Lecture 5: Role of bacterial virulence factors

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  • Created on: 03-01-19 13:39
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  • Bacterial Virulence Factors
    • Definitions
      • Pathogencity = ability of an OG to cause disease. Virulence = degree of pathogencity.
      • Virulence factor = enhance adhesion, invasion and colonisation of host, enhance virulence by breaking down host tissues, provide protection to pathogen. Any bacterially derived enzyme which enables pathogen to do 1) Invade 2) Adhere 3) Colonise
    • 1. Invasion of the host
      • Naturally occurred points of entry - nose, mouth, eyes, anus. Skin = wounds however not in arthropod hosts, fleas, louse, tick (blood)
        • Skin = impermeable dry outer layer, degree of insulation, protects body and maintains sensory communica-tion.
        • Adhesins =  determinants of pathogen location and effectors of infection. Receptors - confer specificty to binding - comprised of oligo of TM glycoproteins/ECM proteins
        • Respiratory tracts: Mucociliary blanket (ciliated cells with goblet cells and mucus secreting glands), foreign particles are trapped in mucus and borne to lungs by cilia. Alveoli = no cilia/mucus
        • GI tract = faster the rate of flow of intestinal contents, the less opportunity for growth. Reduced flow rate = increased growth.
        • Spread of microbes: via lymphatics. Proteins >capillaries >lymph node > vessels become dilated and leucocytes are extravasated so nodes become swollen and tender.
    • 2. Adherence to host
      • Allows them to stick to surface. Small intestine has lots of flow through by peristalsis, no adherence they would be washed away (motility) - niche
      • Adhere to mucous membranes - stick to adhesins - often bind to comp. receptor sites on host cell surfaces
      • Adherence methods: Lectins, Ligands, Capsule, Slime, Fimbriae
    • 3. Colonise the host
      • Colonisation = active replication and persistence of a bacterial strain at given site. Location = skin (boils/abscesses), mucous membranes, lymph nodes, dissemination - collagenase, haemolysins, elastase
      • If a bacterial site is repeatedly isolated from faecal samples over 3 weeks, must have replicated within intestinal tract = colonising strain
      • Once bacteria adhered to host = infection may become localised at point of adherence - bacteria may disseminate
    • Toxin production
      • Exotoxin = extracellular proteins - travel through host and cause damage. Endotoxin = LPS component of Gram NEG - released in large amounts when bacterial cells are lysed - cause fever - stimulate HC to make pyrogens
      • EPEC: severity of disease ranges from diarrhoea to hem. colitis. Causes HUS = lysis of erthrocytes and acute renal failure.
      • Hallmark of EPEC = ability to create an A/E lesion - bacteria make intimate contact, distort apical membrane of enterocytes = destruction of intestinal border. Attachment by BFP bundle forming pili -mediate EPEC-EPEC host attachment
    • Type III secretion system
      • Injectisome (hypodermic needle), injects protein, encoded on PAI (called LEE), syringe composed of: EspA, EspB, EspD. Tir receptor injected into host, penetrates CM and binds to intimin.
      • Forms a pedestal - then bacteria replicate and new cells adhere and colonise further, more toxin production = fluid loss


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