Chapter 15: Microbial Mechanisms of Pathogenicity

Key Concepts

• Microbes have specific properties that contribute to their ability to cause disease.
• Microbes are not intentionally harmful; they are simply living and reproducing.
• Presence of microbes can induce symptoms in the host.
• Pathogenicity: Ability of a microorganism to cause disease (pathogenic vs. non-pathogenic).
• Virulence: Degree of pathogenicity; some microbes are more virulent than others.

Portals of Entry

• Most microbes have a preferred portal of entry:
  • Mucous Membranes: Common entry points, e.g., respiratory tract (easy via inhalation), digestive system (often neutralized by stomach acid), and genital-urinary tract.
  • Conjunctiva: The eye membrane connected to the respiratory system via tear ducts.
  • Skin: Effective barrier unless broken. Microbes can enter through hair follicles, sweat ducts, or open wounds.
  • Parenteral Route: Directly deposited into tissues through punctures, injections, bites, or cuts.

Factors Affecting Pathogenicity

• Pathogenicity depends on the portal of entry.
  • Example: Streptococci inhaled can cause pneumonia but not when swallowed (neutralized by stomach acid).
  • Some pathogens can cause disease through multiple entry points (e.g., anthrax).
• Infectious Dose (ID50): Number of microbes required to infect 50% of a population, varies by entry route.
• Lethal Dose (LD50): Toxicity measurement, different toxins have different potencies.

Adherence

• Pathogens need to adhere to host cells to cause infection:
  • Adhesins: Proteins on pathogens that bind to host cell receptors.
  • Biofilms: Communities of microbes that enhance adherence and resistance to phagocytosis.
  • Example: E. coli attaching to urinary tract cells via pili in UTIs.

Mechanisms of Evasion and Penetration

• Pathogens evade host defenses through various mechanisms:
  • Capsules: Thick glycocalyx layers that inhibit phagocytosis.
  • M Protein: Helps bacteria attach and resist phagocytosis.
  • Waxy Lipids (Mycolic Acid): Found in acid-fast bacteria, protecting against digestion.
  • Enzymes: Coagulases (form clots), kinases (break clots), hyaluronidase, collagenase (break down tissue).
  • Antigenic Variation: Pathogens change surface antigens to evade immune response.
  • Invasins: Produce ruffling in host cells to allow entry.
  • Survival inside Phagocytes: Alter pH or escape phagosome before fusion with lysosome.

Damage to Host Cells

• Pathogens can damage host cells by:
  • Using host nutrients (e.g., siderophores to capture iron).
  • Direct damage through waste products.
  • Toxins, which are critical in pathogenicity.

Types of Toxins

• Exotoxins: Secreted proteins from mainly gram-positive bacteria (e.g., botulinum toxin causing paralysis, tetanus toxin causing muscle contraction).
• Endotoxins: Part of the gram-negative bacteria cell wall (lipid A); released during cell lysis.
• Superantigens: Cause intense immune response leading to cytokine storms.
• Genotoxins: Cause DNA damage, leading to potential cancer.

Immune Response and Interferons

• Interferons are released by infected cells to protect neighboring cells and inhibit viral replication.

Other Pathogenic Organisms

• Fungi: Produce toxic metabolic products and can induce allergic reactions.
• Protozoa: Can cause disease through their presence and waste products (e.g., malaria).
• Helminths (Worms): Cause extensive cellular damage and block lymphatic circulation (e.g., elephantiasis).
• Algae: Produce toxins like saxitoxin during red tide, which can cause poisoning in humans.

Portals of Exit

• Infections typically exit via the same route they entered:
  • Respiratory (coughing/sneezing), gastrointestinal (feces/saliva), urinary (urine/secretions), skin (contact), and blood (insect bites or shared needles).

Summary

• Microbes must adhere to host tissues and evade defenses to cause disease.
• They typically exit the body through the same portal of entry.