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BDS4 CDS Oral Surgery > microbiology and antimircrobials > Flashcards

microbiology and antimircrobials Flashcards

1
Q

aerobic bacteria

A

need oxygen to grow

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2
Q

capnophilic bacteria

A

need CO2 to grow

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3
Q

faculatative bacteria

A

can grow with and without oxygen

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4
Q

strictly anaerobic bacteria

A

can only grow without oxyegn (can be toxic for some)

Metronidazole only works on them

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5
Q

gram positive bacteria appear

on stain

A

purple on

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6
Q

gram negative bacteria appear

on stain

A

red/pink

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7
Q

cocci

A

round shape

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8
Q

bacilli

A

rod shape

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9
Q

e.g. gram positive cocci

A

S.anginosus

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10
Q

e.g. gram negative cocci

A

veillonella species

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11
Q

e.g. gram positive bacilli

A

actinomyces israelli

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12
Q

e.g. gram negative bacilli

A

prevotella intermedia

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13
Q

WHO defintion of anitmicrobial resistance

A

“Antimicrobial resistance occurs when microorganisms such as bacteria, viruses, fungi and parasites change in ways that render the medications used to cure the infections they cause ineffective.”

black pigmented – prevotella intermedia

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14
Q

2 main mechanisms of resistance through resistance genes

A

intrinsic resistance

acquired resistance

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15
Q

acquired resistance from resistance genes can be either

A

mutation or acquisition of New DNA

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16
Q

3 types of acquisistion of new DNA for resistance genes

A

transformation

transduction

conjugation

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17
Q

3 main mechanisms of antiobiotc resistance

A

altered target site

enzyme inactivation

decreased uptake

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18
Q

altered target site mechanism for resisstance

A

Bacteria have changed the shape of antibiotics receptor – no longer able to bind

  • E.g.
    • Viridans group Streptococci
      • E.g. S. mitis
    • Penicillin resistance due to modified penicillin binding proteins
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19
Q

ezyme inactivation mechanism for resistance

A

Enzymes destroy antibiotics or prevent them binding to target sites

E.g.

  • Prevotella and Fusobacterium species against penicillin and amoxicillin (e.g. Penicillin V)
  • mostly beta-lactamases
  • Penicillin used – bacteria evolved penicillinase*
  • Penicillinase resistant drugs made – beta-lactamase evolved*
  • Chemist further modified the (extended spectrum beta-lactamases) and bacteria then evolved extended spectrum beta-lactamases (ESBL) to breakdown the new AB*
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20
Q

decreased uptake mechanism of resistance

A

Large capsule around bacteria – affecting uptake of AB

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21
Q

how many forms of resistance can bacteria utilise

A

multiple

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22
Q

type of infection that odontogenic ones are (e.g. acute periapical infection)

exo or endo

A

endogenous infection

bac orginate from us

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23
Q

single or multi organism infection for odotogenic infection

A

often multi/mixed infections

aerobic and anaerobic, work in symmetry

strict anaerobes are key to them

e.g. Streptococcus anginosus (common in acute dentoalveolar infection)​, Prevotella intermedia (gram negative, strict anaerobe)

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24
Q

ideal specimen for odontogenic infection

A

pus aspirate

can be hard to get in general practices

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25
Q

common bac in periodontal abscess

A

Anaerobic streptococci​, Prevotella intermedia

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26
Q

tx principles for localised dental infection

A
  • Establish a diagnosis & document it​
  • Remove the source of infection
    • Pulp extirpation or incision and drainage or extraction
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27
Q

microbiology for periocornitis

A

Predominantly mixed oral anaerobes, e.g, P. intermedia​, S. anginosus group

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28
Q

tx pericornitis

A
  • Local measures
  • Systemic (only if systemic signs/symptoms)
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29
Q

dry socket microbiology

A
  • Localised alveolar osteitis​
  • Mixed oral flora​
  • Extremely painful
  • Does not ​require antibiotic​ treatment
    • LA, debridement and pack with antimicrobial gels/strips
30
Q

osteomyelitis of jaw

predisposed by

A
  • Biphosphonate therapy (BRONJ/MRONJ)​
  • Impaired vascularity of bone (radiotherapy, Pagets disease)​
  • Foreign bodies (implants)​
  • Compound fractures ​
    • Communication either intra or extra orally
  • Impaired host defences (diabetes)
31
Q

what happened here

A

Post-dental extraction infection osteomyelitis of the jaws

  • 48 removed
  • 2nd x-ray – post op review, pt complained of dry socket, which was managed locally
  • 3rd x-ray – pt developed infection which extended into ramus and border of mandible
    • Needed to go back to surgical theatre and bone curetted out and then long course IV AB (6 weeks)
32
Q

micrbiology in osteomyleitis of jaw

A

Anaerobic Gram negative rods​

  • Anaerobic streptococci​
  • Streptococcus anginosus​
  • Staphylococcus aureus ​
    • Worry – effect AB choice, difficult to tx, need prolonged course of AB

Is aseptic necrosis of bone first or infection first?

Common bacteria cause of cultured bone specimens (difficult as get contamination by oral micro flora)

  • S.angiosus
  • Mixed anaerobes
  • Actinomyces iraelii

SDCEP guidelines – Oral health management of pt at risk of MRONJ

33
Q

microbiology of salivary gland infection

A
  • S. aureus​
  • Mixed anaerobes​
34
Q

tx salivary gland infection

A
  • Dx and Drainage ​
  • Flucloxacillin &​ metronidazole
35
Q

for all odontogenic infections - what you MUST do (4)

A
  1. Systematic history and examination. Document your diagnosis​
  2. Document Ab choice, dose, route & duration​
  3. Document a review date​ (24-48hr for acute)
  4. Document deviation from guidance​

​

36
Q

Ludwig’s angina defintion

A

bilateral infection of submandibular space

37
Q

most common bacteria involved in ludwig angina

A
  • Anaerobic Gram negative bacilli​
  • Streptococcus anginosus​
  • Anaerobic streptococci​

Severe odontogenic infections, watch for S.aureus

38
Q

why is taking specimen imp

A

not always the same common bacteria causing odontogenic infections

  • important to take specimens for culture and sensitivity testing so can modify AB tx

Severe odontogenic infections, watch for S.aureus

39
Q

sepsis

each hour delay in giving AB

A

For each hour delay in AB administration mortality increases by nearly 10%

  • sooner given AB – better survival rate

Reassess antimicrobials daily:

  • Optimise
  • Reduce Resistance
  • Avoid Toxicity
  • Reduce costs
40
Q

sepsis =

A

SIRS + suspected/confirmed infection

need to go to hospital

41
Q

sepsis defintion

A

life threatening organ dysfunction caused by dysregulated host response to infection

42
Q

SIRS

A

systemic inflammatory response syndrome

2 or more of

temp <36 or >38

pulse > 90/min

resp rate >20/min or PaCO2 <4.3

WCC <4 or >12

43
Q

septic shock =

A

sepsis + unresponsis to fluid resuscitation

44
Q

septic shock defintion

A

subset of sepsis with circulatroy and cellular/metabolic dysfunction associated with higher risk of mortality

45
Q

sepsis in scotland

A
  • Kills around 3,500 people in Scotland every year (any source)
    • 1 person every 4 hours
  • Mortality rates from sepsis have fallen by 21% since 2012
  • Many public campaigns to spread knowledge of noticing signs
    • sepsis 6
46
Q

primary care tx principles for SOI and Ludwig’s angina

A

hx, exam, dx

seek advice/help - maxfax unit

47
Q

secondary care tx principles for SOI and Ludwig’s angina

A
  • Diagnosis
  • Sepsis 6
    • High flow oxygen
    • Take blood cultures
    • Give IV antibiotics
    • Give a fluid challenge
    • Measure lactate
    • Measure urine output
  • National Early Warning Score (NEWS – 2)
48
Q

sepsis 6

A
  • High flow oxygen
  • Take blood cultures
  • Give IV antibiotics
  • Give a fluid challenge
  • Measure lactate
  • Measure urine output
49
Q

what is more effective for localised infection

surgical tx or antibiotics

A

surgical tx (removal of source and good drainage)

need appropriate dx

50
Q

antimicrobial resistance - biological defintion

A

Resistance definitions usually based on in-vitro quantitative testing of bacterial suspensions to antibacterial agents

  • Minimum inhibitory concentration noted on e strips
  • Automated susceptibility testing system (tests are usually automated now)
51
Q

breakpoint defintion

A

chosen concentration (mg/L) of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic

52
Q

antimicrobial resistance clinical defintion

A

When infection is highly unlikely to respond even to maximum doses of antibiotic (EUCAST)

53
Q

confounding variable when working out resistance

A

need to try standardise them

  • Laboratory​
    • Inoculum size, growth phase, planktonic (in solution), pH, atmosphere…​
    • Breakpoint calling​
    • -Biofilm​ (most infections in this form – bacteria grow slower, metabolic rates are slower, sometimes need 1000 times usual dosage of AB disinfectant to kill biofilm bacteria)
  • Clinical​
    • Co-morbidities, pus collections (imp in acute dentoalveolar infections, hard to get AB to penetrate into pus – need to surgically remove pus when possible), foreign bodies, site of infection
    • Biofilm​ – almost impossible to tx due to changes in bacterial phenotypes
    • Pharmacokinetics​ – distributed through body
    • Pharmacodynamics – antibiotic classes interact with bacteria

European resistance rate different to US – artificial due to differences in definitions used, careful when looking at data

54
Q

surveillance of microbiology of acute dentoalveolar infections

needs to be

A

continually done

constantly evolving

55
Q

how to improve surveillance of bacteral dental infections for AMR (3)

A
  1. Agree definitions of resistance for common isolates ​in SEVERE odontogenic infections (SOI’s)
  2. Standardised specimen collection, processing &​ reporting for SOI’s (Surveillance)​
  3. Return to 1st choice Penicillin V IF antibiotics required
56
Q

antimicrobial stewardship

A
  • Teamworking

aim

  • ‘preserve antimicrobial medicines by taking measures to promote their control’
57
Q

good OH aid in antimicrobial stewardship

A

revents infection from spreading, reducing the need for antibiotics which helps limit antibiotic resistance

58
Q

5 strategic objectives of the WHO global action plan on antimicrobial resistance

A
  • Improve awareness and understanding
  • Strengthen the knowledge through surveillance and research
  • Reduce the incidence of infection
  • Optimise the use of antimicrobial medicines
  • Ensure sustainable investment

One health – work with colleagues, environment, animals (vets and farmers) to reduce antimicrobial resistance

59
Q

UK action plan for AMR 2019-2024

key way to help

A

Reducing need for, and unintentional exposure to, antimicrobials (prevention of disease)

60
Q

3 reasons for inappropriate AB prescribing

A
  • 30% prescribed due to time/workload pressures​
  • 47% prescribed when unsure of diagnosis​
  • 72% prescribed where treatment had to be delayed​
61
Q

wrong tx for acute pulpitis

A

AB

antibiotics ineffective

62
Q

wrong tx for chronic gingivitis

A

AB

antibiotics ineffective

63
Q

wrong tx for sinusitis due to dental cause

A

AB

antibiotics ineffective

64
Q

wrong tx for dry socket

A

AB

antibiotics ineffective

65
Q

wrong tx for chronic perio

A

AB

antibiotics ineffective

66
Q

pencillin and amoxicillin connection

A

same class

both beta-lactamase antiobiotics

67
Q

1st line AB for dental alveolar infections

A

beta-lactamase agent (e.g. pencillin, amoxycillin)

not metronidazole

68
Q

should dentists prescribe metronidazole

A

no

not 1st line AB for dental alveolar infection (not beta-lactamase agent)

drives selection of metronidazole strict anarobes - worry

69
Q

amoxicillin or penicillin for dental-alevolar infections?

A

Main ab prescribed in Scotland is beta-lactame amoxicillin

  • Wide spectrum agent
    • Evidence to suggest that is more likely encourage development of resistance

Soon to switch to Pen V as 1st line

  • Narrower spectrum
  • Evidence as Norway and Sweeden have been doing this for decade
70
Q

3 ways to contribute to slow AMR

A
  1. Prevent dental disease
  2. Prevent spread of disease
    1. Wash hands/SICPs
    2. Get vaccinated against flu
  3. Antibiotics don’t cure toothache

BDS4 CDS Oral Surgery (19 decks)

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