lectures 8-13 Flashcards

1
Q

define what is meant by an antiseptic

A

a product that destroys or inhibits growth of microorganisms in or on living tissues

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2
Q

define what is meant by sterilisation

A

a physical or chemical process that completely destroys or removes all microbial life including spores

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3
Q

define what is meant by an antibiotic

A

a low molecular substance often produced by a microorganisms that at a low concentration inhibits or kills other bacteria

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4
Q

define what is meant by an antimicrobial

A

any substance of natural, semi-synthetic, or synthetic origin that kills or inhibits the growth of microorganisms but causes little or no damage to the host

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5
Q

what are some sources of antimicrobials?

A
  • plants
  • metal based
  • nanotechnology based
  • animal
  • microbe
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6
Q

what plant derivatives are used in the modern day?

A
  • alkaloids
  • aldehydes
  • alcohols
  • terpenes
  • steroids
  • tannins
  • phenotic compounds
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7
Q

how can essential oils be encapsulated for use?

A
  • polymer-based nanocarriers
  • lipid based nanocarriers
  • molecular complexes
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8
Q

what is curcumin used for?

A
  • anti-tumour
  • anti-inflammatory
  • antimicrobial
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9
Q

what metal ions are used as antimicrobials?

A
  • copper
  • silver
  • gold
  • platinum
  • palladium
  • zinc
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10
Q

what animal based compounds can be used as antimicrobials?

A
  • escapin from sea hares
  • snake venom (C-amino acid oxidase)
  • chitosan from crustacean shells
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11
Q

what is biofilm?

A

an assembly of microbial cells associated with a surface and enclosed in an extracellular matrix

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12
Q

what is biofilm primarily made up of?

A

polysaccharides

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13
Q

what are the principle functions of biofilm?

A
  • provides stability
  • contains pores and channels
  • fills spaces between cells
  • contains localised gradients
  • contains synergistic micro-consortia
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14
Q

Is antibiotic resistance in Gram negative bacteria intrinsic or acquired?

A

intrinsic and acquired

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15
Q

how are Gram negative bacteria intrinsically resistant to antibiotics?

A

they have a double membrane structure that makes up a cellular envelope

alterations can occur to envelope structure (such as porin loss) which reduces permeability to antibiotics

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16
Q

are porin and efflux pump alterations specific or non-specific antibiotic resistance mechanisms?

A

they are non specific

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17
Q

how do porins and efflux pumps confer antibiotic resistance to a bacterium?

A
  • porins can be lost or reduced in number via mutation
  • efflux pumps can mutate so they efflux antibiotics at a high rate
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18
Q

what are the 2 main classes of antibiotic action?

A
  • cell wall synthesis inhibition
  • nucleic acid synthesis and protein synthesis inhibition
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19
Q

what antibiotics use cell wall synthesis inhibition and how is it carried out?

A
  • beta lactam antibiotics utilise this
  • binding to DD-transpeptidases inhibits crosslinking of the cell wall
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20
Q

what 4 methods can lead to the resistance of beta lactam antibiotics?

A
  • mutation of PBP, lowering its affinity for penicillin
  • downregulation of porins
  • acquisition of beta-lactamase
  • up-regulation of efflux pumps
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21
Q

which antibiotics inhibit nucleic acid synthesis and how do they do this?

A
  • quinolone antibiotics do it
  • they bind to topoisomerases and convert them to enzymes that fragment the bacterial chromosomes
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22
Q

how do some bacteria confer resistance to quinolones?

A

1 - mutations in gyrase and topo IV weaken quinolone action
2 - plasmid-encoded Qnr proteins decrease topoisomerase-DNA binding
3 - a plasmid-encoded enzyme acetylates ciprofloxacin, decreasing effectiveness
4 - plasmid-encoded efflux pumps decrease quinolone concentrations in the cell

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23
Q

how do antibiotics inhibit protein synthesis?

A
  • chloramphenicol binds to the 50S ribosomal subunits and inhibits the formation of peptide bonds
  • tetracycline binds to the 30S subunit and interferes with the binding of tRNA to the ribosomal complex
  • aminoglycosides bind to the 30S subunits and cause codon misreading
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24
Q

how do some bacteria confer resistance to aminoglycosides?

A
  • aminoglycosides can be modified by acetyltransferases
  • methylation of the 16s tRNA by ribosomal methyltransferase prevent aminoglycosides from binding to this target
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25
Q

what is a nosocomial infection?

A

an infection developing in a patient as a result of healthcare contact, and had no signs of infection within the first 48hrs of admission

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26
Q

what is a non-nosocomial infection?

A

an infection acquired outside the healthcare setting
- when in hospitals this includes those diagnosed within 48hrs of admission

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27
Q

what are the 5 main types of nosocomial infection?

A
  • central line associated bloodstream infections
  • catheter associated UTIs
  • nosocomial pneumonia
  • surgical site infection
  • gastrointestinal infections
28
Q

what are the risk factors for nosocomial infection regarding the environment?

A

poor hygienic conditions and inadequate waste disposal from healthcare settings

29
Q

what are the risk factors for nosocomial infection regarding susceptibility?

A
  • immunosuppression
  • underlying health problems
  • age
  • use of medical devices
  • drug treatment
  • pain management
  • length of stay
30
Q

what are the risk factors for nosocomial infection regarding unawareness?

A
  • improper use of injection techniques
  • poor knowledge of infection control
  • inappropriate use of invasive devices
  • lack of control points
31
Q

describe the features of the Clostridium difficile bacteria

A
  • Gram positive
  • toxin producing
  • anaerobic bacillus
32
Q

what does Clostridium difficile cause?

A

responsible for a variety of GI manifestations ranging from asymptomatic damage to mild diarrhoea, and rarely bowel perforations and death

33
Q

how is C. diff transmitted?

A

faeco-oral

34
Q

what are the risk factors for C. diff transmission?

A
  • antibiotics
  • co-morbidities
  • gastric acid suppressants
35
Q

what are the features of Klebsiella spp.

A

Gram negative
rod shaped
facultative anaerobe

36
Q

what is Klebsiella spp. resistant to?

A

carbapenem last line antibiotics

37
Q

does Klebsiella spp. have a high or low mortality rate?

A

high

38
Q

what are the symptoms of Klebsiella spp.?

A
  • high fever
  • pleuritic chest pain
39
Q

what is the therapy used to treat Klebsiella spp.?

A

antibiotics

40
Q

what are the features of Streptococcus pneumoniae bacteria?

A
  • Gram positive
  • facultative anaerobe
  • haemolytic
  • more than 90 different strains
41
Q

what are the causes of Streptococcus pneumoniae infection in non invasive and invasive infections?

A

non-invasive: bronchitis, otis media, sinusitis
invasive: bacteraemia, septicaemia, meningitis, pneumonia

42
Q

what control is used to limit the spread of Streptococcus pneumoniae?

A
  • there are 3 licensed vaccines
  • masks, distancing, isolation
43
Q

what is a superbug?

A

any strain of bacteria that has become resistant to the antibiotics that are used to treat it

44
Q

what are some anthropogenic drivers of antibiotic resistance?>

A
  • farming practises
  • horticultural practises - spraying crops with tetracycline
  • veterinary practises
  • healthcare practises
45
Q

what classes can bacteria be typed by?

A
  • Gram stain
  • biochemical typing
  • antibiotyping
  • phage-typing
  • serotyping
46
Q

describe the features of Pseudomonas aeruginosa

A
  • Gram negative rods
  • found in water samples
47
Q

what does Pseudomonas aeruginosa cause?

A
  • pneumonia
  • septic shock
  • UTIs
  • GI infections
48
Q

what does RFLP stand for?

A

restriction fragment length polymorphism

49
Q

how is RFLP carried out?

A

1 - A DNA sample is prepared
2 - the DNA is digested with one or more restriction enzymes that recognise and cut DNA at specific sites
3 - a loading buffer with a blue dye is added and the samples are applied to the gel
4 - a current is applied, and the DNA fragments are separated on the basis of size

50
Q

why is RFLP carried out?

A

to detect differences in homologous DNA sequences

51
Q

what is pulsed field gel electrophoresis?

A
  • a variation of gel electrophoresis in which a voltage is periodically switched among 3 directions equally
  • this results in a net forwards migration of the DNA
52
Q

what is the drawback of using pulsed field gel electrophoresis?

A

it is very hard to reproduce

53
Q

what does MLST stand for?

A

multilocus sequence typing

54
Q

what is MLST used for?

A

used for the typing of multiple gene loci

55
Q

how is MLST carried out

A
  • relatively small fragments are amplified using specific PCR primers
  • for each gene, the different sequences present within a bacterial species are assigned as distinct alleles, and for each isolate the alleles at each loci define the allelic profile or sequence type
56
Q

how can bacteria resist the action of carbapenem?

A

1 - downregulate porins
2 - reduce porin number
3 - acquisition of carbapenemases
4 - up-regulation of efflux pumps

57
Q

how can streptococcus and staphylococcus be differentiated?

A

1 - by growth habits
2 - by a catalase assay - staphylococcus contains catalase, streptococcus does not

58
Q

when was the first recorded case of MRSA

A

1961

59
Q

how have cases of MRSA been reduced in europe?

A
  • improved hospital screening
  • better infection control
  • better barrier precautions
  • increasing knowledge of environmental reservoirs
  • introduction of the antibiotic vancomycin
60
Q

what are the 4 main types of MRSA reservoirs?

A
  • healthcare associated
  • livestock associated
  • community associated
  • fomite associated
61
Q

why is MRSA difficult to eradicate in hospitals?

A
  • it is carried by patients, staff, and on surfaces
  • it can survive on sterile goods packaging for more than 38 weeks
  • it is resistant to ethanol hand washes
62
Q

what makes a person at higher risk of catching community acquired MRSA?

A
  • sports participants
  • msm
  • crowded conditions
  • sharing personal items
  • touching contaminated surfaces
  • being HIV +
63
Q

what does SCCmec stand for?

A

staphylococcal cassette chromosome mec

64
Q

what proportion of MRSA isolates had SCCmec type IV and the PVL toxin gene?

A

98%

65
Q

what is the significance of MRSA possessing SCCmec?

A

it carries the mecA gene which codes for methicillin resistance

66
Q

what is the significance of MRSA possessing PVL toxin gene?

A

it produces Panton-Valentine leukocidin
- an exotoxin that stimulates apoptosis of monocytes
and secretres alpha-toxin