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.
How does surface modulation benefit bacterial survival in hostile environments?
It allows bacteria to dynamically alter adhesin presentation and evade immune detection, thus increasing survival and transmission.
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 one ecological advantage of altering surface properties?
It enables bacteria to switch between adhesion and detachment, facilitating colonisation 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.
Which genetic mechanisms underlie these variations?
Mechanisms include homologous recombination (e.g. between pilS and pilE), slipped strand mispairing, and RecA-dependent repair processes.
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.
Why is redundancy in adhesins advantageous for Neisseria?
Redundancy ensures that multiple adhesins can compensate if one is downregulated, ensuring persistent colonisation.
How does homologous recombination contribute to pilin antigenic variation?
Recombination between multiple silent pilS copies and the expressed pilE locus generates diverse pilin variants.
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 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 is meant by genetic redundancy in the context of bacterial surface proteins?
It refers to multiple genes performing similar functions so that inactivation of one does not eliminate a critical phenotype.
How does redundancy in adhesins enhance virulence?
It allows bacteria to maintain attachment and colonisation even if one adhesin is targeted by the immune system.
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.
Why is continuous variation important for long-term survival of pathogenic bacteria?
It enables rapid adaptation to changing host environments and immune pressures, ensuring persistent colonisation and transmission.
Why do bacteria modulate their surface structures?
They modulate surfaces to adapt to different niches, respond to host factors, enhance colonization, and evade the immune response.
How does surface modulation benefit bacterial survival in hostile environments?
It allows bacteria to dynamically alter adhesin presentation and evade immune detection, thus increasing survival and transmission.
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 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.
Which genetic mechanisms underlie these variations?
Mechanisms include homologous recombination (e.g., between pilS and pilE), slipped strand mispairing, and RecA-dependent repair processes.
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 gonorrhea.
How do Neisserial adhesins contribute to colonization?
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.
Why is redundancy in adhesins advantageous for Neisseria?
Redundancy ensures that multiple adhesins can compensate if one is downregulated, ensuring persistent colonization.
How does homologous recombination contribute to pilin antigenic variation?
Recombination between multiple silent pilS copies and the expressed pilE locus generates diverse pilin variants.
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 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 is meant by genetic redundancy in the context of bacterial surface proteins?
It refers to multiple genes performing similar functions so that inactivation of one does not eliminate a critical phenotype.
How does redundancy in adhesins enhance virulence?
It allows bacteria to maintain attachment and colonization even if one adhesin is targeted by the immune system.
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.
Why is continuous variation important for long-term survival of pathogenic bacteria?
It enables rapid adaptation to changing host environments and immune pressures, ensuring persistent colonization and transmission.
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.
What role do pili play in Neisseria adhesion?
Pili facilitate initial attachment to host cells and can undergo antigenic variation to evade immune responses.
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.
Why is N. meningitidis associated with bloodstream infections more often than N. gonorrhoeae?
The polysaccharide capsule of N. meningitidis provides protection from immune clearance in the bloodstream.
How does Neisseria evade complement-mediated killing?
By modifying its lipooligosaccharide (LOS) structure and binding host complement regulatory proteins.
What is the role of Opa proteins in Neisseria infections?
Opa proteins mediate tighter adhesion to epithelial cells and influence immune evasion.
How does Neisseria meningitidis cause meningitis?
It crosses the blood-brain barrier by interacting with endothelial cells and triggering inflammation.
Why is antigenic variation crucial for Neisseria gonorrhoeae?
It allows the bacterium to reinfect hosts multiple times by evading immune memory.
How does phase variation contribute to immune evasion?
It enables reversible switching of gene expression, leading to transient loss or gain of surface antigens.
What is the significance of lipooligosaccharide (LOS) in Neisseria infections?
LOS mimics host molecules, reducing immune recognition and contributing to inflammation.
How does Neisseria gonorrhoeae cause chronic infection?
Through antigenic variation, phase variation, and immune suppression mechanisms.
What host factors influence Neisseria colonization?
Mucosal surface composition, iron availability, and immune system status.
Why is genetic recombination important in Neisseria species?
It increases genetic diversity, allowing adaptation to host defenses and antibiotic pressures.
What is the relationship between Neisseria and horizontal gene transfer?
Neisseria species are naturally competent, readily acquiring foreign DNA from their environment.
How does immune selection pressure shape Neisseria evolution?
By favoring bacteria with antigenic diversity that escape immune detection.
What is the role of porins in Neisseria pathogenicity?
Porins regulate ion exchange and contribute to immune evasion by interfering with host signaling.
Why is gonorrhea difficult to eradicate with vaccines?
High antigenic variability of surface proteins makes it challenging to develop a universal vaccine.
What antibiotic resistance mechanisms are seen in Neisseria gonorrhoeae?
Efflux pumps, beta-lactamase production, and mutations in target enzymes.
What are pili composed of, and why are they important?
Pili are made of pilin subunits and are essential for adhesion, motility, and immune evasion.
How does capsule switching in N. meningitidis affect disease outbreaks?
It can lead to immune escape and new epidemic strains.
What are the main virulence factors of Neisseria species?
Pili: Mediate adhesion to host cells.
Outer membrane proteins (OMPs): Facilitate invasion and immune evasion.
Porins: Aid in nutrient acquisition and protection from host defenses.
Lipooligosaccharide (LOS): Triggers inflammation and immune system evasion.
IgA protease: Cleaves immunoglobulin A, helping bacteria evade mucosal immunity.
Capsule (in N. meningitidis): Protects from phagocytosis and enhances survival in the bloodstream.
How does Neisseria affect epithelial cells during infection?
Neisseria attaches to epithelial cells using pili and surface proteins, causing inflammation and tissue damage.
What diagnostic methods are used to detect Neisseria infections?
Methods include culture, PCR, Gram stain, serological tests, and immunofluorescence
Why do some Neisseria infections remain asymptomatic?
Asymptomatic infections occur due to immune evasion, low bacterial load, or host immune factors.
What genetic mechanisms lead to antibiotic resistance in Neisseria?
Resistance arises from mutations, horizontal gene transfer, efflux pumps, and target site modifications.
How does Neisseria interact with neutrophils?
Neisseria triggers inflammation and may survive phagocytosis, evading immune defenses.
What role does the host microbiome play in Neisseria colonization?
The microbiome influences Neisseria colonization by competing for resources and modulating the immune response.
What is the significance of the meningococcal serogroups?
Meningococcal serogroups (A, B, C, W, X, Y) determine the strain’s virulence and are used for vaccination strategies.
