L1 – Variation of Bacterial Surface Structures Flashcards
Why do bacteria modulate their surface structures?
They modulate surfaces to adapt to different niches, respond to host factors, enhance colonisation and evade the immune response.
In what way does host immune pressure drive surface variation?
Constant immune surveillance selects for variants with altered surface antigens, preventing effective recognition and clearance.
What is antigenic variation and how does it occur?
Antigenic variation involves genetic changes—often through recombination or slipped strand mispairing—that alter surface proteins.
How does phase variation differ from antigenic variation?
Phase variation refers to reversible on/off switching of gene expression, while antigenic variation results in structural changes in proteins.
What is antigenic drift?
Antigenic drift is the gradual accumulation of random mutations in surface antigens over time.
Which genetic mechanisms underlie Pili, opc, opa, and capsule variations?
Mechanisms include RecA-dependent homologous recombination (e.g. between pilS and pilE), RecA-independent Opa (slipped strand mispairing), and repair processes.
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What is the key difference between Neisseria meningitidis and Neisseria gonorrhoeae?
N. meningitidis is encapsulated and primarily causes systemic infections like meningitis, whereas N. gonorrhoeae lacks a capsule and typically causes gonorrhoea.
How do Neisserial adhesins contribute to colonisation?
They mediate attachment by overcoming charge barriers using pili and outer membrane proteins such as Opa and Opc.
What is the significance of the capsule in N. meningitidis?
The capsule enhances immune evasion and is a major virulence factor in systemic disease.
What role does RecA play in Neisseria surface variation?
RecA facilitates homologous recombination, ensuring genetic diversity and repair that underpin both antigenic and phase variation.
Describe the mechanism of slipped strand mispairing (SSM).
SSM occurs during DNA replication when repetitive sequences (CTCTT) misalign, resulting in the gain or loss of repeat units and altering gene expression.
How can changes in coding repeat numbers affect protein expression?
Variations may shift the reading frame, leading to truncated or non-functional proteins, thereby modulating the presence of surface antigens.
What additional strategies do Neisseria employ to evade host defences?
They utilise surface sialylation, mimic host molecules, and shed excess outer membrane components to divert antibodies.
What is one ecological advantage of altering surface properties?
It enables bacteria to switch between adhesion and detachment, facilitating colonization of new sites within the host.
What is antigenic variation and how does it occur?
Antigenic variation involves genetic changes—often through recombination or slipped strand mispairing—that alter surface proteins.
How does phase variation differ from antigenic variation?
Phase variation refers to reversible on/off switching of gene expression, while antigenic variation results in structural changes in proteins.
What is antigenic drift?
Antigenic drift is the gradual accumulation of random mutations in surface antigens over time.
Why is redundancy in adhesins advantageous for Neisseria?
Redundancy ensures that multiple adhesins can compensate if one is downregulated, ensuring persistent colonization.
What role does RecA play in Neisseria surface variation?
RecA facilitates homologous recombination, ensuring genetic diversity and repair that underpin both antigenic and phase variation.
How can changes in coding repeat numbers affect protein expression?
Variations may shift the reading frame, leading to truncated or non-functional proteins, thereby modulating the presence of surface antigens.
What additional strategies do Neisseria employ to evade host defenses?
They utilize surface sialylation, mimic host molecules, and shed excess outer membrane components to divert antibodies.
How does the absence of a capsule affect N. gonorrhoeae’s pathogenicity?
Without a capsule, N. gonorrhoeae relies more on antigenic variation and immune evasion mechanisms to persist in the host.
How does iron acquisition contribute to Neisseria survival?
Neisseria species have specialized receptors to acquire iron from host proteins, which is essential for growth and pathogenicity.
What are the key iron-binding proteins targeted by Neisseria?
Transferrin, lactoferrin, and hemoglobin are key sources of iron for Neisseria.
