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Microbiology > Bacterial pathogenesis > Flashcards

Bacterial pathogenesis Flashcards

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Biology 101 flashcards
1
Q

Where are our normal microbiota normally found and what are their functions? (4)

A
  • Restricted to our body surfaces (external facing surfaces and membranes)
  • Provide nutrient
  • Protective against infection from other microorganisms by competition
  • Acquired at birth
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2
Q

Difference between normal microbiota and pathogen? (2)

A
  • Pathogens express virulence factors, normal microbiota don’t.
  • Pathogens can mediate adhesion, anti-phagocytic, damage
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3
Q

When was helicobacter pylori discovered and what does it cause? (2)

A
  • First cultured in 1982 by Barry Marshall and Robin Warren

- Associated with gastritis and is leading factor in pathogenesis of peptic ulcers and gastric cancer.

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4
Q

What must pathogens do to cause disease? (5)

A
  • Enter the body
  • Colonise the host
  • Evade host defences
  • Multiply and disseminate
  • Cause damage to host
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5
Q

What are some physical barriers pathogens must overcome? (5)

A
  • High salt, fatty acids, dryness of skin
  • Acid in stomach
  • Mucous and cilia in lower respiratory tract
  • Peristalsis of GIT
  • Soluble mediators like lysozyme in tears
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6
Q

What are some barriers of the innate immune system pathogens must overcome? (3)

A
  • Complement system
  • Phagocytosis (neutrophils/macrophages)
  • Inflammation (triggered by TLC, cytokines via recognition of bacterial products)
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7
Q

What does colonisation of the host involve? (2)

A
  • Pathogens establish themselves within the host by overcoming physical barriers and innate immune response, outcompeting normal microbiota.
  • Normally requires adherence to mucosal surface (host specific and tissue specific).
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8
Q

What are the steps of bacterial adherence? (3)

A
  • Loose attachment to mucosal surface via pili or fimbrae
  • Close adhesion to epithelial cells via afimbrial adhesins
  • Invasion of epithelial cells
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9
Q

Describe the structure of pili/fimbriae and how it functions to adhere to host cell. (3)

A
  • Rod shaped, hollow cylinder, ordered helical array of protein subunits of pilin
  • The tip of the pilus (pilin or other protein) mediates adhesion
  • May be all over cell (peritrichous) or polar
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10
Q

What can pathogenic E.coli cause?

A
  • Normal microbiota of human digestive system that can cause digestive infections (diarrhoea), UTI, septicaemia or meningitis.
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11
Q

How does enterotoxigenic E.coli (ETEC) produce disease? (5)

A
  • Colonisation mediated by specific pili on ETEC called colonisation factor antigen (CFA).
  • It allows bacteria to attach to host cell but not invade epithelial cells.
  • ETEC then produces heat-liable toxins (LT) or heat-stable toxins (ST) or both types of enterotoxins which target epithelial cells of small intestine.
  • The toxins stimulate secretion of electrolytes into the lumen of the gut and H20 follows cuasing diarrhoea.
  • Toxins are plasmid encoded so can undergo horizontal gene transfer.
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12
Q

Describe an afimbrial adhesin. (3)

A
  • Establish close association with host cell
  • Usually membrane-embedded proteins (typically cell envelope component-gram positive or outer membrane proteins- gram negative or a capsule)
  • Can bind to protein or carbohydrate receptors on host cell
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13
Q

Describe a capsule and its function in adherence. (3)

A
  • Made of polysaccharide (or sometimes protein), well organised, difficult to wash off, occur in both types of bacteria.
  • Can help prevent desiccation and can help avoid phagocytosis.
  • It is sticky so aids in adherence
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14
Q

What is dental plaque and how does it form? (3)

A
  • Biofilm that develops on the surface of teeth.
  • Formation initiated by attachment of salivary proteins followed by attachment of bacteria.
  • Provide anaerobic environment for some bacteria to flourish.
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15
Q

Reasons to invade host cell? (4)

A
  • Obligate intracellular parasite
  • Hide from immune system
  • escape from normal microbiota
  • disseminate to deeper tissues
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16
Q

What are invasins and what is their function? (3)

A
  • single proteins or complexes of proteins
  • Binding to host cell receptor causes internalisation of the bacteria
  • Can be passive or active uptake
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17
Q

How does listeria monocytogenes cause disease? (2)

A
  • Through zipper mechanism, binding of internalin to host cell receptor (cadherin) causes clustering of host receptor and formation of phagocytic cup.
  • This bacterium invades the intestinal epithelial cells
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18
Q

How does salmonella typhimurium cause disease? (2)

A
  • Through trigger mechanism where it directly injects invasins into the host cell to activate membrane ruffling (SipA and SipC) and then uptake of bacteria by macropinocytosis and endomal trafficking occurs.
  • It invades intestinal epithelial cells and intestinal macrophages.
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19
Q

How is the membrane attack complex formed and what does it do? (2)

A
  • End result of complement activation/fixation.

- Kills bacteria by puncturing the cell membrane.

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20
Q

What are some ways bacteria avoid complement fixation? (2)

A
  • Use of capsule prevents binding of complement proteins.

- Bind antibody by Fc end of antibody so complement can’t bind to it.

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21
Q

What is host mimicry and provide an example of a bacterium that uses it. (3)

A
  • Displaying of similar surface sugars.
  • N-meningitidis type B has a capsule made up of sialic acid which is a common component of our cell surface sugars.
  • The bacteria flourishes and releases huge amounts of LPS causing septic shock
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22
Q

What is a privileged site and what happens when it is colonised? (2)

A
  • A sterile site that has poor access to immune system.

- Colonisation here can form granuloma (M.tuberculosis) or a biofilm (Salmonella Typhi)

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23
Q

What does oxygen dependent killing involve? (2)

A
  • Killing bacterium using reactive oxygen species generated by NADPH oxidase
  • Occurs on the membrane of vacuole
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24
Q

What does oxygen independent killing involve? (5)

A
  • Low pH (lysosome)
  • Proteolytic enzyme
  • Lysozyme
  • Lactoferrin
  • Membrane damaging proteins
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25
Q

What is major impediment of pathogen? (2)

A
  • The normal microbiota poses as competition for space and nutrients.
  • Since pathogenic bacteria are chemoheterotrophs, they require iron to survive
26
Q

What does dissemination of pathogen mean?

A
  • Escape from normal microbiota/immune system and travel to immune privileged or other body sites to open up new sources of nutrients
27
Q

What aids in dissemination pathogen? (2)

A
  • Virulence factors such as collagenase and hyaluronidase, elastase, protease, phospholipase
  • Travelling in bloodstream inside phagocytes or just by itself (serum resistance bacteria)
28
Q

What are some mechanisms of iron uptake? (4)

A
  • Siderophores are high affinity iron chelators (hydroxamate or catecholates)
  • Iron binding proteins (high molecular weight membrane proteins)
  • Receptors for iron binding proteins of the host (transferrin and lactoferrin receptors)
  • toxins ( haemolysins that release iron from intracellular stores).
29
Q

What is an exotoxin and list a few examples. (2)

A
  • A secreted toxin, usually protein (often in vaccines)

- A-B toxins (simple VS compound), membrane disrupting toxins (pore forming, enzymatic), superantigens (immunopathology)

30
Q

What is A-B toxin? (3)

A
  • A= catalytic active subunit
  • B= binding subunit
  • Linked by disulphide bond
31
Q

What is an example of a simple AB toxin and how does it work? (2)

A
  • Diphtheria toxin secreted by corynebacterium diphtheriae which colonise our upper respiratory tract and back of our throats.
  • It has an ADP-ribosyltransferase as its catalytic subunit which transfers ADP-ribose groups onto target protein (EF2) and halts protein synthesis thereby killing the cell.
32
Q

What is an example of a compound AB toxin and how does it work? (5)

A
  • Cholera toxin secreted by vibrio cholerae which ultimately results in fluid lost causing diarrhoea.
  • It binds to GM1 ganglio site receptors on surface of host cell membrane.
  • Once in vacuole, low pH causes cleavage of A subunit into A1 and A2.
  • A1 subunit (an ADP-ribosyltransferase) causes ADP-ribosylation of GTPase resulting in GTPase being locked into the “on” form.
  • This causes increased levels of adenylate cyclase activity and increased levels of cAMP in cell leading to secretion of ions into lumen.
33
Q

How does the simple neurotoxin botulinum toxin work? (3)

A
  • Botulinum toxin secreted by clostridium botulinum binds to synaptotagamin 2 receptor on neuronal cells resulting in flaccid (no muscle tension) paralysis.
  • The bacteria colonises anaerobic environment (eg. tinned food) and ingestion of active toxin causes disease.
  • Causes cleavage of SNARE proteins so acetylcholine can no longer bind.
34
Q

How does the neurotoxin tetanus toxin work? (2)

A
  • Tetanus toxin secreted by clostridium tetani causes spastic (rigid/unable to release muscle contraction) paralysis.
  • It binds to inhibitory interneurons preventing the release of glycine and relaxation of muscle which causes diregulation in the release of acetylcholine into the synaptic junction.
35
Q

How does an enzymatic lysis work? (2)

A
  • Membrane disrupting toxin
  • Anaerobic bacteria, clostrisium perfringens release alpha toxin (phospholipase C) to hydrolyse phosphatidylcholine in target host membrane.
  • This leads to tissue necrosis and production of gas and swelling in tissues as well.
36
Q

How does cholesterol-dependent cytolysins work? (2)

A
  • Membrane disrupting toxin of gram positive pathogens.

- Inserts beta barrel pore into host cell membrane and functions similarly to membrane attack complex.

37
Q

What is an example of small-pore forming toxin and how does it work?

A
  • alpha haemolysins from staphylococcus aureus inserts into host cell membrane resulting in tissue necrosis and pus.
38
Q

What pathogen produces superantigens and how do they work? (3)

A
  • S.aureus and S-pyogenes
  • It links MHC 2 and TCR non-specifically (no antigen or presentation where there normally should be) causing massive overactivation of the immune system. eg. release of cytokines increases
  • Results in organ failure and shock
39
Q

What is an endotoxin? (2)

A
  • Structural component of pathogen that is embedded in outermembrane (not free floating)
  • In gram negative cell envelope (LPS)
40
Q

What does LPS cause?

A
  • Fever, massive inflammatory response, release of IL-1 and TNF.
41
Q

What results from severe infection? (2)

A
  • endotoxic (septic) shock

- can result in vascular collapse and multiple organ failure

42
Q

What are some examples of indirect damage to host cells? (4)

A
  • Allergic reactions (mediated by IgE)
  • Formation of immune complexes
  • Autoimmunity (host cell mimicry)
  • Cell mediated damage (cell death, granulomas)
43
Q

What are some ways bacteria become pathogens? (4)

A
  • Plasmids
  • Bacteriophages
  • Transposons
  • Pathogenicity islands
44
Q

What does enterohemorrhagic E.coli (EHEC) cause and how does it cause disease? (2)

A
  • Cause food-borne diarrhoea, bloody diarrhoea and haemolytic uraemic syndrome (HUS)
  • Encodes virulence factors including Shiga toxin (Stx) which causes the bloody diarrhoea/HUS
45
Q

Difference between bacteriocidal vs bacteriostatic.

A
  • Kills bacteria

- Prevent bacterial growth

46
Q

What are properties of magic bullets?

A
  • Ideal properties of antimicrobials include: selectively toxic for microbes, broad spectrum of activity (target both gram +/-), kills the microbe, non-toxic to host, long half life, good tissue distribution/penetration, oral and parenteral forms, no interference with other drugs
47
Q

What are ways to test for minimum inhibitory concentration? (3)

A
  • disc diffusion
  • broth serial dilutions
  • e-tests
48
Q

What do antibiotics target? (4)

A
  • cell wall synthesis
  • protein synthesis
  • DNA synthesis
  • cell membrane function
49
Q

What microbe does penicillin come from and how does it work? (5)

A
  • Produced by penicillium chrysogenum
  • Inhibits peptidoglycan synthesis by binding to the penicillin binding proteins (good against gram + but less active against non-dividing cells)
  • Not active against bacteria without peptidoglycan (mycoplasma) or who have an impenetrable cell wall (mycobacteria)
  • Bactericidal
  • Toxicity through allergy
50
Q

What antibiotic inhibits cell wall synthesis? (2)

A
  • B-lactam antibiotics

- penicillins, cephalosporins, carbapenems

51
Q

What are ways which pathogens can resist B-lactam antibiotics? (3)

A
  • Alteration in target sites (PBPs)
  • Alteration in access to target site (porins)
  • Production of B-lactamases (but can be inhibited by clavulanic acid which prevent bacteria form destroying amoxycillin)
52
Q

Which microbe produces aminoglycosides and what does it do? (5)

A
  • Streptomyces spp a gram positive filamentous soil bacteria
  • They are amino acid/sugar complexes which inhibit protein synthesis. eg. streptomycin, kanamycin, neomycin
  • They interfere with fmet-tRNA binding to ribosome (30S subunit function)
  • Bactericidal
  • Not well absorbed in gut so uses IV
53
Q

What are ways which pathogens can resist aminoglycosides? (4)

A
  • efflux
  • Modified outer membrane leading to reduced entry
  • ribosomal mutation leading to reduced binding
  • enzymatic modification leading to reduced entry
54
Q

Which microbe produces chloramphenicol and how does it work? (5)

A
  • Produced by streptomyces spp
  • Targets translation by binding to 50S subunit and blocking action of peptidyl transferase, preventing peptide bond formation
  • Bacteriostatic
  • Has high affinity for bacterial peptidyl transferase (compared to the mammalian enzyme)
  • Can be used to treat Salmonella Typhi but could result in toxic affects on bone marrow which could lead to aplastic anaemia.
55
Q

What are ways which pathogens can resist chloramphenicol?

A
  • Acquisition of a resistance gene encoding inactivation mediated by chloramphenicol acetyl transferase which adds acetyl group to the drug rendering it unable to bind to target.
56
Q

What are 3 ways of inhibiting nucleic acid synthesis?

A
  • Inhibit synthesis of nucleotide precursor
  • Inhibit DNA replication
  • Inhibit RNA polymerase
57
Q

What substance can inhibit synthesis of nucleotide precursor and how does it do that? (3)

A
  • Sulfoamides a synthetic sulfa drug that is an analogue of PABA.
  • It competes for active site of dihydropteroate synthetase preventing PABA being converted into the next molecule in the pathway and so inhibits folic acid production.
  • bacteriostatic
58
Q

List the steps (4) in synthesis of nucleotide precursors.

A
  • PABA -> dihydrofolic acid -> folic acid -> purines and pyrimidines
59
Q

What substance can inhibit DNA replication and how does it do that? (4)

A
  • Quinolones is a synthetic substance which interacts with bacterial DNA gyrase blocking the DNA coling mechanism during replication.
  • Broad spectrum activity
  • Can be bacteriostatic (Nalidixic acid) or bactericidal (fluoroquinolones).
  • Possibly toxic affecting cartilage growth
60
Q

What substance inhibits cytoplasmic membrane function and how does it do that? (3)

A
  • Polymyxins produced by gram +, is a cyclic peptide that act as a cationic detergent disrupting the PM.
  • Active against gram negative outer membrane
  • Bactericidal
61
Q

Which plasmid encodes multiple resistance genes? (3)

A
  • R100
  • Affect uptake or inactivate drug
  • Self trasmissible via conjugation
62
Q

Where do mobile resistance genes come from?

A
  • Spontaneous mutation in a gene with similar function (random, low frequency events)
  • From microbe that make the antibiotic naturally

Microbiology (8 decks)

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