Mech of Bacterial Pathogenosis: Exotoxins Flashcards
Commensal organism
Lives in host
no harm/no gain
NORMAL FLORA
Mutualism
Lives in host - BOTH BENEFIT- no harm
Parasitism
lives in host and CAUSES HARM
opportunistic pathogen
When host immune defence is LOW - may cause infection/asymptomatic carriage
PATHOGENIC MECHANISMS OF MICROBES
adhesins : promote colonisation
toxins: endo and exotoxins
capsules : avoid immune detection
enzymes : proteases
PROPERTIES OF THE HOST: DEFENCE MECHANISMS
natural barriers: skin, chemical
defensive cells : immune cells (phagocytes)
complement activation
immune response: innate and adaptive
What are kochs postulates?
Exceptions?
For an organism of be a PATHOGEN causing disease:
- must be ISOLATED
- must be CULTURED
- must REPRODUCE DISEASE in animal
- must be ISOLATED from the NEW infected organism and shown to be the same
Cannot be proven for non-culturable organisms
Cannot be proven for organisms that cause disease via toxin release (food poisoning)
Types of infection that you may have:
Examples of:
Local?
Invasive?
Systematic?
Immunopathology?
Local: surface/epithelial infection - V. cholera/gonorrhoea
Invasive: penetrate the barriers and spread - shigella, staph aureus
Systemic: via the BLOOD - meningitis, S, typhi ]
Immunopathology: inflammation, cross reactive antigens, granuloma e.g. TB
Examples of Adhesins?
Strep pyogenes?
Gonorrhea?
Strep pyogenes: M protein
Gonorrhea: Fimbriae
What are the stages of infection?
Adhesion
Colonisation
Penetration
Multiplication
Immune evasion
Damage
Transmission
Resolution
Examples of virulence factors?
Adhesins - M protein, Fibriae (pili)
Capsule - avoid immune system
Endo/Exotoxin release
Invasion Factors: Surface components and secreted effector proteins
Siderophores : iron binding factors to compete with the host for iron, hemoglobin, transferrin, lactoferrin
Type 1 Exotoxin
Mechanism:
Examples
Acts at the cell surface
Causes intracellular signalling - increase in cGMP
Examples:
E Coli - enterotoxin - travellers diarrohoea
SUPERANTIGEN
- Staph Aureus : TSST
- Strep pyogenes : toxin locates to skin, erythematous rash, strawberry tongue, desquamation, complications: cellulitis and septicemia
Type 2 Exotoxin
Examples: x 3
Forms a pore and goes into the cell membrane - disruption of enzymes OR neurotoxin
Examples:
Staph A :
heptamer - damages cell membranes/matrices
Disrupts ion transport and leads to cell lysis
Clostridium perfringens :
virulence factors: a lecithinases, phospholipase C (lipid membrane damage), kills WBC and RBC - severe hemolysis and death
Necrotising fasciitis : Strep pyogenes
M proteins and lipoteichoic acid
Streptococcal pyogenic exotoxins
Capule (hylarunoic acid) blocks opsonisation
streptolysin - pore and kills cells
2 examples of neurotoxin
mechanisms
Botulinum toxin: causes - BLOCK of Ach at synapses - no muscle contraction = floppy baby
ingestion of spores
Tetanus: causes block of GABAergic inhibition of muscle contraction - leads to CONSTANT EXCITATION - paralysis
Type 3 exotoxin
Mechanism
Examples x 4
Mechanism - translocation of active unit into cell which results in intracellular signalling
Example:
E.Coli - AB5
A = ACTIVE
5 = 5 binding domains
Shigella - AB5
cleaves adenosine from 28S RNA
Diphtheria: AB type
Toxin Receptor - goes into CELL - cleavage releases A subunit
Pertussis: AB type
invasive toxin - superantigen - tracheal cytotoxin
overcomes host defences and damages muco-ciliary clearance mechanism
Pathology of diptheria
Non-invasive multiplication
Toxin is PRODUCED locally but acts at distance with systemic effects due to absorption via lymphatics - damages the heart kidneys nerves and adrenals
Leads to exudate
Respiratory obstruction
Bull neck
