Hypersensitivity and its types.pptx
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A brief description over Hypersensitivity and its types.
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Hypersensitivity and its types.pptx
- 1. SARDAR PATEL MAHAVIDYALAYA CHANDRAPUR DEPARTMENT OF MICROBIOLOGY 2021-2022 Hypersensitivity and its types A Seminar on PRESENTED BY DEEPAK CHAWHAN (M.Sc. II Yr. Semester- IV)
- 2. CONTENTS Introduction Classification of Hypersensitivity Type I Hypersensitivity- Causes, Signs of Hypersensitivity, Diagnosis and Treatment Type II Hypersensitivity- Example, Diagnosis and Treatment Type III Hypersensitivity- Example, Diagnosis and Treatment Type IV Hypersensitivity- Example, Diagnosis and Treatment References
- 3. INTRODUCTION Hypersensitivity (also called as Hypersensitivity reaction or intolerance). It refers to excessive, undesirable, damaging, discomfort- producing and sometimes fatal reactions produced by the normal immune system, including allergies and autoimmunity. Hypersensitivity reactions require pre-sensitized (immune) state of the host.
- 4. Classification of Hypersensitivity Type I (Immediate/Atopic/Anaphylactic) Type II (Cytotoxic Hypersensitivity/ Antibody Mediated Hypersensitivity) Type III (Immune Complex/Arthus Hypersensitivity) Type IV (Cell Mediated/ Delayed Type of Hypersensitivity)
- 5. Type I Hypersensitivity Type I Hypersensitivity also known as Immediate/Atopic/Anaphylactic Hypersensitivity. This develops within few minutes of exposure to the allergen. The reaction is mediated by Immunoglobulin E and other factors involved in inflammation. The primary cellular component in this hypersensitivity is the mast cell or basophils.
- 6. Causes - The allergens are considered to be the cause of hypersensitivity. The allergens are the non-parasite antigens that stimulate the type I hypersensitivity response.
- 7. Signs of Type I Hypersensitivity The reaction may involve skin (urticaria and eczeema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthama) and gastroinestinal tract (Gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death.
- 8. Diagnosis of Type I Hypersensitivity Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specific IgE antibodies against the suspected allergens. Total IgE and specific IgE antibodies are measured by a modification of enzyme immunoassay (ELISA). Increased IgE levels are indicative of an atopic condition, although IgE may be elevated in some non-atopic diseases (e.g., myelomas, helminthic infection, etc).
- 9. Treatment of Type I Hypersensitivity Drugs- > Non-steroidal anti-inflammatories (NSAIDs) > Antihistamines block histamine receptors. > Steroids> Theophylline OR epinephrine -prolongs or increases CAMP levels in mast cells which inhibits degranulation. Immunotherapy- > Desensitization (hyposensitization)also known as allergy shots. > Repeated injections of allergen to reduce the IgE on Mast cells.
- 10. Type II Hypersensitivity Type II Hypersensitivity also known as Cytotoxic Hypersensitivity/ Antibody Mediated Hypersensitivity. This may affect a variety of organs and tissues. This develops within minutes to hours of exposure to the allergen. The reaction is mediated by antibodies of Immunoglobulin M or Immunoglobulin G Class and complements.
- 11. Hemolytic disease in Newborn -
- 12. Diagnosis of Type II Hypersensitivity Diagnostic tests for detection of circulating antibodies against the tissues involved by immunofluoresence. Stainning procedures also used in the diagnosis.
- 13. Treatment of Type II Hypersensitivity Drugs- > Non-steroidal anti-inflammatories (NSAIDs) > Immunosuppresive Agents.
- 14. Type III Hypersensitivity Type III Hypersensitivity also known as Antigen- Antibody Immune Complex/Arthus Hypersensitivity. This may affect capillaries, joints and trigger inflammation. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs(e.g., aspergillosis), joints (e.g., rheumatoid arthritis) or other organs. This develops within 3 - 10 hours after exposure to the antigen. The reaction is mediated by immune complexes mostly of Immunoglobulin G, although Immunoglobulin M Class may also be involved.
- 15. Signs of Type III Hypersensitivity -
- 16. Diagnosis of Type III Hypersensitivity Diagnosis involves examination of tissue biopsies for the deposit of Immunoglobulins and complement by immunofluoresence microscopy. The presence of immune complexes in the serum and depletion in the level of complement are also diagnostic.
- 17. Treatment of Type III Hypersensitivity Drugs- > Non-steroidal anti-inflammatories (NSAIDs)
- 18. Type IV Hypersensitivity Type IV Hypersensitivity also known as Cell Mediated/ Delayed Type of Hypersensitivity. This reaction peaks within 48 hours after the injection of antigen. There are two different types of reactions capable of causing tissue injury in this way. 1.delayed type hypersensitivity is mediated by CD4+ helper Tcells 2. cell mediated cytotoxicity, is mediated by CD8+ T cells.
- 19. Signs of Type IV Hypersensitivity -
- 20. Diagnosis of Type IV Hypersensitivity Diagnostic test involves Montoux test Patch test (for contact dermatitis) Mitogenic response Interleukin- 2 production
- 21. Treatment of Type IV Hypersensitivity Drugs- > Corticosteroids > Other Immunosuppresive agents
- 23. References Immunology and Medical Microbiology, R.P. Singh Textbook of Microbiology& Immunology, 2nd Edition, Subhash chandra Parija
- 24. Thank you…..
Editor's Notes
- Good Morning Everyone, My Seminar topic is on Hypersensitivity and its types.
- These are the contents of the seminar:
- Hypersensitivity (also called as Hypersensitivity reaction or intolerance). It refers to excessive, undesirable, damaging, discomfort- producing and sometimes fatal reactions produced by the normal immune system, including allergies and autoimmunity. Hypersensitivity reactions require pre-sensitized (immune) state of the host.
- Based on the duration and mechanism of the reaction Hypersensitivity is classified as- Type I (Immediate/Atopic/Anaphylactic) Type II (Cytotoxic Hypersensitivity/ Antibody Mediated Hypersensitivity) Type III (Immune Complex/Arthus Hypersensitivity) Type IV (Cell Mediated/ Delayed Type of Hypersensitivity)
- Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. It develops within few minutes of exposure to an allergen. Anaphylactic reactions are mediated by IgE and other factors involved in inflammation (inflammation means the protective response of the tissues to the damage or destruction of cells). When the body is exposed to an allergen, the IgE immunoglobulins are produced.- These immunoglobulins bind with the surface receptors of mast cells and basophills (Mast cells are the granulated wandering cells found in connective tissue and circulating basophils.) beneath the mucous membrane in the throat, lungs and eyes. During subsequent exposure of the body to the same allergen, the allergen IgE antibody reaction takes place. (Have a look over the picture). This leads to degranulation of mast cells and basophils, with the release of some chemical mediators such histamine.
- The allergens are considered to be the cause of hypersensitivity. The allergens are the non-parasite antigens that stimulate the type I hypersensitivity response. This is some of the list of allergens commonly associated with type I hypersensitivity.
- The chemical mediators produce the hypersensitivity reactions such as fall in blood pressure (due to vasodilatation), obstruction of air passage and difficulty in breathing (due to bronchoconstriction) and shock. The reaction may involve skin (urticaria and eczeema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthama) and gastroinestinal tract (Gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death.
- Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specific IgE antibodies against the suspected allergens. Total IgE and specific IgE antibodies are measured by a modification of enzyme immunoassay (ELISA). Increased IgE levels are indicative of an atopic condition, although IgE may be elevated in some non-atopic diseases (e.g., myelomas, helminthic infection, etc). (Normal level of IgE is <75kU/L
- Drugs- > Non-steroidal anti-inflammatories (NSAIDs) > Antihistamines block histamine receptors. > Steroids> Theophylline OR epinephrine -prolongs or increases CAMP levels in mast cells which inhibits degranulation. Immunotherapy- > Desensitization (hyposensitization)also known as allergy shots. > Repeated injections of allergen to reduce the IgE on Mast cells.
- Type II hypersensitivity is also known as cytotoxic hypersensitivity and Antibody Mediated Hypersensitivity.This may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) that can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia, thrombocytopenia are such examples. Penicillin allergy also belongs to this class. The reaction time is minutes to hours. The reaction is mediated by antibodies of Immunoglobulin M or Immunoglobulin G Class and complements.
- Let us understand with an example- Hemolytic disease in Newborn If the mother is Rh (–ve) and the foetus is Rh (+ve) Rh factor incompatibility IgG antibodies to Rh an innocuous rbc antigen > Rh+ baby born to Rh- mother first time fine. 2ndtime can have antibodies to Rh from 1st pregnancy. > Antibodies crosses placenta and baby kills its own rbcs.> Treat mother with antibody to Rh antigen right after birth and mother never makes its own immune response.
- Diagnosis of Type II Hypersensitivity- Diagnostic tests for detection of circulating antibodies against the tissues involved by immunofluoresence. Stainning procedures also used in the diagnosis.
- Drugs- > Non-steroidal anti-inflammatories (NSAIDs) > ImmunoSuppresive Agents.
- Type III hypersensitivity is also known as Antigen- Antibody Immune Complex/Arthus Hypersensitivity. IgG mediated Large amount of antigen and antibodies form complexes in blood. If not eliminated can deposit in capillaries or joints and trigger inflammation. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs(e.g., aspergillosis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms. The reaction may take 3 - 10 hours after exposure to the antigen. It is mediated by soluble immune complexes. They are mostly of the Ig G class, although Ig M may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE).The antigen is soluble and not attached to the organ involved TYPE III PMNs and macrophages bind to immune complexes via FcR and phagocytize the complexes. BUT If unable to phagocytize the immune complexes can cause inflammation via C' activation ---> C3a C4a, C5a and "frustrated phagocytes".
- Signs of Type III Hypersensitivity involve SLE (subcutaneous lupus erythematosus), Various disease asssociated with the fungus aspergillus., Arthus reaction, rheumatoid arthritis are observed.
- Diagnosis involves examination of tissue biopsies for the deposit of Immunoglobulins and complement by immunofluoresence microscopy. The presence of immune complexes in the serum and depletion in the level of complement are also diagnostic.
- Drugs- > Non-steroidal anti-inflammatories (NSAIDs) > ImmunoSuppresive Agents.
- Type IV Hypersensitivity also known as Cell Mediated/ Delayed Type of Hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction which peaks 48 hours after the injection of antigen (tuberculin) Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. There are two different types of reactions capable of causing tissue injury in this way. 1.delayed type hypersensitivity is mediated by CD4+ helper Tcells2. cell mediated cytotoxicity, is mediated by CD8+ T cells. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the damage. The delayed hypersensitivity lesions mainly contain monocytes and a few T cells.
- Signs of Type IV Hypersensitivity involves Contact dermatitis, Poison ivy.
- Diagnostic test involves Montoux test Patch test (for contact dermatitis) Mitogenic response Interleukin- 2 production
- Drugs- > Corticosteroids > Other Immunosuppresive agents
- This is the brief over Hypersensitivity and its types
- These are the references
- Thank You