Adhesion and Invasion Flashcards

1
Q

Define adhesin and give two examples.

A

Microbial surface molecules or structures that bring microbes to their host (ex. fimbrial adhesin type 1, afimbrial adhesin)

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2
Q

Discuss the role of adherence in bacterial infection.

A

Allows bacteria to colonize and establish infection

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3
Q

List and describe adherence forces that bring bacteria to host cells or extracellular matrix.

A

Non-specific adherence forces
- Hydrophobic interaction
- Electrostatic attraction
- Ionic interaction
- Brownian movement
- Trapping

Specific adherence forces
- Involves bacterial adhesins and host cell receptors
- Can be demonstrated by interaction of an isolated adhesin with its receptor or inhibition of binding by isolated adhesin or receptor or by antibody

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4
Q

Explain how a specific binding mechanism differs from a non-specific binding mechanism.

A

Specific binding mechanisms invovle bacterial adhesins and host cell receptors
- Determines what host cells or tissues are targeted by bacterial pathogens,
- Specific target cells

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5
Q

Define tissue tropism.

A

The tendency of a virus or prokaryotic microorganism to migrate within a host to a specified tissue

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6
Q

Explain how binding specificity contributes to tissue tropism for a bacterial pathogen. Give one example.

A

Binding specificity involves host cell receptors and bacterial adhesins, so if specific host cell receptors are found in a particular tissue, a bacterial pathogen will likely infect that tissue.
- Ex. E. coli causing UTIs

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7
Q

Describe extracellular matrix, fibronectin, and integrin and their interactions with bacteria.

A
  • ECM: network of proteins and polysaccharides between cells in a tissue
  • Fibronectin: a large glycoprotein of the extracellular matrix that plays a role in cellular adhesion
  • Integrin: a class of cell surface proteins that act as receptors and may be involved in cell-cell interactions, attachment of cells to tissues, or receptors for plasma proteins
  • Bacteria can use the ECM as a self-mask; can bind to integrins/fibronectins
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8
Q

Explain the function of the fimH gene in the Escherichia coli fim operon.

A

Acts as an invasin that allows E. coli to adhere to and get internalized by bladder epithelial cells

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9
Q

Reading assignment: Explain why gentamicin was used for the experiment shown in Fig. 7.

A

To prove that E. coli was an intracellular pathogen (gentamicin can’t kill the bacteria inside host cells)

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10
Q

Describe the structure and functions of M protein found in Streptococcus pyogenes.

A

Structure
- About 500 amino acids long
- Anchored in cell membrane
- Project from cell wall as helical fibrils

Functions
- Adherence to extracellular matrix proteins
- Role in invasion of epithelial cells
- Resistance to phagocytosis
- Resistance to complement opsonization

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11
Q

Define serotype.

A

Distinct variation within a species of bacteria

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12
Q

Reading assignment: Discuss the role of M1 protein and/or fibronectin in invasion of human epithelial cells by Streptococcus pyogenes serotype M1 based on the data presented in Figs. 1 and 4.

A

Both are necessary for internalization (both are critical, but just M1 or just Fn is not sufficient)

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13
Q

Reading assignment: Explain whether the experiment for Fig. 4 was necessary.

A

Yes, because idk to prove something/be thorough

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14
Q

Describe potential advantages and disadvantages to bacteria that are internalized by host cells.

A

Advantages
- Escape from extracellular host defense mechanisms
- Antimicrobial agents that can’t penetrate host cells

Disadvantages
- Oxidative and non-oxidative
intracellular killing
mechanisms
- Intracellular nutrients

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15
Q

Describe challenges that face clinicians and patients in dealing with infections caused by intracellular bacteria.

A
  • Recurrent infections
  • Cell-mediated immunity
  • Effectiveness of drug
    therapy
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16
Q

Reading assignment: Describe the cell cycle of L. monocytogenes (Fig. 1).

A
  1. Adhesion: InIA-E-cadhein interaction
  2. Endocytosis
  3. Lysis through listeriolysin O (pore-forming cytotoxin)
  4. Actin polymerization
  5. Cell-to-cell spread
17
Q

Reading assignment: Define the role of L. monocytogenes listeriolysin O in the intracellular survival of the bacterial pathogen.

A

Allows L. monocytogenes to get inside host cells and establish infection

18
Q

Reading assignment: Explain why direct invasion of neighboring host cells by L. monocytogenes is regarded as a protective mechanism for the pathogen.

A
  • Evade host defenses in blood/tissue
  • Access to nutrients
  • Avoid antibiotics
19
Q

Reading assignment: Describe how the InIA-E-cadherin interaction leads to internalization of L. monocytogenes (Figs. 2 and 3).

A

E-cadherin is a cell adhesion molecule (bacteria bind to it and get inside cell)

20
Q

What is the function of Type III secretion in bacterial infection?

https://www.youtube.com/watch?v=OBf64TEo7gA

A
  • Inject proteins directly into host cell cytoplasm
  • Allows the bacteria to invade the host cell and become an intracellular parasite
21
Q

Reading assignment: Describe the routes of dissemination of Salmonella from the intestinal lumen to extraintestinal sites in the mouse (Fig. 1).

A
  1. After reaching the
    distal ileum, the majority of Salmonella invade M cells that overlie PPs.
    2–4. Most bacteria are likely to reach the MLN by carriage within DCs
    via the lymphatic system. DCs transport Salmonella from the PPs (2), intestinal lumen (3) or lamina propria (LP) (4)
  2. It is possible that
    Salmonella can be transported directly from the PPs to the liver and spleen, but large numbers of bacteria are unlikely to migrate out of the
    MLN (6)
  3. Salmonella can also be carried directly from the intestine to the liver and spleen via a haematogenous route involving carriage
    within CD18+ phagocytes, most likely monocytes or DCs.
  4. After prolonged infection, Salmonella can be transported between organs via the
    bloodstream.
  5. Bile excretion from the liver also carries bacteria to the gall bladder
    10./ Gall bladder colonization presumably leads to re-infection of the intestine through bile secretion.
22
Q

Compare and contrast the two invasion mechanisms above (Salmonella).

A

M Cells in Peyer’s Patches:
- Location: In the small intestine’s Peyer’s patches.
- Invasion: Direct transcytosis of Salmonella.
- Protection: Offers a relatively unprotected route.
- Advantages: Bypasses gut-associated lymphoid tissue (GALT) defenses for direct access to Peyer’s patches.
- Outcome: Can lead to systemic dissemination.

Mesenteric Lymph Nodes:
- Location: In the mesentery of the small intestine.
- Invasion: Crossing the epithelial barrier and lymphatic vessels to reach lymph nodes.
- Protection: Involves navigating through the lamina propria.
- Advantages: Provides access to lymphoid tissue.
- Outcome: Results in local infection and inflammation, and can lead to systemic dissemination.

(from Chat GPT)