Lec 29 - VFs Colonisation Flashcards
What are the 4 things that successful pathogens MUST be able to do?
- invade
- colonise new niches
- evade host defences
- multiply & grow
How are virulence factors classified?
into COLONISATION and DAMAGE to the host
Why are healthy mucosal surfaces virtually impervious to bacteria?
- consistently washed with anti bac / chemical agents and antibodies
- mechanistic properties eg coughing, sneezing, mucociliary action also prevent colonisation
What are the 4 main ways that pathogens can invade and colonise?
- chemotaxis and motilitiy
- secreting IgA protease
- adherence
- acquisition of nutrients
Describe how motility and chemotaxis allow the pathogen to survive?
- to survive on mucosal surfaces (eg ileum, mouth) pathogens need to reach the epithelial surfaces to acquire nutrients etc
- to do this they have flagella motility (directional swimming) along a nutrient gradient, sensed by chemotaxis
- the flagella helps to push the pathogen through the mucosal layer towards the epithelial cells
How does chemotaxis in pathogens work?
TCS senses ligands in the medium , activated RRs bind to the gflagellar motor and direct the swimming. As flagella constantly changes position on the exterior for random directions of movement, nutrient sensing stops the flagella chanigng position as frequently and therefore cell is propelled in same direction for longer
What does mutations in the genes involved in chemotaxis/flagella synthesis do?
renders the pathogen unable to colonise/ loss of Virulence
Which cells secrete IgA and what is its purpose?
IgA secreted by mucosal cells of the mucin layer. binds to bacteria as well as interacting with mucin and prevents growth of bacteria
How is the action of IgA combatted by bacteria? Draw a diagram
- bacteria in mucin layer secrete igA protease which cleaves the hinge region of IgA
- stops IgA interactng with mucin
- fabulation of bacterium - covered in Fab parts of antibody therefore prevents binding of other functional antibodies
At what stage of infection is adherence the most important?
early stages for infection - new target for antimicrobials?
Define..
- adhesins
- pili/fimbriae
- receptors
- extracellular bacterial structures that are adhesive - fimbrial or afimbrial
- Gram -ve pili. Gram +ve = fibrils
- complementary receptors/structures on host cells are bound by bacterial surface structures (adhesin)
Describe pili
- filamentous structures that are grouped together based on morphology, antigens, sequence
- made up of 1000s of pilin monomers
- interact w/ host cell receptors
Sites of infection can depend on _____ ____ (tropism)
receptor localisation
What are afimbrils?
do not group together to form pili & can bind protein receptros on host cells.
specific OM cell surface proteins that bind specific receptors
Give an example and function of an exopolysaccharide secretion in Gram +ve bacteria
- Streptococcus mutans
- Secrete a dextran exopolysaccharide made from dietary glucose that binds to and anchors it to teeth
What is fibronectin and give an example of when a bacteria utilises a protein to bind to it. Draw a diagram
- extracellular and matrix glycoprotein
- Str pyogenes produces Protein F which binds to fibronectin and promotes its adhesion and colonisation via bridging
How do siderophores work to acquire Fe?
- chelate Fe3+ with high efficency
- Fe3+ then transported into the cell via an OM protein (siderophore-iron receptor) -> PP then -> cytoplasm via ABC transporter
Draw a diagram to highlight how the TbpA and B complex works to acquire Fe from transferrin (completed by bacterial menningitis)
