Pathogenesis Stages and Infections

Pathogenesis Stages

• Exposure (Contact): Encounter with a pathogen. Exposure doesn't guarantee infection; pathogens need a portal of entry (skin, mucous membranes, or parenteral route).
• Adhesion: Pathogens attach to host cells using adhesion factors (like pili or glycoproteins).
• Invasion/Colonization: Pathogens enter tissues. Exoenzymes and toxins facilitate this, causing damage and spread.
• Intracellular Pathogens: Some pathogens enter cells and use host nutrients to evade the immune system. For example, H. pylori neutralize stomach acid using urease.
• Infection: Successful invasion leads to pathogen multiplication. Infections can be:
  • Local: Infection confined to the entry site (e.g., boil, UTI).
  • Focal: Infection spreads to a secondary site (e.g., gum infection spreading).
  • Systemic: Infection spreads throughout the body (e.g., Varicella Zoster).

Secondary Infections

• Opportunistic Pathogens: These pathogens cause disease in immunocompromised hosts.
• Conditions impacting hosts: Factors that make hosts vulnerable include breaks in skin, weakened immune system (like AIDS), microbiome imbalances, age, pregnancy, and chemotherapy.
• Normal Microbiota: Disruptions in normal microbiota can lead to opportunistic infections (e.g., E. coli from the gut causing a UTI).
• Decreased Immunity: Fighting a primary infection can weaken the immune system, leading to secondary infections. Antibiotics can kill pathogens, but also disrupt the normal microbiome which can lead to secondary infections.

Pathogen Exit

• Pathogens must exit the host to be transmitted to a new host (e.g., skin, respiratory, urogenital, or GI tract).

Virulence Factors

• Virulence Factors: Attributes that increase pathogenicity. These help pathogens adhere, invade, and evade the host's defenses.
  • Adhesins: Promote attachment to host cells.
  • Exoenzymes: Aid tissue penetration and cell damage.
  • Toxins: Harm host cells and interfere with functions.

Virulence Factors: Exoenzymes

• Hyaluronidase: Breaks down hyaluronic acid, allowing tissue penetration.
• Nucleases: Break down DNA, aiding spread.
• Phospholipases: Break down phospholipids and cell membranes.
• Proteases: Breakdown proteins, potentially inactivating antibodies.
• Collagenase: Breaks down collagen, aiding spread.

Virulence Factors: Toxins

• Endotoxins: Released on pathogen death, causing inflammation or organ failure.
• Exotoxins: Protein toxins, often highly potent and deadly.
  • A-B Toxins: Composed of an active (A) and binding (B) component.
  • Membrane-disrupting toxins: Create pores.
  • Superantigens: Trigger massive immune responses (cytokine storms).

Virulence Factors: Evasion of Phagocytosis

• Capsules: Prevent immune cells (phagocytes) from engulfing pathogens.
• Proteases: Break down antibodies.
• Fimbriae: Can block complement proteins.
• Antigenic Variation: Changes in surface proteins to evade recognition (e.g., Borrelia burgdorferi, influenza).

Explore the critical stages of pathogenesis, from initial exposure to systemic infection. This quiz delves into how pathogens invade and colonize host tissues, detailing local, focal, and systemic infections. Understand the role of opportunistic pathogens and their impact on health.