Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Human Health and Disease I > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define prokaryotic cell and provide examples of prokaryotic organisms

A

Prokaryotic cell – a cell that do not contain a nucleus or membrane bound organelles.

Examples:

  • Bacteria
  • Archaea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the two basic forms of prokaryotic cell

A

Two basic forms of prokaryotic cell:

  • Bacteria:
    • Peptidoglycan cell wall for rigidity and shape
    • Cell membrane
    • Lack of organized nucleus but may have plasmids
    • May be parasites
  • Archaea:
    • Similar morphology to bacteria but no peptidoglycan
    • Similar metabolism and genetics to eukaryotes
    • No known archaea pathogens or parasites

No internal membranes or organelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Recall the basic prokaryotic (bacterial) cell structure (8 points)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define eukaryotic cell and provide examples of eukaryotic organisms

A

Eukaryotic cell – a cell which contains a nucleus and membrane bound organelles.

Examples:

  • Animals
  • Plants
  • Fungi
  • Protazoa (single-celled)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the 4 basic forms of eukaryotic cell

A

Four basic forms of eukaryotic cell:

Eukaryote cell structure – animal:

  • Typically smaller than plant cells (10-30 micrometres in length)
  • Phospholipid bilayer cell membrane with no cell wall
  • Various shapes: cuboidal, columnar, squamous, dendritic, etc.
  • Highly differentiated: nerve cell, muscle cell, epithelial cell, blood cells, etc.

Eukaryote cell structure – plant:

  • Typically larger than animal cells (10-100 micrometres in length) and cuboid in shape
  • Extra components of plant cell:
    • Plasmodesmata (communicating pores), chloroplasts, vacuole, cellulose cell wall.

Eukaryotic cell structure – fungal:

  • Yeast cells – unicellular
  • Key differences to animal cell and bacterial cell:
    • Chitin cell wall
    • Vacuole
    • Nucleus
    • Moulds – multiple hyphae

Eukaryotic cell structure – protozoa:

  • Single-celled eukaryote
  • Free living or parasite (not classified as animal, but exhibits animal-like behaviours: predation, motility)
  • Example: amoeba
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Recall the basic eukaryotic (animal) cell structure (12 points):

A

Eukaryote (animal) cell structure:

  1. Nucleus (contains genetic material)
  2. Nucleolus (synthesis of RNA/assembly of ribosome)
  3. Cell membrane (lipid bilayer with proteins and sugars)
  4. Cytoplasm (80% water, suspends organelles)
  5. Mitochondria (double membrane, supplies ATP for cell)
  6. Golgi apparatus (processes and packages proteins into vesicles)
  7. Smooth ER (lipid synthesis and metabolism)
  8. Rough ER (studded with ribosomes, protein metabolism)
  9. Ribosome (site of protein synthesis)
  10. Lysosome (contains enzymes, breakdown of waste products of cell)
  11. Peroxisome (contains catalase to reduce 2H2O2 → 2H2O + O2)
  12. Cytoskeleton (to give cell shape and mechanical resistance).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Compare bacteria, archaea, and eukarya with reference to the following 5 features:

  • Cell membrane
  • Gene structure
  • Internal cell structure
  • Metabolism
  • Reproduction
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Compare Gram-positive cell wall vs Gram-negative cell wall

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define virus and provide examples

A

Virus – obligate intracellular parasite:

  • Not cellular
  • Viruses contain DNA or RNA
  • Virus replicate only within living cells – use the cells ‘machinery’ to replicate
  • Some viruses (bacteriophages) directly infect bacterial cells

Examples:

  • HIV
  • Coronavirus
  • Influenza
  • Herpes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the basic structure of a virus

A

Virus structure:

  • Nucleocapsid:
    • Protein and genome complex – DNA or RNA
    • Three shapes:
      • Icosahedral e.g. Herpes
      • Helical e.g. Ebola
      • Complex e.g. HIV
    • May have a lipoprotein envelope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define prion and provide a key example

A

Prions – proteinaceous infection particles:

  • Not cellular
  • Do not contain DNA or RNA
  • Promotes refolding of native (host) proteins → pathology
  • Infect nerve cells

Key example – Ceutzfeldt-Jakob disease:

  • Transmissible spongiform encephalopathy
  • Humans who develop this disease will slowly lose the ability to think and to move properly and will suffer from memory loss and progressive brain damage until they can no longer see, speak or feed themselves.
  • Very difficult to destroy (even by standard sterilization techniques)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List the main oral habitats for microbes (7 points)

A

Oral habitats:

  1. Teeth
  2. Gingival sulcus
  3. Tongue
  4. Cheeks
  5. Hard palate
  6. Soft palate
  7. Tonsils.

Changes occur over time – deciduous teeth exfoliation, orthodontic appliances, prostheses.

Stagnation areas – occlusal fissures, poor restorations, misaligned teeth, orthodontic appliances, prostheses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Summarize the oral microbiome (4 points)

A

Oral microbiome (4 points):

  1. Bacteria – mostly bacterial (500-700 common species); ~50% culturable
  2. Fungi – yeasts (Candida albicans – esp. associated with dentures); filamentous and dimorphic fungi
  3. Viruses – Herpesviruses, Adenoviruses, Rhinoviruses, Papovaviruses, Orthomyxoviridae (influenza)
  4. Protozoa – Entamoeba gingivalis (amoeba prevalent in 95% patients with gingivitis).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the flora of the oral cavity

A

Gram-positive cocci:

  • Aerobic streptococci:
    • Streptococcus mutans, S. salivarius, S. anginosus, S. mitis
  • Anaerobic streptococci

Gram-positive rods and filaments:

  • Lactobacilli, Propionibacterium
  • Actinomyces

Gram-negative cocci:

  • Neisseria, Veillonella

Gram-negative rods – facultative anaerobes:

  • Haemophilus, Aggregatibacter, Eikenella, Capnocytophaga

Gram-negative Rods – obligate anaerobes:

  • Porphyromonas, Prevotella, Fusobacteria, Leptotrichia, Wolinella, Selenomonas, Treponema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain the 4 main factors affecting the growth of microorganisms in the oral cavity

A

Modulating factors affecting growth of oral microbiome – “SLAM”:

  1. Saliva and gingival crevicular fluid:
    • Flushing microbes
    • Complex mix of organic and inorganic components
    • Source of microbial nutrients (e.g. carbohydrates and proteins)
    • Growth inhibitions (e.g. lysozyme, lactoferrin, IgA)
    • Buffering capacity maintaining pH (acidic saliva favours cariogenic bacteria)
  2. Local environment
    • Moisture (i.e. mouth breathing in athletic population)
    • Local pH
    • Antimicrobial therapy
    • Diet (i.e. sugars)
    • Fluoride
  3. Anatomy – hard to clean areas:
    • Shape and alignment of teeth
    • Quality of restorations
    • Periodontal condition may favour proteolytic bacteria
  4. Microbial factors – composition of microbial flora and competition between commensal and pathogenic organisms (i.e. colonization resistance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe colonization resistance within the oral microbiome

A

Colonization resistance:

  • Commensal oral flora inhibits non-oral organisms
    • Competition for receptors for adhesion (e.g. to hard tissues)
  • Production of toxins - Streptococcus salivarius produce enocin which inhibits Streptococcus pyogenes
  • Production of metabolic products (e.g. acids which lower pH)
  • Use of metabolic products (e.g. Veillonella spp. - use acids produced by Streptococcus mutans)
  • Plaque biofilm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List some common bacterial, viral, and fungal infections of the oral cavity

A

Bacterial:

  • Caries, gingivitis, periodontitis, strep throat

Viral:

  • Herpes simplex type I

Fungal

  • Oral candidiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain the process of microbiological sampling and provide examples of specimens

A

Microbiological sampling

Aim: to assist the clinician in reaching a definitive diagnosis

Process (4 key steps):

  1. Clinical request
  2. Collection and transport of specimens
  3. Laboratory analysis
  4. Interpretation of the microbiology report

Outcome: clinician assisted in making treatment decision.

Avoid contamination of samples - difficult for oral specimens.

Examples of specimens:

  • Aspirate of pus from purulent infection
  • Deep gingival smear for acute ulcerative gingivitis
  • Rinse for quantifying oral Candida
  • Paper point samples for periodontal pockets for molecular identification (gene probing using PCR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the 3 main types of lab analysis of microbiological samples

A

Lab analysis of microbiological samples:

  1. Non-cultural methods:
    • Microscopy
    • Gene probing
  2. Cultural methods – not all microbes will grow in the lab:
    • Solid or liquid media to grow bacteria and fungi
      • Identify bacteria using biochemical tests or genotyping
    • Cultured cells to grow viruses (obligate intracellular parasites)
  3. Immunological methods:
    • Identify organisations using antibodies
    • Detect antibodies in serum – important if microbes hard to grow.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the qualitative and quantitative susceptibility testing methods

A

Qualitative susceptibility test method (zones of inhibition):

  • Agar plate with paper discs impregnated with antibiotic on the plate
  • After incubation, growth of bacteria is observed
  • Areas around the antibiotic disc where no bacterial growth can be seen are known as ‘zones of inhibition’.

Quantitative susceptibility test method (minimum inhibitory concentration)

  • Tests minimum inhibitory concentration (MIC) of antimicrobial agent needed to inhibit growth of microorganism (e.g. MIC50 ⇒ conc. for 50% inhibition)
  • Microorgansms are cultured in a 96-well plate with a concentration gradient of antimicrobial agent
  • Where wells do not turn cloudy, this indicates inhibition of microorganism growth and the specific minimum concentration of antimicrobial agent can be determined quantitatively
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Recall the classification of Gram-positive bactera

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Recall the classification of Gram-negative bactera

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe aerobic, facultative, and anaerobic growth of bacteria

A

Aerobic, facultative, and anaerobic growth:

  • Obligate aerobe – oxygen essential for growth: Mycobacterium tuberculosis
  • Facultative anaerobe - grows in the presence or absence of oxygen: mutans streptococci
  • Obligate anaerobe - grows only in the absence of oxygen: Porphyromonas gingivalis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain bacterial spore formation

A

Bacterial spore formation – hard to kill (contains DNA, cell membrane, some cytoplasm, water, keratin coat):

Occurs in response to adverse conditions e.g. scarce nutrients: Bacillus and Clostridium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the properties of biofilm (4 points)

A

Properties of biofilm:

  1. Bacteria growing in biofilms have different properties to the same bacteria growing planktonically (i.e. free-floating in bodily fluids)
  2. Biofilms are more resistant to antibiotics and chemotherapeutic agents
  3. Mechanical cleansing effective at removing biofilm:
    • Subgingival cleansing – ultrasonic debridement
    • Supragingival cleansing – toothbrushing
  4. Disruption of biofilm not always clinically appropriate:
    • Pseudomonas aeruginosa in cystic fibrosis
    • Legionella in stagnant water pipes
    • Removal of a central venous catheter with suspected colonization of S. epidermidis (removal from vein can result in shear force which breaks off biofilm adhered to the plastic → venous bacterial shower in veins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define oral biofilm (9 points)

A

Oral biofilm (i.e. dental plaque) is an adherent mass of diverse micro-organisms in a muco-polysaccharide matrix. It cannot be rinsed off but can be removed by brushing.

Biofilms are made up of symbiotic communities of different micro-organisms.

They develop in a structured way and are spatially and functionally organized.

The species within communicate with each other (i.e. quorum sensing).

They are less susceptible to host defences and antimicrobial agents than planktonic bacteria.

Resident bacteria can dampen the immune response via communication with host mucosal cells

If this balanced coexistence breaks down disease can occur (e.g. caries, gingivitis, periodontitis).

It forms in 5 key stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List the key consequences of oral biofilm formation (3 points)

A

Consequences of oral biofilm depends on niche site – 3 key dental plaque-mediated diseases:

  1. Caries
  2. Gingivitis
  3. Periodontitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the risk factors for oral biofilm formation

A

Risk factors for oral biofilm formation:

  • Poor oral hygiene (↓mechanical disturbance, ↓Fl- load)
  • Anatomical areas protected from host defences and where mechanical action fails to remove bacteria (i.e. niche sites):
    • Occlusal fissure (leading to occlusal caries)
    • Interproximal space (leading to interproximal cares)
    • Cervical surface (esp. if root exposed, leading to root caries)
    • Gingival sulcus (leading to acute gingivitis)
    • Periodontal pockets (progressing from gingivitis to periodontitis)
  • Increased risk of oral biofilm formation where there is reduced oral function:
    • ↓​Salivary flow rate
    • ↓Muscular movement
    • ↓Immune mechanisms
    • ↓Commensal microflora competition
  • Reduced function may be as a result of increased age, disease, drug-induced, congenital abnormality, trauma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

List the key stages of oral biofilm formation (5 points)

A

Key stages of oral biofilm formation:

“Adhesive Colonies Are Created Dynamically”

  • Adhesion – conditioning film
  • Colonization – linking film
  • Accumulation – co-aggregation and re-conditioning film
  • Complex community – further accumulation and maturation film
  • Dispersal – remodelling and shedding film
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Key stages of oral biofilm formation – stage 1

Describe the following oral biofilm formation stage:

Adhesion – conditioning film(3 points)

A

Adhesion – conditioning film:

  • Salivary glycoproteins selectively adhere to naked tooth surface to form acquired pellicle – helps to protect teeth from acids
  • Planktonic microbial cells reversibly adhere to acquired pellicle via a balance of electrostatic attraction (i.e. van der Waals forces) and electrostatic repulsion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Key stages of oral biofilm formation – stage 2

Describe the following oral biofilm formation stage:

Colonization – linking film (4 points)

A

Colonization – linking film:

  • Irreversible adhesion and linking up (polymer bridging) between pioneer species and acquired pellicle to form microcolonies on acquired pellicle
  • Key pioneer species of microcolonies: S. oralis group – S. sanguinis, S. oralis, S. mitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Key stages of oral biofilm formation – stage 3

Describe the following oral biofilm formation stage:

Accumulation – co-aggregation and re-conditioning film (4 points)

A

Accumulation – co-aggregation and re-conditioning film:

  • Additional early colonizers co-aggregate to the pioneer species to increase diversity and re-condition biofilm (microbial composition varies between niches)
  • Bacteria communicate with each other (via quorum sensing) and multiply in ecological succession → further reconditioning to reflect the local changes of niche environment
  • Quorum-sensing molecules:
    • Secretion of extra polysaccharide matrix
    • Modulation of bacterial metabolism deep in the biofilm
    • Production of virulence factors e.g. drug-destroying genes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Key stages of oral biofilm formation – stage 4

Describe the following oral biofilm formation stage:

Complex community – further accumulation and maturation film (4 points)

A

Complex community – further accumulation and maturation film:

  • If left undisturbed, there is continued accumulation (microbial succession, growth and an increased species diversity by late colonizers) resulting in a ‘mature’ or climax type of biofilm within a week
  • Overall composition of biofilm complex depends on the niche:
    • Occlusal fissure
    • Interproximal space
    • Cervical surface (esp. if root exposed)
    • Gingival sulcus
    • Periodontal pocket.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Key stages of oral biofilm formation – stage 5

Describe the following oral biofilm formation stage:

Dispersal – remodelling and shedding film (6 points)

A

Dispersal – remodelling and shedding film:

  • The ‘mature’ (climax) biofilm is susceptible to hydrodynamic shearing and mechanical disturbance from masticatory forces – results in passive dispersal
  • Limited access to nutrients at the core of the biofilm leads to dispersal signalling and biofilm structure remodelling to maintain an optimal surface area/volume ratio to facilitate diffusion of nutrients and removal of metabolic end-products – results in active dispersal
  • Bacteria may disperse as microcolonies or become planktonic again – cyclic nature.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

List the microbial species in oral biofilm linked to dental caries (4 points)

A

Organisms in biofilm linked to dental caries:

  • Mutans streptococci – initiating organism of caries
  • Lactobacillus spp. – involved in deeper lesions; pioneer organism in advancing front of caries
  • Actinomyces spp. – associated with root caries.

Lactic acid bacteria include Streptococci spp. and Lactobacilli spp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Compare the microbial species in oral biofilm linked to gingivitis vs. periodontitis

A

Biofilm ecological shift from gingivitis → periodontitis

Microbial species in oral biofilm linked to gingivitis:

  • ~55% Gram-positive with occasional spirochetes and motile rods
  • Examples of bacteria:
    1. Streptococcus sanguinis
    2. Fusobacterium nucleatum
    3. Veillonella spp.

Micobiral species in oral biofilm liked to periodontitis:

  • ~75% Gram negative of which 90% anaerobic motile rods and spirochaetes
  • Examples of bacteria:
    1. P. gingivalis
    2. P. intermedia
    3. F. nucleatum
    4. T. forsythia
    5. Aggregatibacter spp.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the main source of nutrients of the oral biofilm?

A

Saliva is the main source of nutrients of oral bacteria – formation of glucose to lactate by lactic acid bacteria

Increased sucrose load in the oral environment (i.e. when eating) correlates with a net formation and metabolism of glucose to lactic acid (reduced pH)

The lactic acid is produced because the micro-organisms wish to survive

Excess sugar can kill bacteria (sugar kill) and to avoid this they have to metabolize the fermentable carbohydrates as rapidly as possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the overall process of dental caries and the associated microorganisms (6 points)

A

Overall process of dental caries:

  • Localized destruction of tooth tissue by bacterial fermentation of dietary carbohydrates (i.e. sucrose) which produces acids
  • Caused by normal oral commensal flora
  • Dynamic process of cyclic mineralization and demineralizaiton of tooth surface over time
  • Considered pathological when there is an imbalance in favour of net demineralization of enamel and later dentine.

Protective factors vs pathological factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Recall the ecological plaque hypothesis for dental caries

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the microbiology of normal periodontal health

A

Microbiology in normal periodontal health:

  • Mainly Gram-positive cocci:
    • S. oralis group – S. sanguinis, S. oralis, S. mitis.
  • Actinomyces naeslundii
  • Actinomyces viscosus
  • Veillonella spp. (Gram –ve anaerobic cocci)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe periodontal disease and the associated micro-organisms

A

Spectrum of disease from acute (reversible) gingivitis → chronic (irreversible) periodontitis:

  • Direct action of microbes
  • Indirect action of host immune system

Microorganisms:

  • Gingivitis (~55% Gram +ve bacteria):
  • Periodontitis (~75% Gram -ve bacteria):
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Recall the four principal phases of plaque-associated periodontal disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Four principal phases of plaque-associated periodontal disease

Describe the inital lesion (2–4 days) of periodontal disease (3 points)

A

Initial lesion (2–4 days of initial plaque accumulation):

  1. No inflammation evident microscopically (gingivitis not clinically evident)
  2. Histologically clinically healthy gingival tissues
  3. Slightly elevated vascular permeability and vasodilatation:
    • GCF flows out of gingival sulcus leading to flushing action
    • Migration leukocytes (primarily neutrophils) in small numbers through gingival connective tissue into sulcus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Four principal phases of plaque-associated periodontal disease

Describe the early lesion (4–7 days) of periodontal disease (6 points):

A

Early lesion (4–7 days of continued plaque accumulation):

  1. Gingivitis that is now clinically evident
  2. Increased vascular permeability, vasodilatation, and GCF flushing
  3. Proliferation of JE cells
  4. Large numbers of infiltrating leukocytes (neutrophils and also lymphocytes)
  5. Degeneration of fibroblasts (fibroblasts play a key role in collagen formation and wound healing)
  6. Start of collagen destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Four principal phases of plaque-associated periodontal disease

Describe the established lesion (2–3 weeks) of periodontal disease (6 points):

A

Established lesion (2–3 weeks of continued plaque accumulation – chronic gingivitis):

  1. Dense inflammatory cell infiltrate – plasma cells (antibody response), lymphocytes, neutrophils
  2. Elevated release of matrix metalloproteinases which degrade extracellular matrix components, including collagens which make up connective tissues (i.e. periodontal ligament, gingival fibres)
  3. Elevated release of lysosomal contents of neutrophils → further hydrolytic activity of enzymes in ECM
  4. Significant collagen depletion → increased mobility and drifting of tooth
  5. Proliferation of epithelium → formation of pocket epithelium containing large numbers of neutrophils
  6. Results in ‘false pocketing’ on basic periodontal examination (BPE).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Four principal phases of plaque-associated periodontal disease

Describe the advanced lesion (transition from gingivitis to periodontitis) of periodontal disease (6 points):

A

Advanced lesion (marks the transition from gingivitis to periodontitis):

  • Determined by bacterial challenge, host inflammatory response and other susceptibility factors
  • Further destruction of collagen subjacent to the JE, with fibrosis at distant sites
  • Predominance of inflammatory cells in connective tissues
  • Predominant immune cells are plasma cells (antibody-mediated response, IgA)
  • Extension of the lesion into the periodontal ligament and supportive alveolar bone (visible on radiograph), exhibited as clinical attachment loss and pocket formation (periodontal defects).
  • Considered periodontitis from this point onward
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Recall the ecological plaque hypothesis for periodontal disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe necrotizing ulcerative gingivitis (5 points)

A

Necrotizing ulcerative gingivitis:

  1. Acutely inflamed, red, shiny, and bleeding gingivae
  2. Irregularly shaped ulcers on the interdental papillae
  3. Painful condition – pseudomembranous slough (offensive smell)
  4. Linked to poor OH, stress, smoking, malnutrition, immunosuppression
  5. Anaerobic, polymicrobial infection (fusospirochaetal complex):
    • Fusobacterium nucleatum
    • Spirochaetes spp.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe leprosy

A

Leprosy:

  • Mycobacterium leprae
  • Atrophy of the anterior nasal spine, saddle nose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

List 9 infections associated with Streptococcus pyogenes (group A)

A

Streptococcus pyogenes causes a number of spreading infections with minimal local suppuration; the most notable are:

  1. Tonsillitis
  2. Pharyngitis
  3. Necrotizing fasciitis (streptococcal gangrene; ‘flesh eating bacteria’)
  4. Scarlet fever
  5. Mastoiditis
  6. Sinusitis
  7. Otitis media (middle-ear infection)
  8. Wound infections leading to cellulitis and lymphangitis
  9. Impetigo and erysipelas (a brawny, massive skin infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

List the complications associated with Streptococcus pyogenes (group A) infection

A

Complications associated with Streptococcus pyogenes (group A) infection

After an episode of infection, some patients develop complications which may have long-lasting effects:

  1. Rheumatic fever
  2. Glomerulonephritis
  3. Erythema nodosum

Virulence factors:

  1. In cellulitis, hyaluronidase (spreading factor) mediates the subcutaneous spread of infection
  2. Erythrogenic toxin causes the rash of scarlet fever
  3. Post-streptococcal infection:
    • Rheumatic fever ⇒ immunological cross-reaction between bacterial antigen and human heart tissue (type 2 ‘cytotoxic’ hypersensitivity)
    • Acute glomerulonephritis ⇒ immune complexes bound to glomeruli (type 3 ‘immune complex deposition’ hypersensitivity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the morphology of candida albicans (2 points)

A

Candida albicans – responsible for > 90% of human candida infections

Morphology:

  1. Yeast → mobile properties
  2. Pseudohyphae → invasive properties
53
Q

List the risk factors for oportunistic candidal infection (5 points)

A

Rarely causes disease in absence of risk factors:

  1. Ill-fitting or poor hygiene of oral appliance
  2. Disturbed oral ecology e.g. xerostomia or antibiotic therapy
  3. Immunological or endocrine disorder e.g. diabetes mellitus
  4. Malignant or chronic systemic disease
  5. Heavy smoking
54
Q

List 3 candida virulence factors

A

Viurlence factors:

  1. Candida adhesins → host cell receptors
  2. Secreted aspartyl peptidase → destroys host salivary sIgA
  3. Hyphae development → invasion of host (hyphae shape is also harder to phagocytose)
55
Q

List the clinically distinct forms of oral candidiasis (4 points)

A

Clinically distinct forms of oral candidiasis:

  1. Pseudomembranous candidiasis (i.e. thrush) → friable (i.e. wipes off)
  2. Acute erythematous candidiasis
  3. Chronic erythematous candidiasis
  4. Chronic hyperplastic candidiasis
56
Q

List 3 candida-associated infections

A

Candida-associated infections (3 points):

  1. Denture stomatitis:
    • Inflammation of the gum tissue that is covered by dentures
  2. Angular cheilitis:
    • Inflammation of angles of mouth
  3. Median rhomboid glossitis:
    • Symmetrical-shaped area in midline of dorsum of tongue
57
Q

Describe median rhomboid glossitis (6 points)

A

Median rhomboid glossitis

  1. Symmetrical-shaped ‘diamond’ in the midline of the dorsum of the tongue
  2. The infection is a chronic and presents as atrophy of the filiform papillae.
  3. Erythematous patches of atrophic papillae located in the central area of the dorsum of the tongue are considered a form of chronic atrophic candidiasis.
  4. When these lesions become more nodular, the condition is referred to as hyperplastic median rhomboid glossitis.
  5. Considered to be a manifestation of chronic oral candidiasis.
  6. Recovery is high and the infection is strongly associated with smoking and use of inhaled steroids.
58
Q

Describe Ludwig’s angina (5 points)

A

Ludwig’s angina:

  1. Type of severe cellulitis involving the floor of the mouth
  2. Cause is often odontogenic (~75% to 90% of cases)
  3. Infections of the lower second and third molars are usually implicated due to their roots extending inferiorly below the mylohyoid muscle
  4. Periapical abscesses of these teeth also result in lingual cortical penetration, leading to submandibular infection.
  5. Rapid onset (hours) and can result in massive swelling and a potentially life-threatening complication involving airways compromise
59
Q

List 6 key types of Human Herpesvirus (HHV)

A

Human Herpesviruses (HHV):

  1. HHV-1 (or herpes simplex virus 1, HSV1):
    • Primary infection – herpetic gingivostomatitis
    • Secondary – herpes labialis (cold sore)
  2. HHV-2 (or herpes simplex virus 2, HSV 2):
    • Genital herpes
  3. HHV-3 (varicella-zoster):
    • Primary infection – chicken pox
    • Secondary infection – shingles
  4. HHV-4 (Epstein-Barr virus):
    • Infective mononucleosis (glandular fever)
    • Hairy leukoplakia (non-friable; associated with HIV)
  5. HHV-5:
    • Cytomegalovirus
  6. HHV-8:
    • Kaposi’s sarcoma (associated with HIV).
60
Q

Describe Coxsackieviruses (Group A)

A

Coxsackievirus (Group A) – papulovesicular lesions:

  • Hand, foot and mouth disease
  • Herpangina
61
Q

Describe paramyxovirus

A

Mumps – enlargement of one or more parotid glands

62
Q

List 4 key oral manifestations of HIV

A

HIV oral manifestations – opportunistic infections:

  1. Candidiasis
  2. Oral hairy leukoplakia
  3. Kaposi’s sarcoma
  4. Necrotising periodontitis.
63
Q

Define colonization

A

Colonisation – presence of microbes but with no pathological changes and no clinical signs or symptoms

64
Q

List 4 key proteins produced by micro-organisms to evade the host immune defence

A

Evasion of host defence:

  1. Leukocidins (pore-forming)
  2. Proteases (tissue degrading)
  3. Cytotoxins (cell killing)
  4. Siderophores (iron transporting – scavenge host iron reserve)
65
Q

Define bacteraemia and sepsis

A

Bacteraemia – presence of bacteria in the blood:

  • May be produced by cleaning teeth or chewing – usually asymptomatic
  • Also extractions, endodontics, periodontal treatment

Sepsis – systemic inflammatory response to microbial products in the blood

66
Q

Outline the dento-alveolar infection progression (5 points)

A

Dento-alveolar infection (caries origin):

Enamel caries

↓

Deep caries

↓

Pulpal inflammation (reversible pulpitis → irrevserible pulpitis)

↓

Periapal abscess

↓

Ludwig’s angina/cellulitis/sepsis

67
Q

Define antiseptic

A

Antimicrobial substance applied to living tissue/skin (topical) to reduce risk of infection

68
Q

Define antibiotic

A

Antimicrobial substance active against bacteria (i.e. antibacterial)

69
Q

Define antiviral

A

Antimicrobial substance active against viruses

70
Q

Define antifungal

A

Antimicrobial substance active against fungi

71
Q

Describe the key target sites and mechanisms of action of antibiotic agents (2x2 points)

A

Key antibiotic target sites – selective toxicity (2 points):

  • Cell wall synthesis (bactericidal); protein synthesis (bacteriostatic)
  • Broad spectrum less selective – associated with diarrhoea due to GI commensal flora disturbance

Key antibiotic mechanisms of action (2 points):

  • Inhibition of cell wall synthesis (transpeptidase enzyme); damage to DNA, protein and cell membrane
  • Inhibition of protein synthesis (50s and 30s ribosome subunits)
72
Q

List the main antibiotic classes listed in the dental formulary of BNF 76

A

Main antibiotics classes listed in dental forumlary of BNF 76:

Bactericidal antibiotics:

  • Penicillins
  • Cephalosporins
  • Metronidazole

Bacteriostatic antibiotics:

  • Macrolides
  • Lincosamides
  • Tetracyclines
  • Fusidic acid
73
Q

Describe the dose-dependant antimicrobial effects of chlorhexidine and the benefits of the pin-cushion effect

A

Chlorhexidine (bisbiguanides) – two positive charges at its polar ends (dicationic)

Dose-dependant antimicronial effects:

  • Low concentrations of chlorhexidine ⇒ bacteriostatic (sublethal dose)
    • Reversible leakage of low molecular weight particles (e.g. K+) from cell cytoplasm via disrupted inner microbial cell membrane
  • High concentrations of chlorhexidine ⇒ bactericidal (lethal dose)
    • Irreversible co-agulation of microbial cell cytoplasm

Pincushion effect:

  • Creates a barrier between acquired salivary pellicle and adhesive bacteria
  • Enables substantivity → a unique property of chlrohexidine which prolongs action over a period of hours due to binding to acquired salivary pellicle (so not easily washed away)
74
Q

Describe the mechanism of action of penicillins and provide key examples

A

Bactericidal – lysis of bacteria

Amoxicillin, ampicillin, benzylpenicillin (penicillin G), flucloxacillin, phenoxymethylpenicillin (penicillin V)

ß-lactam antibiotics

Penicillins target bacterial cell wall synthesis by binding irreversibly to a transpeptidase, which cross-links peptidoglycans in the bacterial cell wall.

75
Q

Describe the mechanism of action of cephalosporins and provide key examples

A

Bactericidal – lysis of bacteria

Cefaclor, cefalexin, cefotaxime, cefuroxime

ß-lactam antibiotics

Mechanism of action similar to penicillin – interferes with cross-linking of the peptidoglycan bacterial cell wall. Shows cross-reactivity with penicillins (0.5–6.5% of penicillin-allergic patients will also be allergic to cephalosporins).

76
Q

Describe the mechanism of action of metronidazole

A

Bactericidal

Prodrug which is activated by anaerobic bacteria to cytotoxic products which damage the helical structure of DNA, protein, and the cell membrane

Therefore used against anaerobic bacteria (and also protozoa)

77
Q

Describe the mechanism of action of macrolides and provide key examples

A

Bacteriostatic

Clarithromycin, erythromycin, azythromycin

Macrolides prevent the translocation of the 50S subunit of the bacterial ribosome along the mRNA and so inhibits the formation of peptide bonds (transpeptidation), resulting in inhibited protein synthesis

(Erythromycin also stimulates gastrointestinal motility, via binding to motilin receptors, and so is associated with nausea)

78
Q

Describe the mechanism of action of clindamycin

A

Bacteriostatic

Clindamycin inhibits protein synthesis by a similar mechanism to the macrolide antibiotics – prevents the translocation of the 50S subunit of the bacterial ribosome along the mRNA and so inhibiting the formation of peptide bonds (transpeptidation) resulting in protein synthesis.

79
Q

Describe the mechanism of action of tetracyclines and provide key examples

A

Bacteriostatic

Doxycycline, tetracycline

Tetracyclines inhibit protein synthesis, by binding to the 30S subunit of the bacterial ribosome and preventing tRNA from binding at the acceptor (A) site.

80
Q

Fusidic acid

A

Bacteriostatic

Inhibits bacterial protein synthesis by binding elongation factor G (EF-G) on the ribosome, which results in the inhibition of both peptide translocation and ribosome disassembly

81
Q

Describe the mechanism of action of aciclovir

A

Aciclovir – the only antiviral in DPF

Mechanism of action:

  • Aciclovir triphosphate is a guanosine analogue which blocks herpes viral DNA polymerase due to abscence of free 3’-OH group needed for DNA synthesis – resulting in termination of viral DNA synthesis
  • Aciclovir has high affinity for viral thymidine kinase (viral specificity)
  • Aciclovir is initially converted by viral thymidine kinase to aciclovir monophosphate, which is then converted by host kinases to aciclovir triphosphate.
82
Q

Describe the mechanism of action of azole antifungals and provide examples

A

Azole antigungals:

  • Miconazole
  • Fluconazole
  • Ketoconazole
  • Itraconazole

Mechanism of action:

  • Targets fungal cell membrane synthesis
  • Inhibits ergosterol synthesis
  • Miconazole is also bacteriostatic against S. aureus

Selective toxicity of antifungals difficult to achieve as fungal and host cells are both eukaryotic.

83
Q

Describe the mechanism of action of polyene antifungals and provide examples

A

Polyene antifungals:

  • Nystatin
  • Amphotericin B

Mechanism of action

  • Binds to the sterols in fungal cytoplasmic membrane
  • Alters cell wall permeability → leakage of cell contents and cell death

Selective toxicity of antifungals difficult to achieve as fungal and host cells are both eukaryotic.

84
Q

Describe the properties of disinfectant agents used in dentristry

A
  • Halogen compounds e.g. Domestos:
    • Hypochlorites and povidone-iodine are oxidising agents which release halide ions
    • Readily corrode metal and quickly inactivated by organic matter
    • Sodium hypochlorite (NaOCl) gold standard for disinfecting root canals
  • Phenolic compounds e.g. Stericol, Clearsol, Dettol:
    • Phenolic disinfectants for gross decontamination but poorly viricidal and sporicidal
    • Chloroxylenol antiseptic (e.g. Dettol) limited to domestic disinfection as poor activity against many bacteria
85
Q

Describe MRSA

A

Meticillin-resistant Staphylococcus aureus – MRSA:

  • Found on skin and in nose
  • Causes poor wound healing, septicaemia and endocarditis
  • Associated with hospital care due to:
    • Point of entry through skin
    • Density of ‘at-risk’ population
    • Elderly and immune-compromised.
86
Q

Describe pseudomembranous colitis

A

Pseudomembranous colitis – antibiotic related colitis

  • Colitis – inflammation of the colon
  • Due to toxin produced by Clostridium difficile (C. diff)
  • C. diff is resistant to many antibiotics e.g. clindamycin, cephalosporins, co-amoxiclav
  • Clindamycin – 13 fatalities reported through Yellow Card Scheme 2004–2014

Clostridium difficile – C. diff:

  • Found in GI tract
  • Causes pseudomembrane colitis
  • Associated with over 65s
  • Associated with the use of ‘4Cs’:
    • Co-amoxiclav
    • Clindamycin
    • Cephalosporins (3rd generation)
    • Ciprofloxacin.
87
Q

List the 3 key antibiotic resistance mechanisms

A

Three key bacterial resistance mechanisms to antibiotics:

  1. Breakdown – enzymes break down antibiotics
  2. Deactivate – enzymes deactivate antibiotics
  3. Efflux – proteins pump antibiotics out of the bacterial cell
88
Q

Describe how bacteria acquire new DNA to become resistant

A

Bacteria mutate and evolve:

  • Bacteria acquire new DNA via 2 key methods:
    1. Random DNA mutations
    2. Acquired DNA from other bacteria
  • New DNA → new genes → new proteins (e.g. enzymes or protein pumps) are coded for by new genes
  • New proteins confer resistance
89
Q

List the 3 key mechanisms bacteria acquire new extrinsic DNA (3 points):

A

Mechanisms of acquiring new extrinsic DNA – exchange of genetic material (3 points):

  1. Conjugation
  2. Transformation
  3. Transduction
90
Q

Describe the mechanism of bacterial conjugation

A

Conjugation:

  • Plasmid can pass directly from one bacterium to another
  • “Horizontal transmission”
91
Q

Describe bacterial transformation

A

Transformation:

  • DNA from dead bacteria can be taken up from the environment
  • That DNA may include a resistance gene
92
Q

Describe bacterial transduction

A

Transduction:

  • Certain viruses can pick up DNA from one bacteria and pass it to another
  • This is exploited by scientists as a laboratory technique for targeted gene insertion
93
Q

List 5 key adverse drug reactions (ADRs) associated with antimicrobial drugs prescribed in dentistry

A

5 key ADRs encountered in dentistry:

  1. Allergic reaction (e.g. anaphylaxis)
  2. Antiobiotic sensitivity (e.g. nausea and diarrhoea)
  3. Opportunistic infection (e.g. candidiasis)
  4. Stevens Johnson syndrome (SJS)
  5. Toxic epidermal necrolysis (TEN)
94
Q

List 7 respiratory tract infections of clinical relevance to dentistry

A

Respiratory tract infections of relevance to dentistry:

  1. Strep throat and scarlet fever
  2. Rheumatic fever – including link to endocarditis
  3. Diphtheria
  4. Otitis media and sinusitis
  5. Bronchitis and pneumonia
  6. Legionnaire’s disease – Legionella pneumophilia
  7. Tuberculosis – Mycobacterium tuberculosis
95
Q

Describe legionnaire’s disease in terms of symptoms, transmission and prevention

A

Legionnaire’s disease – Legionella pneumophilia:

  • Symptoms:
    • Mild influenza to severe pneumonia with mental confusion
  • Transmission:
    • Water aerosols
    • Impossible to eradicate from water as it’s ubiquitous
    • Potential link to stagnant water in hot water taps and dental unit water lines
    • Reduce risk of transmission by isolating dental water from the mains using a bottle unit, and by regularly flushing the waterlines at the start of each session.
96
Q

Describe tuberculosis disease in terms of symptoms, transmission and prevention

A

Tuberculosis – Mycobacterium tuberculosis:

  • Symptoms:
    • Caseating granulomas especially of lungs
    • Oral cavity is site of secondaries
  • Transmission:
    • Droplet spread (coughing)
  • Resides in cells of the reticuloendothelial system e.g. macrophages
  • Pandemic:
    • Developing world linked to HIV/AIDS
    • 15-20% of people with HIV/AIDS may have TB
  • Prevention:
    • PPE
    • BCG Vaccination
97
Q

List 10 gastro-intestinal tract infections of clinical relevance to dentistry

A

Gastro-intestinal tract infections of relevance to dentistry:

  1. Campylobacter
  2. Shigella
  3. Salmonella
  4. Escherichia coli
  5. Staphylococcus aureus
  6. Clostridium welchii
  7. Cholera
  8. Clostridium difficile (and probiotics as prevention)
  9. Bacillus cereus
  10. Enteric fever – typhoid/paratyphoid
98
Q

Describe Clostridium difficle infection (C. diff) in terms of cause, symptoms and treatment

A

Clostridium difficile (C. diff)

  • Antibiotic treatment may disturb the gut microbiome:
    • Can result in a range of symptoms, most notably, diarrhoea
    • Clostridium difficile is one organism that may colonize the GI tract after antibiotics
  • Clostridium difficile-related disease varies from:
    • asymptomatic infection
    • diarrhoea
    • colitis
    • pseudo-membranous colitis
    • death
  • Treatment is expensive – substantial financial burden on the medical system
  • Short-term use of probiotics:
    • Appears to be safe and effective when used along with antibiotics
    • In patients who are not immunocompromised or severely debilitated.

Probiotics – organisms thought to improve the balance of gut organisms:

  • Thought to counteract gut microbiome disturbances and reduce the risk of pathogen colonization:
    • Lactobacillus acidophilus
    • Bifidobacterium bifidum
    • Streptococcus thermophilus
99
Q

List 2 cardiovascular infections of clinical relevance to dentistry

A

Cardiovascular system infections of relevance to dentistry:

  • Bacteraemia, septicaemia, and sepsis
  • Infective endocarditis (IE)
100
Q

Explain prophylaxis against infective endocarditis

A

Patients identified as high-risk are prescribed prophylactic antibiotics to prevent infective endocarditis (IE):

  • High risk factors for (IE): prosthetic valve, MHx IE, MHx congenital heart disease (CHD), Hx IVDA
101
Q

Describe the aetiology of infective endocarditis (4 points)

A

Infective endocarditis (IE) aetiology:

  1. Inflammation of the endocardium of the heart valves resulting from an infection
  2. Bacteraemia – bacteria in the blood:
    • E.g. tooth brushing, chewing
  3. Acute IE linked to S. aureus and S. pyogenes
  4. Chronic IE linked to Viridians streptococci
102
Q

Describe the pathology of infective endocarditis (3 points)

A

Infective endocarditis (IE) pathology:

  1. Vegetations on the valves:
    • Left side valves – more common (↑O2; ↑turbulent blood flow; ↑congenital abnormalities)
    • Right side valves – IV drug users (venous return contains drug and contaminants, e.g. talc)
  2. High mortality/morbidity
  3. Long hospital stays and extended antibiotic regimens​
103
Q

List the signs and symptoms of infective endocarditis (5 points)

A

Infective endocarditis (IE) signs and symptoms:

  1. Fever (> 38 degrees Celsius)
  2. SOB
  3. Heart murmurs
  4. Petechiae
  5. Splinter haemorrhage (e.g. on nails)
104
Q

List the risk factors for infective endocarditis (5 points)

A

Infective endocarditis (IE) risk factors:

  1. Acquired valvular heart disease with stenosis or regurgitation
  2. Hypertrophic cardiomyopathy
  3. Past medical history of infective endocarditis
  4. Structural congenital heart disease
  5. Valve replacement
105
Q

Outline the empirical treatment options for infective endocarditis (5 points)

A

Infective endocarditis (IE) empirical treatment (awaiting swab and blood cultures):

  • Native valve endocarditis, consider amoxicillin (or ampicillin) with/without low-dose gentamicin
    • If penicillin-allergic, or if meticillin-resistant Staphylococcus aureus suspected, or if severe sepsis, cosnider vancomycin + low-dose gentamicin
  • If severe sepsis with risk factors for Gram-negative infection, consider vancomycin + meropenem
  • If prosthetic valve endocarditis, consider vancomycin + rifampicin + low-dose gentamicin
106
Q

Describe the signs and symptoms of syphilis with reference to its clinical relevance in dentistry

A

Genito-urinary tract infections of relevance to dentistry:

  • Syphilis:
    • Congenital syphilis (dental pathology):
      • Hutchinson’s incisors
      • Mulberry Molars
    • Primary syphilis:
      • Single chancre e.g. in the mouth – 3 weeks after initial infections
    • Secondary syphilis:
      • Scaly rash on hands and feet (ensure holistic visual assessment)
    • Tertiary syphilis:
      • Severe immune response e.g. formation of gumma
      • Neurosyphilis
      • Cardiovascular syphilis
      • Liver, joints, testes
    • Latent syphilis:
      • No symptoms
107
Q

List 6 skin and wound infections of clinical relevance to dentistry

A

Skin and wound infections of relevance to dentistry:

  • Staphylococcal skin infections — S. aureus, S. epidermidis:
    • Cellulitis
    • Folliulitis
    • Boils
    • Angular cheilitis
  • Streptococcal infections – S. pyogenes (group A)
    • Erythrogenic toxin → scarlet fever (strawberry tongue)
  • Human papilloma virus (HPV)
    • HPV-16 associated with oropharyngeal cancer
108
Q

Summarize the causes, symptoms, diagnosis, treatment, pathology of varicella zoster virus (12 points)

A
109
Q

List 3 systemic viral infections of clinical relevance to dentistry

A

Systemic viral infections of relevance to dentistry:

  1. Hepatitis B virus (HBV)
  2. Hepatitis C virus (HCV)
  3. Human immunodeficiency virus (HIV)
110
Q

Recall the hepatitis B virus (HBV) etymolgy and viral structure

A

Hepatitis B virus (HBV) etymology and structure:

  • Hepadnaviridae ­
    • Hepa- (liver); -dna- (DNA)
  • Viral structure:
111
Q

Describe the aetiology and pathology HBV with reference to transmission, signs, and recovery

A

HBV aetiology:

  • Transmission:
    • Hepatitis B virus is spread when blood, semen, or other body fluid infected with the HBV enters the body of a person who is not infected
  • Signs of HBV infection:
    • Hepatic dysfunction
    • Jaundice
  • Recovery following infection usually within few weeks:
    • Serological markers remain – antibodies to components of HBV
    • 2–5% of patients fail to clear HBV by 6–9 months → chronic carriers:
      • Chronic persistent hepatitis – not infectious
      • Chronic active hepatitis – extremely infectious and susceptible to cirrhosis and carcinoma.
112
Q

List and describe the 7 key stages of HBV life cycle

A

Quick list of HBV life cycle:

“Excited Unicorns Charged Towards The Ancient Ruins”:

  1. Entry
  2. Uncoating
  3. Conversion (rcDNA to cccDNA)
  4. Transcription
  5. Translation
  6. Assembly
  7. Release

Description of HPV life cycle (7 points):

  1. HPV enters hepatocyte via endocytosis
  2. Uncoating and release of nucleocapsid (virus core) into cytoplasm
  3. Nucleocapsid releases relaxed, partially double-stranded, circular DNA (rcDNA) → rcDNA enters the cell nucleus
  4. In the nucleus, viral rcDNAs are converted into a covalently closed circular form, cccDNA – serves as a template for the transcription of viral RNA
  5. Viral RNA undergoes ribosomal translation in the cytoplasm to produce viral proteins
  6. Viral proteins and other synthesized compoenents are assembled in the cytoplasm via the endoplasmic reticulum
  7. Immature complete HBV partciles are released from hepatocytes into the host extracellular space to restart life cycle in other hepatocytes
113
Q

What does a positive blood test result for Hepatitis B Surface Antigen (HBsAg) mean?

A

Person is a carrier and potentially infective

114
Q

What does a positive blood test result for antibody to HBsAg (anti-HBsAg) mean?

A

Long lived antibody indicating immunity

115
Q

What does a positive blood test result for Hepatitis B Core Antigen (HBcAg) mean?

A

Indicates active disease or high infectivity

116
Q

What does a positive blood test result for antibody to Hepatitis B Core Antigen (anti-HBcAg)

A

Indicates active or very recent infection

117
Q

What does a positive blood test result for antibody to Hepatitis B e-antigen (anti-HBeAg) mean?

A

Indicates partial recovery and a low level of infectivity

Longer lived than other antibodies – sensitive indicator of previous exposure

118
Q

Recall the serum HBV antigen and antibody graph

A
119
Q

Explain which members of the dental team are at greater risk of clinical exposure to HBV

A

Risk is greater among oral surgeons and periodontists than GDPs:

  • HBV concentrates intraorally in gingival sulcus
  • Continuous serum exudate greater in those with periodontal disease
120
Q

Outline the criteria that healthcare professionials infected with HIV must meet before they can perform exposure prone procedures (EPPs)

A

Health care professionals infected with HIV must meet the following criteria before they can perform exposure prone procedures:

  • Either:
    • be on effective combination antiretroviral therapy (cART), and
    • have a plasma viral load <200 copies/mL
  • Or:
    • be an elite controller (not taking ART and undetectable)
  • AND
    • be subject to plasma viral load monitoring every three months and
    • be under joint supervision of a consultant occupational physician and their treating physician, and
    • be registered with the UKAP Occupational Health Monitoring Register (UKAP-OHR).
121
Q

List 3 key vehicles of transmission

A

Vehicle of transmission (3 points):

  • Drops/droplets of body fluids e.g. saliva or blood (aerosols)
  • Contaminated instruments and surface (fomites)
  • Sharps injury
122
Q

List 9 standard infection control procedures

A

Standard infection control procedures:

  1. Hand hygiene – only touch what you need (avoid touching face, hair, sores/abrasions)
  2. Respiratory hygiene
  3. Personal protective equipment (PPE) – e.g. gloves, eye protection, face masks, scrubs, bare below the elbows
  4. Occupational exposure management e.g. safe use and disposal of sharps
  5. Management of care equipment e.g. sterilization in autoclave
  6. Safe care of linen including uniforms
  7. Control of environment – ventilation, avoid carpeted floorings
  8. Safe clinical waste disposal
  9. Immunizations
123
Q

List the 9 occupation health screening tests

A

Occupational health screening before performing exposure prone procedures:

  1. Hep B:
    • Surface antigen and core antibody test (anti-HBsAg and anti-HBcAG)
    • Surface antibody titre (if previous immunised for Hep B)
  2. Hep C antibody screen
  3. HIV screen
  4. TB screen
  5. MMR evidence of immunity
  6. History of vaccination tetanus, polio, diphtheria
  7. Varicella history born and raised in UK
  8. Non-UK varicella screening
  9. Influenza
124
Q

Define exposure prone procedure (EPP)

A

Exposure prone procedure:

  • Any invasive procedure where there is a risk that injury to the health care worker could result in the exposure of the patient’s open tissue to the blood of the worker (i.e. bleed back)
  • As defined by the Department of Health:
    • “Procedures where the health care worker’s gloved hands may be in contact with sharp instruments, needle tips or sharp tissues inside the patient’s open body cavity, wound or confined anatomical space where the fingertips may not be completely visible at all times”.
125
Q

Define decontamination in the context of dentistry

A

Decontamination:

  • Process by which reusable instruments are made safe for further use
  • Minimises the risk of cross-infection
  • HTM 01-05:
    • Decontamination of instruments, surfaces and equipment
    • General hygiene e.g. hand washing, personal protective equipment
    • Impressions and prostheses
126
Q

Describe sterilization in the context of dentistry

A

Sterilization:

  • Process that kills or removes all organisms (and their spores) in something
  • Reusable equipment must be sterilised
127
Q

Define disinfection in the context of dentistry

A

Disinfection:

  • Process that kills or removes pathogenic organisms (but NOT spores) so that they pose no threat of infection
  • Renders equipment safe for handling and inspection
  • Alcohol based methods:
    • Rapidly bactericidal, they are also effective against TB, fungi and viruses
    • Virucidal against ‘enveloped’ viruses, such as HIV and hepatitis B and against the ‘non-enveloped’ viruses, such as poliovirus rhinoviruses and hepatitis A
  • Non-alcohol based methods:
    • Target types of quaternary ammonium compounds known as ‘quats’
    • Generally regarded as ineffective against TB bacteria and non-enveloped viruses such as polio
128
Q

Define antisepsis in the conext of dentistry

A

Antisepsis

  • Application of a chemical agent on a live surface (e.g. skin or mucosa) to destroy organisms or inhibit their growth
  • All antiseptics can be used as disinfectants – but not vice versa (due to toxicity)
129
Q

Recall the sterilization and disinfection schematic pathway

A

Human Health and Disease I (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions