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Microbiology > Antimicrobial Resistance > Flashcards

Antimicrobial Resistance Flashcards

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1
Q

what are forms of natural resistance?
(resistance against antibiotic)

A
  • target not present
  • target not accessible
  • developmental structure/state
  • metabolism (metabolic resistance so antibiotic not activated)
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2
Q

what are examples of when bacteria naturally resistant due to target not present?

A

Mycoplasma = no cell wall
Lactobacillus = D ala- D lactate side chain in cell wall & glycopeptides cannot bind

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3
Q

what are examples of when bacteria naturally resistant due to target not accessible?

A

OM gram -ve prevents vancomycin entry

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4
Q

what are examples of when bacteria naturally resistant due to developmental structure/state?

A

c.difficile spore
persistor cells & biofilms more resistant

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5
Q

what are examples of when bacteria naturally resistant due to metabolism?

A

metronidazole uptake & action require anaerobic conditions

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6
Q

what is biofilom?

A

organism that behaving as part of multi-cellular community that’s associated with surface (increases habitat range) and allows it to cooperate with environment and allows for development & differentiation

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7
Q

what can biofilm be permeated by?

A

water channels

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8
Q

is biofilm evenly distrubuted?

A

no, it has spacial heterogeneity (uneven concentrations)

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9
Q

what substance contains interfaces?

A

biofilm - means there’s biofilm at areas where different properties meet e.g. liquid & air, solid - liquid etc)

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10
Q

what are incorporated into biofilm?

A

environmental components incorporated into structure e.g. EPS, matrix, key extracellular components

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11
Q

what processes does biofilm go under?

A

development, differentiation, specialisation

co-operation, coordination and competition also occurs

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12
Q

what are some key features of persistor cells?

A
  • induce tolerance = not classical resistance
  • metabolically inert = very slow growth, dormant or non-dividing
  • sub-population of cells = they live in : transient state, planktonic & biofilm populations or enriched biofilms
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13
Q

how are biofilms and persistor cells related?

A

biofilm enriches for perisitor cells (persistor cells are found in biofilm)

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14
Q

how much genetic variation does biofilm have?

A

lots - very important to know

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15
Q

how can resistance arise?

A

by mutation or gene transfer e.g. acquisition of a plasmid, natural transformation & transduction

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16
Q

what can resistance provide?

A

a selective advantage (greater chance of survival & reproducing than the available alternatives)

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17
Q

how many steps does resistance result from?

A

multiple or single steps

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18
Q

what is cross resistance?

A

resistance resulting from a single step -> closely related to antibiotics

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19
Q

what is multiple resistance?

A

resistance resulting from multiple mechanisms ->unrelated to antibiotics

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20
Q

how do we determine resistance?

A
  • minimum inhibitory concentration = one that stops growth
  • minimum bacteriacidal concentration (MBC) = one that’s killing

(MBC usually higher)

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21
Q

what is the selective pressure for evolution of anti-microbial resistance?

A

exposure to antibiotics

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22
Q

when is bacteria resistant?

A

when drug is no longer active against entire population of cells

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23
Q

what can increase variation of bacteria?

A

horizontal gene transfer

24
Q

what is horizontal gene transfer?

A

increase of variation by passing DNA between organisms (different organisms have different amounts of horizontal gene transfer)

25
Q

what are the 3 ways of horizontal gene transfer?

A
  1. Natural competence = take up from environment
  2. sex pili = through contact
  3. Bacteriophage = through phage transfer
26
Q

what is the process of selective pressures & evolution?

A

variation arises and causes selective pressure which leads to evolution resistance and then gene transfer spread & variation

27
Q

what are the resistance mechanisms of bacteria?

A
  1. impaired influx (block antibiotic from entering)
  2. efflux (gets antibiotic to flow out)
  3. target mutation (change in active site so antibiotic no longer fits)
  4. target modification (add something like a molecule to active site so antibiotic can’t bind)
  5. overproduction of target mimic (bacteria multiplies lots so too much bacteria for antibiotic to target)
  6. factor-associated protection (factor binds to active site so antibiotic can’t bind)
  7. drug modification (add something to antibiotic so it can’t bind)
  8. drug degredation →secretion of beta-lactamases (breakdown of antibiotic so it can’t bind)
28
Q

how does active efflux of anti-microbial drug resistance occur?

A

(addition of) Energy dependent pump e.g. tetracycline

29
Q

how does altered permeability affect drug resistance?

A

altered permeability = altered influx
so changes number or type of proteins in outer membrane (reduced quinolones) to prevent antibiotic from entering (target not altered)

30
Q

how is inactivation of antibiotics done by anti-microbial drugs?

A

by beta-lactamases
-> extended spectrum beta-lactamases (ESBL)

31
Q

what are 2 subtypes of beta lactamase?

A
  1. penicillinase (include clavulanic acid sensitive & insensitive)
  2. cephalosporinase (include clavulanic acid sensitive & insensitive)
32
Q

what are beta lactamases inhibtors examples?

A

clavulanic acid (usually 1st line of use to inhibit beta lactamase)
examples= co-amoxyclav (amoxicillin & clavulanic acid - oral & IV)

Tazobactam
examples = piperacillin & tazobactam (IV)
= ceftolozane & tazobactam (Resistant urinary tract infections)

33
Q

what are 3 examples of beta-lactamases?

A
  • penicillinase
  • extended spectrum b-lactamase (ESBL)
    -cerbapenemase (CPE)
34
Q

what are penicillinase resistant to and what spectrum?

A

resistant = early penicillins such as amoxicillin
→Largely Gram-positive distribution

penicillinase= type of beta-lactamases

35
Q

what are extended spectrum beta-lactamases (ESBL) resistant to and where are they found (what distribution)?

A

resistant = all penicillins
→Extends to 3rd generation cephalosporins, & monobactams

36
Q

what are carbapenems (CPE) resistant to and where are they found (what distribution)?

A

resistant = all penicillins, all cephalosporins & carbapenems

  • Serine based & metalloenzyme based (different active site structures)
    →Carbapenems, such as meropenem, were considered “antibiotics of last resort”
37
Q

what is metalloenzyme?

A

metallo beta lactamse
= type of carbapenemase which was mostly in gram -ve (like e.coli & k.pneumoniae)

  • caused big scare as they thought unbeatable enzyme
38
Q

what treatment works for metalloenzyme?

A

colistin treatment
= targets outer membrane gram -ve’s
= IV dosing is difficult

39
Q

what does MRSA stand for?

A

methicillin resistant S.aereus (methicillin is now replaced by flucloxacillin so MRSA also resistant to flucloxacillin)

40
Q

how does MRSA show resistance?

A

= altered target site (altered penicillin binding protein): has mecA gene that produces penicillin binding protein (PBP2a) that has low affinity for antibiotic

41
Q

what is generally used for MRSA?

A

vancomycin (reserved for very serious infections)

42
Q

what are the threats to antimicrobials & vaccine success?

A

*AMR
* Emerging Diseases
* Climate Change
* Vaccine hesitancy
* Vaccine failure
* Discovery of role of pathogens in
conditions/pathologies
* Gastric Cancer, HPV, GI cancer
* Alhzeimer’s disease

43
Q

what’s an important factor for when resistance emerges?

A
  • which pathogen
  • where e.g. community or nosocomial (in hospital)
44
Q

how can resistance emerge?

A
  • germs develop new cell processes that avoid antibiotic target
  • germs change or destroy the antibiotics with enzymes (proteins that break down drug)
  • germs restrict access by changing entryways or limit number of entryways
  • germs get rid of antibiotic using a pump
  • germs change the antibiotic target so drug can no longer fit
45
Q

how do we tackle AMR?

A
  • drug development
  • alternative therapies = you need to understand the role of microorganisms(vaccination, phage, antibodies, probiotics)
  • prevention ( public health, isolation, infection control)
  • prescribing ( education, innappropriate prescribing)
46
Q

what are important factors in reducing infection?

A

Infection control (HAI’s transmission of AMR strains, surveillance)

Public health ( food poisining, water sources, vectors)

colonisation of AMR microbes (environment, food)

47
Q

why should you use narrow spectrum antibiotics whenever possible?

A

to reduce emergence of resistance (stop resistance of lots of differengt pathogens) & c.difficile (when all gut biome wiped out, easy for c.difficile spore to colonise)

48
Q

where should you consider no prescribing or only back up prescribing?

A

upper respiratory tract infections & uncomplicated lower UTI’s in females

49
Q

what are some innappropriate prescribing themes?

A

certain viral infections (respiratory tract infections, sinisitus/sore throat, UTI’s)

fungal infections (not common source of inappropriate prescribing)

mild/self limiting conditions (will it go away by itself)

prophylaxis (dental - tooth extraction, surgery - pre & post op, recurrent UTI)

50
Q

what are some urgent scenarios you would most likely prescribe antibiotics?

A
  • Sepsis
  • Cellulitis
  • Meningitis
  • Infective Endocarditis
51
Q

what are the access drugs?

A

quite easy access

  • amoxicillin
  • co-amoxiclav
  • benzyl penicillin
  • Penicillin V
  • flucloxacillin
  • 1st generation cephalosporin
52
Q

what ares some watch drugs?

A
  • temocillin
  • piperacillin/ tazobactam
  • 2nd, 3rd, 4th gen cephalosporin
  • carbapenems (some)
53
Q

what drugs are on the alert NHS tayside list?

A
  • gentamicin
  • meropenem (carbopenem)
  • piperacillin/tazobactam
  • ciprofloxacin
  • temocillin
54
Q

what do we want to do to get drugs that don’t have resistance?

A

we want to prolong the life of already existing drugs like trying to combine things or adapt
(finding whole new antibiotics that fit all the right boxes would be too difficult)

55
Q

what does CPE stand for?

A

CPE (carbapenemase-producing Enterobacterales) = bacteria in gut

-> big threat

56
Q

what does ESBL stand for?

A

ESBL stands for Extended Spectrum Beta-Lactamase.

57
Q

what does VRE stand for?

A

Vancomycin-resistant Enterococcus

Microbiology (6 decks)

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