MICRO Bacterial Pathogenesis

Question 1

A vs B Component of Intracellular Toxins

Answer 1

A = active - actively causes effect desired by bacteria
B = binding - tricks host receptor into letting bacteria into cells

Question 2

Coagulase function

Answer 2

Clots blood by converting fibrinogen into soluble fibrin

Question 3

What enzyme converts fibrinogen into fibrin for clots?

Answer 3

Coagulase

Question 4

Streptokinase function

Answer 4

Dissolves clots

Question 5

What enzyme dissolves clots?

Answer 5

Streptokinase

Question 6

What enzyme directly degrades ECM?

Answer 6

Hyaluronidase

Question 7

Hyaluronidase function

Answer 7

Degrades ECM

Question 8

DNAse fnction

Answer 8

Breaks down NETs

Question 9

What enzyme breaks down NETs?

Answer 9

DNAse

Question 10

Example of coagulase-producing bacteria

Answer 10

S. aureus.

Question 11

Example of staphylokinase producing bacteria

Answer 11

S. aureus.

Question 12

Example of urease producing bacteria

Answer 12

H. pylori.

Question 13

Example of IgA producing bacteria.

Answer 13

N. gonorrhoeae.

Question 14

Explain complement evasion mechanism of bacteria.

Answer 14

• Proteolytic enzymes (mentioned above)
• C3 bound to bacterial surface to prevent opsonisation, phagocytosis, chemotaxis & lysis
• Binding of human complement inhibitors via Factor H

Question 15

How does antigenic variation change the immune response?

Answer 15

Leads to wave-like immune responses with each trough corresponding to a change in pathogenic surface antigens.

Question 16

Explain host mimicry mechanism in bacteria.

Answer 16

• Bind host molecules onto the pathogen’s surface via Fc receptor
• Anti-phagocytic capsules – mimic host polysaccharides

Question 17

Pili/fimbriae vs afimbrial adhesions

Answer 17

Closer associated btw pathogen & host for afimbrial adhesions.

Question 18

Techniques of phagocytosis avoidance

Answer 18

• Killing of phagocytes – via toxins
• Prevention of opsonisation – by binding Fc portion of antibody
• Capsule – prevents contact w phagocytic surfaces, masks bacterial surface antigens & binds factors H to prevent opsonisation.

Question 19

Techniques of phagocytosis invasion & colonisation

Answer 19

• Prevention of phagosome-lysosome formation – bacterial secretion systems inject effector proteins into the host cell that subvert host cell processes in forming lysosome to ultimately colonise phagosome (e.g., Legionella pnemophila).
• Escape from phagosome before phagosome-lysosome fusion to colonise phagocyte
• Survival in phagolysosome – express catalase to breakdown H2O2, secrete proteases to breakdown antimicrobial peptides and colonise phagosome.

Question 20

Techniques of non-phagocytic invasion & colonisation

Answer 20

• Zipper mechanism – interaction of bacterial surface components (e.g., adhesins) w eukaryote surface
• Trigger mechanism – molecular syringe/secretion system injects effector proteins into the cytoplasm of target cell to invite pathogen intracellularly

Question 21

Explain how bacteria can gain intercellular motility abilites.

Answer 21

Harnessing of host actin to build a ‘comet tail’ and move via polymerisation (with great enough force can penetrate double-membrane to avoid extracellular bacterial defence mechanisms and move from one cell to another.

Question 22

What are endotoxins?

Answer 22

LPS component of outer membrane of gram -ve bacteria.

Question 23

3 classifications of exotoxins

Answer 23

Superantigens, toxins targeting extracellular molecules, toxins targeting intracellular molecules.

Question 24

Function of superantigens

Answer 24

Superantigens (SAgs) non-specifically bind to MHCII and TCR to activate T cells to cause massive cytokine release and may cause cytokine storm, hypotension, toxic shock, multiple organ failure.

Question 25

Function of phospholipases

Answer 25

• Phospholipases behave as enzymes destroying the cell membrane

Question 26

Function of pore-forming cytolysins

Answer 26

• Pore-forming cytolysins punch holes in cell membranes to break permeability barrier and cause cell death

Question 27

Toxins types which target extracellular molecules

Answer 27

• Phospholipases behave as enzymes destroying the cell membrane
  o (e.g., C. Perfringerns).
• Pore-forming cytolysins punch holes in cell membranes to break permeability barrier and cause cell death
  o (e.g., S. Aureus).

Question 28

Example of phospholipase

Answer 28

C. Perfringens.

Question 29

Example of pore-forming cytolysins

Answer 29

S. Aureus.

Question 30

Toxins targeting intracellular molecules

Answer 30

Simple A-B toxin/compound A-B toxin.

Question 31

Examples of simple A-B toxins

Answer 31

Corynebacterium diptheria, V. cholerae, C. tetani, C. botulinum.

Question 32

Structure of capsule (what is it composed of?)

Answer 32

High molecular weight polysaccharides.