The ability of an organism to cause disease by harming the host.
The degree of pathogenicity, indicating how severe the disease caused by a pathogen can be.
Molecules, structures, or systems that enable microorganisms to cause disease.
A type of virulence factor; these are substances produced by bacteria that are harmful to host cells.
Bacteria use motility mechanisms (e.g., flagella) to reach entry sites like wounds.
Facilitates invasion by weakening barriers or immune responses.
Accesses nutrients through lysed host cells.
Reduces competition by eliminating other microbes.
Aids dissemination via symptoms like diarrhoea or coughing.
Sometimes, damage is accidental.
Highly virulent pathogens: Consistently cause disease.
Less virulent pathogens: Cause disease in weakened hosts or when present in large numbers.
Break down connective tissues, aiding bacterial spread, increasing the severity of infections and allowing for greater invasion of host tissues.
Coagulase induces clot formation, shielding bacteria.
Kinase dissolves clots, allowing dissemination.
Found in Gram-negative bacteria; released upon bacterial death.
Composed of lipopolysaccharides (LPS).
Trigger strong immune responses, potentially leading to septic shock.
Secreted by both Gram-positive and Gram-negative bacteria.
Highly potent and specific; can act far from the infection site.
Examples include toxins causing diphtheria, botulism, and tetanus.
Target and destroy host cells.
Example: Staphylococcus aureus α-toxin forms pores in cell membranes, leading to cell lysis.
Bypass normal antigen presentation, activating a large proportion of T-cells.
Cause massive cytokine release, leading to toxic shock syndrome.
Consist of two parts: A (active) and B (binding).
The B subunit binds to host cells, allowing the A subunit to enter and disrupt cellular functions.
Often interfere with protein synthesis or signal transduction.
Produced by: Vibrio cholerae.
Mechanism:
Binds to GM1 ganglioside receptors on intestinal cells.
Activates adenylate cyclase, increasing cAMP levels.
Leads to chloride and water efflux, causing severe diarrhoea.
Produced by: Clostridium botulinum.
Mechanism:
Blocks acetylcholine release at neuromuscular junctions.
Results in flaccid paralysis.
Applications:
Used medically to treat muscle spasms and cosmetically to reduce wrinkles.
Produced by: Clostridium tetani.
Mechanism:
Inhibits release of inhibitory neurotransmitters (e.g., glycine).
Causes continuous muscle contraction (spastic paralysis).
Prevention:
Vaccination with tetanus toxoid.
Toxoids: Inactivated toxins that retain their antigenicity.
Usage:
Employed in vaccines (e.g., Diphtheria, Tetanus, Pertussis) to elicit immune responses without causing disease.