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Questions and Answers
What is the primary function of hyaluronidase in relation to pathogens?
What is the primary function of hyaluronidase in relation to pathogens?
Which type of toxin is known for triggering excessive immune responses?
Which type of toxin is known for triggering excessive immune responses?
How do capsules contribute to a pathogen's virulence?
How do capsules contribute to a pathogen's virulence?
Which virulence factor is essential for breaking down host cell membranes?
Which virulence factor is essential for breaking down host cell membranes?
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What allows pathogens to evade recognition from the immune system through antigenic variation?
What allows pathogens to evade recognition from the immune system through antigenic variation?
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What must occur for a pathogen to cause infection after exposure?
What must occur for a pathogen to cause infection after exposure?
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What term describes pathogens that can cause disease only in immunocompromised hosts?
What term describes pathogens that can cause disease only in immunocompromised hosts?
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Which of the following is an example of a focal infection?
Which of the following is an example of a focal infection?
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What role do exoenzymes play in the invasion of pathogens?
What role do exoenzymes play in the invasion of pathogens?
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What characterizes a systemic infection?
What characterizes a systemic infection?
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Which of these factors is a virulence factor that aids in the adhesion of pathogens?
Which of these factors is a virulence factor that aids in the adhesion of pathogens?
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What happens to normal microbiota during antibiotic treatment?
What happens to normal microbiota during antibiotic treatment?
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To prevent transmission to a new host, what must pathogens do?
To prevent transmission to a new host, what must pathogens do?
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Study Notes
Stages of Pathogenesis
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Exposure (Contact): Encounter with a pathogen. Exposure alone isn't infection; pathogen needs a portal of entry (skin, mucous membranes, parenteral).
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Adhesion: Pathogens attach to host cells using adhesion factors (pili, glycoproteins).
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Invasion/Colonization: Pathogens enter tissues; aided by exoenzymes (damage/spread) and toxins.
- Intracellular Pathogens: Enter cells, use host nutrients, evade immune system
- H. pylori Example: Produces urease to neutralize stomach acid; penetrates lining.
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Infection: Pathogen multiplies after successful invasion. Infection can be:
- Local: Infection at entry site (e.g., boil, UTI, pneumonia).
- Focal: Infection spreads from entry site to secondary location (e.g., gum infection spreading).
- Systemic: Infection spreads throughout the body (e.g., varicella zoster).
Secondary Infections
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Opportunistic Pathogens: Cause disease in immunocompromised hosts.
- Factors affecting hosts: Breaks in skin (wounds/burns), weakened immune systems (AIDS), microbiome imbalance, age (young/old), pregnancy, chemotherapy, post-surgery.
- Normal Microbiota: Can become opportunistic if balance is disrupted (e.g., E. coli from gut to urinary tract).
- Decreased Immunity: Primary infection weakens immune system, increasing risk of secondary infections; antibiotics can kill pathogens but also normal microbiome.
Pathogen Exit
- Pathogens must exit host to spread (skin, respiratory, urogenital, GI tracts).
Virulence Factors
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Virulence Factors: Enhance pathogenicity, help with adhesion, invasion, evasion.
- Adhesins: Attachment to host cells.
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Exoenzymes: Help penetrate tissues and damage cells.
- Hyaluronidase: Breaks down hyaluronic acid, tissue penetration.
- Nucleases: Break down DNA, spread.
- Phospholipases: Break down phospholipids, damaging cell membranes.
- Proteases: Break down proteins (inactivate antibodies).
- Collagenase: Breaks down collagen, tissue penetration.
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Toxins: Harmful to host cells, interfering with body functions.
- Endotoxins: Released from dead pathogens, inflammatory response, organ failure.
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Exotoxins: Proteins, often potent and deadly.
- A-B Toxins: Two parts (A=activity, B=binding; A enters cell, B attaches).
- Membrane-disrupting toxins: Create pores, damage membranes.
- Superantigens: Trigger excessive immune responses, cytokine storm.
Virulence Factors: Evasion of Phagocytosis
- Capsules: Prevent phagocytosis (engulfment).
- Proteases: Degrade host antibodies.
- Fimbriae: Block complement binding.
- Antigenic Variation: Alter surface proteins to avoid recognition (e.g., Lyme disease, influenza).
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Description
Test your knowledge on the stages of pathogenesis, including exposure, adhesion, invasion, and types of infections. Understand how pathogens interact with host cells and the role of opportunistic infections. This quiz is essential for students of microbiology and infectious diseases.
