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HYMS Block 9 > Bacterial Infections > Flashcards

Bacterial Infections Flashcards

1
Q

BACTERIAL STRUCTURE

  1. what is the function of the flagellum?
  2. what is the role of pili?
  3. what is a plasmid?
  4. What is the nucleoid?
A
  1. motility
  2. adhesion
  3. extra-chromosomal DNA
  4. circular, double-stranded piece of DNA which is not surrounded by a nuclear membrane
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2
Q
  1. what colour do gram positive bacteria stain?
  2. what colour do gram negative bacteria stain?
  3. describe the cell walls of:
    a) gram negative bacteria
    b) gram positive bacteria
  4. what are acid fast bacteria?
  5. why do bacteria such as mycoplasma and chlamydia not stain with gram staining?
A
  1. purple
  2. pink

3a. thin peptodoglycan layer. Outer layer consisting of LPS
3b. no LPS. Thin layer comprised of teichoic acid. Thick peptidoglycan layer

  1. bacteria that have large amounts of mycoloc acids which resist gram staining
  2. they lack a conventional cell wall
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3
Q
  1. what are spores?

2. what bacteria produce spores?

A
  1. stripped down, dormant form containing genetic material, that is resistant to heat, desiccation and chemicals
  2. gram positive
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4
Q

Nutritional Properties

  1. aerobic
  2. anaerobic
  3. microaerobic
  4. fastidious
  5. name 6 other nutritional requirements of all bacteria
A
  1. require oxygen
  2. require anaerobic conditions
  3. require limited amount of oxygen
  4. has a requirement for specific nutrients
  5. carbon. nitrogen. phosphate. sulphate. minerals. trace elements (e.g. iron)
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5
Q
  1. how do bacteria grow?
  2. describe the following mechanisms of horizontal gene transfer:
    a) transformation
    b) transduction
    c) conjugation
    d) transposons
A
  1. binary fission
    2a) free DNA is taken up by the cell
    b) a phage mediates the transfer of non phage DNA between bacteria
    c) bacteria having sex; a conjugative plasmid moves from one bacteria to the other
    d) jumping genes - DNA sequence that can change its position within a genome, creating mutations. can jump from chromosomal to plasmid DNA and back
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6
Q
  1. what is infectivity?
  2. what is virulence?
  3. what is an infective dose?
  4. exposure leads to infection depening on:
    a) what host factors? (3)
    b) what bacterial factors? (4)
A
  1. the ability of a pathogen to establish an infection
  2. the ability to infect or damage a host
  3. the amount of pathogenic agent that will cause infection in susceptible subjects
    4a) immune status of host
    prior exposure
    genetic predisposition
    b) site of infection
    route of inoculum
    size of inoculum
    specific traits of bacterial strain (virulence factors, metabolism, growth characteristics)
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7
Q
  1. what is an overt pathogen?
  2. what is an opportunistic pathogen?
  3. what is faculative pathogen?
A
  1. only associated with human disease; not found as members of normal healthy flora
  2. members of normal flora that only cause disease when introduced into unprotected sites
  3. can grow and survive in environment as well as host
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8
Q
  1. what strategies must a bacteria have to establish infection and cause disease? (6)
  2. what are virulence factors?
  3. name 6 examples of virulence factors
  4. which genetic components are virulence factors associated with? (3)
A 
1. attachment and entry into the body
local and general spread in the body
multiplication
evasion of host defences
shedding in body
causing damage to host
  1. molecules produced by bacteria that facilitate colonisation, growth and sptread in the host, and evasion of the host immune system
  2. adhesions - fimbriae, pili
    flagella - motility; penetrate mucin
    factors that help obtain essential nutrients
    toxins
    capsule
    type III secreted molecules (found in in several gram negative bacteria. enables them to secrete molecules into host cells.
    • transposons and phages
      - pathogenicity islands (extra genome sequences which can encode virulence factors)
      - black holes
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9
Q
  1. what is an obligate pathogen?

2. what is a non-obligate pathogen?

A
  1. . pathogens that must cause disease to be transmitted between hosts. Must infect a host in order to survive.
  2. do not require hosts to survive
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10
Q
  1. is streptococcus pneumoniae gram + or -
  2. what diseases can it cause following invasion?
  3. which tissue is it particularly invasive of?
  4. describe 5 virulence factors of S. pneumoniae
A
  1. gram +
  2. pneumonia, meningitis, septacemia
  3. lungs (host response to bacteria causes pneumonia)
  4. capsule - prevents phagocytosis
    surface adhesions - enable attachment to respiratory lining
    secretory IgA protease - cleaves IgA and promotes spread of infection
    neuraminidase - cleaves terminal acetylated neuraminic acids from sugar residues which aids motility through respiratory tract mucous
    pneumolysins - pore forming toxin > tissue damage
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11
Q
  1. what is an endotoxin?
  2. what is an exotoxin?
  3. what is an enterotoxin?
  4. what is beta haemolysin?
  5. give 2 examples of intracellular bacterial pathogens
A
  1. LPS of gram negative bacteria; responsible for causing general symptoms
  2. proteins released extracellularly. Highly toxic with high specificity.
  3. group of exotoxins that act on the small intestine
  4. exotoxin produced by streptococcus pyrogenes. results in complete breakdown of haemoglobin
  5. salmonella enterica. listeria monocytogenes
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12
Q

BACTERIAL IMMUNE EVASION STRATEGIES

  1. hide
  2. antigenic variation
  3. phase variation
  4. molecular mimickry
  5. modification of host response
A
  1. enter cell and stay intracellulae
  2. change surface antigens so they are no longer recognised by the immune system
  3. ability to turn antigens on/off so that they are not recognised by the immune system
  4. molecules have partial chemical identity with host molecules
  5. e.g. capsule prevents phagocytosis; interference with host signalling pathways. IgA protease to cleave IgA antibodies
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13
Q
  1. what is the microbiome?
  2. give examples of normal flora found on:
    a) upper respiratory tract
    b) skin
    c) GI tract
A
  1. collection of micro-organisms that resides on or within a number of tissues and biofluids
    2a) H. influenzae
    b) S. aureus
    c) E.coli
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14
Q
  1. name 5 ways in which commensal organisms promote health

2. how can commensal species cause infection

A
  1. development/stimulation of the immune system
    prevent colonisation with pathogens (compete with pathogens for space/nutrients)
    produce beneficial nutrients/components
    transformation of natural compounds
    metabolising xenbiotic substances/destroying toxins
  2. spread to sterile parts of the body
    expand population size numbers
    disturbed normal balance
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15
Q
  1. how can commensal organisms provide resistance against colonisation against pathogens
    a) direct mechanism
    b) indirect mechanism
  2. what are the characteristics of C. difficile
  3. how does it react in the presence of antibiotics?
  4. how can antibiotic treatment lead to C. diff associated diarrhoea
A

1a) nutrient competition; direct toxicity
1b) immune induction; metabolic products

  1. gram positive, anaerobic spore former
  2. naturally relatively antibiotic resistant’ flourishes under antibiotic selective pressure
  3. eliminates commensal bacterial species - antibiotic resistant bacteria thrive due to loss of colonisation resistance
    - normally, microbiome metabolise primary bile salts which prevents the formation of toxin containing spores
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16
Q
  1. what is dysbiosis?
  2. what are prebiotics?
  3. what are probiotics?
A
  1. imbalance of normal gut biota composition
  2. non digestable food ingredient that stimulates the gtowth and or activity of one or a limited number of bacteria
  3. living non-pathogenic organisms used as food ingredients
17
Q
  1. what are broad spectrum antibiotics?

2. what are narrow spectrum antibiotics?

A
  1. antimicrobial effective against a large number of bacterial genera
  2. antimicrobial effective against a limited number of bacteria genera
18
Q
  1. how is the peptidoglycan cell wall synthesised?
  2. which two classes of antibiotic inhibit peptidoglycan synthesis?
  3. How do they do this?
A
  1. cell wall units formed as precursors and linked to lipid in cytoplasm. Penicillin binding proteins facilitate linkage of unit to growing chain. Transpeptidation occurs, forming a mesh
  2. Beta lactams (penicillins and cephalosporins) and glycopeptides
  3. beta lactams - inhibit penicillim binding proteins
    glycopeptides - bind to the terminal end of the growing chain
19
Q
  1. what is the difference between bacterial and eukaryotic ribosomes?
  2. name 2 30s inhibitors
  3. name 3 50s inhibitors
  4. name 2 tRNA inhibitors
  5. Name elongation factor inhibitor
A
  1. bacteria have 30s and 50s ribosomes. Eukaryoties have 60s and 40s ribosomes
  2. aminoglycosides (e.g. gentamycin); tetracyclines
  3. chloramphenicol, erythromycin (macrolide), clindamycin
  4. puromycin, pupirocin
  5. fusidic acid
20
Q
  1. describe the folic acid metabolic pathway
  2. how is this pathway different in bacteria and humans?
  3. Name 2 antibiotics that interfere with this pathway and how they do this
A
  1. PABA > DHF > THF
  2. DHF is synthesised by bacteria; humans can’t do this therefore take DHF up
  3. sulphonamides - inhibits production of DHF from PABA (pathway unique to bacteria)
    trimethoprim - inhibits DHF reductase - higher affinity for bacterial enzyme
21
Q

What is the MOA of:

  1. fosfomycin
  2. quinolones
  3. rifamycins
  4. polymyxins
A
  1. inhibits enzyme required for synthesis of N-acetyl muramic acid
  2. inhibits DNA replication
  3. inhibits mRNA synthesis
  4. acts like a membrane detergent. Mainly topical
22
Q
  1. Name 3 examples of narrow spectrum antibiotics

2. name 3 examples of broad spectrum antibiotics

A
  1. older penicillins; macrolides; vancomycin

2. aminoglycosides, quinolones, some synthetic penicillins

23
Q
  1. what is Minimum inhibitory concentration?

2. is this an in vitro or in vivo value? What does this mean?

A
  1. minimum concentration of the antibiotic agent in a given culture medium below which bacterial growth is not inhibited
  2. in vitro. Pharmacokinetic properties play no role
24
Q

Describe the following mechanisms of resistance

  1. modifying the antibiotic target
  2. limiting access of the antibiotic
  3. enzymatic inactivation of the antibiotic
A
  1. mutation of protein target of the antibiotic (change in lock) - e.g. beta lactam resistance (change in penicillin binding protein)
  2. reduced penetration or increased efflux (upregulation of pumps)
  3. produce an enzyme that degrades the antimicrobial - e.g. beta lactam resistance (production of beta lactamase)

HYMS Block 9 (9 decks)

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