TROPICAL DERMATOLOGY

NANDA EARLIA
BAGIAN / SMF ILMU KESEHATAN KULIT DAN KELAMIN
FK. UNSYIAH / RSUD DR ZAINOEL ABIDIN
BANDA ACEH
2014
 TROPICAL DERMATOLOGY

 Tropical diseases  commonly affect the

skin  affecting > 50% of the population :
1. Infestation (Scabies, Pediculosis, CLM)
2. Bacterial infection (Pioderma)
3. Viral Infection
4. Fungal Infection (Dermatomycosis)
5. Leprosy (Morbus Hansen)
 CHANCROID

GRANULOMA INGUINALE
CHLAMIDIAL
MMP/CPINFECTION
CHICKEN POX
(Varicella) 2001
MEASLES
TRICHOMONIASIS
AECP PYODERMA
1992
SMALL POX LGV
(Variola) OCP
SIPHYLIS
GONORE IMPETIGO
CP (B-P) 1986
MOLLUSCUM 1957
CONTAGIOSUM

FURUNKEL
ENTEROVIRUS
(Hand Foot Mouth Disease)
ERISIPELAS

LEPROSY
MYCOSIS

INFESTATION :
ECTOPARASIT (Scabies, Pediculosis &
HELMINTHIC
(Cutaneous Larva Migrans)
 4

NANDA EARLIA
Department of Dermato Venereology
Faculty of Medicine Syiah Kuala University / Dr Zainoel Abidin Hospital Banda aceh
E-mail: [email protected] [email protected]
Phone : 08126900979
Date of birth : June 19th, 1975
Place of Birth : Sigli, Aceh province, Indonesia
Address : Jl Thayeb Peurelak No 29, Lamprit, Banda Aceh
Clinic : Nayla Skin Center, Jl Tgk Thayeb peurelak No 29, Lamprit, Banda Aceh
Education
2000, MD. University of SyiahKuala, Banda Aceh
2009, Registration Dermatologist of Airlangga University , Surabaya
Professional Experiences
2001– 2002, Internship , Meuraxa Hospital, Banda aceh
2003 – 2005, Internship, Zainoel Abidin Hospital Banda Aceh
2006 – 2009, Resident Dermatology, Airlangga University Surabaya
2010 – now, Medical Staff, Department of Dermatology, Zainoel Abidin Hospital, Banda Aceh
2010 – now, Lecturer , Medical Faculty, Syiah Kuala University
2010 –now, chief of PERDOSKI Aceh
VIRAL INFECTION

1. VARICELLA
2. HERPES ZOSTER
3. HERPES SIMPLEKS
4. VERRUCA VULGARIS
5. KONDILOMA ACCUMINATA
6. MOLLUSCUM CONTAGIOSUM
Poxviruses That Infect Humans* and Cause Disease
VZV : VARICELLA

( CHICKEN POX )
 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

8
 EPIDEMIOLOGY

 Age of onset  90% < 10 years of age

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

9
 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

11
 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

12
 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 : 10-21 days
 Prodrome : absent or mild.
 Exanthem appears : 2-3 days.
 Skin symptoms : pruritic exanthem

14
 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 lesions—that is, erythematous papules, vesicles (“dewdrops on rose

petals”), crusts, and erosions at sites of excoriation—is 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 Chickenpox on the palate. Notice the
vesicle on the skin, the classic "dew glistening, water-drop characteristic of
drop on a rose petal" appearance. the chickenpox vesicle on the palate.
 DIFFERENTIAL DIAGNOSIS

 Herpes Zoster Disseminata

 Smallpox (variola)
 Bullous impetigo
 Bullous pemphigoid
 Hand foot mouth disease
 Dermatitis herpetiformis

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 Differential Dx - Chickenpox

VARIOLA (SMALL POX) VARICELLA (CHICKEN POX)

Variola (Smallpox)  Begins on the face and

 Begins centrally, then scalp, spreads to the
spreads outward to face trunk  centrifugal
and extremities
 All lesions are always  Lesions in various
in a single stage of stages of development
development can simultaneously be
 Associated with severe present on the patient's
constitutional skin
symptoms
 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
22
 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

24
 PREVENTION

 Vaccination
 Varicella-zoster immune globulin

25
 VARICELLA VACCINE

26
VZV : HERPES ZOSTER

SHINGLES)
 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 (Hutchinson’s
sign) → involvement of the nasociliary nerve of V1
(ophtalmic) branch
Crusted ulcerations 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.

Varicella zoster virus infection:

ophthalmic herpes zoster
 EPIDEMIOLOGY

More than 66% are older than 50 years of age

Cumulative life time incidence 10-20%
Risk factors :
Malignancy
Immunosuppresion
Radiotherapy
HIV
Typical grouped vesicles
and pustules with
erythema and edema of
three contiguous
thoracic dermatomes on
the posterior chest wall.

Varicella-zoster virus infection:

herpes zoster in T8 to T10
dermatomes
 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
herpes zoster with
cluster of grouped
vesicles Grouped and
confluent vesicles
surrounding erythema
on the chest wall

VARICELLA ZOSTER VIRUS

INFECTION
 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 transmissible STD.
 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.
A. A. 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. HERPES LABIALIS
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 Lesion
Most clinical lesions are minor breaks in the mucocutaneous epithelium,
presenting as erosion, abrasion and fissures.
The classically described finding are uncommon

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

PRIMARY HERPES SIMPLEX

A. Genital herpes:
recurrent infection of the
penis. Group of vesicles
with early central crusting
on 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.
RECURRENT GENITAL HERPES
 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 Detection : Viral Culture/Modified Culture

 HSV Antigen Detection
 PCR
 Antibodies to HSV
 ELISA
 Tzanck Smear
 Dermatopathology
Herpes simplex virus:
positive Tzanck smear.
A giant, multinucleated
keratinocyte on a
Giemsa-stained smear
obtained from a 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 TZANCK SMEAR HSV
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
. of HSV-2 infections are asymptomatic
 70%
 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.
Multiple mucosal warts
extending to the
vermillion border where
they become highly
keratinized.

MUCOSAL WART
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 1-
5%
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 Verruca vulgaris in an

periungually on the dorsum of a finger. immunocompromised individual
Confluent, skin-colored,
verrucous papules,
forming a mosaic,
disrupting the normal
dermatoglyphics of the
plantar foot.

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

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

FILIFORM WART
MOLUSCUM CONTAGIOSUM
 DEFINITION

 Moluscum Contagiosum is common viral infection of chilhood,

characterized by discrete, umbilicted, pearly-white papules.

EPIDEMIOLOGY
 Age : Children, ussualy between 3-16
years
 Gender : M>F
 Incidence : Common
 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.
 Symptoms are absent.
 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.
A. Discrete, solid, skin-
colored papules, 1–2
mm in diameter with
central umbilication.

B. Multiple, scattered,
and discrete lesions,
some of which are
inflamed.

MOLLUSCUM CONTAGIOSUM
 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 Giemsa’s 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.
 PIODERMA

1. IMPETIGO
2. FOLLICULITIS
3. FURUNKLE & CARBUNKLE
4. ERISIPELAS &CELLULITIS
5. EKTIMA
6. S4
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
 The resistance of the body
 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. Note
blisters filled
with cloudy fluid
and lesions that
have ruptured,
leading to
erosions and
crusting.

BULLOUS IMPETIGO
BULLOUS
IMPETIGO

Bullous impetigo in a child. Blisters are initially

filled with cloudy fluid and later rupture, resulting
in erosions and crusting.
Staphylococcus
aureus: superficial
folliculitis. Multiple
pustules confined to
the beard area.

FOLLICULITIS
 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.
ERYSIPEL
AS

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

Late stage of staphylococcal scalded-skin Advanced stage of staphylococcal

syndrome. Generalized desquamation with scalded-skin syndrome showing a flaccid,
large sheets collapsed bullae
(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.
STAPHYLOCOCCAL SCALDED SKIN SYNDROME
 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 ……….