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MB3008 > Immunity to Bacteria > Flashcards

Immunity to Bacteria Flashcards

1
Q

What makes bacteria and fungi differ from viruses?

A
  • pathogenic bacteria and fungi are free living - don’t usually enter cells
  • reproduce on mucous surfaces
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2
Q

Examples of pathogenic bacteria

A
  • Mycobacterium tuberculosis - TB (infects macrophages in lung)
  • Mycobacterium leprae - Leprosy
  • Salmonella enterica - food poisoning
  • Listeria monocytogenes - food poisoning
  • Brucella abortus - triggers abortion in cows
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3
Q

TB

A
  • common in HIV patients whom are not on HAART anti-viral treatments
  • infects macrophages in lungs - hypersensitivity response forms nodules (tubercles) - chronic inflammation
  • treatment - antibiotic (months)
    • Isoniazid (rifampin + Pyrazinamide + Ethambutol)
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4
Q

Gram + Bacteria

A
  • streptococcus pneumonias (lungs)
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5
Q

Gram - bacteria

A
  • helicobacter pylori (gastric ulcers)
  • mycobacteria (TB)
  • spirochetes (treponema pallidum) - syphilis
  • susceptible to lysis by complement
  • peptidoglycan degradation by lysozyme
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6
Q

Adaptive immune responses to extracellular micro-organsims

A
  • neutralisation
  • opsonisation and fc-receptor mediated phagocytosis
  • inflammation
  • lysis of microbe
  • macrophage activation - phagocytosis
  • ab response

*don’t have to kill cell but rather the bacteria itself

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7
Q

Gram + cell wall

A
  • increased amount of peptidoglycan
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8
Q

Gram - wall

A
  • 2 membranes
    • inner cytoplasmic membrane
    • small peptoglycan layer in between
    • outer membrane
  • main component - LPS
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9
Q

Bacterial Cell Wall Differences

A
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10
Q

Role of Ab

A
  • neutralisation of toxins - e.g. Tetanus toxoid from clostridium tetani
  • secretory IgA (sIgA) - protection of mucosal surfaces
    • sIgA dimers secreted onto intestinal lumen surface by plasma cells
    • prevents new luminal invasion by same pathogen
  • binding of Fe by lactoferrin - required for bacterial growth
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11
Q

How do macrophages and DCs recognise bacteria?

A
  • PRRs
  • mannosyl-fucose receptors - bind sugars on surface of microbes
  • CD14r - remove microbes coated with LPS
  • Fcr - bind abs to pathogens - IgG, IgM, IgA
  • Complement receptor CR1/CD35 - binds complement microbes
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12
Q

Abs that are capable of activating complement

A
  • IgM
  • IgG1
  • IgG3
  • promotes complement mediated lysis of bacteria
  • promotes opsonisation of bacteria and fungi - phagocytosis
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13
Q

Main mechanisms for removing bacteria

A
  • abs
  • phagocytosis
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14
Q

Cationic proteins & Lysosomal enzymes

A
  • Defensins, Cathepsin G, Lysosome, Lactoferrin
  • O2-dependant killing

Mechanism:

  • alkaline environment required for cationic proteins in phagosome
  • when phagosome fuses with lysosome - acidification - acidic environment required for lysosomal enzymes
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15
Q

Describe killing of pathogens by phagocytosis

A
  • production of RO intermediates (ROI)
    • hydroxyl radical
    • H202
    • hypochlorous acid
    • NO
    • Superoxide anion
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16
Q

Evasion mechanism of bacteria

A
  • secretion of anti-chemotaxis signals
  • capsule that inhibits phagocytosis - strep pneumoniae
  • inhibition of phagosome/lysosome fusion and acidification - m.tuberculosis
  • production of catalase - breakdown H202
  • blocks IFNy effects - mycobacterium
  • Impaired MHC - salmonella
  • tough outer coat scavenges free radicals - mycobacterium

*only way to kill this type of bacteria is by antibiotics

17
Q

Sepsis

A
  • body’s response to infection damages its own tissues
  • predisposition to infection - young to old age, immunosuppressive diseases, cancer, immunosuppressive medications, diabetes
  • Treatment : timely initiation of appropriate antibiotic therapy
    • not treated in time - increased LPS, inflamm response (cytokine storm) - irreversible
  • circulatory collapse and disseminated intravascular coagulation
    • NF-endothelial cell adhesion
    • activation of clotting and complement cascades - microthrombi formation
  • massive vasodilation - loss of plasma volume
  • shock from dramatic drop in bp - organ failure
  • important trigger
    • LPS on gram - bacteria (TLR4 binds to LPS)
    • monocytes respond by cytokine storm - TNFa, IL-1, IL-6
18
Q

Drug used to counteract vasodilation in sepsis

A
  • noradrenaline - vasopressor
    • contacts blood vessels and raises bp
19
Q

Therapies under investigation for sepsis

A
  • LPS removal via polymyxin B haemo-perfusion
  • anti-TNF-a mabs

*anti-sepsis medication is time critical

20
Q

Immunity to Fungi

A
  • mainly NFs, macrophages and DCs
  • through TLRs and Dectin-1
    • Dectine-1 binds to β-glucan on surface of Candida albicans
    • TH17 response

Superficial mycosis

MB3008 (9 decks)

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