Flashcards in Micro-organisms in disease: infection Deck (23):
What are the requirements for pathogenicity?
Establisment in or on a host
What is the chain of infection?
Reservoir -> Exit -> Transmission -> Entry -> Susceptible host -> Pathogenic organism
What is virulence and how does it differ from pathogenicity?
May be used interchangeably. Sometimes defined as the degree to which a organism is able to cause to disease ie relative description.
What are Koch's postulates?
- Organism should be present in disease but not in health
- Organism should be isolated from the diseased animal and grown in pure culture
- Organism should cause the same disease in newly inoculated animal
- Organism should be re-isolated from the experimentally infected animal
What are the possible routes of transmission?
Direct contact - hand to hand, mucous membranes
What is infectivity?
The ability of a micro-organism to become established on/in a host. (microbial ligand/host cell surface repair)
Describe some common ligand-receptor interactions that occur between micro-organisms and host.
- E. coli P fimbriae binds to glycolipids on human uroepithelial cells - express specific adhesins
- S. pyogenes protein F binds to fibronectin - large multifunctional protein found in connective tissue on cells surfaces and in various body fluids
- Influenza haemagglutinin - resp. epithelial sialic acid receptors
What are virulence factors?
Components of micro-organisms that result in harmful effects.
What are potential virulence mechanisms?
Facilitation of adhesion
Interference with host defence mechanisms
Facilitation of invasion
Modulation of the host cytokine response
Sometimes referred to as adhesins, aggressins,
interferins, modulins etc..
What is an endotoxin?
Component of the Gram neg bacterial cell wall. E. coli, N, meningitidis etc. Released from damaged/dead cells. Active component is LPS.
What are the effects of LPS on the body?
- uncontrolled T-lymph response (cytokine release, ie TNF, IFN, IL-1)
- cardiac/renal failure
- uncontrolled activation of clotting cascade
- depletion of clotting factors
- uncontrolled activation of complement
Why does limb loss occur in meningoccocal septicaemia?
Endotoxin-mediated increase in vascular permeability causes loss of protein, fluid and plasma into the tissues with pathological compensatory vasoconstriction.
What are exotoxins?
Proteins produced by living bacteria. Usually have quite specific effects on health.
What is the mode of action of botulinum toxin?
Cleaves SNARE proteins of secretory vesicles at NMJ - flaccid paralysis.
What is the mode of action of tetanus toxins?
Cleaves SNARE proteins of GABA secretory vesicles within inhibitory neurones - tetany.
What are the symptoms of botulism?
Diplopia, dysphagia, dysarthria, dry mouth, death from respiratory failure
What are the symptoms of tetanus?
Tetanospasm - produced on germination of spores
Opisthotonos - arched back
Give examples of other exotoxin-mediated infections.
Corynebacterium diptheriae - phage infected
C. diff - diarrhoea/colitis
E. coli O157 hemorrhagic colitis
Staph scolded skin syndrome - epidermolysin
Scarlet fever (Strep. pyogenes)
What is the key to treating a bacterial toxin-induced disease?
Given Abx to kill organism and anti-toxin.
What are the various S. pyogenes syndromes?
scarlet fever (erythrogenic toxin - phage encoded).
Give examples of S.pyogenes virulence factors.
Hyaluronidase and streptokinase - break down connective tissue components, facilitate tissue invasion
C5a peptidase - inactivates complement
Streptolysins O and H - lyse red, white blood cells and platelets
Erytrogenic toxin (phage encoded) - scarlet fever
How might bacteria inhibit phocytosis?
S.pyogenes - M-protein binds fibrinogen and masks bacterial surface - blocks complement and opsonisation
S.pneumoniae - polysaccaride capsule inhibits opsonisation