Bacterial Pathogenesis Flashcards
How does virulence differ from pathogenicity?
Virulence is measurable
Define virulence.
The relative capacity for a microbe to cause damage to the host.
Name the 3 overarching bacterial virulence factors
Structural components (e.g. adherence factors; motility) Ability of evade host defences (e.g. Antiphagocytic/-complement strategies) Gene expression (e.g. Invasion factors; exotoxins/enzyme production)
How does Streptococcus pneumoniae evade host defences?
The bacteria encapsulates itself preventing macrophages from accessing its receptors and thus avoids phagocytosis
List 4 possible host immunity evasion mechanisms used by bacteria
Capsules
Detection avoidance
Damage to immune cells
Resistance to killing immune cells (avoiding action of lysing enzymes)
By what mechanism do Pneumococcus, Meningococcus and Haemophilus evade the immune system?
Resistance to phagocytosis
By what mechanism do Legionella, Mycobacterium and Taxoplasma evade the immune system?
Resistance to macrophage killing
By what mechanism does Pseudomonas evade the immune system?
Secretes a leukotoxin to kill neutrophils
By what mechanism does Clostridium difficile evade the immune system?
Makes itself inaccessible to the immune system by proliferating in the gut lumen.
What type of bacterial toxin am I? I am: Actively produced Relatively unstable Highly toxic Synthesised by plasmids
I am an exotoxin!
Do exotoxins directly or indirectly harm host cells?
Directly
What type of toxin am I? I am: Released in bacterial death Weakly toxic Found in gram -ve cell walls A lipopolysaccharide complex
I am an endotoxin!
What 3 pathways can endotoxic activation take?
Activation of coagulation cascade
Release of prostaglandins and leukotrienes
Activation of the complement cascade
What will likely result from endotoxic activation of the coagulation cascade?
Acute respiratory distress syndrome
OR
Disseminated intravascular coagulation
What will likely result from endotoxic activation of prostaglandin and leukotriene release?
Endothelial damage and potential multi-organ failure
What will result from endotoxic activation of the complement cascade?
IL-1 release and fever (normal inflammatory response)
What does the tracheal cytotoxic Bordetella pertussis cause?
Whooping cough
List the 4 mechanisms of action by which exotoxins can cause cellular injury
Cell or tissue degrading enzymes
Alter cell signalling pathways
Act as neurotoxins
Act as Superantigens
What impact does a Superantigen have on the host?
It causes an excessive immune response activating a high number of T-cells, which activate large numbers of IFN-gamma, which activates macrophages, which over-produce pro-inflammatory cytokines IL1, IL-6 and TNF-alpha - can cause shock or multi-organ failure
By which mechanism of action do Type I exotoxins function?
Disrupt the cell homeostasis by interfering with the cell membrane causing loss of ions and water. They act on the membrane from OUTSIDE the cell.
By which mechanism of action do Type II exotoxins function?
One of two ways:
1) form pores in cell membrane, creating a channel and disrupting the membrane potential
2) destroy the integrity of membrane phospholipids by use of enzymes
By which mechanism of action do Type III exotoxins function?
Interfere with host cell from WITHIN via two possible means:
1) injecting secretions into host cells via ‘secretion apparatus’
2) receptor-mediated endocytosis i.e. A-B toxins
For A-B toxins which is the active component and which is the binding component?
A = Active B = Binding
Name 3 diseases caused by exotoxins from Gram -ve bacteria
Diarrhoea - E. coli (enterotoxin)
Cholera - Vibrio cholerae (enterotoxin)
Whooping cough - Bordetella pertussis (pertussis toxin)
Name 3 diseases caused by exotoxins from Gram +ve bacteria
Pharyngeal diphtheria - Corynebacterium diphtheiae
Toxic shock or Scaled-skin syndrome - Staph. aureaus
Diarrhoea - Clostridium difficile (Toxin A)
