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CMBM Exam 3: Immunology > Bacterial Pathogenesis > Flashcards

Bacterial Pathogenesis Flashcards

1
Q

Define what a pathogen is?

A

An organism that has the capacity to cause disease

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2
Q

What are opportunisitic pathogens and what populations are susceptible?

A

Pathogens that rarely cause disease in healthy hosts but can regularly cause disease in a compromised person. This includes burn victims, HIV patients, and hospitalized patients on broad spectrum antibiotics

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3
Q

What are primary pathogens?

A

Pathogens that cause disease in healthy individuals. They have virulent mechanisms to overcome the immune response.

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4
Q

What factors determine whether a disease due to a pathogen will result?

A
  1. Virulence of pathogen: evasion factors
  2. Environmental factors
  3. Host factors: medications, age, pregnancy, other diseases/conditions
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5
Q

What are 3 virulence determinates/properties that allow an organism to enter, replicate, and persist in a host?

A
  1. Expression of capsule, LPS, or Pili
  2. Elaboration of exotoxins that kill WBCs, proteases, and siderophores
  3. Generation of DNA inversions that lead to antigenic and phase variation
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6
Q

What are 3 types of ways that a pathogen may be transmitted?

A
  1. Exogenous: encounter from an outside source
  2. Endogenous: normal microbiota infecting from a sterile site
  3. Congenital: transmission from mother to child
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7
Q

Define colonization

A

The ability to resist physical removal during infection

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8
Q

Through what 2 mechanisms is establishment of pathogen at the site of infection mediated by?

A
  1. Specific receptor interactions

2. Biofilm formation (non-specific adhesion)

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9
Q

What are 2 specific examples of receptor mediated adhesion molecules or structures located on bacteria?

A
  1. Fimbriae (Pili)

2. Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs)

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10
Q

What are MSCRAMMs?

A

They are a subfamily of surface adhesions that target host ECM proteins such as fibrinogen, fibronectin, and collagen for adhesion

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11
Q

What 3 things do biofilms make the bacterial within them resistant to?

A
  1. Antibiotics
  2. Being flushed away
  3. Phagocytosis and complement attack
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12
Q

What 3 exoenzymes can mediate dissemination of a bacterial infection?

A
  1. Hyaluronidase: breakdown hyaluronic acid (ground substance in connective tissue)
  2. DNases: thins pus made viscous by DNA released by dead WBCs
  3. Streptokinase: activates plasminogen to plasmin thus destroying fibrin clots and allows the bacteria to spread
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13
Q

What are 2 mechanisms by which bacteria can acquire iron?

A
  1. Siderophores: compound secreted by bacteria that chelates iron for transport into the bacterium
  2. Membrane proteins that function as receptors to bind transferrin, lactoferrin, hemopexin, as well as other iron containing compounds.
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14
Q

Direct damage due to infection can be the result of what 4 things?

A
  1. By products of bacterial growth (acids, gas=>gangrene)
  2. Exoenzymes which breakdown cells and intracellular matrices of host tissues
  3. Secretion or elaboration of bacterial toxins (either exo or endo)
  4. Damage by the immune response (Host-mediated pathogenesis): example is granuloma formation during a M. tuberculosis infection
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15
Q

Compare and contrast endotoxins and exotoxins. 9 characteristics

A

Endotoxin Exotoxins
1. LPS, Lipid A moiety Proteins
2. Gram (-) Gram (-) and (+)
3. Gram (-) outer memb. Extracellular
4. Chromosomal Prophage/plasmid
5. Weakly antigenic Highly antigenic
6. No toxoid Toxoid vaccines made
7. Weakly neutral by Ab Neutralized by antibody
8. Stable at high temp Unstable at high temp
9. Same effect regardless Effects vary depending on
of the origin origin

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16
Q

What is one of the most potent stimulators of the innate immune response?

A

Lipid A

17
Q

What pattern recognition receptor (PRR) detects Lipid A?

A

TLR4

18
Q

What is the molecular process by which Lipid A is recognized by the immune system and what is the result?

A
  1. Lipid A binds to LPS binding protein
  2. LPS binding protein complexed with Lipid A bind to CD14
  3. CD14 then interacts with TLR4
  4. TLR4 triggers an intracellular signaling cascade which results in the activation and transcription of NFkB
  5. NFkB is a transcription factor that upregulates TNF(alpha) and IL-1 (proinflammatory)
19
Q

LPS activities

A
  1. Triggers IgE to bind and cross react on Mast cells which release mediators => increased vascular permeability => hypotension => shock
  2. Activates platelets which release similar vasoactive mediators as Mast cells, also => disseminated intravascular coagulation (DIC) thrombosis
  3. May => clotting => DIC thrombosis
  4. Alternative complement activation => release of C3a and C5a => shock
  5. Stresses the liver => hypoglycemia, also causes release of acute phase proteins => fever, also increases TNFa and IL-1 => decreased Fe availability, endothelial cells increase vascular permeability, fever, and T cell activation => IFN-gamma => macrophage activation => even more TNFa and IL-1
  6. Activates polymorphonuclear lymphocytes
  7. Directly activates macrophages
  8. Directly causes endothelial cells to increase vascular permeability
20
Q

What are 4 characteristics of exotoxins?

A
  1. Secreted or membrane bound and released upon lysis
  2. Specifically destroy or inhibit cellular functions or tissue components
  3. Vary in specificity (neurotoxin, cytotoxin, enterotoxin)
  4. Many (but not all) possess enzymatic activity
21
Q

What is the basic structure of an exotoxin?

A

Composed of an active (A) unit and a binding (B) unit and can be dimeric, trimeric, tetrameric, etc.

22
Q

What are the 2 mechanisms by which exotoxins enter the host cell and cause it’s effect?

A
  1. Exotoxin B unit binds to a host cell surface receptor which triggers pinocytosis. The endosome then fuses with the lysosome with acidification leading to the dissociation of the A unit into the cytoplasm where it can exert its effect (known as an AB toxin)
  2. Exotoxins may be directly injected to the host cell via a Type III secretion system which may cause the host to engulf the bacterium
23
Q

What are 2 types of exotoxins that exert their deleterious effect at the cell surface?

A
  1. Pore-forming toxins: act by cleaving phospholipids of the cell membrane or oligimerize. Both result in the influx of water and efflux of ions => cell death
  2. Superantigens: cause an inappropriate locking of MHC II with TCR leading to CD4+ T cell activation which creates a cytokine storm. They produce similar symptoms as endotoxins
24
Q

How does Diphtheria toxin enter and affect the cell?

A

Enters by receptor mediated endocytosis via the B unit. The A unit then inactivates elongation factor-2 causing inhibition of translation => cell death

25
Q

How does Cholera toxin enter and affect the cell?

A

Same mechanism as Diphtheria toxin since it is also an AB toxin. The B unit binds to ganglioside receptors on intestinal epithelial cells. The A unit causes stimulation of a Gs protein => upregulation of adenylate cyclase => increase cAMP => efflux of Na, K, Cl, HCO3 and water thus creating a watery diarrhea

26
Q

What are hemolysins?

A

Toxins that damage cell membranes enzymatically or by the insertion of pore-forming molecules

27
Q

What exotoxin does clostridium perfringens use to exert its effect?

A

Phospholipase C which acts as a hemolysin

28
Q

How does a superantigen influence a T cell population?

A

The inappropriate interaction is promiscuous thus acting on many different clones of T cells. Because there is no memory component to the activation they end up eliminating a large population of T cells that the person might need in the future.

29
Q

For bacterial infections where the disease is toxin mediated, what is a good choice for antibiotic mechanism of action?

A

Antibiotics that inhibit protein synthesis

30
Q

List properties of the immune system (adaptive and innate) and describe how a bacteria might overcome them

A
  1. Stomach acidity: H. pylori uses urease to cleave urea to NH3 which is basic, thus increasing the pH allowing the bacteria to thrive
  2. Opsonization: S. aureus uses protein A to bind Fc region of antibody
  3. Phagocytosis: any organism that can produce a capsule
  4. Phagolysosome: M. tuberculosis can inhibit phagolysosomal fusion, some organisms contain catalase which neutralizes ROS allowing them to survive
  5. IFN gamma: Mycobacterium block the release of IFN gamma
  6. Antibodies: Hiding by going to an intracellular residence, antigen/phase variation, bind antibody, elaboration of IgA protease, and molecular mimicry

CMBM Exam 3: Immunology (21 decks)

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