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Microbiology for dentists > Theme III: Control of microorganisms > Flashcards

Theme III: Control of microorganisms Flashcards

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Biology 101 flashcards
1
Q

Difference between colony forming units and number of cells in a population

A
  • CFU are only viable cells, not dead
  • colonies may join together
  • some may not form a colony or be visible
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2
Q

What agar is staphylococcus aureus grown on and how can it be identified. Other techniques to identify it.

A
  • Grown on high salt agar (Mannitol agar). Gold colour because it produces a gold pigment - staphyloxanthin.
  • Also by coagulase, catalase, DNAase tests
  • alpha hameolysis on blood agar so green tinge
  • Gram positive so purple gram stain
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3
Q

What is methicillin and why is methicillin Resistant Staphylococcus aureus significant. What gene is involved in resistance.

A
  • It is a narrow-spectrum Beta lactam antibiotic of the penicillin family. It targets the transpeptidase protein that is involved in the cross linking in peptidoglycan formation.
  • S. aureus has mecA gene that encodes penicillin binding protein 2a (a transpeptidase involved in peptidoglycan formation)
  • Modification of the mecA gene reduces binding to B lactams, makes them resistant to methicillin.
  • PBP2a has lower affinity for methicillin so is less sensitive to the action of methicillin.
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4
Q

What is the difference between minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) for antibiotics. What is used for antibiotics

A
  • MIC - lowest conc of an antibiotic required to inhibit bacteria growth, so will be lower than MBC as this is how much it takes to kill.
  • We want least possible side effects so MIC is used and allows the immune system to do the rest of the bacteria killing
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5
Q

What do tetracycline antibiotics target

A

-small 30S ribosome during translation so targets elongation phase of protein synthesis

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6
Q

Where does hydoxyfluoride accumulate on the tooth

A
  • Pits and fissures. Plaque either holds F close to the enamel.
  • The outer layer of the enamel, to protect inner layers
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7
Q

Tests for staphylococcus epidermis

A
  • Has no coagulase

- Gram positive so purple on gram stain

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8
Q

What form of fluoride enters the bacteria cells

A

-Hydrofluoric acid. It is uncharged so can cross the membrane

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9
Q

What antibiotic is used for treating anaerobic infection

A

-Metranzidadol

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10
Q

Describe what bactericidal, bacteriostatic and bacteriolytic antibiotics are. Give examples

A
  • Bacteriostatic = inhibits growth of bacteria. Held at a stationary phase (sulphonamides, tetracycline, macrolides)
  • Bactericidal = kill all viable bacteria. (B lactam, fluoroquinolone)
  • Bacteriolytic = kills viable cells and removes all dead cells
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11
Q

How do penicillins work.

A
  • Contains a beta lactam ring that interacts with peptidoglycan of gram positive bacteria which weakens the cell wall and causes it to swell and rupture.
  • It inhibits transpeptidase enzyme, which is involved in the cross linking of NAG and NAM amino sugars into glycol chains
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12
Q

What is beta lactam resistance. What drug can inhibit this enzyme

A
  • Bacteria produce B lactamase which hydrolyses the Beta lactam ring in penicillin. Therefore the penicillin is ineffective at destroying peptidoglycan
  • Beta lactamase can be inhibited by clavulanic acid. This can be given along side amoxicillin, in order to prevent resistance. (co-amoxiclav)
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13
Q

How do sulphonamides work

A
  • Inhibit folate metabolism and therefore DNA synthesis of bacteria
  • Binds to dihydropteroate synthetase
  • Bacteriostatic
  • Not used anymore due to photosensitivity, haematopoietic disturbances, stevens Johnson syndrome
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14
Q

How do fluoroquinolones work

A
  • Target DNA replication via Type II topoisomerase so inhibits DNA synthesis
  • Inhibits DNA gyrase (supercoiling) and DNA topoisomerase IV (2 daughter chromosomes don’t separate)
  • Bacteriocidal
  • Rarely used due to hypersensitivity and GI disturbances
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15
Q

How do macrolides work. Bacteriostatic or bactericidal

A
  • Bind to large 50S ribosomal subunit so blocks translocation
  • Bacteriostatic
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16
Q

What folate biosynthetic enzyme does sulphonamide target to produce antimicrobial effects

A

dihydropteroate synthetase

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17
Q

Is the folate antagonist trimethoprim bacteriostatic or bactericidal? Why is this?

A

-Bacteriostatic. Stops replication but does not kill the bacteria

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18
Q

Name the amino sugars essential for the formation of the peptidoglycan bacterial cell wall

A
  • NAM = N-acetylmuramic acid

- NAG =N-acetylglucosamine

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19
Q

What enzyme do B lactam antibiotics target

A

-Transpeptidase

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20
Q

What is antibiotic resistance. How does it develop

A

-ability of a microbe to resist the effects of medication that could perviously eradicate it

  • bacteria in biofilms mutate constantly and these mutant cells are more resistant than others. Biofilms also contain slow growing resistant persister cells that are also resistant.
  • After a course of antibiotics, susceptible cells die, while these resistant cells can survive and continue to grow with less competition. Shift in population causes infection
  • more microbials= increased chance of these resistant cells remaining and replicating, causing resistance and infection.
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21
Q

What factors affect increased resistance

A
  • inappropriate prolonged use of antibiotics - over prescribing
  • people not finishing full courses. Take them at later dates
  • Increasing use due to ageing population
  • Used in agriculture
  • International travel spreads resistance
  • Poor infection control and hygiene
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22
Q

How to combat antimicrobial resistance

A
  • Prevent infection in the first place by promoting infection control, immunisation
  • Monitor resistance by public health systems
  • Monitor use of antimicrobials - make sure prescribed appropriately
  • Develop new antimicrobials and agents (however companies don’t gain much money from these drugs as they are not long term drugs)
  • no over the counter antibiotics
  • educate the public.
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23
Q

Difference between antibiotic cross resistance and multi resistance

A
  • Cross resistance = resistance to 1 antibiotic leads to resistance of other antibiotics in the same class with similar mechanisms
  • Multi resistance = resistance to several antibiotics in different classes via independant mechanisms
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24
Q

How do bacteria gain resistance (Intrinsic and acquired)

A
  • Intrinsic = innate characteristics that make them naturally resistant which is seen in all strains of the species. Eg. Vancomycin have large membrane so drug cannot enter. having thick peptidoglycan so less likely to die from B lactam antibiotics
  • Acquired = gain resistance genes by chromosomal mutations or horizontal genes transfer. Only seen in some strains.
25
Q

Describe the 3 types of horizontal gene transfer

A
  • Transformation: When a cell dies it releases its DNA into the environment. This donor DNA is taken up by recipient cell
  • Transduction: DNA transmitted via bacterial viruses (bacteriophages) that infect recipient cell
  • Conjunction: DNA plasmid transferred via pili. Requires direct contact
26
Q

Give examples of properties that make bacteria resistant to antibiotics

A
  • Lack of permeability: (eg. Vanomycin has thick membrane so antibiotics cannot gain entry)
  • Produce enzymes that degrade the antibiotics (B lactamase hydrolyse Beta lactam)
  • Cell pumps out antibiotic via drug efflux pumps
  • Alter the structure of drug target (like ribosomes) so drug cannot bind
  • Alters drug’s metabolic pathway
  • alterations in mecA gene which encodes Penicillin binding protein 2a (a transpeptidase), which reduces binding to B lactams
27
Q

What percentage of antibiotics prescribed in NHS is by dentists. What is the most prescribed antibiotic by dentists and what is it usually used for

A

5%, so a lot

  • Amoxicilin is a penicillin that breaks down peptidoglycan
  • Treats abscesses, sinusitis, pericoronitis if it is causing systemic infection and after local measures such as draining have failed.
28
Q

What makes viruses hard to target using drugs, compared to bacteria

A
  • fewer drug targets, less cellular properties for drugs to act on
  • Replicate in host cells and use their metabolic machinery so drugs need to be selective so don’t cause damage to host (selective toxicity)
  • Viruses can be latent so not actively replicating so cannot be killed unless replicating
  • Rate of replication or mutation can be high so hard to disrupt
  • Incubation of viruses can be short so virus would already have caused damage before showing symptoms
  • genetic variability
29
Q

What is the main target of antiviral drugs

A

-Viral replication: binding & entry, uncoating, transcription, nucleic acid synthesis, translation, assembly of functioning proteins, release of the virus

30
Q

What is acyclovir used for treating and how does it work

A
  • Treats the acute phase of Human herpes virus (HSV1 & 2, HHV 3)
  • Less effective on latent stage as it is not replicating
  • It blocks viral replication. It is a nucleoside analogue so mimics a nucleotide and blocks others being added in the DNA strand. Chain termination so no elongation
31
Q

How is acyclovir activated

A
  • Phosphorylated by thymidine kinase in the virus so cannot be activated in uninfected cells
  • Activated into acyclovir triphosphate
32
Q

How does HAART manage HIV. What 5 things does it target

A

-Drugs suppress replication but cannot eradicate it

  • Highly active antiretroviral therapy (HAART) uses a combination of drugs to target different things:
    1. Inhibition of CCR5 receptors on T cells (blocks entry)
    2. Fusion inhibition (prevents entry)
    3. integrase inhibitors prevent the insertion of of viral genome into host
    4. Reverse transcriptase inhibitors (DNA replication)
    5. protease inhibitors (protein synthesis)
33
Q

What 2 types of drugs can treat Hep B and C and how

A
  • Immunomodulator drugs: enhance the host’s immune response to infection to reduce progression but cannot eliminate.
  • Direct antiviral drugs (nucleoside analogues): target viral replication
34
Q

What 2 types of drugs can treat influenza.

A
  • Neuraminidase (Zanamivir and oseltamivir): prevent release of virus from cell
  • Amantadines inhibit the uncoating of viral RNA in an infected cell so inhibits replication
35
Q

What drugs have been used for treating SARS CoV2

A
  • Remdesivir: used early on in the pandemic. nucleoside analogue so causes chain termination but conflicting evidence
  • Molnupiravir: nucleoside analogue. Mimics 2 base pairs so tricks the virus so can cause lethal mutagenesis. Effective and safe
36
Q

Standard infection control procedures in dentistry

A
  • Hand hygiene: 20-30s for general procedure. Before & after patient contact, before and after treatment, after touching contaminated objects
  • PPE: gloves, mask, apron, eye protection (FFP3 mask for AGP)
  • Sharp safety
  • Disinfection & sterilisation
  • Surgery design
  • Ventilation
  • Monitoring & disinfecting waterlines
  • Waste management
  • Vaccines and screening
37
Q

What is the difference between disinfection and sterilisation. And the methods used

A
  • Disinfection causes reduction in viable organisms to the point where risk of infection is acceptable. Used for surfaces without saliva or blood. Heat, pasteurisation (66C), chemical disinfection
  • Sterilization kills all viable organisms. Autoclaving (doesn’t kill prions), radiation, gases, chemicals
38
Q

What types of bacteria can live in dental water lines

A

-Pseudomonads, legionella, pneumophila

39
Q

What are the 3 types of transmission of infectious agents (nosocomial, iatrogenic, idiopathic)

A
  • Nosocomial: acquired in a hospital
  • Iatrogenic: caused by medical examination or treatment
  • Idiopathic: of unknown cause
40
Q

What 3 things does transmission of infectious agents require. And give examples of each.
(6 types of routes)

A

1-Source of infection: patient incubating a disease, from environment, commensal microflora causing bacteraemia

2-A vehicle: blood, saliva, direct contact, objects.

3- A route: in utero, inhalation, ingestion, implantation (broken skin), inunction (skin to skin), injection

41
Q

What can be done to reduce infection risk during AGPs

A

-Ventilation, high volume suction, rubber dams, no pre-procedural mouth rinses, leaving enough time between patients so aerosols can settle and be disinfected

42
Q

What 3 ways does fluoride prevent caries

A

1-Reduces demineralisation: fluoride incorporated into outer layers, and in pits/ fissures. It can replace OH in calcium hydroxyapatite to make fluorapatite which is more stable and less acid-soluble

2-Promotes remineralisation: presence of fluoride in saliva speeds up crystal precipitation, even at low pH, forming HA to mineralise the enamel.

3-Inhibits cariogenic bacteria: low plaque pH converts F to hydrofluoric acid which is taken up by bacteria. F ions released inside the cell which decrease microbial growth, metabolism and acid production by inhibiting enzymes

43
Q

What affects can fluoride have on cariogenic bacteria

A
  • inhibits pyruvate kinase and other enzymes to inhibit glycolysis so reduction in nutrients and reduction in lactic acid production
  • inhibits ATP-ase proton pumps so less acidogenic
  • Inhibits urease so bacteria less acidoduric
44
Q

Explain outbreak, epidemic and pandemic

A
  • Outbreak = the occurrence of a large number of cases of a disease in a short period of time
  • Epidemic =the occurrence of a disease in unusually high number in a localised population
  • Pandemic= disease prevalent worldwide
45
Q

-What is influenza. Family of viruses. Symptoms. Structure.

A
  • The flu - seasonal infection
  • An acute respiratory infection caused by influenza viruses.
  • Part of the orthomyxoviridae family
  • Enveloped with 8 linear segments of RNA genome, with spike proteins (H and N)

-Symptoms: fever, muscle ache, drowsiness, cough. (no runny nose) Risk of serious secondary bacteria infection occurring.

46
Q

What does the different types of influenza depend on

A
  • Subtypes A - D depending on antigenicity of inner proteins.
  • Further classified depending on the spike glycoproteins on the surface: (eg. H1N1, H3N2)
47
Q

What spike glycoproteins are on influenza virus and what are their functions. How many varieties are there of each protein.

A
  • Haemagglutinin: facilitates attachment and entry into host cell. Binds to sialic acid. (18 varieties)
  • neuraminidase: facilitates exit from cell. (11 varieties).
48
Q

Explain antigenic drift and shift. How shift is caused and its impact in a population

A
  1. Antigenic drift: minor antigenic changes in the H and N spike proteins causing gradual change over time
  2. Antigenic shift: change in the subtype. So H & N change eg. from H1N1 to H3N2. Creates novel viruses where people are not immune to so susceptible to infection.
    - It occurs due to reassortment of RNA segments when 2 different viral strains from 2 different animals infect a cell of another animal.
49
Q

3 key influenza pandemics. When and their H and N class

A
  • Spanish flu = 1918-19. H1N1. Most devastating influenza pandemic of all time.
  • Asian flu = 1957. H2N2
  • Swine flu = 2009-10. H1N1
50
Q

What is risk, risk factor, risk determinant and risk marker. Mutable/modifiable factors. Social factors. (in relation to disease)

A
  • Risk: the probability an individual will develop a disease in a particular time period
  • Risk factor: factor that increase the likelihood that someone will develop a disease
  • Risk determinant: factor that cannot be modified- immutable (genetics, race, gender)
  • Modifiable risk factor: smoking, diet etc.
  • Social factors: socio-economic status, education, income, family history)
  • Risk marker: associated with disease risk but not necessarily on the casual pathway.
51
Q

what is the odds ratio (OR) for disease risk factors. What if the value of OR is equal or less that 1.

A

-Odds ratio represents the odds that an outcome (disease) will occur given a particular exposure (risk factor), compared to the odds occurring without the factor.

  • OR = 1: factor causes no effect to odds of outcome (health is maintained)
  • OR <1 factor is a risk factor for disease

**Lower the number, higher the risk.

52
Q

Difference between specificity and sensitivity of biological assays.

A
  • Sensitivity: how effective it is at detecting positive individuals. Proportion of true positives that go on to develop disease. Ability to correctly identify diseased.
  • Specificity: making sure there are no false positives. Proportion of true negatives that remain disease free. Ability to correctly identify non-diseased.
53
Q

What enzymes does fluoride inhibit

A
  • Enolase, urease, heme catalase & peroxidase, ATP-ase, phosphatase
  • inhibiting glycolysis so less acid production, and inhibiting pumping out of acid.
54
Q

How are gram negative bacteria, and strep aureus resistant to penicillin

A

-Gram-negative bacteria are intrinsically resistant to early penicillins due to:
lack of permeability through the outer membrane, multidrug efflux pumps, B-lactamases enzymes which can breakdown beta lactam.

-Acquired resistance in Staphylococcus aureus:
plasmid-borne, B-lactamase
modification of mecA gene encoding PBP2a, reduced binding to B-lactams (methicillin resistance)

55
Q

What makes biofilms so resistant to antibiotics

A
  • polymicrobial so lots of bacteria to kill
  • slow growing dormant persister cells. (Antimicrobials target cell division)
  • poor penetration through biofilm
  • antibiotic may be altered/ antagonised by waste products in the biofilm
  • B lactamase can deactivate penicillin
56
Q

SARS-CoV2. What receptors it binds to, and where. RNA or DNA. Structure. Alpha, beta, gamma or delta. initial and severe symptoms

A
  • ACE2 and TMPRSS2 in RS, GI, kidneys, vessels, tongue, saliva glands.
  • Single stranded positive RNA virus
  • enveloped. Helical nucleocapsid.
  • Beta coronavirus.
  • High infectivity that MERS and SARS but less fatal.
  • Initial respiratory disease: binding to epithelium in respiratory tract then replicates and travels to alveoli and causes damage.
  • Excessive dysregulated immune response to infection causes cytokine storm which spreads systemically. Fibrotic lungs, acute respiratory distress syndrome (ARDS), prolonged myocardial inflammation
57
Q

What are type A-D inluenza virus

A
  • Type A: common human infection. Only one that has caused epidemics/ pandemics
  • Type B: human infection. Mainly in children. Less severe outbreaks
  • C = causes mild illness
  • D = affects cattle
58
Q

Basic facts about SARS CoV, MERS CoV and SARS CoV2. (origins, year, deaths)

A
  • SARS CoV: China. Severe Acute respiratory Syndrome. 2002. Killed 800
  • MERS CoV: Middle Eastern Respiratory syndrome. Saudi Arabia. 2012
  • SARS CoV2: Wuhan, China. 2019.

Microbiology for dentists (5 decks)

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