PATHOLOGY OF

INTEGUMENT SYSTEM

By :

Djoko Legowo, MKes., drh

Departemen Patologi Veteriner FKH

Universitas Airlangga
 INTRODUCTION

Skin is not only the largest organ in the body,

but one of the most important. Without the
skin, terrestial mammalian life could not exist
MORPHOLOGY AND THE FUNCTION
OF THE SKIN
 MORPHOLOGY OF THE SKIN

-THE SKIN IS THE LARGEST ORGAN IN THE BODY AND

HAS HAIRED AND HAIRLESS PORTIONS

-HISTOLOGIC STRUCTURE VARIES GREATLY AMONG

DIFFERENT SITES AND SPECIES
- THE SKIN CONSISTS OF :

1. EPIDERMIS
2. DERMIS
3. SUBCUTIS
4. ADNEXA (HAIR FOLLICLES; SEBACEOUS; SWEAT GLAND)
Gambar 17.1. Kulit Tipis
Kulit tebal
 Distribution and Portion ;
nose; lips; handpats; footpats

Kuli tipis Kuli tebal

 EPIDERMIS

- DIVIDED INTO LAYERS BASED ON THE MORPHOLOGY OF

KERATINOCYTE
- EPIDERMIS OF HAIRED SKIN CONSISTS OF 4 LAYERS
- EPIDERMIS OF HAIERLESS SKIN CONSISTS OF 5 LAYERS
- THE LAYERS OF EPIDERMIS :
1. STRATUM BASALE
2. STRATUM SPINOSUM
3. STRATUM GRANULOSUM
4. STRATUM LUCIDUM ( ONLY FOUND IN HAIRLESS SKIN)
5. STRATUM CORNEUM
 DERMIS (CORIUM)

- GENERALLY DIVIDED INTO TWO PORTION :

- UPPER PART (STRATUM PAPILARE)
- LOWER PART (STRATUM RETICULARE)
- CONSISTS OF COLAGEN AND ELASTIC FIBERS
- FUNCTION  SUPPORTS OF :
- HAIR FOLLICELS
- GLANDS (SEBACEUOUS AND SWEAT)
- VESSEL
- NERVES ( MEISRNERS AND PACINIANS CORPUSCLES )
 SUBCUTIS (HYPODERMIS, PANNICULUS)

- THE SUBCUTIS ATTACHES THE DERMIS TO SUBJECENT

MUSCLE OR BONE.
- CONSISTS OF ADIPOSE TISSUE AND COLAGENOUS AND
ELASTICS FIBERS, WHICH PROVIDE FLEXIBILITY.
- ADIPOSE TISSUE INSULATES AGAINST TEMPERATURE
VARIATION AND, IN THE CASE OF FOOTPADS IN SHOCK
ABSORPTION).
 FUNCTIONS OF THE SKIN

1. PROVIDES A PROTECTIVE BARRIER AGAINST FLUID LOSS,

MICROBIOLOGIC AGENTS, CHEMICALS, AND PHYSICAL INJURY

A. PARTICIPATES IN INFLAMATION AND REPAIR

B. PARTICIPATES IN INNATE AND ADAPTIVE IMMUNITY

2. REGULATES TEMPERATURE AND BLOOD PRESSURE.

3. PRODUCES VITAMIN D

4. ACTS AS SENSORY ORGAN

5. STORES NUTRIENTS

6. ABSORPTIVE SURFACE
Skin is composed of a number of interdependent cell types and structures
that work toward a common protective goal :

1. Squamous epithelial cells (keratinocytes)

Function : - production of keratin protein
- major sites for the biosynthesis of soluble molecules
(cytokines) that are important in the regulation of
adjacent epidermal cells as well as cells in the dermis
2. Melanocytes within the epidermis are cells
Function : production of a brown pigment (melanin) that represents

an important endogenous screen against harmful

3. Langerhans cells (epidermal dendritic cells)
Function : take up and process antigens and communicate
critical information to lymphoid cells
4. Merkel cells (reside within the basal cell layer)
Function : serve as mechanoreceptors or may provide
neuroendocrine
5. Specialized dermal cells (dendrocytes)
Function : engineered for antigen presentation and
production of molecules (e.g., factor XIIIa) that
important in the early stages of wounds healing
Schematic representation of dynamic interaction between the epidermal layer and the dermal layer.
Keratinocytes at the edge of an ulcer (A) produce cytokines and factors that influence both
keratinization and the function of underlying dermal cells (B). In turn, dermal cells (B), such as mast
cells, also release cytokines (green granules) and proteases (red granules), which may regulate
both endothelial cells and overlying keratinocytes. Perturbations in these interactions between
epidermal cells and dermal cells may contribute to pathologic processes, such as psoriasis (C), in
which both compartments become morphologically abnormal.
 EXOGENOUS

FACTORS THAT INFLUENCE

OF THE NORMAL SKIN

ENDOGENOUS
AGENT ON SKIN DISEASES

Bacterial Skin Diseases

Fungal Skin Diseases

Parasitic Skin Diseases

Viral and Protozoal Skin Diseases

 PORTAL OF ENTERY INTO THE SKIN

ABSORBTION THROUGH STRATUM CORNEUM

EPIDERMIS
AND EPIDERMIS (TRAUMA; UV; DIRECT CONTACT
WITH IRRITANT, HEAT, COLD, MICROBIAL AGENT)

PENETRATION THROUGH THE MFOLLICULAR OPENING

ADNEXA ; RUPTURE OF FOLLICLE, GLAND

DERMIS VESSELS (HEMATOGENOUS) : DRUG OR TOXINS;

EMBOLISM ; LEUKOCYTE TRAFFICKING

NERVE MIGRATION FROM GANGLION ALONG SENSORY NERVES

PENETRAION TRAUMA FROM BONE FRACTURE;

SUPPORT INFECTION FROM AJECENT LYMPH NODE, GLAND,
STRUCTURE MUSCLE AND EXTENSIVE O TUMOR
 DEFENSE MECHANISMS AGAINST INJURY

1. PHYSICAL  BARRIER FUNCTION OF EPIDERMIS

- KERATIN INTERCONECTING NETWORK OF KERATINOCYTE;
DESMOSOME

2. IMMUNOLOGIC  INNATE AND ADAPTIVE IMMUNITY

- INNATE : - ANTIMICROBIAL PEPTIDA (DEFENSIN ; CATHELICIDIN)
- NORMAL FLORA OF NON PATHOGENIC BACTERIA
- ADAPTIVE : CYTOKINES ; TNF α ;GROWTH FACTORS

3. REGENERATION AND REPAIR MECHANISM

KERATINOCYTE PLAY A CENTRAL ROLE

 COMMON MANIFESTATIONS OF SKIN DISEASE
CONGENITAL NO INFLAMATORY
1. ALOPECIA OR HEREDITY REACTION

ACQUAIRED INFLAMATORY
REACTION
2. DERMATITIS
INFLAMATORY OF THE SKIN CUASE NUMEROUS
FACTORS

3. PRURITUS
THE UNPLEASENT SENSATION OF IRRITATION WITHIN
THE SKIN PROVIDE DISIRE TO SCRATCH
 DIAGNOSA OF SKIN DISEASES

Depend on :
- Accurate description of the clinical appearance of
the skin at a macroscopic and microscopic level
- Spesific test (exp. Biopsy)
 DEFINITIONS OF MACROSCOPIC TERMS

1. Callus : thick, hard, hairless plaque with increased skin creases.

example : trauma over bony prominence such as elbow or sternum
2. Comedo : plug of stratum cornuem and sebum within the lumen of hair

folikel
ex : canine actinic dermatosis, hiperadrenocorticism
3. Crust : dried exudate on skin surface
ex : chronic state of pustular diseases suchas staphylococal
infection or pemphigus foliceaus
Dermatophytosis. thick, grayish-white crusts on
face and neck.
4. Pustule epidermal
Elevated superficial accumulation of purulent fluid
within the epidermis (arrow).
Example : bacterial infection, pemhigus foliaceus.
5. Cyst : cavity lined by epithelium and filled with liquid or semisolid
material and located in the or subcutis.
Example : follicular cyst, dermoid cyst.
5. Epidermal Collarette
flat to minimally elevating (arrows) of scale that enlarges
peripherally.
example : superficial bacterial infection, insect bite, fungal infection.
6. Erosion : loss of part of the epidermis
depressed, moist, glistening (arrows)
example : secondary to vesicle or pustula rupture or secondary to
surface trauma.
7. Excoration
linear loss of epidermis (arrows)
ex : abrasion or scratch.
8. Fissure
linear crack or break (arrows) from the epidermis to the dermis.
example : footpad fissure seen in pemphigus foliaceus, superficial
necrolytic dermatitis, or digital hyperkeratosis.
9. Lichenification
rough, thickened epidermis secondary to persistent rubbing,
scratching, or irritation.
example : chronic dermatitis.
CAUSE OF
10. Macula
flat, circumscribed area that is a change in the color of the skin, < 1
cm in diameter.
example : hemorrhage, lentigo, vitiligo.
11. Neoplasm
“an abnormal mass of tissue, the growth of which exceeds and is
uncoordinated with that of normal tissue manner after cessation of
the stimuli, which evoked the change” .
Example : lipoma, mast cell tumor, squamous cell carcinoma.
12. Nodule
Elevated , firm, circumscribed lesion 1-2 cm in diameter.
Example : bacterial, parasitic or fungal infection, infectious or sterile
granuloma.
nodule cause by parafilaria bovicola worm on cow that transmitted by
musca genus fliesh bites
Serious bleeding after musca bite became a portal entry of parafilarial worm
13. Papula
Elevated, firm, circumscribed area < 1 cm in diameter (arrows).
Example : insect bite, papilloma, superficial folliculitis,
Small papula as seen on cow demodecosis
14. Plaque
Elevate, firm, lesion with a flat top surface.> 1 cm in diameter.
Example : calcinosis cutis, reactive histiocytosis, eosinophilic
plaque.
16. Scale
Fragmented, keratinized cells, flaky skin, irregular, thick or thin, dry
or oily.
Example : cornification disorders, sebaceous adenitis, ichthyosis.
17. Scar
Thin to thick fibrous tissue that replaces normal skin ollowing injury or
laceration to the dermis.
Examples : healed wound, surgical scar.
18. Ulcer
Loss of epidermis and basement membrane with eposure of dermis.
Example : ischemic lesions resulting from vasculitis, indolent ulcer,
feline herpesvirus infection, feline ulcerative dermatosis syndrome.
 FAECOLITH
An ulceration due to ischemic necrosis following the contraction of dry faeses
on tail

Dry faeses Develop constraction on skin

Resulting of blood vessel constriction ischemic necrosis

19. Vesicle and bulla (larger than vesicle)
Vesicle elevated, circumscribed, fluid-filled lesion < 1 cm in diameter
Example : burn, viral inection, immune mediated diseases such as
bullous pemphigoid.
20.Wheal
Elevated, irregular-shaped area of cutaneous edema, solid, transient
Example : insect bites, allergic reacion.
 CUTANEOUS URTICARIA

Wheal raised on face and soulder of FH cow following

Hipersensitivity reaction
Wheal on face of simental cow due to snake bites or bee sting

Hyperemic muzzle
 HAEMATOMA
Fluctuating fluid-fills swelling due to subcutaneus hemorrhage

Initially soft, painless, cold and appear sunddenly

Common sites are points where bruising of the skin against a bon can occur
e.g. over pelvic prominances, spines, flank, or shoulder

Untreated Hematome resulting on abcess

 LESSION DEFINITIONS
OF MICROSCOPIC TERMS
 DEFINITIONS OF MICROSCOPIC TERMS
Hyperkeratosis : Thickening of the stratum corneum,
often associated with a qualitative abnormality of the
keratin.
Hypergranulosis / Hyperplasia : Hyperplasia of the
stratum granulosum.

Papillated Hyperplasia
(Cotaneus papilloma) on cow
HP appereance : Like-finger Projected of stratum papilare with
colagen core of papillated hyperplasia (arrow)
 PSEUDOCARCINOMATOUS
HYPERPLASIA

HP appereance : elongated epidermis through dermis

layer (arrow); normal thick of stratum corneum,
ETYOLOGI : Chronic injury of skin ; ulcera
Sarcoid : Hyperplasia of the epidermis and dermis
layer
Hydropic swelling (ballooning) : Intracellular edema of
keratinocytes, often seen in viral infections.
Acantholysis : Loss of intercellular connections resulting in
loss of cohesion between keratinocytes.
Papillomatosis : Surface elevation caused by hyperplasia and
enlargement of contiguous dermal papillae

Dyskeratosis : Abnormal keratinization occurring prematurely

within individual cells or groups of cells below the stratum
granulosum

Spongiosis : Intercellular edema of the epidermis.

Parakeratosis : Modes of keratinization characterized by the

retention of the nuclei in the stratum corneum. On mucous
membranes, parakeratosis is normal.
Ulceration : Discontinuity of the skin exhibiting complete loss of
the epidermis and often of portions of the dermis and even
subcutaneous fat.

Lentiginous : Referring to a linear pattern of melanocyte

proliferation within the epidermal basal cell layer. Lentiginous
melanocytic hyperplasia can occur as a reactive
change or as part of a neoplasm of melanocytes
 DEFINITION ON DERMIS AND SUBCUTIS
DISORDER

DERMATITIS : inflamation on dermis layer

FOLLICULITIS : inflamation on hair follicel , Histologically

devide into :
1. Perifoliculitis
2. Mural folliculits
3. Bulbitis
4. Luminal folliculits.
SEBACEOUS ADENITIS : Inflamation on sebacea gland, often
found on dog demodecosis. In chronic
case resulted Hyperkeratosis

PANNICULITIS : Inflamation on subcutaneous lipid tissue

 BULBITIS

- Inflamation on hair pulp (deepest part of hair)

- Causing damaging of hair (Dystropia) and Alopesia
 LUMINAL FOLLICULITIS

Inflamation on wall and lumen of hair, often resulted hair

ruptur (furunculosis)

Causa : Demodex, Stapylococci , dermatophytes ,

Microsporum
SEBACEOUS ADENITIS
 Disorders of Pigmentation
and Melanocytes

Focal or widespread loss of normal protective pigmentation not

only renders individuals extraordinarily vulnerable to the harmful
effects of sunlight (as in albinism), but has also resulted in
severe emotional stress and, in some cultures, profound social
and economic discrimination.
 VITILIGO

Vitiligo is a common disorder characterized by partial or

complete loss of pigment-producing melanocytes within the
epidermis.

Clinical lesions are asymptomatic, flat, well-demarcated

macules and patches of pigment loss; their size varies from
few to many centimeters. Vitiligo often involves the hands;
axillae; and perioral, periorbital, and anogenital skin.

A curious phenomenon called koebnerization often occurs in

vitiligo where lesions develop primarily at sites of repeated
trauma.
Immunochemistry for S-100
protein revealing positively
stained melanocytes within the
basal cell layer of the
epidermis ; these cells are
decreased or absent in vitiligo
Pathogenesis

(1) Autoimmunity
(2) Neurohumoral factors toxic to melanocytes and released by nearby nerve

endings
(3) Self-destruction of melanocytes by toxic intermediates of melanin synthesis.

Most evidence supports autoimmune causation, focusing on the presence of

circulating antibodies against melanocytes and the association of vitiligo with
other autoimmune disorders, such as pernicious anemia and Autoimmune
thyroiditis. Abnormalities in macrophages, and in T lymphocytes suggesting
that
aberrations in cell-mediated immunity may also be operative in the
Pathogenesis of vitiligo.

The impact of therapy with UV light of the A wavelength coupled with use of the
photosensitizing drug, psoralen (a therapy known as PUVA). Suggesting that
melanocyte precursors harbored within the uppermost follicular epithelium are
 Albinism

Albino : loss of the whole body pigmentation

resulted of tyrosine (enzime needed for melanin
production) depletion.

In Albinism melanocyte existed but fail to

produce melanin
 LENTIGO

The term lentigo (plural, lentigines) refers to a common benign localized

hyperplasia of melanocytes occurring at all ages but often in infancy and
childhood.

Cause and pathogenesis are unknown.

These lesions may involve mucous membranes as well as the skin, and
they appear as small (5 to 10 mm across), oval, tanbrown patches and do
not darken when they are exposed to sunlight.
 MELANOCYTIC NEVUS
(PIGMENTED NEVUS/ MOLE)
The term nevus denotes any congenital lesion of the skin (e.g., birthmark).
Melanocytic nevus, however, refers to any congenital or acquired neoplasm
of melanocytes.

In clinical appearance, common acquired melanocytic nevi are tan to brown,

uniformly pigmented, small (usually <6 mm across), solid regions of
relatively flat (macules) to elevated skin (papules) with well-defined,
rounded borders

Morphology. Melanocytic nevi are initially formed by melanocytes that

have been transformed from highly dendritic single cells normally
interspersed among basal keratinocytes to round cells that grow in
aggregates, or "nests," along the dermoepidermal Junction. Nuclei of
nevus cells are uniform and rounded in contour, contain inconspicuous
nucleoli, and show little or no mitotic activity.
nevus cells
Nevocellular nevus
Junctional type

Nevocellular nevus
compound type
 DYSPLASTIC NEVI

Are larger than most acquired nevi (often >5 mm across) and may occur as
hundreds of lesions on the body surface.

Morphology : flat macules, slightly raised plaques with a "pebbly " surface, or
target-like lesions with a darker raised center and irregular flat periphery.
They usually show variability in pigmentation (variegation) and borders that
are irregular in contour. Unlike ordinary moles, dysplastic nevi have a
tendency to occur on non-sun-exposed as well as on sun-exposed body
surfaces.

Dysplastic nevi have been documented in multiple members of families

prone to the development of malignant melanoma
 MALIGNANT MELANOMA
As with epithelial malignant neoplasms of the skin, sunlight appears to play
an important role in the development of skin malignant melanoma.

Lightly pigmented individuals are at higher risk for the development of

melanoma than are darkly pigmented individuals.

Other predisposing factors :

- a pre-existing nevus (e.g., a dysplastic nevus)
- hereditary
- exposure to certain carcinogens
Clinical Features :
- Usually asymptomatic, the majority of lesions are greater than 10 mm
- The most important clinical sign are change in color, size, or shape in a
pigmented lesion.
- Exhibit striking variations in pigmentation, appearing in shades of black,
brown, red, dark blue, and gray
These solar induced squamous cell carcinomas that developed in a beagle dog
living outdoors at high altitude region where The level of UV lights is increased
High-power view of malignant melanoma cells
 ALOPECIA
Alopecia (atrichia) : is partial or complete lack of hairs in areas
Where they are normaly present

Etiology : any diseases that resulted pruritus and pain

or affect hair follicels commonly cause hair loss.
There are two broad etiologic categories of alopecia
: congenital or heredity and acquired

Diseases that can directly cause damage to hair follicel

include :
- Bacterial skin diseases
- Dermatophytosis
- Demodecosis
- Severe inflamatory diseases of dermis,
- Traumatic
- Poisoning (rarely) by mercury, thalium and Iodine
Diseases that can directly inhibit or slow hair follicel growth
include :
- Nutritional deficiencies (particurarly : protein dificiencies)
- Hypotyroidsm
- Hyperadrenocortism
- Excessive estrogen production or Administration

Temporary alopecia can occour in horse, sheep and dog when

pregnancy, lactation or, several weeks after severe illness or fever
 Alopesia cause of Hormone

hypothyroidsm

Cushing's diseases
 DISEASES OF THE SKIN

CONGENITAL AND HEREDITARY DISORDER

ALLERGIC SKIN DISEASES
DISORDERS OF PIGMENTATION AND MELANOCYTES

BACTERIAL SKIN DISEASES

VIRAL SKIN DISEASES

FUNGAL SKIN DISEASES

PARASITIC SKIN DISEASES

NEOPLASTIC SKIN DISEASES

 I. CONGENITAL AND HEREDITARY DISORDER

1. CONGENITAL ALOPECIA AND HYPOTRICHOSIS

- Hyphotrichosis is : amount of hair less than normal

In some animal this condition often allowed the defect of other
body system, exp. brachygnathism (smallness of mandibula),
genital abnormalities, or dental growht abnormalities)
-Deferrential diagnose : follicular dysplasia (never allowed with
other organ abnormalities and it detect years after birth)
Congenital hypotrichosis with anodontia
 No hair folicel present at dermis

Animal with hypotrichosis are suspectable to extreme of

temperatures and infection due to the lack of hair coat
2. COLLAGEN DYSPLACIA (HYPERELASTOSIS)

- Cause : defects of ezymes that sythesis of collagen

- clinical sign : hyperextensible of skin
- histologiclly : abnormal stucture of dermal
- often occur in dog

-Clinical manifestation :
- skin tend to wound even
handle normally
3. EPITHELIOGENESIS INPERFECTA (APLACIA CUTIS)

- Result from the failure of the stratified squamous epithelium

of skin, adnexa, to developed completely
- Cause genetic defect
- affected skin easily traumatized and infected
- Lesions are located most often on the face, extrimities,
and mocous membrane
AFFECTED SKIN GROSSLY RED AND MOIST (ARROW)

EPITHELIOGENESIS INPERFECTA (APLACIA CUTIS) ON CALF

 NORMAL

AFFECTED SKIN

HISTOLOGICALLY OF EPITHELIOGENESIS INPERFECTA

 II. ALLERGIC SKIN DISEASES

1. ATOPIC DERMATITIS (ALLERGIC INHALANT DERMATITIS)

- Tipe I hypersensitivity and affected more than 10% of domestic dog

- Etiology : allergens from environment enter via inhalasi, GI tract or skin
evoke allergan-specifig IgE production
-Strong breed such as Golden Retrievers often more sensitive
- Predominat clinical sign : pruritus (dog affected manifest by face rubbing
and food licking) and in feline pruritus on face and general allowed with
allopecia
Lession : excoriation, eritrema, and alopecia
2. FLE and MOSQUITO BITE HYPERSENSITIVITY

- The most most common hypersensitivity dermatitis on dog and cat

- It is mediated by Tipe I and IV hypersensitivity reaction
- Cutaneous lession cause fle bite occur on along dosal lumbosacral
area, ventral abdomen, caudomedial, flank, and neck
- Gross : papular dermatitis with excoriation and in chronic lession
include licheification, alopic nodules.
- Mosquito bite commonlly occur in cat (Tipe I) and cause lession
primary on nose, periocular, nasal planum
- Lession due to mosquito bite begin as erythrematous papula and
progress to crust, erosion, ulcers, and alopecia
3. PEMPHIGUS FOLIACEUS

- Pemphigus is a group of diseases that clinically characterized

by transient vesicles or bullae and histologically by acantholysis
- between keratocyte of dermis, cause of immune-mediated injury or
with neutrophylic enzymatic destruction
- PEMPHIGUS FOLIACEUS Is the most common of pemphigus in
domestic animals include : dog, cat, hores and goat
- Result as adverse reaction to drug therapy
-Lession : transient vesicles that rapidly become pustules
- location of lession : spesific on nose; periocular, foodpat, clawbed
 PARASITIC SKIN DISEASES
1. MANGE IN DOGS ( CANINE DEMODECOSIS) :
Etilogy : Demodex canis
In small numbers this mites are part of the normal flora of the dog
Demodecosis also occur on bovine, goat, sheep, horse, and cat

Clinical sign occurs when large number of mites inhabit hair follicels,
sebaceous gland or apocrine sweat gland, include : alopecia, papula,
pustula, and crusting

Lession are ussualy agravated by secondary bacterial infection

Lession in bovine particularly found at neck, back, flank and absent of
pruritus

There are two clinical form :

a. Localized (occur in < 1 years old dog) 90% resolve spontaneusly
b. Generalized
Demodex canis
In follicular luminal

Limfocyte infiltration
In perifollicular of
Hair
 SCABIES
Kausa : Sarcoptes Scabies

Sangat contagious, ektoparasit yang penting pada :

babi , anjing.kucing,kuda,sapi,kambing.
.
Parasit : bersembunyi dalam liang ( tunnel )
pada st. corneum epidermis → sangat gatal.
Lesi dimulai pada telinga luar, kepala , wajah → merata seluruh tubuh

Mikros : disekitar parasit banyak sel eosinofil, limfosit

dan spongiois ringan → kerak.

Kronis : Acantolisis, hyperkeratosis, parakeratosis

 Gejala klinis

1. Pruritus nokturna (gatal malam hari )

akibat udara lembab dan parasit aktif.
2. Ada kunikulus (saluran ) panjang 1cm ,putih
keabuan berisi prsit , ujungnya ada papula
/vesikula.
3. Infeksi sekunder staphylococcus albus terjadi
Pustula
Early state of ring worm showed alopecia and eritrema
SWINE POX
Kausa :pox virus.
Infeksi bisa kontak atau
transplacental.
Lokasi : lateral dan ventral
abdomen. Bentuk lesi :
erythematous ;papula.bisa
menginfeksi umbilicus
(Pusar ) menimbulkan
pustula Umbilikus.
Mikroskopis :
Balloning degenerasi dan
inclusion bodies eosinophilic
cytoplasma
Terima kasih