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MFD Theme 1 Flashcards

1
Q

what is evolution

A

process of change over time that results in new varieties and species of organisms

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2
Q

what is phylogeny

A

 Evolutionary relationships between organisms

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3
Q

how can relationships be deduced in different specimens

A

by comparing the genetic information

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4
Q

what is excellent for determining phylogeny

A

ribosomal RNA (rRNA)

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5
Q

where is rRNA present

A

in all cellular life forms

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6
Q

what is contained in rRNA that can be used to differentiate between species

A

highly variable regions

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7
Q

what is the benefit of DNA sequence analysis

A

it provides an insight into evolution and diversity of the organisms

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8
Q

how can you measure evolution and diversity

A
  1. isolate DNA from each organism
  2. make copies of rRNA gene by PCR
  3. sequence DNA
  4. analyse sequence
  5. generate phylogenetic tree
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9
Q

what dominates the tree of life

A

microorganisms

v few macroorganisms

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10
Q

what are the classifications in the tree of life

A 
Domain
Kingdom
Phylum 
Class 
Order 
Family 
Genus 
Species
Strain
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11
Q

what are the top taxonomic levels

A 
Archaea
Bacteria
Eukaryota
Viruses 
Viroids
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12
Q

are prions living or non living

A

non-living proteinaceous infectious agents

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13
Q

what are Protozoa and fungi

A

groups within the eukaryotes

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14
Q

what are prions

A

Misfolded proteins that cause correctly folded proteins to gradually fold abnormally

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15
Q

when does disease occur as a result of a prion

A

when a host-encoded a-helical protein (PRPC) is converted to b-pleated sheet form (PRPSc)

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16
Q

what does Exogenous PRPSc do

A

triggers disease

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17
Q

what is further conversion of PRPC

A

autocatalytic

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18
Q

what can prions cause

A

transmissible spongiform encephalopathies (e.g. vCJD)

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19
Q

what do transmissible spongiform encephalopathies do

A

Loss of voluntary and autonomic function

Degeneration leads to death

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20
Q

what is PRPSc is extremely resistant to

A

heat (including autoclaving), proteases etc

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21
Q

why is extreme care needed in the case of PRPSc in regards to dentists/medics

A

iatrogenic transmission

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22
Q

what are some characteristics of viruses

A

Can only replicate inside cells using cells’ machinery
Small genomes
Evolve rapidly

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23
Q

what are some examples of viruses

A

HIV, herpes simplex, influenza, cytomegalovirus

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24
Q

what is Archaea

A

Previously thought to be a type of bacteria but actually are closer to eukaryotes

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25
Q

what features do archaea share with eukaryotes

A

DNA replication is initiated at multiple origins

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26
Q

what is the role of archaea in the mouth

A

unknown

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27
Q

which patients are archaea particularly found in

A

patients with severe periodontal disease

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28
Q

what is protozoa

A

Single celled eukaryotes

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29
Q

where are protozoa found

A

Single celled eukaryotes

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30
Q

what do protozoa do

A

Graze on bacteria

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31
Q

what are common examples of protozoa

A

amoeba, plasmodium

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32
Q

what are the Oral protozoa

A

Trichomonas tenax and Enamoeba gingivalis

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33
Q

what is the only serious pathogenic oral protozoan

A

Leishmania

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34
Q

what are fungi

A

Simple eukaryotes

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35
Q

which fungi can form multicellular structures

A

mushrooms, pin moulds

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36
Q

what forms do some fungi transition between

A

yeast and hyphal forms

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37
Q

how are microbial processes related to the environment

A 
Creation of the Earth’s atmosphere
Nitrogen cycle
Decomposition
Metal ore recovery
Sewage digestion
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38
Q

how are microbial processes related to disease

A

Man, animals, plants

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39
Q

how are microbial processes related to food and drink

A

Beer, bread, wine, vinegarm cheese, yoghurt

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40
Q

how are microbial processes related to Biotechnology

A 
Antibiotics
Therapeutics
Genetic engineering
Human gene therapy
Production of drugs, e.g. insulin
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41
Q

what are prions

A

misfolded proteins which form aggregates: proteinaceous infectious particles

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42
Q

why are prions ‘infectious’

A

they spread from cell to cell and in between individuals via contaminated food, blood and surgical instruments

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43
Q

what neurodegenerative diseases can prions cause

A

Cretzfeldt-Jakob Disease (CJD), transmissable spongiform encephalopathies (TSEs)

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44
Q

how are prion diseases caused

A

by proteins whose misfolding is infectious

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45
Q

outline what happens after a protein undergoes a rare change to give an abnormally folded prion

A
  • the protein form of the protein can bind to the normal form making it an abnormal prion
  • abnormal prion proteins propagate and aggregate to form amyloid fibrils
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46
Q

what can amyloid fibrils do

A

they disrupt brain cell function causing neurodegenerative disorder

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47
Q

what is significant about the amyloid fibres

A

they’re protease resistant and resistant to autoclaving for long periods

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48
Q

what does stacking of Beta sheets allow for

A

some misfolded proteins to aggregate into amyloid fibres

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49
Q

what are some protein diseases in man

A

spontaneous- sporadic CJD
inherited- familial CJD
acquired- vCJD, Kuru

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50
Q

what are the consequences of of protein diseases in man

A
  • very long incubation periods- slow replication
  • symptoms progress rapidly and disease is always fatal
  • form insoluble aggregates visible as plaques in tissue
  • neuronal dysfunction and tissue death visible as holes
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51
Q

what don’t prion diseases do

A

induce an inflammatory response

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52
Q

what is the most common prion disease

A

sporadic CJD

occurs at a freq of 1-2 per million population worldwide

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53
Q

what can other misfolded proteins e.g. amyloid proteins contribute to

A

non-infective tissue degenerative disorders e.g. alzheimer’s, parkinson’s, huntington’s, atherosclerosis, type 2 diabetes

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54
Q

what are enveloped proteins

A

have a nucleocaspid containing the viral genome lipid layer from host with envelope proteins

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55
Q

what are non-enveloped proteins

A

nucleocaspid proteins only

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56
Q

what do viral genomes encode

A

viral structural proteins
proteins that interact with the host:
-proteases, DNA/RNA polyermase, reverse transcriptase, immune system inhibitors-see IAH

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57
Q

*what are the structural properties of viral genomes RNA and DNA

A

single stranded

double stranded

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58
Q

*what shape are viral genomes

A

linear, circular or segmented

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59
Q

why do viruses have a variety of replication mechanisms

A

have many different nucleic acid structures

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60
Q

what are most viruses that cause human disease

A

double stranded DNA (e.g. herpes viruses) or single stranded RNA (e.g. retroviruses such as HIV)

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61
Q

what is the life cycle of a virus with a dsDNA genome

A
  • The virus first enters the cell by binding to receptors on the surface of the cell
  • The virus’ DNA is released into the cell
  • The DNA is replicated to produce multiple copies
  • The copies are transcribed and translated to produce new viral particles (coat protein)
  • Assembly of the new virus particles occurs
  • Viral particles then break free out of the host cell by causing cell lysis
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62
Q

what is the life cycle of retrovirus (ssRNA genome)

A
  • Once the retrovirus has entered the host cell, reverse transcriptase enzyme is used to converted the viral RNA to DNA
  • The reverse transcriptase then synthesises a complementary DNA strand to make dsDNA
  • The DNA is then integrated with the host DNA
  • Transcription and translation occur, producing new viral particles (coat proteins, envelope proteins, reverse transcriptase)
  • The new viruses are assembled and then break free from the host by causing lysis
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63
Q

what can viruses be classified into

A

DNA
RNA
Subcategories

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64
Q

what are the types of RNA and and examples

A

enveloped- HIV/influenza A/B

non enveloped- Rhino

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65
Q

what are the types of DNA and and examples

A

enveloped- Herpes

Non-enveloped- Human Papilloma Virus (HPV)

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66
Q

what are the subcategories for viruses

A

SS/DD - nucleocaspid shape

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67
Q

how are viruses involved in oral health and disease

A

some have directly infect the mouth and affect oral health

others colonise the mouth without directly causing oral disease (following release from other tissues)

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68
Q

what viruses have systemic effects but may have oral symptoms

A

measles (rash-Koplik’s spots)
mumps (salivary gland inflammation/swelling of the jaws and neck)
rubella (rash)

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69
Q

what are the viral infections of the mouth

A
  • Hand, foot and mouth disease
  • Human herpes viruses (HHV)
  • Human papilloma viruses (HPV)
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70
Q

what are the consequences of hand, foot and mouth disease

A

enterovirus
(coxsackie A virus) which causes oral blisters
(not the same as foot and mouth disease in cattle)

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71
Q

what is the Human herpes viruses (HHV)

A 
large class of
structurally related viruses
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72
Q

what does the human herpes virus family consist of and what are the diseases

A

HHV1- fever blisters (cold sores)
HHV3- chicken pox/shingles
HHV4- Glandular fever, Hairy leukoplakia, B-cell Lymphoma
HHV5- Congenital defects/pneumonia in AIDS
HHV8- Kaposi’s sarcoma

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73
Q

what are the characteristics of HHV1 (HSV-1)

A

-Infects epithelial cells (oral mucosa) and
neuronal cells
-Exhibits latency
-Causes stomatitis on initial infection, then
fever blisters on reactivation
-Transmission during childhood contact via
saliva

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74
Q

what are different primary oral HSV-1 infections

A

primary palatal herpes

primary herpetic gingivo-stomatitis

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75
Q

what are different recurrent oral HSV-1 infections

A

herpes labialis

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76
Q

what are the characteristics of HHV3 (varicella zoster virus, VZV)

A 
-Very contagious-transmitted via aerosols and
direct contact
-Can cause blisters in the oral mucosa
-Primary disease is chicken pox-can be
reactivated as shingles
-Shingles appears in skin along track of nerve
usual on trunk but can be facial (30% of
shingles cases)
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77
Q

what is an example of primary HHV3 (VZV)

A

chicken pox

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78
Q

what is an example of recurrent HHV3 (VZV)

A

shingles

- follows trigeminal nerve (mandibular divison)

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79
Q

how many types of HPV are there

A

over 150 types

some cause pathology, others are part of the virome of the skin

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80
Q

what can some HPV cause

A

warts of the genital or oral mucosa

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81
Q

which HPV’s associated with papillomas are also associated with cancers e.g. cervical/oral cancer

A

HPV-16

HPV-18

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82
Q

which HPV’s cause focal epithelial hyperplasia are restricted to oral cavity

A

HPV-13

HPV-32

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83
Q

what are the viruses present in the mouth that do not directly cause oral disease

A

Hepatitis B virus (HBV)

HIV

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84
Q

what are the consequences of Hep B

A

 Blood and saliva transmission

  • Causes severe liver disease, including hepatocellular carcinoma
  • Acute and chronic infection phases
  • Carriers often asymptomatic
  • Complex pathogenesis
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85
Q

what is HIV associated with

A
  • Oral candidiasis
  • Necrotising ulcerative gingivitis
  • Viral infections
    e. g.Kaposi sarcoma
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86
Q

what is necrotising ulcerative gingivitis associated with

A

stress, mixed bacterial infection, smoking and HIV

very painful

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87
Q

what are the treatments for necrotising ulcerative gingivitis

A 
plaque control (CHX, ultrasonics, OHI) 
metronidazole
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88
Q

what are the steps of diagnosis of viral infection

A
  1. clinical experience
  2. lab tests immunoassay (ELISA) and sero-conversion (detect antibodies)
  3. microbiology: viral culture
  4. histology of tissues: biopsy (cellular morphology and immunohistochemistry)
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89
Q

how does antiviral health care prevent infection

A

cross infection control and vaccination

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90
Q

what are the treatments of antiviral health care

A

antiviral drugs, e.g. nucleoside analogues (inhibit replication as they are the building blocks of DNA): acyclovir and azidothymidine

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91
Q

outline the features of prokaryotes

A

no internal membranes (organelles)
single chromosomes, no histones
no fusion of gametes (can transfer DNA)

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92
Q

what lengths do bacteria vary from

A

0.2-700 micrometers

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93
Q

what are the major morphologies of bacterial cells?

A 
coccus
rod
spirillum 
spirochete
budding and appendaged bacteria 
filamentous bacteria
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94
Q

what are the major structures of bacteria

A

cell wall
cell membrane
nucleoid/cytoplasm

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95
Q

what are the surface appendages of bacteria

A

flagella, fimbriae, capsule

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96
Q

what are the specialised structures of bacteria?

A

spores

inclusion of bodies

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97
Q

how is light microscopy carried out

A
  1. prepare smear- spread culture in thin film over slide and then dry in air
  2. heat fixing and staining- pass slide through flame and flood slide with stains, rinse and dry
  3. microscopy- place drop oil on slide and examine with 100x lens
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98
Q

what is the procedure and results for staining

A
  1. flood the heat-fixed smear with crystal violet for 1 min- all cells purple
  2. add iodine solution for 1 min- all still purple
  3. decolorize with alcohol briefly -about 20 sec- gram+ purple, gram- colourless
  4. counterstain with safranin for 1-2 min - G+ purple, G- pink to red
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99
Q

what does the gram stain distinguish between

A

major groups of pathogenic organisms

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100
Q

whats is the gram stain bases on

A

presence of outer membrane in gram negatives

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101
Q

*what are some other methods for the gram stain

A

gram - rods

gram + cocci

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102
Q

what is the difference in the gram stain between + and -

A

+ thick cell wall, largely peptidoglycan (retains crystal violet-iodide complex)
- thinner peptidoglycan layer
(permeable to crystal violet-iodide)

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103
Q

what are acid fast bacterial cell walls

A

carbol fuchsin
drive with heat
destain with 3% acid-alcohol
high lipid/wax content (mycolic acids)

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104
Q

what is an example of acid fast bacterial cell walls

A

myobacterium tuberculosis (bacterial cell which causes TB)

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105
Q

what is an example of gram positive cocci

A

streptococcus pyogenes

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106
Q

what % of humans carry streptococcus pyogenes in their respiratory tract

A

5-15%

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107
Q

what acute infections are as a result of streptococcus pyogenes

A

Pharyngitis (severe sore throat) spread by droplets of saliva or nasal secretions

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108
Q

what are the clinical manifestations of Streptococcus pyogenes

A

– 2 to 4 day incubation

– pharyngitis, tonsillitis, malaise, fever, headache, and redness, and lymph node enlargement in throat

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109
Q

what is an example of gram negative rods

A

salmonella enterica

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110
Q

what is the most common foodborne infection

A

salmonellosis

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111
Q

what is the most common form of salmonella enterica, and how long does it like

A

entercocolitis

lasts 2-5 days

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112
Q

what types of salmonella are extremely dangerous

A

S. enterica serovar Typhi - typhoid fever

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113
Q

what are the characteristics of cytoplasmic membrane

A

phospholipid bilayer
thin barrier
6-8nm

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114
Q

what are the characteristics of the outer membrane (gram negative)

A

asymmetrical- phospholipid/LPS

exposed on cell surface

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115
Q

what are the characteristics of flagella

A 
motility
rotates 
long and thin 
can be used for classifications as different patterns 
helical 
protein= flagellin subunits
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116
Q

what is the flagellum

A

a highly complex molecular motor. rotation is coupled to the flow of protons across the membrane

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117
Q

what is fimbriae

A

protein filamentous structure that enables cells to stick to surfaces. it aids biofilm production

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118
Q

what is pilli

A

similar to fimbriae but longer and there are fewer on the cell

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119
Q

why are pilli important

A 
genetic exchange (conjugation)- important in antibiotic resistance 
adhesion of pathogens to host cells
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120
Q

example of pilli

A

neissera spp, s pyogenes

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121
Q

importance of polysaccharide capsule and slime layers

A

aid adherence
evade phagocytosis
protect against desiccation

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122
Q

what can be capsules and slime layers be composed of

A

polysaccaride or protein

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123
Q

what are cell inclusions

A

carbon storage polymers (poly B-hydroxybutyric acid, glycogen)
polyphosphate and sulfur

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124
Q

what are endospores

A

highly differentiated cell- cell almost becomes dormant and resistant to the environment

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125
Q

examples of endospores

A

bacillus anthracis, clostridium

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126
Q

whats needed to grow bacteria

A

anabolic and catabolic
micro and macro nutrients
H, O2, C, N, P, S and selenium pivotal
70% water

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127
Q

energy source for heterotrophs

A

obtain C from organic chemicals

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128
Q

energy source for autotrophs

A

obtain C from CO2

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129
Q

how are autotrophs different from auxotrophs

A

auxotrophs cannot synthesise an essential organic compound

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130
Q

what is fermentation

A

(anaerobic): organic compound used as both electron donor and electron acceptor

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131
Q

what is Respiration

A

(aerobic or anaerobic): electron donor is oxidised with O2 or O2 substitute.

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132
Q

what is the first step in fermentation and respiration

A

glycolysis (glucose –> pyruvate)

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133
Q

how is ATP synthesised in fermentation

A

substrate level phosphorylation

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134
Q

how is ATP synthesised in respiration

A

driven by oxidative phosphorylation

135
Q

what is a major product from h the metabolism of streptococcal bacteria

A

lactic acid

136
Q

what is the F0F1 ATPase

A

Highly abundant protein complex in actively growing bacterial cell walls

137
Q

how does F0F1 ATPase generate ATP

A

from flow of H+ into cells

138
Q

why do oral bacteria (s.mutans) use ATPase to pump H+ out of cells

A

too much H+ reverses ATP generation so protons pumped out to reduce acidic environment

139
Q

what is bacterial growth

A

Irreversible increase in biomass and also, usually, numbers

140
Q

how can bacterial growth be measured

A

microscopy, colony forming units (CFU), absorbance, nitrogen, carbon, DNA, protein

141
Q

what are the methods of measuring bacterial growth

A
  1. microscopic counts
  2. viable counts
  3. turbidimetric methods
142
Q

what is recombinant DNA technology

A

joining together of DNA molecules from two different species

143
Q

what is e.coli

A

harmless resident of the human gut, lives on our skin

144
Q

what is the ecoli K12 genome

A

4.6 million base pairs
encodes 4,400 proteins
40% genes are of unknown function
many genes encoding enzymes clustered into operons
average protein contains approx 300 amino acids

145
Q

what are bacterial plasmids

A

• Small circular DNA present in varying copy number per cell

146
Q

what genes do bacterial plasmids carry

A

genes that are useful but not essential to survival: e.g. genes which make bacteria resistant to antibiotics

147
Q

what are plasmids released by

A

dead bacteria and absorbed by those still living thus genetic information is exchanged.

148
Q

how does horizontal gene transfer occur in bacteria

A

Occurs naturally by transformation, transduction or conjugation

149
Q

what is bacterial sex in dental plaque

A

Genes transferred between bacteria in dental plaque

Occurs naturally by transformations, transduction or conjugation

150
Q

which bacteria in dental plaque can increase its ‘fitness’ after bacterial sex

A

streptococcus mutans

151
Q

how does dna exchange take place between bacteria

A

dna uptake (transformation)
phage-mediated dna transfer (transduction)
mating (pilus-mediated transfer; conjugation)

152
Q

what is dna transformation

A

dna incorporated into the chromosome of the recipient by homologous recombination

153
Q

what the goals of genetic manipulation

A

Biology: To understand the function of a gene
- Knock-¬‐out genes
- Change individual amino acids in protein
- Clone and over-¬‐express proteins
- Construct fusions with reporter genes
Biotechnology:
– Production of recombinant proteins eg insulin
- Develop vaccines eg hepatitis B
- Generate improved probiotic bacteria

154
Q

what is recombinant dna technology

A
  1. creation of recombinant dna- new combinations of unrelated genes in test tube
  2. cloning of recombinant dna
    - amplifying the new dna by introducing it into living cells
  3. using recombinant dna
    - expressing a cloned gene to produce a protein
155
Q

what is in a molecular biologists ‘toolbox’

A
  • Enzymes- to manipulate the DNA/RNA
  • Vectors- act as a vehicle to carry recombinant DNA into host cells
  • DNA/RNA- the raw material- usually purified from tissue/cell culture
  • Cells- to amplify- and sometimes express the recombinant DNA
156
Q

what enzymes are important in the creation of recombinant dna

A

• Restriction enzymes: Cut double-stranded DNA
• DNA Ligase: Sticks fragments of DNA together
• Taq polymerase: PCR
- POLYMERASE CHAIN REACTION, Creates multiple copies of DNA fragment
• Reverse transcriptase: Copies RNA into DNA

157
Q

what are restriction enzymes

A

molecular scissors
Cleave DNA, usually at very specific sequences
Naturally produced by bacteria: self-defence mechanism
many recognise 4-8 base pair palindromic sequences

158
Q

what are the general properties of vectors

A

contain unique restriction sites for insertion of new dna
introduced into host easily
Contain a gene to allow selection of cells which contain the plasmid – eg an antibiotic resistance gene
regulatory sequences

159
Q

what is can be used as a vector

A

plasmid (most common)
bacteriophage- virus which infects bacteria
cosmids/phagemids- genetically engineered hybrids which replicate as a plasmid but can be packaged as a bacteriophage

160
Q

how would we clone a human gene in e.coli

A
  1. create recombinant dna

2. clone recombinant dna

161
Q

how would we create recombinant dna to clone a human gene in e.coli

A

Obtain DNA of interest

Insert DNA of interest into vector (eg.plasmid)

162
Q

how would we clone recombinant dna to clone a human gene in ecoli

A
  • Recombinant plasmid is inserted into E.coli host
     By transformation
     Formation of pores in bacterial membrane to aid uptake of DNA, using CaCl2 on ice + heat shock (42°C, 2 mins) or Electroporation
  • E.coli containing plasmid are selectively cultured
     Each bacterial colony arises from a single transformed E coli cell
     Each cell in the colony contains copies of the SAME plasmid
     The cells in the colony are therefore clones
  • Recombinant plasmid is purified or expressed
     Technique may be used in industry to produce large quantities of the recombinant DNA
163
Q

what are the problems with hormones from animal sources

A

animal protein not identical to human- side effects
difficult to purify
possible contamination with pathogens

164
Q

what was the first recombinant drug licensed for human use

165
Q

how is recombinant human insulin produced

A
  • The gene for proinsulin contains 2 introns
  • mRNA is reverse-­‐transcribed to produce pro-­‐insulin cDNA (no introns)
  • joined to plasmid to produce recombinant plasmid and then infected into ecoli
166
Q

what is the SMaRT replacement therapy technology

A

Creation of a genetically altered strain of Streptococcus mutans, called SMaRT, which does not produce lactic acid.

167
Q

what are planktonic cells

A

homogenous, single species, nutrient rich

168
Q

what are surface associated cells

A

limited heterogeneity, single species, nutrient rich. cells at the edge of the colony have access to more nutrients

169
Q

what are natural cells

A

structured community, heterogenous, mixed species, nutrient limited

170
Q

what is a biofilm

A

a community of microbial ells encased within a matrix of polymers and associated with an interface

171
Q

what is the difference between a biofilm and a broth culture

A

broth cultures have no matrix

172
Q

where do most bacteria grow

A

in biofilms

173
Q

what are the characteristics of planktonic culture

A 
homogenous 
single species 
uniform growth rate in chemostat
even distribution of O2, nutrients and waste etc
cells well-separated 
no ECM
174
Q

what are the characteristics of a biofilm (heterogenous)

A 
mixed species which all interact 
mixed growth rate 
uneven distribution of O2, nutrients, waste 
cells are in close contact
ECM present
175
Q

what is the difference between biofilms and pure broth cultures

A
  • biofilm bacteria are up to 1000 times more resistant to antibiotics than planktonic cells
  • biofilms difficult to remove
  • bacterial communities more pathogenic
  • bacteria in biofilms can hide from host immunity
  • biofilms provide a range of niches
176
Q

where are biofilms found

A

anywhere there is an:

interface, moisture, nutrients/energy source

177
Q

what is an example of biofilms at air liquid interfaces

A

surfaces of ponds, oceans

178
Q

what is an example of biofilms at air solid interfaces

A

tree trunks, rocks, solids particles

179
Q

what is an example of biofilms at solid-liquid interfaces

A

internal surfaces of pipes (including dental unit waterlines), river beds, indwelling catheters, teeth

180
Q

what is the structure of a biofilm

A

3 dimensional, mushroom like structures, contain serum, open structures often with channels permeating the matrix, heterogenous (cell distribution is not uniform), nutrients and wase products non-uniformly distributed

181
Q

outline the growth of a biofilm

A
  • attachment- adhesion of few motile cells to suitable solid surface
  • colonisation- intercellular communication, growth, and polysaccharide formation
  • development- more growth and polysaccharide
  • active dispersal- triggered by environmental factors such as nutrient availability
182
Q

what is the structure of a biofilm- heterogenicity

A

range of different niches
anaerobic bacteria can grow in parts of the biofilm that contain lower levels of O2
may be pockets in biofilm with aerated areas and those with low nutrients

183
Q

what are the structures in the biofilm matrix

A

macromolecules form the basic structure
small molecules trapped in the matrix
biofilm growth and resistance to antimicrobials

184
Q

what are the diagnostic criteria for biofilm infections

A
  • associated with a surface
  • aggregated cells in cell clusters incased in matrix
  • infection confined to particular site in host
  • recalcitrance to antibiotic treatment
  • catheter infections often recalcitrant to antibiotics
  • used a model containing artificial urine flowing over discs of catheter infections
  • inoculated with pseudomonas aeruginosa and tested antibiotic sensitivity of biofilm bacteria and compared them with planktonic cells.
185
Q

what were the results of the diagnostic criteria test for biofilms

A

results: biofilms reduced with tobramycin
when you treat a planktonic culture with 50mg per mil you wipe it out and when you treat a biofilm with 1000 mg per mil you dont wipe it out

186
Q

why are biofilm bacteria so resistant

A 
slow growing 
persister cells present 
sequestration from immune system 
elevated expression of efflux pumps 
poor penetration of antibiotics
187
Q

what does antibiotic sensitivity vary with

A

stage of growth

188
Q

are antibiotics that target cell wall more effective against biofilms or planktonic cells

A

planktonic cells

189
Q

are antibiotics that target protein or RNA synthesis more effective against biofilms or planktonic cells

A

equally effective against both

190
Q

what are persister cells

A

inactive/dormant cells

191
Q

why are persister cells dangerous

A

they are very difficult to kill with antibiotics

192
Q

what happens when dormant cells become a significant proportion of biofilm bacteria

A

can become responsible for the reactivation of infections

193
Q

what are SCVs and what are they responsible for

A

small colony variants- formed on agar by persister cells

may be responsible for infections on replacement hips 15-20 years after the operation

194
Q

what is the difference between slow growth and persisters

A

in persister cells there are one or two highly resistant persister cells in the population whereas in slow growth there are many cells

195
Q

why are biofilms highly resistant to phagocytosis

A

inflammatory cells cannot penetrate the matrix and if they do, they do not ingest the bacteria effectively

196
Q

what adaptive responses in biofilms or communities can protect bacteria

A
  • pseudomonas spp. produce rhamnolipids in biofilms, which can kill neutrophils.
  • interactions with oral streptococci induce production of a complement-evading protein by aggregatibacter actinomycetemcomitans
  • up regulation of efflux pumps
197
Q

what do efflux pumps do

A

kick out drugs e.g. cancer cells kicking out drugs

198
Q

in which biofilms are antibiotic efflux pumps up-regulated

A

biofilms formed by E.coli, P.aeruginosa, Candida albicans

199
Q

are efflux pumps effective against all antibiotics

A

no

up-regulation of efflux pumps is not universal

200
Q

why are biofilm bacteria so resistant

A 
slow growing
persister cells 
sequestration from the immune system 
more efflux pumps 
poor penetration of antibiotics
201
Q

how is mass transfer measured in biofilms

A

using fluorescently labelled latex beads, dyes or labelled proteins

202
Q

what is the consequence of diffusion being impeded by the biofilm matrix

A

not v significant for small molecules
even large molecules are weakly limited
molecules are carried through water channels

203
Q

how are electrostatic and vdw interactions important in biofilms

A

the matrix acts as an ion channel resin e.g. metal cations become trapped in the anionic matrix

204
Q

is tobramycin impeded by the matrix in biofilms

A

yes as its positively charged

205
Q

is ciprofloxacin impeded by the matrix in biofilms

A

no as its neutral

206
Q

when does reduced penetration of the biofilms occur

A

in non-mucoid strains (don’t produce the carbohydrate alginate)

207
Q

how can protection against tobramycin be achieved

A

adding extracellular DNA to biofilms enhances protection

208
Q

what are the bacterial cell-cell interactions in oral biofilms

A

signalling, synergism, antagonism

209
Q

what is the human microbiome

A

microorganisms within the human body- colonised by 10 trillion bacteria (10% human)

210
Q

what was the first microbial gene sequenced

A

haemophilus influenza

211
Q

what is the ORF

A

the part of the reading frame which has the potential to be translated

212
Q

how is a list of ORFs obtained from the reading frame

A
  1. computer finds possible start codons then stop codons
  2. computer counts codons between start and stop
  3. computer finds possible RBS
  4. computer calculates codon bias in ORF
  5. computer decides if ORF is likely to be genuine
  6. List of probable ORFs
213
Q

what are the 2 components of the bacterial genome

A

core genome

pan genome

214
Q

what is the core genome

A

shared by all strains of the species

215
Q

what is the pan genome

A

all optional extras in some but not all strains of the species

216
Q

what are chromosomal islands

A

region of bacterial chromosome of foreign origin that contains clustered genes for some extra property such as virulence or symbiosis (thought to be acquired by horizontal gene transfer)

217
Q

what are pathogenicity islands

A

chromosomal islands containing genes for virulence (disease) acquired by horizontal gene transfer

218
Q

what can transposons do

A

jump to other places in the chromosome

219
Q

how is the human microbiome important in health

A

its essential for healthy immune system
predictions can be made from analysis of microbial community types
oral community types correlate with gut communities

220
Q

which community type is least stable

A

oral is less stable than microbial community types in the gut or vagina

221
Q

how is the human microbiome important in disease

A

analysis of microbiome is used to identify biomarkers for disease
many diseases result from shifts in microbial community types rather than infection by a single agent

222
Q

what do probiotics do

A

introduce a microbe into the human body for its beneficial qualities

223
Q

what is the difference between chromosomal islands and the rest of the genome

A
  • chromosomal islands believed to have a foreign origin

- base composition and codon usage varies in chromosomal islands from the rest of the genome

224
Q

what is a microbiome

A

the total compliment of microorganisms in an environment

225
Q

how can microbial communities be analysed

A

metagenomic sequences- obtains information about all DNA present

226
Q

how can bacterial pathogens be identified

A

sequencing of 16S rRNA gene

227
Q

what is the 16S rRNA gene

A

component of the 30S small sub unit of the bacterial ribosome -provides indication of the bacterial species present

228
Q

why doesn’t the sequence analysis of the 16S rRNA gene include viruses or fungi

A

viruses lack rRNA genes

fungi have the 18s rRNA gene

229
Q

what is the diversity of human microbiome

A
  • concordant among measures
  • unique to everyone
  • determined by microbial habitat
  • diversity between individuals at a single body site is generally lower than diversity within individuals at different body sites
230
Q

what is the downside of antibiotics

A

they kill good bacteria as well as those that cause disease

231
Q

what influences the core human microbiome

A 
host lifestyle 
host genotype 
host physiology 
host immune system 
transient community members 
host environment 
host pathobiology
232
Q

how is the human microbiome important in health

A

its essential for a healthy immune system

233
Q

what are the diseases of different systems related to human microbial symbiosis

A 
obesity
IBD
liver disease
emerging infectious disease
diabetes mellitus 
atherosclerosis 
metabolic syndrome
234
Q

what is the relationship between mouthwash and blood pressure

A

it can raise blood pressure due to oral microbiota converting nitrate to nitrite

235
Q

what is disease aetiology

A

the study of causation

236
Q

what is the germ theory of disease

A

the idea that disease is caused by ‘invisible’ creatures dates back to roman times

237
Q

what bacteria is anthrax caused by

A

gram-positive, rod-shaped bacteria known as Bacillus anthracis

238
Q

what are the characteristics of Bacillus anthracis

A

spore forming
highly resistant
resilient

239
Q

what was Koch’s proof that B.anthracis causes infections

A
  • spleen tissue from infected farm animal was given to the mouse and the mouse died
  • proliferated organisms in mouse after the infected tissue had been cultured in a growth medium in the eye
240
Q

what are Koch-Henle Postulates

A
  • the organism must be present in all cases of disease and not present in healthy individuals
  • the organisms must be isolated in pure in culture
  • the isolated organisms must cause disease in a suitable animal
  • the organism must be reisolated from infected animal (shows proliferation)
241
Q

where are legionella bacteria found

A

naturally in the environment, usually in water

242
Q

where do legionella bacteria grow best

A

in warm water e.g.

hot tubs, cooling towers, hot water tanks, large plumbing systems, air conditioning systems

243
Q

how are legionella able to survive in harsh environments

A

they survive within amoobae

244
Q

what harbours legionella pneumophila

A

Protist (Tethymena)

245
Q

when is it not possible to fulfil Koch’s postulate of: The organism must be present in all cases of disease, and not present in healthy individuals

A

there may be asymptomatic carriers (cholera, Neisseria meningitidis)

246
Q

when is it not possible to fulfil Koch’s postulate of: The organism must be isolated in pure culture

A
  • viruses could not be cultured in 1900s. Prions are still difficult/impossible to culture
  • Some infections are polymicrobial (no single aetiological agent)
247
Q

when is it not possible to fulfil Koch’s postulate of: The isolated organism must cause disease in a suitable animal

A

animal models may not be available/may not be representative of human disease

248
Q

when can Koch’s postulates not be applied precisely

A
  • If no infecting organism can be detected
  • If the bacteria cannot be grown in culture
  • If no suitable animal model is available
  • If more than one species of bacterium is involved
  • If it is the level rather than just the presence of the infecting bacterium that is important
249
Q

how do organisms cause disease

A 
Transmission (the 6 ‘I’s)
-       Implantation
-	In utero
-	Ingestion 
-	Inhalation 
-	Injection 
-	Inunction
Pathogenesis
250
Q

how is dna analysis useful in the molecular biology era to detect infectious agents

A

circumvents the isolation of an infectious agent
very sensitive (detects agetns in the absence of disease)
may be quantitative-i.e. can determine load of infectious agents

251
Q

what are many infectious diseases now regarded as

A

imbalances in the microbiota

252
Q

what is meant by commensal

A

an organism that lives in harmless association with its host (‘normal flora’)

253
Q

what is meant by carriage (carrier state)

A

colonisation with a pathogen i.e. this host can act as a source of infection for others, but shows no symptoms themselves

254
Q

what is an opportunistic pathogen

A

an organisms which requires the host to have a pre-existing defect in its defences before it can cause diseases- exists in the body but doesnt cause disease

255
Q

what is virulence

A

a measure of the capacity of an organism to cause disease

256
Q

what are virulence factors

A

properties of a bacterium which contribute to its virulence i.e. toxins created by bacteria

257
Q

what are endogenous infections

A

caused by an infectious agent that is already present in the body, but has previously been inapparent or dormant

258
Q

what are exogenous infections

A

acquired from sources outside the patient (i.e. bacteria which causes tetanus infection).

259
Q

what are some virulence factors that pathogens possess

A

adhesins- stick to the body
invasins- can invade cells
toxins- harm cell types an cause disease
extracellular enzymes

260
Q 
what are the pathogens in
1- whooping cough 
2-gonorrhoea 
3-black death 
4-anthrax
A

1- bordetella pertussis
2-neisseria gonorrhoeae
3-yersinia pestis
4- bacillus anthracis

261
Q

what are opportunist pathogens in
1- catheters/endocarditis
2- burns
3-diarrhoea

A

1-staphylococcus epidermis
2-pseudomonas aeruginosa
3-escherichia coli

262
Q

what are the stages of infection

A 
1- adherence- to skin/mucosa
2- invasion- through epithelium
3- infection/growth-virulence factors and toxins  
4- invasiveness toxicity 
5- damage to host

effect: tissue damage, disease

263
Q

what interactions occur between surface structures of bacteria and the host tissue

A

pilli, fimbrae and surface proteins of bacteria bind to host tissue receptors including to glycoproteins and tissue-specific antigens

flagella is an important virulence factor

264
Q

what are examples of bacteria adhering to the host

A

E.coli with type I pili adgere to epithelial cells in the uniary tract

vibrio cholerae is highly motile, swims through intestinal mucus to attach to receptors in gut wall

265
Q

what are some innate host defences

A
  • Skin (keratinised, shedding of outer layers)
  • Flushing (saliva, urine, peristalsis in gut)
  • Secretions (lysozyme, stomach acid, bile salts)
  • Mucous membranes (cilia)- antibacterial peptides
  • Normal bacterial population (colonisation resistance
266
Q

what are some adaptive host defences

A
  • Phagocytosis
  • Inflammation, fever
  • Antibodies
267
Q

why may you be more vulnerable to infection if you’ve taken omeporazol

A

it increases stomach acid so less bacteria needed to cause disease.

268
Q

how have pathogens overcome the skin as a host defence

A

keratinases, skin penetration

269
Q

how have pathogens overcome flushing

A

adherence, motility

270
Q

how have pathogens overcome secretions

A

lysozyme resistant walls, tolerance to salts, bile, pH

271
Q

how have pathogens overcome mucous membranes

A

degrade or swim through mucin

272
Q

how have pathogens overcome commensal flora

A

metabolic end products, bacteriocins, bacteriophage

273
Q

how have pathogens overcome phagocytosis

274
Q

how have pathogens overcome inflammation/fever

A

heat shock response

275
Q

how have pathogens overcome antibodies

A

breakdown of immunoglobulins kill host defence cells, intracellular growth, antigenic variation

276
Q

what is bacteraemia

A

invasion of bacteria into the blood stream

277
Q

what is septicaemia

A

infection in the blood stream

-release of large number of cytokines which kills the host in the end when its meant to kill the pathogen

278
Q

what is an infection

A

a situation when a microorganism that is not a natural coloniser grows within the host, whether or not it causes damage

279
Q

when does a disease arise

A

when there is damage to the host

280
Q

how do bacteria spread

A
  • Through lungs, gut, urinary tract, blood via sinuses and body cavities
  • Tracking along nerve pathways
  • Direct cell‐to-¬cell
  • Tissue breakdown
281
Q

what are the microbial virulence factors

A

Toxins

  1. endotoxins- lipopolysaccharides cause septic shock
  2. exotoxins - damage the host cells

Tissue degrading enzymes
collagenase/haemolysin/hyaluronidase

282
Q

what are endotoxins, where are they found, when are they released and what do they cause

A
  • Lipopolysaccharide (LPS) is an endotoxin
  • Found only in Gram-negative bacteria
  • Present in the outer layer of the outer membrane
  • Released during growth or when bacteria die and lyse
  • Causes fever, septic shock and local inflammation
283
Q

what are exotoxins and what are they produced by

A
  • Secreted by bacteria
  • Produced by some Gram positive and Gram-negative species
  • Relatively unstable (often heat‐sensitive)
  • Highly toxic - 1 nanogram (10^-9g) of botulism toxin can be fatal
284
Q

why are antibiotics useless to treat e.g. food poisoning by enterotoxin. what should be used to treat it

A

bc damage by exotoxin does not always require bacterial infection. vaccines are needed to target the toxin rather than the infectious agent

285
Q

what do tissue degrading enzymes do and what are some examples

A

Breaks down junctions between skin cells and destroys skin cells

S.pyogenes, hyaluronidase

286
Q

what bacteria causes tetanus and what are its characteristics

A

Clostridium tetani
Gram positive, spore forming rod
Secretes a powerful neurotoxin that blocks the release of neurotransmitters from the pre-synaptic membranes of inhibitory nerve synapses

Found in soil and animal faeces

287
Q

what are the symptoms of tetanus

A
  • ‘lockjaw’, muscular contraction

- can Bend over backwards- snap spine and die

288
Q

what bacteria causes botulism and what are its characteristics

A
  • Clostridium botulinum
  • Found in soil, water, foodstuffs (including honey)
  • Extremely potent toxin (like tetanus) inactivated by cooking.
289
Q

what is the botulism toxin used for

A

botox
Treat muscle conditions
Cosmetics- remove wrinkles, temporary relax muscles
Poison-tip umbrella assassination

290
Q

what bacteria causes diphtheria and what are its characteristics

A

Corynebacterium diphtheriae

  • Makes toxin that stops protein synthesis in cells
  • Toxin gene carried by bacteriophage
  • Inhibits protein synthesis
  • Causes pseudo membranes to be formed in the posterior pharynx
291
Q

how to bacteria cause damage to the host (step 5)

A

Tissue breakdown (Necrotising Fasciitis)
overactive immune response
most common mono infections are Streptococcus pyogenes and MRSA

292
Q

what are factors that influence susceptibility to the disease

A
  • trauma
  • underlying disease or other infections
  • Age
  • Genetic constitution (tissue type etc)
  • Nutrition
  • Hormonal factors and stress
  • Pollutants
293
Q

what does targeted microbiome analysis involve

A

sequencing the 16S rRNA gene for bacteria

tells you what OTU (generally what species it is, doesn’t exactly correlate)

294
Q

what does metagenomics involve

A

sequencing all DNA present in a sample, then using bioinformatics to predict the source/function of the DNA sequences

295
Q

what is the SPH

A

diseases are caused by a single microorganism.

296
Q

what is the N-SPH

A

diseases are caused by the amount of plaque

297
Q

what is the ecological plaque hypothesis

A

disease is caused by interactions of specific microorganisms with the microbial community

298
Q

what are keystone species

A

they disproportionately large effects on their communities given their abundance

299
Q

what does a keystone pathogen do

A

supports and stabilises the dysbiotic state, and triggers an immune reaction even when present at relatively low numbers

300
Q

what is periodontitis initiate by

A

a synergistic and dysbiotic microbiota, within which different members, or specific gene combinations thereof , fulfil distinct roles that converge to shape and stabilise a disease-provoking microbiota

301
Q

what is the gut microbiome

A

of the most diverse microbial communities in the body and is the totality of microorganisms, bacteria, viruses, protozoa, and fungi, and their collective genetic material present in the gastrointestinal tract (GIT).

302
Q

what are differences in the microbiota between individuals associated with

A

obesity, colorectal cancer, inflammatory bowel disease & many systemic conditions

303
Q

what is IBS caused by

A

Host genetics play a key role

Gut microbiome is gaining increasing attention.

304
Q

which is clinical microbiology

A

In vitro diagnosis and management of diseases caused by bacteria, viruses, fungi and parasites

305
Q

what is the role of the clinical microbiology lab

A

accurate information about the presence or absence of microorganisms in a patient sample

aid in the diagnosis and management of diseases caused by pathogenic microorganisms

provide information regarding the antimicrobial susceptibility of the microorganisms detected

Do all this is a clinically relevant timeframe

306
Q

What makes a good diagnostic test in clinical microbiology?

A

Specificity (NO FALSE POSITIVES!)

Sensitivity

Time taken to produce a result

Ease of use

307
Q

what are there different Types of lab tests

A

Identification of a specific microbial product

Detection of specific antibodies to a pathogen

Detection of genes (DNA or RNA) specific to a pathogen in a patient sample

308
Q

what are the Types of lab tests used

A

Direct microscopy

isolation and culture

309
Q

what are the drawbacks of direct microscopy

A

Lacks sensitivity & specificity for many organisms

You needs lots of the pathogen

Usually requires culture confirmation

310
Q

when would you used direct microscopy

A

e.g. Detection of tuberculosis

311
Q

what is required for the identification of bacteria

A

Microscopy: Gram stain and morphology

Growth requirements

Biochemical Identification tests

Antibody-based tests

MALDI-TOF mass spectrometry

PCR/Nucleic acid-based tests (gene specific)

312
Q

what does the oxidase test test for

A

Oxidase Positive bacteria contain cytochrome C oxidase and can therefore use oxygen for energy production with an electron transfer chain

313
Q

what is good about Biochemical Identification tests

A

metabolise sugars oxidatively or fermentatively

produce enzymes which can be easily detected

use a range of substrates for growth.

314
Q

what are limitations of culture-based methods

A

Some organisms grow very slowly in vitro

Some organisms are difficult to grow in vitro

Some organisms don’t grow in vitro

Organisms don’t always grow if the patient has already been treated with antibiotics

315
Q

how can antigens be detected

A

Detection of soluble carbohydrate antigens by antibody-coated latex

316
Q

what can examination of blood serum detect for

A
  • Measles
  • Mumps
  • Mycoplasma
  • Parvovirus
  • Rubella
  • Syphilis
  • Toxoplasma
  • Varicella-zoster
317
Q

when is Nucleic acid-based tests (NATS) used

A

Mainly used in virology
Some application in bacteriology

Very sensitive and specific
Mainly polymerase chain reaction (PCR

318
Q

what are advantages of PCR

A

Rapid testing:
Multiplex detection
Increased sensitivity
Specific detection

319
Q

how is Bordetella pertussis (whooping cough) detected

A

PCR

More rapid and sensitive than culture

320
Q

what is Legionnaires disease

A

Nosocomial or community acquired pulmonary infection

Often causes outbreaks of infection

Transmitted through the inhalation of Legionella from a contaminated environmental source

321
Q

how is Legionellosis detected

A

culture of the organism from clinical samples

Rapid diagnosis by PCR (3-5 hrs) improves the prognosis

322
Q

how is bacterial meningitis detected (N. meningitidis and Streptococcus pneumoniae)

A

Culture doesn’t work

PCR testing used- Sample types CSF, blood

323
Q

what is syndromic testing

A

testing for multiple pathogens at the same time

324
Q

what are PCR arrays

A

Up to +40 targets per sample

Gastrointestinal panel (viral/bacterial/parasitic

Respiratory panel (viral/bacterial)

Viral haemorrhagic fever panel (inc. malaria)

325
Q

what does dysbiosis show

A

shows association, not necessarily disease causing organism

326
Q

what is one condition that differences in the microbiota can be associated with

A

irritable bowel disease

crowns disease and ulcerative colitis

327
Q

how does a healthy microbiome interplay with disease

A

protects agains pathogens
train/stimulates immune function
supplies nutrients, energy, vitamins

328
Q

how does a diseased microbiome affect the individual

A

inflammation, oxidative stress, increase in gram negative bacteria, infection, altered metabolite production

329
Q

what are the treatments used to target the microbiome

A

Careful selection of antibiotics to minimise unwanted shifts in the microbiota
e.g. avoid repeated use of a single antibiotic.

repopulation of the gut with healthy bacteria
(prebiotics and probiotics)

330
Q

what are prebiotics

A

feed the good organisms in gut/mouth (encourage good bacteria to restore balance)

331
Q

what are probiotics

A

deliver the microorganisms into the gut/mouth (e.g. yoghurt)

332
Q

what is Faecal microbiota transplantation

A

separate microorganisms from faeces and give back to someone with the disease (encouraging results for relapsing C. diff. infection but not so clear for IBD).

333
Q

what are the stages of ecological plaque hypothesis and the aetiology of dental caries

A

excess sugar induces acid production (stress)

shift from neutral pH to low pH (environmental change)

s.sanguinis and s.gordinii to s.mutains, lactobacillus spp, and scardovia wiegsiae (ecological shift)

shift from remineralisation to demineralisation (disease)

Stage 2 (16 decks)

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