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BVetMed - Principles of Science > Antimicrobials 1 + 2 > Flashcards

Antimicrobials 1 + 2 Flashcards

1
Q

What is the goal of antimicrobial therapy?

A

Eliminate infectious organism without toxicity to host

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2
Q

What is the most important thing to try and augment when treating bacterial infection?

A

Natural defence mechanism

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3
Q

Give 3 examples of natural defences and when these may be compromised

A
  • mucociliary escalator (cystic fibrosis)
  • flushing effect of urination (catheter placement)
  • normal gut flora (gut dysbiosis)
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4
Q

What are the 4 quadrants targetted by the antimicrobial spectrum? What else may “4 quadrants” of microbes also refer to?

A
  1. G+ aerobes/ G- aerobes/ Obligate anaerobes (G+-)/Penicillinase producing staph
  2. G+/G- aerobes/ G+/G- anaerobes
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5
Q

Give 4 examples of G+ aerobes

A
  • Strep (B haemolytic)
  • Enterococcus
  • Pnumococcus
  • Bacilli (lactobacillus, corynebacterium, listeria, erysopalathrix, arcanobacterium)
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6
Q

Give 6 examples of G- aerobes

A
  • E. Coli
  • Klebsiella
  • Helicobacter
  • Campylobacter
  • Pastuerella
  • Psuedomonas
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7
Q

Give 5 examples of staph

A
  • aureus
  • saphrophyticus
  • epidermis
  • haemolyticus
  • capitis
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8
Q

Give 4 broad examples of anaerobes

A
  • G+ spore forming clostridium (perfringens, botulinum, tetani)
  • G+ bacilli (actinomyces, lactobacillus, bifdobacterium)
  • G- bacilli (fragillis or not fragillis)
  • Cocci (peptococcus niger)
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9
Q

Give 6 examples of atypical bacteria

A
  • Rickettsia (not uk disease)
  • Mycoplasma
  • Chlamydia
  • Borrelia
  • Bartonella
  • Mycobacterium
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10
Q

Where are many antimicrobial substances derived from?

A

Fungus

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11
Q

Give conditions when rational antimicrobial use can be justified

A
  • bacterial infection definitively diagnosed
  • OR highly likely
  • disease will progress without medical therapy
  • would casue critical illness if occourred and not recognised/treated
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12
Q

What essentially useless treatment should be given inlieu of prescribing antibiotics as a placebo because you don’t know what else to do?

A

Vitamin injection

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13
Q

Give some clues of bacterial infection

A
  • heat, redness, swelling
  • pyrexia (could also be viral/fungal/neoplasia)
  • neutrophilia (stress leukogram)
  • bacterial cause COMMON?!
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14
Q

Give 3 examples where ABx are commonly prescribed but a bacterial aetiology is rare

A
  1. V+ D- = acute gastritis due to eating rubbish etc. No bacteria casues V+D-! except helicobacter but v. rare
  2. Hameaturia in young cat <10y = idiopathic cystitis usually due to stress, will resolve within 5-7d. In DOGS haematuria indicates UTI but cat urine so concentrated these are RARE.
  3. Haemotochezia = no evidence of need for antimicrobials unless signs of sepsis seen
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15
Q

What 5 factors influence the success rate of ABx Tx?

A
  • what bugs live where?
  • bacterial susceptibility
  • Pharmacokinetic phase - getting the drug to the infection
  • Pharmacodynamic phase - Local conditions
  • Client comlpliance
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16
Q

Give the 3 main sources of infection with egs.

A
  1. Environment
    - mycobacteria, tetanus, contaminated food (campylobacter, E. Coli)
  2. Other animals
    - Bordatella
  3. Internal
    - GI (E. Coli, G-s, Anaerobes)
    - Skin (Staph - S. Aureus, Strep in horses )
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17
Q

How does previous ABx Tx affect the decision making for rational ABx use?

A

changes susceptibility profile of bugs

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18
Q

How do horses differ from SAs with wound infection risks?

A

Strep ^ risk in horses than staph/

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19
Q

What bacteria usually causes mastitis in cattle?

A

Staph

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20
Q

How should sepsis of unknown origin be treated?

A

Cover all 4 bacterial quadrants

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21
Q

What is the common cause of pneumonia?

A

Difficult to predict bacteria

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22
Q

What is the common cause of endocarditis, arthritis or discospondylitis?

A

Staph -> systemic infection from the skin

23
Q

What is the exception to the rule of bacteria which are resistant to a drug in vitro being resistant in vivo?

A
  • stats based on blood concentration of drug

- > resistence may be overcome by high concentrations achieved in urine/topically

24
Q

Define MIC. How is this used clinically?

A

Minimum inhibitory concentration

  • lowest concentration of a drug to inhibit bacterial growth
  • MIC90 used as therapeutic dose (conc that inhibits 90% bacterial isolates of a specific species eg. e coli, s. pseudointermedius)
25
Q

Give 3 antimicrobials that inhibit cell wall synthesis

A
  • penicillins
  • cephalosporins
  • bacitracin (usually used for eyes and ears)
26
Q

Give 4 antimicrobials that inhibit cell membrane function. What are their usual usage?

A 
- polymixins (eyes)
Usually antifungals:
- amphotericin B 
- imidazoles
- nystatin
27
Q

Give 5 antimicrobials that inhibit protein synthesis

A
  • chloramphenicol
  • macrolides
  • lincosamides
  • tetracylinces
  • aminoglycosides (good for ears)
28
Q

Which antimicrobial class have an ^ risk of side effects and why?

A

Protein synthesis inhibitors (chloramphenicol, macrolides, lincosamides) as act on element of bacterial cell that is similar to mammalian.

29
Q

Give 5 antimicrobial classes that inhibit nucleic acid synthesis

A
  • sulphonamides
  • trimethoprim
  • quinolones (enrofloxacin etc.)
  • metronidazole
  • rifampin (used rarely)
30
Q

Is distinguishing bacteriostatic and bacteriocidal drugs clinically relevant?

A

Not really - just know that bacterioSTATIC = effect reversible once drug removed, and during Tx MIC should be maintained at site of infection throughout dosing interval -> specific dosing schedule and strict instructions necessary. Can work as bactericidal if dose is sufficiently high/prolonged.
- BacterioCIDAL = preferred when concern about site of infection or host defences as technically body defence not necessary. Killing action may be both TIME and CONCENTRATION dependent

31
Q

Give 5 bacteriostatic antimicrobials

A
  • chloramphenicol
  • lincosamides
  • macrolides
  • tetracyclines
  • non-potentiated sulphonamides
32
Q

Give 6 bactericidal antimicrobials. Which are TIME and which are CONCENTRATION dependent?

A 
Time
- penicillins
- cephalosporins 
- TMPS
Concentration
- aminoglycosides
- fluoroquinolones 
- metronidazole
33
Q

Which antimicrobials should not be used in conjuction with bacteriostatics and why?

A

Time dependent bacteriocidal as bacteria need to be multiplying for drugs to be effective

34
Q

Is there any advantage to achieving >2-4x MIC in time dependant ABx?

A

No providing MIC is maintained for long duration

35
Q

How is the efficacy of concentration dependant ABx determined? How does their activity differ to time dependent ABx?

A

Peak concentration OR area under the curve (-> time may play a role)

  • optimum ratio is 8-10x MIC
  • effective against dormant bacteria (don’t need to be multiplying to be effective
  • CAN be used in conjunction with bateriostatics
36
Q

What are the 4 colours used to code ABx activity?

A
  • Green (excellent against most spp. in quadrant)
  • Blue (good activity against many, some spp. resistant)
  • Brown (moderate activity, many spp. resistant)
  • Red (no useful activity against majority of bacteria in quadrant)
37
Q

Which quadrant are good at developing resistance and why?

A

> G- aerobes

  • plasmid transfer means can bypass slow mutation based resistnace
  • produce B lactamase like Staph
38
Q

Which quadrant are stupid when it comes to developing resistnace?

A

G+ aerobes - mutation based resistnace only

39
Q

In tissues with adequate blood supply, what is distribution of a drug limited by?

A

Perfusion

- free drug conc in plasma directly related to interstitial space conc.

40
Q

What may drug distribution be limited by other than perfusion? In which tissues may this be an issue?

A

Permeability
- lipid membrane forms barrier to drug diffusion if no cell pores
- brian
- eye
- prostate
- bronchus
- intracellular
- blood milk barrier
- poorly vascularlised tissues eg. bone fragments and heart valves
(adequate conc usually reached in living bone and synovial fluid)

41
Q

When may normally tight cell junction eg. BBB become less tight? How may this affect therapy?

A

When inflamed eg. in infection

  • > allows more substances than would normally be able to pass through barrier
  • > MAY close junctions soon as infection begins to subside, meaning poor reach of drugs once again before complete clearance of the infection
42
Q

Give 6 intracellular bacteria

A
  • Bartonella
  • Brucella
  • Chlamydophila
  • Mycobacterium
  • Rickettsia
  • Staphylococcus - facultative
43
Q

What may affect a drugs ability to penetrate difficult to access areas?

A

Hydrophilic (less penetrating) v lipophilic (More penetrating)

44
Q

What is the pharmacodynamic phase dependent on?

A

Local conditions

  • abscess
  • pus inactivates TMPS
  • necrotic debris
  • oedema (v concentration at site of infection)
  • foreign material (-> phagocytes degranutalte to try and destroy FB, intracellular bactericidal substances depleted)
  • presence of Hbg v penicillin activity
  • v pH -> loss of activity (erythromycin, clindamycin, fluoroquinolones)
45
Q

What is a glycocalyx?

A

Bacteria can form a biofilm at the site of infection and foreign material can protect bacteria from ABx and phagocytosis

46
Q

What does post operative infection risk depend on?

A
  • degree of contmaination
  • virulence of organism
  • health of patient
  • local tissue health
47
Q

What are the justifications for surgical prophylactic Abx?

A

Wound clean or dirty

  • timing of surgery
  • health of patient (Shock and emaciation, age, BCS, endocrinopathy)
  • level of asepsis
  • presence of implants
  • surgical time (>90mins)
  • surigcal technique (-> trauma)
  • organs involved
  • anaesthesia
  • propofol administration (due to multidose vial?)
  • clipping pre surgery ^ risk of infection
48
Q

Give situations when surgical prophylaxis is indicated

A
  • dental procedure (possibly)
  • patients with leukopenia (viral or drug induced)
  • contaminated surgery
  • orthopaedic/major abdo/thoracic surgery
  • surgical time >90 mins
  • serious consequences of infection (play it safe!)
49
Q

Can antiseptics compensate for lack of aseptic technique?

A

No

50
Q

How should surgical prophylaxis be administered?

A
  • should be present in wound at time of contamination
  • no use 3-5 hours post surgery
  • only single dose needed (not 5d course)
51
Q

What are the most likely contaminants of surgical wounds?

A
  • skin: staph aureus

- GIT: anarobes and G- aerobes

52
Q

What are the 2 most useless drugs for surgical prophylaxis in SA?

A

> Amoxycillin (aminopenicillin)
- Useless against penicillinase producing staph - most common wound infection in SA. (Not the same in horses as staph (G+ aerobe) most common infectant.
Long acting form of amoxycillin (LA)- takes 12 hrs to reach therapuetic doses

53
Q

What is the commonest best drug for surgical prophylaxis? What is this influenced by?

A
  • Influenced by type of surgery
    > 2nd gen cephalosporin eg. cefuroxamine (Zinacef) [not vet registered]
    > 1st gen cephalosporin [okay, not great]
  • give IV at time of induction if possible
  • If SC/IM give at least 1-2hrs pre-surgery

BVetMed - Principles of Science (27 decks)

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