Immunity to infections.

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Immunity to infections.

• Prof. Mohamed Osman Gad El Rab.
• College of Medicine KKUH.

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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 .
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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 ).

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Primary immune response

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

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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 ).

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Nature of infecting microbe determine type of
response .

• extracellular microbes .
• ( bacteria)
• Th 2 helper cells.
• antibody- mediated immunity.

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

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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 .

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The balance between TH1 TH2
is important in immunity. It
determine the clinical
presentation of the disease .
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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 .

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Immunity to bacterial infections

• extracellular.
  intracellular.
• protection by
• antibody- mediated cell-mediated
• immunity.
  immunity.
  

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Adherence
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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 .

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Penetration into the host Cell
Salmonella entering epithelial cells via
invasins
Figure 15.2
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Protective functions of antibodies.
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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.

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. In chronic intracellular infections e.g.
T.B. excessive CMI responses lead to
granuloma formation .
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Granuloma formation ( T.B. )
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Complications of immune responses .

• In some cases disease is not caused by
• the bacteria but rather by the immune
• response.

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

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immunity to viral infections

• initially
• 1. interferon, secreted by
• - infected cells.
• - inflammatory cells.
• 2. NK- cells.

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Antibody- mediated immunity

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

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adaptive immune mechanisms

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

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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.

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Influenza virus .
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1. Antigenic drift gradual minor change in HA
NA.

• 2. Antigenic shift
• sudden major change in HA NA .
• ( new subtype emerge )

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• Immunity to parasitic infections

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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.

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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
  )

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Life cycle of malaria
3-stages.
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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.

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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.

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Immunity to parasitic worms (helminthes)

• Helminthes are large multicellular
• organisms e.g. Schistosoma (Bilharzia ).
• Have complex life- cycle .

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

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Humoral immune responses to parasitesare
characterized by

• 1. elevated IgE.
• 2. blood eosinophilia .
• Eosinophils mediate ADCC to
• damage the parasite.