10. Bacterial colonisation Flashcards
mutualism
both parties benefit
mutualism example
gut bacteria breaking down nutrients
commensalism
one party benefits the other is neutrally effected
commensalism example
skin flora
parasitism
one party benefits the other is harmed
parasitism example
bacterial pathogens
what are the 3 relationships between bacteria and humans?
mutualism, commensalism and parasitism
what steps are essential for colonisation?
adhesion
local spread
growth
evasion of host defences
exit from host - transmission
damage to host
what are the colonisation steps unique to pathogens?
damage to host
how are capsules used for adhesion?
sticky so stick to the host cell
how are slime layers used for adhesion?
sticking
how are flagella used for adhesion?
to drive deeper into tissues and through mucus layers
how are pili/fimbriae used for adhesion?
get through mucus layers
no gram -ve and +ve
how are lipoteichoic acids and carbohydrates used for adhesion?
attach to cell host cells
how are bacterial outer membrane proteins used for adhesion?
stick to ECM protein like fibronectin and fibrinogen
what do bacteria bind to on host cells?
surface receptors
ECM proteins
secreted proteins and carbohydrates
calcified components
implants and prostheses
Why are epithelial cells a big target for bacteria?
Because of the massive mucosal epithelium surface area
why are fibroblasts targetted by bacteria?
they are in the sub dermal layer and help with wound healing and tissue repair
what are the cell types targetted by bacteria?
epithelial cells
fibroblasts
phagocytic cells
Endothelial cells
why are phagocytic cells targetted by bacteria?
to disrupt their function to continue disease progression
why are endothelial cells targetted by bacteria?
target blood vessels for distribution and sepsis
how do humans Initially defend against bacteria?
lysozymes in the saliva
mucus to wash away pathogens
acidic environments like the stomach
what causes the most pain in a bacterial infection?
the inflammation response of the immune system
where can you get gonorrhoea?
sexual organs
throat
blood stream
skin
what can gonorrhoea cause?
Infertility
arthritis
Proctitis
why are cases of gonorrhoea rising?
very drug resistant and super gonorrhoea cannot be treated
Development of HIV prophylactic treatment means people are being less careful about other STIs
stages of gonococcal infections
- Initial exposure at the epithelium
- at the basal surface and interact with macrophages
- activation of pro-inflammatory cytokines leading to chronic inflammation
- Tissue damage
- cell damage - dead and dying epithelium and neutrophilsh
what are the pro inflammatory cytokines?
TNFa and IFNy
what percentage of gonorrhoea cases can be asymptomatic?
10-30%
what virulence factors are involved in gonorrhoea pathogenesis?
Pili binding to integrins and possibly CD46
Opa porins - beta barrels
LPS bind to glycoprotein receptors and complement and cause inflammation
what is different about enteric bacteria LPS?
no O-antigen repeats but shorter oligosaccharide region
what is the toxic part of LPS?
aceylated lipid A
how do you get diversity in LPS?
phase variation of LPS
upto 14 types of different LPS
why do bacteria express lactoneotetraose?
to mimic host cells and avoid the immune system
what does siayl transferase do ?
transfers sialic acid from host membranes to the bacteria and add to lactoneotetraose?
when is siayl transferase expressed?
when the lactoneotetraose is present in the membrane
what are the complement inhibitor points?
C4b binding protein
Factor H
Vitronectin
what is the function of complement inhibitors?
they protect the host by preventing membrane attack complexes binding to host cells
how have bacteria like gonorrhoea evolved to use complement inhibitors?
they bind the inhibitors to protect themselves from the complement
how does gonorrhoea bind factor H?
can express the galactose needed to bind host sialic acid so the body thinks it is a host cell
this means factor H will bind to it and prevent membrane attack complexes forming on the gonorrhoea bacteria
what is unstable resistance?
resistance that can be phased on or off depending on the presence of a variable like galactose
what porins do gonorrhoea produce?
Por1A and Por1B
trimeric outer membrane proteins
what is the function of porins in gonorrhoea?
nutrient uptake and invasion
how do porins cause apoptosis?
translocation from bacterial membrane to mitochondrial membrane
activating the intrinsic apoptosis pathway
what is a positive about the porins?
it is a potential target for vaccines
how do the porins contribute to host mimicry?
Factor H can bind the porins preventing complement activation and no membrane attack complex formation
what is stable resistance?
the resistance is dependant is something that is nearly always expressed
what else binds to gonorrhoea porins to prevent classical activation of the complement?
Por1A and Por1B can bind C4 binding protein preventing membrane attack complex formation
what is a trade off for this resistance?
sialic acid coats bacteria in negative charge which can repel nutrients and other useful molecules
cannot bind Opa
what are sialic acid binding lectins?
often on immune cells
interactions can subvert neutrophil functions
what are the roles of LPS?
target receptors
damage to host - lipid A toxin
immune evasion - factor H
