Allergy Reaction immunity microbiology bpt 2nd year
Reading File
Now let me search the medical library for allergy, hypersensitivity reactions, and immunity topics relevant to BPT 2nd year microbiology.
Finding Sources
Finding Sources
Excellent! Jawetz Medical Microbiology is perfect for BPT 2nd year. Let me now read the key sections in parallel.
Finding Sources
Reading File
I have excellent content. Let me read more to get all 4 types fully covered, plus search for immunity basics and images.
Reading File
Searching Images
hypersensitivity types I II III IV allergy classification diagram
Let me get the rest of the hypersensitivity content (Types II, III, IV) and immunity basics.
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.