Bacteriology - random essay questions Flashcards
How do pathogenic bacteria avoid being killed by macrophages?
Avoid contact with macrophages
Inhibit engulfment by macrophages.
Survive within macrophages.
Kill or lyse phagocytes
Avoiding contact with macrophages
In lumen of glands/bladder, unbroken skin.
Avoiding provoking inflammatory response.
Inhibit macrophage chemotaxis.
Avoid recognition.
Inhibiting engulfment by macrophages.
Polysaccharide capsule Group A streptococci Alginate slime O polysaccharide LPS of E coli, and K antigen S. Aureus soluble protein A.
Survival inside macrophages
Entry
Early escape from phagosome. Prevent phagosomal maturation.
Inhibit phagosomal/lysosomal fusion.
Survive within phagosome
Kill phagocytes.
Before ingestion
After ingestion.
Avoiding contact with macrophages; avoiding inflammatory response.
Decrease cytokine production
Prevent maturation of cells.
Avoiding contact with macrophages; avoiding inflammatory response. DECREASE PROINFLAMMATORY CYTOKINE RESPONSE.
cholera toxin
EF, LFb
SptP
Pertussis toxin
Avoiding contact with macrophages; avoiding inflammatory response. INHIBIT MATURATION OF CELLS.
cAMP signalling toxins inhibit proper maturation of dendritic cells.
Avoiding contact with macrophages; avoiding inflammatory response. Decrease proinflammatory response, cholera toxin.
decreases TNFa production by 80 times
Avoiding contact with macrophages; avoiding inflammatory response. Decrease proinflammatory response, SptP.
–> carboxy terminus tyrosine phosphatise is thought to dampen down pro-inflammatory response
Avoiding contact with macrophages; avoiding inflammatory response. Decrease proinflammatory response, EF and LFb.
decrease TNFa, IL-12 etc
Avoiding contact with macrophages; avoiding inflammatory response. Decrease proinflammatory response, pertussis toxin.
CD11b/CD18 myeloid cells –> Stops proper differentiatioN, reduces LPS induced TNFa, IL-12 production, Increases LPS induced: IL-6, IL-10
Vibrio cholerae pathogenicity
• Signalling – quorum sensing o Signalling pathways o Inactive virulence o Active colonization and biofilms o Cyclic dipeptides, QseE • Colonisation o Biofilms general + Vps pathway o TCP for adhesion. Toxin coregulated type IV pili. • Toxins o Synthesis – control using ToxRS and TcpP/H system acting on ToxT. o Delivery to cell o Action o Other toxins – cholera RTX, zonula occludens toxin, accessory cholera toxin. • Flagella for movement o Important for access to new hosts o Monotrichous.
How do bacteria subvert and manipulate small GTPases in the mammalian host cell. What are the consequences?
Ways to manipulate
• Upstream – binding receptors. E.g. Yersinia binding B-integrins leads to Rac1 remodelling.
• Interactors – GEFs, GAPs, GDIs.
o YOP mimics
o Chamlydia recruitment via Tarp phosphorylation pathway.
o PIP pathways. Salmonella SopB.
• Direct modification
o To RhoGTPases
CNF, Legionella SidM pathway, Salmonella SopE and SptP.
Small G proteins and toxins.
Consequences
• Uptake
o RhoA, Rac1, Cdc42.
o Can be by other e.g. that work directly on cytoskeleton, but rarer.
• Vacuolar delivery – Rabs important.
o Keeping targeting to recycling endosome (Rab 1, 4, 11)
o Movement or arrest. Recruitment Rab7 salmonella perinuclear. Prevention of recruitment mycobacterium arrest.
o Lysosomal effectors. Listeria and Rab5.
o Maintenance of modified vacuole Chlamydia Rab1b.
• Small G proteins.
o Altering cAMP levels, cholera and pertussis.
How does the Agr gene regulator signaling pathway control virulence gene expression in Staph aureus?
• Intro: quorum sensing • Draw pathway • Different promoters • RNA III control o Dual function, positive regulation of Hla, negative regulation of rot. o Translated to give d-hemolysin. • Other controls such as sigma factors.
