BACTERIA 4

Cards (18)

  • Routes of entry
    Sites of vulnerability
    →Respiratory tract ( breathing in) 
    Intestinal tract ( eating food) 
    Urogenital tract ( UTI as STI ) 
    Conjunctiva ( eyes) 
  • Physical removal strategies- ways your body responds to invasion 
    Coughing and sneezing
    Vomiting and diarrhea
    Urination
    Tear production
  • Attributes involved in effective host colonisation
    →1.  Adhere to host cells and resist physical removal 
    → 2. Invade host cells.
    → 3. Compete for iron and other nutrients.
    → 4. Evade the immune system
  • Fimbriae and Pili promote attachment and resistance to physical removal 
    • Gram –ve pathogens NEGATIVE
    • Fillia fimbriae  made out of protein called PILIN
    • Bind to sugar receptors on HOST CELL
    • Can colonize gut and urinary tract – diarrhea and UTI
    • Adhere to host cells and resist physical removal
  • Fimbriae and Pili promote attachment and resistance to physical removal  EXAMPLE : E. COLI - fimbriae and pili HAS A LOT TO CAUSE DAMAGE AND RESISTANCE
  • Adhesins also enable attachment and resistance to physical removal for POSITIVE
    • Has Protein F factor  that binds to fibronectin on the host cell 
    • Lipoteichoic acid binds to fibronectin on epithelial cells.
    • M-protein also functions as an adhesin
    • Adhesins also enable attachment and resistance to physical removal for POSITIVE VERY CLOSE TO ATTACH AND
    • EXAMPLE = Streptococcus
  • Motility  helps to colonization at mucosal surfaces- bacteria that are motile
    • Gram –ve pathogen Negative 
    • Urease = produces ammonia from urea
    • Ammonia passes into periplasmic space – buffer against acidic pH of the gut 
    • Helicobacter pylori
  • Motility  helps to colonization at mucosal surfaces- bacteria that are motile 
    • Gram –ve pathogen Negative 
    Using  chemotaxis bacteria  able to swim to host cell with flagella 
    Flagella pushing down and adherence 
    • Flagella help move bacteria through the mucus attach to gut epithelial cell 
  • Virulence factors involved in these processes in both Gram –ve and Gram +ve bacteria include
    Pili
    Flagella
    Adhesins e.g. M protein
    Invasins
    Siderophores
    Altering the chemistry of the cell envelope
    → Secreted enzymes e.g. coagulase
    Surface proteins that interfere with antibody function
  • Invasins are molecules that activate the host cell's cytoskeleton and promote cell entry by phagocytosis
    • They promote entrance via phagocytosis
    • Facilitate the growth and spread of the pathogen/ spread within hosts 
  • bacterial secretion systems.
    • Gram-negative bacteria.
    • forms an injectosome that delivers effector molecules to host cells.
    • Effector molecules interfere with the host cell's cytoskeleton.
    • This interference encourages phagocytosis, allowing bacteria to enter host cells.
    • It can also lead to cell lysis, releasing food sources for bacteria.
  • Bacterial invasion of epithelial cells/ how do bacteria cause damage to host cell 
    • Bacterial secretion systems co-opt the functions of the host cell (Gram +ve and Gram –ve) = example = E.coli
  • Extra-cellular proteases also help with invasion of host tissue
    → enzyme that breaks protein 
    metalloprotease
    → punch holes in the cell 
    → gain access to host cell
    catalytic domain and binding
    • Bacteria compete with host cells for iron, an essential nutrient.
    • They produce siderophores, which strongly bind to iron.
    • Siderophores scavenge iron from host glycoproteins like Lactoferrin, Transferrin, and Hemoglobin.
    • This theft of iron allows bacteria to thrive, as iron must be bound for bacterial uptake.
  • Coagulase production also allows evasion of phagocytosis→ mechanism to stop phagocytosis
    • Coagulase → Causes fibrinogen to fibrin which causes clotting
    • Fibrin coats the surface of the bacteria which allows evasion of phagocytosis 
    • Gram-positive bacteria, with their thick peptidoglycan cell walls, are vulnerable to lysosomal action.
    • They employ N-deacetylation to protect against lysozymes, preventing breakdown by these enzymes.
    • Listeria bacteria use N-deacetylation to survive in the host after phagocytosis.
  • Certain bacteria can interfere with antibody function.
    some bacteria have the ability to change the epitome
    • Protein A can change how antibodies bind to the bacteria.
    • It effectively "swaps" antibodies around, causing them to bind in the wrong orientation.
    • This prevents recognition by immunological cells, allowing the bacteria to hide from the host's immune system and proliferate.