microbiological veiw of hypersensitivity 4

2. Type iv : Delayed hypersensitivity
 These are typically provoked by the intracellular
microbial infections or Haptens (simple chemicals
applied on the skin).
 They evolve slowly and consist of mixed cellular
reactions involving lymphocytes and macrophages.
 The reaction is induced by sensitised T cells not by
antibodies.
 It cannot passively transferred by serum but can be
transferred by lymphocytes or the transfer factor.

3. Mechanism

4. Mechanism
Activation of T lymphocytes by APC
Release of cytokines from T helper cells &
macrophage activation.
T cell mediated Cytotoxicity.

5. Types
• Two types of delayed hypersensitivity are
recognised
1.Tuberculin (infection) type
2.Contact dermatitis type

6. Tuberculin (infection) type
• When a small dose of tuberculin is injected
intradermally .
• In an individual sensitised to tuberculoprotien by
prior infection or immunisation,an indurated
inflammatory reaction develops at the site within
48-72 hrs.
• No response is seen in unsensitised individuals.
• This test differs from skin test of type1 hypersensitivity by
longer interval for appearance,morphology and histology.

8. Cutaneous basophil hypersensitivity
• It is formerly known as Jones-mote
reaction.
• A local reaction resembling the tuberculin
response may be produced by the
intradermal injection of some protein
antigens.
• It can be passively transferred by serum.
• Histology charecterised by prominent
basophil infiltration.

9. Contact dermatitis
• Delayed hypersensitivity sometimes results from skin
contact with a variety of chemicals-
• * Metals- Nickel& chromium.
* simple chemicals-dyes,
picryl chloride,dinitrochlorobenzene
* Drugs-pencillin
* plant allergen (parthenin)

10. • Sensitisation is particulary liable when contact is with
an inflammed area of skin and when a chemical is
applied on the oily base.
• The substances ivolved are in themselves not antigenic
but may acquire antigenicity on combinatioin with
skin protiens.
• Antibiotic ointments applied on patches of dermatitis
frequently provoke sensitisation.
• Sensitisation requires percutaneous absorption.
• Method of entry of allergens is by passage along the
sebaceous glands, as they are mostly fat soluble.

11. Symptoms
# Varying lesions
* macules
* papules
* vesicles
# vesicles breakdown,leaving behind
raw weeping areas
(typical of acute eczematous
dermatitis)
Allergen is applied to the skin under an adherent dressing
sensitivity indicated by ictching
apppearing in 4 to 5 hrs.
local reaction which vary
from erythema to vesicle or blister
formation after 24-28hrs.

12. Type v : Stimulatory hypersensitivity
• The antibody activates receptor sites and enhances
the activity of the cell.
Ex;- 1. Long acting thyroid stimulator(LATS)
2. Stevens Johnson syndrome
3. Sulphonamide-induced morbillifrom rash.