Bacteriology - random essay questions Flashcards Preview

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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

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
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.
• 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.


Compare and contrast the structures, modes of host cell entry, and mechanisms of action of diphtheria toxin and shiga toxin

• Intro. Endo versus exo. These are both exo.
• Corynebacterium and Shigella bacterium summary
• Diptheria toxin and Shiga toxin basics (synthesis, AB toxins etc).
• Mode of host cell entry.
• Mechanism of action
• Purpose


Listeria and Shigella with cell cytoskeleton.

Intro – types of bacteria.
1) Describe host cytoskeleton
a. Intracellular matrix that supports both shape and function.
b. Actin polymerisation
c. Rho GTPases
d. PIPs.
2) Zipper vs trigger
a. Shigella Trigger. Virulence plasmid, effectors.
b. Listeria zipper. Binding proteins.
3) Survival in vacuole followed by escape and motility.
4) Intracellular spread.


Describe the structure, assembly and function of the bacterial flagella.

• Intro
• Function – movement, biased random walk, chemotactic control. Motility
• Motility – action, swimming, swarming, dispersal, role in pathogenesis, relationship to virulence
• Structure
o Macro: distribution
o Basal body
o Hook
o Filament
• Assembly
o Order
o Control
o Powering


How does UPEC colonise and cause damage to the host?

Intro: importance
Section 1: colonization
Chemoattraction in E. Coli.
Adhesion mechanisms
Afimbrial adhesins
Intracellular colonies
FAK cascade.
Src and Rho cascade
Different options inside.
Extracellular UPEC
Avoiding the immune system
Section 2: damaging the host
Presence of bacteria – immune response, exfoliation.
Protein toxins
Cytolysins – HlyA
Cytotoxic necrotizing factor
Vacuolating autotransporter.


Discuss S. aureus pathogenicity

QS system (Agr, kin selection, biofilms, virulence)
Virulence - control, types of toxins, mechanisms of action of HlyA
Avoiding immune system.


QS essay

1) QS in increasing virulence –
a. pseudomonas aeruginosa (LasI, LasR, RhlI-RhlR, PqsABCDH-PqsR)
b. staph aureus
i. Classic TCS system.
2) QS in decreasing virulence – cholera DIAGRAM (CqsS and LuxPQ systems)
3) interactions with other systems
a. Pseudomonas aeruginosa systems
b. Staph aureus
c. Vibrio cholera – cyclic (Phe-pro) decreases virulence.
4) Interactions with other species
a. Staph aureus
b. Humans
i. QseE
c. Cyclic dipeptides
5) Problems with these as anti-microbials;


Discuss bacterial signalling essay

General: in response to what? Altering transcription, altering translation.
Altering transcription: RNAP by sigma factors, TFs, promoters and small molecules.
TFs by phophorylation (HAP), small ligand binding (Fur) and second messengers.
Altering translation - riboswitches (GEMM) and riboregulators (Qrr and RNAIII)


Bordetella pertussis pathogenicity

Afimbrial adhesions.
Toxin CyaA, pertussis toxin.
Bvg control of virulence.