Allergy Reaction immunity microbiology bpt 2nd year
Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Searching Images
hypersensitivity types I II III IV allergy classification diagram
Reading File
Searching Images
IgE mast cell degranulation type I hypersensitivity anaphylaxis
I now have all the core content needed. Let me compile the comprehensive answer for BPT 2nd year students.
Allergy, Hypersensitivity Reactions & Immunity - BPT 2nd Year Microbiology
1. Basic Concepts of Immunity
The immune system is divided into two broad arms:
| Feature | Innate Immunity | Adaptive (Acquired) Immunity |
|---|---|---|
| Speed | Immediate | Delayed (days) |
| Specificity | Non-specific | Highly specific |
| Memory | None | Yes (immunological memory) |
| Key cells | Macrophages, NK cells, neutrophils | T cells, B cells |
| Key molecules | Complement, interferons | Antibodies (immunoglobulins), cytokines |
Humoral immunity is mediated by B lymphocytes and their antibodies (IgG, IgM, IgA, IgE, IgD). Cell-mediated immunity (CMI) is mediated by T lymphocytes.
2. Hypersensitivity - Overview
Hypersensitivity is a condition in which an exaggerated or augmented immune response occurs that is harmful to the host. It requires a presensitized state - reactions typically occur after the second exposure to a specific antigen (allergen).
In 1963, Coombs and Gell classified hypersensitivity into four types:
- Types I, II, III - Antibody mediated
- Type IV - T-cell mediated
3. Type I: Immediate Hypersensitivity (Allergy)
Also called: Anaphylactic / IgE-mediated / Atopic hypersensitivity
Timing: Occurs within seconds to minutes after antigen exposure.
Mechanism:
- First exposure (sensitization): Antigen induces formation of IgE antibody
- IgE binds by its Fc portion to high-affinity IgE receptors (FcεRI) on mast cells and basophils
- Second exposure: The antigen cross-links cell-bound IgE molecules
- This triggers degranulation and release of pharmacological mediators
Mediators:
Primary mediators (preformed):
- Histamine - causes vasodilation, increased capillary permeability, bronchospasm
Secondary mediators (newly formed from arachidonic acid):
- Prostaglandins - edema, bronchoconstriction
- Leukotriene B4 - chemoattractant, recruits leukocytes
- Leukotrienes C4 and D4 - vasodilation, vascular permeability
- TNF-α and IL-4 also act as secondary mediators
Clinical Manifestations:
| Local | Systemic |
|---|---|
| Hay fever (rhinitis) | Anaphylaxis (most severe) |
| Asthma | Urticaria (hives) |
| Eczema | Angioedema |
| Food allergy | - |
Atopy:
- Strong familial/genetic predisposition
- Associated with elevated IgE levels
- Triggered by environmental allergens: pollens, ragweed, house dust, shellfish
- Common manifestations: hay fever, asthma, eczema, urticaria
Treatment of Anaphylaxis:
- Epinephrine (drug of choice - reverses bronchospasm, maintains BP)
- Antihistamines (block histamine receptors - effective in rhinitis)
- Corticosteroids (reduce inflammation)
- Maintain airway, artificial ventilation if needed
- Prevention: Identify antigen by skin test or IgE serology → avoid trigger
4. Type II: Cytotoxic Hypersensitivity
Mediated by: IgG (or IgM) antibodies directed against cell surface antigens or extracellular matrix
Timing: Hours to days
Mechanism:
- Antibody binds to cell surface antigen → complement activation → cell lysis
- Or antibody to cell surface receptor alters cell function without lysis
Clinical Examples:
| Condition | Mechanism |
|---|---|
| Hemolytic anemia | IgG against RBC surface antigens |
| ABO transfusion reactions | Preformed antibodies destroy donor RBCs |
| Rh hemolytic disease | Maternal IgG crosses placenta, destroys fetal RBCs |
| Goodpasture syndrome | Antibody to basement membrane of kidney & lung → complement activation, severe membrane damage |
| Graves disease | Autoantibody binds TSH receptor → hyperthyroidism (stimulatory - no cell injury) |
| Penicillin-induced hemolysis | Drug attaches to RBC surface → antibody formation → hemolysis |
5. Type III: Immune Complex (Serum Sickness) Hypersensitivity
Mediated by: IgG antibodies forming antigen-antibody immune complexes
Timing: 6-21 hours (subacute)
Mechanism:
- Immune complexes normally cleared, but when they persist and deposit in tissues (kidneys, joints, vessels), they activate complement → macrophage/neutrophil migration → inflammation and tissue injury
Two major forms:
-
Arthus Reaction (local):
- Low-dose antigen injected into skin → IgG produced → local complement activation → mast cells and neutrophils release mediators
- Occurs within 12 hours
-
Systemic Immune Complex Disease:
- Example: Acute poststreptococcal glomerulonephritis
- Onset weeks after Group A β-hemolytic streptococcal infection
- Streptococcal antigen-antibody complexes deposited in glomeruli → complement fixed → neutrophil attraction → kidney damage
- Low complement level (C3 consumed)
- Lumpy deposits of immunoglobulin + C3 seen on immunofluorescence along the glomerular basement membrane
Other examples:
- Serum sickness (after foreign protein injection)
- SLE (nephritis, arthritis, vasculitis from "self" antigen-antibody complexes)
- Rheumatoid arthritis
6. Type IV: Cell-Mediated (Delayed) Hypersensitivity
Mediated by: T lymphocytes (NOT antibodies)
Timing: 48-72 hours after antigen contact (hence "delayed")
Mechanism:
- Antigen presented to sensitized T cells
- T cells proliferate and release cytokines: IFN-γ and IL-2
- Macrophages are activated → inflammation and tissue injury
Subtypes:
A. Contact Hypersensitivity:
- Sensitizing agents: nickel, formaldehyde, poison ivy/oak, topical sulfonamides
- Results in contact dermatitis (skin redness, vesicles, itching)
B. Tuberculin (Tuberculosis) Reaction:
- Injection of purified protein derivative (PPD/tuberculin) in a sensitized person
- Hard, raised lesion peaks at 48-72 hours
- Basis of the Mantoux test for TB screening
C. Granulomatous Hypersensitivity:
- Most severe form of Type IV
- Occurs when the antigen cannot be cleared by macrophages
- Results in granuloma formation (e.g., tuberculosis, sarcoidosis, leprosy, schistosomiasis)
7. Summary Comparison Table (Coombs & Gell Classification)
| Feature | Type I | Type II | Type III | Type IV |
|---|---|---|---|---|
| Name | Immediate / Anaphylactic | Cytotoxic | Immune Complex | Delayed / Cell-mediated |
| Mediator | IgE | IgG / IgM | IgG / IgM complexes | T cells |
| Target | Mast cells, Basophils | Cell surface antigens | Tissue deposits | Any cell with antigen |
| Timing | Seconds-minutes | Hours | 6-21 hours | 48-72 hours |
| Complement | No | Yes | Yes | No |
| Key examples | Anaphylaxis, Asthma, Hay fever | Transfusion reactions, Goodpasture, Graves | SLE, Post-strep GN, Arthus reaction | TB test, Contact dermatitis, Granulomas |
| Transfer | Serum (IgE) | Serum (IgG) | Serum | Cells (lymphocytes) |
8. Key Points for Exams
- IgE is the hallmark antibody in Type I hypersensitivity (allergy)
- Epinephrine is the FIRST-LINE treatment in anaphylaxis
- Antihistamines work in Type I by blocking H1 receptors
- Type II involves complement activation by cell-bound antibody
- Type III immune complexes activate complement in vessel walls, kidney, joints
- Type IV is the ONLY type NOT mediated by antibodies - it is purely T-cell dependent
- Mantoux/PPD test is the classic example of Type IV hypersensitivity
- Granuloma formation = most severe Type IV reaction
Source: Jawetz, Melnick & Adelberg's Medical Microbiology, 28th Edition, pp. 151-154
This is a shared conversation. Sign in to Orris to start your own chat.