(3) Pathogens & Host Defenses Flashcards

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1
Q

What is defined as pathogens?

A

Microorganisms causing DAMAGE to the host

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2
Q

What is virulence?

A

Measure of the ability to cause damage

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3
Q

What are the 5 virulence factors pathogens use?

A
  • Adhesins (attachement to host cell surface)
  • Capsule (protects [from host immune cells] & attachement)
  • Enzymes (extracellular enzymes to invade tissues or to protect pathogen)
  • Invasins (surface or injected proteins that trigger endocytosis of pathogen)
  • Type 3 & Type 4 Secretion Systems (injects effectors that take control of the host cell)
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4
Q

What are the 6 extracellular enzymes pathogens might use?

A

H.C.L-P.C.L.

  • Hyaluronidase (destroys hyaluronic acid = saccharides holding cells together)
  • Collagenase (degrades collagen in connective tissues)
  • Lecitinase (degrades lecithin [phosphatidylcholine] of cell membrane)
  • Leucocidin (cause lysis of WBC [protects agains immune sys.])
  • Protease (degrase complement proteins & antibodies of immune syst.)
  • Coagulase (cloaks the pathogen with insoluble fibres)
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5
Q

What are the differences between T3SS & T4SS? (Secretion Systems)

A

Type 3: form a channel, acts as a syringe

Type 4: acts as a gun, shoots effectors

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6
Q

What are the two main ways pathogens damages the host?

A

Invasiveness (microorganism establishes itself in the host and speads into the tissues)
Toxigenicity (microorganism produces toxins damaging the host’s tissues)

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7
Q

What are the 5 steps of an infection?

A
Exposure
Attachement/adherence
Invasion
Colonization & Growth (Toxicity/Invasiveness)
Tissue damage
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8
Q

What are the 2 categories of disease related with toxigenicity?

A
Infectious disease (infected w/ bacteria producing toxins damaging the host)
Intoxication (ingest [a food containing] toxins damaging the host; the bacteria do not infect the host)
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9
Q

What are the two types of toxins and their characteristics? (4&5)

A
  • Exotoxins
    a) secreted or released [when organism lyse]
    b) usually heat-labile proteins
    c) highly immunogenic (big antibody response)
    d) AB toxins (B = binds to SPECIFIC receptor of host cell; A = enzymatic part modifying & damaging the host cell)
  • Endotoxins
    a) are part of the pathogen (lipid A of LPS)
    b) heat stable
    c) weekly immunogenic (no antibody produced)
    d) activate the complement
    e) induce vasodilation->inflammation->fever->SEPTIC SHOCH
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10
Q

Which type of toxin can be used to make vaccines?

A

Exotoxins (produce antibody response and can be inactivated by heat to form… TOXOID)
Endotoxins cannot be inactivated and cannot be converted to a toxoid

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11
Q

What type of toxin is produced by Clostridium Botulinum & Vibrio cholerae and how do they differ?

A

Both are AB toxins => exotoxins
Botulinum toxin: target motor neurons, inhibits muscle contraction (stops the heart)
Cholera toxin: produce cAMP in intestinal epithelial cells; block Na intake and induces ions mvmnt to the lumen; water is attracted into the lumen (instead of into the blood with normal Na flow); massive fluid loss (diarrhea)

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12
Q

When it comes to host’s defenses, what are the two main types of defenses?

A
Innate defenses (always present in the host and are non-specific defenses)
Adaptive defenses (relies on DETECTION & RESPONSE to infection; are specific to FOREIGN ANTIGENS)
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13
Q

What consist of the Innate First barrier defenses? (4)

A

Skin (thick layer of dead cell)
Mucosa (mucus + ciliated cells of airways)
Normal microbiome (occupies sites, produces bacteriocin [kills other invading bacteria])
Antimicrobial substances (lysozymes [cleavage of peptidoglycan], antimicrobial peptides [creates pores in membranes])

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14
Q

Of what is composed the Innate Second line of defense? (3)

A

Complement system (protein inducing lysis by pore formation)
Phagocytes (digests pathogens)
Inflammation (vasodilatation [inc. blood flow], inc. fluid, recruitment of immune cells [complement, macrophages])

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15
Q

How does the complement system works?

A

Set of blood proteins activated by classical pathway (antibodies) or alternative pathway (microbial cell component [LPS]) resulting in the formation of membrane attacking complex (MAC) causing lysis of bacteria.
MAC complex consist of C(5b)(6)(7)(8)(9) proteins

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16
Q

Which bacteria are more sensitive to the complement system (MAC)?

A

Gram-negative bact. (target Outer membrane)

17
Q

Which cells undergo phagocytosis and how (2,4)?

A

Macrophage & Neutrophil

  • Attachement
  • Ingestion
  • Killing:
    a) lysozyme fuses w/ phagosome (injested bact.)-> hydrolytic enzymes-> degradation/lysis
    b) oxidative by reactive oxygen species (ROS)-> oxidizes bact.
  • Digestion
18
Q

What is the role of fever in the Innate Second line of defense?

A

Activated by IL-1 released by macrophages;

Increases temperature to inhibit growth of some pathogens

19
Q

What are the 3 characteristics of the adaptive defenses?

A
  • Specificity: each immune cell is specific to one antigen
  • Memory: exposure of an antigen to immune cells induces their reproduction; Subsequent exposure illicit a stronger and faster response
  • Tolerance: immune cells are tolerant to host’s (self) antigens (so don’t attack yourself)
20
Q

What are antigens?

A

molecules of microorganisms that can be recognized by the immune system

21
Q

What are T cells, what do they do and how do they get activated?

A

T-helper (T-h) cells: Big chiefs; T Cell Receptor (TCR) recognize antigen from MHC-2 (from macrophage or B cells) -> release IL-2 -> reproduction & differentiation into T-h and memory T cells; Once activated by IL-2, releases TNF-α -> activates macrophages into ANGRY KILLER CELLS
T-cytotoxic (T-c) cells: Killers; TCR recognizes antigen from MHC-1 (from any cell) -> releases IL-2 -> reproduction & differentiation into T-c and memory T cells; Once activated by IL-2 -> releases PERFORINS & GRANZYMES -> induces apoptosis (controlled death of infected cell presenting antigen on MHC-1)

22
Q

What are the two ways antigen are presented to and by the immune system?

A

With the Major Histocompatibility Complex (MHC):
{you are 1 with the cell = comes from inside {infection}; you are 2 with the cell = different, comes from outside (phagolysosome)}
MHC-1: (expressed by all cells) Presents antigen originating from inside cell (infection); recognized by T-c cells
MHC-2: (expressed by macrophages and B cells) Presents antigen processed in the phagolysosome; recognized by T-h cells

23
Q

What happens when macrophages are affected by TNF- α?

A

They become Angry Killer Cells -> produce lot of oxidative stress and oxidizes everything on their way (even themselves)

24
Q

What are B cells, what do they do?

A

B cells have antibodies on their surface to recognize antigens. Once antigen recognized -> phagocytosed and then presents it on MHC-2 -> antigen recognized by T-h cells -> T-h releases IL-4 -> induces reproduction & differentiation of B cells into Plasma cells & Memory B cells; Plasma cells produces antibodies

25
Q

What do Plasma cell do? (1->3)

A

They produce antibodies which:
Neutralizes toxins and adhesins
Triggers opsonisation (flags pathogen to increase phagocytosis)
Increases Complement system activity

26
Q

Who releases IL-4?

A

T-h cells

27
Q

Who releases IL-2?

A

T-h cells

28
Q

Who has MHC-2 and who recognizes it? (3,1)

A

Macrophages, Neutrophiles, B cells;

TCR of T-h cells

29
Q

Who releases IL-1?

A

Macrophages

30
Q

Who releases antibodies?

A

Plasma cells (differentiated B cells)

31
Q

Who releases perforins & granzymes?

A

T-c cells

32
Q

Who releases TNF-α?

A

T-h cells

33
Q

Who has MHC-1 and who recognizes it?

A

All cells have MHC-1 and is recognized by TCR of T-c cells

34
Q

By which pathway do antibodies activate the Complement System?

A

Classical pathway (not alternative = microbial cell component)

35
Q

What are the three ways one can get Immunity?

A

Acquired & Active immunity: (production of memory cells) Vaccine or Infection
Acquired & Passive immunity: (acquires antibodies) Colustrum {first milk} or serum
Natural immunity: already have it (born with it) -> incompatibility between host and pathogen