MICRO Bacterial Pathogenesis Flashcards
A vs B Component of Intracellular Toxins
A = active - actively causes effect desired by bacteria
B = binding - tricks host receptor into letting bacteria into cells
Coagulase function
Clots blood by converting fibrinogen into soluble fibrin
What enzyme converts fibrinogen into fibrin for clots?
Coagulase
Streptokinase function
Dissolves clots
What enzyme dissolves clots?
Streptokinase
What enzyme directly degrades ECM?
Hyaluronidase
Hyaluronidase function
Degrades ECM
DNAse fnction
Breaks down NETs
What enzyme breaks down NETs?
DNAse
Example of coagulase-producing bacteria
S. aureus.
Example of staphylokinase producing bacteria
S. aureus.
Example of urease producing bacteria
H. pylori.
Example of IgA producing bacteria.
N. gonorrhoeae.
Explain complement evasion mechanism of bacteria.
- Proteolytic enzymes (mentioned above)
- C3 bound to bacterial surface to prevent opsonisation, phagocytosis, chemotaxis & lysis
- Binding of human complement inhibitors via Factor H
How does antigenic variation change the immune response?
Leads to wave-like immune responses with each trough corresponding to a change in pathogenic surface antigens.
Explain host mimicry mechanism in bacteria.
- Bind host molecules onto the pathogen’s surface via Fc receptor
- Anti-phagocytic capsules – mimic host polysaccharides
Pili/fimbriae vs afimbrial adhesions
Closer associated btw pathogen & host for afimbrial adhesions.
Techniques of phagocytosis avoidance
- 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.
Techniques of phagocytosis invasion & colonisation
- 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.
Techniques of non-phagocytic invasion & colonisation
- 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
Explain how bacteria can gain intercellular motility abilites.
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.
What are endotoxins?
LPS component of outer membrane of gram -ve bacteria.
3 classifications of exotoxins
Superantigens, toxins targeting extracellular molecules, toxins targeting intracellular molecules.
Function of superantigens
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.
Function of phospholipases
- Phospholipases behave as enzymes destroying the cell membrane
Function of pore-forming cytolysins
- Pore-forming cytolysins punch holes in cell membranes to break permeability barrier and cause cell death
Toxins types which target extracellular molecules
- 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).
Example of phospholipase
C. Perfringens.
Example of pore-forming cytolysins
S. Aureus.
Toxins targeting intracellular molecules
Simple A-B toxin/compound A-B toxin.
Examples of simple A-B toxins
Corynebacterium diptheria, V. cholerae, C. tetani, C. botulinum.
Structure of capsule (what is it composed of?)
High molecular weight polysaccharides.
