2. LEARNING OBJECTIVES:
• At the end of this unit students will be able
to:
– Define hypersensitivity
– Explain the four different types of
hypersensitivity
3. HYPERSENSITIVITY:
“Exaggerated or inappropriate immune response”.
Types:
Hypersensitivity reactions can be subdivided into
four main types.
– Type 1 or Immediate or anaphylactic hypersensitivity
– Type 2 or Cytotoxic hypersensitivity
– Type 3 or Immune complex
– Type IV or Delayed or cell-mediated hypersensitivity
• Types I, II, and III are antibody-mediated,
whereas type IV is cell-mediated
4. Type 1 or Immediate or anaphylactic hypersensitivity
On first exposure Ag induces formation of IgE antibodies
Binding of IgE antibody to mast cells & basophils
On 2nd exposure cross reaction of the cell-bound IgE
Degranulation & release of mediators within minutes
Allergic reaction
6. Type 1 or Immediate or Anaphylactic hypersensitivity
Antibody Time of
Onset
Mediators Reactions
Reaction is
mediated
by IgE
Minutes • Histamine
• Serotonin
• Slow-reacting substance
of anaphylaxis (SRS-A)
• Prostaglandins
• Platelet-activating factor
(PAF)
• Eosinophil chemotactic
factor of anaphylaxis
(ECF-A)
• Food allergy
Such as peanuts and
shellfish,& bee venom
• Allergic asthma.
• Allergic conjunctivitis
• Allergic rhinitis (“hay
fever”)
• Drug allergies
especially penicillin,
• eczema (atopic
dermatitis)
7.
8. • The most severe form of type I
hypersensitivity is systemic anaphylaxis, in
which severe bronchoconstriction and
hypotension (shock) can be life-threatening.
• A sense of doom and dizziness can occur.
• Other symptoms include wheezing due to
bronchoconstriction, hoarseness due to
laryngeal edema, pruritis, and urticaria.
Tachycardia, arrhythmia, cyanosis, and
cardiac arrest can occur
9. TREATMENT & PREVENTION
• Treatment of anaphylactic reactions include
drugs to counteract the action of mediators
• Maintenance of an airway
• Support of respiratory and cardiac function.
• Epinephrine
• The treatment typically involves antihistamines
along with nasal decongestants.
• Prevention relies on identification of the
allergen by a skin test and avoidance of that
allergen.
10. Antibody Time of
Onset
Reactions Examples
IgG or IgM Hours to
days
Antigen on cell surface react with
Abs
complement activation or
antibody-dependent cell-
mediated cytotoxicity
destruction of foreign cell or host
cells carry antigen on their surface
• Blood
transfusion
reactions
• ABO transfusion
reactions
• & Autoimmune
hemolytic
anemia.
Type 2 or Cytotoxic hypersensitivity occurs when antibody directed at
antigens of the cell membrane activates complement . This generates a membrane
attack complex, which damages the cell membrane. The antibody (IgG or IgM)
attaches to the antigen via its Fab region and acts as a bridge to complement
via its Fc region. As a result, there is complement mediated lysis
12. • Type III reaction involve antibodies against
soluble antigens circulating in the serum in
contrast, type II immune reactions are
directed against antigens located on cell or
tissue surfaces.
• Antigen-antibody complexes are deposited
in organs and cause inflammatory damage.
13. Type Antibody Time of Onset Reactions Examples
Type 3 or
Immune
complex
Reactions
Immune
complex
hypersensitiv
ity occurs
when
antigen–
antibody
complexes
induce an
inflammator
y response in
tissues
IgG or
IgM
2 to 3 weeks Antibodies bind to
antigens to form
immune
complexes in
circulation
immune complexes
subsequently
deposit in tissues.
Complement
activation & Release
of lysosomal
enzymes
Tissue damage
Systemic
Lupus
Erythematosu
s
& Post-
streptococcal
Glomerulonep
hritis
15. Type Antibody Time of
Onset
Reactions Examples
Type IV or
Delayed
or cell-
mediated
hypersensi
tivity
Cell-
mediated
response
T cells are
involved
2 to 3
days
T Lymphocytes
activation upon 2nd
exposure
Lymphokines
release
Cells inflamatted
Tuberculin -
type
Hypersensitivit
y,
Type-1
diabetes &
Allergic
contact
dermatitis
16. • Response is delayed due to time is required
by the participating T cells and macrophages
to migrate to and accumulate near the
foreign particles
17.
18. REFERENCES:
• Gladwin, M., & Trattler, B. (2009). Clinical
Microbiology: Made Ridiculously Simple. Miami,
FL: Medmaster. Inc. Pub.
• Levinson, W. (2014). Review of Medical
Microbiology and Immunology. McGraw-Hill
Education.
• Tortora , Jerard J. (2010). Microbiology: An
Introduction
