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BDS stage 2 > Microbiology for dentists theme 3 > Flashcards

Microbiology for dentists theme 3 Flashcards

1
Q

What is a bacteriostatic mode of action ?

A

holds bacterial cells in steady state of growth- stopped from increasing further
total number of cells stays in a straight line

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2
Q

What is a bacteriocidal mode of action ?

A

rupture and burst cell wall so bacteria degrade
host immunity recognises this and removes it
total number of cells doesnt chage but virulent decreases

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3
Q

What is a bacteriolyitc mode of action ?

A

agent allows the body to recognise the invading organism- removes cells and total cells drop

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4
Q

Which antibiotic class targets cell wall ?

A

penicillin

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5
Q

Which antibiotic class targets protein synthesis ?

A

macrolides and tetracycline

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6
Q

Which antibiotic targets DNA synthesis >

A

fluoroquolines

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7
Q

Which antibiotic targets folate metabolism ?

A

sulphonamides

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8
Q

What is the structure of penicillins ?

A

beta lactam ring
heteroatomic ring with 3C and 1N
lactam is cyclic amide

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9
Q

What is benzylpenicillin ?

A

penicillin with benzene ring

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10
Q

What are the characteristics of benzylpenicillin ?

A

not very active against gram negatives
easily altered in the stomach- acid - changes the chemical structure
doesnt get to GI tract either

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11
Q

What does benzylpenicllin work against ?

A

narrow spectrum

works mainly against gram positives and a few gram negatives

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12
Q

What is amoxicillin ?

A

penicillin was altered to include an amino group
facilitates penetration of the outer membrane of gram negative
broad spectrum and more absorbed

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13
Q

What are beta lactamse resistant antibiotics ?

A

some forms of penicllin are resistant against beta lactamase

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14
Q

What is beta lactamase ?

A

bacteria produce beta lactamase
destroys Beta lactam ring of penicllin
some penicillins are resistant against

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15
Q

What is extended spectrum penicllin ?

A

effective against pseudomonas species

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16
Q

What are reverse spectrum penicillins ?

A

greater activity against gram negatives

than gram positives

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17
Q

What does transpeptidase do ?

A

catalyses formation of cell wall
cross links in peptidoglycan- pentaglycines
bacterial cell wall looses rigidity
cells swell and rupture

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18
Q

What do beta lactam antibiotics do to transpeptidase ?

A

they inhibit transpeptidase

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19
Q

What is the gram positive cell envelope like ?

A

thick peptidoglycan cell wall and cytoplasmic membrane

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20
Q

What is the gram negative cell envelope like ?

A

cytoplasmic membrane
periplasm
outer membrane

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21
Q

What is a peptidoglycan monomer made of ?

A

N-acetylmuranic acid
N-acetlyglucosamine
side chain of 4 amino acids

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22
Q

How do side chains of amino acids join together in peptidoglycan ?

A

via pentaglycines
cross links between amino acid side chains
glyceine with lysine

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23
Q

What is penicillin absorption like ?

A

vary when given orally

delayed release preparations can be given

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24
Q

What is penicillin distribution like ?

A

widely distributed

doesnt enter CSF- not good for meningitis

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25
Q

What is penicllin metabolism like ?

A

short half lives- need many doses

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26
Q

What is penicillin excretion like ?

A

90% kidney tubualr secretion

clearance reduced in neonates

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27
Q

What are adverse reactions to penicillin ?

A

rashes
fever
altered gut flora
blood clotting

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28
Q

What do sulphonamides target ?

A

folate metabolism and hence DNA synthesis

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29
Q

What is the folate pathway ?

A 
pABA
Folate
tetrahydrofolate
synthesis of thymidylate
DNA
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30
Q

Which enzymes work on the folate pathway ?

A

dihydroptrtoate synthetase from pABA to folate

dihydrofolate reductase from folate to tetrahydrofolate

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31
Q

Where do sulphonamides work ?

A

at dihydropteroate synthetase

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32
Q

What do fluoroquinolones target ?

A

broad spectrum- affecting gram positive and negative bacteria
targrt DNA replication - type II topoisomerases

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33
Q

What is DNA gyrase ?

A

regulates amount of torsional stress in DNA

facilitates movement of transcription and replication mechanisms through DNA helix

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34
Q

How is DNA gyrase targeted ?

A

quinolones inhibit in gram negatives

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35
Q

What does DNA topoisomerase IV do ?

A

homologue of gyrase
separates topologically linked daughter chromosomes
during terminal stage of DNA replication

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36
Q

How is DNA topoisomerase IV targeted ?

A

quinolones inhibit DNA topoisomerase IV in gram positives

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37
Q

What is the mechanism of action of sulphonamides?

A

act as false substrates - like P-aminobenzen will act on enzyme that makes folate- stop pABA binding
mimic pABA
inhibit production at dihydropteroate synthetase

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38
Q

Why are sulphonamides selective ?

A

human cells take up b9 and produce folic acid internally
bacterial cells cant take up folate so must make internally which is where sulphonamides act to stop cellular folate production

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39
Q

What is sulphonamide absorption like ?

A

80% of drug id given orally and absorbed from the stomach

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40
Q

What is sulphonamide distribution like ?

A

widely distributed including CNS

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41
Q

What is sulphonamide excretion like ?

A

in urine

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42
Q

What are some adverse reactions to sulphonamides ?

A

photosensitivity
stevens johnson syndrome
haemopoietic disturbances

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43
Q

What is the most effective administration of fluoroquinolones ?

A

oral

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44
Q

What is quinolone distribution like ?

A

well absorbed by GI tract

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45
Q

What is quinolone metabolism like ?

A

potent inhibitor of CYP1A2

taking quinolones will effect drugs that are metabolised by the same enzyme

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46
Q

What are adverse reactions to quinolones ?

A

hypersensitivity and GIT disturbance

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47
Q

What are macrolides ?

A

target bacterial ribsomes and protein synthesis

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48
Q

What size are eukaroyitc ribsomes ?

A

80S

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49
Q

What size are prokaryotic ribosomes ?

A

70S

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50
Q

What are the subunits in 70S ribsomes ?

A

50s and 30s

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51
Q

Where is the main site of protein synthesis in prokaryotes ?

A

50s sub unit of the 70s ribosome

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52
Q

Which part of protein synthesis do macrolides target ?

A

translocation part

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53
Q

What is translocation ?

A

forming the new peptide bond

ribsome will move along to form new peptide bonds

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54
Q

What do macrolides do ?

A

bind to site near RNA exit tunnel and cause peptidyl transferase to drop off

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55
Q

What does oral administration of macrolides require?

A

protected tablets to avoid inactivation by gastric juice

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56
Q

What is macrolide distribution like ?

A

diffuses to most tissues bit not BBB

crosses placenta

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57
Q

How are macrolides metabolised ?

A

by demethylation via the CYP3A4 drug

potentiate effects of other drugs

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58
Q

How are macrolides excreted ?

A

in the bile

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59
Q

What are adverse reactions to macrolides ?

A

GIT disturbances
auditory imapirment
cholestatic hepatits after erythromycin estolate

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60
Q

What are tetracyclines ?

A

target bacterial ribsomes

and protein synthesis

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61
Q

What do tetracyclines do ?

A

interrupt elongation phase

stop tRNA binding to ribosome

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62
Q

What is tetracycline absorption like ?

A

greater in fasting state

absorption inhibited by digestion of dairy products

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63
Q

What is tetracycline distribution like ?

A

distributed widely

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64
Q

What is tetracycline metabolism like ?

A

excreted via bile and kidneys by glomerular filtration

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65
Q

What is tetracycline excretion like ?

A

long half live

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66
Q

What is antibiotic resistance ?

A

ability of a microbe to resist effects of medication that could have previously been used to eradicate the microbe

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67
Q

How does antibiotic resistance occur ?

A
  1. population of bacterial cells that show variation- some are more resistant than others
  2. antibiotics used will kill bacteria but resistant strains will remain - antibiotics select for resistant strains
  3. Resistant bacteria multiply and resistance spreads
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68
Q

What is intrinsic resistance ?

A

innate property of bacteria seen in all strains

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69
Q

Why are gram negatives more resistant to B lactams ?

A

cell envelope is different

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70
Q

Why are gram positives resistant to vancomycin ?

A

too large to cross cell membranes

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71
Q

What is acquired resistance ?

A

drug resistance is selected for by antibiotics

use of drug leads to genes encoding resistance

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72
Q

What is cross resistance ?

A

resistance to 1 antibiotic leads to resistance to another

antibiotics often in the same class

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73
Q

What is multi resistance ?

A

resistance to several via independent mechanims

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74
Q

What were the FAA plates with vancomycin and neomycin selecting for ?

A

fusobacterium - it is resistant to vancomycin and neomycin

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75
Q

Why is fusobacterium resistant to vancomycin and neomycin ?

A

intrinsically resistant

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76
Q

Why is fusobacterium resistant to vancomycin ?

A

vancomycin is a large glycopeptide

cant cross gram negative membrane

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77
Q

Why is fusobacterium resistant to neomycin ?

A

an aminoglycoside
targets ribosomes
requires an electron transport chain to be taken up
anaerobic bacteria like aminoglycosdies dont have an electron transport chain- cant take up neomycin

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78
Q

What is VISA ?

A

vancomycin insensitive S aureus

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79
Q

What is CA MRSA ?

A

community acquired MRSA

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80
Q

How does acquired resistance spread ?

A

through genetic transfer

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81
Q

What is vertical gene transfer ?

A

between generations in binary fission

resistant strains passed on to next generation

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82
Q

What is horizontal gene transfer ?

A

between cells

one strain gets resistance and passes on to others via transformation, transduction and conjugation

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83
Q

How does acquired resistance start ?

A

through mutations

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84
Q

What does a chromosomal mutation do ?

A

results in genetically altered population

DNA is altered and provides an evolutionary advantage

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85
Q

What is transformation ?

A

DNA taken up into bacterial cell from the environmrtn
free DNA from lysis - released into environment (ECM)
genetically similar bacteria take up DNA

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86
Q

What is transduction ?

A

DNA transmitted via bacteriophages

DNA picked up by virus and transferred to another cell

87
Q

What is conjugation ?

A

between a donor cell with a conjunctive plasmid and a recipient without
via a pilus - only donor has a pilus

88
Q

What are the 3 mechanisms of antibiotic resistance ?

A

1- modification of the antibiotic to inactivate it
2- Modification of the target so the antibiotic doesnt work
3- Sequester the antibtiotic from the target to prevent it reaching the target

89
Q

How were gram negative bacteria intrinsically resistant to early penicillin ?

A

penicllin not permeable through membrane
efflux pumps- sequester
Beta lactamases encoded which break beta lactam ring

90
Q

How did acquired resistance come about in S. Aureues ?

A

plasmid boune beta lactamases- modify antibiotic

modification of the mecA gene- encodes for pencillin binding protein- reduced binding to beta lactams

91
Q

What are beta lactamases ?

A

they are modified pencillin binding proteins
bind to beta lactam ring
and hydrolyse it

92
Q

How can some beta lactamases be inhibited ?

A

by clavulanic acid

augmetnin- amoxicillin and clavulanic acid

93
Q

What are carbopneomes ?

A

potent beta lactams

94
Q

What is NDM1 ?

A

new delhi metallo beta lactamase
break down carbaponemes
gene that encodes it is present on a plasmid which can be transferred between bacteria like E.coli in dental tourism

95
Q

How can there be a reduced concentration of antibiotic in the periplasm or cytoplasma ?

A

reduced import due to outer mebrane

increased export via efflux pumps

96
Q

Why can their be increased export of a drug ?

A

antibiotic specific drugs

multidrug efflux pumps

97
Q

What are oral biofilm antibiotic resistance mechanisms ?

A

antibiotic reaction with ECM- modifes antibiotic
slow growth rate in plaque
exclusion of drug by matrix
up regulation of efflux pumps

98
Q

What are the 3 mechanisms of biofilm resistance ?

A

slow penetration
resistant phenotype
altered microenvironment

99
Q

What does slow penetration mean ?

A

antibiotic cant penetrate surface layers

antibiotic deactivated by beta lactamase on membranes

100
Q

What are persisters ?

A

some bacteria differentiate into protected phenotype

these are persisters

101
Q

How can altered microenvironment lead to resistance ?

A

microscale gradient of nutrietns and waste can antagonise antibiotics

102
Q

What are some factors that have lead to spread of antibiotic resistance ?

A

excessive and prolonged use in chronic illnesses
over counter availability
animal feeds
medical tourism

103
Q

What are the most common antibiotics used ?

A

penicillins
tetracyclines
macrolides

104
Q

Why do dentists over prescribe antibiotics ?

A 
time pressure
lack of up to date knowledge 
miscocneption 
demand 
poor training 
patient pressure
105
Q

What are common errors in prescrbing antibiotics ?

A

unecessary use
inappropriate dose
incorrect length of treatment
failure to check MH

106
Q

How can we treat bacterial dental infections ?

A 
local measures - before anything else
drain pus 
tooth extraction 
access and drain root canals 
debride perio pockets
107
Q

What is the carriage of Staphylococcus aureus ?

A

30 %

anterior nares, throat and groin

108
Q

Where does each CFU originate from ?

A

from 1 cell

109
Q

Why is the number of CFU not the same as the number of cells ?

A

dead cells in CFU

each cell divides

110
Q

What type of antibiotic is methicillin ?

A

broad spectrum

111
Q

How did MRSA become resistant ?

A

acquird the mecA gene that encodes the PBP2a

112
Q

What does PB2A do ?

A

allows transpeptidase activity in the presence of methicillin

113
Q

Why are gram negative bacteiria resistant to vancomycin ?

A

intrinsic resistance through LPS

vancomycin is a large molecule

114
Q

What is amoxicillin ?

A

moderate spectrum
effective against gram positve
limited effectiveness agaisnt gram negative

115
Q

What is metronidazole ?

A

active against gram positive and gram negative

116
Q

What is clavulanic acid ?

A

binds to beta lactamase enzyme that makes bacteria resistant - stops it hydrolysing the beta lactam
mixed with amoxicillin to make augmentin

117
Q

How do you work out the MIC and the MBC ?

A

broth culture of bacteria
make dilutions of antibiotics
add bacteria
incubate overnight

118
Q

What is the MIC ?

A

minimum inhibitory concentration

min conc needed to inhibit growth of bacteria

119
Q

What is MBC ?

A

minimum bacteriocidal concentration
concentration needed to kill bacteria
difficult to distinguish between killing and inhibiting

120
Q

What are MIC and MBC useful for ?

A

drug efficacy

resistance

121
Q

What is the zone of inhibition ?

A

diameter relates to the sensitivity of the bacteria to the antibiotic

122
Q

What are bacteria in the ZOI known as ?

A

breakout colonies

they have resistance to the antibiotic

123
Q

What makes staph aureus produce golden colonies ?

A

has a pigment called staphloxanthin

protects cells from oxidate stress

124
Q

How can we distinguish between staph aureus and epidermidis ?

A

epidermidis makes white colonies

aureus has postive catalase and DNase test

125
Q

In what form does fluoride enter cells ?

A

HF - uncharged so passes membrane

126
Q

How is vancomycin absorbed and why is this significant in treamtent of clostridium dificile ?

A

vancomycin is poorly absorbed in the gut - keeps the drug at site of infection of the enteric bacterium

127
Q

How does fluoride prevent caries ?

A

reduces demineralisation
promotes remineralisation
inhibit cariogenic bacteria

128
Q

What is the mineral component of dentine and enamel ?

A

impure calcium hydroxyapatitte

biological apatite

129
Q

How does fluoride make enamel less soluble ?

A

fluoride replaces the hydroxyl groups in the centre of the crystals making it less soluble
also fills gaps left by hydroxyl groups

130
Q

What is the structure of the unit cell ?

A

calcium forms columns
and makes calcium triangles stabilised by phosphate
OH ions are very large and polar so are displaced
dispalced are exposed and can be exchanged

131
Q

Replacing the hydroxide ions in enamel with fluoride ions creates what ?

A

calcium fluorapatite

132
Q

Where does fluoride incorporate in the tooth ?

A

in the outer layers
pits and fissures
fluoride distribution is uneven

133
Q

Why do pits and fissures hold more fluoride ?

A

pits and fissures have more plaque so theplaque is able to hold the fluoride close to the tooth
these areas have more dissolution leaving only fluorapatite which remineralises

134
Q

What happens with age to the fluoride distribution in teeth ?

A

fluoride in different areas of the tooth changes

135
Q

What is the process of enamel remienralisation ?

A

apatite dissolves in acidified plaque liquid raising the local concentration of Ca P and F
CFA forms
CFA has a lower solubility

136
Q

What are the practical applications of fluoride ?

A

fluoride toothpastes increase local F

Acidulated phosphate fluoride - makes acidic conditions where HFA will remineralise - more stable

137
Q

When is fluoride uptake by bacteira the highest ?

A

in acidic pH -pKa is 3.45

138
Q

How does fluoride enter bacteria ?

A

as HF which is small and uncharged

pass through membranes

139
Q

What happens to the pH of plaque fluid in a cariogenic challenge

A

pH lowered

140
Q

What happens when HF is taken up by bacteria ?

A

bacterial cytoplasm is neutral so it favours the dissociation of HF- release fluoride ions

141
Q

What does fluoride to do S mutans ?

A

inhibits growth and acidogenicity

142
Q

What effect does fluoride have on enzymes ?

A

fluoride binds to specifc sites on enzymes and inhibits them

143
Q

Give some examples of enzymes that fluoride inhibits ?

A 
urease
arginase dehydrolase 
enolase
F ATPasse 
Pyruvate kinase
catalase
144
Q

What is the role of enolase ?

A

bacterial glycolysis

glucose uptake

145
Q

What is the role of F ATPase ?

A

removes H from the cell

146
Q

What is the role of pyruvate kinase ?

A

glycolysis

147
Q

What does inhibting catalase do ?

A

limits the ability of the organism to deal with the oxidate stress from Hydrogen peroxide

148
Q

What does fluoride do with metals ?

A

fluoride ions bind to metals to make complexes
complexes bind to enzymes to stimulate/inhibit them
enzymes require metal co factros but they have now been removed

149
Q

How does fluoride act as a transmemebrane proton carrier ?

A

reduced uptake of key nutrients and export of macromolecules

150
Q

Is fluoride resistance seen ?

A

not clinically

in some strains in labs

151
Q

When is fluorie binding to enzymes enhanced ?

A

in acidification

152
Q

What is the effect of inhibiting F ATPase ?

A

protons arent removed from the cell

reduced acudurcity

153
Q

What are some characteristics of fluoride resistant species ?

A

higher F ATPase activity
stronger enolase activity and higher glucose uptake
fluoride exporters

154
Q

What are standard infection control procedures in dentistry ?

A 
hand hygeine 
PPE
sharps safety
sterilisation and disinfection 
waste management 
screening and vaccines
155
Q

What are examples of infectious agents ?

A

blood bourne virus - HIV and HepB
respiratory virus - infleuenza and cold
bacteria- mycobacterium TB, MRSA, Legionella
prions

156
Q

Which types of species have a greater resistance to destruction ?

A

prions
spores
mycobacterium

157
Q

Which species have a low resistance to destruction ?

A 
enveloped virus (HepB)
gram positive bacteria - strep, staph and enterococcus
158
Q

What are the 3 types of transmission ?

A

nosocomial- hospital- MRA
iatrogenic- due to physician/therapy- chemotherapy
idiopathic- unknown cause

159
Q

What does transmission require ?

A

source of infection - person, contaminated instrument
vehicle - blood,saliva
route -

160
Q

What are the sources of infection ?

A

overtly infected people
people incubating a disease- prodromal stage - like measles
health carriers- convalescent carriers are reservoirs of infection or asymptomatic carriers
environmental microorganisms- legionella
normal commensal flora- staph aureus and epidermidis

161
Q

Who are more prone to infections ?

A

immunocompromised patients

162
Q

What are the vehicles of transmission ?

A

blood- HIV and hepB
saliva- epstein barr - also if blood is in saliva
direct skin contact- stpah
objects- crubs and instrumenrs

163
Q

What are the routes of transmission ?

A 
in utero 
inhalation 
ingestion 
injection 
implantation 
inunction
164
Q

What is in utero transmission ?

A

placenta is a barrier for most microbes except cytomegalovirus and rubella

165
Q

What is inhalation ?

A

aerosol droplets

inhale strep pyogenes and TB

166
Q

What is ingestion ?

A

food drink become infected
instruments in mouth can introduce
strep pyogenes and TB

167
Q

What is implantation ?

A

trauma to mucosa can implant microorganisms into tissues

stap epidermidis and aureus

168
Q

What is inunction ?

A

microbes driven into tissue by open wounds and rubbing

169
Q

What is injection ?

A

biting - plasmodoum-malaria

needle stick

170
Q

Which pathogens cane be inhaled ?

A 
pneumonic plague- yersinia pestis 
TB- can be resistant to antibiotics 
infleunza- coughing 
legionnaires disease-
SARS
171
Q

Where can you find legionnella penumophilia ?

A

A/C
dental water lines
water lines

172
Q

How can we keep surface clean ?

A

disinfection of surfaces

single use instruments

173
Q

What is sterilisation ?

A

killing/removal of viable microorganisms

174
Q

What is disinfection ?

A

reduction in viable microorganisms to a point where infection risk is acceptable

175
Q

What is the formula for efficiency ?

A 
N=k/CT
N= number of microoganims 
K- constant 
C- cocnetration 
T- time applied
176
Q

What does K depend on ?

A

species
physiological state
organic material- clean before disinfection

177
Q

What is accepted as sterile ?

A

less than 1x106 chance of a single microorganism being present

178
Q

What are methods for disinfection ?

A

boiling water - kills bacteria not spores
pasteurisation- heat to 66/71- kills TB but not heat resistant
chemical- glutaraldehyde, chlorine , alcohol, chlorhexidine

179
Q

What does the functionality of chemical disinfectants rely on ?

A

concentration
temperature
pH
chemicals can be toxic and corrode instruments

180
Q

What are the methods of sterilisation ?

A 
dry heat-oven 
moist heat- autoclave
radiation-cobalt 60- for single use 
gases0 s02
filtration
181
Q

What is the process of autoclaving ?

A

high pressure saturated steam

121 for 15 minutes

182
Q

How do we safeguared agaisnt prion disease ?

A

endodontic files are single use

183
Q

Do prions have a nucleic acid ?

A

no

184
Q

What is risk ?

A

the probability an individual will develop a disease in a particular time period
usually expressed as a percentage

185
Q

What is risk factor ?

A

increases the likelihood that an individual will develop a disease
can be modified or immutable
can be part of the causal pathway

186
Q

What is a risk determinant ?

A

risk factor that cant be modified

187
Q

What is a risk marker ?

A

associated with the disease but not in the causal pathway

188
Q

What are host risk factors for periodontitis ?

A 
age 
genetics 
host response 
illness
local plaque retentive factors 
occlusion
189
Q

What are environmental risk factors for periodontitis ?

A 
smoking 
poor OH
nutrition
drugs- can impact on saliva 
dental attendance
190
Q

What are bacterial risk factors for periodontitis ?

A

plaque composition- red complex bacteria

plaque amount

191
Q

What are social risk factors for periodontitis ?

A

socio economic status
income
attitude
education

192
Q

What is the odds ratio ?

A

represents the odds that an outcome will occur given a particular exposure compared with the odds of not having the exposure

193
Q

What does it mean if the OR=1 ?

A

exposure doesnt affect outcome

194
Q

What does it mean if OR>1 ?

A

exposure associated with higher odds of outcome

195
Q

What does it mean if OR<1 ?

A

exposure associated with lower odds of outcome

196
Q

What is the odds ratio used for ?

A

comparing if an exposure is a risk factor

comparing the magnitude of risk

197
Q

How can you test the significance of the odds ratio ?

A

p value

198
Q

What is the advantage of assessing the risk at population level ?

A

targeted at risk populations

199
Q

What is the advantage of assessing risk at an individual level ?

A

treatment and preventitive strategies specific to the individual

200
Q

How can we assess individual risk ?

A

patient history
clinical examination
biological assay

201
Q

What is the validity of a test ?

A

test measures what it is intended to measure

202
Q

What is the reliability of a test ?

A

test is consistent when used at different time

203
Q

What is the quantifiability of a test ?

A

can be analysed statistically

204
Q

What is the sensitivity of a test ?

A

true positive rate

ability of a test to pick up all individuals who have the disease

205
Q

What is the specificity of a test ?

A

true negative rate

proportion of people who have false negatives

206
Q

Which periodontal markers can be assessed ?

A 
pathogenic bacteria
host response factors
tissue breakdown factors
host enzymes
inflammatory mediators
207
Q

What does the BANA test measure ?

A

proteolytic enzyme activity due to
p.gingivalis
T.Forsytha
T.denticola

208
Q

Give some antimicrobials used in the UK ?

A

iodine
chlorhexidine
SLS
triclosan

209
Q

What are the characteristics of chlorhexidine ?

A

cationic- attracted to the negative charge of phospholipids in cell wall
has a high substantivity

210
Q

What are the benefits of Chlorhexidine ?

A

plaque growth almost inhibited

gingivitis inhibited

211
Q

What are the problems of chlorhexidine ?

A

tooth staining

allergy can be severe

212
Q

What are the characteristics of tirclosan ?

A

lower substantivity than chlorhexidine
lipid soluble - penetrate skin and mucosa
reduces inflammation

213
Q

How does triclosan act as a broad spectrum antimicrobial ?

A

targets lipid synthesis - enoyl reductase
inhibits glycolysis - pyruvate kinase and lactate dehydrogenase
inhibits Proton ATPase- cellular pH falls

BDS stage 2 (28 decks)

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