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Microbio final > third colloq > Flashcards

third colloq Flashcards

1
Q

Five stages of infectious disease

A
  1. incubation stage
  2. prodromal stage
  3. invasive stage
  4. decline stage
  5. convalescence stage
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2
Q

Types of infection according to…

A
  • origin (endogenous, exogenous)
  • spread (localized, systemic)
  • Symptoms
  • Duration
  • quantity of species
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3
Q

Transmission routes of infections

A
  • contact
  • fecal-oral
  • alimentary
  • aerogenic
  • transplacental
  • via vectors
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4
Q

Occurrence of infections in society

A
  • sporadic (isolated)
  • endemic (regular and continuing with no time Limit)
  • epidemic (increased within localities and time periods)
  • pandemic (increased with no limitations)
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5
Q

lethal doses

A

Dosis lethalis minima
Dosis lethalis certa
letalis dosis 50

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6
Q

bacterial toxins

A

Exotoxins: actively secreted
Endotoxins: part of outer membrane, not released unti bacterium is killed; can cause Inflammation

toxinosis: pathogenesis caused by the bacterial Toxin alone

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7
Q

types of acquired immunity

A

natural active immunity (after infection)
natural passive immunity (antibodies from mother to Infant)

artificial active immunity (vaccines)
artificial passive immunity (immune Serums)

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8
Q

Types of innate immunity

A

1- constituitive: barriers, Body temp.)
2- Recruitment: complements, chemokines
3- Pathogen triggered (neutrophils, macrophages, NK)

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9
Q

Secondary lymphoid Organs and their functions

A

LYMPH NODE

  • filters fluid
  • where Antigen presentation occurs

SPLEEN

  • filters fluid
  • Antigen presentation
  • removes old RBCs and platelets
  • filters Antigens, Bacteria, viruses

MALT

  • filters fluid
  • Antigen presentation
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10
Q

Nonspecific defense vs specific defense

A

NONSPECIFIC

  • mechanical barriers
  • chemical/ humoral factors
  • cellular facotrs
  • pathophysiological processes (Inflammation, Fever…)

SPECIFIC

  • cellular (T and B cells)
  • humoral (antibodies)
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11
Q

Humoral factors of innate immunity (9)

A
  • defensins –> kill pathogens
  • lysozymes –> hydrolysis of peptidoglycan
  • ß-Lysin –> Lysis of bact. cell
  • lactoferrin –> competes for iron
  • lactoperoxidase –> bactericidal activity
  • Properdin –> activates complement
  • Interferons –> cell killing
  • Mannose-binding proteins –> activate complement
  • Complement –> phagocytosis, Lysis, inflammation
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12
Q

Cellls of the innate immunity

A
  • neutrophils: phagocytose and kill
  • eosinophils: against parasites and in allergies
  • basophils: in allergic Response, release histamine…
  • Monocytes: MHC II and phagocytose in blood
  • Macrophages: same only in tissues
  • Dendritic cells: MHC I and II in tissues and lymph nodes
  • NK cells: kill Virus infected or Tumor cells
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13
Q

Process of inflammation

A
  1. Activation of dendritic cells, macrophages, NK cells
  2. Vasodilation
  3. Increased vascular permeability –> neutrophils into tissue
  4. Exudation of fluid, proteins, RBCs and WBCs into tissue
  5. Vascular stasis to allow chemical Mediators and infalmmatory cells to collect and response
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14
Q

Process of Fever

A
  • increased Body temp. by pyrogenes –> effect on Hypothalamus
  • exogenous pyrogens stimulate release of endogenous pyrogens from macrophages
  • Fever lowers the Plasma iron Levels
  • pagocytosis, incr. Interferons, breakdown of lysosomes
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15
Q

Process of Acute Phase response

A

–> increased production of specific blood proteins called acute Phase proteins (CRP, MBP)

  • inititate complement
  • initiate or accelerate Inflammation
  • stimulate Chemotaxis of the phagocytic cells
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16
Q

Helper T cells and their functions

A

TH1: early and local –> increased inflamm. Responses
TH2: late and systemic –> decreased inflamm. Responses
TH17: Epithelium and neutrophils

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17
Q

CD8 T cells and their functions

A

CTLs:
- eliminating infected cells

Suppressor T cells:
- antigen-specific Regulation of helper T function

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18
Q

Characteristics of antigen

A

T DEPENDENT ANTIGEN –> must be presented to T and B cells for Ab production
T INDEPENDENT AG –> with large, repetitive structures, can directly activate B cells resulting in production of IgM

  • contain Epitopes –> are the actual structures that interact with single antibody molecule
  • TCR can only recognize linear Epitopes conformational epitopes
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19
Q

Bacterial antigens

A 
- bacterial structure components
somatic (O) Antigen
capsular (K) Antigen
Flagellar (H) Antigen
- bacterial exoenzymes
- bacterial exytoxins
- bacterial superantigens
20
Q

IgD

A
  • on Surface of B cells together with IgM

- activates B cell growth

21
Q

IgM

A
  • on Surface of B cells with IgD
  • activates complement pathway
  • pahgocytosis and bacteriolysis
  • monomeric igM vs pentameric IgM connected with J chain
22
Q

IgG

A
  • crosses the placenta
  • important in the anamnestic repsonse
  • Chemotaxis, faciliates phagocytosis, fixes complement
  • four subclasses
23
Q

IgA

A
  • as momomer, dimer, trimer, multimers with J chain
  • Serum IgA and secretory IgA
  • secretory IgA for localized immunity
24
Q

IgE

A
  • receptor for Allergens and parasite Antigens
  • when enough UgE is on mast cells, they release histamine, prostaglandin, platelet activating factor, cytokines
  • in type I hypersensitivity reactions!
25
Q

Activation of T cell responses

A
  1. First Signal: Antigen specific, MHC-TCR
    2- Second Signal: enhances previous Signal
    3- Third Signal: for production of Interleukins –> T cell is activated
26
Q

Mechanisms of the antibacterial immunity responses

A 
1- Infection
2- Innate Responses
  --> neutrophils
  --> monocytes, macrophages
  --> acute Phase respones
3- Antigen-specific 
 --> early (B-cells, Interleukins, Interferons)
  --> later (B-cells, Memory cells)
27
Q

Mechanisms of the antivrial immunity responses

A 
1- infection
2- innate Responses
 --> NK cells
 --> dendritic cells
3- Antigen specific 
  --> early (B-cell)
  --> leater (B cell, Memory cell)
28
Q

Activation of B cell responses

A

Th1 and Th2 make B cells develop intp Plasma cells which produce antibodies

29
Q

Table of hypersensitivity reactions

A

look in summary

30
Q

Type I hypersensitivity

A 
1- exposure to Antigen
2- activation of Th2 cells
3- production of IgE antibodies
4- binding to mast cells --> sensitisation
5- re-exposure to Antigen
6- release of mediators
31
Q

Mechanism of desensitization

A
  1. denatured allergen under Skin
  2. T-reg –> no production of IgE
    3- Th1 for IgG –> IgG secreted
    4- IgG Abs intercept antigen
32
Q

Type II hypersensitivity reaction

A

IgG and IgM
leads to cell Lysis, tissue Damage, loos of functions, Agglutination of blood cells

  1. complement activation via classical pathway
  2. antibody dependenet cell-meidated cytotoxicity
  3. anti-receptor activity
33
Q

Type III reaction

A

1- Ag-Ab complex is formed
2- IC is deposited in tissue –> activating complement
3- This attracts neutrophils –> release lysosomal Enzymes –> inflammation

34
Q

type IV reaction

A
  • delayed, cell-mediated
  1. Th1 recognize Antigen Bound to APCs
    2- release of cytokines –> mediating immune Response
    3- CTLs_ destroy target cells on contact
  • -> overreaction of helper T and overprocution of cytokines
  • -> Damage of tissues, Inflammation, cell death
35
Q

Types of vaccines

A
  • live vaccines: waekened from of pathogen
  • subunit: made from other small peices taken from pathogen
  • inactivated /Killed: not as strong, we Need more than one shot
  • DNA vaccines: contain DNA that codes for specific Antigens from a pathogen
36
Q

Comparison of live and inactivated vaccines

A

LIVE VACCINES

  • low doses and single shot
  • Long term
  • IgG, IgA
  • good cell mediated Response
  • labile in tropics
  • occasional interference, mild Symptoms, Reversion to virulence

INACTIVATED VACCINES

  • high dose, multiple shots
  • short term
  • IgG
  • poor cell mediated Response
  • no heat lability in tropics
  • no interference, no Reversion
  • occasional sore arm
37
Q

Immunological assays

A
  • Tests that measure the presence of concentration of a molecule through the use of an antibody
  • molecule detected –> analyte
38
Q

Agglutination reactions

A

–> based on Formation of bridges btw. bivalent (IgG) or multivalent (IgM) antibides and antigenic particles with multiple Epitopes

DIRECT
- Antigen on RBCs bind to antibodies

INDIRECT

  • Antigen is absorbed on Surface (Latex, colloid Gold)
  • Antigens bind with antibodies
39
Q

Toxin-Antitoxin reaction

A
  • Neutralization reactions can detect bacterial toxins and antibodies to certain viruses
  • in botulism: animals are infected with pathogen; then they are given Variety of Antitoxins
  • if animal survives, then Antitoxin was successful
40
Q

Percipitation reaction

A

IN FLUID

  • Ab in Bottom
  • soluble Ag added
  • Zone of equivalence –> precipitin ring

IMMUNODIFFUSION

  • Ab and Ag both in agar gel
  • diffuse towards another and precipitin bands form

IMMUNOELETROPHORESIS

  • Ag in agar gel with Electric current –> spread
  • through of antobody in middle
  • curved precipitin bands form

RADIAL IMMUNIDIFFUSION

  • gen containing antobody
  • wells with Antigens
  • precipitin rings form
  • Diameter of the ring is proportional to the logarithm of the Ag concentration
41
Q

Complement Fixation test

A

–> to detect the presnece of either specific antibody or speific Antigen in a patients Serum

Serum (either with antibody or not)
1- Add Antigens
2- Add free complement
3- Add red blood cells with attached antibodies

—> RBCs are either lysed by free complements or not

42
Q

Immunofluorescence assay

A

DIRECT

  • to target unique Antigens present in the Bacteria but not present in mammals
  • cell Surface has Antigens and antibody with fluorescnent dye binds to ot

INDIRECT

  • secondary antobidy with dye binds to Primary antibody –> are for example Cancer markers
  • used to Diagnose autoimmune blistering diseases –> detects autoantibodies
43
Q

ELISA (Enzyme linked immunosorbent Assay)

A

AB DETECTION
- Ag + Serum
+ antiimmunoglobulin Enzyme
+ Substrate

AG DETECTION

  • Ab + specimen
  • second antiviral antobody
  • antiimmunoglobulin Enzyme
  • substrae
44
Q

Immunoblotting method

A
  • -> to detect posttranslational modifications (HIV, proteins in Tumors)
  • -> using antibody-based probes to obtain Information about target proteins
  • mix of proteins is separated with the help of gel-electrophoresis (charge, size, …)
  • bands become visible
45
Q

PCR

A
  • -> to make several copies of a specific DNA Segment by DNA polymerase
  • -> for testing genetic carriers, identification of microorganisms
  1. denaturation –> heating, cleaving
    2- annealing –> cooling, primers bind
    3- Extension –> DNA polymerase makes copies

TYPES

  • hot start PCR
  • fast PCR
  • real time PCR
  • nested PCR
46
Q

MALDI-TOF Mass spectomentry

A
  • sample is mixed in large quantity of Matrix
  • Matrix absorbs UV light and converts it to heat Energy
  • small part og Matrix is vaporized together with sample
  • charged Ions of various sizes are on sample slide
  • lighter Ions move faster through the drift space until they reach the detector
  • -> for identification of Bacteriaof all Kinds, fungi, mycobatera
  • -> for antimicrobial susceptibility test

Microbio final (6 decks)

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