TROPICAL DERMATOLOGY

dr Nanda Earlia, sp.kk

BAGIAN / SMF ILMU KESEHATAN KULIT DAN KELAMIN
FK. UNSYIAH / RSUD Dr ZAINOEL ABIDIN
BANDA ACEH
2013

TROPICAL DERMATOLOGY
Tropical diseases that most
commonly affect the skin.
Skin disease is extemely common in
the tropics, affecting up to 50% of
the population

O
L
O
T
A
M
DER

CHICKEN POX
(Varicella)

CHANCROID
GRANULOMA INGUINALE

CHLAMIDIAL
MMP/CPINFECTION
MEASLES

SMALL POX
(Variola)

2001

TRICHOMONIASIS
AECP

1986

1957

ENTEROVIRUS
(Hand Foot Mouth Disease)

MYCOSIS

LGV

SIPHYLIS
OCP

GONORE
CP (B-P)

MOLLUSCUM
CONTAGIOSU
M

PYODERMA

1992

I A

I N

I O

IMPETIGO

FURUNKEL
ERISIPELAS

LEPROSY

INFESTATION :
ECTOPARASIT (Scabies, Pediculosis
& HELMINTHIC
(Cutaneous Larva Migrans)

VIRAL INFECTION
1.
2.
3.
4.
5.
6.

VARICELLA
HERPES ZOSTER
HERPES SIMPLEKS
VERRUCA VULGARIS
KONDILOMA ACCUMINATA
MOLLUSCUM CONTAGIOSUM

Poxviruses That Infect Humans* and Cause Disease

( CHICKEN POX )

VZV : VARICELLA

DEFINITION
VARICELLA :
The highly contagious primary infection caused by

Varicella-Zoster Virus (VZV)

Characterized pruritic vesicles pustules & crust
Accompanied by mild constitutional symptoms
Primary infection in adulthood pneumonia &
encephalitis
7

EPIDEMIOLOGY

Age of onset 90% < 10 years of age

< 5% > 15 years of age
Transmission airborne droplets & direct
contact

TRANSMISSION
Airbone droplet
Direct contact
Patient are contagious several days
before varicella exanthem appear &
until last crop of vesicles
Crust are not infectious
VZV can be aerosolized from skin of
person with HZ varicella in
susceptible contact

PATHOGENESIS OF PRIMARY INFECTION WITH VZV

10

PATHOGENESIS

VZV enter through mucosa of respiratory system

& oropharinx Colonies the upper respiratory tract
Replicates in the regional lymph nodes, 4-6 days
later a primary viremia to reticuloendothelial cells
One week a secondary viremia disseminates the
virus to the skin & mucous membranes

11

PATHOGENESIS
Localization of VZV in the basal cell
layer of epidermis is followed by
virus replication, balloning
degeneration of epithelial cells, and
accumulation of edema fluid with
vessiculation
During the course of varicella, VZV
passes from the skin lession to the
sensory nerve sensory ganglia
establish latent infection

PHYSICAL EXAMINATION
HISTORY
Incubation period
Prodrome
Exanthem appears
Skin symptoms

:
:
:
:

10-21 days
absent or mild.
2-3 days.
pruritic exanthem

13

PHYSICAL EXAMINATION
Skin lession :
Vesicular lession : papule vesicle
pustule crust erosion (8-12h)
heal (1-3 weeks)
Distribution : face -> scalp trunk
extremities
Mucous membrane palate >>

VARICELLA

A. A full spectrum of lesionsthat is, erythematous papules, vesicles (dewdrops

on rose petals), crusts, and erosions at sites of excoriationis seen in a child
with a typical case of varicella. B. A wider range of lesions, including many large
pustules, is seen in a 21-year-old female who was febrile as well as toxic and
had varicella pneumonitis.

Varicella (Chickenpox)

Chickenpox vesicle behind the ear.

Notice the translucent quality of the
vesicle on the skin, the classic "dew
drop on a rose petal" appearance.

Chickenpox on the palate. Notice the

glistening, water-drop characteristic of
the chickenpox vesicle on the palate.

DIFFERENTIAL DIAGNOSIS

Herpes Simplex Virus Infection

Enterovirus infections
Bullous form of impetigo
Smallpox
Exzema herpeticum

18

Differential Dx - Chickenpox

VARIOLA (SMALL POX)

VARICELLA (CHICKEN POX)

Variola (Smallpox)
Begins centrally, then
spreads outward to face
and extremities
All lesions are always in
a single stage of
development
Associated with severe
constitutional symptoms

Begins on the face

and scalp, spreads to
the trunk
Lesions in various
stages of
development can
simultaneously be
present on the
patient's skin

COMPLICATION
Children < 5 years secondary
bacterial infection
Children 5-11 years Varicella
encephalitis Reye syndrome
Fetal varicella syndrome
Immunocompromized : hepatitis,
encephalitis, pneumonia

LABORATORY FINDING

VZV antigen detection (Direct Fluorescein Antibody)

Viral culture (Isolation of virus on virul culture from
vesicular skin lession)
Tzanc smear (Cytology of fluid ar scrapping from base of
vesicle)
Serology

THERAPY

Antiviral therapy
Symptomatic therapy
Treatment of bacterial superinfection
21

TREATMENT
IMMUNIZATION
SYMPTOMATIC THERAPY
ANTIVIRAL AGENTS
Decrease severity if given within 24 hours of onset
Neonates : acyclovir 10 mg/kg every 8h for 10 days
Children (2-28 yrs) : Valacyclovir 20 mg/kg every 8h for 5 days or
Acyclovir 20 mg/kg every 6 h for 5 days
Adolescent : Valacyclovir 1 gr PO every 8h for 7 days
Immunocompromised : Valacyclovir 1 gr PO for 7-10 days; or Acyclovir
800mg by mouth 5 times a day or Famciclovir 500 mg by mouth every 8h
for 7-10 days
Severe immunocompromised : acyclovir 10 mg/kg IV every 8h for 7-10
days
Acyclovir resistent : Foscarnet 40 mg/kg IV every 8h until resolution

PROGNOSIS

Healthy children with varicella have excellent prognosis

In adult ; prodromal symptoms are common and may be

severe, with prolonge periode of recovery

Neonatal varicella mortality rates 30%

Complication :
Children < 5 y.o : bacterial superinfection
5-11 y.o : varicella encephalitis and Rey syndrome

23

PREVENTION

Vaccination
Varicella-zoster immune globulin

24

VARICELLA VACCINE

25

SHINGLES)

VZV : HERPES ZOSTER

DEFINITION

Herpes Zoster :
Acute dermatomal infection associated with
reactivation of Varicalla Zoster Virus (VZV) latent in
the dorsal
nerve root following the infection of varicella
Characterized : unilateral pain and vesicular or bullous
eruption, limited to dermatomal
innervated by
corresponding sensory ganglion.

Ophtalmic nerve zoster :

The eye is afected in 2/3 cases
When vesicle on the side of the nose (Hutchinsons
sign) involvement of the nasociliary nerve of V1
(ophtalmic) branch

Varicella zoster virus infection:

ophthalmic
zoster
Crusted ulcerationsherpes
and vesicles
on the right forehead and
periorbital area in the ophthalmic branch of the trigeminal
nerve; marked facial edema is also present. Vesicles on
the tip of the nose indicates nasociliary involvement.
Hutchinson's rule: involvement of the nasociliary nerve
suggests that eye involvement may occur.

EPIDEMIOLOGY
More than 66% are older than 50 years of age
Cumulative life time incidence 10-20%
Risk factors :
Malignancy
Immunosuppresion
Radiotherapy
HIV

Varicella-zoster virus infection:

herpes zoster in T8 to T10
dermatomes
Typical grouped vesicles and pustules with erythema and
edema of three contiguous thoracic dermatomes on the
posterior chest wall.

PATHOGENESIS
VZV passes from lession in the skin and mucosa via
sensory fibers sentripetally to sensory ganglia.
In the ganglia, virus established lifelong latent infection
Reactivation occurs in those ganglia in which VZV has
achieved the highest density and is triggered by
immunosuppresion, trauma, tumor, or irradiation
Virus multiple & spreads centrifugally, antidromically
down the sensory nerve to skin/mucosa where it produce
the characteristic vesicles

PHYSICAL EXAMINATION
HZ manifest in 3 distinct clinical stages :
1. Prodrome : pain (Allodynia : hightened sensitivity to mild stimuli;
zoster sine herpete : nerve involvment without cutaneous zoster),
tenderness, paresthesia in the involve dermatome precede the
eruption
2. Active infection (dermatomal lession) : papule (24h)
vesicle/bulla (48h) pustule (96h) crust (7-10 days) resolve (2-4
weeks).
New lession continue to appear up to 1 week.
Distribution : unilateral, dermatome
Sites of predilection : thoracic (>50%) ; trigeminal (10-20%),
lumbosacral &cervical (10-20 %)
Mucous membran : vesicle & erosion occure in mouth, vagina, bladder
3. PHN : constant, severe, stabbing, burning, dysesthetic pain may
persist for month or years

VARICELLA AND HERPES

ZOSTER

A. During primary VZV infection (varicella or chickenpox), virus

infects sensory ganglia. B. VZV persists in a latent phase within
ganglia for the life of the individual. C. With diminished immune
function, VZV reactivates within sensory ganglia, descends sensory
nerves, and replicates in skin.

DERMATOMES
The cutaneous fields of peripheral nerves

HISTORY
Duration of symptoms

Prodromal stage : neuritic pain 2-3 weeks

Acute vesiculation : 3-5 days
Crust formation : days to 2-3 weeks
PHN : months to years

Skin symptoms

Prodromal stage : pain, tenderness, parestesia

Active vesiculation : pruritic and no painfull
Chronic stage : PHN

Constitutional symptoms

Prodromal stage & active vesiculation : flu like symtoms

Chronic stage : depression

PHYSICAL EXAMINATION
Skin lesion : papul, vesicle, bullae, pustule, crust based
on erythematous and edematous skin
Distribution : unilateral, dermatomal
Site of predilection : thoracic, trigeminal, lumbosacral
Mucous membrane within the affected dermatomes are
also involved
Sensory or motor nerve changes : detectable by
neurologic examination
Eye : uveitis, conjunctivis, retinitis, optic neuritis,
glaucoma, proptosis, cicatricial lid retraction, extarocular
muscle palsies

VARICELLA ZOSTER VIRUS

INFECTION
herpes zoster with cluster of grouped vesicles
Grouped and confluent vesicles surrounding erythema on
the chest wall

DIFFERENTI AL
DIAGNOSIS
Prodromal stage / localized pain :
can mimic migrain
Dermatomal eruption :
contact dermatitis
erysipelas
bullous impetigo

LABORATORY
EXAMINATION
VZV antigen detection
Viral culture
Tzanc smear
Serology
Dermatopathology

DIAGNOSIS
Prodromal stage :
Suspect HZ in older or imunocompromised
individual with unilateral pain
Active vesiculation :
Clinical appearance classic enough to be
diagnostic
- Tzanck test
- Viral culture
PHN :
- History and clinical finding

COMPLICATION
Ocular complication
Bacterial infection of damage skin
Ramsay Hunt syndrome
Encephalitis or Meningoenchephalitis : elderly, the
immunosupressed and in
association with
disseminated zoster

RAMSAY HUNT SYNDROME

PROGNOSIS
Most patient :
self limited course without permanent sequele
Ocular involvement, damage to the eyes, and loss of
vision may occur unless ophthalmology care obtained

MANAGEMENT
Uncomplicated infection :
- Antiviral therapy oral Acyclovir 800 mg 5 times for 7 days
or valacy clovir1g every 8h for 7 days
or Famsiclovir 500 mg every 8h for 7 days
- Suportive therapy Analgesics

Immunocompromised patient and disseminated

infection :
- IV Acyclovir 10 mg/kg IV every 8h for 7-10 days
Ophthalmology evaluation on ocular involvement or lession are present
on the eyelid or nose
PHN : gabapentin, pregabalin, tricyclic antidepressant, i.e doxepin,
capsaicin cream. Nerve block

HERPES ZOSTER

A.

Early involvement of a thoracic dermatome with erythema within the dermatome and
areas of grouped vesicle formation. B. Later involvement with crusted sites on the back,
where the eruption first appeared, and many confluent hemorrhagic vesicles and bullae on
the lateral chest wall, where the eruption appeared more recently; some vesicles are also
seen outside the involved dermatome, representing hematogenous dissemination, a not
uncommon occurrence. C. Ophthalmic zoster. Note the involvement of the tip of the nose,
which frequently signals involvement of the eye.

HERPES SIMPLEKS VIRUS

DISEASE

HERPES SIMPLEKS
Herpes genitalis (HG) is a chronic sexually
transmitted viral infection, characterized by
asymptomatic.
When symptomatic, primary HG may present
with grouped vesicles at the site of inoculation
associated with significant pain and regional
lymphadenopathy.
When aware of HG , individualist may notice
mild symptoms, uncommonly of recurring
outbreaks of vesicles at the same site.
Most symtoms from HG relate to the
psychological stigma of having a chronic

EPIDEMIOLOGY
Age of Onset
young, sexually active adults.
Incidence
nuns, 3%
middle class, 25%
heterosexuals at an STD clinic, 26%
homosexuals, 46%
lower classes, 46-60%
prostitutes, 70-80%
Transmission
Usually skin-to-skin contact.
Risk increases with number of sex partners.
Most patients with genital ulcers have HG, syphilis, or chancroid

PATHOGENESIS
HSV infection is transmited through close contact with a persons
shedding virus at a peripheral site, mucosal surface, or secretion.
HSV is inactivated promptly at room temperature; aerosol or fomitic
spread unlikely.
Infection occurs via inoculation onto susceptible mucosal surface or
break in skin.
Subsequent to primary infection at inoculation site, HSV ascends
peripheral sensory nerve and enters sensory or autonomic nerve
root ganglia, where latency is established.
Latency can occurs after both symptomatic and asymptomatic
primary infection.
Recrudescences may be clinically symptomatic or asymptomatic.

HERPES LABIALIS
With primary herpes simplex virus infection, virus replicates in the oropharyngeal epithelium and ascends
peripheral sensory nerves into the trigeminal ganglion.
B. B. Herpes simplex virus persists in a latent phase within the trigeminal ganglion for the life of the individual.
C. C. Various stimuli initiate reactivation of latent virus, which then descends sensory nerves to the lips or
perioral skin, resulting in recurrent herpes labialis.
A. A.

HERPES SIMPLEX

Herpes simplex virus

infection:
recurrent
herpes
labialis.
Grouped
and
confluent
vesicles
with an erythematous
rim on the lips 24
hours after onset of
symptoms.

HISTORY
Incubation : 2-to 20-day (average 6).
Primary
: Most individuals with primary
infection are asymptomatic.
Recurrent : New symptoms may result from old
infection.
Systemic Symptom
Symptoms of aseptic HSV-2 meningitis can occur
with primary or recurrent HS.

PHYSICAL EXAMINATION
Skin
Skin Lesion
Lesion
Most clinical lesions are minor breaks in the mucocutaneous epithelium,
presenting as erosion, abrasion and fissures.
The classically described finding are uncommon
General
General Finding
Finding
Regional Lymph Nodes :
Inguinal/femoral lymph nodes enlarged, firm, nonfluctuant, tender; usually
unilateral.
Sign of Aseptic Meningitis :
Fever, nuchal rigidity. Can occur in the absence of GH. Pain along sciatic
nerve.

PHYSICAL EXAMINATION

Primary GH
An erythematous plaque is often noted initially, followed soon by
grouped vesicles, which may evolve to pustules; these become eroded as
the overlying epidermis sloughs.
Erosions are punched out and may enlarge to ulcerations, which may be
crusted or moist.
These epithelial defects heal in 2 to 4 weeks, often with resulting
postinflammatory hypo- or hyperpigmentation, uncommonly with
scarring.
Recurrent GH
Lesions may be similar tp primary infection but on a reduced scale.
Often a 1-2cm plaque of erythema surmounted with vesicles, which
rupture with formation of erosions. Heals in 1 to 2 weeks.

PRIMARY HERPES SIMPLEX

A. Primary genital herpes with vesicles. Primary herpetic
vulvitis.

A. Genital herpes: recurrent infection of the penis. Group

RECURRENT
GENITAL
of vesicles
with early central
crusting on HERPES
a red base arising
on the shaft of the penis. This textbook presentation,
however, is much less common than small asymptomatic
erosions or fissures. B. Genital herpes: recurrent vulvar
infection. Large, painful erosions on the labia. Extensive
lesions such as these are uncommon in recurrent genital
herpes in an otherwise healthy individual.

PHYSICAL EXAMINATION

Distribution
Males
Primary infection : glans, prepuce, shaft, sulcus, scrotum,
thigh, buttocks.
Recurrences : penile shaft, glans, buttocks.
Females
Primary infection : labia majora/minora, perineum, inner
thighs.
Recurrences : labia majora/minora, buttocks.
Anorectal infection
Occurs in male homosexuals, characterized by tenesmus,
anal pain, proctitis, discharge, and ulcerations as far 10 cm
into anal canal.

DIFFERENTIAL DIAGNOSIS

Trauma
Candidiasis
Syphilitic chancre
Fixed drug eruption
Cancroid

LABORATORY EXAMINATION

HSV
HSV Detection
Detection :: Viral
Viral Culture/Modified
Culture/Modified Culture
Culture
HSV
HSV Antigen
Antigen Detection
PCR
PCR
Antibodies
Antibodies to
to HSV
HSV
ELISA
ELISA
Tzanck
Tzanck Smear
Smear
Dermatopathology
Dermatopathology

Herpes simplex virus: positive Tzanck smear.

A giant, multinucleated keratinocyte on a
Giemsa-stained
smear
obtained from a
TZANCK SMEAR
HSV
vesicle base. Compare size of the giant cell to
that of neutrophils also seen in this smear.
Another smaller multinucleated acantholytic
keratinocyte is seen as well as acantholytic
keratinocytes. Identical findings are present
in lesions caused by varicella-zoster virus.

DIAGNOSIS

Because in most cases intermittent asymptomatic

shedding is occurring and lesions are atypical (not
grouped vesicles on erythematous base), HS must
be confirmed by viral culture or DFA.

COURSE AND PROGNOSIS

GH may be recurrent and has no cure
.
70%
of HSV-2 infections are asymptomatic
HSV-2 GH recurs approximately 6 times/year
HSV-1 GH usually recurs, on the average, only once/
year
The rate of recurrence is 20% higher in men than
women

MANAGEMENT
Topical Antiviral Therapy : No significant efficacy
Oral Antiviral Therapy :
First clinical episode (primary or first symptomatic)
Acyclovir
400mg tid or 200mg 5 times daily for 7-10
days
Valacyclovir 1gm bid for 10 days.
Famciclovir 250mg bid for 10 days.
Recurrent episodes
Acyclovir
400mg PO tid for 5 days or 800mg PO bid for
5 days
Valacyclovir 500mg bid for 5 days
Famciclovir 250mg bid for 5 days
Prevention
Education about sexual transmission

CONDILOMA ACCUMINATA

CONDYLOMA
ACCUMINATA
An epidermal manifestation attributed to the epidermotropic
human papillomavirus (HPV)
Benign, superficial specially on genital area

ETIOLOGY
HPV Papova virus DNA Virus
HPV > 80 types,related to condyloma :
6,11,16,18,30,31,33,35,39,41,42,44,51,52 and 56. 90% related to HPV
type 6 & 11
Some related to increased neoplastic risk
High neoplastic risk : HPV 16,18

EPIDEMIOLOGY
US : Annual incidence : 1%
Young adults in third decade
World : variably, at least as common as in US
Sex : female = male
Age : 17-33 years, peak 20-24 years

PREDILECTION AREA
Male : Perineum, anal region, sulcus coronarius, glands
penis, distal and shaft of penis, OUE
Female : Vulva, introitus vagina, cervix

PATHOGENESIS
HPV
Cell of basal layer of epidermis
Penetrate skin
Mucosal microabrasions
Latent phase
no sign & symptoms
Month years
Production of viral DNA, capsids & particles
Infects host cell
Morfologic atypical koilocytosis of CA

HISTORY
Single/multiple lesions
Incubation : 3 week 8 months
Complaint : painless bumps, pruritus +/Lesions: regress,remain the same or progress
History of anal intercourse perianal lesions
Urethral bleeding/urinary obstruction

CLINICAL MANIFESTATION
Single or multiple papular eruption
Pearly, filliform, fungating, cauliflower, or plaquelike
Quite smooth, verrucous, or lobulated
Involvement: multiple sites
Perianal lesions: immunosuppression or anal
intercourse.
Color : same the skin / erythema, hyperpigmentation.

MUCOSAL WART
Multiple mucosal warts extending to the vermillion border
where they become highly keratinized.

DIFFERENTIAL DIAGNOSIS

Condyloma latum
Squamous cell Ca

LABORATORIUM
Test for other STDs : HIV, GO, chlamydia, syphilis
Pap smear
Acetowhitening, colposcopy
Histo PA
Anoscopy
Filter hybridization, in situ hybridation, PCR for Dx &
HPV typing

MANAGEMENT
General :
Personal higiene
Do save sexual contact
Specific :
Chemoteraphy: podofilin 25%, TCA 50%, Fluorourasil 15%
Imunoterapi: Interferon, Imiquimod krim 5%.
Surgery: cryotheraphy, electrocauter, scissor excision,
laser treatment

PROGNOSIS
>> fail to respond to treatment or recurs after adequate response
Recurrence rate exceed 50% after 1 year (residif).

CUTANEOUS WART

DEFINITION
Discrete benign epithelial hiperplasia
with varying degress of suface
hiperkeratosis.
Manifestasi as papule-plaques
Lession may become confluent
became mosaic
The extent of the lession is
determined by immune status of the
host

VERRUCA VULGARIS
A. Common wart, periungual. Multiple, confluent, keratotic papules
around the proximal periphery of the fingernails. B. Common wart,
verruca plantaris with black dots of thrombosed capillaries. C. Common
wart, mosaic plantar. A large hyperkeratotic plaque is seen on the heel,
made up of multiple small coalescing warts.

VERRUCA VULGARIS
Periungual Hyperkeratotic papules
located periungually on the dorsum
of a finger.

Verruca vulgaris in an
immunocompromised individual

VERRUCA PLANTARIS
Confluent, skin-colored, verrucous papules, forming a
mosaic, disrupting the normal dermatoglyphics of the
plantar foot.

VERRUCA PLANA
Flat-topped, pink papules with sharp margination and
minimal hyperkeratosis on the dorsa of the hands and
fingers.

FILIFORM WART
Multiple, elongated keratotic papules on the face of a
child; note the clustering on the eyelids.

MOLUSCUM
CONTAGIOSUM

DEFINITION

Moluscum Contagiosum is common viral infection of chilhood,

characterized by discrete, umbilicted, pearly-white papules.

EPIDEMIOLOGY
Age
: Children, ussualy between
Gender
: M>F
Incidence
: Common

3-16 years

 Transmision
Skin to skin contact. In sexually active adults, the primary
genetal location of the lesions suggest is spread sexually.
Risk Factors
Increase insidence in young children, swimmers, and in
children who bath together. Also increase in
immunocompromised individuals.

HISTORY

Moluscum lesions typically

appear anywhere from 14 days
to 6 month after exposure.they
can spread by inoculation, but
typically self-resolve in a few
months. The lesions are
asymptomatic or mildly pruritic
and can look inflamed prior to
spontaneous involution.

PHYSICAL EXAMINATION
Skin findings
Type
: papuls to noduls with central
umbillication.
Size
: 2-5 mm, rarely 10-18 mm lesions
Color
: pearly-white or flesh colored
Shape
: round, oval, hemispherical,
umbilicated number : isolated single
lesion or
multiple scattered discrete
lesions
Site of predilection : axillae, antecubital and
crural
folds.

MOLLUSCUM CONTAGIOSUM
A. Discrete, solid, skin-colored papules, 12 mm in
diameter with central umbilication.
B. Multiple, scattered, and discrete lesions, some of which
are inflamed.

DIFFERENTIAL
DIAGNOSIS

The diagnosis of moluscum contagiosum can be made

if characteristic dome shape papules with central
umbilication are noted. With smaller lesions or
atypical cases,
Moluscum can be confused with :
* Nevi
* Wart
* Acne
* Basal cell Ca (in adult)

LABORATORY
EXAMINATION
Dermatopathology :
skin biopsy will reveal molluscum bodies
(epithelial cells with large intracytoplasmic
inclusions, Henderson-Petterson bodies)
Skin scrape :
A simple skin srape of the central core, obtained
by pointed scalpel without local anesthesia,
reveals molluscum with Giemsas staining.

MANAGEMENT

Molluscum are common in children and often self resolve.

Management :
Prevention: avoid skin-to-skin contact with individual having
molluscum.
Supportive: In immunocompetent children and sexullay active adults,
molluscum regress spontaneusly; painful aggressive agrevise therapy is
not indicated.

MANAGEMENT

Treatment :
Imiquimod 5% cr applied 3 time/ week
Curettage
Cryosurgery freezing lesion 10-15s
KOH 20%

MUCOSAL WART

A. Multiple condylomata
acuminata on the shaft of the
penis B. Erythroplasia of the
glans with exophytic SCC
extending onto prepuce. C.
Multiple perianal condylomata
in a child. Sexual abuse must
be considered. D. Oral florid
papillomatosis with multiple,
large verrucae. E. Multiple
confluent condylomata on the
labia minora, majora, and
fourchette.

" thank you "

1.
2.
3.
4.
5.
6.

IMPETIGO
FOLLICULITIS
FURUNKLE & CARBUNKLE
ERISIPELAS &CELLULITIS
EKTIMA
s4

PIODERMA

CUTANEOUS BACTERIAL
INFECTION
PYODERMA
A.Staphylococcusaureus
B.Streptococcus betahemolyticus
NON-PYODERMA
A. Corynebacterium
B. Mycobacterium
C.Other bacteria

PYODERMA
Pyoderma is usually caused by
staphylococcal, streptococcal, or combined
infection.

Pyoderma is a group of cocci

infections in the skin, including
impetigo, ecthyma, folliculitis,
furuncle, carbuncle, erysipelas and
cellulitis.
The quantity and the toxicity of the
bacteria

IMPETIGO
Occur most frequently on the exposed
parts of the body
Contagious
Occur most frequently in childhood
Mostly during summer

PATHOGENISITY
Coagulasepositive Staphylocuccus
aureus Group A beta-hemolytic
streptococci
Group A beta-hemolytic streptococci
and the phage type 71 and 80/81 S.
aureus skin infections are sometimes
followed by glomerulonephritis.
Enviroment: humid weather
Body: itching skin diseases

CLINICAL TYPE
Impetigo vulgaris
impetigo bullosa
Impetigo neonatorum
Granuecthyma

IMPETIGO KONTAGIOSA
Feature of the lesion: erythematous macula or
papula, pustula, erosion, crusts

Subjective symptom: itching seriously

Course of disease: about one week
Systemic symptom: fever and lymphangitis may
occur in serious disease, and more seriously
septicaemia and acute glomerulonephritis may occur
in disease.

Staphylococcus aureus:
impetigo. Erythema and
crusting on the nose and
moustache area (A),
which can spread to
involve the entire
centrofacial region (B).

IMPETIGO

BULLOUS IMPETIGO
Childhood, Summer
Impetigo often complicates miliaria,
hidradenitis and insect bites
Bullae:pellucid to turbid exudate, like half
bottle of water, after these lesions rupture,
the exudate dries to form crusts and
hyperpigmentation.
Impetigo circinata

Bullous impetigo in a child.

BULLOUS IMPETIGO
Note blisters
filled with cloudy
fluid and lesions that have
ruptured, leading to erosions
and crusting.

Bullous impetigo in a child. Blisters

are initially filled with cloudy fluid
and later rupture, resulting in
erosions and crusting.
BULLOUS IMPETIGO

FOLLICULITIS
Staphylococcus aureus: superficial
folliculitis. Multiple pustules
confined to the beard area.

FURUNKLE

A. Furuncle of the upper lip. The lesion is nodular, and the central necrotic
plug is covered by purulent crust. Several small pustules are seen lateral
to the center of the lesion. B. Multiple furuncles. Multiple abscesses on the
buttocks of long standing in a young man with inflammatory bowel
disease. The lesions healed with scarring after a prolonged course of
dicloxacillin.

CARBUNCLE

This lesion
represents
multiple confluent
furuncles draining
pus from multiple
openings.

ERYSIPELAS

There is painful,
warm erythema of
the lower
extremity with
well-defined
borders.

ERYSIPELAS
Erysipelas. Painful,
edematous
erythema with
sharp margination
on both cheeks and
the nose. There is
tenderness, and
the patient has
fever and chills.

CELLULITIS

A. Cellulitis after puncture trauma. The forearm is swollen,

erythematous, and tender; there is abscess formation. B. Cellulitis
arising at the site of a surgical excision: Staphylococcus aureus. Note
discharge of pus.

FURUNKEL / KARBUNKEL
Definisi :
Furunkel : peradangan folikel rambut dan
jaringan subkutan sekitarnya
Karbunkel : kumpulan furunkel
Penyebab: Staphylococcus aureus
Umur : anak, dewasa muda, dewasa
Sex : anak >>
Predileksi : daerah banyak gesekan dan keringat
(hidung, leher, wajah,ketiak, pantat)

FOLIKULITIS
Definisi : peradangan folikel rambut
Penyebab : Staphylococcus aureus
Umur : semua umur, >> anak-anak
Sex
:=
Tipe
:
Superfisialis : terbatas di epidermis
Profunda
: sampai subkutan
Lokasi : daerah berambut kulit kepala
& anggota gerak >>

 Klinis :
Superfisialis : papula atau pustule eritematus
ditengahnya terdapat rambut
Profunda : seperti superfisialis + infiltrate
subkutan
Penatalaksanaan :
jaga kebersihan
antibiotik topikal
bila berat antibiotika sistemik

Klinis :
Nyeri
Nodul eritematosa bentuk kerucut, ditengahnya
ada pustul melunak jadi abses isi pus dan
jaringan nekrotik memecah
Penyulit :
Furunkel : sepsis, meningitis
Bila di bibir atas / pipi trombosis sinus
kavernosus
Karbunkel : sepsis
Penatalaksanaan :
- obat topical : - lesi basah / kotor kompres
- lesi bersih antibitika
- obat sistemik : antibiotika missal : injeksi penisilin
G, ampisilin, amoksilin, kloksasilin, dikloksasilin,
eritromisin, linkomisin

ERISIPELAS
Definisi : infeksi akut pada epidermis
dan dermis yang biasanya disebabkan
Streptococcus
Penyebab: Streptococcus hemolyticus
>>
Umur
: anak dan dewasa
Sex
: =
Predileksi: tungkai bawah, wajah

 Klinis

sering didahului luka kecil di kulit

panas badan, malaise
macula eritematus, batas tegas, panas pada
perabaan, nyeri, bisa ada bula atau vesikula
diatasnya

Penatalaksanaan :
istirahat (tungkai bawah dan kaki ditinggikan)
topikal kompres terbuka
sistemik antibiotika

SELULITIS
Definisi : radang akut pada kulit dan subkutis
Penyebab : Streptococcus hemolyticus >>
Staphylococcus aureus
Umur : anak dan orang tua
Sex
: =
Predileksi : wajah dan anggota gerak
Klinis : - demam, malaise
- infiltrat difus di subkutan, tanda
radang
akut (+)
Penatalaksanaan : sama dengan Erisipelas

ECTIMA
Deep and inflammatory vesicle or
vesicopustule, ruptures to form ulcer and
dark brown crusts
Causalgia, regional lymphonodi swell
Autoinoculation infection
The lesions tend to heal after 2-4 weeks,
leaving scars or granulomatous lesions

ECTYMA
Staphylococcus
aureus:
ecthyma.
Multiple
thickly
crusted ulcers on the
leg of a patient with
diabetes and renal
failure. Ecthymatous
lesions
were
also
present on the other
leg, the arms, and the
hands.

STAPHYLOCOCCAL SCALDED
SKIN
Advanced
stage of
Late stage of staphylococcal
staphylococcal scalded-skin
SYNDROME
scalded-skin syndrome.
Generalized desquamation with
large sheets

syndrome showing a flaccid,

collapsed bullae

STAPHYLOCOCCAL SCALDED SKIN SYNDROME

(A) erythema, more superficial blisters with desquamation of large
sheets. B. Superficial erosions around the eye with underlying
denuded skin. C. Characteristic crusting with superficial erosions
noted on face of this 10-month-old child with SSSS.

MANAGEMENT
Clean the skin and cure the wound and
itching skin diseases
Systemic treatment: sulfanilamide antibiotics
or other antibiotics

Topical therapy: Principle: sterilize, diminish

inflammation, astringe and desiccate ;
mupirocin oint, fusidic acyd cream

Ecthyma : Remove the crusts, topical

antibiotics ointment
Isolation and disinfection

Thank you
.