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Sem 2 year 2 > The Public > Flashcards

The Public Flashcards

1
Q

What is inflammation?

A

A critical innate defence between microbial invaders and their hosts
Body’s primary method of defence against infection

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2
Q

What characterises inflammation

A

Increase vascular permeability which:
allows diffusible components to enter the site of infection
Cellular infiltration by chemotaxis
Movement if inflammatory cells to site of injury

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3
Q

Which types of cells are involved in acute inflammation?

A

neutrophils, Allergy, eosinophils, mast cells

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4
Q

Whuch types of cells are involved in chronic inflammation?

A

Macrophages, lymphocytes

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5
Q

What is the difference in chemical mediators in acute and chronic inflammation?

A

Acute - complement, kinins, prostaglandins, leukotrienes, cytokines (IL-1 IL-6), interferon
Chronic - cytokines but different

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6
Q

Describe a acute inflammation visible lesion

A

Rash, pus, absess

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7
Q

Describe a chronic inflammation visible legion

A

Rash, fibrosis, granuloma

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8
Q

Give 2 examples of acute inflammation clinical examples

A

Abscesses

Allergic reaction

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9
Q

Give 2 examples of chronic inflammation clinical examples

A

Autoimmune conditions

Cystic fibrosis

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10
Q

6 types of inflammatory diseases

A 
IBD
COPD
Heart disease/atherosclerosis
Alzheimers Disease
Rheumatoid arthritis
Cancer
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11
Q

What are monokines

A

Cytokines secreted by mononucclear phagocytes

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12
Q

What are lymphokines

A

Cytokines secreted by activated T cells (especially T helper)

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13
Q

What are interleukins

A

Cytokines mediating signalling between white blood cells

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14
Q

What are four functions or cytokines

A

Development of cellular and humoral immune responses
Induction of inflammatory response
Regulation of haematopoiesis
Wound healing

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15
Q

What do the cytokines secreted during acute inflammation do?

A

Activate NK and CTL cells

Supress tumour

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16
Q

What do the cytokines secreted during chronic inflammation do?

A

Tumour cells escape immine response so tumour progression

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17
Q

What is stress?

A

A specific response by the body to a stimulus that disturbs or interferes with normal physiological equilibrium/homeostasis

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18
Q

What does stress affect?

A

Affects the hypothalamus - high levels of glucocorticoids so more supression of pro inflam cytokines and chemokines

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19
Q

What happens to the glucocorticoids during chronic stress?

A

The levels dont matter anymore because the signals are not taken notice of by the body
Reactive oxygen species produced which can oxidise to cause mutations

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20
Q

How does cortisol impair immune function?

A

Changes cytokine secretion - decreases levels of tumor necrosis factor
Decreases IL-2
Induces WBC death
Decreases inflammatory response

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21
Q

What changes in the adipose tissue when obese?

A

More leptin, less adiponectin

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22
Q

What does leptin do?

A

When levels increase, it signals us to stop taking any more food for energy as we don’t need it

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23
Q

Which types of macrophages are found in lean people vs obese people?

A

M2 - lean

M1 - obese and produce inflammatory cytokines

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24
Q

In what ways does obesity facilitate the development of autoimmune diseases?

A

Cause chronic inflammation
Upregulate T helper 17 cells – produce pro inflame cytokines
Down reg of deregulatory cells
Development of antibodies that lead to autoimmune complications
Macrophages that do not support cells death (inhibit it) – leads to lipolysis leading to aggregates, recognised by immune system as foreign – autoimmune
Some autoantibodies produced – recognise some of our cells as foreign
Alterations in gut - Accumulations of strains of bacteria that are not helpful
Vitamin B not enough levels- can lead to cells which loose myelin which protects neurones from microenvironmental stresses – multiple sclerosis can occur

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25
Q

Outcomes of dysregulation (inflammation not terminated properly)

A 
Allergy/asthma
Type 1 diabetes
MS
IBD
Psoriasis
Obesity
Arterioscleosis
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26
Q

Outcomes of homeostasis (inflammation maintained)

A

Immunity
Health
Well-being
Prolonged living

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27
Q

What do antibodies do as drugs?

A

Attach to non-physiological cells and attract NK cells

The mechanism of attack involves the release of cytoplasmic granules containing perforin and granzymes

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28
Q

Internal factors affecting immune responses to therapeutic proteins

A 
Genetic factors - modulating the immune response and related to gene defect
Age related
Disease related
Concomitant treatment
Treatment related
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29
Q

External factors affecting immune responses to therapeutic proteins

A

Protein structire
Formulation and packaging
Aggregation and adduct formation
Impurities

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30
Q

Ways to reduce immunogenicity

A

Change AA sequence of glycosylation patterns
Link proteins to polymers
Use humanized versions of the proteins
Reduce the immunogenic response by immunosuppresive treatments
Use another route of admin

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31
Q

What is antisense therapy?

A

Designing an antisense molecule against the mutated part of DNA
Blocks that bit from being read and copied

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32
Q

Advantages of antisense therapy

A

Same effect as enzyme inhibitor or receptor antagonist
Highly specific where the oligonucleotide is 17 nucelotides or more
Smaller dose levels required
Potentially less side effects

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33
Q

Disadvantages of antisense therapy

A

Must target exposed sections of mMRNA
Instability and polarity of oligonucleotides
Short lifetime of oligonucleotides and poor absorption across cell membranes

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34
Q

What is micro-RNA (miRNA) and how does it work?

A

Short segments of double stranded RNA
RISC makes it single stranded (siRNA)
siRNA binds to complementary mRNA region
mRNA is cleaved by enzyme complex- degregated so no gene product sythesised

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35
Q

What are the hallmarks of cancer?

A 
An inflammatory environment
Insensitivity to growth inhibitors
Limitless replicative potential
Sustained angiogenesis
Self-sufficiency in growth signals
Evasion of apoptosis
Tissue invasion and metastasis
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36
Q

What drives the hallmarks of cancer processes?

A

Signal transduction and the activity of tyrosine kinases

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37
Q

What is the signal transduction process?

A

Signal, reception, amplification, transduction, response

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38
Q

What converts an external signal to intra-cellular signals?

A

Conformational changes in the structure of the receptor

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39
Q

What are Tyrosine Kinase Receptors?

A

Receptors with an extra-cellular and intra-cellular domain

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40
Q

What does the intracellular domain in RTK’s do?

A

Phosphorylates tyrosine residues in target proteins which can initiate signal cascades and cause changes in expression of genes

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41
Q

What are the 3 essential RTK components?

A 
Ligand binding site (extracellular domain)
Transmembrane domain (α helix)
Domain with tyrosine kinase activity (cytosolic)
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42
Q

In what two ways can you modulate kinase activity?

A

Disruption of ligand-receptor interactions

Inhibition of kinases

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43
Q

Give two drugs the disrupt ligand receptor interactions and explain how they work

A

Bevacizumab - binds to growth factor and prevents it binding so tumour blood vessel development disrupted (colorectal cancers)
Trastuzumab(herceptin) prevents binding of EGF to HER2 receptor so no signal transduction - onlt if this gene overexpressed

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44
Q

Give two drugs that inhibit kinase activity and explain how they work

A

Imatinib mesylate - inhibits ATP binding to the bcr/abl fusion protein
Gefitinib prevents ATP binding to EGFR - so no dimerisation

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45
Q

Give examples of targeted cancer therapies

A

Disruption of oestrogen and receptor interaction
Inhibiting MAPK signalling (Dabrafenib and vemurafenib)
Inhibit pro-tumour inflammation
Promote anti-tumour inflammation

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46
Q

Summarise anti-tumour immune activation

A

Endogenous tumour antigens released during tumour lysis (by chemo or local radiation)
These are captured by dendritic cells, activated by GLAAS technology t generate an anti tumour immune respone
Immune system attacks the primary tumour and distal metastases

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47
Q

Summarise promoting anti tumour inflammation

A

T cell responses controlled by immune checkpoints to protect the body from damaging immune responses
Develop drugs to target these checkpoints which stops anti tumour T cell mediated responses

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48
Q

What is anti-CTLA4 therapy?

A

monoclonal antibody (ipilimumab) binds to CTLA4 checkpoint blocking signalling and allowing activation of anti tumour T cell response

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49
Q

What is PD-1/PD-L1 therapy?

A

Monoclonal antibodies (Nivolumab) block signal so enables T cell response, T cell proliferation and therefore anti-tumour activity

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50
Q

Explain the dental caries process

A

Sugar meets plaque, acid is release
Acid causes minerals (calcium phosphate) to be lost from the tooth surface into saliva (demineralisation)
Saliva bicarbonate neutralises the acid so minerals go back into the tooth and remineralise it

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51
Q

Give 3 predisposing and 3 protective factors of caries

A
  1. Frequent sugar intakes
  2. Acid producing bacteria
  3. Reduced saliva flow
  4. Fluoride
  5. Saliva
  6. Time
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52
Q

What are the risk factors for General and Oral Health?

A 
Diet
Stress
Control
Hygiene Smoking
Alcohol
Exercise
Injuries 
Obesity
Diabetes
Cancers
Cardiovascular Disease
Respiratory Disease
Mental Illness
Dental Caries
Periodontal Disease
Skin Disease
Trauma-Teeth and Bones
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53
Q

How many baby teeth do we have and how are they split up?

A

20

Into 4 quadrants - A,B,C,D,E

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54
Q

How are permanent teeth identified?

A

1-7

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55
Q

Which numbers correlate to which teeth?

A

1, 2 - incisors
3 - canine
4, 5 - premolar
6,7 - molar
Potentially another 4 wisdom teeth which are molars too
Potentially 32 permanent teeth altogether

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56
Q

What bacteria is found in plaque?

A

Streptococcus mutans

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57
Q

What will be affected if you floss incorrectly?

A

Periodontitis membrane

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58
Q

How does fluoride reduce caries?

A

Held in the enamel and plaque. When the pH drops during an acid attack, the reservoir acts as a source of free fluoride ions.
Calcium fluoride is incorporated into the enamel as hydroxyfluorapatite of fluorapatite as part of remineralisation

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59
Q

How old do you have to be to be prescribed Fluoride toothpaste?

A

2,800 ppm - over 10

5,000 - over 16

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60
Q

What is plaque called above and below the gumline?

A

Above - supragingival

Below - subgingival

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61
Q

What is the aquired pellicle of dental plaque?

A

A conditioning film of saliva on the teeth in the polymicrobial biofilm, which is removed when brushing

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62
Q

What is the initial phase of human caries and is it reversible?

A

‘White spot’ and it IS reversible at this stage

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63
Q

Why do we get human caries? What is the cause?

A

Eating sugar
Low salivary flow
Low exposure to fluoride
Bacteria involved in the formation of lesions on the basis of their function

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64
Q

Which bacteria are best at being acidoduric and acidogenic and what do these terms mean?

A

Mutans streptococci
Lactobacilli
Acidogenic - ferment sugar to produce acid
Acidoduric - survive acidic conditions

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65
Q

Which pH puts you at risk of caries?

A

A pH lower than 5.5

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66
Q

How can we break the caries cycle?

A 
Eat less sugar 
Good oral hygiene 
Antimicrobial agents
Raise Ph of mouth
Oral probiotics
Increase salivary flow
Increase fluoride exposure
Repair enamel
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67
Q

What is periodontal disease?

A

Disease of the supporting tissues of the tooth

68
Q

Describe the environment of the gingival crevice

A 
Anaerobic
Abundance of protein in the environment
Sometimes a hostil inflammatory response
Further down has less oxygen
Have to be able to cope with inflammation
69
Q

What are the four main types of periodontal disease?

A

Gingival disease
Chronic periodontis
Necrotising periodontal disease
Aggressive periodontitis

70
Q

What is gingivitis and what causes it?

A

Reversible inflammation of the gums due to poor oral hygiene, hormonal disturbances, drug therapy or smoking
(pre-cursor for periodontal disease)

71
Q

What is chronic periodontis?

A

Untreated
Cause of teeth loss
Loss of attachment - irreversible
Alveolar bone loss = increased depth and BOP

72
Q

How deep is the periodontal pocket normally?

A

2mm

73
Q

What are the ‘RED’ pathogens for periodontal disease?

A

Porphyromanas gingivalis
Treponema denticola
Tannerella forsythia

74
Q

Where do periodontopathogens come from?

A

Some can attach to the mucosa and have been isolated from the tounge biofilm

75
Q

What is necrotizing periodontal disease and what symptoms does it have?

A

An underlying systemic infection
Painful and bad breath
Grey pseudo-membrane on the gingivae

76
Q

What is responsible for aggressive periodontitis?

A

Aggregatibacter actinomycetemcomitans (AA) leukotoxin

77
Q

What is the treatment for aggressive periodontitis?

A

Tetracycline
Metronidazole - preffered as targets anaerobes
Amoxicillin

78
Q

What other types of periodontal disease are that occur in certain groups?

A

Pregnancy gingivitis
Group A streptococcal gingivitis
Diabetes Gingivitis
HIV periodontal disease

79
Q

What is the process that causes periodontal disease?

A

Plaque accumulates
Host inflammatory response
Flow of GCF increases
Delivery of nutrients and fluid available
Proteolytic bacteria proliferate
Local pH increases (alkaline products from metabolism) - redox reduces
Up regulation of bacteria virulence factors
A change in the resident microflora

80
Q

Which other health factors are people with periodontal disease more likely to have?

A 
CVD
Respiratory diease
Diabetes
Risk of premature labour
Risk of low birth weight (then leads to more risks in life)
81
Q

Oral bacteria can enter the bloodstream, give 3 examples of what this can cause

A

Streptococci and endocarditis
Infectious atherosclerosis
Aspiration pneumonia

82
Q

Which surfactant causes toothpaste to foam?

A

Sodium Lauryl Sulphate

83
Q

What is the role of fluoride and what is the optimum ppm?

A

Influences remineralisation of enamel

Inhibits metabolism of some plaque bacteria

84
Q

What is substantivity of antimicrobials?

A

How long an antimicrobial can maintain its activity for

85
Q

Wht might an antimicrobial be used?

A

if people cannot maintain oral health using mechanical methods

86
Q

What is chlorhexadine, what is it for and what is it found in?

A

A broad spectrum anitmicrobial (antiseptic) that reduces plaque, caries and gingivitis
In mouthwash, gel, varnish only

87
Q

What is triclosan and how does it work?

A

A broad spec bisphenol
Selectively inhibits obligately anaerobic gram negative bacteria
Inhibits acid production, reduces inflammation, inhibits bacterial fatty acid metabolism
Need fatty acids to make membrane so membrane indirectly disrupted
Can be enhanced by formulation with a co-polymer or zinc citrate
NOT FOR MOUTHWASHES (but can be)

88
Q

Give examples of enzymes in dental care and their role

A

Dextranases and glucanases - modify plaque matrix
Glucose oxidase and amyloglucosidase - boost salivary peroxidase system
Menthol, thymol and eucalyptol can penetrate plaque
Oils - disrupt cell membranes and inhibit enzymes
Plant extracts

89
Q

What are QAC’s and how do they work?

A

Quaternary Ammonium Compounds
e.g. Cetyl-pyridium chloride
Broad spec, substantive
Binds to bacterial cell membranes and disrupts integrity
Inhibits glucan synthesis and co-aggregation
MOUTHWASH ONLY

90
Q

Are metal salts more potent that triclosan, CPC ect?

A

No, not as potentally antimicrobial

91
Q

What do zinc salts in dental formulations do?

A

Inhibit bacterial glycolysis so reduce acid production in the mouth

92
Q

What does zinc lactate in dental formulations do?

A

Inhibits VSC production so reduce smell

93
Q

What do stannous fluorides in dental formulations do?

A

Inhibit caries formation

Reduce dental hypersensitivity

94
Q

What properties does Sodium Lauryl Sulphate have?

A

Detergent - disrupts lipids

Bactericidal - inactivates bacterial enzymes

95
Q

What is the role of arginine in dental products?

A

Arginine salts used
Arginine metabolised to ammonia by oral bacteria
Raises pH in mouth, keeping it above the critical caries level
Also a sensitivity agent so blocks dental tubules

96
Q

Why is sugar free gum beneficial?

A

increase salivation, no sugar so no acid, shear force on oral cavity

97
Q

Give examples of sugar substitutes.

A

Aspartame

Saccharin

98
Q

Which sugar substitutes are found in sugar free gum?

A

Sorbitol, mannitolm lactitol

99
Q

What are probiotics and why might they be used? Give an example

A

beneficial bacteria that you put on or in you in the hope of having a beneficial affect
Potential life long protection
E.g. - non pathogenic mutans streptococci

100
Q

Which pathogen most commonly causes UTI’s and in what % of cases?

A

E.coli

85% cases

101
Q

Which other bacteria can cause UTI’s in more vulnerable/immunocompromised people?

A 
Staphylococci spp (UT surgery, catheter)
Proteus spp (GIT)
Klebsiella spp (GIT)
Pseudomonas spp (Hospital acquired)
102
Q

Why do women get UTI’s more often?

A

Shorter urethra so bacteria have less distance to travel

Predisposed to ascending infection with Grm –ve bacteria from the GI tract

103
Q

What are the symptoms of a UTI?

A

Frequency
Dysuria
Urgency
Haematuria

104
Q

How are UTI’s managed?

A

OTC potassium and sodium citrate (alkaline)
OTC analgesia
Public health role (differential diagnosis, pregnancy)

105
Q

When should you refer someone with a suspected UTI?

A

Pregnancy
Recurrent or non-resolving/worsening cystitis
Children and men
Symptoms suggestive of ascending infection (pyelonephritis)
Diabetes

106
Q

What are the features of pyelonephritis and how do they differ from a normal UTI?

A

Ioin pain
Fever
Malaise (no temp with regular UTI)

107
Q

Does the bladder naturally have bacteria in?

A

NO, completely sterile

108
Q

What should stop urine flow back up to the kidney?

A

Sphincter

109
Q

In which groups doe pyelonephritis need hospital referral?

A

Pregnant women
Dehydration/unable to keep fluids down
Recurrent pyelonephritis
Men (in whom there is no obvious cause)

110
Q

When might further investigation into pyelonephritis be needed?

A

Recurrent UTI
>45 with haematuria (blood in urine) that persists after UTI treated
>60 with unexplained non-visible haematuria and raised WCC on dipstick

111
Q

How is a UTI diagnosed?

A

Symptoms
Urine dipstick for nitrites, leukocytes, protein and blood
Mid Stream Sample of Urine (MSSU)

Treat when symptomatic and urine dipstick is positive (except pregnancy)

112
Q

Why are recurrent UTI’s a risk?

A

They carry an increased risk of renal damage

113
Q

How many episodes of UTI’s per year can you have before investigation is requires?

A

3

114
Q

Why might UTI’s be recurring?

A

Kidney stones
Local obstruction - benign growth, enlarged prostate, congenital

Restricting urine flow

115
Q

What is classified as an uncomplicated UTI?

A

Women (inc pregnancy)

Single episode in children

116
Q

What is classified as a complicated UTI?

A

Men
Structural abnormality - - indwelling catheter, stent, nephrostomy tube, vesicouteric reflux, prostatic hypertrophy, ect ect

117
Q

What is Vesicouteric reflux? What may be the cause in children?

A

Faulty sphincter
Urine back up ureter taking bacteria with it
May just not be fully developed in children yet

118
Q

What advice on UTI prevention and symptom control should be given?

A 
Fluids to pas through and clear bladder
Avoid caffeine and alcohol
Empty bladder often and ensure full emptying
Wipe front to back
Empty bladder after sex
Analgesia
119
Q

Why are UTI’s a risk in pregnant women?

A

Very common and often asymptomatic

Risk of progression to pyelonephritis

120
Q

When are pregnant women screened for UTI’s?

A

At their first midwife appointment (bacteruria screening)

121
Q

If a woman is found to have a UTI during pregnancy, what happens?

A

Treated with antibiotics even if no symptoms
Urine culture 7 days after antibiotic
Monthly urine cultures after this

122
Q

When should a UTI for children be treated?

A

When a dipstick is positive

123
Q

How long is treatment for a child with a UTI?

A

if cystitis/lower UTI treat for 3 days

if at risk of pyelonephritis or upper UTI treat for 10 days

124
Q

How long is treatment given for a UTI in adults?

A

3 days treatment

125
Q

If an antibiotic is given for a UTI, what influence the choice of which one to use?

A 
Local resistance patterns and formularies
Previous exposure
Culture results
Allergy status/intolerances
Renal function
Likelihood of interactions
126
Q

Why does renal function affect the use of antibiotics for a UTI?

A

Antibiotics are having a local effect
Need to get large concs of antibiotics in the bladder
They wont reach the bladder in large concs if not producing enough urine

127
Q

Which antibiotics are given for a regular UTI?

A 
Trimethoprim 
Nitrofurantoin
Cephalosporins
Co-amoxiclav
Quinolones
Gentamicin – IV ONLY
128
Q

How long are antibiotics given for a complicated and uncomplicated UTI?

A

3-5 days
(uncomplicated)

7 -10 days
(complicated)

129
Q

Which antibiotics are given for a recurrent UTI?

A 
Treat as UTI, 
Trimethoprim 
Nitrofurantoin
Cephalosporins
Co-amoxiclav
Quinolones
Gentamicin – IV ONLY
BUT consider prophylaxis with Trimethoprim
130
Q

How long are antibiotics given as prophylaxis for a recurrent UTI?

A

3-6 months

131
Q

Which antibiotics are given to treat acute pyelonephritis?

A

2nd-generation cephalosporin – BROAD SPEC
Quinolone
Gentamicin

132
Q

Give examples of 2nd gen cephlosporins used in pyelonephritis?

A

Ceflacor (oral)

Cefuroxime (IV)

133
Q

Which antibiotics are used to treat asymptomatic bacteruria?

A

Pregnancy
1st line: nitrofurantoin (avoid at term)
2nd line: cefalexin

134
Q

How long are antibiotics given to treat asymptomatic bacteruria?

A

7 days

135
Q

How long are antibiotics given to treat acute pyelonephritis?

A

14 days

136
Q

Why is Trimethoprim contraindicated in the first trimester of pregnancy?

A

It is a folate antagonist

137
Q

What are the side effects of Trimethoprim?

A

Blood disorders long term

Bone marrow suppression

138
Q

What are the side effects of Nitrofuratoin?

A

Nausea, GI disturbance
Many people vomit
Rarely, pulmonary reactions, peripheral neuropathy- stop immediately
Contraindicated in renal impairment

139
Q

What are the side effects of Cephalosporins/penicillins?

A

GI disturbances

C diff risk

140
Q

What are the side effects of 4-quinolones?

A

Rarely arthralgia, tendon damage
Caution in epilepsy
broad spectrum so C diff risk

141
Q

What are the side effects of Gentamicin?

A

Nephrotoxic, ototoxic

142
Q

What is the Pharmacists role regarding UTI’s?

A 
Differential diagnosis and referral
OTC treatments (analgesia, alkanising agents)
Lifestyle advice
Advice on use of antibiotics
Monitoring for side effects
143
Q

Which antibiotics target Cell wall synthesis?

A 
Cycloserine
Vancomycin
Bacitracin
Penicillins
Cephalosporins
Monobactams
Carbapenems
144
Q

Which antibiotics target Folic acid metabolism?

A

Trimethoprim

Sulfonamides

145
Q

Which antibiotics target DNA gyrase?

A

The Quinolones Nalidixix acid and Ciprofloxacin

Novobiocin

146
Q

Which antibiotics target RNA elongation

A

Actinomycin

147
Q

Which antibiotics target Cytoplasmic membrane structure and function?

A

Polymyxins

Daptomycin

148
Q

Which antibiotics target DNA directed RNA polymerase?

A

Rifampin

Streptovaricins

149
Q

Which antibiotics target Protein synthesis 50s?

A

Erythromycin (macrolides)
Chloramphenicol
Clindamycin
Lincomycin

150
Q

Which antibiotics target Protein Synthesis 30s?

A 
Tetracyclines
Spectinomycin
Streptomycin
Gentamycin
Kanamycin
Amikacin
Nitrofurans
151
Q

Which antibiotics target lipid biosynthesis?

A

Platensimycin

152
Q

Which antibiotics target protein synthesis (tRNA)?

A

Mupirocin

Puromycin

153
Q

What is Isoniazid used to treat?

A

TB

154
Q

What is antibiotic resistance?

A

The acquired ability of a microorganism to resist the effects of a chemotherapeutic agent to which it is normally sensitive (some are naturally resistant before exposure)

155
Q

What is the difference in generation time of human vs human-associated bacteria?

A

Human: 10-15 million minutes

Human-associated bacteria: 20-100 minutes

156
Q

What is the difference in abundance of human vs human-associated bacteria?

A

Human: 6.070,000,000

Human-associated bacteria: 697,000,000,000,000,000,000,000

157
Q

What are 5 biochemical mechanisms of antibiotic resistance

A 
Overproduction/alteration of target
Alternative pathway (bypass)
Decreased influx/increased efflux
Drug modification
Drug destruction
158
Q

How do bacteria get antibiotic resistance genes?

A

Mutation - spontaneous

Horizontal gene transfer

159
Q

Summarize the three types of horizontal gene transfer

A

Transformation - free DNA into bacterial cell (can be plasmids)
Conjugation - plasmid transfer cell to cell
Transduction - involves bacteriophages

160
Q

Are plasmids independent of chromosomal DNA?

A

Yes

161
Q

Can plasmid replication occur independently?

A

Yes

162
Q

Do plasmids only carry genes for normal growth? Which types of genes do they carry?

A

No

Normal, extra, genes for

163
Q

How does conjugation occur?

A

Ferility factor - transfer pilius connects 2 organisms together and DNA can transfer down the tube

164
Q

What issue do microbial biofilms have?

A

The organism is susceptible when screened but when embedded in a biofilm it is not susceptible to antimicrobials

165
Q

Antibiotic resistance increases with:

A

Use and time

166
Q

What are the next steps against antibiotic resistance?

A

Antimicrobial stewardship
Combination therapy
Develop new antibiotics

Sem 2 year 2 (9 decks)

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