Microbial Mechanisms of Pathogenicity
Objectives of Microbial Mechanisms of Pathogenicity:
Identify main portals of entry for pathogens
Describe adherence of microbes to host cells
Explain how pathogens evade host defenses and penetrate tissues
Discuss damage to host cells and types of toxins
Contrast exotoxins vs. endotoxins
Mechanisms of A-B toxins and membrane disrupting toxins
Use ID50 and LD50 for commenting on virulence
Virulence: Measure of a microbe's ability to cause disease
ID50: Infectious Dose 50 (number of microorganisms causing infection in 50% of a test population)
LD50: Lethal Dose 50 (number of microorganisms that kill 50% of the population)
Portals of Entry:
Main portals: mucous membranes, skin, parenteral routes
Specific pathogens have specific entry portals based on host receptors
Adherence:
Pathogens use adhesins (e.g., fimbriae, spike proteins) for binding to host tissues
Specificity to host tissue affects pathogenicity
Evasion of Host Defenses:
Mechanisms include:
Capsules: Prevent phagocytosis (e.g., Streptococcus pneumoniae)
M proteins: Aid in adherence and evade immune response (e.g., Staphylococcus aureus)
Enzymes: Break down host tissues (e.g., collagenase)
Antigenic variation: Changes in antigens to avoid immune detection
Types of Damage:
Exotoxins: Secreted proteins that damage host cells (A-B toxins) or disrupt membranes
Endotoxins: Components of Gram-negative bacteria's cell wall (e.g., Lipid A) released upon cell lysis
Toxin Mechanisms:
A-B Toxins: Binding (B) and active (A) components; A alters cell function (e.g., inhibiting protein synthesis)
Membrane-disrupting Toxins: Cause direct damage by lysing host cells
Competitiveness for Resources:
Pathogens may compete for iron in host tissues (via siderophores)
Portals of Exit:
Typically same as portals of entry (e.g., respiratory tract, skin)
Defense Against Toxins:
Antitoxins: Antibodies that neutralize toxins
Toxoids: Inactivated toxins used for vaccines
Identify main portals of entry for pathogens
Pathogens primarily enter through mucous membranes, skin, or parenteral routes. Each pathogen typically has specific entry points based on host receptors.
Describe adherence of microbes to host cells
Pathogens use structures called adhesins (like fimbriae and spike proteins) to bind to host tissues, which affects their pathogenicity based on the specificity for host tissue.
Explain how pathogens evade host defenses and penetrate tissues
Pathogens employ various mechanisms to avoid host defenses, such as:
Capsules that prevent phagocytosis (e.g., Streptococcus pneumoniae)
M proteins that facilitate adherence and evade immune responses (e.g., Staphylococcus aureus)
Enzymes like collagenase that degrade host tissues
Antigenic variation to alter antigens and avoid detection by the immune system.
Discuss damage to host cells and types of toxins
Damage is typically executed via toxins:
Exotoxins: Secreted proteins that can damage host cells (e.g., A-B toxins) or disrupt membranes.
Endotoxins: Components found in the cell wall of Gram-negative bacteria (e.g., Lipid A) released upon cell lysis, causing damage to the host upon immune activation.
Contrast exotoxins vs. endotoxins
Exotoxins are actively secreted proteins that damage host cells, whereas endotoxins are part of the bacterial cell wall and only induce damage when the bacteria die and release their components.
Mechanisms of A-B toxins and membrane disrupting toxins
A-B Toxins: Consist of two components: the binding (B) component which attaches to host cells and the active (A) component which alters cell function (e.g., inhibiting protein synthesis).
Membrane-Disrupting Toxins: Directly damage host cells by lysing them or disrupting cell membranes.
Use ID50 and LD50 for commenting on virulence
ID50 (Infectious Dose 50): Refers to the number of microorganisms required to cause an infection in 50% of a test population, measuring the potency of infection.
LD50 (Lethal Dose 50): Refers to the number of microorganisms needed to kill 50% of a population, indicating the lethality of the pathogen and thus its virulence.