Section B (Bacteria): Practice exam questions Flashcards
Compare how Shigella and Listeria manipulate the host actin cytoskeleton to facilitate intracellular movement and intercellular spread.
Describe the trigger and zipper mechanisms of entry.
Outline key effectors (e.g., IpaC, ActA) and their interactions with host actin regulators.
Discuss actin tail formation and intracellular propulsion.
Explain how actin-based motility contributes to immune evasion and pathogenesis.
Discuss the mechanisms by which pathogenic bacteria alter their surface structures to persist within the host and evade immune detection.
Explain antigenic and phase variation mechanisms (e.g., recombination, SSM).
Provide examples such as pilin variation in Neisseria or LOS sialylation.
Analyse how transcriptional and translational control contributes to surface diversity.
Consider the implications for vaccine development and diagnostic testing.
Evaluate how genome-wide association studies (GWAS) have improved our understanding of bacterial pathogenesis and host-pathogen interactions.
Describe how GWAS identifies genotype-phenotype associations.
Provide examples where GWAS has uncovered virulence or resistance loci.
Explain how GWAS has been used to predict clinical outcomes or transmission.
Discuss current limitations and the future potential of GWAS in pathogen surveillance.
Describe how Gram-negative and Gram-positive bacteria use distinct secretion systems to export virulence factors. Discuss how these systems are adapted to their envelope structures.
Compare Sec-dependent and Sec-independent systems across Gram types.
Detail specific systems (e.g., T3SS in Gram-negatives, T7SS in Gram-positives).
Analyse how these systems deliver toxins or effectors into host cells.
Evaluate the relevance of these systems in therapeutic development.
How do bacterial toxins disrupt host cell signalling and function to promote infection and dissemination? Provide examples of distinct mechanisms and toxin families.
Describe AB toxins and their enzymatic activities (e.g., diphtheria, cholera toxins).
Explain pore-forming toxin mechanisms and effects on membranes.
Provide examples of toxins that manipulate host signaling (e.g., CNF, CDT).
Discuss the role of toxins in transmission, immune evasion, and tissue damage.
Explain how bacterial phase and antigenic variation contribute to immune evasion and chronic infection.
Define mechanisms of phase and antigenic variation.
Describe genetic mechanisms (e.g., SSM, recombination).
Provide examples like Neisseria pili or Haemophilus LOS.
Analyse how variation impairs immune memory and vaccine efficacy.
Discuss how bacterial toxins contribute to disease pathology and dissemination within the host.
Classify toxins (e.g., AB, membrane-disrupting, superantigens).
Describe cellular effects such as protein synthesis inhibition or apoptosis.
Provide case studies (e.g., diphtheria, cholera, pertussis).
Analyse how toxins facilitate tissue invasion or immune modulation.
Evaluate the role of bacterial secretion systems in virulence, focusing on how effector proteins manipulate host cell signalling.
Describe different secretion systems (T3SS, T4SS, etc.).
Highlight examples of effector proteins (e.g., SopE, CagA).
Explain how they target host pathways like Rho GTPases, NF-kB.
Assess the contribution of these systems to disease severity.
Describe the mechanisms through which intracellular bacteria survive within host the cells and avoid destruction.
Compare vacuole modification (e.g., Salmonella, Legionella) vs cytoplasmic escape (e.g., Listeria).
Discuss manipulation of phagosome maturation and autophagy.
Explain immune evasion strategies (e.g., preventing detection, antigen presentation).
Analyse the impact of intracellular survival on disease persistence.
How does proteomics enhance our understanding of bacterial pathogenesis and host-pathogen interactions?
Describe key proteomics techniques (e.g., MS/MS, 2D gels).
Explain how host and bacterial proteins are identified during infection.
Provide examples of discovered virulence factors or host targets.
Discuss integration with transcriptomics and systems biology.
Critically evaluate the use of transcriptomics to study infection. What are the advantages and limitations of this approach?
Define transcriptomics and techniques (e.g., RNA-Seq).
Explain how it reveals host and bacterial gene expression changes.
Highlight insights into virulence regulation and immune responses.
Discuss limitations: RNA stability, indirect protein-level inference.
Compare the “trigger” and “zipper” mechanisms of bacterial entry into non-phagocytic host cells.
Define each mechanism and key molecular players.
Use Listeria (zipper) and Shigella (trigger) as examples.
Explain actin polymerization initiation pathways.
Discuss how these strategies influence intracellular niche establishment.
How can bacterial secretion systems be engineered for medical applications such as vaccine delivery or cancer therapy?
Describe the potential of secretion systems to deliver therapeutic proteins.
Highlight engineered T3SS or T4SS in biotechnology.
Analyse challenges such as specificity and immune response.
Provide examples of current experimental therapies.
Explain how WGS is transforming clinical microbiology, with examples from outbreak tracking and resistance profiling.
Describe how WGS identifies pathogens and AMR genes.
Provide case studies from hospital outbreaks or foodborne pathogens.
Explain how it reveals transmission chains.
Discuss integration into routine clinical workflows and challenges.
Discuss how the concept of the evolutionary arms race applies to bacterial immune evasion strategies.
Define the arms race and co-evolution with host immunity.
Provide examples of immune evasion mechanisms (e.g., antigenic variation, secretion of immunomodulators).
Highlight evolutionary pressure on both host and pathogen genomes.
Discuss how this influences vaccine design and long-term control.
Discuss how bacterial recombineering has advanced our ability to study gene function and pathogenesis.
Define recombineering and tools like Red/ET systems.
Explain how targeted gene knockouts or insertions are made.
Highlight applications in virulence gene discovery.
Discuss the role in building attenuated or reporter strains.
Evaluate how bacterial manipulation of host GTPases contributes to cytoskeletal rearrangement and pathogenesis.
Describe how Rho family GTPases control actin dynamics.
Explain bacterial effector functions (e.g., SopE, IpaC).
Use examples of pathogens like Salmonella and Shigella.
Discuss implications for immune evasion and dissemination.
How has proteomics revealed novel biomarkers and therapeutic targets in infectious diseases?
Describe proteomic profiling of infected tissues or fluids.
Identify bacterial or host response proteins as biomarkers.
Provide examples of identified targets for therapy or diagnostics.
Discuss advantages over genomics alone.
Critically assess the utility of GWAS in understanding bacterial virulence and predicting patient outcomes.
Explain the principles and statistical foundations of GWAS.
Highlight discoveries in virulence genes or host-pathogen interactions.
Describe the links between bacterial genotype and clinical severity.
Discuss challenges like population structure and phenotype definition.
Using examples, discuss how commensal bacteria can cause disease through toxin production and what this implies about microbial pathogenesis.
Define opportunistic pathogenesis and context-dependent virulence.
Describe toxins from commensals (e.g., Bacteroides fragilis enterotoxin).
Explain host/environmental triggers for pathogenicity.
Reflect on the blurred lines between commensals and pathogens.
