T. mentagrophytes
T. megnini
Tinea Capitis
Inflammatory Type
Begins as erythematous, scaly, papular eruptions
w/ loose & broken off hairs
A. Kerion- localized spot w/ pronounced
swelling, creating a boggy & indurated area
exuding pus

B. Favus- concave, sulfur-yellow crust
forming around loose wiry hairs
Hyphae & air spaces within the hairshaft
Bluish-white fluorescence
Tinea Capitis
Treatment
Griseofulvin x 2-4 mos or at least 2 weeks after
negative microscopic and culture examinations
Terbinafine 250mg/ Tab x 2 weeks (Trichophyton)
and 4 weeks (Microsporum)
Itraconazole 100mg/caps, 2 caps/day x 4-6 weeks
Ketoconazole 200mg/tab x 4-6 weeks
Others: short courses of systemic steroids for
inflammatory type; Selenium sulfide Shampoo or
Ketoconazole Shampoo left for 5 mins 3x a week
Tinea Barbae
Clinical Manifestations- usually on the neck
&/or beard area

1. Deep Type

2. Superficial, crusted Type
Tinea Barbae
1. Deep Type
Develops slowly
Does not usually involve the upper lip except the
mustache
Produces nodular thickenings & kerion-like
swellings, which are confluent & form diffuse
boggy infiltrations w/ abscesses
Overlying skin is inflamed
Hairs are loose or absent
Pus may be expressed through the remaining
follicular openings

Tinea Barbae
1. Superficial, crusted Type
Mild pustular folliculitis
With broken off hairs
Without broken off hairs

Hairs are loose, dry, brittle & when
extracted, the bulb appears intact

Tinea Barbae
Treatment
Micronized or Ultramicronized Griseofulvin
500-1000mg/ day x 4-6 weeks
Terbinafine 250mg/ Tab x 2 weeks
(Trichophyton) and 4 weeks (Microsporum)
Itraconazole 100mg/caps, 2 caps/day x 4-6
weeks
Ketoconazole 200mg/tab x 4-6 weeks


Tinea Barbae
Treatment
Topical Antifungals: miconazole, clotrimazole,
oxiconazole, sulconazole, econazole,
ketoconazole, naftitine, terbinafine, ciclopirox
olamine BID x 2-4 weeks
Affected areas washed with soap and water
Healthy areas maybe shaved or clipped


Tinea Faciei
Erythematous, slightly scaling patches or
plaques with indistinct borders & with
slight central regression
Tinea Faciei
Treatment
Topical Antifungals: miconazole, clotrimazole,
oxiconazole, sulconazole, econazole,
ketoconazole, naftitine, terbinafine, ciclopirox
olamine BID x 2-4 weeks
Oral Antifungals:
Micronized or Ultramicronized Griseofulvin 500-1000mg/ day x 4-6
weeks
Terbinafine 250mg/ Tab x 2 weeks (Trichophyton) and 4 weeks
(Microsporum)
Itraconazole 100mg/caps, 2 caps/day x 4-6 weeks
Ketoconazole 200mg/tab x 4-6 weeks


Tinea Corporis
Sites: neck, upper & lower extremities and
trunk
Characterized by one or more circular,
sharply circumscribed, slightly
erythematous, dry, scaly plaques w/
central clearing
Borders are usually elevated & more
inflames & scaly than the central part
Tinea Corporis
Lesions may widen to form rings,
sometimes making concentric rings or
rings of intricate patterns (Tinea imbricata)

Disseminated patches of both dry
(macular) & moist (vesicular) types of
Tinea circinata
Tinea Corporis
Treatment
For Extensive lesions
Micronized or Ultramicronized Griseofulvin 370-750mg/ day x
4-6 weeks
Terbinafine 250mg/ Tab x 2 weeks
Itraconazole 200mg/day x 1 week
Fluconazole 150mg/tab once a week x 4 weeks

For Localized lesions
Topical Antifungals: miconazole, clotrimazole, oxiconazole,
sulconazole, econazole, ketoconazole, naftitine, terbinafine,
ciclopirox olamine BID x 2-4 weeks

Tinea Cruris
Aka Jock Itch
Sites: upper & inner surfaces of the thighs
Begins as a small erythematous and scaling or
vesicular & crusted patch that spreads
peripherally & partly clears in the center
Curved with well-defined border particularly on
its lower edge
Border: vesicles, pustules or papules
Extends: downward- thighs & backwards-
perineum or anus
Tinea Cruris
Treatment
Same as Tinea Corporis
Reduce perspiration and enhance
evaporation on crural area
Area should be kept dry by wearing loose
underclothing and trousers, application of
plain talcum powder or antifungal powder
Tinea Pedis
Aka Atheletes Foot
Most common dermatophytosis
Consists of maceration, slight scaling &
occasional vesiculation & fissures between
& under the toes
Most common site: third toe web
If untreated: ulcerative, exudative process
affecting web spaces or entire sole
Tinea Pedis
Types:
1. Non-inflammatory
Dull erythema & pronounced scaling (moccasin or
sandal appearance)

2. Inflammatory
Acute vesicular or bullous eruption
Vesicles contain clear tenacious fluid w/ glycerin
consistency which dries up leaving yellowish
brown crusts
Symptoms: burning & itching
Tinea Pedis
Treatment
Reduce perspiration and enhance
evaporation on the interdigital areas
Toe webs & soles should be dried
immediately after bathing
Use antiseptic powder on the feet after
bathing ( eg Tinactin powder or Zeasorb
Medicated Powder)
Plain tlac, cornstarch or rice powder maybe
dusted to the socks & shoes to keep feet dry
Tinea Pedis
Treatment
Severe Tinea Pedis
Micronized or Ultramicronized Griseofulvin 370-
750mg/ day x 4-6 weeks
Terbinafine 250mg/ Tab x 2 weeks
Itraconazole 200mg/day x 1 week
Fluconazole 150mg/tab once a week x 4 weeks
*** With severe maceration: One part Aluminum
Acetate to 20 parts of water as dressing
***Secondary Infections: Oral or Topical
antibacterial
Tinea Pedis
Treatment
Localized Tinea Pedis
Topical Antifungals: miconazole, clotrimazole,
oxiconazole, sulconazole, econazole,
ketoconazole, naftitine, terbinafine, ciclopirox
olamine BID x 2-4 weeks
Keratolytic Agents (eg Salicylic Acid, Lactic Acid
Lotions) for areas protected by thick layers of
underlying skin

Tinea Manum
Dry, scaling, erythematous or may be
verrucous

Moist, vesicular and eczematous
Tinea Manum
Treatment
Severe Tinea Manum
Micronized or Ultramicronized Griseofulvin 370-
750mg/ day x 4-6 weeks
Terbinafine 250mg/ Tab x 2 weeks
Itraconazole 200mg/day x 1 week
Fluconazole 150mg/tab once a week x 4 weeks
*** With severe maceration: One part Aluminum
Acetate to 20 parts of water as dressing
***Secondary Infections: Oral or Topical
antibacterial
Tinea Manum
Treatment
Localized Tinea Manum
Topical Antifungals: miconazole, clotrimazole,
oxiconazole, sulconazole, econazole,
ketoconazole, naftitine, terbinafine, ciclopirox
olamine BID x 2-4 weeks
Keratolytic Agents (eg Salicylic Acid, Lactic Acid
Lotions) for areas protected by thick layers of
underlying skin

Onychomycosis
Types
1. Distal Subungal Onychomycosis
2. Superficial White Onychomycosis
3. Proximal Subungal Onychomycosis
4. Candidal Onychomycosis
Distal Subungal Onychomycosis
Involves the distal nail bed & hyponychium
w/ sec involvement of the underside of
nailplate
Whitish-yellowish discoloration starting at
the distal corner of the nail & involves the
junction of the nail & its bed and becomes
brown-black in color
Later: opaque, thickened, friable & raised
by underlying hyperkeratotic nail bed
Superficial White Onychomycosis
Aka Leukonychia Trichophytica
Invasion of the toenail plate on the surface
producing chalky white nail plate
Maybe eroded: nail loss
Proximal Subungal Onychomycosis

Involves the proximal nail fold
White spot appears from beneath the PNF
which gradually fills the lunula & moving
distally
Maybe an indicator of HIV infection
Candidal Onychomycosis

Aka Total Dystrophic Onychomycosis
Involves the whole nail plate
Fingernails>toenails
Begins under the lateral & proximal nail
fold & the adjacent cuticle is pink, swollen
& tender on pressure\
Neighboring nail becomes dark, ridged &
separated from the nail bed
Candidal Onychomycosis

Later: total onycholysis
Nail plate doe not become white, yellow or
friable
Seen in chronic mucocutaneous
candidiasis
Onychomycosis Therapy
Terbinafine 250mg/day x 6 weeks for fingernails
and 12 weeks for toenails
Itraconazole Pulse Treatment: 200mg BID for 1
week of each month for 2 months for fingernails
and 3 months for toenails
Fluconazole 150-300mg once a week x 6-12
months
Griseofulvin 350mg TID with meals x 4-6 months
for fingernails and 10-18 months for toenails
(note: not used for Candidal Onychomycosis)
Dermatophytid
Id reaction to the fungal antigen
especially the inflammatory types
Diagnosis depends on presence of fungal
infection at site different from the lesion
Pruritic vesicles on the hand & sides of fingers-most
common site esp of Tinea Pedis
Acute widespread eruption usually follicular, lichenoid
& scaly papules on the trunk esp of Tinea Capitis
Erysipelas-like dermatophytid on the shin esp of toe
web tinea
*** resolves once infection subsides
Pityriasis/Tinea Versicolor
Etiology:
Malassezia furfur or Pityrosporum orbiculare
Short thick fungal hyphae &spores (spaghetti & meatballs)
Clinical Manifestation
Yellowish or brownish macules in pale skin or
hypopigmented macules in dark skin
Coalesce to form patches
Delicate scaling (grattinage)
Mild itching & minimal inflammation

Pityriasis/Tinea Versicolor
Clinical Manifestation, contd
Sites of Predilection
Sternal region & sides of chest
Abdomen
Back
Pubis
Neck
Intertriginous areas
*** Hypopigmentation- fungus compels production of
abnormally small melanosomes which are not
transferred to the keratinocytes properly

Pityriasis/Tinea Versicolor
Diagnosis
Woods Lamp: yellowish or brownish
fluorescence
Skin Scarping w/ 10% KOH: spaghetti &
meatballs
Pityriasis/Tinea Versicolor
Treatment
1. Topicals
Imidazoles- Ketoconazole Shampoo
Selenium Sulfide Shampoos
Ciclopirox Olamine Shampoo
Zinc Pyrithione Shampoo
Sulfur Preparations
Propylene Glycol lotions
Benzoyl Peroxide
Terbinafine Cream or Sprays
Pityriasis/Tinea Versicolor
Treatment
2. Oral
Ketoconazole 200 mg/day x 10 days
Fluconazole 400mg single dose
Itraconazole 200mg x 5-7 days

*** hypopigmentation will take time to resolve and
is not a sign of treatment failure
Candidiasis
Aka candidosis, moniliasis, thrush or
oidiomycosis
Etiology: Candida albicans
Features:
Normal inhabitant at various sites (skin, nails, mucous
membranes & viscera), until there is some change in
the state of the area then it becomes a pathogen
Areas: perianal and inguinal folds, interdigital, nail
folds & axillae
*** warmth, moisture & maceration permit the organism to
thrive
Candidiasis
Types:
1. Oral
2. Perleche
3. Candidal Vulvovaginitis
4. Candidal Intertrigo
5. Pseudodiaper rash
6. Congenital Cutaneous Candidiasis
7. Perianal Candidiasis
8. Candidal Paronychia
9. Chronic Mucocutaneous Candidiasis
Oral Candidiasis
Newborn/ Infant
Grayish white membranous plaques w/ reddish base
on mucous membrane of mouth
Angles of the mouth
Adults
Buccal mucosa and tongue
Papillae of tongue atrophied w/ smooth, glazed and
bright red surface
*** elderly, debilitated & malnourished
*** often 1
st
manifestation of HIV
Oral Candidiasis
Treatment
Clotrimazole troches
Fluconazole 100-200mg/day x 5-10 days
Itraconazole 200 mg OD x 5-10 days
Perleche/Angular Cheilitis
Maceration w/ transverse fissuring of the oral
commisures

Early lesions: ill-defined, grayish white thickened areas
w/ slight erythema of mucous membrane at oral
commisure

More developed lesions: bluish white ot mother of pearl
color, contiguous w/ a wedge shaped erythematous
scaling dermatitis of skin portion of commisure fissure,
maceration & crust formation
Perleche/Angular Cheilitis
Also seen in Riboflavin deficiency & in
malocclusion caused by ill-fitting dentures
Can be bilateral
Candidal vulvovaginitis
Labia: erythematous, moist & macerated
Cervix: hyperemic, swollen & eroded with
small vesicles on the surface
Sx: severe pruritus, irriattion, extreme
burning
Vaginal Discharge: thick & tenacious

























Candidal vulvovaginitis
Pregnancy, In diabetes or secondary to
broad spectrum antibiotic therapy
Frequent recurrences
Male partner should be examined
Candidal vulvovaginitis
Treatment
Fluconazole 150mg single dose or 100mg/day
x 5-7days
Itraconazole
Topical Antifungals
Antifungal Vaginal Tablets
Candidal Intertrigo
Arises between folds of genital, in groins
or armpits, between buttocks, under large
pendulous breasts, over hanging
abdominal folds or umbilicus
Pinkish intertriginous moist patches
surrounded by a thin, overhanging fringe
of macerated epidermis (collarette of
scale)
Characteristic Satellite Lesions
Pseudo Diaper Rash
Perianal region spread over entire area
enhanced by maceration produced by wet
diapers

Scaly macules & vesicles w/ maceration:
pruritus, burning & extreme discomfort

Erythematous desquamating satellite or
daughter lesions scattered along edges
Congenital Cutaneous
Candidiasis
Infection of an infant during passage
through a birth canal infected with C.
albicans
Erythematous macules progress to thin
walled pustules, that rupture, dry &
desquamate
Lesions are widespread, involving even
the nailfolds.
Oral cavity & diaper area are spared
Perianal Candidiasis
(+) pruritus ani
Erythema, oozing & maceration
Svere pruritus & burning
Maybe precipitated by oral antibiotic tx
Treatment:
Imidazoles
Topical corticosteroids
Antipruritic meds
Candidal Paronychia
Chronic inflammation of nailfold produces
discharge of pus
Involves all nail plate
Cushion-like thickening of paronychial
tissue
Slow erosion of lateral NF
Gradual thickening & brownish
discoloration of nailplate
Transverse ridges, one nail
Candidal Paronychia
Sual: dishwashers & diabetics
Treatment
Oral Fluconazole weekly
Itraconazole in pulse doses
Anticandidal lotions
*** continued for 2-3months to prevent
recurrence
Chronic Mucocutaneous
Candidiasis
Chronic but superficial
Before age of 6
Oral Lesions: diffuse perleche & lip
fissures
Nail: thickened & dystrophic, (+)
paronychia
Skin: hyperkeratotic, horn-like or
granulomatous lesions
Chronic Mucocutaneous
Candidiasis
Adult onset: heralds the occyrence of
Thymoma
Inherited or sporadic
Viral Infections with
Cutaneous Manifestations
Purely Cutaneous Involvement
Molluscum contagiosum

Verruca/Wart
Molluscum contagiosum
Etiologic Agent:
Molluscum contagiosum virus (poxvirus)

Epidemiology:
MCV 1: general population
MCV 2: 60% among HIV patients
3 groups: young children, sexually active
adults & immunosuppressed patients (HIV)
Direct skin to skin contact
Molluscum contagiosum
Clinical Presentation

Lesions:
smoothed surface, firm, dome-shaped, pearly
papules
3-5mm in diameter (giant: 1.5cm)
Characteristic: central umbilication
Molluscum contagiosum
Children Adults
Usually STDs
Few to >100 <20 lesions
Location: face, trunk & extremities Location: lower abdomen, upper
thighs and penile shaft (men)
May occur in genitals as part of wide
distribution; if restricted- sexual abuse
maybe considered
Mucosal involvement is uncommon
Molluscum contagiosum
Differential Diagnoses
Wart
Syringoma (benign sweat gland tumor on face
around the eyes)
Sebaceous hyperplasia (sebaceous gland
hyperplasia in seborrheic areas of face)
Basal Cell Carcinoma (skin cancer)
Molluscum contagiosum
Complications
Secondary bacterial infection
Eczematous reaction in 10% (molluscum dermatitis)
Conjunctivitis or keratitis
Cutaneous horn (MC cornuatum)

Histopathology
Eosinophilic and later basophilic inclusion bodies
(Molluscum bodies or Henderson-Paterson
bodies) are formed in the cytoplasm of spinous cells
Molluscum contagiosum
Diagnosis
Clinical: centrally umbilicated dome-shaped
lesion

Diagnostics:
Cryotherapy: umbilication appears clear against a
white (frozen) background
Shelleys method for visualization
Expression of pasty core lesion
Squash between 2 glass slides
Methylene blue stain

Molluscum contagiosum
Treatment
Surgical nicking with comedone extractor***
Removal by curettage
Surgical tape after bathing x 16 weeks (90% cure)
Topical Tretinoin 0.05% ODHS
Imiquimod Cream ODHS***
TCA 35%-100% application
10% KOH
Light cryotherapy
Anthradin x 4-8 hours
Oral Cimetidine 40mkday x 2 mos (90% cure)
Molluscum contagiosum
Treatment, contd

Adults w/ genital molluscum
Mandatory screening for STD
Screen sexual partners
Cryotherapy
Podophyllotoxin 0.5% cream BID x 3 days per
weeks x 12 weeks
Curettage
Molluscum contagiosum
Course and Prognosis

Spontaneous resolution in 2-4 months

Average duration: 2 years
Human Papillomavirus/Wart
Etiologic Agent:
Human Papillomavirus (HPV)
80 types to date
Only few are pathogenic to men
Human Papillomavirus/Wart
Clinical Presentation:
Verruca Vulgaris/Common Wart
Verruca Plana/ Flat warts
Verruca Plantaris/ Plantart wart
Conduloma acuminata/Genital Wart
Verruca Vulgaris

Most common: HPV type 2
Less frequent: HPV type 1,4,7
Age: 5-20 years old (15% occur after 35)
Children: 5%
Risk Factors:
Frequent immersion of hands in water
Meat handlers


Verruca Vulgaris

- Spontaneous resolution
- 50% by 1 year
- 60-70% by 2 years

- Predilection sites
- Hands (fingers & palms)
- Nail biters: periungal, lips & tongue



Verruca Vulgaris
Lesions
size: pinpoint to 1 cm (ave:5mm)
increase in size: weeks to months
elevated, rounded papules with rough,
grayish surface
tiny, black dots on surface w/ thrombosed
capillaries
no dermatoglyphics (vs calluses)


Verruca Plana

Most common: HPV type 3
Less frequent: HPV type 10, 27 & 41
Children & young adults
Lesions:
2-4mm flat topped papules, slightly erythematous or brown
on pale skin & hyperpigmented on darker skin
Generally multiple
Grouped on face (forehead, cheeks, nose, perioral), neck,
dorsa of hands, wrists or knees
Highest rate of spontaneous resolution

Verruca Plantaris
Most common: HPV type 1
Less frequent: HPV type 2, 4
Appear at pressure points on ball of foot esp
midmetatarsal area
Soft pulpy cores are surrounded by firm, horny ring

Mosaic wart: contiguous warts appearing as one
Verruca Plantaris
Myrmecia wart: smooth-surfaced, deep, inflamed &
tender papules or plaques on palms or soles, beside
or beneath nails or pulp of digits
- dome shaped
- bulkier beneath the surface
- HPV 1
- DDx: paronychia or digital mucinous cyst

Verruca Plantaris
Ridged wart:
- peculiar type, HPV 60
- dermatoglyphics persits
- slightly elevated, skin-colored, 3-5mm papules
- non weight bearing areas
Plantar verrucous cysts:
- HPV 60
-1.5-2cm epithelium lined cysts on plantar area
-weight bearing areas

Condyloma Acuminata
Common sexually transmitted disease
among sexually active young adults
Infection rate: 50%
Lifetime risk: 80%
Subclinical and latent infections-
recurrences & transmission

Condyloma Acuminata
Benign Genital Warts: HPV 6 & 11
Cervical Dysplasia: HPV 16 & 18 (98%)

Human Papillomavirus/Wart
Differential Diagnosis:
Molluscum contagiosum-umbilicated surface
Syringoma- benign sweat gland tumor of the face
Seborrheic Keratoses-stuck-on hyperkeratotic,
pigmented papules & plaques
Acrochordon-skin tag; skin-colored, soft exophytic
papule
Callus & corn-maintained skin lines, absent
thrombosed capillaries/black dots

Genital warts vs condyloma lata
Human Papillomavirus/Wart
Treatment
Few lesions
Light cryotherapy
Topical Salicylic Acid
Electrodessication
More extensive
Topical Tretinoin 30-100% OD-BID
5 Fluorouracil cream 5% BID

Human Papillomavirus/Wart
Treatment
Refractory
Pulse dye laser before electrodessication (reduced risk of
scarring)
Genital
Podophyllin 25% in tincture of benzoin weekly, washed off 4-
8 hours later.
Trichloroacetic acid 35-85% weekly or biweekly. Safe in in
pregnancy.
Cryotherapy w/ liquid nitrogen every 1-3 weeks, 1 or 2
freeze-thaw cycles. Safe in pregnancy.
Electrofulguration or electrocauterization
Minor surgical removal
CO2 laser- more costly & highly technical

With Systemic Involvement
Varicella/Chickenpox
Herpes Zoster/Shingles
Herpes Simplex
Measles/Rubeola
Rubella/German Measles

Varicella
Etiology
Primary infection of VZV

Epidemiology
90%- children <10 years in temperate
countries; adults & adolescents in tropical
Summer months
Varicella
Pathogenesis
Aerosol or direct contact

Inoculation of respiratory mucosa replication in
regional nodes (innate defenses) primary viremia:
replication in liver & spleen & RESSecondary
Viremia: mononuclear cells transport virus to skin &
mucous membranes (fever & malaise) Virus
released into respiratory secretions replication in
epidermal cells

Transported to Dorsal Root Ganglia: Latency
Varicella
Clinical Characteristics
Incubation Period: 10-21 days
Transmission: direct contact & respiratory
route
Infectious: 4 days before & 5 days after
exanthem
Prodrome: low grade fever, malaise &
headache
Lifelong immunity
Varicella
Differential Diagnosis
Drug eruption (drug intake, monomorphous)
Allergic Contact Dermatitis (symmetrical, localized)
Blistering diseases- Dermatitis Herpetiformis & Linear
IgA dermatoses

Diagnostics
Tzank smear- multinucleated giant cells
Direct fluorescent Ab test- rapid & confirmatory
Varicella
Congenital Neonatal Immuno
compromised
-hypoplastic limbs,
cutaneous scars, ocular
& CNS diseases
-extremely severe & even
fatal
-necrotic & ulceration
-maternal infections: 20
weeks AOG
-in utero- zoster
postnatally during 1
st
2
years of life

-maternal infections: 5
days before & 2 days
after delivery
Prevention: vaccination
Varicella
Treatment
Antiviral Therapy (Aciclovir, Valaciclovir &
Famciclovir)
Within 24 hours of appearance of eruption
Acyclovir 800mg 5x a day x 7days
Valacyclovir 1 gm TID x 5days
Immunocompromised
Mild: Aciclovir 800 mg 5x/D x 7-10 days
Severe: Aciclovir 10mkdose IV q8 x 7 days or
longer
Acyclovir resistant: Foscarnet 40mkdose IV q8
until healed
Varicella
Treatment
Antiviral Therapy (Aciclovir, Valaciclovir &
Famciclovir)
Within 24 hours of appearance of eruption
Acyclovir 800mg 5x a day x 7days
Valacyclovir 1 gm TID x 5days
Immunocompromised
Mild: Aciclovir 800 mg 5x/D x 7-10 days
Severe: Aciclovir 10mkdose IV q8 x 7 days or
longer
Acyclovir resistant: Foscarnet 40mkdose IV q8
until healed
Varicella
Treatment, contd
Supportive: topical antipruritic lotions, oatmeal baths
& cool light clothing
Antibiotics- secondary bacterial infections

Complications
Secondary bacterial infection w/ Staph or Strep
Cerebellar ataxia & encephalitis
Asymptomatic myocarditis & hepatitis
Reyes syndrome- Aspirin is CI
Purpura Fulminans-low levels of protein C & S
Herpes Zoster
Etiology:
Varicella Zoster Virus Secondary infection
Latency in DRG replicates & travels down
sensory nerve into skin

Epidemiology:
Increases with age, sun exposure, smoking,
trauma, stress & immunocompromised states
Herpes Zoster
Classically occurs unilaterally within the
distribution of cranial or spinal sensory
nerve

Dermatomes:
Thoracic- 55%
Cranial-20% (Trigeminal)
Lumbar- 15%
Sacral- 5%
Herpes Zoster
Clinical Presentation
Eruption is preceded by pain over affected areas
Papules & plaques of erythema in dermatome,
followed by blisters within hours
Lesions maybe hemorrhagic, necrotic or bullous
Duration: depends on age, severity of eruption &
underlying immunosuppression ( 2-3 weeks in
younger & up to 6 weeks in elderly)
Herpes Zoster
Pregnancy Disseminated Ophthalmic
-Antivirals: risk-benefit
ratio
-> 20 lesions outside the
affected dermatome

-Ophthalmic division of
CNV
-Acyclovir has been
commonly given during
pregnancy without direct
effect to the fetus

-in old & debilitated -Hutchinsons Sign:
vesicles on side & tip of
the nose (external
division of nasociliary
nerve w/ involvement of
eyeball)

-Usually localized to the
skin & does not affect
the fetus

-fever, protration,
headache, signs of
meningeal irritation or
viral meningitis

- Ocular involvement:
uveitis (92%) & keratitis
(50%)

Herpes Zoster
Diagnosis
Histopathology: intraepidermal vesicles, balloon cells
which are degenerated cells of spinous layer, marked
intercellular & intracellular edema
Treatment
Supportive:
Bedrest- prevention of neuralgia in middle aged &
elderly
Warm compresses
Herpes Zoster
Treatment, contd
Antiviral Therapy
Cornerstone in management, reduces zoster-
associated pain

Intitiated within 3-4 days
Acyclovir 800mg 5x/day x 7days
Valacyclovir 1 gm TID x 7 days
Famciclovir 500 mg TID x 7days

Herpes Zoster
Complications
Ramsay-Hunt Syndrome: facial & auditory nerves
Herpetic inflammation of geniculate ganglion
Zoster of external ear or tympanic membrane
Herpes auricularis, facial paralysis & auditory symptoms
Post herpetic Neuralgia; zoster associated pain until 1
month from resolution of lesions
Major complication of zoster
Age or severity dependent
Treatment:
Tricyclic Antidepressants-1
st
line
Anticonvulsants: phenothiazines & carbamazepine 200-400mg OD
Gabapentin in escalating doses up to 3200mg OD
Herpes Simplex
Etiology
Orolabial: HSV Type 1
Genita; : HSV Type 2

Epidemiology
One of the most prevalent STI worldwide
80% are seropositive for HSV-1
HSV-2 at onset of sexual activity
Herpes Simplex
Clinical Presentation
Orolabial Herpes
Herpetic Whitlow
Genital Herpes
Intrauterine & Neonatal Herpes***
Eczema Herpeticum
HSV in immunocompromised
Orolabial Herpes
High fever, regional lymphadenopathy & malaise
Cold sore or fever blister
Grouped blisters on erythematous base
involving the lips near vermillion border
Trigger for recurrence: UV exposure
Sunscreens reduces recurrence
Herpetic Whitlow
Infection of the pulp of the fingertip
Bimodal:
Children: < 10 years old
Adults: 20-40 years old

Tenderness & erythema, of lateral nail fold
followed by formation of deep seated blisterd 24-
48 hours after
Genital Herpes
Spread by skin to skin contact usually during
sexual activity
Incubation period: 5 days
Primary Infection
Grouped blisters & erosions in vagina, rectum or
penis w/ continued devt of new lesions over 7-14
days
Bilaterally symmetrical w/ bilaterally enlarged inguinal
LN

Genital Herpes
Recurrence
Prodrome; burning, itching or tingling
Papules in 24 hoursvesicles in another 24 hours
erosions in 24-36 hours and heals in 2-3 days
Milder than 1
st
due to antibodies
Common site: upper buttocks
Heals without scarring unless secondarily infected
Chronic suppressive therapy- reduces asymtomatic
shedding by 95%

Eczema Herpeticum
Herpes infection in:
Atopic dermatitis
Severe Seborrheic dermatitis
Scabies
Dariers Disease
Blistering Diseases: Benign Familial
Pemphigus, Pemphigus, Pemphigoid
Wiskott-Aldrich syndrome
Burns
Eczema Herpeticum
Hundreds of umbilicated vesicles with
fever & regional adenopathy

Self-limited
HSV in immunocompromised
Erosions or crusts
Hallmarks: pain, active vesicular border &
scalloped periphery
Visceral dissemination is unusual
Herpes Simplex
Diagnostics:
Tzanck Smear
Most common procedure done
Nonspecific
HSV & VZV results in formation of multinucleate giant cells
Accurate rate: 60-90%
Direct Fluorescent Ab test
Viral Culture
Polymerase Chain Reaction
Herpes Simplex
Diagnostics:
Skin Biopsy
Intraepidermal blisters
Ballooning degeneration of epidermal cells to produce
acantholysis
Minute eosinophilic intranuclear bodies occur in nuclei of
epithelial cells, coalescing to occupy majority of nucleus as
inclusion body
Herpes Simplex: Treatment
Disease Antiviral Therapy Others
Orolabial Herpes Acyclovir 200mg 5x OD x 5 days Topical Treatment w/ drying
agents: Benzoyl Peroxide,
Zinc Oxide, Sunscreen
Genital Herpes
Primary Acyclovir 200-400mg 5x OD x 5-7
days
Famciclovir 250 mg TID x 5-7 days
Valacyclovir 1gm BID x 5-7 days
Recurrence Episodic Treatment
Acyclovir 200mg 5x OD x 5 days
Valacyclovir 500 mg BID x 5 days
Famciclovir 125-250 mg BID x
5days

Suppressive (> 6
episodes/year)
Acyclovir 200mg TID or
400 mg BID
Herpes Simplex: Treatment
Disease Antiviral Therapy Others
Intrauterine &
Neonatal Herpes
IV Acyclovir 250mg/m2 q8 x 7
days
Deliver via ceasarean
section within 4 hours of
membrane rupture, and if
during labor, there are
active lesions.
Immunocompromised Acyclovir 200-400 mg 5x daily or
IV acyclovir 5 mg/kg
Suppressive Therapy:
Acyclovir 400mg BID
Valacyclovir 500 mg BID
Famciclovir 250 mg BID
Measles
Etiology
Paramyxovirus

Epidemiology
Worldwide distribution
Usually infects young children
Transmission: respiratory droplets
Incubation period: 9-12 days
Measles
Pathogenesis
Virus enters cells of respiratory tract
replicates locally & spreads to regional
lymph nodes disseminates
hematogenously to skin & mucous
membranes

Viral replication also occurs in skin &
mucosa
Measles
Clinical Presentation

Prodrome: fever, malaise, conjunctivitis &
prominent upper respiratory symptoms
(nasal congestion, sneezing, coryza &
barking cough)
Measles
Clinical Presentation
Rash
1-7 days after prodrome
Macular or maculopapular
Anterior scalp line & post auricular
Discrete erythematous papules that coalesce,
spreads quickly over face extending down the
trunk to extremities (cephalocaudal &
centrifugal)
Clears in 6-7 days after appearnce w/ fever
lysis
Measles
Clinical Presentation
Kopliks Spots
Pathognomonic
Appears during the prodrome
Location: buccal mucosa nearest to the lower
molars, spreading to involve other areas of
buccal mucosa & pharynx
1mm white papules on erythematous base
Measles
Diagnosis
High fever, Kopliks spots, conjunctivitis,
upper respiratory sx & typical exanthem
Lymphopenia is common

Histopathology
Syncytial keratinocytic giant cells
Measles
Treatment
Vitamin A in high dose (reduces morbidity &
mortality of hospitalized children w/ measles)
Retinyl palmitate 200,000 IU OD x 2 doses
Bed rest
Analgesics
Antipyretics
Measles
Complications
Otitis media, pneumonia, encephalitis,
thrombocytopenic purpura
In Malnourished & T cell deficiencies
Exanthems are less prominent in HIV-infected
children
Special Cases
Pregnant- associated w/ fetal deaths
Partially immune host( prior infection, persistent
maternal antibodies or immunization)
Milder, shorter, less confluent exanthems, (-) Kopliks spots
Rubella
Etiology
Togavirus

Transmission
Respiratory secretions
Rubella
Clinical Presentation
Incubation Period: 12-23 days (15-21 days)
Prodrome
1-5 days
Fever, malaise, sore throat, eye pain, headache,
red eyes, runny nose, post auricular LAD
Pain on lateral & upward eye movement

Rubella
Clinical Presentation
Exanthem
Begins on the face progressing caudad, covering
the entire body in 24 hours
Resolves by 3
rd
day (3-day measles)
Pale pink, morbilliform macules, smaller than
measles
Enanthem
Pinhead-sized red macules or petechiae on soft
palate and uvula (Forscheimerss sign)
Rubella
Complication
Arthritis or Arthralgias- adult women lasting
for > 1 month
Skin Infestations
1. Scabies
2. Pediculosis
Scabies
Sarcoptes scabiei var hominis

Produces diffuse, pruritic eruption after an
initial IP of 6-8 weeks

Pathognomonic Clinical Feature: burrow
produced by tunneling of the mite in the
stratum corneum
Scabies
Transmission
Close physical contact
Fomite



Scabies
Pediculosis
1. Pediculosis Capitis (Head Lice)
2. Pediculosis Corporis (Body Lice)
3. Pediculosis Pubis
Pediculosis Capitis
Pediculosis humanus var capitis
Spread: close physical contact & sharing
of head gears, combs, brushes & pillows
Site: occipital and retroauricular
Symptom: pruritus
Diagnostic Sign: live nits on proximal hair
shaft
Pediculosis Capitis
Pediculosis Corporis
Pediculosis humanus var humanus
Spread: contaminated clothing or bedding
Site: waist, buttocks & thighs
Symptom: pruritus
Diagnostic Sign: maculae cerulea- slightly
slate colred macule


Pediculosis Corporis
Treatment
Single application of Permethrin 5%
cream/lotion, left on for 8-10 hours and then
washed off thoroughly
All household contacts
Pediculosis Pubis
Pthirus pubis
Spread: STD or direct contact
Site:pubic hair & any other hair-bearing
region
Symptom: pruritus
Diagnostic Sign:microscopic examination
of plucked hair


Pediculosis Pubis

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