TROPICAL MEDICINE SYSTEM

PBL MODULE 1 REPORT

CASE ‘RED PATCHES ON THE SKIN’

GROUP 3
 RIZKA PURNAMASARI C11108196
 REZKI MIFTAHUL JANNAH C11108234
 GOPINATH NADARAJAN C11108753
 MUHAMMUD LUQMANUL HAKIM BIN SULAIMAN C11108765
 NUR ANIESSA BT ABD RAHMAN C11108777
 NUR AFEEZA BINTI ABDUL MUTALLID C11108802
 NIMMELEN KASAVA MOORTHI C11108789

MEDICAL FACULTY
HASANUDDIN UNIVERSITY
MAKASSAR
 2011
SCENARIO

A housewife aged 30 years came to health centers with symptoms of redness on the chest
area experienced from a week ago.

KEYWORDS
 Female
 House wife
 30 y.o
 Redness on chest for the last 1 week
 Skin redness is a condition which is characterized by redness of the skin due to congestion of
the capillaries.

QUESTIONS
1.Anatomy and physiology of skin.
2.Etiology of redness
3.Physical examination that can be done
4.Primary skin lesions.
5.Pathomechanisme of redness.
6.Differential diagnosis-A.Candidiasis
B.Herpes Zoster
C.Scabies.
D.Dengue Hemorrhagic Fever
E.Tinea corporis

1. Anatomy and Physiology of Skin

The skin is the interface between humans and their environment. It is the largest organ in
the body. It weighs an average of 4 kg and covers an area of 2 m2. It acts as a barrier, protecting
the body from harsh external conditions and preventing the loss of important body constituents,
especially water.
The skin has two layers. The outer is epithelial, the epidermis, which is firmly attached
to, and supported by connective tissue in the underlying dermis. Beneath the dermis is loose
connective tissue, the subcutis/hypodermis which usually contains abundant fat.

A. Epidermis
 The outermost layer of the skin is the epidermis.
 The cells of the epidermis continually undergo mitosis and are replaced approximately every
30 days.
 The epidermis contains sensory receptors for touch, temperature, vibration, and pain.
 The main component of the epidermis is the protein keratin, produced by cells called
keratinocytes. Keratin is an extremely durable, tough substance that is insoluble in water.
Keratin prevents loss of body water and protects the epidermis from irritants and infection-
causing microorganisms. Keratin is the main component of the skin appendages: the nails
and the hair.

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 Melanocytes are present at the base of the epidermis. Melanocytes synthesize and secrete
melanin in response to stimulation by melanocyte-stimulating hormone, which is produced
by the anterior pituitary. Melanin is a black pigment that disperses throughout the epidermis
to protect cells from ultraviolet radiation.
 Immune cells, called Langerhans' cells, are present throughout the epidermis. Langerhans'
cells recognize foreign particles or microorganisms that enter the skin and present them to T
lymphocytes as the first step in initiating an immune attack. Langerhans' cells may be
responsible for recognizing and eliminating dysplastic or neoplastic skin cells. Langerhans'
cells are physically associated with sympathetic nerves, suggesting a relation between the
nervous system and the ability of the skin to fight off infection or prevent skin cancer. Stress
may affect the functioning of Langerhans' cells by increasing sympathetic stimulation.
Ultraviolet radiation may damage Langerhans' cells, reducing their ability to prevent cancer.

B. Dermis
 Lying immediately under the epidermis, the dermis is considered loose connective tissue and
is composed of fibroblast cells that secrete the proteins collagen and elastin.
 The collagen and elastin fibers are arranged haphazardly, giving the dermis distensibility and
resilience.
 A gel-like substance, hyaluronic acid, is secreted by the connective tissue cells. Hyaluronic
acid surrounds the proteins and gives the skin elasticity and turgor (tension).
 Throughout the dermis are blood vessels, sensory and sympathetic nerves, lymphatic vessels,
hair follicles, and sweat and sebaceous glands.
 Mast cells, which release histamine during injury or inflammation, and macrophages, which
phagocytize dead cells and microorganisms, are also present.
 Blood vessels in the dermis supply the dermis and epidermis with nutrients and oxygen and
remove waste products. Dermal blood flow offers a means for the body to control its
temperature. With a decrease in body temperature, sympathetic nerves to the blood vessels
are activated and increase the release of norepinephrine, causing constriction of the vessels
and a conservation of body heat. If body temperature is too high, sympathetic stimulation of
the dermal blood vessels is reduced, dilating the vessels and allowing for the transfer of body
heat to the environment.
 Arteriovenous (AV) connections, called anastomoses, are present on some blood vessels. AV
anastomoses facilitate skin temperature regulation by allowing blood to bypass the upper
layers of the dermis in times of severe cold.
 Sympathetic nerves to the dermis also innervate sweat glands, sebaceous (oil) glands, and
hair follicles.

C. Subcutaneous Layer
 Lying beneath the dermis, the subcutaneous layer of the skin is composed of fat and
connective tissue and acts as both a shock absorber and a heat insulator.
 The subcutaneous layer is a calorie reserve station as well: fat can be stored in this layer and,
if needed, broken down to serve as an energy source.

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The skin immune system
The horny layer of the skin is able
both to prevent the loss of fluid and
electrolytes, and to stop the penetration of
harmful substances. It is a dry mechanical
barrier from which contaminating
organisms and chemicals are continually
being removed by washing and
desquamation. Only when these breach the
horny layer do the cellular components,
described below, come into play.

A. Some cellular components of the skin

immune system:

1. Keratinocytes
Their prime role is to make the
protective horny layer and to support to the
outermost epithelium of the body but they
also have immunological functions in their
own right. Keratinocytes produce large
numbers of cytokines, and can be induced

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by γ-interferon to express HLA-DR. They can also produce α-melanocyte-stimulating hormone,
which is immunosuppressive. Keratinocytes play a central part in healing after epidermal injury

2. Langerhans cells
These dendritic cells come from the bone marrow and circulate through the epidermis,
the dermis, lymphatics (as ‘veiled cells’), and also through the T-cell area of the lymph nodes
where they are called ‘dendritic’ or ‘interdigitating’ cells. Langerhans cells have a key role in
antigen presentation.

3. Dermal dendritic cells

These poorly characterized cells are found around the tiny blood vessels of the papillary
dermis. They bear MHC Class II antigens on their surface and, like Langerhans cells, probably
function as antigen presenting cells.

4. T lymphocytes
These develop and acquire their antigen receptors (Tcell receptors, TCR) in the thymus.
They differentiate into subpopulations, recognizable by their different surface molecules (cluster
of differentiation markers), which are functionally distinct.
a. T-helper (TH)/inducer cells
These help B cells to produce antibody and also induce cytotoxic T cells to recognize and
kill virally infected cells and allogeneic grafts. TH cells recognize antigen in association
with MHC Class II molecules and, when triggered by antigen, release cytokines that
attract and activate other inflammatory cells. They are CD4+. Helper T cells are divided
into type 1 (TH-1) and type 2 lymphocytes (TH-2) according to the main cytokines that
they produce. Some skin diseases display a predominantly TH-1 response (e.g. psoriasis),
others a mainly TH-2 response (e.g. atopic dermatitis).
b. T-cytotoxic (TC) cells
These lymphocytes are capable of destroying allogeneic and virally infected cells, which
they recognize by the MHC Class I molecules on their surface. They are CD8+.
c. T-cell receptor and T-cell gene receptor rearrangements
Most T-cell receptors are composed of an α and β chain, each with a variable (antigen
binding) and a constant domain, which are associated with the CD3 cell surface
molecules. Many different combinations of separate gene segments, termed V, D and J,
code for the variable domains of the receptor. An analysis of rearrangements of the gene
for the receptor is used to determine whether a T-cell infiltrate is likely to be malignant or
reactive. The identification of a specific band, on analysis of DNA from the lesion, which
is not matched by the patient’s DNA from other sites, indicates monoclonal T-cell
proliferation, and suggests either malignancy or a T-cell response to a single antigen.

5. L cells/null (non-T, non-B) cells

These leucocytes have properties between those of T and myelomonocytic cells. Most
have receptors for FcIgG. This subpopulation contains natural killer (NK) and killer (K) cells.
a. Natural killer cells
These are large granular leucocytes that can kill virally infected cells, or tumour cells that
have not previously been sensitized with antibody.
b. Killer cells

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 These are not a separate cell type, but rather cytotoxic T cells, NK cells or monocytic
leucocytes that can kill target cells sensitized with antibody. In antibody-mediated
cellular cytotoxicity, antibody binds to antigen on the surface of the target cell: the K cell
binds to the antibody at its other (Fc) end by its Fc receptor and the target cell is then
lysed.

6. Mast cells
These are present in most connective tissues, predominantly around blood vessels. Their
numerous granules contain inflammatory mediators. Skin mast cells play a central part in the
pathogenesis of urticaria.

B. Molecular components of the skin immune system:

1. Antigens and haptens

Antigens are molecules that are recognized by the immune system thereby provoking an
immune reaction, usually in the form of a humoral or cell-bound antibody response. Haptens,
often chemicals of low molecular weight, cannot provoke an immune reaction themselves unless
they combine with a protein. They are important sensitizers in allergic contact dermatitis.

2. Superantigens
Some bacterial toxins (e.g. those released by Staphylococcus aureus) are prototypic
superantigens. Sensitization to such superantigens is not necessary to prime the immune
response. Superantigens align with a variety of MHC Class II molecules outside their antigen
presentation groove and, without any cellular processing, may directly signal to different classes
of T cells within the large family carrying a Vβ type of T-cell receptor.
By these means, superantigens can induce massive T-cell proliferation and cytokine production
leading to disorders such as the toxic shock syndrome. Streptococcal toxins act as superantigens
to activate T cells in the pathogenesis of guttate psoriasis.

3. Antibodies (immunoglobulins)
a. Immunoglobulin G (IgG) is responsible for most of the secondary response to most
antigens. It can cross the placenta, and binds complement to activate the classical
complement pathway. IgG can coat neutrophils and macrophages (by their FcIgG
receptors), and acts as an opsonin by cross-bridging antigen. IgG can also sensitize target
cells for destruction by K cells.
b. IgM is the largest immunoglobulin molecule. It is responsible for much of the primary
response and, like IgG, it can fix complement but it cannot cross the placenta.
c. IgA is the most common immunoglobulin in secretions. It does not bind complement but
can activate complement via the alternative pathway.
d. IgE binds to Fc receptors on mast cells and basophils, where it sensitizes them to release
inflammatory mediators in type I immediate hypersensitivity reactions.

4. Cytokines
Cytokines are small proteins secreted by cells such as lymphocytes and macrophages, and
also by keratinocytes. They regulate the amplitude and duration of inflammation by acting
locally on nearby cells (paracrine action), on those cells that secreted them (autocrine) and

6
occasionally on distant target cells (endocrine) via the circulation. The term cytokine covers
interleukins, interferons, colony-stimulating factors, cytotoxins and growth factors. Interleukins
(IL) are produced predominantly by leucocytes, have a known amino acid sequence and are
active in inflammation or immunity.

5. Adhesion molecules
Cellular adhesion molecules (CAMs) are surface glycoproteins that are expressed on
many different types of cell; they are involved in cell–cell and cell–matrix adhesion and
interactions. CAMs are fundamental in the interaction of lymphocytes with antigen-presenting
cells, keratinocytes and endothelial cells and are important in lymphocyte trafficking in the skin
during inflammation. CAMs have been classified into four families: cadherins, immunoglobulin
superfamily, integrins and selectins.

6. Histocompatibility antigens
Like other cells, those in the skin express surface antigens directed by genes of the MHC.
The human leucocyte antigen (HLA) region lies on chromosome 6. In particular, HLA-A, -B and
-C antigens (the Class I antigens) are expressed on all nucleated cells including keratinocytes,
Langerhans cells and cells of the dermis. HLA-DR, -DP, -DQ and -DZ antigens (the Class II
antigens) are expressed only on some cells (e.g. Langerhans cells). They are poorly expressed on
keratinocytes except during certain reactions (e.g. allergic contact dermatitis) or diseases (e.g.
lichen planus). Helper T cells recognize antigens only in the presence of cells bearing Class II
antigens. Class II antigens are also important for certain cell–cell interactions.
On the other hand, Class I antigens mark target cells for cell-mediated cytotoxic reactions, such
as the rejection of skin allografts and the destruction of cells infected by viruses.

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2. Etiology of redness

Skin redness (erythema) is a condition which is characterized by redness of the skin due
to congestion of the capillaries. The abnormal redness of the skin, often signalling a pathological
condition, such as inflammation, infection, exposure to heat, insect bites, infections, allergy, non-
ionizing radiation (sunlight, UV) and ionizing radiation (X-ray, nuclear radiation).
Erythema may appear within a few hours after acute exposure to radiation with a skin
dose of about 2 to 3 gray (Gy) for radiation energies encountered in X ray machines used for
interventional procedures, whereas 6 to 8Gy with 200 kV radiation used in radiation therapy are
required for erythema to occur.

 Some causes of local redness include:

- Rash
- Flushing
- Haemorrhagic rash
- Burn
- Sunburn
- Actinic keratosis
- Dermatitis
- Contact dermatitis
- Eczema
- Palmar erythema - red palms
- Erytrasma

 Some causes of generalized redness include:

- Fever
- Viruses
- Body rash

• Certain medications; Drugs, medications, substances or toxins are some of the possible
causes of redness as a symptom.

• Medications causing general redness may include:

- Aspirin
- Penicillin

3. Physical examination that can be done

A. Inspection
• Defloration
• Shape, size, border, surface
• Location

B. Palpation
• Pain
• Heat

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 • Surface(Reguler/Ireguler)

4 .Primary skin lesions

Primary skin lesion Characteristic

Macula • A change in surface color, without elevation or depression
• Non palpable
• Less than 10mm in diameter of widest point
Patches • A large macule
• equal or greater then 10mm
• May have some subtle surface change, such as fine scale or wrinkling
• Non palpable
Vesicle • A circumscribe, fluid containing, epidermal elevation
• Generally considered less then 10mm
Bulla • A large vesicle
• Containing serous or seropurulent fluid
• Equal or greater then 10mm
Pustule • A small elevation of skin
• Containing cloudy or purulent material
Papule • A circumscribed, solid elevation of skin
Nodule • Morphologic similar to papule
• Greater then 10mm
• Most frequently centered in the dermis or subcutaneous fat

5.Pathomechanisme of redness
Immune response

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 Innate immune system has two stadiums which are vascular and cellular. White blood
cells-neutrophil, basinophil, eosinophil, monosit and macrophage are involved in this system.
Inflammation responses stimulated after an injury or infection. White blood cells and
thrombosites will then move to the site of injury or infection to repair the damage. Vascular
stadium occurs immediately right after an injury, infection or exposure to the toxins. Arteriols
near to the site of infection will go through a brief constriction followed by a long vasodilation.
The brief constriction will then pull away the endotel cells from the arteriol wall, which allows
the white blood cells to move to the site of infection or injury. Mast cells and chemical mediators
will be released.

6.Differential Diagnosis

Disease Age Gender Location Efflorescence

Herpes zoster Any age but more F=M Depend on Papule until crust
common >50 infection
years old
Candidiasis Any age F=M Mouth, nail, Redness, pustule
armpit, umbilical,
genital
Tinea Any age F=M Arms, legs, face Annular lesion and squama
corporis and other exposed with vesicular boundaries
body areas
Scabies Any age F=M Hands, feet, wrists, Superficial burrows tracks
elbows, back, often linear to the point that a
buttocks, under the neat line of 4 or more closely-
breast of women placed and equally developed
and external genital mosquito-like bites
Dengue Any age F=M Skin Petechiae
Hemorrhagic
Fever

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HERPES ZOSTER

A. Introduction
 Herpes zoster is an infection of the vericella zoster virus who attack at the nervus spinalis and
nervus cranialis.
 It is a prognosis of the chicken pox
 Normally the pain is unilateral base on infected dermatome
 It can be recurrent base on human immune status

B. Risk factors
 Immune response decrease due to age > 55 y.o
 Malignancy.
 Immunosuppressant – lymph proliferative disease.
 Chemotherapy.
 HIV.

C. Sign and symptoms

 3-4 days before herpes zoster attack
− fatigue
− shivering
− Fever
− Nausea
− diarrhea
− sometimes feel pain and itchy
 Swelling of the lymph nodes
 Papule (24 hours) à bulla- vesicle (48 hours) à pustule (96 hours) à crust (7-10 days)
 After the crust formation, the fluid that contain in the pustule will spread to the other region
of the body within 1 week
 The area of infected will leave the pain for month to years due to damaged by VHV
especially during extreme weather

D. Pathomechanism

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12
Example of the skin effloresion in herpes zoster

E. Treatment

Systemic therapeutic :
1. Analgesic
2. Antibiotic
3. Antivirus
→ Acyclovir 5 x 800 mg/day (7 days)
→ Valacyclovir 3 x 1000 mg/days (7 days)
4. Imunostimulator → Isoprinosin

Topical therapy :
 Vesicle → talcum (preventing secondary infection)
 Ulcers → Antibiotic cream

F. Complication
1. Post herpetic neuralgia
2. Ptosis paralytic
3. Keratitis
4. Skleritis
5. Uveitis
6. Optic neuritis
7. Gangrene

CANDIDIASIS

A. Etiology
 Candidiasis or moniliasis is caused by opportunistic yeasts from the genus Candida, most
frequently, C. albicans.

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  Infections may be superficial or deep, involving of the skin, mucosa, or the internal
organs. The course may be acute, subacute or chronic.
 Candidiasis occurs worldwide; it causes up to 25% of the superficial mycoses involving
nails (35%), skin (30%), and the mucosae (20%).
 There is no predilection for race, sex, or age. It affects 4-8% of newborns.
− Candida vulvovaginitis is more common between age 20-30 years of age, and is
present in 20-30% of gynaecological infections.
− Balanitis occurs in adult and elderly men.
− Oral candidiasis occurs in persons with immune incompetence, in children under 10,
and in the elderly.
− The intertrigous and onychomycotic forms are more frequent in women
− Interdigital candiasisis is more common in the tropics.

B. Pathogenesis
This opportunistic fungus can become a pathogen. For example, Candida from the
oropharyngeal mucosa may be swallowed and passed to the rectum, from which it can infest the
vaginal mucosa.

Other modes of infection are also possible; all require certain conditions such as:
 An immunocompromised host;
 Immunodeficiency disorders of the T-cell system;
 Therapy with corticosteroids and/or immunosuppressive agents that suppress
lymphocytopoiesis;
 Agranulocytosis (severe neutrophil deficiency);
 Antibiotic therapy that suppresses and disrupts the balance of oral and gastrointestinal flora;
 Endocrine disorders (primarily diabetes mellitus).

Virulence factors include:

 Formation of hyphae;
 Hyphae-forming pathogens adhere more readily to the target cells, and their surface proteases
and lipases make them particularly invasive;
 Lectin-like adherence factors;
 Molecular mimicry; the pathogens bind thrombocytes with their fibrinogen ligands, creating
a surface “camouflage” that renders them invisible to immune defenses.

C. Classification
1. Localized forms: mouth, big folds, small folds, diaper area, genitals, nails and periungual
region.
2. Disseminated and deep forms: chronic mucocutaneous candidiasis and granuloma.

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3. Systemic forms: septicemia from Candida, iatrogenic candidemia and fungal invasive
dermatitis.
D. Presentation

1. Oral candidiasis
One or more whitish adherent plaques (like bread sauce)
appear on the mucous membranes. If wiped off they
leave an erythematous base. Under dentures, candidiasis
will produce sore red areas. Angular stomatitis, usually
in denture wearers, may be candidal.

2. Candida intertrigo
A moist glazed area of erythema and maceration appears
in a body fold; the edge shows soggy scaling, and
outlying satellite papulopustules. These changes are
most common under the breasts, and in the armpits and
groin, but can also occur between the fingers of those
whose hands are often in water

3. Genital candidiasis
Most commonly presents as a sore itchy vulvovaginitis,
with white curdy plaques adherent to the inflamed
mucous membranes, and a whitish discharge. The
eruption may extend to the groin folds. Conjugal spread
is common; in males similar changes occur under the
foreskin and in the groin. Diabetes, pregnancy and
antibiotic therapy are common predisposing factors.

4. Paronychia
Acute paronychia is usually bacterial, but in chronic
Sites susceptible to Candida
paronychia Candida may be the sole pathogen, or be infections
found with other opportunists such as Proteus or
Pseudomonas. The proximal and sometimes the lateral nail folds of one or more fingers become
bolstered and red. The cuticles are lost and small amounts of pus can be expressed. The adjacent
nail plate becomes ridged and discoloured. Predisposing factors include wet work, poor
peripheral circulation and vulval candidiasis.

5. Chronic mucocutaneous candidiasis

Persistent candidiasis, affecting most or all of the areas described above, can start in infancy.
Sometimes the nail plates as well as the nail folds are involved. Candida granulomas may appear
on the scalp. Several different forms have been described including those with autosomal
recessive and dominant inheritance patterns. In the Candida endocrinopathy syndrome, chronic
candidiasis occurs with one or more endocrine defects, the most common of which are
hypoparathyroidism, and Addison’s disease. A few late-onset cases have underlying thymic
tumours.

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6. Systemic candidiasis
This is seen against a background of severe illness, leucopenia and immunosuppression. The skin
lesions are firm red nodules, which can be shown by biopsy to contain yeasts and pseudohyphae.
**Cutaneous candidiasis causes patches of red, moist, weepy skin, sometimes with small
pustules nearby.

E. Investigations
 Biopsy is not necessary, but when performed:
− The superficial forms show, in the thick stratum corneum, the microorganism as
filaments and yeasts that are more evident with PAS or Gomori-Grocott.
− In the dermis there is mild edema. With deep involvement, there are abscesses and a
granulomatous reaction.
− The intradermal reaction to candidin is not useful because it is positive in all the
individuals who have had previous contact with the fungus (60%).
 Direct examination with KOH, Lugol’s solution or distilled water reveals pseudohypha,
hypha and blastospores 2-4 µm in diameter.
 Also a smear, stained with Gram, periodic acid-Schiff (PAS) or methylene blue is useful.
 Cultures in Sabouraud, with or without addition of antibiotics, support abundant colonies
of Candida. These species are sensitive to cycloheximide (Actidione): C. tropicalis, C.
krusei, and C. parapsilosis. Chlamydospores in potato-carrot agar or corn meal indicates
C. albicans. It is possible to make physiologic determinations (auxonogram and
zymogram) through systems available commercially.
 Immunological and serum filamentation are more specialized.
 Serological tests involve immunodiffusion, latex agglutination, complement fixation,
ELISA or fluorescent antibodies. They are useful in deep and systemic forms.

Morphology
In tissue sections, C. albicans demonstrates yeastlike forms (blastoconidia),
pseudohyphae, and true hyphae. Pseudohyphae are an important diagnostic clue for C. albicans
and represent budding yeast cells joined end to end at constrictions, thus simulating true fungal
hyphae.
Pathogen identification: include
slightly basophilic organisms under
hematoxylin and eosin stain and purplish red
organisms in a periodic acid-Schiff reaction
(A). The fungus may be present in the form of
an oval yeast (A1), a pseudomycelium with
pseudo-hyphae (A2), and occasionally one
with septate mycelia as well.

F. Treatment
 Predisposing factors should be sought
and eliminated; e.g. denture hygiene
may be important.

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  Infected skin folds should be separated and kept dry. Those with chronic paronychia
should keep their hands warm and dry.
 Amphotericin, nystatin and the imidazole group of compounds are all effective topically.
 For the mouth, these are available as oral suspensions, lozenges and oral gels. False teeth
should be removed at night, washed and steeped in a nystatin solution.
 For other areas of candidiasis, creams, ointment and pessaries are available. Magenta
paint is also a useful but messy remedy for the skin flexures.
 In chronic paronychia, the nail folds can be packed with an imidazole cream or drenched
in an imidazole solution several times a day.
 Genital candidiasis responds well to a single day’s treatment with either itraconazole and
fluconazole. Both are also valuable for recurrent oral candidiasis of the
immunocompromised, and for the various types of chronic mucocutaneous candidiasis.

G. Prevention
 Good general health and hygiene help prevent candida infections.
 Keep the skin clean and dry.
 Drying powders may help prevent fungal infections in people who are susceptible to
them.
 Weight loss and good sugar control in diabetics may help prevent these infections.

H. Complications
 Infection of nails may cause nails to become oddly shaped and may cause infection
around the nail
 Recurrence of candida skin infection
 Disseminated candidiasis may occur in immunocompromised individuals

I. Prognosis
Typically, in otherwise healthy people with superficial candidiasis, a properly treated
infection goes away without leaving permanent damage. Candidiasis is unlikely to return as long
as the person remains healthy and well nourished.
In people with chronic illnesses or weakened immune systems, episodes of candidiasis
may be more resistant to treatment and may return after treatment ends.
In people with deep candidiasis, those who are diagnosed quickly and treated effectively
have the best prognosis, especially if their infection can be stopped before it spreads to major
organs.

SCABIES

A. Introduction
Scabies is a contagious skin infection that occurs among humans and other animals. It is
caused by a tiny and usually not directly visible parasite, the mite Sarcoptes scabiei, which
burrows under the host's skin, causing intense allergic itching. The mite cannot live more than
three days without a human host, but it can survive up to a month when living on a human. The
mite also lays eggs in human skin, which hatch and grow into adult mites. This means that
symptoms of the condition can last for months or even years.

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B. Risk factor
Scabies affect everyone regardless of age, gender, race, social class, or personal-hygiene
habits. However, it is most common among household members and sexual partners of affected
individuals. Scabies is also common in congested areas, such as nursing homes and hospitals,
where it can spread widely. In people who have poor immune systems or who are malnourished,
scabies can cause a syndrome called "crusted scabies" or "Norwegian scabies," which causes
skin thickening and a scaly rash. Scabies is usually transmitted by direct skin-to-skin physical
contact. It can also be spread through contact with other objects, such as clothing, bedding,
furniture, or surfaces with which a person infected with scabies might have come in contact, but
these are uncommon ways to transmit scabies. Animals can harbour a similar mite, but when the
animal mite is passed to people, it cannot reproduce and dies within a few days

C. Symptoms
The characteristic symptoms of a scabies infection include intense itching and superficial
burrows. The burrow tracks are often linear, to the point that a neat "line" of four or more
closely-placed and equally-developed mosquito-like "bites," is almost diagnostic of the disease.
The itching that is worse by warmth and is usually experienced as being worse at night, possibly
because there are fewer distractions. The superficial burrows of scabies usually occur in the area
of the hands, feet, wrists, elbows, back, buttocks, under the breasts of women and external
genitals. The burrows are created by excavation of the adult mite in the epidermis. In most
people, the trails of the burrowing mites show as linear or “s-shaped” tracks in the skin, often
accompanied by what appear as rows of small pimple-like mosquito, or insect bites. The
symptoms typically appear 2-6 weeks after infestation for individuals never before exposed to
scabies. For those having been previously exposed, the symptoms can appear within several days
after infestation. However, it is not unknown for symptoms to appear after several months or
years.

D. Diagnosis
For diagnosis, to detect the burrow the suspected area is rubbed with ink from a fountain
pen or a topical tetracycline solution, which glows under a special light. The skin is then wiped
with an alcohol pad. If the person is infected with scabies, the characteristic zigzag or "S" pattern
of the burrow will appear across the skin; however, interpreting this test may be difficult, as the
burrows are scarce and may be obscured by scratch marks. Sometimes a doctor confirms a
diagnosis by looking for signs of mites on a sample of your skin. The doctor gently scrapes some
dry skin from an affected area and then looks at it under a microscope.

E. Treatment
First of all, the doctor may recommend a cream, permethrin 5% which contains
chemicals that kill scabies. The patient has to use it twice a week. Permethrin is generally
considered safe for children and adults of all ages, including women who are pregnant or
nursing. Besides that, there is also has lindane. It is also a chemical treatment that is available as
a cream, lotion and shampoo. Like permethrin, it's usually applied in two treatments, spaced
about a week apart but, this medication isn't safe for children younger than age 2 years, women
who are pregnant or nursing, or people with weakened immune systems. Crotamiton is non-
chemical medication that is applied once a day for two to five days. The doctor may recommend

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it if your baby has scabies. Although these medications kill the mites promptly, you may find
that the itching doesn't stop entirely for several weeks. The doctors sometimes prescribe the oral
medication ivermectin (Stromectol) for people with altered immune systems, for people who
have crusted scabies, or for people who don't respond to the prescription lotions and creams.
The medication usually apply the medication over all your body, from your neck down,
and leave the medication on for at least eight hours. Because scabies spreads so easily, your
doctor may recommend treatment for all family members and other close contacts, even if they
show no signs of scabies infestation.

DENGUE HEMORRHAGIC FEVER

A. Introduction
Hemorrhagic dengue; Dengue shock syndrome; Philippine hemorrhagic fever; Thai
hemorrhagic fever; Singapore hemorrhagic fever
Dengue hemorrhagic fever is a severe, potentially deadly infection spread by certain
species of mosquitoes (Aedes aegypti). Dengue hemorrhagic fever is characterized by a fever that
lasts from two days to a week and is accompanied by symptoms seen in the milder dengue
infection known as dengue fever. These include headache, eye pain, musculoskeletal pain, and
easy bleeding or bruising. As the fever goes away, fluid begins to leak from the tiny blood
vessels known as capillaries. The fluid can collect in the abdominal cavity or around the lungs.
Intravenous fluids are then needed to support the circulatory system.
Aedes aegypti, the principal mosquito vector of dengue viruses is an insect closely
associated with humans and their dwellings. People not only provide the mosquitoes with blood
meals but also water-holding containers in and around the home needed to complete their
development. The mosquito lays her eggs on the sides of containers with water and eggs hatch
into larvae after a rain or flooding. A larva changes into a pupa in about a week and into a
mosquito in two days.
It is very difficult to control or eliminate Ae. aegypti mosquitoes because they have
adaptations to the environment that make them highly resilient, or with the ability to rapidly
bounce back to initial numbers after disturbances resulting from natural phenomena (e.g.,
droughts) or human interventions (e.g., control measures). One such adaptation is the ability of
the eggs to withstand desiccation (drying) and to survive without water for several months on the
inner walls of containers. For example, if we were to eliminate all larvae, pupae, and adult Ae.
aegypti at once from a site, its population could recover two weeks later as a result of egg
hatching following rainfall or the addition of water to containers harboring eggs.
It is likely that Ae.aegypti is continually responding or adapting to environmental change.
For example, it was recently found that Ae. aegypti is able to undergo immature development in
broken or open septic tanks in Puerto Rico, resulting in the production of hundreds or housands
of Ae.aegypti adults per day. In general, it is expected that control interventions will change the
spatial and temporal dispersal of Ae. aegypti and perhaps the pattern of habitat utilization. For
these reasons, entomological studies should be included to give support before and throughout
vector control operation
There are no specific treatments for dengue hemorrhagic fever other than relieving
symptoms and replacing fluids and blood as needed.

B. Causes, incidence, and risk factors

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 Four different dengue viruses are known to cause dengue hemorrhagic fever. Dengue
hemorrhagic fever occurs when a person catches a different type dengue virus after being
infected by another one sometime before. Prior immunity to a different dengue virus type plays
an important role in this severe disease.
Worldwide, more than 100 million cases of dengue fever occur every year. A small
number of these develop into dengue hemorrhagic fever. Most infections in the United States are
brought in from other countries. It is possible, but uncommon, for a traveler who has returned to
the United States to pass the infection to someone who has not traveled.
Risk factors for dengue hemorrhagic fever include having antibodies to dengue virus
from prior infection and being younger than 12, female, or Caucasian.
Dengue hemorrhagic fever is caused by a dengue virus, specifically known as DENV-1,
DENV-2, DENV-3 or DENV-4. The virus is transmitted to humans by mosquitoes. There have
been reports of transfer of the virus though organ transplants and blood transfusions, as well as
transfer from a pregnant mother to her baby, but these cases are rare.
Dengue hemorrhagic fever is not considered contagious; it is not spread from person to
person.

C. Symptoms
Early symptoms of dengue hemorrhagic fever are similar to those of dengue fever, but
after several days the patient becomes irritable, restless, and sweaty. These symptoms are
followed by a shock -like state.
Bleeding may appear as tiny spots of blood on the skin (petechiae) and larger patches of
blood under the skin (ecchymoses). Minor injuries may cause bleeding.
Shock may cause death. If the patient survives, recovery begins after a one-day crisis
period.
Initial symptoms of dengue hemorrhagic fever include high fever, headache, eye pain,
musculoskeletal pain, and easy bleeding or bruising. Later symptoms include rash, restlessness,
sweating, red to reddish-purple spots or patches on the skin, and cold, clammy skin.

i. Early symptoms of dengue hemorrhagic fever last for a few days to a week and include:
• Aches in the muscle, joints or bones
• Cold, clammy skin
• Eye pain
• Fever
• General ill feeling
• Headache
• Loss of appetite
• Nausea with or without vomiting

ii. Later symptoms of dengue hemorrhagic fever indicate that the infection is entering a crisis
phase. These symptoms include:
• Abdominal pain
• Easy bleeding or bruising
• Irritability and restlessness
• Rash
• Red to reddish-purple spots (petechiae) or patches (ecchymoses) on the skin

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 • Persistent vomiting
• Sweating

Serious symptoms that might indicate a life-threatening condition:

• Bleeding from the nose or gums
• Bloody stool (the blood may be red, black, or tarry in texture)
• Change in level of consciousness or alertness, such as passing out or unresponsiveness
• Change in mental status or sudden behavior change, such as confusion, delirium,
lethargy, hallucinations and delusions
• High fever (higher than 101 degrees Fahrenheit)
• Irritability and restlessness
• Persistent vomiting
• Red to reddish-purple spots (petechiae) or patches (ecchymoses) on the skin
• Seizure
• Severe abdominal pain
• Vomiting blood or black material (resembling coffee grounds)

D. Signs and tests

i. A physical examination may reveal:

• Enlarged liver (hepatomegaly)
• Low blood pressure
• Rash
• Red eyes
• Red throat
• Swollen glands
• Weak, rapid pulse

ii. Tests may include:

• Arterial blood gases
• Coagulation studies
• Electrolytes
• Hematocrit
• Liver enzymes
• Platelet count
• Serologic studies (demonstrate antibodies to Dengue viruses)
• Serum studies from samples taken during acute illness and convalescence (increase in
titer to Dengue antigen)
• Tourniquet test (causes petechiae to form below the tourniquet)
• X-ray of the chest (may demonstrate pleural effusion)

E. Treatment
Because Dengue hemorrhagic fever is caused by a virus for which there is no known cure or
vaccine, the only treatment is to treat the symptoms.
• A transfusion of fresh blood or platelets can correct bleeding problems
• Intravenous (IV) fluids and electrolytes are also used to correct electrolyte imbalances

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 • Oxygen therapy may be needed to treat abnormally low blood oxygen
• Rehydration with intravenous (IV) fluids is often necessary to treat dehydration
• Supportive care in an intensive care unit/environment

F. Expectations (prognosis)
With early and aggressive care, most patients recover from dengue hemorrhagic fever. However,
half of untreated patients who go into shock do not survive.

G. Complications
• Encephalopathy
• Liver damage
• Residual brain damage
• Seizures
• Shock

TINEA CORPORIS

A. Definition
Tinea corporis is a skin infection due to fungi. It is also
called ringworm of the body.

Causes
Tinea corporis is a common skin disorder among
children. However, it may occur in people of all ages. It is
caused by mold-like fungi called dermatophytes. Scientific
names for the most common of the dermatophyte fungi that
cause ringworm include Trichophyton rubrum, Trichophyton
tonsurans, Trichophyton interdigitale, and/or Trichophyton
mentagrophytes, Microsporum canis, and Epidermophyton
floccosum.
Fungi thrive in warm, moist areas. The following raise
the risk for a fungal infection:
• Long-term wetness of the skin (such as from sweating)
• Minor skin and nail injuries
• Poor hygiene

B. Patomechanism
When fungus affects the skin of the body, it
often produces the round spots of classic ringworm.
Sometimes, these spots have an "active" outer border as
they slowly grow and advance. It is important to
distinguish this rash from other even more common
rashes, such as nummular eczema. This condition, and
others, may appear similar to ringworm, but they are
not due to a fungal infection and require different
treatment.

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Risk factors
Tinea corporis can spread easily to other people. You can catch the condition if you come
into direct contact with an area of ringworm on someone's body, or if you touch contaminated
items such as:
• Clothing
• Combs
• Pool surfaces
• Shower floors and walls
The fungi can also be spread by pets (cats are common carriers).

Symptoms
 Symptoms may include itching.
 The rash begins as a small area of red, raised spots and pimples. The rash slowly becomes
ring-shaped, with a red-colored, raised border and a clearer center. The border may look
scaly.
 The rash may occur on the arms, legs, face, or other exposed body areas.

Signs and tests

Tinea corporis can often diagnose tinea corporis by how the skin looks.
In some cases, the following tests may be done:
• Looking at a skin scraping of the rash under the microscope using a KOH (potassium
hydroxide) test
• Skin lesion biopsy

C. Treatment
Antifungal medications are used to cure ringworm. Ringworm can be treated topically
(with external applications) or systemically (for example, with oral medications):
 Topical treatment: When fungus affects the skin of the body or the groin, many antifungal
creams can clear the condition in around two weeks. Examples of such preparations include
those that contain clotrimazole (Cruex cream, Desenex cream, Lotrimin cream, lotion, and
solution), miconazole (Monistat-Derm cream), ketoconazole (Nizoral cream), econazole
(Spectazole), naftifine (Naftin), and terbinafine (Lamisil cream and solution). These
treatments are effective for many cases of foot fungus as well. Many of these antifungal
creams are available as over-the-counter preparations. It is usually necessary to use topical
medications for at least two weeks.
 Systemic treatment: Some fungal infections do not respond well to external applications.
Examples include scalp fungus and fungus of the nails. To penetrate these areas and in cases
of particularly severe or extensive disease, oral medications can be used.

For a long time, the only effective antifungal tablet was griseofulvin (Fulvicin, Grifulvin,
and Gris-PEG). Now, other agents are available that are both safer and more effective. These
include terbinafine, itraconazole (Sporanox), and fluconazole (Diflucan). Oral medications are
usually given for a three-month course.

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Prognosis
Ringworm usually responds to topical medications within 4 weeks. Severe or resistant
cases usually respond quickly to antifungal medicines taken by mouth.

Complications
• Bacterial skin infections, cellulitis
• Skin disorders such as pyoderma or dermatophytid
• Spread of tinea to feet, scalp, groin, or nails
• Whole-body (systemic) side effects of medications

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References
1. John Hunter et. al, Clinical Dermatology 3rd Edition
2. Roberto Arenas et. al, Landes Bioscience Vademecum Tropical Dermatology
3. Riede / Werner, Color Atlas of Pathology © 2004 Thieme
4. Kumar et. Al, Robbins Basic pathology, 8th Edition
5. http://symptomchecker.about.com/od/Diagnoses/candidiasis.htm

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