Microbial Mechanisms of Pathogenicity

Microbial Mechanisms of Pathogenicity

• Pathogen: A microorganism that can cause disease.
• Pathogenicity: The ability of a pathogen to cause disease by overcoming the host's defenses.
• Virulence: The degree of pathogenicity, a measure of a pathogen's ability to cause disease.

Stages of Microbial Pathogenicity

• Portals of Entry: Microbes enter the body through various portals: skin, mucous membranes (respiratory, gastrointestinal or genitourinary tract or the conjunctiva), and the parenteral route.
• Adherence: Microbes attach to host cells by binding their ligands/adhesins to host cell receptors via complementary chemical interactions.
• Penetration or Evasion of Host Defenses: Microbes evade host defenses, such as phagocytosis, by using capsules, cell wall components, enzymes, antigenic variation, or invading host cells.
• Damage to Host Cells: Microbes damage host cells by using host nutrients (siderophores), direct damage through their metabolism, or by releasing toxins.
• Portals of Exit: Microbes generally use the same portals of entry for exit but can also use arthropods or syringes.

Numbers of Invading Microbes

• ID50 (Infectious Dose): The number of microbes required to infect 50% of inoculated animals.
• LD50 (Lethal Dose): The number of microbes required to kill 50% of inoculated animals.

Adherence

• Colonization: The establishment of a pathogen at the appropriate portal of entry.
• Adherence: Microorganisms attach to cells using receptors and ligands.
• Bacterial Adhesins: Can be found in capsules, cell walls, glycocalyx, pili or fimbriae.
• Viral Adhesins: Found in viral capsids or envelope components.
• Host Receptors: Often glycoproteins located on the cell membrane or tissue surface.
• Specificity: The interaction between ligand and receptor can determine the specific host cells the microbe can infect.
• Avirulence: Inability to produce attachment proteins or adhesins can render the microorganisms avirulent.

Biofilms

• Biofilms: Masses of microbes and their extracellular products that facilitate the attachment of free-floating microorganisms to a surface using cell adhesion structures.
• Quorum Sensing: Bacteria in biofilms communicate with each other to coordinate activities.
• Antibiotic Resistance: Biofilms are often associated with antibiotic resistance.

How Bacterial Pathogens Penetrate Host Defenses

• Capsules: Prevent engulfment by phagocytes (e.g., Streptococcus pneumoniae, Haemophilus influenzae, Bacillus anthracis).
• Cell Wall Components: Proteins in the cell wall can facilitate adherence or prevent phagocytosis.
  • M protein: Resist phagocytosis in Streptococcus pyogenes.
  • Opa protein: Inhibits T helper cells in Neisseria gonorrhoeae.
  • Mycolic acid: (waxy lipid) resists digestion in Mycobacterium tuberculosis.

How Bacterial Pathogens Damage Host Cells

• Using the Hosts's Nutrients: Siderophores are specialized molecules that bind iron, an essential nutrient for many bacteria.
• Direct Damage: Pathogens metabolize and multiply inside host cells, damaging host cells without toxins.
• Toxins: Most bacterial damage is caused by toxins.

Toxin Production

• Toxins: Poisonous substances produced by microorganisms.
• Toxigenicity: The ability to produce toxins.
• Toxemia: The presence of toxins in the blood.
• Exotoxins: Proteins produced by bacteria and released into the surrounding medium.
• Endotoxins: Components of the outer portion of the cell wall (lipid A) of gram-negative bacteria.

Exotoxins

• Cytotoxins: Kill or damage host cells.
  • Membrane-disrupting toxins: Create pores in cell membranes or disrupt phospholipid bilayers.
• Neurotoxins: Interfere with nerve impulses.
• Enterotoxins: Affect the lining of the gastrointestinal tract.
• Antitoxins: Provide immunity to toxins.
• Superantigens: Overstimulate the body's immune response, leading to cytokine release and symptoms like fever, nausea, vomiting, diarrhea, shock, and death.
• Toxoids: Altered toxins used as vaccines (e.g., diphtheria and tetanus).

Endotoxins

• Lipid A: The lipid portion of lipopolysaccharides (LPS) found in the outer membrane of gram-negative bacteria.
• Release: Endotoxins are released when bacterial cells die due to autolysis, external lysis, phagocytosis, or antibiotics.
• Effects: Fever, shock, blood clotting, tissue death, and death.
• Blood-Brain Barrier: Endotoxins can weaken the blood-brain barrier, allowing bacteria to cross it.

Exotoxin vs. Endotoxin

Plasmids, Lysogeny, and Pathogenicity

• Plasmids: Can carry genes for antibiotic resistance, toxin production, capsule formation, and fimbriae.
• Lysogenic Conversion: Bacteriophages can integrate their DNA into bacterial chromosomes, altering the bacteria's properties.
• Toxins and Capsules: Lysogeny can lead to the production of toxins and capsules by bacteria.

Pathogenic Properties of Viruses

• Attachment: Viruses gain access to cells by binding to receptors on the host cell surface.
• Immune Evasion: Viruses hide within host cells to avoid the immune system.
• Cytopathic Effects: Visible effects of viral infections.
  • Cytocidal effects: Cell death.
  • Noncytocidal effects: Damage but not death.
• Cytopathic Effects: Include:
  • Inhibition of mitosis
  • Lysis (release of lysosomal enzymes)
  • Transformation (abnormal cell growth)
  • Inclusion bodies (viral components accumulating within cells)
  • Cell fusion
  • Antigenic changes
  • Chromosomal changes

Pathogenic Properties of Fungi, Protozoa, and Algae

• Fungi: Secrete enzymes, produce toxins, and cause allergic responses.
• Protozoa: Damage host tissue, release metabolic waste products, and can change surface antigens to avoid the immune system.
• Algae: Some algae produce neurotoxins.

Portals of Exit

• Exit Portals: Microbes leave the body through the respiratory tract (coughing, sneezing), gastrointestinal tract (saliva, feces), genitourinary tract (vaginal or penile secretions), or through arthropods or syringes (in blood).

Explore the complex world of microbial pathogenicity in this quiz. Understand key concepts such as pathogen mechanisms, portals of entry, and how microbes evade host defenses. Dive deep into the stages that contribute to disease and enhance your knowledge of microbiology.