Bacterial Pathogenicity Flashcards
What are the 2 groups of bacterial pathogens?
Opportunistic pathogen
Primary pathogens
What makes a bacteria able to cause disease?
It’s virulence determinants, usually multifactorial
What are the different parts of a bacteria and what are their function?
Fimbrae/pili: proteins involved in adherence of bacteria to host’s cells
Envelope proteins: for adhesion, nutrition and immune system evasion
Flagella: motility
Capsule: made of PLS, protect against phagocytes
LPS/endotoxins: in gram -ve only, promote tissue damage immune system evasion
What are the bacterial disease processes?
Colonisation (nutrients acquisition and adhesion) Invasion of tissues Avoidance of host defence Tissue damage Transmission
Where do bacteria adhere?
Mostly on mucosal surfaces but also no tooth surface (streptococci) and plastic catheters (staphylococci)
State and explain the different stages of adhesion.
1st stage: association . It involves non-specific forces like charge and hydrophobicity, weak and reversible
2nd stage: adhesion. It involves specific binding between bacterial adhesins and host receptors, strong and irreversible.
Subsequent stages may result in bacterial biofilm production which cause chronic infections very difficult to treat with antibiotics
Give examples of bacterial adhesins and host receptors.
Bacterial adhesins: fimbrae (rod like protein,E.coli) ; polysaccharide adhesion (oral streptococci)
Host receptors: blood group antigens and extracellular matrix proteins (fibronectin and collagen)
What are the 2 main iron uptake systems of bacteria?
Siderophores: when bacteria sense low iron,it produces siderophores which gets out into the host circulation and displace ferric ions form transferrin due to its higher affinity. It then take it back into the bacteria and ferric iron gets reduced to ferrous iron which has a lower affinity to siderophores, so it unbind it and let it go back into circulation to get more.
Direct binding of iron transport proteins: bacteria has transferrin binding receptors which bind to transferrin and take up ferric ion which gets reduced to ferrous ion
How are gram -ve bacteria able to avoid the complement proteins?
- The liposaccharides on the bacterial surface stoically hinder access of activated complement proteins to bacterial membrane
- capsules also interfere with complement binding (E.coli)
- surface proteins also inhibit complement binding (M protein in strep pyogenes)
Also staph aureus produce factors that interfere with complement activation