What are the three main types of bacteria–host relationships?
Mutualism, commensalism, parasitism.
What is mutualism?
A relationship where both bacteria and host benefit (e.g., gut flora).
What is the first obligatory step in bacterial colonisation?
Attachment/entry into the host body.
What are the six steps of bacterial colonisation?
- Attachment 2. Local/General spread 3. Growth 4. Immune evasion 5. Shedding 6. Host damage.
What structures enable bacterial adhesion to hosts?
Pili/fimbriae, adhesins, flagella, LPS, surface virulence proteins.
Which bacterial attachment structures are common in Gram-negative species?
Pili/fimbriae and LPS.
What host structures do bacteria most commonly recognise?
Host cell receptors (integrins, cadherins), mucin/carbohydrates, ECM proteins, calcified tissues, prosthetics.
Which host cell type is the most common colonisation target?
Epithelial cells at mucosal surfaces.
Why are mucosal epithelial cells highly targeted?
Large surface area (200–400 m²), warm, nutrient-rich environment.
What are the three non-epithelial cell types targeted during colonisation?
Fibroblasts, phagocytic cells, endothelial cells.
Why is bacterial colonisation considered non-linear?
Adhesion, invasion, and immune evasion occur simultaneously and are adaptive.
What organism causes gonorrhoea?
Neisseria gonorrhoeae, a Gram-negative diplococcus.
Why is N. gonorrhoeae highly variable?
It lacks a capsule and compensates with extensive antigenic variation.
What are the key steps of early N. gonorrhoeae infection?
Enter mucosa → enter subepithelial space → evade phagocytes → move back to surface → transmit via contact.
Which adhesin is essential for initial attachment of N. gonorrhoeae?
Pili, which bind CD46, integrins, and CD47.
Which host receptors do Opa proteins bind?
CEACAMs (CD66), HSPG, and matrix proteins/integrins.
What are the four main roles of LOS in N. gonorrhoeae?
Receptor binding, inflammation, antigenic variation, complement evasion.
What is the significance of sialylation of LOS?
Allows LOS to bind Factor H, blocking complement MAC formation.
Which enzyme allows sialylation of LOS?
Bacterial sialyltransferase (adds sialic acid from host CMP-sialic acid).
Why is LOS-mediated complement resistance unstable?
LOS is not always expressed or sialylated.
How do Por1A and Por1B contribute to immune evasion?
They bind Factor H and C4b-binding protein, blocking C3 convertase formation.
What is a key consequence of LOS sialylation on bacterial adhesion?
Prevents Opa and LOS from binding CEACAMs and asialoglycoprotein receptors.
How can sialylated N. gonorrhoeae still interact with host cells?
By binding Siglecs on monocytes and neutrophils, facilitating uptake.
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Intro to immunity20
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Defense against infection23
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Innate defenses20
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Humoral responses30
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Cellular responses25
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Extracellular pathogens25
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Intracellular pathogens43
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Bacterial colonization23
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Emerging bacterial infections22
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Melioidosis25
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Salmonella28
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Shigella & Listeria32
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Mycobacterium tuberculosis31
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Persistent bacterial infections18
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Defenses at mucosal surfaces25
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Viral infection20
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Viral immunopathology24
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Influenza23
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Emerging viruses21
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Smallpox20
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HIV29
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Innate viral evasion0
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Epidemiology0
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Viral vaccines24
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Adaptive viral evasion0
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NGS & Proteomics0
