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Questions and Answers
How does antigenic variation contribute to bacterial virulence?
How does antigenic variation contribute to bacterial virulence?
- By releasing toxins that directly damage host cells, overwhelming the immune system.
- By preventing phagocytosis through the production of a thick capsule.
- By altering surface antigens, allowing evasion of the host immune response. (correct)
- By directly neutralizing host antibodies through enzymatic degradation.
What is the primary mechanism by which bacterial capsules enhance virulence?
What is the primary mechanism by which bacterial capsules enhance virulence?
- Protecting bacteria from phagocytosis by immune cells. (correct)
- Interfering with complement activation, thus preventing opsonization.
- Neutralizing host antibodies through enzymatic degradation.
- Promoting bacterial adhesion to host cells.
Which of the following best describes the role of Protein A in bacterial virulence?
Which of the following best describes the role of Protein A in bacterial virulence?
- Degrading IgA antibodies in mucosal secretions.
- Binding to the Fc portion of IgG to inhibit phagocytosis. (correct)
- Disrupting the complement cascade to prevent opsonization.
- Acting as a superantigen to induce excessive T-cell activation.
How do siderophores contribute to the virulence of certain bacterial pathogens?
How do siderophores contribute to the virulence of certain bacterial pathogens?
What is the role of the Type III secretion system (T3SS) in bacterial pathogenesis?
What is the role of the Type III secretion system (T3SS) in bacterial pathogenesis?
How does the 'cord factor' produced by Mycobacterium tuberculosis contribute to its virulence?
How does the 'cord factor' produced by Mycobacterium tuberculosis contribute to its virulence?
What is the significance of the LD50 (Lethal Dose 50) in assessing bacterial virulence?
What is the significance of the LD50 (Lethal Dose 50) in assessing bacterial virulence?
What is the role of IgA protease in bacterial virulence, and which bacteria utilize it?
What is the role of IgA protease in bacterial virulence, and which bacteria utilize it?
How do bacterial toxins like LPS (lipopolysaccharide) induce systemic effects such as shock and hypotension?
How do bacterial toxins like LPS (lipopolysaccharide) induce systemic effects such as shock and hypotension?
Sulfatides produced by Mycobacterium tuberculosis inhibit phagolysosome fusion. What is the consequence of this inhibition?
Sulfatides produced by Mycobacterium tuberculosis inhibit phagolysosome fusion. What is the consequence of this inhibition?
Flashcards
Virulence
Virulence
Quantifiable pathogenicity of an organism; helps determine disease severity after exposure.
Infectious Dose 50 (ID50)
Infectious Dose 50 (ID50)
Quantifies the number of pathogens required to cause disease in 50% of those exposed.
Lethal Dose 50 (LD50)
Lethal Dose 50 (LD50)
Quantifies the number of pathogens required to kill 50% of those exposed.
Virulence Factors
Virulence Factors
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Capsule
Capsule
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Endotoxin (LPS)
Endotoxin (LPS)
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Phase Antigenic Variation
Phase Antigenic Variation
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Protein A
Protein A
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Protein M
Protein M
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Injectisome
Injectisome
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Study Notes
Virulence vs. Pathogenicity
- Virulence quantifies an organism's pathogenicity, helping doctors gauge disease severity and time-based effects after exposure.
- Infectious Dose 50 (ID50) measures the pathogen quantity needed to cause disease in 50% of those exposed.
- Lethal Dose 50 (LD50) measures the pathogen quantity needed to kill 50% of those exposed.
- Enteropathogenic E. coli has an LD50 of 1 million cells, while anthrax has an LD50 of less than 10 spores.
Virulence Factors
- Virulence factors relate to infection processes like adhesion and invasion.
- These factors help microbes evade the immune system.
- Capsules, produced by bacteria like S. pneumoniae and N. meningitidis, act as anti-phagocytic factors.
- Bacterial toxins, such as endotoxin LPS, trigger macrophage activation and cytokine release, leading to shock, hypotension, and thrombosis.
- Host responses can amplify the virulence of bacterial infections.
- Pathogens use phase antigenic variation, altering surface antigens to evade the host immune system.
Specific Virulence Factors
- Protein A, from Staphylococcus, binds to the Fc portion of immunoglobulin G to prevent phagocytosis.
- Protein M, from Group A streptococci, prevents phagocytosis and plays a role in molecular mimicry, rheumatic heart disease, and rheumatic fever.
- IgA protease, an enzyme released by bacteria like S. pneumoniae and H. influenzae (remember "chin"), facilitates colonization by preventing IgA from attaching to the mucus of the GI and respiratory tracts.
- Injectisomes, used by Pseudomonas, E. coli, Salmonella, and Shigella (remember "PESS"), deliver toxins into host cells via the type three secretion system.
- Cord factor, used by Mycobacterium, activates macrophages and releases tumor necrosis factor alpha, forming granulomas.
- Sulfatides, also from Mycobacterium, inhibit phagosome-lysosome fusion, helping the bacteria survive within macrophages.
- K capsule, used by E. coli, reduces complement deposition and inhibits opsonization.
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