PBL GROUP REPORT

"WHITE SPOTS"
TROPICAL INFECTION BLOCK

Tutor : dr. Zulfahmidah

ARRANGED BY:
Group 14

Eka Dewi Mulyani 11020160003

M. Arif Munandar K 11020160030
Zulfikar Anand Pratama 11020160034
Suci Ramadhani 11020160083
Muh. Agung Gunadi 11020160096
Ratu Sri Bestari 11020160104
Rahmawaty Kurnia Putri 11020160111
Gita Ananda Pratiwi 11020160117
Hartina Burhan 11020160155
Firmawati AR 11020160171

MEDICAL FACULTY
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2018
A. SCENARIO

A 32 years old man came to the Puskesmas with complaints of white spots in thigh fold area,
uneven in shape with mild itching. Small round patches of 1-3 cm in diameter accompanied by
smooth scale since 2 weeks ago. This white spots is surrounded by red spots, but the middle part
of the skin lesion looks calm and smooth scales.

B. CLARIFICATION OF KEYWORDS
Keywords :
1. A 32 years old man
2. Complaints of white spots in thigh fold area
3. Uneven in shape, mild itching
4. Small round patches of 1-3 cm, smooth scale since 2 weeks ago.
5. White spots is surrounded by red spots
6. The middle part of the skin is calm and smooth scales.

C. IDENTIFICATION OF PROBLEMS
Question
1. Explain the kinds of tropical diseases with complains of white spots !
2. Explain the pathomechanism of itching, white spots, and squama !
3. Explain the etiology of the white spots !
4. How to diagnose based on scenario ?
5. Mention the differential diagnosis according to the scenario!
6. Islamic perspective according to the scenario!
D. ANSWER QUESTION
1. Explain the kinds of tropical diseases with complains of white spots !
Answer :
a. Tinea Versocolor or tinea versicolor
Pitiriasis versicolor is a mild chronic superficial fungal infection caused by malassezia
fungus with clinical features or Confluent, body parts, often found in the armpit, between thighs,
upper limbs, neck, face and scalp.
b.Vitiligo
Vitiligo is a loss of pigment obtained and established by histology where it is found that
there is no epidermal melanocytes. Vitiligo is an idiopathic hypomelanosis that is acquired by the
presence of clinical symptoms in the form of white macules which can be widespread and can
affect all parts of the body containing melanocyte cells, such as hair and eyes.
c. Ptyriasis alba
Pityriasis alba is often found in children aged 3-16 years, many women and men. Lesions
are oval and round. At first the lesion is pink or in accordance with the color of the skin with a
fine scale on it. After the erythema disappears the lesions that are found are only hypopigmented
with a fine squamous. Lesions can be found in the extremities and body. Lesions are generally
asymptomatic but can also be itchy and hot.
d.Morphea
Rare skin conditions that cause white spots or spots on the skin without pain. Usually,
these skin changes appear on the abdomen, chest, or back. But it can also occur on the face,
arms, or legs. This skin disorder has a connection with genetic and environmental factors.
Morphea is associated with increased collagen and also the extracellular matrix of the dermis
layer of the skin. Morphea is more common in women and people with white skin.
e. Leprosy / Morbus Hansen
The characteristics are macula hypostesia, alopecia, anhidrosis and atrophy. Lesions can
be one or many, with strict limits with varying sizes. There is thickening of the peripheral nerves.
This disorder occurs because of decreased activity of melanocytes.

Reference : Menaldi SL, Bramono K, Indriatmi W, editor. Ilmu Penyakit Kulit dan Kelamin.
Edisi ke Jakarta: Badan Penerbit FKUI; 2015
2. Explain the pathomechanism of itching, white spots, and squama !
Answer :
ANATOMY AND HISTOLOGY

Figure 1 : Anatomy of the skin Figure 2 : Histology of the skin

The distribution of skin is broadly composed of three main layers, namely : Epidermis layer,
dermis apical, and subcutaneous layer.
a) Epidermal layer
 The stratum corneum (horn layer) is the outermost layer of the skin and consists of dead,
nucleated, and keratin cells.
 Stratum lusidum is a layer of nucleus flat cells with protoplasm which has become a
protein called eleidine. The layer is more pronounced in the palms and feet.
 Stratum granulosum (keratohialin layer), which is two or three layers of sprawl cells with
coarse and nucleated grain cytoplasm. These coarse grains consist of keratohialin. The
mucosa usually does not have this layer. Stratum granulosum is also evident in the palms
and feet.
 Stratum spinosum (Malphigi strata) consists of several layers of cells that are polygonal
in shape with different magnitudes due to the mitotic process. Among the cells of the
stratum spinosum are intercelullar bridges consisting of protoplasm and tonofibril or
keratin. Between cells spinosum cells also have Langerhans cells.
  Stratum basale is formed by cube (columnar) cells arranged vertically and lined up like a
fence (palisade).
b) The dermis layer
This layer is under the epidermis layer and thicker than the epidermal layer. This layer
consists of elastic and fibrous layers dense with cellular elements and hair follicles. Broadly
divided into two parts, namely:
 Pars papillare, which is the part that protrudes into the epidermis which contains the ends
of nerve fibers and blood vessels.
 Pars retikulare, which is the part that protrudes into the subcutaneous direction which
contains supporting fibers for example: collagen fibers, elastin, and reticuline.
c) Subcutting layer
This layer is a continuation of the dermis consisting of loose connective tissue containing
fat cells. The layer of fat cells is called paniculus adipose which functions as a food reserve.
In this layer there are peripheral nerve endings, blood vessels, and lymph.

Adnexa of the skin consists of glands of the skin, hair, and nails.
a) The skin glands in the dermis layer consist of :
 Sweat glands (sudorifera glands) there are two types, namely the small eccrine gland
located superficially in the dermis with dilute secretions and the larger apocrine glands
located deeper with a thicker secretion. The eccrine gland has been perfectly formed at
28 weeks of gestation and is only functioning 40 weeks after birth. The channel of this
gland is spiral and empties directly on the surface of the skin. Found throughout the
palms and feet, forehead and axilla. Secretion depends on several factors and is
influenced by cholinergic nerves, heat factors, and emotional stress. The apocrine gland
is affected by adrenergic nerves, found in axillae, areolamame, pubis, labia minora, and
outer ear canal. Sweat contains water, electrolytes, lactic acid, and glucose, usually PH
around 4-6.
 It Palate glands (sebaceous glands) are located on the entire surface of the human skin
except the palms and feet. This gland is also called the holocrine gland because it does
not have dust and the secretion comes from the decomposition of glandular cells. Paly
 glands are usually located next to the root of the hair and the mouth is on the root lumen
of the hair (hair follicles)
b) Nails are the terminal part of the horn layer (stratum corneum) which thickens. The part of
the nail that is immersed in the skin of the finger is called the nail root, the part that opens on
the base of the soft tissue of the skin at the tip of the finger is called the nail plate, and the
end is the free part of the nail. Nails grow at around 1mm per week. The side of the nail is
slightly bent to form the nail groove (up the grove). The thin skin covering the nails in the
proximal part is called the eponikium while the skin covered with the free part of the nail is
called hyponikium.
c) Hair has a part that is immersed in the skin (hair roots) and parts that are outside the skin
(hair shaft). There are two types of hair, namely Lanugo is fine pigmented hair in infants and
the terminal is hair that is coarser with lots of pigments and has a medulla in adults. Hair
grows cyclic, the anagen phase (growth) lasts 2-6 years with a speed of about 0.35 mm per
day. The telogen phase (rest) lasts several months. Between these two phases there is a
catagen phase. In adult humans besides hair on the head, there are also lashes, armpit hair,
pubic hair, mustache, and beard whose growth is influenced by sex hormones (androgens).

SKIN PHYSIOLOGY
1. Protection function
The skin keeps the inside of the body against physical or mechanical disturbances, such
as pressure, friction, pulling, chemical disturbances, for example chemicals, especially those
that are irritants, for example lysol, carbolic acid, other strong acids and alkalis, heat
disturbances such as radiation, stings ultra violet rays, disorders of external infections,
especially germs / bacteria and fungi.
The above is made possible due to the presence of fat pads, the thickness of the skin layer
and supporting tissue fibers which act as a protector against physical disturbances.
Melanocytes play a role in protecting the skin against exposure to sunlight by holding
tanning. Chemical stimulation protection can occur because of the impermeable nature of
the stratum corneum to various chemicals and water, besides that there is a layer of skin
acidity that protects chemical contact with skin. The acidity of this skin may be formed from
the excretion of sweat and sebum, the acidity of the skin causes the pH of the skin to range
 at PH 5-6,5 so that it is a chemical protection against bacterial and fungal infections. The
creatinization process also acts as a mechanical barrier because dead cells disengage
regularly.
2. Absorption Function
Healthy skin is not easy to absorb water, solution and solid objects, but volatile liquids
are more easily absorbed, as well as fat soluble. Skin permeability of O2, CO2 and water
vapor allows the skin to take part in the function of respiration. The ability of skin
absorption is influenced by the thickness of the skin, moisture hydration, metabolism and
type of vehicle. Absorption can take place through the gap between cells, penetrating
epidermal cells or through the mouth of the gland, but more through the cells of the
epidermis than through the mouth of the gland.
3. Excretion Function
The skin glands secrete useless substances or metabolic waste in the body in the form of
Nacl, urea, uric acid and ammonia. Fat glands in the fetus under the influence of androgen
hormones from their mothers produce sebum to protect their skin against ammonion fluid, at
birth they are found as vernixcaseosa. Sebum produced protects the skin because this sebum
layer besides oiling the skin also prevents excessive water evaporation so the skin does not
dry out. Fat glands and sweat products cause skin acidity at PH 5-6,5.
4. Perception Function
The skin contains dermal and subcutaneous sensory nerve endings. The heat stimulation
is played by ruffini bodies in the dermis and subcutaneously. The cold is played by krause
bodies located in the dermis. The meisner tactile body located in the dremic papilla acts on
palpation, as well as the body of mercury ranvier located in the epidermis. While the
pressure is played by the body paccini in the epidermis. Sensory nerves are more numerous
in erotic areas.
5. Body Temperature Setting Function (Thermoregulation)
The skin performs this role in a way to sweat and contract (the muscles contract) the
blood vessels of the skin. The skin is rich in blood vessels so that it can get good nutrition.
Vascular tonsus is affected by the sympathetic nerve (acetylcholine). In infants, blood vessel
walls are not yet fully formed, resulting in fluid extravasation, so baby's skin looks more
edematous because it contains more water and Na.
6. Pigment Formation Function
Cells of pigment formation (melanocytes), located in the basal layer and these cells come
from nerve rigi. Comparison of the number of melanocyte basal cells is 10: 1. The number
of melanocytes and the amount and magnitude of the pigment granules (melanosomes)
determine the race's skin color as well as individuals. This cell is clear in shape round and is
a dendritic cell, also called clear cell. Melanosomes are formed by the golgi with the help of
tyrosinase, cu and O2 enzymes. Exposure to sunlight affects the production of melanosomes.
Pigments are spread to the epidermis through the hands of dendrites while the skin layer
below is carried by melanofag cells (melanofor). Skin color is not entirely affected by skin
pigments, but also by the thin skin thickness, Hb reduction, and carotene.
7. Keratinization Function
The adult epidermal layer has 3 main cell types namely keratinocytes, langerhans cells,
melanocytes. Keratinocytes starting from basal cells make division, the other basal cells will
move up and change shape to spinosum cells, the more up the cell becomes more flat and
granules into granulosum cells. The longer it disappears and the keratinocytes become
amorphous horn cells. This process continues for life, and until now it has not been fully
understood. Maltosy argues that keratinocytes may go through the process of synthesis and
degradation into a horn layer. This process lasts normally for about 14-21 days, and protects
the skin from infection mechanically physiologically.
8. Formation Function Vit D
It is possible to change 7 hydroxy cholesterol with sunlight. But the body's need for
vitamin D is not enough just from that, so the provision of systemic vitamin D vitamin is
still needed.

PATHOMECHANISM OF ITCHING
Fungus is one of the causes of itching. This causative agent produces enzymatic
keratinases, which justify invasion of the epidermal horn cell layer. The body's immune response
will hinder deeper invasions. Causes prey to feel itchy or slightly hot in the area due to
inflammation and irritation. The risk factor for early infection or recurrence is to wear tight or
wet clothing. Excessive sweat in certain areas. The method of transmission of fungi can be
directly or indirectly. Direct transmission can be fomites, epithelium, fungal-containing hair from
humans, animals, or soil. Indirect transmission can be through plants, wood plagued with fungi,
dust clothes. The causative agent can also be transmitted through contamination with clothing,
towels or sufferers or autoinoculation bed sheets from tinea pedis, tinea unguium, and tinea
manuum. This fungus produces keratinase which digests keratin, so it can facilitate invasion of
the stratum corneum. The infection begins with colonization of the hyphae or branches in the
dead keratin tissue. These hyphae produce keratolytic enzymes that diffuse into epidermal tissue
and cause an inflammatory reaction. Its growth with a radial pattern in the stratum corneum
causes the appearance of skin lesions with clear and elevated boundaries (ringworm). The initial
skin reaction is in the form of papules which develop into an inflammatory reaction.

PATHOMECHANISM OF WHITE SPOT

White spot abnormalities in the skin are a decrease in melanin or the absence of melanin
from melanocytes. Broadly speaking, white spot abnormalities in the skin are divided into two,
namely the absence or decreased number of melanocytes. There is no or decrease in melanin
production, but the normal amount of melanocytes. Other conditions such as adding tyrosinase
enzyme inhibitors can also reduce melanin production. There are several factors that affect the
production of melanin which causes general skin discoloration. These factors include the
following.
1. Trauma
2. Inflammation
3. Poor physiological conditions
 4. Autoimmunity
5. Neurohormonal
6. infections of microorganisms
7. Environmental factors (such as misuse of cosmetics)

inhibit the reduce the

action of the hypopigmen
production
tyrosinase tation
enzyme of melanin
trigger
factors
lesions that the tyrosinase
cover the enzyme to melanin to hypopigmen
surface of remain in an not form tation
the skin inactive state

Various conditions above can lead to hypopigmentation. The mechanism of action can be
divided into two processes. First, the presence of trigger factors will inhibit the action of the
tyrosinase enzyme. This tyrosinase enzyme plays an important role in melanocyte cell melanin
synthesis. This situation will then reduce the production of melanin so that the amount decreases
and causes hypopigmentation. Second, when there are trigger factors that cause lesions that
cover the surface of the skin which causes the tyrosinase enzyme to remain in an inactive state
causing melanin to not form so that hypopigmentation occurs

PATHOMECHANISM SQUAMA
Living cells in the basal stratum. Then it moves upward (the stratum corneum) into dead cells
that are complete keratin. In the stratum corneum the horn cells produce keratocytes called
keratinization. But because of an inflammatory process that causes the process of keratinization
to be disrupted. Horn cells that have died have accumulated and then cause a squamous
formation on the skin.
 there is an the process of squamous
dead horn cells
inflammatory keratinization to formation on the
accumulate
reaction be disrupted skin

Reference :
1. Junqueira LC, Carneiro J. Histologi Dasar Teks & Atlas. 10th ed. Jakarta: EGC; 2007.
2. Tortora G, Derrickson B. Principles of Anatomy and Physiology. 11th ed. USA: John Wiley
& Sons Inc; 2006. p. 145-70
3. Djaenudin Natadisastra dr.Sp.Park. Parasitologi Kedokteran Ditinjau dari Organ Tubuh yang
Diserang. Penerbit Buku Kedokteran EGC. Jakarta. 2009. hlm 274-276
4. Tabri, Farida, dkk. 2016. Tatalaksana Bercak Putih pada Kulit Anak. Makassar.
5. Champion RH. Eksim, lumensifikasi, Prurigo, dan Ertroderma. Di:Champion RH
eds. Rook's, buku teks dermatologi, Washington;Publikasi Ilmiah Blackwell.

3. Explain the etiology of the white spots !

Answer :
Etiology of white spots

The cause of white spots on the skin can differ depending on the organism that causes it, for
example because there are bacterial and fungal infections.

1. Fungi
Some fungi, both dermatophytes and nondermatophytes, can cause white patches on the skin.
Nondermatophytic fungi such as Malassezia furfur, which with indirect morphological and
immunophlorency examination were found to be identical to Pityrosporum orbiculare. This
fungus can cause Pityriasis versicolor disease which is characterized by white and itchy patches,
higher (50%) in tropical regions with warm and humid temperatures. Factors that can trigger
abnormal growth of M.furfur include exogenous factors including heat and humidity. This is the
cause so many pitiriasis versicolor are found in the tropics and in the same season in the
subtropical regions. Other exogenous factors are skin closure by clothing and cosmetics.
Endogenous factors include malnutrition, seborrheic dermatitis, chusing syndrome,
immunospatial therapy, hyperhidrosis and a positive family history.

2. Bacterial Infection
The growth and development of bacteria is influenced by three factors: (1) port the entry and
skin defense function, (2) host defense and inflammatory response to microbial invasion, (3) and
pathogenic substances produced by bacteria. Basically, bacteria cannot penetrate the keratin
layer on normal skin. If maceration and occlusion occur, it can cause an increase in PH, high
carbon dioxide, and fluids in the epidermis, causing an increase in normal bacteria on the skin.
Gram negative bacteria can be found in several places on the skin, where dry skin that tends to
normal skin limits the growth of these bacteria, especially gram-negative bacilli bacteria.

In gram-positive bacteria such as some groups of Streptococcus and M. leprae are bacteria
that generally are not included in the normal flora of the skin. Streptococcus group bacteria can
invade the skin and are thought to cause Pityriasis alba disease, where the disease is
characterized by erythema in the skin which then disappears and causes depigmentation (white
spots). While M. leprae bacteria are gram-positive bacteria that can cause leprosy. Symptoms
vary depending on the type.

Reference : Menaldi SL, Bramono K, Indriatmi W, editor. Ilmu Penyakit Kulit dan Kelamin.
Edisi ke Jakarta: Badan Penerbit FKUI; 2015.

4. How to diagnose based on scenario ?

Answer :
a. General history

According to the patient's personal data: name, age, address and occupation. Ask what
causes the patient to come to the doctor (main complaint)

b. Guided Name

 Ask when the skin disorder begins to appear. Digging deeper into the onset, the duration
of the abnormality, whether it arose or settled, how the initial lesion was described,
 where it was originally located, how the lesions were developing and the distribution of
the lesions later.

 Ask whether there is a burning sensation in the lesion or not, is there a fever or not.

 Ask whether it is accompanied by itching or not

 Ask whether this skin disorder has anything to do with work before

 Ask if there are other complaints felt by the patient. If there is ask: When it starts
happening, does it happen suddenly or not. Do appear together or after.

 Ask whether the patient has experienced the same complaint in the past.

 Ask about the contact history with patients with the same symptoms, history of contact
with insects or plants.

 Asking for a history of medication that has been received from a doctor and a drug
purchased by a patient without a doctor's prescription

 Ask about socio-economic family, number of family members, way of life, and illness in
the family or in individuals around them.

 Inquire whether the occurrence of a disease is related to a cause, for example due to
work, injuries due to certain objects, relationships with seasons, or a result of a factor in
the environment.

Physical examination

Inspect and palpate existing lesions or skin abnormalities (using a magnifying glass). Pay
attention to its efficiency.

1. Location and / or distribution of existing abnormalities

2. Individual lesion characteristics:

 Characteristics of lesions: macules, papules, nodules, plaques, vesicles, bulls, pustules,

ulcers, urticaria.
 Surface characteristics of lesions: squamous, crusting, hyperkeratosis, eschoriation,
maceration and lichenification
  Size, shape, edges and boundaries. Size should be measured precisely, rather than just
comparing it with peas, oranges or coins. Lesions can have various forms, for example
round, oval, anular, linear or "irregular"; straight or angled edges may be caused by
external factors.
 Color, there is always the benefit of making notes about colors: red, purple, brown, solid
black and so on
 Surface Depiction. Browse whether the surface of the lesion is smooth or rough, and to
distinguish crusting (serum that dries) from squamous (hyperkeratosis); some searches on
the screen can help, for example there is silvery color of padapsoriasis.
 Teksture. Shallow, deep. Use fingertips on the surface of the skin; estimate the depth and
location whether inside or under the skin; lift scales or crusts to see what's under it; try to
make the lesion paler with pressure.

3. Examination of "secondary" locations

Look for abnormalities in other places that can help the diagnosis. For example:

 Finger and wrists on scabies

 Side between toes in fungal infections
 Mouth on lichen planus

4. "Special" examination techniques

Special technical techniques are needed in conducting skin checks such as skin scrapings
with Potassium Hydroxide to check for hyphae and spores for examination of fungi on the skin.

Supporting Examination

1. Examination with Wood Lamp

Which is a ray with a wavelength of 320-400 nm (365 nm) (colored purple). This
examination is to determine the fluorescence of various pathogenic germs, such as in infections:
Malassezia furfur (golden yellow to orange), P. ovale (greenish yellow), erythrasma: C.
minutissimun (reddish yellow). This examination is also to find out the depth of pigmentation in
melasma, if the irradiation with the lights of Woods the pigmentation limit looks clearer than
direct examination, shows epidermal pigmentation, and vice versa in dermal pigmentation, the
results of Wood's lamp examination will appear blurred.

2. Examination of blood, urine, or routine stool, blood chemistry (liver function, kidney function,
blood glucose), serology (herpes simplex infection, syphilis, HIV), molecular biology (PCR
(polymerazed chain reaction) skin tuberculosis DNA).

3. Skin biopsy to find out the type or process of disease pathology.

Reference : Menaldi SL, Bramono K, Indriatmi W, editor. Skin and Venereal Diseases. Edition
to Jakarta: FKUI Publishing Agency; 2015 Langkah-Langkah Diagnosis Bercak Putih pada Kulit

5. Mention the differential diagnosis according to the scenario!

Answer :
A. Tinea Cruris
Tinea kruris is superficial mycosis or also called Eczema marginatum, Dobie itch, Jockey
itch, Ringworm of the groin, which belongs to the group of dermatophytosis in the groin,
perineal area, and around the anus. This disorder can be acute or chronic, it can even be a disease
that lasts a lifetime. Tinea kruris is superficial mycosis or also called Eczema marginatum, Dobie
itch, Jockey itch, Ringworm of the groin.15 which belongs to the group of dermatophytosis in
the groin, perineal area, and around the anus. This disorder can be acute or chronic, it can even
be a disease that lasts a lifetime.

Tinea cruris is dermatophytosis in the thighs, genitalia, pubic region, perineum and
perianal. Trichophyton rubrum (T. Rubrum) is the main cause, followed by Trichophyton
mentagrophytes and Epidermophyton floccosum (E. Floccosum). Trichophyton rubrum,
Trichophyton mentagrophytes and Epidermophyon floccosum are dermatophytes that like warm
and moist areas of intertriginous and occlusive skin like thigh interrupts.

Skin disorders that appear between the thighs are well-defined lesions. Inflammation on
the edges is more pronounced than the middle part. Eflorescence consists of various forms of
primary and secondary (polymorphy). If the disease becomes chronic, it can be a black spot with
a few scales. Erosion and discharge are usually due to scratching
Epidemiology

Tinea cruris can be found throughout the world and most in the tropics. The incidence is
more common in adults, especially men than women. This fungus often occurs in people who
pay less attention to cleanliness or dirty and humid surroundings.

In Indonesia, dermatophytosis is 52% of all dermatomycosis and tinea cruris and tinea
corporis is the most dermatophytosis. The incidence of dermatomycosis in various medical
teaching hospitals in Indonesia which shows the percentage of all cases of dermatophytosis
varies from 2.93% (Semarang) to the lowest to 27 , 6% (Padang) the highest. Men after puberty
are more affected than women, usually regarding ages 18-25 years and 40-50 years.

Etiology

The main causes of tinea cruris are Epidermophyton floccosum and Trichophyton
rubrum. In addition it can also be caused by Trichophyton mentagrophytes and although it is
rarely caused by microsporum gallinae.

Factors that influence the occurrence of tinea cruris

The factors that influence the occurrence of this fungal infection are hot, humid climate,
sanitary hygiene, nylon clothing, excessive sweating, skin trauma, and the environment.
Maseration and occlusiveness in the cruric region contributes to the condition of moisture which
causes the development of fungal infections. Tinea cruris is highly contagious and minor
epidemics can occur in schools and other similar communities. Tinea cruris generally results
from other dermatophytosis infections in the same individual through direct contact with the
patient such as shaking hands, sleeping together, and sexual intercourse. But it can also be
through indirect contact. through contaminated objects, "clothes, towels, bed linen, pillows, etc.".

Pathogenesis

Tinea kruris usually occurs after contact with an infected individual or animal. Spread
may also occur through objects such as clothing, furniture, and so on. Tinea kruris generally
occurs in men. Maseration and occlusion of the groin skin increases the temperature and
humidity of the skin, making it easier for infection, but it can also occur due to the spread of
infection from other body parts. Dermatophytes have an incubation period of 4-10 days.
Dermatophyte infections involve three main steps: attachment to keratinocytes, penetration
through and between cells, and development of host responses.

a. The attachment of the superficial fungus must pass through various obstacles to be attached to
the keratin tissue including UV light, temperature, humidity, competition with normal flora and
sphingosin produced by keratinocytes. Fatty acids produced by the sebaceous glands are also
fungistatic.

b. Penetration. After attachment, the spores must develop and penetrate the stratum corneum at a
speed faster than the desquamation process. Penetration is also aided by the secretion of
proteinases, lipases and mucinolytic enzymes, which also provide nutrients for fungi. Trauma
and maceration also help fungal penetration into keratinocytes. A new defense arises when the
fungus reaches the deepest layer of the epidermis.

c. Development of host response. The degree of inflammation is influenced by the immune status
of the patient and the organisms involved. Type IV hypersensitivity reactions, or Delayed Type
Hypersensitivity (DHT) play a very important role in fighting dermatophytes. Patients who have
never been infected with a dermatophyte before, Primary infection causes inflammation and the
trichopitin test results are negative. The infection produces a small amount of erythema and
squamous resulting from an increase in changes in keratinocytes. There is a hypothesis that the
dermatophyte antigen is processed by Langerhans epidermal cells and is expressed in T
lymphocytes in the lymph nodes. T lymphocytes proliferate and migrate to the infected site to
attack the fungus. At present, the lesion suddenly becomes inflamed, and the epidermal barrier
becomes permeable to transferrin and migrating cells. Immediately the fungus disappears and the
lesion spontaneously heals.
Clinical features

Patients feel itchy and abnormalities of lesions in the form of a firm bounded placard
consist of various skin efflorescence (polymorphic). This diverse form of lesion can be a little
hyperpigmentation and a chronic squeeze. The abnormalities seen in the clinic are round or oval
lesions, well-defined, consisting of erythema, squamous, sometimes with vesicles and papules on
the edge of the lesion. The area in the center is usually quieter, while the one at the edge is more
active which is often called central healing. Sometimes erosion and crusting are seen due to
scratching. Skin disorders can also be seen polycyclic, because some skin lesions become one.
Lesions can expand and provide a picture that is not typical especially in immunodeficient
patients.

Diagnosis

The diagnosis is based on clinical features, namely the presence of skin abnormalities in
the form of well-defined lesions and inflammation where the edges are more pronounced than
the middle part. Mycological examination found fungal elements in microscopic examination of
skin scrapings directly using 10-20% KOH solution. KOH examination is most easily obtained
by sampling from the lesion boundary. The positive 10% KOH microscopic examination results,
namely the presence of fungal elements in the form of branching and or arthrospores.
Mycological examination to get mushrooms requires clinical ingredients, which can be scrapings
of skin, hair, and nails.
Histophatology

Figure 3 : Histophatology of Tinea Cruris

Management

Management of tinea cruris can be divided into two: hygiene sanitation and
pharmacological therapy. Through hygiene sanitation, tinea cruris can be avoided by preventing
risk factors such as used underwear, it can absorb sweat and be replaced every day. Groin or
groin area must be clean and dry. Avoid wearing narrow and tight pants, especially those that are
used for a long time. Keeping the groin area or groin dry and not moist is one of the factors that
prevent infection in tinea cruris.

Nowadays, Dermatophytis in general can be overcome by giving fungistatic griseofulvin.

The griseofulvin treatment dosage chart is different. In general, griseofulvin in the fineparticle
form can be given with a dose of 0.5-1 g for adults and 0.25-0.5 g for children a day or 10-25 mg
per kg body weight. Duration of treatment depends on the location of the disease and the
condition of the patient's immunity.

Side effects of griseofulvin are rarely encountered, which is a major complaint is

cephalgia found in 15% of patients. Other side effects can be digestive tract disorders such as
nausea, vomitus, and diarrhea. The drug is also photosensitive and can interfere with liver
function.
a. Topical: antimicotic ointment or cream. The location of this location is very sensitive, so the
drug concentration must be lower than other locations, such as salicylic acid, benzoic acid, sulfur
and so on.

b. Systemic: given if the lesion is widespread and chronic; griseofulvin 500-1,000 mg for 2-3
weeks or ketoconazole100 mg / day for 1 month.

Complications

Tinea cruris can be secondary to other candida or bacteria. In chronic fungal infections
lichenification and skin hyperpigmentation can occur.

Prognosis

The prognosis of this disease is good with the right diagnosis and therapy as long as the
moisture and cleanliness of the skin are always maintained.

B. Pitiriasis Versicolor

Definition

Pitiriasis versicolor is a mild chronic superficial fungal infection caused by malassezia

fungus with discrete or Confluent clinical features. Has scaly, colorless or non-pigmented
features and without inflammation. Pitiriasis versicolor is most dominant about the upper body,
but often found in the armpit, between thighs, upper limbs, neck, face and scalp.

Epidemology

Pitiriasis versicolor is the most common superficial fungal infection. The prevalence of
pitiriasis versicolor in the United States is estimated at 2-8% of all residents. The prevalence of
pitiriasis versicolor is higher in the tropics with hot temperatures and relative humidity. In the
world the prevalence of pitiriasis versicolor reaches 50% in hot and humid areas and 1.1% in
cold areas. This disease is often found at the age of 13-24 years. In Indonesia this disease is often
called phlegm and the incidence in Indonesia is unknown but in Asia and Australia a general trial
was carried out in 2008 which was a high number because of the climate in Asia.
Etiology

There are several normal flora in the skin including lopopilic fungi. It can be a single
polymorphic species such as Pityrosporum ovale or Pityrosporum oblicular, but it is now
recognized that the genus name is invalid, and this fungus has been reclassified in the genus
Malassezia as a single species, Malassezia furfur. However, genetic analysis demonstrates that it
is now far more complex. At present there are at least 12 separate species of lophilic mushrooms
that can be explained, and only 8 can infect human skin. Species dependent on fat are M.
sympodialis, M. globosa, M. restricta, M. slooffiae, M. fufur, M. obtusa, and most recently found
M. dermatis, M. japonica, M. yamotoensis, M. nana, M. carpae, and M. equina. There is a
lipophilic one that is not completely dependent on fat, M. pachydermatis is often found in animal
skin. What we previously knew as M. fufur actually consisted of several species.

Figure 4. Malassezia furfur Figure 5. Colony of Malassezia furfur

Some studies on normal skin and skin with lesions, especially those suspected of
malassezia, have been tested using microscopy and culture, because of the different sampling
techniques that very little can be compared. Some researchers found that M. globosa was the
species most often found in pitiriasis versicolor, but other researchers found that M. furfur and
M. sympodialis were predominant species and M. sympodialis was often found on normal skin.
From microscopic examination, the scales of pitiriasis versicolor mushrooms are almost always
thick-walled, round shape and buds from the base of a narrow shape according to the image of
M. globosa and mycelium bersepta and composed of thin filament filaments. In the tropics
mycelium appears with oval-shaped fungi that sprout from the base morphologically similar to
M. furfur or M. obtusa. In the beginning it was very impossible to describe the mycelial phase of
the malassezia species in living things. But in 1977 three successful groups of researchers
showed fungi and mycelial forms with several media.
 The case related to M. furfur occurs because of the flora present in the host but it can also
be due to transmission from other people. Pitiriasis versicolor in some cases occurs due to
imbalance or host and flora of the fungus. There are several factors that contribute to disturbing
the balance. Several species are known. Malassezia turns into mycelial and has a greater level.
Some families with a positive history of getting pitiriasis versicolor are more often affected by
the disease, this is not yet known due to genetics or due to the greater exposure risk factors of M.
furfur.

Predesposing factors that affect the development of pitiriasis versicolor vary, which need
to be considered are environmental factors and host factors. In warm climates, hyphae were
associated with malassezia fungi on normal skin. Gender is a factor that has no effect but there
are differences at different ages. In zones with warm temperatures it is very rare in children, but
most often in adolescents and young adults. Pitiriasis versicolor is claimed to be a serious
disease, very susceptible to malnutrition. Pregnancy and oral contraception are also a factor in
the emergence of Pitiriasis versicolor.

Colonies of M. furfur itself are usually found on the scalp, upper limbs, and folds, areas
that are rich in sebaceous glands and their secretions under certain conditions, malassezia will
develop from sporophyte fungus forms into a miselial and pathogenic form. The conditions that
affect the balance between the host and the fungus are endogenous and exogenous factors.
Endogenous factors include sebaceous gland production and sweat, genetics, malnutrition,
immunological factors and drug use, while the most important exogenous factors are skin
temperature and humidity.

Sebum production

An increase in sebum secretion by the sebaceous glands will affect the overgrowth of these
lipophilic organisms.14 Production of sebum differs from age to age. The incidence occurs when
the sebaceous glands are most active, namely puberty and early adulthood.15 The organisms that
are usually found are M. furfur.

Sweat Production
People with hyperhidrosis have a tendency to develop this fungus. The Startum corneum will
soften in a wet and moist state so that M. furfur is easily entered.

Genetics

Genetic predesposition occurs in families that are susceptible to fungal infections

Malnutrition

Lack of some nutrients will facilitate the growth of opportunistic fungi.

Immunological factors

The incidence of fungal infections is increasing in a number of patients with immune system
suppression, for example in cancer patients, kidney transplants and HIV / AIDS and can occur in
people with cushing's disease.

Topical and systemic material

The use of topical ingredients containing oil can cause occlusion of the sebum gland ducts
thereby facilitating M. furfur growth in that place. Some systemic drugs such as antibiotics, oral
contraceptive steroids and immunosuppressant drugs are factors that facilitate the overgrowth of
culinary fungi.

Temperature and humidity

Tropical regions with high temperatures and high humidity will increase the production of
sebum glands and sweat so that M. furfur growth increases.

Pathomechanism

Dermatophytic fungi based on the affinity for a particular host are divided into 3 namely
zoophilic, anthropophilic, and geophilic fungi. Zoophilic fungi mainly infest animals and
sometimes infect humans, such as M. canis in dogs and cats. Anthropophilic fungi mainly infect
humans, for example T. rubrum. Whereas in geophilic fungi, namely fungi that live on the
ground, for example M. gypseum.
 Dermatophytic fungi often live in dead cells, skin stratum corneum, hair and nails and in
general do not attack the layers beneath the epidermis. Although the dermatophytes have been
captured by the mechanism of immunity intermediate cells, the dermatophytes can penetrate into
the deeper dermis and bloodstream that has been protected by the host's non-specific defense
mechanism. This mechanism includes serum inhibitor factors and complementary activity and
polymorphonuclear leukocyte activity. Dermatophytes have keratinase and other enzymes that
allow fungi to attack the deeper layers of the stratum corneum. The skin responds to the
mechanism of this infection by increasing proliferation as a result the skin looks scaly and the
epidermis thickens.

Basically the ability of the fungus to cause a disease in the host depends on the ability of
the fungus to adapt to the host environment and to fight non-specific and specific body defense
mechanisms.

Clinical Overview

Pitiriasis versicolor abnormalities are often found in the upper part of the chest and extend to the
upper arms, neck, back, and upper or lower limbs. Patients in general. Complaints felt by patients
are generally mild itching when sweating. Hypopigmented or hyperpigmented macules, shaped
regularly to irregular, well-defined and diffuse.

Some of the most common forms are:

a. Forms of patches that expand with a smooth top above with no elevated edges, this is a type of
macular.

b. Forms like specks of water that often arise around hair follicles, these are follicular types.

Figures 6 and 7. Pityriasis versicolor shows hyperpigmented lesions in Caucasian lesions (left)
and hypopigmentation in Australian Aborigines (right).

Pitiriasis versicolor in general does not give complaints to patients or often called
asymptomatic. Patients more often experience mild itching but usually sufferers are treated for
cosmetic reasons caused by hypopigmentation spots. Hypopigmentation in these lesions occurs
because decarboxylic acid produced by malassezia is a competitive inhibitor of the tyrosinase
enzyme and has a cytotoxic effect on melanocytes, whereas in Hyperpigmented lesions cannot be
explained.

Diagnosis

Diagnosis is based on clinical features, microscopic examination, and examination using wood
lamps. Typical features include hypopigmenation patches to hyperpigmentation with extensive
spread and firm boundaries.

Check with wood lamps

This examination is done in a room or a dark room so that this method the clinician must
prepare the appropriate room along with the wood lamp that will be used to diagnose the patient.
As a result of this examination the skin affected by pitiriasis versicolor will fluoresce to golden
yellow. This fluorescence can show a clear boundary of the lesion, so that we can know the
extent of the lesion, besides that it can also be used for previous treatment evaluations.

Examination of direct preparation with a light microscope

Preparations of preparations are made from squat scrapes in lesions placed on glass
objects dripped with 20% KOH solution of 1-2 drops, then covered with a glass cover and left
for 15-20 minutes so that the skin epithelium dissolves. After the preparation is ready, then an
examination using a light microscope is carried out with 10x10 magnification, followed by
10x40 magnification. Examination using 10-20% KOH was found in short 2-5µ and bersepta
hyphae, surrounded by 1-2µ-sized spores, this image is typical of sphageti and meatball or
banana and grapes.

Histophatology

Figure 8 : Histophatology of Pityriasis versicolor

Management

There are two types of treatment for pitiriasis versicolor fungal infections, which can be
done topically and systemically. Minimal lesions usually use a type of topical type of treatment.
Topical types of treatment, namely:

1. Selenium sulfide 1.8% in shampoo form 2-3 times a week. The drug is rubbed on the
lesion and allowed to stand for 15-30 minutes before bathing
2. Salicyl spirits 10%
3. Azol derivatives, for example: micozanol, clotrimazole, isoconazole and econazole in
topical form
4. Presipitatum sulfur in 4-20% whipped powder
5. 25% Sodium Tiosulfas solution, applied twice a day after bathing for 2 weeks

Systemic types of treatment, namely:

1. Ketokonazole
Dosage: 200Mg daily for ten days and as a single dose of 400Mg
2. Intracoazole
Dosage: 200Mg daily for seven days
3. Fluconazole
Dosage: 200Mg every day for seven days

Hypopigmentation therapy (Leukoderma)

1. Liquor carbonas detergent 5%, morning / night ointment

2. Medium corticosteroid cream morning and night
3. Dry in the sun ± 10 minutes between 10.00-15.00

Complications

1. Secondary bacterial infection, cellulitis

2. Spread tinea to the feet of the scalp, nails.

3. Pyoderma, dermatophytid

Prevention

To prevent Pityriasis versicolor from occurring, it is recommended to use 50% propylene

glycol in water for prevention of recurrence. In endemic areas it can be recommended to use
ketoconazole 200 mg / day for 3 months or itraconazole 200 mg once a month or use selenium
sulfid shampoo once a week. To prevent recurrence, preventive treatment needs to be given, for
example once a week, a month and so on. Skin color will recover if no reinfection occurs.
Exposure to sunlight and if necessary phototoxic drugs can be used with caution, for example
oleum bergamot or metoxalene to restore the skin color.

Prognosis

The prognosis is good in terms of healing if the treatment is done thoroughly, diligently and
consistently. Treatment must be continued 2 weeks after negative fluorescence with Wood lamp
examination and the direct preparation is negative.

C. Morbus Hansen

Definition
The term leprosy comes from the Indian language, namely leprosy means a collection of skin
symptoms in general. Leprosy is also called Morbus Hansen, according to the name that found
germs, namely Dr. Gerhard Armauwer Hansen in 1874 so that this disease was called Morbus
Hansen. Leprosy, also called leprosy, is a chronic granulomatous infectious disease caused by
Mycobacterium leprae, especially regarding the peripheral nervous system, skin, but can also
occur in the upper respiratory tract mucosa, then it can go to other organs except the central
nervous system.

Epidemiology
In Indonesia sufferers of children under the age of 14 years get ± 13%, but children under
1 year are rarely. The highest frequency is found in the age group between 25-35 years. Leprosy
is everywhere, especially in Asia, Africa, Latin America, tropical and subtropical regions, and
low socio-economic communities. Leprosy is spread throughout the world with different
endemicity. The spread of leprosy from somewhere in the world seems to be caused by the
migration of people infected with the disease. This disease is spread through droplet infections
and has a long shoot period (between 2 months to 40 years).

Etiology
The leprosy-causing bacteria is Mycobacterium leprae. These germs are obligate
intracellular, aerobic, cannot be cultured in vitro, are Gram positive bacilli with a size of 3-8 μm
x 0.5 μm, acid and alcohol resistant. The time for cleavage of Mycobacterium leprae is very
long, ie 2-3 weeks, these germs can reproduce optimally at 27 ° C - 30 ° C in vivo, grow well on
cooler tissues (skin, peripheral nervous system, nose, ear lobe , anterior chamber of eye, upper
airway, legs and testes), and not on warm areas (axillary, inguinal, head, midline backs. 1,2)

Figure 9 and 10 : Microscopic of Mycobacterium leprae

Classification and Clinical Manifestation

According to WHO, leprosy is divided into 2 forms, namely bacillary pausi

(indeterminate and tuberculoid) and multi bacillary (borderline and lepromatous).

Table 1. Chart of Clinical Diagnosis according to WHO.

PB (Pausibasilar) MB (Multibasilar)

Skin lesions (flat 1-5 lesions > 5 lesions

macules, elevated Hypopigmentation / Distribution is more
papules, infiltrates, erythema symmetrical
erythematous plaques, The distribution is not
nocus) symmetrical

Nerve damage (causing Clear sensation loss Nerve damage (causing

loss of muscle loss of muscle
sensation / weakness Only one nerve branch sensation / weakness
 innervated by the innervated by the
affected nerve affected nerve

BTA Negatif Positif

Tipe Indeterminate (I), Lepromatosa (LL),

Tuberkuloid (T), Borderline lepromatous
Borderline tuberkuloid (BL), Mid borderline
(BT) (BB)

Based on Ridley and Jopling's classification, leprosy is divided into:

a. Indeterminate leprosy (I): hypopigmented macules, sometimes erythema macules. There is no

sensory loss. About 75% of patients experience spontaneous recovery, while others will remain
in this form until when immunity decreases, it will change to another form.

b. Tuberculoid leprosy (TT): minimal skin lesions. Usually only one erythematous plaque with
an elevated edge. Predilection of the face, extremities, intertrigosa and head. Dry, squamous,
hypohidrotic and no hair lesions. In this form, the lesion on the skin has undergone anesthesia.

c. Bordeline tuberculoid leprosy (BT): the lesion is the same as the tuberculoid type, but the
lesion is smaller and more numerous. An anesthetic macula or plaque accompanied by a satellite
lesion on the edge. Hypopigmentation, skin dryness and squamous appearance are not clear. The
nerve is not too large and does not cause alopecia too much compared to the tuberculoid type.
This form usually persists, but can return to the type of tuberculoid or progressive towards the
lepromatousform.

d. Borderline borderline leprosy (BB): the most unstable type, also called dimorphic and rarely
found. Many skin lesions, red, are irregular plaques. Lesions vary greatly in size, shape, and
distribution. Punched out lesions can be found, namely hypopigmentation which is oval in the
middle. The distribution resembles a lepromatous form, but is asymmetrical. Regional
adenopathy can occur.
e. Borderline lepromatous leprosy (BL): numerous lesions and consisting of macules, papules,
plaques and nodules. There are annular punched-out lesions. Anesthesia does not occur.

f. Lepromatous leprosy (LL): the initial lesion is a pale macula. Small, diffuse and symmetrical
macula. Anesthesia does not occur in this form, the nerve does not thicken, and hydrotic. The
loss of nerve stimulation is slow and progressive.

Table 2. Clinical, Bacteriological, and Immunologic Features of Leprosy PB

Characteristics Tuberculoid Borderline Indeterminate (I)

Tuberculoid (BT)
(TT)

Lesions

Form The macula or Macula is limited Infiltrate only

macula is limited by infiltrates,
by infiltrates macula only

Total One or several One with satellite One or several

lesions

Distribution Location and asymmetry Varies

asymmetry

Surface Dry, squama Dry, squama Smooth rather

shiny

Anesthesia Clear Clear Nothing until

unclear

Limit Clear Clear Can be clear or

unclear

BTA

In skin lesions Negative Negative, or 1+ Usually negative

 Lepromin test Positive (3+) Weak positive Can be weak
positif or negative

*Lepromin Test to help determine type, the result are only known after 3 weeks

Tabel 3. Clinical manifestation, Bacteriology, dan Imunologic Lepra MB

Characteristics Lepromatosa Borderline Mid-borderline

(LL) Lepromatosa (BB)
(BL)

Lesions

Form Macula, diffuse Macula, papule, Plaque, dome-

infiltrates, plaque shaped lesions,
papule, node punched out lesions

Total Lots of broad Many but healthy Several, healthy

distribution, skin still exists skin (+)
practically n
healthy skin

Distribution Symmetrical Tend to be Asymmetrical

symmetrical

Surface Shine and smooth Shine and smooth A little shine, some
dry lesions

Anesthesia Unclear Unclear Clear

Limit Unclear Rather clear Rather clear

BTA

On skin Many Many A lot

lesions
 Secret on the Many Usually nothing Nothing
nose

Lepromin test Negative Negative Usually negative

Pathogenesis
M. leprae is predilected in relatively cooler areas of the body. The imbalance between the
degree of infection and the degree of disease is caused by a different immune response that
causes a local or overall granuloma reaction that can heal itself or progressively. Therefore
leprosy can be called an immunological disease. The clinical symptoms are more proportional to
the cellular reaction rate than the intensity of the infection. Although the method of entering M.
leprae into the body is still not known with certainty, several studies have shown that the most
common is through skin blisters on cold-temperature parts of the body and through the nasal
mucosa. Influence, M. leprae on the skin depends on a person's immunity factors, the ability to
live M. leprae at low body temperature, long regeneration time, and the avirulent and nontoxic
nature of germ.

M. Leprae enters the body (skin, nose, etc)

Peripheral nerves

Bind to schwan cell of axon

Demyelination of
nerve

Loss of axonal
conductance

Deformity (loss of pain, temperature, touch,

sesation)
Diagnosis

The diagnosis of leprosy is based on clinical, bacteriological and histopathological

features, and is serological. Among the three, clinical diagnosis is the most important and
simplest. Bacteroscopic results require at least 15-30 minutes, while histopathology is 10-14
days. If possible, a lepromin (Mitsuda) test can be done to help determine the type, the results of
which can only be known after 3 weeks. Skin disorders in uncomplicated leprosy can only take
the form of macules, infiltrates, or both. Inspecting other diseases, the presence or absence of
anesthesia is very helpful in determining the diagnosis, although it is not very clear. This is easily
done by using a needle against pain, cotton against feeling palpable, and can also with a sense of
temperature, namely heat and cold with a test tube. Also note the presence or absence of
dehydration in the area of the lesion that can be confirmed by using an ink pencil (Gunawan's
sign). How to scratch it from the middle of the lesion to normal skin. It can also be noted for
alopecia in the lesion area. And found one or more cardinal signs of patients from endemic areas,
skin lesions with leprosy character with or not numbness, accompanied by peripheral nerves, and
found M. leprae.

EXAMINATION OF SUPPORT
1.Bacteroscopic examination

Used to help establish diagnosis and observation of drugs. The preparation was made
from skin tissue scrapings or nasal mucosal swabs that were colored with Ziehl Neelson staining.
Bacteriacopic negative in a patient does not mean that the person does not contain M. leprae
bacilli. First, the lesion on the skin must be determined which is expected to be the most dense
by the bacillus after first determining the exact amount taken. For research, 10 sites can be
examined and routine should be at least 4-6 places, namely the two lower ear lobes and 2-4 other
most active lesions, which mean the most erythematous and most infiltrative. Selection of ear
lobes regardless of the presence or absence of lesions in the place because the ear lobe is usually
found in many M. leprae.

2.Histopathological examination
Macrophages in tissues originating from monocytes in the blood have special names, and
those from the skin are called histiocytes. If the SIS is high, the macrophages will be able to
phagocyte M. leprae. The arrival of histiocytes to the germ site is caused by an immunological
process in the presence of chemotactic factors. If it comes in excess and no more has to be
phagocyted, the macrophage will transform into an immobile epitheloid cell and then it can turn
into a cell datia Langhans.

Figure 11 : Histophatology of Morbus Hansen/Leprosy

3. Serological examination
Based on the formation of antibodies on the body of a person infected with M. leprae.
The antibodies formed can be specific to M. leprae, namely anti phenolic glycolipid-1 (PGL-1)
antibodies and 16kD and 35kD antiprotein antibodies. While non-specific antibodies include
anti-lipoarabinomanan (LAM) antibodies, which are also produced by M. tuberculosis.

Management
The main goal is to break the chain of transmission to reduce the incidence of disease,
treat and cure patients, prevent the onset of disease, to achieve these goals, the main strategies
carried out are based on early detection and treatment of patients.2
Treatment of leprosy is recommended to use the Multi Drugs Therapy (MDT) program
with a combination of rifampicin, clofazimine, and DDS, recommended by WHO since 1981.
The aim of the MDT program is to overcome increasing dapsone resistance, reduce drop-out
rates and patient disobedience. The most widely used anticancer drugs currently are DDS,
clofazimine and rifampicin. In 1998 WHO added 3 other antibiotic drugs for alternative
treatments namely ofloxacin, minocycline, and clarithomycin.
Rehabilitation
Medical rehabilitation efforts that can be carried out for disability include surgery and
physiotherapy. Although the results are not perfect back to origin, but the function can be
corrected cosmetically. Another way is to work, that is to give jobs that match their bodily
disabilities, so that they can achieve and can increase self-confidence, in addition psychological
therapy can be performed (psychiatric) .

Prognosis
Quo ad vitam is ad bonam because MH is not life threatening even though it is chronic and
requires long-term treatment. Quo ad fungsionam is dubia ad bonam because MH also does not
cause disruption of bodily organs in these patients, although it can cause deformity in some cases
that are late in getting treatment. Quo ad sanationam in this patient is dubia ad bonam because
the patient has sufficient education and is able to understand the importance of long-term
treatment of the disease.

Reference :

1. Janik, M. P., &Heffernan, M. P. Superficial Fungal Infection : Dermathopytosis,

Onycomycosis, Tinea nigra, Piedra . In: Fitzpatrick Dermatology in General Medicine.
McGraw-Hill: USA. 2008. p 1807-1822.
2. Bramono Kusmarinah, Unandar Budimuljah. Pitiriasis versicolor. Ilmu penyakit Kulit dan
Kelamin. FK UI. Edisi ke 7. 2015. Hal 103-105
3. A.Kosasih, I Made Wisnu, Emmy Sjamsoe – Dili, Sri Linuwih Menaldi. Kusta. Dalam:
Djuanda,Adhi dkk.(ed). Ilmu Penyakit Kulit dan Kelamin. Edisi Kelima. Jakarta: Balai
Penerbit FKUI; 2010.h. 73-88.
4. Buxton K.P. ABC of Dermatology, 4th ed (BMJ Books); 2003.p.109-10.
5. Lewis S. Leprosy. Update 4 Februari 2010. Diunduh dari:
http://emedicine.medscape.com/article/1104977-overview#showall, 19 Juni 2016.
6. Wolff K, Goldsmith LA, Katz SI, Fritzpatrick’s Dermatology in General Medicine. 6th
Edition. Mc Graw Hill; 2008.h. 665-71.
7. World Health Organization. WHO model prescribing information: drug used in leprosy.
Diunduh dari: http://apps.who.int/medicinedocs/en/d/Jh2988e/1.html, November 2018
6. Islamic perspective according to the scenario!

Rasulullah saw said : Indeed Allah SWT is kind, He likes kindness, God is clean, He likes
cleanliness, God is noble, He likes glory. God is generous, He likes charity, then cleanse your
places. (H.R. Tirmidzi)