Stages of Pathogenesis Quiz

Stages of Pathogenesis

• Exposure (Contact): Encounter with a pathogen. Exposure alone isn't infection; pathogen needs a portal of entry (skin, mucous membranes, parenteral).

• Adhesion: Pathogens attach to host cells using adhesion factors (pili, glycoproteins).

• 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.

• 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

• 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

• Virulence Factors: Enhance pathogenicity, help with adhesion, invasion, evasion.
  • Adhesins: Attachment to host cells.
  • 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.
  • Toxins: Harmful to host cells, interfering with body functions.
    • Endotoxins: Released from dead pathogens, inflammatory response, organ failure.
    • 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).