CSII Exam 2

What are the limitations of Koch's Postulates?

Asymptomatic carriers, unculturable microbes, host variability, and ethical constraints.

What are the five components of the chain of infection?

Reservoir, portal of exit, mode of transmission, portal of entry, susceptible host.

What defines a virulence factor under Molecular Koch's Postulates?

Present in pathogens, deletion reduces virulence, restoration restores virulence, expression confers virulence.

What is colonization resistance?

Commensals prevent pathogen expansion via nutrient competition, SCFAs, immune stimulation, and anaerobic/pH maintenance.

How does Salmonella overcome colonization resistance?

Induces inflammation to generate electron acceptors (e.g., tetrathionate) that favor Salmonella growth.

How does Helicobacter pylori penetrate gastric mucin?

Flagellar motility and helical shape allow movement through mucus.

What adhesins allow Staphylococcus aureus nasal colonization?

ClfB, WTA, and SREC receptor interactions.

What is a biofilm?

Structured surface-attached bacterial community in an extracellular matrix.

What are the steps of biofilm formation?

Reversible attachment, irreversible attachment, microcolonies, maturation, dispersion.

Why are biofilms antibiotic resistant?

Slow growth, diffusion barriers, efflux pumps, horizontal gene transfer.

What does Salmonella SPI-1 T3SS do?

Injects effectors that induce actin rearrangements and epithelial invasion.

What does Salmonella SPI-2 T3SS do?

Modifies SCV for intracellular survival and replication.

What are bacterial effector proteins?

Secreted proteins that manipulate host cytoskeleton, trafficking, immunity, and signaling.

How does Listeria escape the vacuole?

LLO forms pores; PlcA/B degrade membranes.

What is the function of ActA in Listeria?

Drives actin polymerization for intracellular motility and cell-to-cell spread.

What are spreading factors?

Enzymes like hyaluronidase, collagenase, and streptokinase that degrade tissue barriers.

How does Staphylococcus aureus evade complement?

Efb blocks C3; staphylokinase activates plasmin to degrade C3b.

How does Protein A help S. aureus evade immunity?

Binds Fc region of IgG backwards, preventing opsonization.

What are superantigens?

Toxins that cause massive nonspecific T‑cell activation and cytokine storm.

What is antigenic variation?

Alteration of surface antigens to evade immunity (e.g., Borrelia gene conversion).

What is selective pressure?

Environmental forces eliminating susceptible populations (antibiotics, immunity).

What is selective advantage?

Mutation or gene that improves survival under selective pressure.

What is the central dogma?

DNA → RNA → Protein.

What are the components of a bacterial gene?

Promoter, RBS, ORF, terminator.

Which mutations alter protein function?

Missense, nonsense, and frameshift mutations.

How do mutations cause antibiotic resistance?

Alter targets, efflux, permeability, or regulatory pathways.

What is bacterial transformation?

Uptake of naked DNA and recombination into chromosome.

What did Griffith's experiment show?

DNA is the transforming hereditary material.

How is transformation identified experimentally?

DNase-sensitive, no cell contact required.

What is generalized transduction?

Lytic phage packages random host DNA fragments.

What is specialized transduction?

Temperate phage excises imprecisely, carrying adjacent host genes.

What is lysogenic conversion?

Prophage-encoded virulence factors (e.g., diphtheria toxin).

How is transduction identified experimentally?

DNase-resistant and no cell contact.

What is conjugation?

Plasmid-mediated gene transfer requiring direct cell contact.

What is an F+ cell?

Contains F plasmid; transfers plasmid only.

What is an Hfr cell?

F plasmid integrated; transfers chromosomal genes.

What is an F′ plasmid?

F plasmid carrying host genes due to faulty excision.

How do you identify conjugation experimentally?

Requires contact (U‑tube negative) and is DNase‑resistant.