JOITIBA COLLEGE OF NURSING

Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

BY: MS. SWITY JOSHI

 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

 Subject: microbiology

 Placement: 1st year P.B. B.sc nursing

 Teaching method: Lecture, discussion and demonstration

 A.V aids: P.P.T, black board, tranceperancy.

 General objective: at the end of lecture student will able to understand hypersensitivity and they will

use their knowledge in day to day life.

 Specific objective:
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

 To define hypersensitivity

 To explain types of hypersensitivity

 To explain clinical disorder of hypersensetivity

objective Time content Method A.V Method

of aids of
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

teaching evaluati
on
To define 1 min What is hypersensitivity? Lecture PPT, Question
the It is excessive immune response which leads to and trance- and
hypersense undesirable consequences, i.e. tissue or organ discussion Parncy answers
tivity damage/ dysfunction.
Black
To explain Types :
types of Type Ⅰ hypersensitivity(anaphylactic) Board
hypersense IgE mediated, immediate hypersensitivity/
tivity allergy
Major features:
 React and disappear quickly on re-exposure to Ag
 Dysfunction rather than severe tissue and cell
damage occurs
 Obvious individual difference and genetic
correlation
Component and cells
Allergen: An antigen that causes allergy.
 Hapten can turn into allergen by carrier effect
(hapten +carrier →immunogen)
 Common allergen: inhalant allergen (grass
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

pollen, animal dander, feces from mites in house

dust, etc.), some kinds of food and drugs
Reaginic antibody (IgE)
The main anaphylactic Ab in human
IgE can bind FcεRⅠon mast cells and basophils
by its CH4 domain, cause anaphylaxis
Mast cells
Express high affinity IgE Fc receptor FcεRⅠ,
granules contain mediators.
Distribution: connective tissues, mucosa, skin
Anaphylaxis is triggered by clustering of IgE
receptors (FcεRⅠ) on mast cells and basophils
through cross-linking
IgE-binding Fc recepors
FcεRⅠ: high affinity receptor of IgE on mast cell/
basophil, activate mast cell/ basophil
FcεRⅡ:low affinity
Mediators released by mast cells
Primary mediators (preformed): heparin,
histamine, neutral protease, eo-sinophil &
neutrophil chemotactic factors, provoke early
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

phase(immediate) reaction
Secondary mediators(newly synthesi-zed) :
leukotrienes(LTB4, LTC4 and LTD4), PGD2, PAF,
CKs(IL-4, GM-CSF), induce late phase reaction
Mechanism of typeⅠhypersensitivity
Allergen→host→specific B-cell→IgE→Fc
fragment of IgE binding FcεRⅠon mast cells/
basophils
Allergen once again enter the host →binding IgE
→cross-linking of IgE → cross-linking of FcεRⅠ→
mast cell activation→ degranulation→ mediators
release→ anaphylaxis symptoms
 Early phase response: short-lived, resolve within
1 hr. Increase of vasopermeability, smooth
muscle contraction, gland hypersecretion and
vasodilation
 Late phase response: inflammation, peak at
around 5 hrs, last for several days. Eosinophils,
mast cells, basophils, T-cells and neutrophils
infiltration.
Typical diseases of anaphylaxis
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

Systemic anaphylaxis(anaphylactic shock): fatal,

venom from bee, wasp; drugs such as penicillin,
antitoxins, etc.
Localized anaphylaxis(atopy): the tend-ency to
manifest localized anaphylaxis is inherited and
called atopy. typical diseases: asthma, hayfever,
eczema, food allergy, etc.
Atopy
Allergic rhinitis: Hay fever, airborn allergens,
symptoms include shedding tears, sneezing,
coughing, etc.
Asthma: airborn/blood-born allergens. Occur in
lower respiratory tract
 Cardinal clinic and physiological features:
variable airflow obstruction, bronchial hyper-
responsiveness.
Therapy of typeⅠhypersensitivity
Allergen avoidance: best if possible, but often
impractical. Skin test
Hyposensitivity: repeated injection of increasing
doses of allergen. Allergic rhinitis
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

Drug: antihistamines; epinephrine (also called

adrenaline), etc. Immediate injection of
adrenaline could rescue anaphylactic shock
Type Ⅱ hypersensitivity(cytotoxic)
Mediated by IgG and/or IgM
Mechanism:
 Ag present on the surface of cells→ im-munity
activation→Ab→tissue damage/ dysfunction
 Tissue damage caused by:
 Opsonic adherence: phagocytosis
 Complement: membrane damage
 ADCC: cell destruction
Type Ⅱ associated diseases
Transfusion reaction: mismatched blood
transfusion cause complement-mediated
hemolysis.
 ABO blood group: isohemagglutinins(IgM)
 Prevention: cross-matching between donor and
recipient blood
Heamolytic diseases of newborn
Rh incompatibility: Rh blood groups
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

 Rh- mother has the first Rh+ baby→ mother

sensitized by baby’s erythrocy-tes →anti-Rh IgG
 Mother has the second Rh+ baby→ IgG enter the
fetus through placenta→ destruction of fetal RBC
Drug-induced hemolytic anemia
Drug adsorb RBC proteins→Anti-RBC
IgG/IgM→complement, opsonization, ADCC
→RBC lysis, anemia
Grave’s disease and myasthenia gravis
Special class of type Ⅱ hypersensitivity,
Autoimmune diseases, tissue/organ dysfunction
Grave’s disease: anti-TSH receptor
Myasthenia gravis: anti-acetylcholine receptors
Type Ⅲ hypersensitivity
Participate by IgG/IgM, induced by de-position of
immune complex (IC)
Formation of IC: Excess of antigen over a
protracted period
Deposition frequently observed: blood-vessel
walls, synovial membrane of joints, glomerular
basement of kidney
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

Tissue damage caused by:

 Complement activation and attraction of neu-
trophils: release tissue damaging mediators
 Stimulation of Mφ: release proinflammatory
cytokines
 Aggregation of plate-lets: cause microthrombi
and vasoactive amine release
Type Ⅲ associated diseases
Localized type Ⅲ reaction: the Arthus reaction,
erythematous and edematous, intense
neutrophil infiltration
Generalized type Ⅲ reaction:
 Serum sickness: injection of foreign protein
(horse serum)
 SLE: systemic lupus erythematosus, DNA/ anti-
DNA/ complement
Type Ⅲ associated diseases
 Rheumatoid arthritis: rheumatoid factor (RF):
anti-IgG autoantibodies, usually IgM. IgM-IgG
complex deposit in joints
 Immune complex glomerulonephritis: Ag-Ab-C3
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

deposit glomerular basement membrane

 Others: drug reactions, infectious diseases
Type Ⅳ hypersensitivity
Delayed-type(DTH), T-cell mediated, 24-72 hr
after Ag contact, Ab not involve
Results from excessive CMI, secondary response,
chronic granuloma
Mechanism:
 CD4+Th1: Tm→Ag:MHCⅡ→effector T-cell→MCP-
1, IFN-γ, TNF, IL-2→Mφ attraction and
activation→tissue damage
Immune pathogenesis
CD8+CTL: primed CTL→Ag:MHCⅠ→ perforin/
Fas-FasL→target cell death
Type Ⅳ associated diseases
Insulin-dependent diabetes mellitus (IDDM):
insulin-producing βcells
Multiple sclerosis(MS): central nervous system,
myelin Ag
Contact dermatitis: foreign low molecular weight
materials, hapten-carrier, topical
 JOITIBA COLLEGE OF NURSING
Lalji Park, Bhandu,Ta: Visnagar, Dist: Mehsana. – 384120. (Guj.)

Infectious diseases: tuberculosis

Others: hashimoto’s thyroiditis, IBD

Bibliography:

A. Ananthanarayan “Text book of microbiology” 7 th edition, university press pvt ltd, page
no:24-18
B. Sharma PHBS “PV A text book of microbiology” peevee publication, page no:37-39
C. Gupte satish “A short text book of medical microbiology, 9 th edition, page no:19-21