the importance of cell biology & AMR for vet med Flashcards

1
Q

define infection

A

the invasion and/or colonisation by and subsequent multiplication of pathogenic microorganisms in a bodily part or tissue
- can produce subsequent tissue injury and progression to overt disease through a variety of cellular or toxic mechanisms

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2
Q

what is the daily impact of microbiology for veterinarian

A
  • revention of infectious disease (vaccines, probiotics, owner education)
  • treatment of infectious disease ( diarrhea, skin infections, bite wounds - do they need antibiotics?)
  • sterilisation of instruments
  • biosecurity
  • epidemiology
  • antimicrobial stewardship
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3
Q

describe the hierarchy of antibiotics - should we be routinely using critically important human antibiotics in animals

A

to be able to assess antibiotic usage we need to understand which antibiotics are seen as critically important in human medicine and hence should only ever be a last resort in animal medicine if used at all

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4
Q

describe how microbes can cause disease

A
  • infection (colonise or invade tissues)
  • produce toxins and poision the host (often associated with infection but sometimes just ingestion of pre-formed toxin)
  • cause a host response (allergic reaction)
  • combination of above
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5
Q

what 3 words can be used to classify the prevalence of pathogens

A
  • sporadic
  • enzootic (regularly affecting animals in a particula district or at a particular season)
  • endemic ( term that relates to humans but also used in vet med - regularly found among particular group of people or in a certain area)
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6
Q

define latency

A

the pathogen goes inert in the animals. reactivation may occur if the pathogen is switched back on (i.e herpes)

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7
Q

define carriage

A

the animal tolerates the pathogen without disease and is capable of transmitting the organism (host can control pathogen but not clear it or causes disease in one species but is carried in another)

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8
Q

define reservoir of infection

A

any animal, human, environment in which an infectious agent normally lives and multiplies

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9
Q

what is an acute infection

A

pathogen cleared shortly after inefection

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10
Q

what is a chronic infection

A

pathogen is detectable for lifetime of host
- immune response takes effect (or treatment) and reduces but does not clear infection)

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11
Q

what is a latent infection

A

infectious agent disappears (indetectable) but can be reactivated by a number of factors.

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12
Q

what features do antibiotics use as points of attack on bacteria

A
  • cell wall synthesis
  • cell membrane structure and function
  • translation/protein synthesis
  • transcription
  • DNA synthesis and replication
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13
Q

how do antibiotics target the cell wall and give examples of antibiotics that do this

A

a cell wall is a good target because it contains components unique to bacteria (target peptidoglycan instead of body cell)
- beta lactams inhibit transpeptidation by binding to penicillin binding proteins on maturing peptidoglycan strands (cause decrease in peptidoglycan)
- promote autolysin activity (BACTERICIDAL)

EXAMPLES:
- penicillin (beta lactam)
- ampicillin (beta lactam)
- vancomycin (glycopeptide)

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14
Q

describe how antibiotics target the cell membrane. give examples of antibiotics that do this
what are the disadvantages of these antibiotics?

A

cell membrane is a good target becuase distrupted functional integrity of cell membrane leads to escape of macromolecules and ions from the bacterial cell => bactericidal
disadvantages: high level of similarity between bacterial and animal cell membranes => more toxic to animal cells and often last resort

examples:
polymixin and colistin
- both target the outer membrane of Gram negative bacteria

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15
Q

why is nucleic acid synthesis a good target for antibiotics, how does it work and give examples of antibiotics that target this

A

organisation and replication of bacterial DNA and RNA is different to eukaryotics - bacteriostatic (dont kill but prevent from growing/replicating so immune system can take over)
Examples:
Quinolones and Novobiocin both act on DNA gyrase which separates DNA strands during bacterial replication. quinolones interfere with changes in DNA suoercoiling by binding to topoisomerase II or topoisomerase IV
rifampin interferes with DNA-dependant RNA polymerase activity and prevents RNA synthesis

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16
Q

what is protein synthesis a good target for antibiotics, how do they work (give examples of antibiotics)

A

there are differences in ribosome structure between eukaryotes and prokaryotes - bacteriostatic (doesnt kill, prevents growth and replication so immune system can take over)

examples;
tetracycline blocks tRNA molecule attachment on 30 s subunit
erythromycin and chloramphenicol both block 50 s subunit activity preventing growth of polypeptide chain
aminoglycosides bind to 30 s subunit and inhibit proofreading and initiation (ex. spectinomycin, streptomycin, neomycin)

17
Q

describe the 4 antibiotic resistance mechanisms

A
  1. enzymes that degrade or inactivate antibiotic (beta lactamases that degrade penicillin/ampicillin)
  2. alteration of target site (altered ribosome structure)
  3. elimination of antibiotic from bacterial cell (efflux pump)
  4. bacterial cell impenetrable for antibiotic (gram negative cell wall inpenetrable for penicillin)
18
Q

how does antibiotic use lead to increased antibiotic resistance

A

antibiotics are an environmental stress and cause selection pressure, leading to only resistant bacteria surviving and subsequently replicating, resulting in the next generation of bacteria being highly resistant as only the strongest survived to divide

19
Q

how can we uphold antimicrobial stewardship

A
  • only use if necessary
  • evaluate risk of selecting multidrug resistance
  • avoid last resort/critically important antibiotics for human medicine
  • prevention rather than cure (herd health)
  • “use as little as possible and as much as necessary”