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Immunity to infectious diseases.

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Acute glomerulonephritis : ... Only 22% of the children have detectable antibodies to sporozoites. In adults 84% have such antibodies. In general, the ... – PowerPoint PPT presentation

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Title: Immunity to infectious diseases.


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

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

3
  • Immunity to viral infections .

4
  • Innate (natural) immunity
  • many viruses induce
  • 1. production of type 1 interferons.
  • ( INF- alpha INF - beta.)
  • 2. activation of NK - cells .

5
dsRNA produced during viral replication
induce the expression of interferons by
the infected cells.
  • monocytes , macrophages fibroblasts
  • also synthesize interferons .

6
Viruses initiate infection by binding to
specific host - cell membrane molecules .
  • e.g.
  • 1. influenza virus bind to cell membrane
  • glycoproteins .
  • 2. rhinoviruses bind to intercellular
  • adhesion molecules (ICAMs).

7
Mechanism of action
  • Interferons bind to receptors that activate
  • JAK-STAT pathways.
  • These induce several genes .
  • One gene activate a ribonuclease that
  • degrade viral RNA .

8
2. Other genes activate protein kinases
which inhibit protein synthesis .
  • 3. binding of INFs to NK-cells induce
  • lytic activity .
  • IL-12 produced by macrophages also
  • enhance NK-cell activity .

9
Antibody- mediated immunity
  • Anti-viral antibodies
  • 1. prevent spread during acute infection.
  • 2. protect against reinfection .

10
Protective functions of antibodies
  • 1. secretory IgA blocks viral attachment .
  • 2. complement - fixing antibodies may
  • cause lysis of enveloped viruses
  • 3.IgM antibody agglutinate viral particles .

11
Cell mediated immunity is important for
control clearance of viral infections .
  • CTL activity arises within 3 - 4 days,
  • peak by 7-10 days then decline
  • when the infection is cleared .

12
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.

13
3. Measles ,CMV HIV reduce MHC
-11 levels .
  • 4. A large no. of viruses cause
  • generalized immunosuppression.
    .
  • e.g. mumps , measles , EBV., CMV.,
  • HIV.

14
Influenza virus .
15
Antigenic variation of influenza virus .
  • In 1918-1919 an influenza pandemic
  • killed over 20 million people .
  • The structure of the virus contain
  • Hemagglutinins (HA ).
  • Neuraminidase (NA ).

16
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17
Shifting Nature of Influenza
  • Antigenic drift small, ceaseless changes in the
    genetic structure. New strains continually
    replace old strains.
  • Antigenic shift major change, usually occurs
    when species hosting virus trade viral genes.
    Novel strain appears without natural immunity in
    host population.

18
1. Antigenic drift gradual minor change in HA
NA.
  • 2. Antigenic shift
  • sudden major change in HA NA .
  • ( new subtype emerge )

19
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20
1918 Hemagglutinin Causes Severe Lung Damage.
M88/Hsp
M88
Kobasa et al. Nature 2004431703
21
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22
  • Immunity to bacterial infections.

23
  • If the inoculum (dose ) is small and the
  • virulence of the bacteria is low .
  • Tissue phagocytes may eliminate
  • the bacteria .

24
The humoral response (antibody) is the
main protective response against
extracellular bacteria .
  • Antibodies act in several ways
  • 1. neutralize toxins .
  • 2.activate complement .
  • - generates anaphylatoxins.
  • -release chemotactic agents
    .

25
Protective functions of antibodies.
26
Intracellular bacteria
  • Initially activate NK cells which
  • provide early defense .
  • Final control is by
  • cell - mediated immunity .
  • ( this involve activated macrophages )

27
Cell-mediated immunity involve activated
macrophages.
28
Bacteria can by-pass host defense
  • 4 steps in bacterial infections
  • 1. attachment .(adherence).
  • 2. proliferation .
  • 3. invasion of host tissues .
  • 4. toxin - induced damage.

29
Adherence
30
Penetration into the Host Cell
Salmonella entering epithelial cells via invasins
Figure 15.2
31
Secretory IgA block attachment , but some
bacteria secrete proteases that break IgA .
  • Opsonization phagocytosis prevent
  • proliferation , but some bacterial
    surface structures inhibit phagocytosis,
  • ( polyssacharide capsule ,Strp.pneum.)

32
Strep.pneumonae. Inhibit phagocytosis.
33
3. Some bacteria resist complement lysis .
  • 4. Mycobacteria survive intracellularly by
  • resisting oxidative attack ,some prevent
  • lysosomal fusion .

34
Complications of immune responses .
  • In some cases disease is not caused by
  • the bacteria but rather by the immune
  • response.

35
Endotoxins of gram ve bacteria activate
macrophages which release high levels of
IL-1, TNF - alpha, these may cause
Septic shock .
  • In staphylococcal food poisoning ,
  • enterotoxins act as superantigens
  • and cause direct massive T-cell
    activation . This may cause
  • Toxic shock syndrome .

36
Endotoxin
Contrast the nature and effects of exotoxins and
endotoxins.
Figure 15.4b
37
Exotoxins
Figure 15.4a
38
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39
3.Complications of streptococcus pyogenes
throat infections
  • 1. Rheumatic fever antibodies formed against
    antigen in the strep. cell wall cross react with
    the sacrolemma of
  • Human heart .Granuloma form in the heart
    (Aschoffs
  • nodules).
  • 2. Rheumatic heart disease repeated attacks
    by strep. with different M types can
    result in damage to the heart valves.( certain
    children have a genetic predisposition
  • to this immune-mediated disease ). ( high
    A.S.O. titer ).

40
  • 3. Acute glomerulonephritis
  • antibodies to strep . components combine to
    form
  • immune- complexes which then deposit in the
    kidney
  • glomeruli .

41
4. In chronic intracellular infections e.g.
T.B. excessive CMI responses lead to
granuloma formation .
42
Granuloma formation ( T.B. )
43
The balance between TH1 TH2 is
important in immunity. It determine
the clinical presentation of the
disease .
44
5. Immunological response in leprosy
  • The response decide the type of disease
  • 1.In tuberculoid leprosy the patient mount an
    effective
  • cell-mediated response.Macrophages destroy the
    bacilli
  • and contain the infection .
  • 2. In lepromatous leprosy the patient is unable
    to produce
  • a cell-mediated response and organisms
    multiply and
  • spread in the tissues gt

45
  • Immunity to parasitic infections

46
  • A. Protozoal diseases .
  • These are unicellular organisms .
  • e.g. malaria , trypansomiasis , toxoplasma,
  • They have complex life - cycles.
  • some stages are free in the blood ,
  • other stages are intracellular.

47
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.

48
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 .

49
Life cycle of malaria
3-stages.
50
During the life- cycle, many antigens appear
  • 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.

51
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.

52
In endemic areas
  • Only 22 of the children have detectable
  • antibodies to sporozoites.
  • In adults 84 have such antibodies.
  • In general, the degree of immunity to
  • Malaria is not complete .

53
Trypansomiasis ( sleeping sickness).
  • As the parasite multiply , an
    effective
  • antibody response develop to
    the
  • glycoprotein coat called variant
    surface
  • glycoprotein (VSG).
  • These antibodies eliminate most of
    the
  • Parasite from the blood
    by
  • 1. complement lysis.
  • 2. opsonization
    phagocytosis .

54
Trypansomes, (T. cruz,)
55
However , 1 of the parasite with
different antigen (VSG ) escape the
antibody response. These
proliferate and a new wave of
parasites invade the blood .
  • This is called antigenic shifts.
  • (a characteristic feature of
    Trypansomes ).

56
Immunity to parasitic worms (helminths)
  • Helminths are large multicellular
    organisms e.g. Schistosoma (Bilharzia ).
  • Have complex life- cycle .
  • Cercaria enter the blood stream and
    become schistosomules which enter
  • capilleries.then pass to the lungs
    liver.
  • then become adult worms.

57
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58
Immune responses are not sufficient
to eliminate the adult worms .
  • Adult worms evade immune responses
  • by coating themselves by host
  • glycoproteins .

59
Humoral immune responses to parasites are
characterized by
  • 1. elevated IgE.
  • 2. blood eosinophilia .
  • Eosinophils mediate ADCC to
  • damage the parasite.

60
A chronic state develop in which
adult worms persist and induce
cell-mediated delayed hypersensitivity
reactions
  • This eventually result in the formation of
  • large granulomas .

61
  • Immunity to fungi .

62
  • Fungal infections of man fall into 4 types
  • 1.superficial mycoses .
  • 2.subcutaneous mycoses.
  • 3.respiratory mycoses.
  • 4.candida albicans .
  • Recovery is based on cell-mediated immunity.
  • There is also evidence for neutrophil involvement
  • In immunity to some respiratory mycoses.

63
Immunology quiz no 4.
64
A.
  • A12-year old girl has been receiving cytotoxic
    drugs for
  • Acute leukemia. Although there is evidence
    that the leukemia is responding, she has become
    neutropenic
  • ( neutrophils were less than 0.5 x10 ml )
    .Early in the evening she was found to have
    fever, within half an hour
  • she collapsed and was found to have features
    of sock
  • (tachycardia and hypotention ).
  • Blood was taken for culture which later grew
    E. coli. She
  • was started on antibiotics and fluid
    replacement .She
  • gradually improved during the next 12 hours .

65
1. What is the diagnosis of this patient
? 2. What is the predominant cell
involved in this condition ?
  • 2. Describe the underlying
    immunopathology.?

66
B.
  • What is the recommended childhood immunization
  • schedule in Saudi Arabia ?
  • What are the indications for passive
    immunization ?
  • Mention 2 infectious and 1 non-infectious
    condition
  • for which passive immunization may be
    required ?

67
Practical points
68
  • Routine tests in microbial serology .
  • 1. Widal test for diagnosis of typhoid fever.
  • standard tube agglutination test (STA)
  • -patient serum in dilution mixed with
  • salmonella suspension .
  • 2.A.S.O. test.
  • anti- streptolysin O test.
  • -toxin anti-toxin neutrallization test for
  • diagnosis of streptococcal infections .
  • (patient serum neutralize toxin therefore
    indicator R.B.C . not lysed )

69
3. T.P.H.A.test.
  • Treponema pallidum hemagglutination test.
  • -for diagnosis of syphilis.

70
Trypansomes,life cycle.
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