Pathogenesis Flashcards

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1
Q

Pathogen

A

microbe causes disease

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2
Q

Pathogenicity

A

ability of a microorganism cause disease to other organism

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3
Q

Opportunistic pathogen

A

cause disease by accessing to tissue or body sites where they are not usually found

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4
Q

True pathogen

A

cause disease by producing toxin or damaging compound

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5
Q

Virulence

A

Measurement of pathogenicity

High virulent, more likely to cause disease

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6
Q

Indicators of virulence

A

Median infectious dose (ID50)

Median lethal dose (LD50)

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7
Q

Median infectious does (ID50)

A

number of pathogen cells required to activate infection in 50% of inoculated animals

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8
Q

Median lethal dose (LD50)

A

number of pathogen cells required to kill 50% of infected animals

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9
Q

Steps of pathogenesis

A
  1. Entry: with number of invading microbes + adherence
  2. Penetration or Evasion of Host Defenses
  3. Damage Host cell
  4. Exit: usually same with entrance
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10
Q

Factors of virulence

A
Adhesion
Colonization
Toxigenesis
Invasiveness
Resistance and immune system evasion
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11
Q

Adhesion

A

Process that bacteria attach to cell, tissue, and biological subtances

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12
Q

Colonization

A

adherence, multiplication, and establishment of bacteria at entrance

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13
Q

Toxigenesis

A

ability to produce toxins

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14
Q

Invasiveness

A

ability to forcingly enter tissues

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15
Q

Resistance and immune system evasion

A

ability of bacteria to resist antimicrobial compounds or to escape containment of host immune system

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16
Q

Steps of immune system

A
  1. Innate immunity: rapid, halts infection, no memory

2. Adaptive immunity: slower, clears infection, memory

17
Q

Antigen

A

Foreign particle elicit immune response

18
Q

Epitope

A

A segment of antigen where antibody recognize and bind to.

19
Q

How antibodies work?

A

Neutralization
Opsonization
Complement activation

20
Q

Neutralization

A

Antibodies bind their target

21
Q

Opsonization

A

Macrophage or neutrophil consume the target. When enough bacterial cells, antibodies will conjugate and form polymers to stick large amount of pathogen to prevent them from getting away and to localize them

22
Q

Complement activation

A

Series of protein damages microbe

23
Q

How are microbes digested?

A
  1. Phagosomes cover microbes.
  2. H+ pumps on phagosomes surface pump into phagosome mixture
  3. Lysosomes are activated by low pH and digest microbes.
24
Q

Ways of invasion

A

Injecting multiple protein into host cell to disrupt, kill, or make the cell work differently.
Causing cytoskeletal reorganization which engulf the bacteria.
Disrupting intercellular attachment molecules.
Using surface protein to bind to host cell surface and induce its own endocytosis

25
Q

How pathogen can survive from being digested?

A

Block lysosome

Stop the digestion by inhibiting enzyme or producing opposite phasing proton

26
Q

Compare types of toxin

A
Lipopolysaccharides (LPSs): endotoxin
Proteins:
- Tissue sites
- Extracellular diffusible toxins
- Heat-labile
27
Q

What include in the production of inflammatory cytokines?

A

Tumor necrosis factor (TNF)
Interleukin-1Beta (IL-1Beta)
Gamma interferon (IFNy)
Chemokines

28
Q

What happen with overzealous production of inflammatory cytokines?

A

Lead to cytokine storm

Contribute to mortality consecutive to sepsis or toxic shock syndrome

29
Q

What the production of inflammatory of cytokines do?

A

Guide anti-infectious innate immune response

30
Q

Endotoxin

A
  • Inflammatory bc they auto-amplificatory loops after monocytes activate
  • Cell wall of Gram-negative
  • Heat-stable
31
Q

Why endotoxin is the most potent microbial mediator?

A
  • Small does within a localized tissue space can make antimicrobial defense and stimulate bacterial clearance mechanism.
  • Sudden release of large amount can release a massive, dysregulated, and potentially lethal inflammatory response such as endothelial injury, low blood flow, disseminated intravascular coagulation, low blood pressure
32
Q

Exotoxin

A
  • Gram-positive

- Cell lysis

33
Q

How exotoxin work?

A
  1. Bacterium produces and release exotoxin
  2. B component binds host cell receptor
  3. A-B exotoxin enters host cell by endocytosis
  4. A-B exotoxin close pinched-off potion of plasma membrane during pinocytosis
  5. A-B exotoxin separate. A component inhibit protein synthesis and affect cell function. B component release from host cell
34
Q

A-B exotoxin (binary toxin)

A
  • 2-component protein complex secreted by pathogenic bacteria
  • Comprise of heavy and light chain
  • Connect by disulfide bond
  • Ex: botulinum toxin
35
Q

How botulinum toxin affect nerve cell function?

A
  • Flaccid paralysis: neurological weakness, paralysis, reduce muscle tone (even breathing one)
  • Reduce wrinkle
  • Unsuccessfully used as bioterror agent
36
Q

5 Types of botulism

A
  • Foodborne
  • Wound
  • Infant
  • Adult intestinal toxemia: rare
  • Iatrogenic: too much botulinum toxin in cosmetic
37
Q

Cholera

A
  • Non-toxigenic: in water

- Toxin-producing: infected with ctx gene bacteriophage

38
Q

Mechanism of cholera

A
  1. Catalytic portion find G-proteins of cellular signaling and attach ADP molecule to them
  2. G-protein convert into permanently active state to send never-ending signal
  3. The cell confuses and transports a lot of water and sodium to outside
  4. Intestine is flood
39
Q

What CFTR do?

A

Movement of chloride ions in and out of cell