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3rd BDS IHD > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are Protozoa

A

Unicellular eukaryotes
Many are Free-living
Often with parasites

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2
Q

What are eukaryotes

A

Cellular organisms with membrane bound organelles
DNA in the form of chromosomes in a nucleus
Complex metabolic function

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3
Q

example of protozoa

A

trypanosomiasis (chagas disease)
malaria
cryptosporidium
Toxoplasma gondii

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4
Q

how big are protozoa generally

A

2-100 micrometers

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5
Q

what does Bordetella pertussis cause

A

whooping cough

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6
Q

how to streptococcus cause infection

A

release Streptolysin O toxin
haemolysis

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7
Q

what shape is streptococci and staphylococci

A

strep = line of circles
staph = bunch of circles

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8
Q

what is a protkaryote

A

single-celled organism that lacks a nucleus, and other membrane-bound organelles.

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9
Q

compare gram positive and negative bacteria

A

Gram negative have 2 membranes separated by a very thin layer of peptidoglycan which cannot sustain the gram stain leaving it its natural histological pink colour.

Gram positive microbes have a very thick peptidoglycan wall which can hold the stain, leaving it purple.

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10
Q

explain the structure of peptidoglycan (3)

A

Peptidoglycan is a polymer of N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)
crosslinked via amino acid pentapeptides and anchored to the cell wall.

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11
Q

what part of bacteria does penicillin attack

A

the cross linking of the peptidoglycan in cell walls

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12
Q

compare flagella and Pili

A

Flagella rotate in different directions to propel the bacteria in a direction
Pilli have sticky ends that adhere to host surfaces and contract to bring closer
both for movement of bacteria

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13
Q

what is a pathogen

A

disease causing organism

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14
Q

what is a commensal

A

an organism that lives freely in a host that does not cause disease in normal circumstances

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15
Q

what is an opportunistic pathogen

A

a commensal that is usually harmless but under certain circumstances e.g. immunocompromised - leads to disease

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16
Q

name some commensals, where they are found and their opportunistic diseases

A

Staph aureus - found in nasal passages = MRSA, endocarditis
Staph Epidermidis - found on skin = catheter related sepsis

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17
Q

how many bacteria are in 1g of GI tract

A

1000,000,000

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18
Q

give the structure and gram stain of E. Coli

A

gram negative rod
commensal

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19
Q

how do we test for mycobacterium and why

A

It is impervious to gram staining due to waxy cell wall
unusual cell wall containing mycolic acid - higher melting point that have a waxy nature - can survive in lungs
Ziehl-Neelsen acid-fast staining procedure: mycobacteria in red.
An example of this would be M.Tuberculosis.

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20
Q

compare the structure of a gram negative wall and a acid fast wall

A

gram negative have 2 membranes separated by a thin layer of peptidoglycan
acid fast walls contain mycolic acid making it waxy

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21
Q

how would we test for M. Tuberculosis or M. Lepore

A

Ziehl-Neelsen acid-fast test under microscope
red rods

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22
Q

what was the first pathogen related to a disease

A

m. Leprae

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23
Q

what is the carrier state and why is it important

A

asymptomatic carriage of pathogenic bacteria
it increases the spread of the disease quickly before people realise they have the disease. Half of gonorrhoea and chlamydia is asymptomatic and even less so in women. But with larger effects on women.

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24
Q

why does washing hands prevent spread of typhoid fever and what causes this (3)

A

Salmonella Typhi causes Typhoid fever
Small amounts of this are kept in the gall bladder which is then excreted
Washing hands after going to the toilet stops spread

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25
Q

what is an Obligate intracellular parasites

A

can survive outside a cell but can only thrive and reproduce within cells.

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26
Q

describe the structure of a virus

A

Nucleic acid (DNA/RNA/Single/Double) encapsulated by proteinaceous capsid
Varying shape and symmetry
Some further coated with lipid coat - enveloped e.g. HIV derived from sometimes host and always virus proteins.
Spike proteins on the surface interact with human cell receptors e.g. Covid = ACE protein

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27
Q

what is a viruses Lytic Cycle

A

the cell cycle tat occurs whilst in the host cell

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28
Q

what is a lentivirus and how do they work

A

another name for retrovirus
inject mRNA and reverse transcriptase turns this into DNA
implemented into Host DNA
when host replicates cell, infectious DNA also replicated and transcribed
pathogen proteins created

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29
Q

how might some infections re-activate over time

A

some pathogens can hide in dorsal root ganglions e.g. chicken pox
when immunocomprimised, re-occurance can occur

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30
Q

why might a patient get a very small portion of shingles on the body

A

chicken pox zoster virus hides in dorsal root ganglions
when these particular nerves are re-activated, shingles occurs along this nerve
can be very smal

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31
Q

what is the most abundant organism on earth

A

bacteriophage 10^31

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32
Q

what are bacteriophages and how might we identify one

A

viruses that kill bacterial cells
place virus on bacterial colonies on agar
if clear, bacteriophage

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33
Q

what are prions and how do they work

A

Prions are proteins made from living organisms/viruses
They act against other proteins and stop them working properally

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34
Q

why are prions a problem for dental materials (endo especially)

A

they are small so very hard to filter
heat resistant so very hard to kill by heat
very sticky and stick to instruments
in animal studies have been found in pulp so endodontic equipment is disposed of

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35
Q

why do we dispose of endodontic equipment

A

animal studies have found prions in pulp
prions are very small and heat resistant
very hard to sterilise the equipment

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36
Q

what is BSE and how does it lead to CJD

A

BSE is a prion infection in the brain of cows
cow brain fed to other cows spreading the BSE
cow brain fed in human food
causing CJD infection in human brain

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37
Q

how does CJD work

A

BSE prion from cow brain
Inhibit nerve and brain function
normal PrPC converted into ‘Rogue’ PrPSC
Aggregate into long fibres and amyloid plaques (the picture on the right is 3 subunits that would stack on top to form a fibre)
Loose ability to move, speak and process information

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38
Q

what antigens can be found on the outside of gram negative bacterial walls

A

H - flagella
K - capsule
O - LPS on outer surface
Peptidoglycan -

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39
Q

what is the H antigen

A

flagella

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40
Q

what is the O antigen

A

LPS outer surface

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41
Q

what is the K antigen

A

capsule

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42
Q

describe the cell wall of a gram negative bacteria

A

Double membrane asymmetric phospholipid bilayer
Thin layer of peptidoglycan in between membranes held to the outer surface with lipoproteins
Lipid A attached to a polysaccharide chain = lipopolysaccharide LPS antigen on outer surface = antigen O which deters complement factors preventing MAC
Polymer capsule antigen K which Deter antibodies and evade antibody binding
Therefor stops opsonization

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43
Q

what is the function of a bacterial capsule Antigen K

A

Deter antibodies and evade antibody binding
Therefor stops opsonization

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44
Q

what is the function of LPS antigen O

A

Deters complement factors preventing MAC

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45
Q

what is the structure and gram stain and main virulence factor of Neisseria and give 2 main examples

A

Gram Negative Diplococci
variable capsule being virulence factor
N. Meningisitis
N. Ghonnorreha

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46
Q

what can N.meningitidis cause and what are the symptoms of this

A

meningitis
symptoms include:
Rash doesn’t blanch
Stiff neck
Cold feet
Fever
Bright light intolerance
Vomiting

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47
Q

what is meningitis

A

Infection of CSF and meninges
Commensal carriage in pharynx/nasopharynx can enter the bloodstream or go directly into the sub-arachnoid plexus
Grow in the CSF
Inflammation of capsules around the brain e.g. meninges put pressure on the brain

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48
Q

what vaccines are used against meningitis and what are the different types

A

N.meningitidis
type A,B,C,Y,W135 based on capsule variance
B vaccine and tetravalent A,C,Y,W135
must be above 2 years old

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49
Q

what is the most common capsule type of N.Meningitidis

A

B capsule serogroup

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50
Q

what % of people will carry meningitis in nasopharynx

A

10-25%
50% in winter seasons

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51
Q

what are the common age/place outbreaks of meningitis

A

1st year of life and 16-23 at university
2/3 of cases are under the age of 5
Sub-saharan - African meningitis belt through mid africa with high prevalence e.g. MECCA

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52
Q

what vaccine must people have before going on a MECCA pilgrimage

A

meningitis ACY135

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53
Q

how do we diagnose meningitis

A

very quick in first 24 hours

CSF has many Polymorphonucelated Leukocytes PMNLs e.g. neutrophils and presence of diplococci

Blood/CFS/nasopharyngeal swab cultures
White cultures on chocolate and blood agar
DNA PCR for meningitis

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54
Q

what is the chance of passing meningitis on to close contact

A

1 in 300

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55
Q

how do we treat meningitis

A

B-lactam antibiotics
sometimes accompanied by corticosteroids
VACCINATION

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56
Q

what are fastidious microorganissm

A

microorganisms that are difficult to grow in the laboratory because they have complex or restricted nutritional and/or environmental requirements

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57
Q

how do we grow Neisseria

A

heated blood chocolate agar with CO2
fastidious

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58
Q

what is the morphology and gram stain of haemophilus influenza

A

gram negative coccus-bacilli (oval shaped)

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59
Q

what can H. Influenza cause and how does it enter the blood

A

meningitis and pneumonia (4 months-2 years)
Non-invasive disease : otitis media, sinusitis (2 - 4 yrs old)
septacaemia

Invasion by penetration of submucosa of nasopharynx

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60
Q

how many survivors of H.Influenza have disability after

A

15-35%

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61
Q

what capsule types can we get with H. Influenza and how do they act

A

A-f and some without capsules = commensals
capsule major virulence factor avoidance of c3b binding

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62
Q

which capsule type of H.Influenza causes 99% of invasive disease

A

B

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63
Q

How can we tell the difference between H.Influenza meningitis and N.Meninigitis

A

We cannot tell clinically
would have to use microscopy or PCR
N. Miningiditis = gram negative diplococci and white colonies on heated chocolate agar
H. Influenza = gram negative bacilli oval shaped

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64
Q

which vaccine works against H.Influenza infections and when is it given

A

Hib - typhoid toxin polysacchardie- protein conjugate vaccine
Haemophilus Influenza Type B vaccine
given at 2, 3, 4 months

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65
Q

what 2 factors does H. Influenzas require to live

A

X (haemin) and V (NADH)

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66
Q

how do we treat meningitis or non-invasive H. INfluenza

A

meningitis: Ceftriaxone/ Cefotaxime
non-invasive: Amoxicillin

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67
Q

what is a pathogens R number

A

its rate of spread from patient to patient

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68
Q

compare the bubonic plague and the pneumonic plague

A

bubonic = 75% death with no person to person spread
Pneumonic= 90% death with high person to person spread

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69
Q

what pathogen causes the plague

A

Yersinia pestis

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70
Q

what are the virulence factors of Yersinia Pestis (4)

A

Gram negative- has LPS (antigen O)
Contains three large virulence plasmids
Encode type III secretion needle for injection of toxins into host cells: suppress immune response, promote bacterial invasion and survival inside host cells
Can degrade C3b and C3a

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71
Q

what pneumonic describes antibiotic resistant bacteria

A

ESKAPE
Enterococcus faecium (G+)
Staph aureus (MRSA) (G+)
Klebsiella pneumoniae (G-)> hospital pneumonia/ sepsis in UK> common in environment
Acinetobacter (G-)> more of a problem in developing countries (but multiply resistant)- common in environment
Pseudomonas (G-)
Enterobacter (G-)
G- are more of a worry as becoming resistant to last resort antibiotic: Carbepenem

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72
Q

what atibiotic are some G- bacteria becoming resistant to, and which bacteria are these?

A

last resort antibiotic Carbepenem
Klebsiella pneumoniae (G-)> hospital pneumonia/ sepsis in UK> common in environment
Acinetobacter (G-)> more of a problem in developing countries (but multiply resistant)- common in environment
Pseudomonas (G-)
Enterobacter (G-)

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73
Q

describe the shape/G stain and relevance of Pseudomonas aeruginosa

A

Gram Negative motile Rod
becoming antibiotic resistant to carbepenem and major killer of cystic fibrosis

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74
Q

where do we find Pseudomonas aeruginosa in the environment and humans

A

soil and ground water
commensal bacteria found in gut

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75
Q

how does Pseudomonas aeruginosa appear on Agar

A

green spreading colonies
grape smell

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76
Q

what is the major killer of cystic fibrosis patients

A

Pseudomonas aeruginosa
leads to septicaemia and gangrene
well adapted to warm, moist conditions e.g lung/burn

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77
Q

how many species of staphylococcus are there

A

40

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78
Q

what is the coagulase test

A

some bacteria produce an enzyme called coagulase that clots blood plasma
plasma is mixed with bacteria to determine if they are coagulase + or -

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79
Q

where do we find most staph

A

nose and skin

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80
Q

what type of staph are important in opportunistic disease

A

coagulase negative
Staph aureus
Staph epidermisis

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81
Q

what are carrier and shedders

A

they carry the same load of microorganism
shedders spread disease quicker as they ‘shed’ the pathogen more

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82
Q

how would we identify Staph. Areus

A

Mannitol salts agar
selective for Gram positive, S.aureus ferments mannitol → yellow droplets on agar

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83
Q

how would we describe staph aureus (3)

A

gram positive
coagulase positive
Beta Haemolytic

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84
Q

what are some virulence factors of Staph aureus

A

Pore-forming toxins (some strains) = penumonia
Proteases = Exfoliation = exfoliation of skin = scalded skin syndrome < 2 year olds
Toxic Shock Syndrome toxin (TSST) stimulates cytokine release- tampons
Protein A (surface protein which binds Ig’s in wrong orientation)

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85
Q

what produces toxic shock syndrome toxin

A

Staph. Arues

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86
Q

what causes scaled skin syndrome

A

staph. Aureus
proteases that reduce connections between cells

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87
Q

what are some pyogenic associations with all staphylococci

A

Wound infections
Abscesses - boils
Septicemia
Endocarditis
Pneumonia
osteomyelitis

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88
Q

what are some toxin mediated associations with Staph Aureus

A

Food poisoning
Toxic shock syndrome
Scalded skin syndrome

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89
Q

what are some associations with coagulase negative staphylococcus

A

Infected implants
Septicemia
Endocarditis

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90
Q

what is the most common coagulase negative and coagulase positive staph

A

+ve = staph aureus
-ve = staph. epidermidis

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91
Q

how would we identify staph epidermidis (4)

A

gram positive (gram stain)
Staphylococcus
Coagulase negative
white colonies on blood again (previously called staph albicans)

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92
Q

how does Staph Epidermidis act

A

opportunistic on skin
forms strong biofilm (main virulence factor) around prosthesis or catheters

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93
Q

someone has an infection around their catheter, resistant to antibiotics. What is the cause

A

staph epidermidis
strong biofilm made preventing antibiotic passage

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94
Q

what is staph epidermidis’ main virulence factor

A

ability to form strong thick biofilms

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95
Q

what are the two main coagulase negative staphyloccous

A

staph epidermidids
staph saprophyticus

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96
Q

what is haemolysis and give the types that bacteria can be and how can we test this

A

haemolysis is the breakdown of blood
Alpha Hemolysis is the process of incomplete destruction of red blood cells in the blood
Beta Hemolysis is the process of complete destruction of red blood cells in the blood. Gamma haemolysis is no break down

Grow on blood agar

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97
Q

what does alpha, beta and gamma haemolytic bacteria present as on blood agar

A

alpha = partial breakdown = green/yellow patches
beta = full breakdown = clear patches
gamma = no breakdown = red

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98
Q

what is the main beta haemolytic, gram positive staphylococcus

A

staph aureus

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99
Q

what is the main alpha haemolytic staphylococcus

A

Staph Intermedius (also coagulase positive )

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100
Q

what causes beta or alpha haemolysis

A

beta = release of haemolysins that break down blood
alpha= release of H202 and reacts with Hb to partially destroy RBC

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101
Q

how do we classify streptococci

A

Haemolysis
Lancefield Grouping

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102
Q

what is Lancefield grouping

A

a method of grouping coagulase negative bacteria based on bacterial carbohydrate cell surface antigens
Lancefield A-H and K-V (A and B most pathogenic)
Antiserum is added to suspension of bacterial colony and clumping indicates recognition = +ve

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103
Q

what Lancefield groups are there and which are most pathogenic

A

Lancefield A-H and K-V
A and B most pathogenic
A = Strep. Pyogenes
B = Strep .agalactiae

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104
Q

how would we identify Strep. Pyogenes

A

Gram positive
Streptococcus
Coagulase negative
Lancefield type A

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105
Q

what can Strep Pyogenes cause

A

Cellulitis
Pharyngitis
tonsillitis
Impetigo
Scarlet Fever

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106
Q

what is Impetigo

A

skin infection leading to sores on the face and skin that burst after about a week and cause yellow, crusty scabs
Strep. Pyogenes

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107
Q

what is scarlet fever

A

red rash that affects skin and tongue often in babies (red on white skin, darker skin no colour change but texture change)
Strep. Pyogenes

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108
Q

what can follow tonsillitis and what can cause this

A

Rheumatic Fever
Strep. Pyogenes

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109
Q

what is rheumatic fever and what can cause this

A

Inflammatory disease of heart, joints, skin, brain. Often follows Strep. throat infection - follows tonsillitis - Strep. Pyogenes

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110
Q

how can we test the likelihood of Strep. Pyogenes leading to more complications like rheumatic fever and Glomerulonephritis

A

anti SLO titre

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111
Q

what are some virulence factors of Strep. Pyogenes

A

Streoptolysins O and S for haemolysis
Streptokinase breaks down clots
C5a peptidase - reduces chemotaxis + vasodilation
Erythrogenic toxin - SPeA – exaggerated response = similar to TSST

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112
Q

explain the Anti SLO titre and what it is used for

A

used to test likelihood of Strep. Pyogenes patients developing rheumatic fever and Glomerulonephritis. Tests amount of anti SLO in patients plasma

ASLO – Antibody against SLO found in plasma
ASLO reacts with SLO (streptolysin O) to neutralise haemolytic activity
Patients serum is serially diluted with constant concentration of SLO & RBCs added
Dilution of serum at which there is is still prevention of hemolysis of RBC = Anti SLO titre

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113
Q

give 2 ways of testing for anti - SLO in blood plasma and what does this tell us

A

ASLO titre with serial dilution of plasa with constant SLO and RBC
ASO rapid test where ASO binds to latex particles and presence of an ASLO titer of >200 IU/mL in the serum = agglutination of the latex particles.

Presence of anti-SLO means recent infection of Group A strep

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114
Q

explain the ASLO rapid test

A

Streptococcal exoenzymes are bound to biologically inert latex particles
If streptococcal antibodies present in the test sample, agglutination occurs.
presence of an ASLO titer of >200 IU/mL in the serum = agglutination of the latex particles.
Pt has antibodies and has had recent infection

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115
Q

where is Strep. Pneumoniae found

A

oro-pharynx of 30% of population

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116
Q

what does Strep. Pneumoniae cause

A

pneumonia, otitis media, sinusitis, meningiti

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117
Q

what are some predisposing factors of Strep. Pneumoniae

A

impaired mucus trapping (e.g. viral infection)
Hypogammaglobulinemia - immunocompromised
Asplenia - immunocompromised

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118
Q

what is Strep. Pneumonia virulence factors

A

Pneumolysin cytotoxin - causes lysis of cells
teichoic acid (choline) - binds to choline helping to bind to host cells
Peptidoglycan - inflammatory
polysaccharide (84 types), antiphagocytic

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119
Q

what are the 2 main vaccines for Strep. Pneumoniae

A

PCV - Pneumococcal conjugate vaccine (protein-polysaccharide conjugate) for children e.g. PCV13 - 13 most common carbohydrates in capsule
PPSV – Pneumococcal polysaccharide vaccine eg ‘PPV23’
polyvalent vaccine – against 23 most common types of capsule polysaccharide
available to >2 year olds at risk of infection and adults

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120
Q

what are viridians strep

A

collective streptococci of the oral cavity

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121
Q

what organisms might be accountable for deep organ abscesses

A

Viridians Strep

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122
Q

what is the tell tale sign of Corynebacterium diphtheriae

A

Pesduomembranes grey/green on tonsils and thick ‘bull neck

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123
Q

how would we grow diptheria

A

potassium tellurite

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124
Q

how do we detect C. Diptheria

A

Elek plate - strip of filter paper with antitoxin and streak suspicious bacteria along the filter paper and form precipitates if the toxin is being released)

Or PCR

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125
Q

other than C. Diptheria, what else can cause Diptheria

A

C. Ulcerans

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126
Q

what is the main cause of osetomyelitis

A

Staph Aureus

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127
Q

what are draughtsman colonies and what causes them

A

white, drafts pieces, raised edges, dimple in middle, colonies on blood agar
S. Pneumoniae

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128
Q

what is blood agar selective for

A

aerobic bacteria

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129
Q

what are the three types of anaerobe

A

obligate anaerobes = harmed by oxygen
Facultative anaerobes = can do both aerobic and anaerobic respiration
Microaerophiles- grow in atmosphere of low oxygen <5%

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130
Q

what is the maximum ATP/mol of glucose possible with aerobic respiration

A

38

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131
Q

instead of entering the oxygen dependant TCA cycle, what happens to pyruvate in anaerobic respiration

A

organic electron acceptors to produce
2ATP
Acids (VolitileFAs) - lactate is produced under extreme exercise
Alcohols

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132
Q

A lot of anaerobes cannot survive in the presence of oxygen due to the radicals produced. How does P.gingivalis survive these radicals?

A

P.Gingivalis reduces superoxide→peroxide→water = survive in oxygen

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133
Q

what is a effective antibiotic for anaerobes? how does it work

A

metronidazole
pre-drug is metabolised by anaerobes and produced metronidazole to kill bacteria

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134
Q

what is the morphology and products of Clostridia

A

Large, straight, Gram-positive bacilli
Produce endospores - inside cell
Produce exo-toxins

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135
Q

how does Cl. Perfringens show on a red blood agar

A

double beta haemolytic
fully clear in middle
encircled by a ring of partial haemolysis

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136
Q

what does Cl. Perfringes cause

A

Gas gangrene
food sickness

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137
Q

what is the leading 3 causes of food poisoning

A

norovirus
salmonella
Cl. Perfringes

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138
Q

what is the incubation period for Cl. Perfringens

A

10-12 hours

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139
Q

what is the incubation period for Cl. Tetani

A

10-14 days

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140
Q

what is the morphology, agar and gram stain of Cl. Tetani

A

drumstick rod with terminal ball end
thin white film on blood agar
gram positive

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141
Q

what is tetanus and how is it caused

A

Acute spastic paralysis caused by a potent bacterial neuro-exotoxin
locked jaw and uncontrolled contraction of muscles in CNS
Cl. Tetani spores enter wound and travel along nerves

142
Q

what is the gram stain, morphology of Cl. Botulinum

A

Bacillus with sub-terminal spores
Gram positive

143
Q

what does Cl. Botulinum cause

A

botulism severe food poisining

144
Q

what is Cl. Botulinum incubation period

A

1-2 days

145
Q

what does Cl. Difficile cause

A

pseudomembranous colitis, hospital/antibiotic related diorrhea

146
Q

what causes Pseudomembranous colitis

A

Cl. Difficile

147
Q

why is Cl. Difficile present in hosptial

A

lots of antibiotics, outcompetes other bacteria after use of antibiotics
very heat resistant and resistant to sterilisation
Travels in Faeces

148
Q

how many toxigenic types are there

A

5 A-E

149
Q

how do we detect toxins

A

Nagler Reaction Plate

150
Q

describe Tetanus Toxin

A

Classic A-B neurotoxin called Tetanospasmin
A domain contains active site - Zinc endopeptidase - inhibits release of inhibitory trasmitter = continuous excitement
B domain> Carbohydrate receptor binding- Sialic acid containing poly-sialic-gangliosides

151
Q

how do we treat tetanus

A

anti toxin
penecillin
metronidazole

152
Q

how do we prevent tetanus

A

toxoid vaccination

153
Q

how many cases of tetanus every year

A

15-30,000

154
Q

how do we get botulism (3)

A

ingestion of the pre-toxin
soil or reheated food that has been left to cool for too long or home tinned foods

155
Q

what does the botulism toxin cause

A

Flaccid paralysis - uncontrolled relaxation
Drooping eyelids, progressive
motor loss, flaccid paralysis;
Neurological symptoms- dizziness
respiratory & cardiac failure

156
Q

describe the botulism toxin

A

potent neurotoxin
AB toxin with 7 types A-g
A B and E most common
A active site Zinc endopeptidase
Affects peripheral cholinergic synapses
blocks release of acetylcholine
IRREVERSIBLE BINDING!

157
Q

how many types of botulism toxin are there and which are most cmmon

A

7 types
A-G
A B and E most common

158
Q

how does the botulism toxin cause uncontrolled relaxation

A

A site is the active site
Zinc Endopeptidase
Irreversibly blocks release of acetylcholine so no excitation

159
Q

how do we treat botulism

A

polyvalent anti-toxin

160
Q

what can we use the botulism toxin for therapeutically

A

t can weaken muscles temporarily when injected in small amounts, used for treatment of spasms and dystonias, e.g
Strabismus (Cross-eyes)
Bruxism (tooth grinding)> linked to bone loss
Torticolis (neck spasms)
Muscle spasms in cerebral palsy
BOTOX cosmetics

161
Q

how do we diagnose Cl. Difficle

A

Stool sample

162
Q

how do we treat C. Difficle

A

remove offending broad spectrum, selective antibiotic e.g. clindamycin/penicillin
vancomycin or metronidazole

163
Q

what are the virulence factors of Cl. Difficle and how do they act

A

TcdA and TcdB
inactivates GTPase Rho family
causes apoptosis and cell damage of intestinal epithelial

164
Q

describe the morphology and gram stain of porphymonamos e.g. P. Gingivalis

A

Gram-negative, non-motile, rod-shaped

165
Q

why do black pigmented anaerobes appear black on blood agar

A

they store oxidised iron which is black

166
Q

what is the morphology and staining of fusobacterium

A

LONG Rod shaped spindle-shaped bacilli, Gram negative

167
Q

where would we find Eubacterium and Bifidobacterium

A

isolated from abdominal infections POST oral/ genital trauma.

168
Q

what relevance does Fusobacterium Nucleate have to cancer

A

Oral infection of F.Nucleatum in the gut is linked to colon cancer
FadA adhesin stimulates oncogenic response in colon- BIG news in microbiology- READ about it….

169
Q

describe the general structure and staining of actinomyces

A

filamentous sometimes branched
gram positive with uneven staining

170
Q

which bacteria is most found in actinomycosis

A

A. Israeli 70%

171
Q

what would A.Meyeri cause

A

brain abscess

172
Q

what type of bacteria are likely to cause brain abscess

A

A. Meyeri

173
Q

name 2 type of actinomycetes found in caries

A

A. odontolyticus
A. gerencseriae

174
Q

how do we grow actinomyces and what does it appear as

A

‘molar colonies’ will grow in an anaerobic brain heart infusion broth due to them being fastidious and facultatively anaerobic

175
Q

how many species of actinomyces are there

A

21

176
Q

where are actinomyces found

A

mouth, gut and vagina
commensals

177
Q

what is Actinomycosis

A

Rather rare infectious agent
Painful slow growing abscesses – months to develop
Affected people have often just had dental treatment, poor oral hygiene, periodontal disease
Large abscesses – can penetrate bone and muscle to the skin where they can break open leaking pus

178
Q

where do most actinomycosis occur

A

55-65% cervicofacial

179
Q

what type of pus do we get from actinomycosis

A

‘sulphur pus’ yellow

180
Q

what does actinomycosis look like histologically (3)

A

Locules of pus and filametous gram positive bacteria
surrounded by fibrous eosinic amorphous club shaped material
surrounded by dense sheets of neutrophils

181
Q

how does an Actinomycosis abscess defend itself (2)

A

Amorphous polysacchardie protein matrix
Splendore-Hoeplli Club shaped cationic protein complex including fibrin and Ag-Ab complexes
Both wall off from host immune system
The characteristic formation of the peri-bacterial or peri-fungal Splendore-Hoeppli reaction prevents phagocytosis and intracellular killing of the insulting agent leading to chronicity of infection.

182
Q

what disease is associate with Splendore-Hoeppli Phenomenon

A

Actinomycosis

183
Q

what are the virulence factors of actinomyces

A

induction of chronic inflammation
walling off from defences
slow growth as large aggregates in a matrix

184
Q

what is treatment for actinomycosis

A

Surgical removal/drainage
6-8 week course of penicillin, amoxicillin o tetracycline

185
Q

what is the structure of candida

A

Trimorphic
blastopore (yeast) - circles
Pseudohyphae - short chains
Hyphae (chlamydospores) - long chains

186
Q

what agar can we use for growth of Candida

A

Sabouraud’s dextrose medium SAB - straw colour
doesnt row bacteria, Candida. Albicans grows white colones

187
Q

what is chromatic agar used for

A

growth of multiple fungi, differentiating by enzyme

188
Q

compare the 3 forms of Candida Albicans

A

Yeast with daughter spores and scars from past spores
Pseudohyphae with mother and rod daughter which are walled off due to environment
Hyphae - no wall between mother and daughter

189
Q

what is the main fungus and bacteria to cause infective endoarditis

A

S. Aureus
C. Albicans

190
Q

What is Candidosis

A

Systemic infection of Candida Albicans
50% fatal

190
Q

What is Candidosis

A

Infection/Colonisation of Candida Albicans on skin/mucosa

Systemic infection of Candida Albicans is uncommon but
50% fatal

191
Q

what causes chronic Atrophic Candidosis

A

Dentures

192
Q

what causes chronic hyperplastic candidosis

A

smoking

193
Q

what causes acute pseudomembranous Candidosis

A

Trush/HIV

194
Q

what causes Erythromatus Candidosis

A

Red patches = HIV

195
Q

give 4 pre-disposing factors of Candidosis

A

Prostheses - no exfoliation, no desquamation, candida proliferation, hyphae
Low saliva - no flow; low soluble defences
Antibiotics - reduced bacterial competition
Immunosuppression - no T-cell defence
diabetes, immunodeficiency
Smoking

196
Q

which type of form is more dangerous in fungi

A

yeast forms = commensals
Hyphae = Pathogenic

197
Q

what pH favour hyphae/Yeast

A

under 6 = yeast
over 6 = hyphae

198
Q

how do candida albicans attach to epithelium

A

Agglutinin-Like Sequence (ALS)
8 family members, ALS3 appears to be most important for adhesion to cells – only expressed by hyphae

199
Q

how do hyphae invaginate into epithelium

A

Secrete inactive candid lysin - A pore forming toxin that kills human cells and also initiates an immune response
Hyphae go into well they create and carry on

200
Q

what is candidolysin

A

A pore forming toxin that kills human cells and also initiates an immune response

201
Q

what is SAP

A

secreted Aspartyl Proteases
secreted by the tip of Hyphal Penetration

202
Q

what are 2 mechanicams important for hyphal penetration

A

SAP - Secreted Aspartyl Proteases
Candidolysin

203
Q

what is the most common cause of hospital-acquired-related death in the US (even greater than MRSA !)

A

systematic Candidiasis
50% mortality

204
Q

why can we use zebra fish ethically and biologically (2)

A

they are not classed as animals and their endothelium is flourescent

205
Q

how does candida cause death

A

Enters blood stream and epithelial attachment occurs ALS (ALS3)
Travels along endothelium until a bend but carries on through endothelium
with SAP and actinolycin
causing infection around body in organs causing organ failure

206
Q

how do we treat candidiosis

A

Fluconazole - antifungals
removal of predisposing factors

207
Q

describe the structure and gram stain of spirochetes

A

gram negative very thin spiral shaped rods

208
Q

how do spirocheates move

A

internal flagella

209
Q

how are different spirochetes identified

A

Identification by Sequence analysis of 16s rRNA gene which is well conserved due to need for function

210
Q

what and where are axial filaments found

A

found in the periplasmic space of spirochaetes
internal flagella

211
Q

how many people have candida albicans

A

40-60% have candida albicans in their mouth

212
Q

what is wild type fungus

A

mixture of yeast forms and hyphae forms

213
Q

what would happen if the internal flagella were removed from spirochaetes

A

this would lead to the spiral shape going and the bacteria becoming straight non-motile

214
Q

do spirocheates have LPS?

A

no

215
Q

what are the three major spirocheates that cause clinical problems

A

Leptospira = Weil’s disease Leptospirosis
Borella = Lyme Disease, Relapsing fever
Treponema = Syphilis, ANUG, Periodontitis

216
Q

what are zoonotic infections

A

They have an animal reservoir of infection that can under certain circumstances infect humans via a zoonotic vector

217
Q

what bacteria causes Lyme’s Disease

A

Borrelia burgdorferi - zoonotic, tics

218
Q

how can we view Borrelia burgdorferi

A

EM or darkfield microscopy

219
Q

how does lymes disease spread

A

spirocheate lives in the midgut of rodents
Uninfected larval ticks feed on rodents and get bacteria in saliva
live in midgut
further move to saliva
ticks bite humans and when they d, they release anaesthetic so we don’t feel it. In doing so, releasing Lymes infected saliva

220
Q

what symptoms is specific to lymes disease

A

Bulls eye rash

221
Q

what happens if a patient goes undetected with lymes disease

A

flu like symptoms
bulls eye rash
30% patients get rash somewhere else on body
1 week to 2 year post infection = arthiritis, neurological problems due to bacteria hiding in joints/nerves

222
Q

how do we treat lymes disease

A

doxycycline 100 mg twice per day or 200 mg once per day 3 weeks
Borrelia burgdorferi

223
Q

how can we prevent Lymes disease

A

wear long clothes
DEET repellents
vaccination (pulled due to antivaxx movement)

224
Q

what is the main virulence factor of Borrelia burgdorferi

A

motility

225
Q

how does Borrelia burgdorferi survive in low iron levels

A

Copes with low-iron levels by using Manganese instead of iron as an enzyme co-factor

226
Q

what is Borrellia Recurrentis and what does it cause and how

A

Spirochaete
recurrent fever of 3-10 episodes
due to genetic variation of surface protein

227
Q

what causes Wiels Disease

A

“Leptospira interrogans

228
Q

describe the shape of Leptospira interrogans

A

very thin, coiled spirochaete
Two terminal Periplasmic flagella

229
Q

where would we find “Leptospira interrogans

A

stagnant water
near dog/rat colonies as in their urine

230
Q

what is Leptospirosis

A

infection of

231
Q

what are the symptoms of Leptosperosis and what can it lead to

A

Febrile, flu-like illness with muscle pain, reddening of eyes, and other symptoms such as diarrhoea and in some cases meningitis and Haemorrhage in Aqueous humour of eye and CSF
10-15% of cases develop Weil’s disease:
kidney failure
Jaundice and liver failure, yellow eyes
Most symptoms caused by damage to blood vessel

232
Q

what are most symptoms of Leptosperosis due to

A

damaged blood vessels

233
Q

How do we reduce cases of Leptospirosis and Wiels Disease

A

Rodent control
Doxycycline
Avoid swimming in infected rivers

234
Q

why do patients with Leproperosis get red eyes

A

Haemorrhage in Aqueous humour of eye due to damaged blood vessels

235
Q

how do we treat necrotising ulcerative gingivitis

A

metronidazole or Hydrogen peroxide washes
deep removal of plaque and bacteria

236
Q

what causes ANUG

A

acute necrotising ulcerative gingivitis
Treponema Vincentii , Rods and fusobacterium (fuso-spirocheatal complex)

237
Q

what are the red complex bacteria

A

Porphyromonas gingivalis
Tannerella forsythia
Treponema denticola

238
Q

describe the structure of T. Denticola

A

spirochete, gram negative, anaerobic

239
Q

what are T. Denticola’s virulence factors

A

Co-adherence with other oral bacteria in mixed biofilm and to the basement membrane
good at invading tissues and oral mucosa
Proteases
Motility due to internal flagella

240
Q

compare narrow and broad spectrum antibiotics

A

narrow only aerobic/anaerobic or only gram positive/negative
broad can be negative AND positive or aerobic AND anaerobic

241
Q

what is selective toxicity

A

where a drug has a high affinity and toxicity to bacteria
but low toxicity to human cells

242
Q

the larger to theraputic index…

A

the safer the drug is for use

243
Q

ideal characteristics of an antimicrobrial

A

High Theraputic index
target is is not present in man
if microorganism has higher affinity for the drug than man
It should be non allergenic to the host.
It should not eliminate the normal flora of the host.
It should be able to reach the part of the human body where the infection is occurring.
It should be inexpensive and easy to produce.
It should be chemically-stable (have a long shelf-life).
Microbial resistance is uncommon and unlikely to develop

244
Q

what three ways can we classify anti-biotics

A

by chemical structure e.g. β-lactam ring
by target site
according to whether they are bactericidal (kill) or bacteriostatic (inhibit growth)

245
Q

how can we test the efficacy of an anti-biotic (2)

A

disc plates on agar
lquid MIC/MBC testing

246
Q

explain MIC MBC testing

A

MIC = minimal inhibitory concentration
MBC = minimum bactericidal concentration
Standardised [bacteria] + different [drug]
MBC usually higher than MIC

247
Q

what are the main targets for antibiotics

A

Cell wall - peptidoglycan
Protein synthesis - ribosomes or enzymes unique to bacteria
Metabolic pathways
DNA
Membranes
Enzymes

248
Q

what is antibiotic resistance

A

an organism that is not inhibited or killed by an antibacterial agent at concentrations of the drug achievable in the body after normal dosage.

249
Q

give three ways of spread of antibiotic resistance

A

Some resistance is by chromosomal mutation, some is coded for by plasmid DNA
Some plasmids are transmissible - between species
Transposons can carry resistance genes and jump between chromosome and plasmids

250
Q

what mechanisms might cause an antibiotic to no longer work (4)

A

The target is structurally altered (by mutation) -Now has a lower affinity for the antibacterial (PBPs) Penicillin-binding proteins

The target is overproduced Dihydropteroate synthetase (bacterial target) and sulphonamide

The drug is not activatedAerobes and metronidazole - intrinsic, not acquired resistance

The drug is removed e.g. Β-lactamase - breaks beta lactam ring produced by bacteria

251
Q

how can we gain a blood sample for testing infections

A

needle aspiration

252
Q

what organisms are likely to be found in pharyngitis

A

Streptococcus pyogenes: beta haemolytic, Coagulase -ve, Lancefield Group A
EBV (glandular fever is virus with no medication)

253
Q

what type of bacteria are likely in a dental abscess

A

Viridans group streptococci
Anaerobes
Gram negative rods

254
Q

what is the centor criteria

A

set of criteria to determine if a sore throat is of viral or bacterial origin

255
Q

what are the set of centor criteria (CENT)

A

Bacterial if:

Cough is absent.
Exudates are present on the tonsils.
Nodes are tender in the anterior cervical region.
Temperature of 100.4 F by history (i.e. fever by history).

256
Q

what determins if the antibiotic can penetrate the site (2)

A

the pH of the site - abscess/infection is low pH
weather the drug is lipid soluble

257
Q

why is infective endocarditis hard to treat (3)

A

build up and infection of bacteria on the heart valves
most antibiotics work via the blood stream
heart valves do not have any blood supply

258
Q

give an example of intrinsic resistance

A

Naturally resistant
pseudomonas is naturally resistant to penicillin

259
Q

give some ways of finding if an antibiotic is effective

A

sensitivity testing with discs
breakpoint testing
tube dilution

260
Q

explain how we can find the MIC of an antibiotic

A

MIC minimum inhibitory concentration
agar plat with cultured bacteria
place strip of increasing [antibiotic]
will form a oval shape, lowest [antibiotic] with clear zone is MIC

261
Q

what are the major 2 determinants of effectiveness of an antibiotic

A

the concentration at the binding sites
the time that the antibiotic remains on these binding sites to allow sufficient inhibition of metabolic processes

262
Q

compare concentration and time dependant killing

A

time dependant is done at a lower concentration, closer to the MIC for a longer time
concentration is done is done or less time at the peak concentration (higher [])

263
Q

give a few ways that horizontal gene transfer can occur

A

Conjugation is where plasmids are shared (not in nucleus) by exocytosis or endocytosis e.g. MRSA
Virus vector damages bacteria and then released DNA spreading bacterial DNA
Transformation when bacteria dies its DNA is released and can be picked up
Resistance start to occur in the gut and where antibiotics have their major effect

264
Q

what is the structure of herpes virus (3)

A

Icosahedral capsid surrounding dsDNA Virus
tegument glycoproteins on outside very important for specificity e.g. binding to oral mucosa

265
Q

what are the three alpha-herpese viruses

A

Type 1 Herpes Simplex Virus
Type 2 Herpes Simplex Virus
Varicella-Zoster Virus (VZV)

266
Q

what are the 3 beta-herpes viruses

A

Cytomegalovirus (HCMV)
Human Herpesvirus 6
Human Herpesvirus 7

267
Q

what are the 2 gamma-herpes viruses

A

B-lymphocytes Epstein-Barr virus (EBV)
Human Herpesvirus 8 (important in HIV)

268
Q

what mucosa does HHV-1 and HHV-2 affect and why does this occur

A

1 = oral mucosa
2 = genital and oral due to cross contamination

due to different tegument glycoproteins on outside

269
Q

what are the two stages of herpes viruses

A

infection
reactivation

270
Q

what are the two stages of HHV-1 (3)

A

Herpes Simplex (infection)
Herpetic Gingivostomatitis

lesions around the tongue causing epithelial damage, becoming latent by transferring from epithelium to the nervous system to the trigemnical ganglion. This stays for ever and is never removed
50% of cases = retrograde infection –>

Herpes Simplex (reactivation)
Herpes Labialis (cold sores)

271
Q

what can cause secondary herpes simplex re-activation

A

in 50% of patients, virus will travel down from the trigeminal ganglion and re-infect the neurones it spread from

this can be caused by many factors:
UV light
Stress
Illness
Immuno- suppression

272
Q

of those infected with primary herpes infection, how many are symptomatic and what would they present with

A

1-10% are symptomatic
herpetic gingivostomatitis

273
Q

what is the incubation, duration and symptoms of herpatic gingivostomatitis

A

Incubation period 3-10 days
Duration 5-14 days
Multiple vesicles - rupture to form extensive sloughing ulcers
Gingivitis with erythema and sloughing
Malaise, pyrexia, lymphadenopathy

274
Q

how could we diagnose gingivostomatitis genetically and histologically

A

genetically = PCR
histologically = ballooning of epithelial cells due to intraepithelial vesicles

275
Q

how do we treat herpatic gingivostomatitis (3)

A

Acyclovir (500mg 5 x daily for 5 days) if found early or in immunocompromised
Fluids and soft diet
Analgesics / antipyretics (paracetamol) Local antiseptics e.g. chlorhexidine Topical analgesics e.g.

276
Q

what is added to cordysol toothpaste apart from flouride

A

CHX

277
Q

how does Acyclovir work (4)

A

mimics structure of guanosine
when HSV replicates, TK enzyme phosphorylates Acyclovir
implemented into DNA translation and acts as a gene terminator
prevents formation of new proteins

278
Q

What is herpes Labialis and what are its clinical features

A

Prodromal irritation - tingling (coming down neurones)
Vesicles at or near mucocutaneous junction of lips (or skin, chin)
Crusting lesions lasting 7-10 days Usually re-occurs at the same

279
Q

what is management of Herpes Labialis

A

5% Acyclovir cream
prophylactic acyclovir very rare - only in immunocompromised patients or if patients are having very frequent problems

280
Q

what are the effects of using prophylactic Acyclovir for Herpes 1

A

reduces duration of cold sores
reduces pain
Reduces re-occurance by 50%

281
Q

what is herpatic whitlow and how can we prevent it

A

very painful herpetic infections of the fingers of those handling patients’ oral tissues with herpes simplex 1 Virus

prevent by wearing gloves and good cross contamination control

282
Q

what is HSV encephalitis and what does it effect

A

swelling of frontal lobes of brains in 1 in 500,000 patients
Usually only people >50 years (HSV-1) and neonates (HSV-2) affected

283
Q

what is the mortality and recovery rate of HSV encephalitis

A

70% - 80% mortality if untreated
Of survivors, only 3% return to normal

284
Q

how might we tell if an adult has HSV encephalitis

A

headaches
change in behaviour over a few days
history of HSV infection

285
Q

what are the two stages of VZV

A

varicella = chicken pox = primary infection
Zoster = shingles = secondary infection

286
Q

at what age do 70% of shingles cases occur

A

> 50

287
Q

what 4 factors lead to increased chances of developing shingles in the future

A

Age (70% >50yrs)
Stress
Illness
Immunosuppression

288
Q

explain the progression of a shingles belt

A

blisters of epithelial balooning cells intracellular vesicles
turns to rash
release and heal
contagious throughout

289
Q

what are the three phases of oral herpes zoster

A

Pre-herpetic neuralgia
Rash
Post-herpetic neuralgia

290
Q

what is oral herpes zoster

A

infection of VZV along the trigeminal nerves from the trigeminal ganglion

291
Q

explain pre-herpetic oral zoster

A

Pain in the distribution of the affected division of the trigeminal nerve
Prior to the development of the rash
May mimic dental pain = think shingles if tooth ache with sound teeth

292
Q

if a patient has sound teeth but is complaining of tooth ache in a lower or upper reigon, what might this be

A

oral zoster pre-herpatic symptoms

293
Q

explain the rash of oral zoster virus

A

Unilateral vesicles in the distribution of a branch of the trigeminal nerve: Ophthalmic, Maxillary, Mandibular
Vesicles break down to form
Ulcers (mucosa)
Crusting lesions (skin)
Last 2-3 weeks

294
Q

which division of the trigeminal ganglion is oral zoster most likely to have severe implications

A

opthalmic divison:
glaucoma, cataract, double vision and scaring of the cornea

= shingles of the eye send to hospital immediately

295
Q

how do we manage oral zoster

A

cyclovir 800mg 5 x daily for 7 days if seen soon after lesions develop
Analgesics
Ophthalmic referral if eye involved
Avoid contact with children

296
Q

what is post-herpetic neuralgia of oral zoster

A

continuous pain after reactivation in the elderly
not well understood
10% of patients go on to get extremely unpleasant intractable burning pain in the distribution of the affected nerve
More common in the elderly
Effective early treatment of zoster may ↓ risk of neuralgia
Treat pain with tricyclic anti-depressants and neuropathic pain drugs

297
Q

how do we treat post-herpetic oral zoster

A

Treat pain with tricyclic anti-depressants and neuropathic pain drugs

298
Q

how many patients with shingles will get post-herpetic neuralgia

A

10%

299
Q

what is EBV

A

Epstein Barr virus affecting B cells
beta-herpes virus
depending on the local environment, can cause 4 different diseases

300
Q

depending on the local environment, can cause 4 different diseases. what are they

A

Infectious Mononucleosis (Galndular Fever) – acute 1º infection with EBV - kissing disease
Burkitt’s Lymphoma – a B-cell malignancy
Nasopharyngeal Carcinoma – an epithelial cell malignancy
Oral Hairy Leukoplakia – seen in AIDS patients and some transplant recipients

301
Q

where does EBV initiate and then where does it remain latent

A

Primary infection EBV replicates in oro-pharyngeal epithelial cells but then establishes latency in B- lymphocytes.

302
Q

how many people have EBV

A

95%

303
Q

what are symptoms of symptomatic EBV

A

Symptoms include sore throat, swollen cervical lymph nodes and mild fever, Petichae on palate (red spots)

304
Q

a young patient has a sore throat, cervicale lymphadenopathy and petechiae. what are they likely to have

A

Infectious mononucleosis (Oral) from EBV

305
Q

where is Burkitts syndrome prelevent and what is it

A

b cell carcinoma caused by EBV
found in tropical Africa at elevations below 1500 metres where malaria is present

306
Q

how do we treat burkitts syndrome and why is this not usually done

A

cyclophosphamide (chemo)
relatively cheap but not available where this disease is prelevent:
tropical Africa at elevations below 1500 metres where malaria is present

307
Q

a child, recently migrated from tropical Africa, has a very swollen jaw/face and is generally ill. what are they likely to have

A

Burkitts syndrome
B cell carcinoma
caused by EBV

308
Q

how does Burkitt’s syndrome often present

A

usually forms a bone tumour on the mandible

309
Q

where is nasopharyngeal cancer related to EBV and why

A

japand
due to high soya eating

310
Q

how might cytomegalovirus present

A

Glandular fever-like illness
Salivary gland swelling
rarely causes illness in healthy individuals

311
Q

what might CMV cause in immunocompromised patients

A

Large ragged oral mucosal ulcers
Salivary gland swelling
Retinitis

312
Q

what is the cause of kapsosis sarcoma in AIDs patients

A

HSV-8

313
Q

what does HSV-8 cause

A

usually has no effect
in very immunocompromised patients (AIDS) the patient will get Kapsosi’s Sarcoma = very large, red swollen gingiva

314
Q

what is HIV

A

human immunodeficiency virus
causes depletion of host immune system resulting in AIDs

315
Q

what is HIV

A

human immunodeficiency virus
causes depletion of host immune system resulting in AIDs
type of lentivirus - slow growing retrovirus

316
Q

what is AIDs

A

Acquired Immune Deficiency Syndrome

317
Q

give 5 ways HIV is transferred

A

sexual contact
blood contamination
placental carriage to uterus
breast milk
infected blood products e.g. meat

318
Q

what are, and compare breifly, the two types of HIV

A

HIV 1 = more common, more symptomatic and more easily tranferred

HIV 2 = less pathogenic and less easily tranferred, localised to western africa

319
Q

why does HIV mutate readily

A

has no proofreading genes
if mistakes are made during reverse transcription, there is nothing to correct these mistakes
forms new genes and new proteins

320
Q

what do M, O and N stand for e.g. HIV-1m

A

m = main/pandemic
n = new
o = outlier e.g. confined to cameroon

321
Q

describe the structure of HIV (5)

A

2 single stranded RNA
reverse transcriptase
proteases

protein core Capsid

Capsule lipid membrane with glycoproteins:
-gp120
-gp41
(begin as one strand, then get cut in two by the proteas)

322
Q

what are the major two glycoproteins on HIV

A

gp120 and gp41
(begin as one protein but then cut in two by a proteas)

323
Q

explain how HIV binds to cells, and which cells

A

CD4 cells macrophages and T-cell
have receptors for gp120 and gp41 expressed by HIV
intial attachment CD4 - gp120
co-receptor attachment CCR5 receptor - gp41

324
Q

how might someone be naturally immune to HIV

A

HIV attaches gp120 to CD4
then co-receptors need to attach gp41 - CCR5 (macrophages)
if pt has mutation in CCR5 protein, co-receptor cannot occur so HIV cannot attach to CD4 cells

325
Q

how many people are immune to HIV and how

A

2-14% europeans (caucasian) , and 15% of Icelandic
mutatin in CCR5 gene that is used by HIV to attach via gp41

326
Q

after binding, how does HIV proliferate

A

uncoated and release capsid releasing RNA strands
reverse transcriptase
into DNA double stranded
incorporated into genes of host immune cell
transcribed when the cell replicates
more replication occurs due to infection, making more HIV which destrosy CD4 cells

326
Q

after binding, how does HIV proliferate

A

uncoated and release capsid releasing RNA strands
reverse transcriptase
into DNA double stranded
incorporated into genes of host immune cell
transcribed when the cell replicates
more replication occurs due to infection, making more HIV which destrosy CD4 cells

327
Q

what is the most important post-translational modification with HIV

A

the snipping of glycoproteins into two seperate glyocproteins gp120 and gp41 for attachment to CD4 and CCR5 (on macropahges, or CXCR4 on T cells) respectivly

328
Q

explain the virus variation during HIV infection

A

Isolates from early in infection- CCR5 (M) macrophage tropic and low cytopathic effect- more transmissable

Isolates from late infection- CXCR4 (T) high cytopathic ability – less transmissable, causes more problems

329
Q

explain the course of HIV infection

A

initial infection peaks CD4 cells
viral load increases to peak at 6 weeks
= flu symptoms
viral load steady level
Cd4 slowly reduce over 3-10 years
when Cd4 < viral, viral laod increases massively
oppertunistic diseases show now

330
Q

what are some AIDs defining illnesses

A

Candidia Albican oral infection
Kapsosis Carsoma HHV-8
HSV- Herpes simplex virus- chronic oral infection
EBV- Hairy leukoplakia, and B- cell lymphomas
Cryptosporidum (chronic diaarhoea)
Toxoplasma gondii (disseminated, including CNS- from Cats) - most common diagnostic disease, can get from cats (Avoiddealing with ctas if pregnant and lower immune system)

331
Q

what is cryptosporidum

A

chronic diarrhea
aids defining

332
Q

what is toxoplasma gondii

A

Common parasite, common in uncooked meats or cat litter
causes toxoplasmosis = gives un-noticed symptoms of flu syptoms for 7 days
in reduced immune system (pregnancy, HIV) can be life threatening
most common diagnostic tool for HIV

333
Q

why should pregnnat women not handle cats

A

prengnancy = immunocompromised
more suseptable to toxoplasmosis caused by the common parasite toxoplasma gondii found in cat litter and blood

334
Q

what would the mouth of a pt with HBV look like

A

hairy, striated leukoplakia on tongue

335
Q

give 4 oral representations of AIDS

A

hairy, striated leukoplakia - HBV
oral candidiasis - thrush
erythematous candidosis - red markings
gingival erythema

336
Q

why does HIV treatment rely on compliance (2)

A

drugs have a short half life so must take regularly
have to take in combination so multiple drugs

337
Q

name some targets for HIV treatment

A

protease inhibitors (no gp120 and gp41)
Reverse transcriptase inhibitors (no DNA)
CCD5 entry inhibitors (no co-receptor)

338
Q

what are NNRTI and NRTI

A

(non) nucleoside reverse transcriptase inhibitors
main tx for HIV

339
Q

how do NRTIs work

A

nucleoside reverse transcriptase inhibitors
similar shape to a nucleotide
implemented into growing nucleotide chain
terminates the chain = no DNA formation

340
Q

what is HAART

A

highly-active anti-retroviral treatment

341
Q

what are zidovudine (AZT), lamivudine (3TC), emtricatabaine (FTC), stavudine (d4T)

A

NRTIs for HIV tx

342
Q

what are Ritonavir, Indinavir (IDV), Fos-amprenavir (FPV) and what are there side effects

A

protease inhibitors
lipodystrophy- fat loss from legs, fat gain-pot belly

343
Q

a pt is on treatment for HIV and also has a pot belly and thin legs. what are they taking

A

protease inhibitors e.g. ritonavir

344
Q

which NRTI do we use less now

A

AZT - zidovudine
headaches and nausea, anaemia, neutropenia

345
Q

what can be a side effect of NNRTIs

A

Stevens Johnson Syndrome: a severe disorder of mucous membranes
teratogenecity

346
Q

what is Stevens Johnson Syndrome and what causes it

A

severe disorder of mucous membranes following flu like symptoms
caused by drugs e.g. Carbamazapine, NNRTIS for HIV and Phenytoin

347
Q

how can we prevent dental contamination with HIV

A

Normal infectious control procedures
Gloves
Sterilise instruments
Dispose of sharps
Suction
Care if blood spillage

If at risk- contact Occupational health physician for prophylactic HAART and HIV testing

If needlestick of HIV + patient» PEP administration ASAP and within 72 hours at longest. (using this method NO NHS employee was infected (last 10y- no sero conversions – out of around 600 incidents).

348
Q

what is PEP

A

post exposure prophylaxis

349
Q

if we get a needlestick with a pt possibly have HIV what do we do

A

PEP < 72 hours
test at 3 months where virus would be at its highest

350
Q

how do we test for HIV

A

ELISA or PCR

3rd BDS IHD (14 decks)

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