Pathogenesis Stages Quiz

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).