Microbiology for Veterinary

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  1. Which two molecules make up peptidoglycan?
    NAG (N-Acytlglucosamine) and NAM (N-Acytlmurmic acdi)
  2. What bonds are formed in peptidoglycan to make it such a ridged structure?
    Short peptide bonds between the NAM molecules
  3. When Gram stained what colour do Gram positive bacteria go?
  4. When Gram stained what colour do Gram negative bacteria go?
    What ever colour the final stain (the counter stain) is, which is typically red
  5. What are the two main differences between Gram negative and Gram positive bacteria?
    Gram positive bacteria have a thicker cell wall and Gram negative bacteria have an outer membrane
  6. Is E coli a Gram negative or Gram positive bacteria?
    Gram negative
  7. Is bacterium Clostridium tetani (the bacteria which causes tetanus) Gram positive or Gram negative?
    Gram positive
  8. What are the three main componants to a lipopolysaccharide?
    Lipid A, core carbohydrates and an O side chain
  9. What is another name for lipid A within a lipopoly saccharide?
  10. name two bacteria which don't stain gram positive or gram negative
    Mycobacteria (due to a waxy coat) and enzoonotic pnemonia (which has no cell wall)
  11. Why do capsules prevent phagocytosis?
    The are charged so repel the phagosome
  12. what are the three strains of fungi?
    Mycelia, yeasts and bimorphic fungi
  13. What is the difference between a yeast and a mycelia fungi?
    Yeasts have single oval bodies while mycelia have hyphae
  14. When classing bacteria on their oxygen requirements what are the 4 classes?
    obligate anaerobes, obligate areobes, microaerobes and faculative anaerobes
  15. What are the most common strips used to identify bacteria?
    API strips
  16. What methods may change a bacterias genome?
    mutations, plasmids, transposons and bacteriophages
  17. what methods do bacteria transfer genes by?
    Transformations (although very uncommon), transduction and conjugation
  18. What are non-specific ways that the body defends itself?
    skin and innate imune system
  19. what are the specific ways that the body defends itself?
    the specific immunesystem aka the adaptive immunity
  20. whats the most comon phagocyte?
    macrophage (the one with the big nucleus)
  21. Name the differences between macrophages and nutrophils
    • nutrophils rapedly form pus (pyogenic), sit in inflamed tissues only, they're short lived, have just one mature form and die after phagocytosis.
    • Macrophages live in healthy tissues, have a variety of mature forms, granulomas form (although slowly with the help of T cells), they are long lasting and survive phagocytosis.
  22. What are the steps to phagocytosis?
    The bacterias O chains are oxidated, they are uptaken into a phagasome, the lysomes bond to the phagosome to form a phagolysome the pH is lowered and chemicals pumped in and activated.
  23. What can phagosomes do without oxygen intermediates?
    Damage bacterial membranes, damage peptidoglycan (i.e. lyzosomes), damage bacterial proteins (proteases) and deprive the bacteria of nutrients (i.e. lactoferrin)
  24. How do phagosomes phagocytose bacteria with capsules?
    The force them to undergo opsonisation
  25. Name some opsonins
    • Inate opsonins: Complement componants, C-reactive proteins, Mannose binding proteins and lipopolysaccharides binding proteins
    • Aquired opsisns: specific immunoglobulin and complement
  26. What are the three complement pathways?
    • Classical- antigen:antibody
    • aquaired- molecules are recognised on the bacteria surface
    • lectin- mannose binding protien
  27. What are the three outcomes to complement pathways?
    The pathogen is killed, opsonisation or inflamatory cells are recruted
  28. What are the main characteristics of bacteria that the immune responce are triggered by?
    Lipid A, peptidoglycan, bacteria lipoprotiens and bacteria DNA
  29. What is the inflamatory responce?
    Macropharges are activated and release TNF- (alpha) (Tumor necrosis factor), this causes increase release of plasma proteins into the tissue though bigger pores in the blood vessels and the lymph vessels become more active
  30. What do T cell 1 and T cell 2 do?
    • T helper cell 1 activates macrophages and attack them.
    • T helper cells 2 activates and secretes antibody and B cells
  31. What are the four main jobs of an antibody during an infection?
    Produce anti toxins, stop the bacteria getting nutrients, stoping adhesion and invasion as well as allowing for opsonisation
  32. What does IgA do?
    It nutralises anti toxin, causes agglutination and anti-adhesion
  33. How does T helper cell 4 activate macrophages?
    Interferon gamma and CD4 liganand attacth to the macrophage causesing the bacteria to be oxidised and the bacteria to be pagocytosed, as well as causing increased nitric oxide
  34. How do T helper 1 and T helper 2 cells inhibit each other?
    T helper 1 produces interferon gamma and T helper 2 cells produce IL-4
  35. What are the three main types of pathogen?
    • Oppertunistic pathogen- this is when the pathogen will only create an infection when the immune system has been compromised
    • secondary pathogens- these are ones which cause infection when room has been made for them i.e. infection to the rispiratory tract after a cold
    • Primary pathogen- this will cause disease even if the host is not compromised
  36. Define Pathogenesis
    The mechanism of disease development
  37. Define Virulence
    The measure of the virus to damage or kill the host
  38. Define virulnce factor
    Componant of bacteria which is involved in pathogenesis, infectivity or virulence
  39. Define infectivity
    The ability of the bacteria to enter, colonise and survive within a host
  40. what is the general life cycle of a bacteria?
    It is taken up by a host, it attaches to a specific cell with its fimbrae, it multiplies (for this to happen it requires nutrients and to fight off the hosts defences) and then needs to be redistrabuted
  41. Describe the 4 steps to Kochs postules
    • 1- The organism should be found in each diseased individual
    • 2- The organism should be isolated and cultured outside of the organism (this can be a downfall)
    • 3- The pure cultured organisms should be innoculated into an individual
    • 4- The organism should be re isolated and cultured
  42. What three ways ar used to detect virulence factors?
    • Molecular- by putting the virulence gene into an a virulent organism
    • Epidemiology- corrolation between the suspected virulence factor and disease
    • Biomolecular- analysis of the virulence factor (i.e. toxin) both invitro and invivo
  43. What is K88 another name for
    The gene which is a common virulance factor as it coads for fimbrae which adhear to cells
  44. What are the two most commonly used methods to detect a virulence factor?
    • Random mutanogenesis- this is where UV is fired at the organisms to create a mutant (worry about healthy genes also being affected
    • Site directed mutanogenesis means that the virulence gene is removed and placed in an a virulent bacteria. they are then compared invitro and invivo.
  45. What are bacterias adheasion techniques?
    • commersial bacteria adhear to mucous
    • some bacteria bind to carbohdrates for example those with K88
    • binding to surface proteins ie invasin proteins
    • binding to matrix proteins i.e. gram positive bacteria
  46. whats the difference between extracellular and intracellular pathogens?
    • extracellular pathogens resist complement and phagocytes (i.e. clostridia or staphloccos aureus)
    • intracellular pathogens resist intracellular destruction (i.e. salmonella or brucella)
  47. How do bacteria survive when extracellular?
    They repel complement by haveing capsules containg salicic acid, the capsule also repelse phagocytes by being charged they also try to be none immunogenic by resembling the host.
  48. how do bacteria gain iron?
    sidephore which collect iron, or transferrin/lactoferrin binding protein
  49. What methods do intracellular pathogens use?
    escaping the phagosome, preventing acidification, preventing lysosome excretion and only coxielle burnetii
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Microbiology for Veterinary
Revision notes for a 3rd year vet student at Glasgow uni
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