Immunology dermatophytosis

Immunology dermatophytosis

Dr. MOH. IFNUDIN. SpKK.

INTRODUCTION

The fungus is an infectious agent in pandangn seruoa tumbuahan in the organization and structure, have properties that are not owned bakkteri dimorphism is the ability of the natural shape of hyphae which branched structures such as branches (vegetative form) are in the network host, round or oval unicellular (yeast form) . This dimorphism is a fungus that can change shape, making it hard for the body's defense system menaggulanginya. The walls of fungi are composed of layers of chitin polsakarida as a capsule and composed of N. acetyl glucosamine causing fungus is difficult in Exterminate by nonspecific immune system. The interaction between the fungus and determine the body's immune response fungus disease.

Immune system that play a role in fungal infection broadly divided into two groups, namely innate immunity (innate immunity) is non-specific and specific acquired immunity (acquired immunity) in the form of humoral and cellular responses.

In fungal infections, the first act is a nonspecific immunity, if this system fails, the immune system got a new specific action. Dermatophyte fungal infection of the skin, hair and nails called dermatophytosis. Included in this group of fungi dermatophytosis are Microsporum, Tricophyton and Ephidermopyiton are pleased with karatin mangandung tissue such as skin, hair and nails due to dermatophytes have keratinase enzyme so that it could destroy the keratin that is used for growth.

This paper will discuss various aspects of the body's immune in the face of fungal infections, especially dermatophytosis.

 

Pathogenesis

Dermatophyte fungal invasion into the epidermis begins with adhesion (adherens) artrokonodia on keratinocytes followed by penetration through or between epidermal cells, giving rise to reactions of the host. Artrokonodia adhesion process to the keratinocytes in the stratum corneum, which takes 2 hours artrokonidia growth and extension of hyphae. Penetration into the epidermis caused by dermatophytes are keritinofilik, have proteolytic enzyme keratinase which can damage the skin keratin, hair, and nails.

To be able to cause disease, the fungus must be able to overcome the body's defense both non-specific or specific. Also as a dermatophyte fungal pathogens, must be able to:

- Sticking to and penetrate the skin or mucus membranes.

- Surviving and adapting to environmental temperature and host tissue

- Growing, breeding and overcome the body's defense sisetm non-specific and specific

- Triggered tissue damage

Dematofit ability to adapt in the host tissue environment and overcome the cellular defenses is an important mechanism in the pathogenesis of dermatophytosis.

The environment in which appropriate patient skin is an important factor for the development of dermatophytosis. The skin is not intact due to trauma, high humidity with maceration are factors that facilitate infection. Tight clothing that does not absorb perspiration can increase the humidity making it easier for the emergence of Tinea pedis.

In the incubation period, dermatodit will grow and develop in the stratum, corneum, although it has not caused clinical abnormalities can be a positive KOH examination. In addition, required to cause disease state where dermatophyte growth rate equal or faster than the epidermal turnover of the epidermis.

Karatinase or other proteolytic enzymes produced by fungal colonization and the influential of these dermatophytes. Dermatophytes also produces catalase and superoxide dismutase that can fight the system myeloperoksidase of phagocyte cells.

Nonspecific immune SYSTEM

Marupakan nonspecific immune system of the body's innate defenses leading in the face of fungal infections because it may provide a direct reaction to antigens that enter, are the specific immune system to recognize antigens time mambutuhkan fungus before they can give his reaction.

Called the nonspecific immune system because it is not specifically directed against entigen atai certain micro-organisms existing and functioning since birth.

Important component of the nonspecific immune system, among others:

a. Physical defense / mechanical form of the skin and mucous membranes are intact and healthy

b. Biochemical defenses that can inhibit fungal skin infections include:

• acidic pH of sweat / vagina

• sebaceous secretion of fatty acids

• enzymes that are antimicrobial

After puberty, the production of saturated fatty acids on the scalp menigkat menyababkan inefksi dermatophyte fungus on the scalp of adults with less frequency.Unsaturated transferrin in serum is a serum inhibitory factor (SIF), capable of binding Fe ions needed for the growth of dermatophytes.

Alpha macroglobulin keratinase keratinase enzyme inhibitors inhibit the work so as to inhibit the growth of dermatophytes.

In short, some non-immunological factors that influence the infection dermatophytosis seen in Table I:

Table I. non-immunological factors that influence the pathogenesis of dermatophytosis

Quoted in the original from the literature 7

c. Pertahana humoral

Defense humorial of nonspecific immune system that play a role manigkatkan facilitate phagocytosis and destruction of fungi, among others: the complement, C-reactive protein (CRP).

• Complements

Complement system consists of 11 components of plasma proteins from nonspecific immune system, circulating in the circulation in a state separate and inactive tetapu every time can be activated by substances such as antigens, immune complex, and so forth. The result of this activation will produce a variety of mediators that are active bilogik in inflammatory processes including vasodilatation, kemotaksis phagocytes, opsonisasi, discharge resulting in tissue damage, destroy microbes and cell lysis.

Antigen-antibody complexes can activate the complement system via the classic route, starting with the activation of C1 in a chain that will activate the next complement so that eventually all the components until the last (C9) becomes active. The end result of complement activation process is the destruction of the cell membrane.

Activation of the complement system can also be through an alternative route starting with C3 activation. Aktifsi of complement leads to:

- The release of phagocytic cell factor resulted kemotaktik attracted to the area of ​​infection

- Opsonisasi that enhances phagocytosis

- Assisting the process of metabolism in inflammatory cells and destruction of infectious agents.

Fungi can activate the complement malalui alternate paths, so that complement activation is expected to:

- Destroy the fungal cell membrane

- Remove the material kemotaktik that mobilize macrophages to the fungus.

- Fungi that settles in perukaan memfagosit mekrofag easier.

The fungus usually have strong Diding impenetrable form of chitin by this complementary mechanism, so that the role of complement in defense against infection is not great dermatophytosis seen in Table II.

• C reactive protein (CRP)

CRP is increased in acute infection, with the help of Ca + + ion can bind to molecules found on the surface fosforikolin fungus that can bind to complement and facilitate phagocytosis. The existence of a fixed high CRP showed a persistent infection.

d. Cellular defense

Cells in the body can do fsagositosis which is a non spesefik defense mainly carried out by mononuclear cells (monocytes and macrophages), polymorphonuclear cells (PMN) or granulocytes, natural killer cells (NK).

Specific immune SYSTEM

In contrast to the nonspecific immune system, immune system able to identify specific agents that are considered foreign to him. Cells that play an important role in specific immune system are lymphocytes T and B lymphocytes

T lymphocytes play a role in the cellular system is B lymphocyte cells play a role in the formation of immunoglobulin are important in humoral immunity system.

Antigenic material from dermatophyte fungi consisting of polysaccharides, keratinase, polypeptides, and ribonucleic acid. Glikopeptida antigen is an antigen with antigenesis palingkuat and has a similar structure of the three dermatophyte fungal genus causing cross reactions. Research on responses to the dermatophyte most developed is against Trichophyton and is considered to represent an immune response against the other dermatophytes.

a. Cellular immune system

System-specific cellular immunity, is the body's defense system is important in combating fungal infections. Patients with T lymphocyte system imunodifesiensi or received immunosuppressive treatment would be more easily infected by fungus.Antigen fungal pathogens, which first appeared daalm loss can be found free or bound to the cell surface of macrophages (antigen presenting cell = APC) for presentation to T lymphocytes often the antigen must be processed first, broken down by the APC into small immunogenic peptide before it can be recognized by T lymphocytes selnjutnya interaction between APC antigen carried by lymphocytes, lead to proliferation, differentiation and activate riboson in the cells to release chemotactic mediators limphokines among other factors, macrophage migration inhibitory factor actifating factor, arming macropage specific factor that is useful to increase the biological activity of phagocytosis and inflammatory processes.

T lymphocytes will have profilerasi and differentiation, forming a specific population of T cells, namely cell effector and memory cells. Memory cell will stay in circulation until a few years and will quickly generate a response when the meet again with the same antigen. So on the specific immune system, occurs sensitization of T lymphocytes and known to be more rapid if the cells for later destruction.

Reaction of cellular immunity involves three stages namely:

• Stage I

The combination of antigen with sensitized T lymphocytes specific.

Include binding of antigen with sensitized lymphocytes, macrophages, which gives basic assisted identification of a specific antigen.

• Stage II

Morphology and biochemical reactions.

Is perunbahan morphology of lymphocyte transformation and mitosis of cells perunahan limfobas and biology of protein synthesis in DNA and RNA.

• Stage III

Biological expressions:

Expression of biology there is a change in stage I and II of the generation of T lymphocyte cell population which T helper cells, suppressor T cells, cytotoxic T cells, T cells which produce mediators cellular immunity and memory cells.

Mediators produced by T lymphocyte cells are called lymphokine cytokine among others:

- Chemotactic factor (CF): attract monocytes / macrophages to the site of infection

- Migration inhibitory factor (MIF) macrophage cells to immobilize sehigga still gathered at the site of infection.

- Macrofag actifating factor (MAF): kemmapuan enhances macrophage activity so that more virulent.

- Specific macropage arming factor (SMAF): arming macrophages to attack specific antigens.

Briefly, after antigen with an intermediary macrophages as APC met with T lymphocytes, the T lymphocytes that will differentiate daapt sebgai following functions:

- Helper T cells help B lymphocyte cells in the production antinodi

- Cell cytotoxic and natural killer cells recognize and destroy infected.

- Mediator cellular immunity among others CF, MIF, MAF, activate phagocytosis of macrophages.

- T cells control the threshold and the quality of the immune system by pressing the activity of other T lymphocytes and B lymphocytes

Premises erspons way inflammation will increase and is expected to manggulangi fungal infections. Macrophages with lymphokine effect will be activated macrophages that have a greater ability to increase phagocytosis.

The process of generating cellular immune system of this nature will spsesifik but the effector mechanisms of phagocytic cells brought nonspecific nature.

To know the immune system that occur dpat spssifik Trichophytin intra-dermal test in patients with infection Trichophytin premises, the visible reaction depends on the mediators that play a role as shown in Table II, namely:

Reaction

Reaction Time% prevelance type mediators

Wheal 30 min 20 I Ig E

Rare 2-12 hr Papule III IgG, C?

Papule 50 IV 1-3 days

No reaction 0-7 days 25 - -

Quoted in the original from the literature 8

Urtika at 30 minutes after injection showed rapid hipertensitivitas reaction (immediate) and IgE mediated type I reaction terjasdi in 20% of patients.

Papel arising 2-12 hours after the injection of type III reacted with IGC mediators and the complement reaction is rare in patients with dermatophytosis terjdi.

Papel arising 1-3 days after the injections showed type IV reaction mediated by lymphocytes without the type I hypersensitivity reactions often occur later than normal in patients with Tinea kruris, Tinea and Tinea capitis due to Trichophyton rubrum korposis by a chronic and resistant, or in patients atopy with high IgE levels.

To determine cellular immunity against the fungus Trichophyton Trichophyton can be evaluated intra-dermal test premises that is read after the 48 hours.

Positive reaction in case of inflammation and induras, a negative reaction should not arise if inflammation and induration. Sisetm this cellular immunity plays an important role in defense against infection dermatophytosis. This can be seen in patients with Trichophyton test that provides intra-dermal induration and inflammation after the 48 hours, mean cellular imnitas already formed, then the inflammatory reaction that happens to be lighter and quicker recovery, and KOH examination or culture negative bias. The relationship between test results with the state of Trichophyton clinic patients can be seen in Table III below in:

Clinical Test result status

Wheal (30 min)

Papole (after 48 hours)

No reaction - Dermatopithosis

Previously infected, resolved

- Previously infected, resolved

Resolving infection

Kerion

Id reaction

Inflamtory tinea pedis

- Never infected

- Chronic Dermatophytosis

- Immunodeficiency disea

Quoted in the original from the literature 8

b. Humoral immune system

B lymphocyte cells are 5 -15% of the total number of lymphocytes in the circulation that serves to produce antibodies. These cells are marked premises of immunoglobulins formed in the cell and then released but some stuck to the surface of cells that then function as resptoe antigens.

In human B lymphocyte cell maturation occurs in the marrow wanderer, after the mature move to the spleen, and tonsils kelnjar limfoit. The effect of antigen malalui T helper lymphocytes that produce B-cell growth factor (BCGF) and B-cell differensiation factor (BCDF), B lymphocytes and differentiated manjadi berfoliferasi plasma cells capable of producing immunoglobulins with spesivitas same as the existing receptors on the surface prekusornya cells. In the plasma cells will occur the transaction process is pentransferans information genetikauntuk immunoglobulin molecules of DNA into mRNA, forming a specific antibody.

Dermatophytosis infection can lead IgG antibody. IgM and IgA and even IgE that can be shown by precipitation reaction of hemagglutination, antibody fixation koplemen and this will soon disappear from circulation when the infection healed.

Humoral immunity has little role in the defense system ajmur dermatophyte infections, this is diy \ show with:

- Patients with lesions of tinea imbrikata premises turned out to have very broad ang high antibody levels.

- Patients with atopy degna high levels of immunoglobulin E, often mn \ enderita dematofitosis chronic.

- Patients with chronic infection, acquired high-titer antibody ayng of IgG, IgM, IgA and even IgE.

In the first infection fungus Trichophyton premises where the patient is on Trichophyton skin test results fast reaction member (immediate) is still negative, clinical symptoms of a mild inflammatory reaction and formation of skuama little.

After his 10-15 days, the rapid reaction of Trichophyton skin test positive start then eraksi inflammatory ayng terjad become heavier and feels more itchy. Glikopeptida of Trichophyton antigens started to be presented by makropang to T lymphocytes resulting in the release of cytokines and other inflammatory mediators that can inhibit the growth of Trichophyton this part though examination of KOH preparations and fungal cultures of the lesion was still positive. When linfosit T cells are sensitized and cellular immunity has been established, the inflammatory reaction becomes greatly reduced even in case of lost and re-infection occurring mild inflammatory reaction and recover faster, KOH examination and culture of the lesions are often negative.

REACTION ID

In dermatophytosis daapt id reaction commonly called dermatophytid a secondary inflammatory reaction in another place from where the primary dermatophyte infection can occur 4-5% of patients. Lesions id reaction is not obtained from dermatofi element, KOH examination and negative culture. The exact mechanism is unknown, suspected as the immunological response against fungal antigens diabsorsi sitemik into the circulation.

Form eruptions eczema esikuler numularis or on the hands and feet associated with slow reaction (48 hours) is positive on the test Trichophytin, was bnetuk sentrifugum erythema and urticaria associated denan immediate reaction (20-30 minutes) is positive.

Kerion

Kerion is a great inflammatory reaction in dermatophytosis is like tumor formation.Trichophytin test usually gives a strong positive hypersensitivity reactions slow. Skin lesions suspected to be an abscess like immediate manifestation of delayed type hipersnsitivitas reaction.

SUMMARY

To be able to cause disease daapt dermatophytes must overcome the defense system of non-specific and specific. Non-specific defense system consists of skin and membranes are intact and healthy landir, biochemical defenses in the form of acid pH, antimicrobial fatty acids and enzymes, humoral pertahana form of complement and CRP serata cellular phagocytosis system.

Specific defense systems that were most responsible is imnitas cellular system involving T lymphocytes, lymphokine and phagocytic cells. Humoral immune system which dihantar by antibody and complement mampunyai a small role and is directed more for diagnostic purposes.

REFERENCES

1. Bratawijaya KG. Basic immunology. 4th Edition. Jakarta: Balai Publisher FKUI; 2000

2. Roitt I, Brostoff J, male D. Immunology. 4th ed. London: Mosby; 1996

3. Hay RJ, Moore M. Mycalogy. In: Champion RH, Burton JL, Burns Da, Breathnach SM, editors. Textbook of Dermatology. 6th ed. Oxford: Blackwell Sciner; 1998.p.1277-350

4. January susilo Immunology fungal infections. In: Budimulya U, Kuswadji, Basuki S, Menaldi SL, Suriadiradja A, Dwihastuti P, editors. Diagnosis and management of dermatomitosis. Jakarta: Balai Publisher FKUI; 1992.h 16-20.

5. Martin AG, Kobayashi. Superficial Fungal Infection. In: freedberg M, Elesen AZ, Wolf KAusten KF, Goldsmith LA SI, et al, editors. Fitzpatrick's xdermatology in General Medicine. 5th ed. New York: McGraw Hill; 1999.p.2337-58

Edting By: EnongXp