A condition in which the immune system reacts abnormally to a foreign substance. Drug allergy An abnormal reaction of the immune system to a medication. Food allergies An unpleasant or dangerous immune system reaction after a certain food is eaten. Contact dermatitis A skin rash caused by contact with a certain substance. Latex allergy An allergic reaction to certain proteins found in natural rubber latex. Allergic asthma Asthma triggered by exposure to the same substances that trigger allergy symptoms. Seasonal allergies An allergic response causing itchy, watery eyes, sneezing and other similar symptoms. Animal allergy An abnormal immune reaction to proteins in an animal's skin cells, saliva or urine. Anaphylaxis A severe, potentially life-threatening allergic reaction. Allergy to mold An abnormal allergic reaction to mould spores.

1. GuidedGuided byby ––
Dr. Anil Govindrao Ghom
Dr. Ajit Mishra
Dr. Shweta Singh
Dr. Savita Ghom
Dr. Anshul Khandelwal
Presented By –
Dr. Bratati Dey
(Dept. of OMR)
PG 1st year

2. CONTENTSCONTENTS
Introduction
Classification
Type I Hypersensitivity
 Anaphylaxis
 Atopy
Type II Hypersensitivity
Type III Hypersensitivity
 Arthus Reaction
 Serum Sickness
Type IV Hypersensitivity
Type V Hypersensitivity
Comparison Of Different Types Of Hypersensitivity Reactions
Conclusion
References

3. TERMINOLOGIESTERMINOLOGIES
 AllergenAllergen – An antigen that can elicit allergic symptom.
 AnaphylacticAnaphylactic – Ana ₌ against backward, phylax ₌ protect,
meaning without protection.
 AngioedemaAngioedema (Angioneurotic edema) – non inflammatory
edema, occurs in response to allergen.

4. TERMINOLOGIESTERMINOLOGIES
 AntibodyAntibody – These substance
response to the administration of
antigen.
 AntigenAntigen – Any substance foreign
to the host is capable of activating
immune.
 AtopyAtopy – A „strange disease‟ a
clinical hypersensitivity state
subject to hereditary influence
Ex- Asthma, Hey fever, Eczema.

5. TERMINOLOGIESTERMINOLOGIES
PruritusPruritus – Itching
UrticariaUrticaria – Vascular reaction of skin, marked by
transient appearance of smooth slightly elevated
patches paler than surrounding.

7. INTRODUCTIONINTRODUCTION
It is an immune response resulting in exaggerated or
inappropriate reactions harmful to host.
In this reaction both the humoral & cell mediated immunity
participate.
Have twoHave two
componentcomponent
PrimingPriming
dosedose
ShockingShocking
dosedose

8. INTRODUCTIONINTRODUCTION
Prince of Monaco 1st observed the deleterious effects of
jellyfish on bathers.
Portier and Richet (1906) suggested a toxin to be responsible
for these effects and coined the term “anaphylaxis”.
Gell and Coombs (1963) classified it into four categories.
– Types I, II, and III are antibody-mediated and are known as immediate
hypersensitivity reactions
– Type IV is cell-mediated immunity (known as delayed hypersensitivity
reactions).

9. CLASSIFICATIONCLASSIFICATION
 Depending on the time taken for the reactions and the
mechanisms
HYPERSENSITIVITYHYPERSENSITIVITY
IMMEDIATE
TYPE I
ANAPHYLAXIS
ATROPIC
TYPE II
TYPE III
ARTHUS REACTIONARTHUS REACTION
SERUM SICKNESS
DELAYED TYPE IV
TUBERCULINTUBERCULIN
INFECTION
CONTACTCONTACT
DERMATITIS

10. Properties Immediate Delayed
Type I, II, III IV
Time to manifest Minutes to hours Days
Mediators Antibody T Cells
Route of sensitization Any route Intradermal
Passive transfer with serum Possible Not possible
Desensitization Easy but short lived Difficult but long lasting

11. Type I (Anaphylactic)Type I (Anaphylactic)
HypersensitivityHypersensitivity
 It is an acute, potentially fatal, and systemic manifestation of
immediate hypersensitivity reaction.
 Antigen bind to IgE resulting in release mediators of
anaphylaxis.

12. Initiator cells in anaphylaxisInitiator cells in anaphylaxis
Plant pollen,
proteins
Food items
Drugs

13. Mediators of AnaphylaxisMediators of Anaphylaxis
HistamineHistamine
Slow reacting substances of anaphylaxisSlow reacting substances of anaphylaxis
SerotoninSerotonin
Eosinophilic chemotactic factor of anaphylaxisEosinophilic chemotactic factor of anaphylaxis
Prostaglandins & ThromboxanesProstaglandins & Thromboxanes

14. Phases of anaphylaxisPhases of anaphylaxis
IMMEDIATE PHASE LATE PHASE
Degranulation & release of
chemical mediators
Histamin, prostaglandin,
leukotriens
4-8 hr after the immediate
phase and persist for 1-2 days
Infiltration of neutrophils,
macrophages, eosinophils, and
lymphocytes
Mediators in late phase
SRS-A LTC4, LTD4, and LTE4
platelet-aggregating factor,
Cytokines

15. SCHEMATIC DIAGRAM OF TYPE ISCHEMATIC DIAGRAM OF TYPE I
HYPERSENSITIVITY REACTIONHYPERSENSITIVITY REACTION

17. Clinical Manifestation ofClinical Manifestation of
AnaphylaxisAnaphylaxis
 Multiple organ
systems are
usually affected,
including the skin
(purities, flushing,
urticaria, and
angioedema).
cardiovascula
r system
(hypotension
and cardiac
arrhythmias).

18. Clinical Manifestation ofClinical Manifestation of
AnaphylaxisAnaphylaxis
 Respiratory
track
(bronchospasm
and laryngeal
edema)
Gastro-
intestinal system
(nausea,
vomiting,
stomach pain)

19. Management of AnaphylaxisManagement of Anaphylaxis
Adrenaline is to be administered 0.5 ml of a 1
in 1000 solution, subcutaneously or
intramuscularly;
The dose being repeated up to a total of 2 ml
over 15 minutes, if necessary

20. AnaphylactoidAnaphylactoid ReactionReaction
 This is clinically similar to anaphylactic reaction but differs
from it it.
 It is not IgE mediated.
 Initiating agent stimulate directly basophils and mast cells to
release mediators.

21.  Injection of peptone, trypsin (iv) and certain
other substances provokes a clinical reaction
resembling anaphylactic shock.
This is termed „anaphylactoid reaction‟.

22. AtopyAtopy
 First coined by Coca (1923)
 High degree of familial predisposition & a high level of IgE.
 Common manifestations –
 Asthma (broncheal asthama),
 Rhinitis (hay fever),
 Urticaria,
 Atopic dermatitis
 It is not transferred by hyphoid cell but by serum

23. HAY FEVERHAY FEVER

25. Difference Between Anaphylaxis andDifference Between Anaphylaxis and
AtopyAtopy
Anaphylaxis Atopy
Acute,
Potentially fatal,
Systemic form
Chronic or recurrent,
Nonfatal,
Typically localized form

26. Management and prevention ofManagement and prevention of
AnaphylaxisAnaphylaxis
Desensitization –
Acute desensitization: involves the
administration of small amounts of antigen to
which the person is sensitive.
The complex of antigen–IgE is produced in small
quantities, hence enough mediators are not
released to produce a major reaction.

27. Chronic desensitization
Long term administration of antigen
to which person is sensitive
Production of IgG, IgA blocking
Prevent subsequent antigen to
binding to mast cell
Preventing the reaction

28. Type II Hypersensitivity (Type II Hypersensitivity (cytotoxiccytotoxic))
 The reactions involve combination of IgG or IgM antibodies
with the cell-fixed antigens
Antibody binds to
antigen on cell
surface
Phagocytosis of
cell
Cytotoxicity by
NK cell
Lysis through
complement
system activation

29. Clinical ManifestationClinical Manifestation
Transfusion
reaction
Erythroblastosis
featalis
Drug induced
hemodialysis
Goodpasture‟s
syndrome
Rheumatic
fever

30. Human ABO Blood TypesHuman ABO Blood Types
GenotypeGenotype RBC PhenotypeRBC Phenotype ABO AntigenABO Antigen SERUM AntibodySERUM Antibody
AAH or AOH A A, H Anti-B
BBH or BOH B B, H Anti-A
ABH AB A, B, H None
OOH O H Anti-B
Anti-A

31. ERYTHROBLASTOSIS FETALISERYTHROBLASTOSIS FETALIS

32. SCHEMATIC DIAGRAM OF TYPE IISCHEMATIC DIAGRAM OF TYPE II
HYPERSENSITIVITY REACTIONHYPERSENSITIVITY REACTION

33. Type III hypersensitivity (immuneType III hypersensitivity (immune
complex)complex)
 Mediated by antigen-antibody immune complex
 Reaction between antigen-antibody give rise to formation of
complement system
 Immune complex are deposited on
 Blood vessels
 Synovial membrane
 glomerular basement membrane of the kidneys,
 choroid plexus of the brain

34. SCHEMATIC DIAGRAM OF TYPE IIISCHEMATIC DIAGRAM OF TYPE III
HYPERSENSITIVITY REACTIONHYPERSENSITIVITY REACTION

35. Clinical Manifestation of type IIIClinical Manifestation of type III
hypersensitivityhypersensitivity
ARTHUS REACTION-
Inflammatory reaction caused by immune complex
as local tissue response.
Named after Dr. Arthus who described arthus
reaction.
This reaction is edematous in early stage later
become hemorrhagic, eventually necrotic.

36. Clinical Manifestation of type IIIClinical Manifestation of type III
hypersensitivityhypersensitivity
SERUM SICKNESS-
 Systemic inflammatory reaction
 Deposition of immune complex at many site of body
 Manifested after high concentration of foreign serum
 Appears a few days to week after injection

37. Immune Complex DiseaseImmune Complex Disease
1. Autoimmune disease
1. SLE
2. Rheumatoid arthritis
2. Drug reaction
1. Allergy to penicillin
2. Sulphonamide
3. Infectious disease
1. Meningitis
2. Hepatitis
3. Infectious mononucleosis
4. Malaria

38. Type IV Hypersensitivity (Delayed)Type IV Hypersensitivity (Delayed)
It is called delayed hypersensitivity because
response is delayed
Initially described by Robert KochRobert Koch in TB
It starts hours or days after primary exposure
Cell mediated- MACROPHAGEMACROPHAGE

39. Type IV HypersensitivityType IV Hypersensitivity
MECHANISM OF ACTION
Activated T Lymphocytes
 Release of cytokines and macrophase activation
 T Cell mediated cytotoxicity

40. SCHEMATIC DIAGRAM OF TYPE IVSCHEMATIC DIAGRAM OF TYPE IV
HYPERSENSITIVITY REACTIONHYPERSENSITIVITY REACTION

41. CLINICAL MANIFESTATIONCLINICAL MANIFESTATION
OF DELAYEDOF DELAYED
HYPERSENSITIVITYHYPERSENSITIVITY
CLINICAL MANIFESTATIONCLINICAL MANIFESTATION
OF DELAYEDOF DELAYED
HYPERSENSITIVITYHYPERSENSITIVITY

42. Delayed Hypersensitivity ReactionsDelayed Hypersensitivity Reactions
CONTACT HYPERSENSITIVITY
 These include drugs, such as sulfonamides and neomycin;
plant products, such as poison ivy and poison oak;
chemicals, such as formaldehyde
 Itching, erythema, vesicle, eczema, or necrosis of skin
within 12–48 hours of the second exposure.

43. Delayed Hypersensitivity ReactionsDelayed Hypersensitivity Reactions
TUBERCULIN-TYPE
HYPERSENSITIVITY REACTION
A typical example of delayed hypersensitivity
Tuberculin skin testTuberculin skin test: This test is carried out to
determine whether an individual has been exposed
previously to Mycobacterium tuberculosis or not.

44. Tuberculin Skin TestTuberculin Skin Test
Result-positive

45. SkinSkinSkinSkin TestTest
Lepromin TestTest--
positive in tuberculoid
leprosy, negative in
lepromatyous leprosy
Frei Test-
positive in lympho
granuloma venerum

46. ImmunofluorescenceImmunofluorescence
Fluorescence is a property of absorbing light
rays of one particular wavelength and emitting
rays with different wavelengths.
Conjugated to antibodies and such labelled
antibodies can be used to locate and identify
antigen in tissue.

47. ImmunofluorescenceImmunofluorescence
USE to identify
Bacteria
Virus
Fungi
Commonly used dye – isothiocynate and
lissamine rhodamine exhibiting blue-green
and orange-red fluorescence respectively

48. Differences Between Contact AndDifferences Between Contact And
TuberculinTuberculin--type Hypersensitivitytype Hypersensitivity
Characteristics Contact
hypersensitivity
Tuberculin-type
hypersensitivity
Site Epidermal Intradermal
Antigen Organic chemicals,
poison ivy, metals, etc
Tuberculin, lepromin,
leishmanin skin tests,
etc.
Reaction time 48–72 hours 48–72 hours

49. TYPE IV HYPERSENSITIVITYTYPE IV HYPERSENSITIVITY
Graft rejection-
Rejection of transplanted organ
Rejection depends on degree to which the graft is
foreign to the recipient
It is based on types of graft

50. Types of graft

51. Type V (Stimulatory Type)Type V (Stimulatory Type)
HypersensitivityHypersensitivity
 It is modification of type II hypersensitivity reaction.
 Antibodies combine with antigens on cell surface
 Type V hypersensitivity reaction plays an important role in
pathogenesis of Graves‟ disease (thyroid hormones are
produced in excess quantity).

52. Comparison of different types ofComparison of different types of
hypersensitivity reactionshypersensitivity reactions
Type I Type II Type III Type IV
Antigen Exogenous Cell surface Soluble Tissue and
organ
Antibody IgE IgG, IgM IgG, IgM None
Reaction time 15–30
minutes
Minutes to
hours
3–8 hours 48–72 hours
Transfer Antibody Antibody Antibody T cells
Conditions Hay fever,
allergy,
Allergic
rhinitis
Erythroblastosi
s fetalis and
Goodpasture‟s
syndrome
SLE, serum
sickness
Tuberculin
test, poison
ivy, etc

53. AsthmaAsthma AllergicAllergic
rhinitisrhinitis
AnaphylaxisAnaphylaxis DrugDrug allergyallergy RapidRapid onsetonset
skinskin reactionreaction
Position
A-B-C.
Definitive-
bronchodilators
aerosol spray i.e. ᵦ
adrenergic agonist
ex-Epinephrine,
Isoprotenol,
metaprotenol.
Inj. Epinephrine
(s.c)
1st to avoid
aerosol
Definitive-
select a anti-
histaminic.
Ex- cetrizine,
Levocetrizine,
A-B-C. basic life
support.
Definitive-
administration of
histamine blockers.
Diphenhydramin
50mg (benadryl
cap/asmicold) or
Chlorpheniramine
4mg (Tab deltacold
or chlortab)
Diphenhydramin
50mg, or inj.
chlorpheniramin 10
mg for adult or i.v
administered
blocker
Then give-tab
diphenhydramine /
chlorpheniramine
4-6hr for 3 days
A-B-C
Basic life
support. Monitor
vital sign in
every 5min
Administered
histamine
blocker
Epinephrin
1:1000 every 5-
20min to total 3
dose, 1ml i.v
1:10000 slow i.v
over 3-5 min
Epinephrine
contraindication-
Diabetes,
hypertension,
ischemic heart
disease.
In such condition
sedation Common side
effects are
dizziness, dry
mouth, dry nose,
constipation
Side effect on
parenteral route are
CNS Depression,
Drowsiness,
fatigue, sedation

55. Immune response is generally protective
process but it may sometimes be injurious to
the host.

56. REFERENCESREFERENCES
Textbook of microbiology – C P Baveja, 101 – 105
Textbook of microbiology and immunology –Subhas
Chandra Parija 2nd edition, 149 – 155
Medical microbiology – David Greenwood Sixteen edition,
143 – 145
Kuby immunology – Owen Punt Stranford 7th edition, 485 –
516
Medical emergency in the dental office – Stanley F.
Malamed 5th edition, 385 – 421
Essential of pharmacology for dentistry – KD Tripathi 3rd
edition, 491 – 492
Textbook of oral medicine – Anil Govindrao Ghom 2nd
edition, 18 – 23

57. Thank YouThank You