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Immunity to infections.

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Immunity to infections. Prof. Mohamed Osman Gad El Rab. College of Medicine& KKUH. During the life- cycle, many antigens appear : Infection begin with mosquito bite. – PowerPoint PPT presentation

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Title: Immunity to infections.


1
Immunity to infections.
  • Prof. Mohamed Osman Gad El Rab.
  • College of Medicine KKUH.

2
Classification of immunity.
  • classification of acquired immunity.
  • active.
    passive.
  • natural. artificial. natural.
    artificial.
  • infections. immuniz. Maternal
    immuno -
  • IgG.
    therapy.

Subclinical. Clinical.
Vaccines.
IgG from mother to fetus.
Ready made antibodies .
3
General features
  • First encounter with any microbe ( at any
  • age )
  • Primary immune response.
  • 4 phases
  • 1. lag .( no antibodies
    )
  • 2. log. ( antibodies
    appear )
  • 3. plateau.( no more
    synthesis )
  • 4. decline.( antibody
    disappear ).

4
Primary immune response
  • 1. takes a longer time ( recognition of
    antigen,
  • differentiation proliferation of
    cells ) .
  • 2. antibody class mainly IgM .
  • 3. memory cells generated .

5
General features
  • Second encounter with same microbe
  • Secondary immune response
  • 1.require small amount of antigen.
  • 2. fast reaction ( memory cells ).
  • 3. high levels of antibody ( IgG ).

6
Nature of infecting microbe determine type of
response .
  • extracellular microbes .
  • ( bacteria)
  • Th 2 helper cells.
  • antibody- mediated immunity.

7
  • intracellular microbes .
  • ( viruses , intracellular bacteria ,
    fungi )
  • Th-1 helper cells .
  • cell- mediated immunity .


8
Th1 , Th2 cells down-regulate each other.
  • 1. each cell type secrete different
  • cytokines.
  • 2. balance between Th1 Th2
  • determine the clinical presentation of
  • the disease .

9
The balance between TH1 TH2
is important in immunity. It
determine the clinical
presentation of the disease .
10
Many factors influence immune response to
infections
  • 1. structure of the microbe antigen.
  • 2. dose of infection (optimum dose, good
    response).
  • 3. route of entry into the tissues .(
    determine
  • site of reaction ).
  • 4. host factors - genetic constitution.
  • - age .

11
Immunity to bacterial infections
  • extracellular.
    intracellular.
  • protection by
  • antibody- mediated cell-mediated
  • immunity.
    immunity.

12
Adherence
13
protective functions of antibodies
  • 1. neutralizing action
  • - prevent pathogens from binding to
  • tissues.
  • - prevent the action of toxins .
  • 2. activate complement .
  • 3. stimulate phagocytosis .
  • 4. stimulate NK-cell-mediated killing .

14
Penetration into the host Cell
Salmonella entering epithelial cells via
invasins
Figure 15.2
15
Protective functions of antibodies.
16
microbial strategies to avoid the immune
system
  • e.g. Pneumococcus.
  • has large polysaccharide coat .
  • can evade phagocytosis .
  • Mycobacteria .
  • have waxy coat secrete catalase.
  • can block respiratory burst.

17
. In chronic intracellular infections e.g.
T.B. excessive CMI responses lead to
granuloma formation .
18
Granuloma formation ( T.B. )
19
Complications of immune responses .
  • In some cases disease is not caused by
  • the bacteria but rather by the immune
  • response.

20
Endotoxins of gram ve bacteriaactivate
macrophages which releasehigh levels of
IL-1, TNF - alpha, these may cause
Septic shock .
21
  • In staphylococcal food poisoning ,
  • enterotoxins act as superantigens
  • and cause direct massive T-cell
    activation . This may cause
  • Toxic shock syndrome .

22
immunity to viral infections
  • initially
  • 1. interferon, secreted by
  • - infected cells.
  • - inflammatory cells.
  • 2. NK- cells.

23
Antibody- mediated immunity
  • Anti-viral antibodies
  • 1. prevent spread during acute infection.
  • 2. protect against reinfection .

24
adaptive immune mechanisms
  • cell-mediated immunity .
  • activation of CD8 T-cells.
  • - inhibit viral replication.
  • - kill infected cells .

25
Viruses can evade host defenses.
  • 1. Hepatitis C virus
  • overcome anti - viral effect of INFs
  • blocking the action of protein kinase.
  • 2.Adenoviruses CMV
  • reduce surface expression of MHC-1.

26
Influenza virus .
27
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28
1. Antigenic drift gradual minor change in HA
NA.
  • 2. Antigenic shift
  • sudden major change in HA NA .
  • ( new subtype emerge )

29
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30
  • Immunity to parasitic infections

31
The type of the immune response
depend on the location of the
parasite in the host .
  • In the blood antibodies may be effective
  • In the intracellular stage CMI may be
  • effective.

32
Immunity to Malaria
  • Caused by genus Plasmodium.
  • P.falciparum is the most virulent
    prevalent.
  • Infect 10 of the population.
  • Causes 1 2 million deaths every year.
  • Have a complex life cycle .
  • ( many antigens appear during infection
    )

33
Life cycle of malaria
3-stages.
34
During the life- cycle, many antigensappear
  • Infection begin with mosquito bite.
  • Sporozoites enter the blood disappear
  • within 30 min.
  • Migrate to the liver after 1
    week
  • release merozoites which infect RBCs.

35
Sporozoites stay for only 30 min. in the
blood, therefore induce a poor immune
response.
  • The intracellular stage in the liver cells
  • and RBC ,reduce the degree of immune
  • activation generated by the pathogen.

36
Immunity to parasitic worms (helminthes)
  • Helminthes are large multicellular
  • organisms e.g. Schistosoma (Bilharzia ).
  • Have complex life- cycle .

37
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38
  • Cercaria enter the blood stream and
    become schistosomules which enter
  • capilleries.then pass to the lungs
    liver.
  • then become adult worms.

39
Humoral immune responses to parasitesare
characterized by
  • 1. elevated IgE.
  • 2. blood eosinophilia .
  • Eosinophils mediate ADCC to
  • damage the parasite.
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