Hendra Gunawan, dr. Sp.KK (K), Ph.D, FINSDV, FAADV

Hendra Gunawan, dr. Sp.KK (K), Ph.D, FINSDV, FAADV

Departmen Dermatologi dan Venereologi Fakultas Kedokteran

Universitas Padjadjaran / Rumah Sakit Dr. Hasan Sadikin Bandung

h.gunawan2016@unpad.ac.idPendidikan :- Fakultas Kedokteran Universitas Padjadjaran Bandung, Indonesia Lulus 1994- Diploma Course in Dermatology Bangkok, Thailand Lulus 2002- Program Spesialis Ilmu Kesehatan Kulit dan Kelamin

Fakultas Kedokteran Universitas Padjadjaran Bandung, Indonesia Lulus 2005- Program Doktoral (S3) Juntendo University Tokyo, Jepang Lulus 2008- Fellowship in Dermatopathology and Dermoscopy

Toranomon Hospital Tokyo, Jepang Lulus 2014

Riwayat Pekerjaan :- Dokter Offshore Pertamina Jakarta Tahun 1994-1995- Kepala Puskesmas Mapin Kebak Sumbawa, NTB Tahun 1995-1998- Dokjter Rumah Sakit M.H. Thamrin Pondok Gede Jakarta Tahun 1998-1999- Staf Departemen I.K. Kulit dan Kelamin FK UNPAD Tahun 2006-2021

Organisasi :- Anggota Ikatan Dokter Indonesia (IDI)- Sekretaris II Kolegium Dermatologi dan Venereologi Indonesia (KDVI)- Koordinator Ujian Tulis Nasional Komisi Evaluasi Nasional KDVI - Anggota Perhimpunan Dokter Spesialis Kulit dan Kelamin Indonesia- Anggota Komisi III Perhimpunan Dokter Spesialis Kulit dan Kelamin Indonesia

(PERDOSKI) Cabang Bandung- Wakil Ketua Kelompok Studi Morbus Hansen Indonesia- Wakil Ketua Kelompok Studi Dermatologi Sosial Indonesia

- Anggota Kelompok Studi Dermatopatologi Indonesia- Anggota Kelompok Studi Imunodermatologi dan Dermatosis

Akibat Kerja- Anggota Komite Etik dan Penelitian Kesehatan Rumah Sakit

Dr. Hasan Sadikin Bandung

Hendra Gunawan, dr., SpKK, PhD

SUMMARY

Immunity to skin infection

Outline

Bacterialskin infection

Fungal skin infection

Viral skin infection

Parasites skin infestation

Clinical manifestation

Lab examination

Management

FORNAS FKTP

< 0.5 mm: eyelids > 5 mm: upper back

Largest organ of body*

1.5 to 2 m2 in area

12% of body weight

Varies in thickness

Introduction:

* High risk to get infection

Hairs

Nails

Gland

Appendages of

Skin

SKIN FUNCTIONS

Aesthetic

Vitamin D production

Sensory function

Excretion

Temperature regulation

Barrier against loss of body fluid

Protectionfirst line of defense against microorganisms.

SKININFECTION

IMMUNITY TO

Pathogens organisms that cause diseases

What are the four major types of pathogen?

bacteria fungi

protozoa

virus

Pathogens organisms that cause diseases

What are the four major types of pathogen?

Skin(pores, hair follicles)

Route of Infection

Wounds(scratches, cuts, burns)

Insect bites

First line of

defense

Immune System

Second line of

defense

Third line of

defense

123

Immune System

• First line of defense:

• Physical barriers

microorganisms must cross:

•Thick keratin

•Sebum (low pH),

•Sweat (low pH, high salt,

lysozyme)

Immune System

• Second line of defense:

• Innate immune system

(no adaptation to specific pathogens)

•Macrophages

•Neutrophils

•Natural killer (NK) cells

Immune System

• Third line of defense:

• Adaptive immune system

(adapts to defend against specific

pathogens using variable receptors)

•B cells: make antibody specific for

antigen

•T cells: cellular responses using

receptors (T cell receptors)

SKININFECTION

BACTERIAL

Bacterial Skin Infections

Pyoderma

Primary

Impetigo

Echtyma

Folliculitis, Furuncle,

Carbuncle

Erysipelas, Cellulitis

Secondary

Non-pyoderma

Erythrasma

Skin tuberculosis

Leprosy

•Caused by a single pathogen affect normal skin.

• Most common primary skin pathogens:

• S. aureus

• β-hemolytic streptococci.

•Occur in skin that is already diseased.

• Because of the underlying disease clinical picture & course of these infections vary.

PRIMARY INFECTIONS SECONDARY INFECTIONS

PYODERMA

•Superficial skin infection with bullae

(bullous) or crusting (non-bullous).

•Caused by Streptococci, Staphylococci,

or both

Impetigo

Vesicles, bullae, & bullae hypopion with surrounding erythema

(4A)

Bullous Impetigo (4A)

Non-bullous Impetigo (Crusted Impetigo)

• Initially a vesicular infection

rapidly evolves into pustules

that rupture

dried discharge forming honey

colored crust on an erythematous base.

(4A)

•Similar to impetigo more

deeply dermis of skin

possibly causing scars.

•Caused by Streptococcus

•Begin as vesicles rupture,

creating circular erythematouslesions with adherent crusts.

Ecthyma (4A)

Ecthyma

• Inflammation at the opening of

hair follicle.

•Erythematous papules & pustulessurrounding individual hairs.

•Caused by S. aureus.

Folliculitis (4A)

•Deep-seated inflammatory nodule

with a pustular center that

develops around a hair follicle

(painful, localized)

•Caused by Staphylococcal.

Furuncle (4A)

Furuncle (4A)

Furunculosis

Crops of boils occur over a longer period of time.

• Involvement of several adjacent

follicles, with pus discharging from

multiple follicular orifices.

•Clusters of furuncles connected

subcutaneously

Carbuncle (4A)

•Painful, fluctuant, red, tender

nodule, on which may rest a

pustule.

Cutaneous Abscesses

•Plaque-like edema of cutaneous

surface involves superficial

dermis.

•Occurs most frequently on legs and

face.

•Most often caused by group

A β-hemolytic streptococci.

Erysipelas (3A)

•Shiny, raised, indurated & tender

plaque-like edema with distinct

margins clear border between

normal & infected skin.

Erysipelas (3A)

Cellulitis

Affects the deeper tissues &less clearly defined than in erysipelas.

(3A)

•Rapidly spreading cellulitis to

fascia & muscle with necrosis of

subcutaneous tissue & overlying

skin.

•Fever, systemic toxicity, & severe

pain.

•Caused by a mixture of aerobic &

anaerobic organisms.

Necrotizing Fasciitis

•~ Lyell's disease

•Caused by epidermolytic toxin of

Staphylococcal.

•Starts as a localized lesion widespread erythema & exfoliation of skin.

•More common in infants than in adults.

Staphylococcal Scalded Skin Syndrome (SSSS)

Staphylococcal Scalded Skin Syndrome (SSSS)

Lab Examination

•Direct microscopy:

Gram stained smear is useful in

case of pus, where cocci are seen.

• Culture and sensitivity test.

Management

Non-medicamentosa therapy

Medicamentosa therapy

Personal Hygiene

Identifying predisposing

factors

Topical

Systemic

Management

FORNAS FKTP

FORNAS FKTP

FORNAS FKTP

FORNAS FKTP

FORNAS FKTP

FORNAS FKTP

FORNAS FKTP

NON-PYODERMA

•Super›cial bacterial skin infection

in intertriginous areas:

toes, armpits, or groin

•Well-de›fined but irregular reddish-brown patches.

•Caused by Corynebacterium

minutissimum.

Erythrasma (3A)

• Wood's lamp:

• Ultraviolet light causes the

organism to fluoresce a characteristic

coral red fluorescence.

Erythrasma (3A)

Management

Localized topical

Benzoyl peroxide gel

Clindamycin or erythromycin gel

Fusidic acid ointment

Widespread/not respond to topical therapy systemic

Oral erythromycin, 250 mg 4 times a day

for 2 weeks

Single dose of 1 g clarithromycin.

FORNAS FKTP

SKIN TUBERCULOSIS

• Caused by M. tuberculosis

• Primary infection: acquiring bacilli for first time.

• Post primary infection: occurs in patient with previous TB or previous BCG vaccination.

LEPROSY

• Caused by M. leprae

• Paucibacillary (PB)

• Multibacillary (MB)

CHRONICBACTERIAL SKIN INFECTION

SkinTuberculosis

Skin Tuberculosis(3A)

Skin Tuberculosis(3A)

Before Treatment

After 3 Weeks Treatment

Management FORNAS FKTP

LEPROSY

PB MB

WHO

Leprosy (4A)

Silva MR CM. Mycobacterial infections. Dermatology. New York: Elsevier; 2008. p. 1114-25.

BORDERLINE

“Cardinal Sign”Leprosy

“Cardinal Sign”Leprosy

Gynecomastia

Madarosis

The other signsof leprosy

• Lesi tunggal atau beberapa

• Hipopigmentasi

• Berkurangnya sensasi (hypoesthetic)

TIPE TUBERKULOID (TT)

BORDERLINE TUBERCULOID (BT)

• Lesi sedikit (< 5)

• Batas tegas

• Asimetris

• Plak eritem

• Berkurangnya sensasi(hypoesthaetic)

BORDERLINE BORDERLINE (BB)

Dimorphous leprosy

Plak eritem, skuama

Berbentuk anular (seperti cincin)

Well-defined internal & external borders

BORDERLINE BORDERLINE (BB)

BORDERLINE LEPROMATOUS (BL)

LEPROMATOUS LEPROSY (LL)

Diffuse infiltrations

LEPROMATOUS LEPROSY (LL)

LEPROMATOUS LEPROSY (LL)

LEPROMATOUS LEPROSY (LL)

PemeriksaanSaraf Tepi

n. aurikularis magnus

n. aurikularis magnus

n. ulnaris

n. ulnaris

n. peroneus komunis

n. peroneus komunis

n. tibialis posteriorn. tibialis posterior

Bakteri

• 2 cuping telinga kanan & kiri

• 1 lesi kulit aktif

• 2 cuping telinga kanan & kiri

• Atas lutut atau punggung tangan

Pemeriksaan BTA

The Presence of Acid-fast Bacilli

1

Bacterial Index & Morphological Index

MI = SOLID BACILLI

TOTAL BACILLI X 100%

The Presence of Acid-fast Bacilli

Management

FORNAS FKTP

FUNGALSKIN

INFECTION

Fungal Skin

Infection

Dermatophytosis

Candidiasiscutis

PityriasisVesicolor

FungalSkin Infection T capitis

T facialis

T corporis

T cruris

T manum

T pedis

T unguium

DERMATOPHYTOSIS

Tinea Capitis

Gray patch

Kerion

Favus

TineaCapitis

‘Back dot’

Childrenmost common cases

(3A)

Black dot type• Large alopecia without inflammation

• Black dot hairs & mild scaling

• Look like alopecia areata

Tinea Capitis

Gray patch type• Inflammatory circumscribed

erythematous scaly patches.

• Nonscarring alopecia with breakage hair

(3A)

Kerion• Inflammed, boggy, & tender

• Fever, adenopathy.

• Scaring alopecia may occur

• May look bacterial

Tinea Capitis

Favus• Severe form of tinea capitis

• Characterized by scutula:yellowish, circular, cup-shaped crusts

grouped in patches ~ honeycomb

(3A)

Normal Hair

Endothrix Exothrix

Direct microscopy:KOH 10%

Lab Examination

Tinea Facialis (4A)

•Erythematous papulosquamous

•Annular

•Scaling

•Crusting

• ‘Ringworm’

Tinea Corporis (4A)

Tinea Cruris (4A)

• Erythema with pronounced scales• Vesicles and bullae

Tinea Pedis Tinea Manus(3A) (3A)

•Types:

1. Distal subungal

2. Proximal subungal

May indicate HIV infection

4. White superficial

5. Candida onychomycosis

Normally hands with accompanying

paronychia

Onychomycosis (2)

Direct microscopy: KOH 10% septate, branching hyphae

Lab Examination

Management

Management

FORNAS FKTP

FORNAS FKTP

PITYRIASIS VESICOLOR

• Etiology: Malassezia

• Numerous, well-marginated, oval-to-

round macules with fine white scales

(when scraped).

• Pigmentary alteration in each individual:

• Redness

• Hypopigmented• Hyperpigmented

Pityriasis Vesicolor (4A)

• Asymptomatic to mildly pruritic

• Scattered over the trunk & neck

• Differential diagnosis:

• Intertrigo

• Erythrasma

Pityriasis Vesicolor (4A)

Woods Light: Yellow green fluorescence pityrialactone (tryptophan derivative).

Pityriasis Vesicolor

Direct microscopy: KOH 10% “spaghetti and meatballs”.

Pityriasis Vesicolor

Management

FORNAS FKTP

FORNAS FKTP

CANDIDIASIS CUTIS

• Etiology: Candida albicans (normal flora)

• Occurs in moist areas

• Primary lesion is red pustules.

• Most Common: red, denuded surface with

satellite lesions.

Candidiasis Cutis (4A)

Candidiasis Cutis (4A)

Candidiasis Cutis

Direct microscopy: KOH 10% pseudohyphae and blastospores

Management

FORNAS FKTP

FORNAS FKTP

VIRALSKIN

INFECTION

Varicella Zoster Virus (Vzv)

Clinical Forms: Herpes zoster

Clinical Forms: Varicella

• Mainly children highly contagious

• Generalized vesicular eruptions on skin

& mucous membranes

• Adults & immune-compromised

severe manifestations

• Prodrome: brief of low-grade fever, URT

symptoms, & mild malaise

• Rapid appearance of pruritic exanthem

Varicella (4A)

• Incubation period: 14-21 days.

• Begin in trunk & scalp spread

peripherally

• Lesions begin as tiny erythematouspapules develop central vesicles

surrounded by red halos

(‘dew drops on a rose petal’)

Varicella (4A)

Varicella (4A)

Management

FORNAS FKTP

• After primary infection virus lies

dormant in sensory nerve root cell.

• Reactivation results in a sensory

neuritis.

• Severity & risk of complications: age

& immunosuppression due to

decline in specific cell-mediated

immune response

Herpes Zoster (4A)

• Postulated triggers:

Mechanical trauma

Thermal trauma

Infection

Immunosuppression

Herpes Zoster (4A)

• PRODROME PHASE :

Pre-eruptive pain (pre-herpetic

neuralgia), unilateral, dermatomal

4 to 5 days precedes the eruption.

Pain/pruritis, tingling, hyperesthesia

Herpes Zoster (4A)

• ERUPTIVE PHASE:

Dermatome does not cross midline.

Red, swollen plaque & spreads to involve

part or all of a dermatome.

Vesicles arise in clusters on erythematous

base purulent fluid by day 3 or 4.

Rupture before forming crusts falls off

in 2 to 3 weeks.

Herpes Zoster (4A)

Direct microscopy:

Tzanck smear: Stain with Giemsa

multinucleated giant cells.

Lab Examination

Management

FORNAS FKTP

•Primary infections:• More severe• Frequently involve systemic signs and

symptoms• Have a higher rate of complications

compared to episodes reactivation

of HSV.

•Pain, burning, or itching at the site of subsequent eruption.

Herpes simplex (4A)

Management

HPV worldwide occurrence.

>150 genotypes of HPV

Affecting people of all ages most common children & young

adults.

Cutaneous warts (3A)

Well-defined, raised papules or plaques,

rough or hard surface, no inflammation.

Most common on hands or feet.

Cutaneous warts

Common warts

Filiform wartsMosaic warts Plane warts

(3A)

Management

Common benign cutaneous infection

due to Molluscum contagiosum virus.

Children most commonly affected.

Discrete firm, dome-shaped papules

have central umbilication.

Molluscum Contagiosum (3A)

Management

PARASITESSKIN

INFESTATION

• Caused by Sarcoptes scabiei var. hominis.

burrows tunnels into epidermis.

• Mites of deposit faeces behind them.

• Female lays eggs in tunnels.

Scabies (4A)

• Mode of Transmission:• Close person-to-person contact• Sexual intercourse• Fomites may transmit the infection

• Clinical Picture:1. Nocturnal pruritus scratching2. Lesions on predilection sites Circle of Hebra3. Attacks group of people

4. Finding mites or its products

Scabies (4A)

Scabies (4A)

• Represents an abnormal host immune

response:

• Mentally retarded (Down’s syndrome)

• Severe systemic diseases (leukemia,

diabetes )

• Severe immunesuppression.

Crusted Scabies (3A)

Crusted Scabies (3A)

• Direct microscopy:

• KOH preparation of skin scrapings

presence of mites, larva, eggs, scibala

within the skin .

Lab Examination

Management

FORNAS FKTP

• Infestation of sucking lice blood-feeding ectoparasitic.

• Lay their eggs on hair shafts or in the seams of clothing

Pediculosis (4A)

• Lice: small gray brown, blood sucking

insects crawl among hairs.

•Head louse nit attached to hair shaft.

Pediculosis capitis (4A)

• Infestations commonly found in homeless individuals.

•Pruritus only sign of body lice is excoriations, often linear.

•Primarily on back, neck, shoulders, & waist.

•Diagnosis presence of nits in lining of clothing, particularly the seams.

Pediculosis corporis

• Best to call “crab lice” rather than “pubic lice”

• Infestations involve other hair-bearing sites:

mustache, beard, axillae, eyelashes, & eyebrows.

• Transmitted by sexual or close contact & fomites.

• Therapy similar to pediculosis capitis.

Pediculosis Pubis (4A)

Management

FORNAS FKTP

• Caused by Ancylostoma braziliense, Ancylostoma caninum

• Tropical countries

• Contact with contaminated soil

• Feet & buttocks

Cutaneous Larva Migrans (4A)

•Typically 1 to 3 serpiginous lesions up to 20 cm in length

•May be vesicobullous; movement up to several cm per day.

• Intense pruritic

Cutaneous Larva Migrans

Management

FORNAS FKTP

• Skin infection can caused by bacteria, fungal, viral, and parasites.

• Clinical manifestation vary from mild to serious condition.

• Accurate medical history & carefully perform physical examination

is fundamental to provide a correct diagnosis.

• Many skin infections require treatment, both non-medicamentosa &

medicamentosa therapy (topical with/without systemic).

Some available in primary health care center.

Summary

HATUR NUHUN

h . a . g . e

h.gunawan2016@unpad.ac.id