Podcast
Questions and Answers
What is the primary function of hyaluronidase in pathogens?
What is the primary function of hyaluronidase in pathogens?
Which type of toxin is associated with the stimulation of an inflammatory response upon pathogen death?
Which type of toxin is associated with the stimulation of an inflammatory response upon pathogen death?
What is the role of proteases in the context of virulence factors?
What is the role of proteases in the context of virulence factors?
Which of the following describes A-B Toxins?
Which of the following describes A-B Toxins?
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How do capsules contribute to the virulence of pathogens?
How do capsules contribute to the virulence of pathogens?
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What mechanism allows microbes to alter their surface proteins to evade the immune system?
What mechanism allows microbes to alter their surface proteins to evade the immune system?
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Which enzyme is responsible for breaking down collagen in tissues?
Which enzyme is responsible for breaking down collagen in tissues?
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What is a characteristic of superantigens?
What is a characteristic of superantigens?
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Which type of virulence factor can directly create pores in host cell membranes?
Which type of virulence factor can directly create pores in host cell membranes?
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What is the effect of nucleases produced by pathogens?
What is the effect of nucleases produced by pathogens?
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What is the first stage in the process of pathogenesis?
What is the first stage in the process of pathogenesis?
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Which of the following best describes a focal infection?
Which of the following best describes a focal infection?
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What role do adhesins play in pathogenesis?
What role do adhesins play in pathogenesis?
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How do opportunistic pathogens typically cause disease?
How do opportunistic pathogens typically cause disease?
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What is a common effect of antibiotic treatment on normal microbiota?
What is a common effect of antibiotic treatment on normal microbiota?
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Which virulence factor is specifically responsible for penetrating host tissues?
Which virulence factor is specifically responsible for penetrating host tissues?
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Which of the following accurately defines systemic infection?
Which of the following accurately defines systemic infection?
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Which of the following can serve as a portal of entry for pathogens?
Which of the following can serve as a portal of entry for pathogens?
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What is the function of toxins produced by pathogens?
What is the function of toxins produced by pathogens?
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What can lead to a patient being more susceptible to secondary infections?
What can lead to a patient being more susceptible to secondary infections?
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Flashcards
Pathogenesis stages
Pathogenesis stages
The process of a pathogen causing disease.
Exposure (contact)
Exposure (contact)
Encounter with a pathogen; does not always lead to infection.
Portal of Entry
Portal of Entry
The way a pathogen enters the body (skin, mucous membranes, etc.).
Adhesion
Adhesion
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Invasion/Colonization
Invasion/Colonization
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Intracellular Pathogen
Intracellular Pathogen
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Infection (Local, Focal, Systemic)
Infection (Local, Focal, Systemic)
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Opportunistic Pathogen
Opportunistic Pathogen
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Virulence Factor
Virulence Factor
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Pathogen Exit
Pathogen Exit
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Hyaluronidase function
Hyaluronidase function
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Exotoxin type
Exotoxin type
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A-B toxin part
A-B toxin part
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Membrane-disrupting toxin action
Membrane-disrupting toxin action
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Endotoxin trigger
Endotoxin trigger
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Collagenase function
Collagenase function
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Capsule evasion
Capsule evasion
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Superantigen effect
Superantigen effect
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Phagocytosis prevention
Phagocytosis prevention
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Antigenic variation
Antigenic variation
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Study Notes
Stages of Pathogenesis
- Exposure (contact): Encounter with a pathogen. Exposure doesn't guarantee infection; a portal of entry (e.g., skin, mucous membranes) is required.
- Adhesion: Pathogens attach to host cells using adhesion factors (e.g., pili, glycoproteins).
- Invasion/Colonization: Pathogens enter tissues; exoenzymes and toxins aid this process, causing damage and spread.
- Intracellular Pathogens: Enter cells, use host nutrients, and evade the immune system. H. pylori, for example, neutralizes stomach acid using urease to penetrate the stomach lining.
- Infection: Pathogen multiplication after successful invasion. Infection can be:
- Local: Confined to the entry site (e.g., boils, UTIs).
- Focal: Spreads from the entry site to a secondary location (e.g., spreading from a gum cut).
- Systemic: Spreads throughout the body (e.g., varicella zoster, affecting mucous membranes and the upper respiratory tract, causing a rash).
Secondary Infections
- Opportunistic Pathogens: Cause disease only in immunocompromised hosts.
- Factors impacting host susceptibility:
- Breaks in skin (e.g., wounds, burns)
- Weakened immune system (e.g., AIDS)
- Issues with the normal microbiome
- Age (young or old)
- Pregnancy
- Chemotherapy
- Post-surgical recovery
- Normal Microbiota: Disrupted balance can make them opportunistic pathogens (e.g., E. coli moving from the gut to the urinary tract).
- Weakened Immunity: Primary infections can compromise the immune system and increase susceptibility to secondary infections. Antibiotic treatment can eliminate pathogens but also disrupt the normal microbiome, leading to opportunistic infections.
Pathogen Exit
- Pathogens must exit the host to be transmitted to a new host (e.g., through skin, respiratory or urogenital tracts, or the GI tract).
Virulence Factors
- Virulence Factors: Enhance pathogenicity by assisting in adherence, invasion, and immune system evasion.
- Adhesins: Promote attachment to host cells.
- Exoenzymes: Aid penetration and damage tissues.
- Hyaluronidase: Breaks down hyaluronic acid, facilitating tissue penetration.
- Nucleases: Break down DNA, promoting spread.
- Phospholipases: Break down phospholipids, damaging cell membranes.
- Proteases: Break down proteins, inactivating antibodies.
- Collagenase: Breaks down collagen, allowing pathogen spread.
- Toxins: Harm host cells and impair bodily functions
- Endotoxins: Released upon pathogen death; stimulate inflammation and can cause organ failure.
- Exotoxins: Protein toxins, often highly potent.
- A-B Toxins: Have two parts (A=activity, B=binding); A enters the cell, B binds to the cell receptor.
- Membrane-disrupting toxins: Create pores in cell membranes.
- Superantigens: Trigger excessive immune response (cytokine storm).
Evasion of Phagocytosis
- Capsules: Prevent phagocytosis (immune cell engulfment).
- Proteases: Degrade host antibodies.
- Fimbriae: Block complement binding.
- Antigenic variation: Alter surface proteins to evade recognition (e.g., Lyme disease, influenza).
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Description
Test your knowledge on the stages of pathogenesis, including exposure, adhesion, invasion, and infection. Understand how pathogens interact with host cells and the different types of infections that can occur. This quiz will help reinforce your learning on the mechanisms of infectious diseases.
