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
what is an Obligate intracellular parasites
can survive outside a cell but can only thrive and reproduce within cells.
26
describe the structure of a virus
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
27
what is a viruses Lytic Cycle
the cell cycle tat occurs whilst in the host cell
28
what is a lentivirus and how do they work
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
29
how might some infections re-activate over time
some pathogens can hide in dorsal root ganglions e.g. chicken pox when immunocomprimised, re-occurance can occur
30
why might a patient get a very small portion of shingles on the body
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
31
what is the most abundant organism on earth
bacteriophage 10^31
32
what are bacteriophages and how might we identify one
viruses that kill bacterial cells place virus on bacterial colonies on agar if clear, bacteriophage
33
what are prions and how do they work
Prions are proteins made from living organisms/viruses They act against other proteins and stop them working properally
34
why are prions a problem for dental materials (endo especially)
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
35
why do we dispose of endodontic equipment
animal studies have found prions in pulp prions are very small and heat resistant very hard to sterilise the equipment
36
what is BSE and how does it lead to CJD
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
37
how does CJD work
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
38
what antigens can be found on the outside of gram negative bacterial walls
H - flagella K - capsule O - LPS on outer surface Peptidoglycan -
39
what is the H antigen
flagella
40
what is the O antigen
LPS outer surface
41
what is the K antigen
capsule
42
describe the cell wall of a gram negative bacteria
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
43
what is the function of a bacterial capsule Antigen K
Deter antibodies and evade antibody binding Therefor stops opsonization
44
what is the function of LPS antigen O
Deters complement factors preventing MAC
45
what is the structure and gram stain and main virulence factor of Neisseria and give 2 main examples
Gram Negative Diplococci variable capsule being virulence factor N. Meningisitis N. Ghonnorreha
46
what can N.meningitidis cause and what are the symptoms of this
meningitis symptoms include: Rash doesn't blanch Stiff neck Cold feet Fever Bright light intolerance Vomiting
47
what is meningitis
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
48
what vaccines are used against meningitis and what are the different types
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
49
what is the most common capsule type of N.Meningitidis
B capsule serogroup
50
what % of people will carry meningitis in nasopharynx
10-25% 50% in winter seasons
51
what are the common age/place outbreaks of meningitis
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
52
what vaccine must people have before going on a MECCA pilgrimage
meningitis ACY135
53
how do we diagnose meningitis
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
54
what is the chance of passing meningitis on to close contact
1 in 300
55
how do we treat meningitis
B-lactam antibiotics sometimes accompanied by corticosteroids VACCINATION
56
what are fastidious microorganissm
microorganisms that are difficult to grow in the laboratory because they have complex or restricted nutritional and/or environmental requirements
57
how do we grow Neisseria
heated blood chocolate agar with CO2 fastidious
58
what is the morphology and gram stain of haemophilus influenza
gram negative coccus-bacilli (oval shaped)
59
what can H. Influenza cause and how does it enter the blood
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
60
how many survivors of H.Influenza have disability after
15-35%
61
what capsule types can we get with H. Influenza and how do they act
A-f and some without capsules = commensals capsule major virulence factor avoidance of c3b binding
62
which capsule type of H.Influenza causes 99% of invasive disease
B
63
How can we tell the difference between H.Influenza meningitis and N.Meninigitis
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
64
which vaccine works against H.Influenza infections and when is it given
Hib - typhoid toxin polysacchardie- protein conjugate vaccine Haemophilus Influenza Type B vaccine given at 2, 3, 4 months
65
what 2 factors does H. Influenzas require to live
X (haemin) and V (NADH)
66
how do we treat meningitis or non-invasive H. INfluenza
meningitis: Ceftriaxone/ Cefotaxime non-invasive: Amoxicillin
67
what is a pathogens R number
its rate of spread from patient to patient
68
compare the bubonic plague and the pneumonic plague
bubonic = 75% death with no person to person spread Pneumonic= 90% death with high person to person spread
69
what pathogen causes the plague
Yersinia pestis
70
what are the virulence factors of Yersinia Pestis (4)
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
71
what pneumonic describes antibiotic resistant bacteria
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
72
what atibiotic are some G- bacteria becoming resistant to, and which bacteria are these?
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-)
73
describe the shape/G stain and relevance of Pseudomonas aeruginosa
Gram Negative motile Rod becoming antibiotic resistant to carbepenem and major killer of cystic fibrosis
74
where do we find Pseudomonas aeruginosa in the environment and humans
soil and ground water commensal bacteria found in gut
75
how does Pseudomonas aeruginosa appear on Agar
green spreading colonies grape smell
76
what is the major killer of cystic fibrosis patients
Pseudomonas aeruginosa leads to septicaemia and gangrene well adapted to warm, moist conditions e.g lung/burn
77
how many species of staphylococcus are there
40
78
what is the coagulase test
some bacteria produce an enzyme called coagulase that clots blood plasma plasma is mixed with bacteria to determine if they are coagulase + or -
79
where do we find most staph
nose and skin
80
what type of staph are important in opportunistic disease
coagulase negative Staph aureus Staph epidermisis
81
what are carrier and shedders
they carry the same load of microorganism shedders spread disease quicker as they 'shed' the pathogen more
82
how would we identify Staph. Areus
Mannitol salts agar selective for Gram positive, S.aureus ferments mannitol → yellow droplets on agar
83
how would we describe staph aureus (3)
gram positive coagulase positive Beta Haemolytic
84
what are some virulence factors of Staph aureus
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)
85
what produces toxic shock syndrome toxin
Staph. Arues
86
what causes scaled skin syndrome
staph. Aureus proteases that reduce connections between cells
87
what are some pyogenic associations with all staphylococci
Wound infections Abscesses - boils Septicemia Endocarditis Pneumonia osteomyelitis
88
what are some toxin mediated associations with Staph Aureus
Food poisoning Toxic shock syndrome Scalded skin syndrome
89
what are some associations with coagulase negative staphylococcus
Infected implants Septicemia Endocarditis
90
what is the most common coagulase negative and coagulase positive staph
+ve = staph aureus -ve = staph. epidermidis
91
how would we identify staph epidermidis (4)
gram positive (gram stain) Staphylococcus Coagulase negative white colonies on blood again (previously called staph albicans)
92
how does Staph Epidermidis act
opportunistic on skin forms strong biofilm (main virulence factor) around prosthesis or catheters
93
someone has an infection around their catheter, resistant to antibiotics. What is the cause
staph epidermidis strong biofilm made preventing antibiotic passage
94
what is staph epidermidis' main virulence factor
ability to form strong thick biofilms
95
what are the two main coagulase negative staphyloccous
staph epidermidids staph saprophyticus
96
what is haemolysis and give the types that bacteria can be and how can we test this
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
97
what does alpha, beta and gamma haemolytic bacteria present as on blood agar
alpha = partial breakdown = green/yellow patches beta = full breakdown = clear patches gamma = no breakdown = red
98
what is the main beta haemolytic, gram positive staphylococcus
staph aureus
99
what is the main alpha haemolytic staphylococcus
Staph Intermedius (also coagulase positive )
100
what causes beta or alpha haemolysis
beta = release of haemolysins that break down blood alpha= release of H202 and reacts with Hb to partially destroy RBC
101
how do we classify streptococci
Haemolysis Lancefield Grouping
102
what is Lancefield grouping
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
103
what Lancefield groups are there and which are most pathogenic
Lancefield A-H and K-V A and B most pathogenic A = Strep. Pyogenes B = Strep .agalactiae
104
how would we identify Strep. Pyogenes
Gram positive Streptococcus Coagulase negative Lancefield type A
105
what can Strep Pyogenes cause
Cellulitis Pharyngitis tonsillitis Impetigo Scarlet Fever
106
what is Impetigo
skin infection leading to sores on the face and skin that burst after about a week and cause yellow, crusty scabs Strep. Pyogenes
107
what is scarlet fever
red rash that affects skin and tongue often in babies (red on white skin, darker skin no colour change but texture change) Strep. Pyogenes
108
what can follow tonsillitis and what can cause this
Rheumatic Fever Strep. Pyogenes
109
what is rheumatic fever and what can cause this
Inflammatory disease of heart, joints, skin, brain. Often follows Strep. throat infection - follows tonsillitis - Strep. Pyogenes
110
how can we test the likelihood of Strep. Pyogenes leading to more complications like rheumatic fever and Glomerulonephritis
anti SLO titre
111
what are some virulence factors of Strep. Pyogenes
Streoptolysins O and S for haemolysis Streptokinase breaks down clots C5a peptidase - reduces chemotaxis + vasodilation Erythrogenic toxin - SPeA – exaggerated response = similar to TSST
112
explain the Anti SLO titre and what it is used for
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
113
give 2 ways of testing for anti - SLO in blood plasma and what does this tell us
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
114
explain the ASLO rapid test
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
115
where is Strep. Pneumoniae found
oro-pharynx of 30% of population
116
what does Strep. Pneumoniae cause
pneumonia, otitis media, sinusitis, meningiti
117
what are some predisposing factors of Strep. Pneumoniae
impaired mucus trapping (e.g. viral infection) Hypogammaglobulinemia - immunocompromised Asplenia - immunocompromised
118
what is Strep. Pneumonia virulence factors
Pneumolysin cytotoxin - causes lysis of cells teichoic acid (choline) - binds to choline helping to bind to host cells Peptidoglycan - inflammatory polysaccharide (84 types), antiphagocytic
119
what are the 2 main vaccines for Strep. Pneumoniae
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
120
what are viridians strep
collective streptococci of the oral cavity
121
what organisms might be accountable for deep organ abscesses
Viridians Strep
122
what is the tell tale sign of Corynebacterium diphtheriae
Pesduomembranes grey/green on tonsils and thick ‘bull neck
123
how would we grow diptheria
potassium tellurite
124
how do we detect C. Diptheria
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
125
other than C. Diptheria, what else can cause Diptheria
C. Ulcerans
126
what is the main cause of osetomyelitis
Staph Aureus
127
what are draughtsman colonies and what causes them
white, drafts pieces, raised edges, dimple in middle, colonies on blood agar S. Pneumoniae
128
what is blood agar selective for
aerobic bacteria
129
what are the three types of anaerobe
obligate anaerobes = harmed by oxygen Facultative anaerobes = can do both aerobic and anaerobic respiration Microaerophiles- grow in atmosphere of low oxygen <5%
130
what is the maximum ATP/mol of glucose possible with aerobic respiration
38
131
instead of entering the oxygen dependant TCA cycle, what happens to pyruvate in anaerobic respiration
organic electron acceptors to produce 2ATP Acids (VolitileFAs) - lactate is produced under extreme exercise Alcohols
132
A lot of anaerobes cannot survive in the presence of oxygen due to the radicals produced. How does P.gingivalis survive these radicals?
P.Gingivalis reduces superoxide→peroxide→water = survive in oxygen
133
what is a effective antibiotic for anaerobes? how does it work
metronidazole pre-drug is metabolised by anaerobes and produced metronidazole to kill bacteria
134
what is the morphology and products of Clostridia
Large, straight, Gram-positive bacilli Produce endospores - inside cell Produce exo-toxins
135
how does Cl. Perfringens show on a red blood agar
double beta haemolytic fully clear in middle encircled by a ring of partial haemolysis
136
what does Cl. Perfringes cause
Gas gangrene food sickness
137
what is the leading 3 causes of food poisoning
norovirus salmonella Cl. Perfringes
138
what is the incubation period for Cl. Perfringens
10-12 hours
139
what is the incubation period for Cl. Tetani
10-14 days
140
what is the morphology, agar and gram stain of Cl. Tetani
drumstick rod with terminal ball end thin white film on blood agar gram positive
141
what is tetanus and how is it caused
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
what is the gram stain, morphology of Cl. Botulinum
Bacillus with sub-terminal spores Gram positive
143
what does Cl. Botulinum cause
botulism severe food poisining
144
what is Cl. Botulinum incubation period
1-2 days
145
what does Cl. Difficile cause
pseudomembranous colitis, hospital/antibiotic related diorrhea
146
what causes Pseudomembranous colitis
Cl. Difficile
147
why is Cl. Difficile present in hosptial
lots of antibiotics, outcompetes other bacteria after use of antibiotics very heat resistant and resistant to sterilisation Travels in Faeces
148
how many toxigenic types are there
5 A-E
149
how do we detect toxins
Nagler Reaction Plate
150
describe Tetanus Toxin
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
how do we treat tetanus
anti toxin penecillin metronidazole
152
how do we prevent tetanus
toxoid vaccination
153
how many cases of tetanus every year
15-30,000
154
how do we get botulism (3)
ingestion of the pre-toxin soil or reheated food that has been left to cool for too long or home tinned foods
155
what does the botulism toxin cause
Flaccid paralysis - uncontrolled relaxation Drooping eyelids, progressive motor loss, flaccid paralysis; Neurological symptoms- dizziness respiratory & cardiac failure
156
describe the botulism toxin
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
how many types of botulism toxin are there and which are most cmmon
7 types A-G A B and E most common
158
how does the botulism toxin cause uncontrolled relaxation
A site is the active site Zinc Endopeptidase Irreversibly blocks release of acetylcholine so no excitation
159
how do we treat botulism
polyvalent anti-toxin
160
what can we use the botulism toxin for therapeutically
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
how do we diagnose Cl. Difficle
Stool sample
162
how do we treat C. Difficle
remove offending broad spectrum, selective antibiotic e.g. clindamycin/penicillin vancomycin or metronidazole
163
what are the virulence factors of Cl. Difficle and how do they act
TcdA and TcdB inactivates GTPase Rho family causes apoptosis and cell damage of intestinal epithelial
164
describe the morphology and gram stain of porphymonamos e.g. P. Gingivalis
Gram-negative, non-motile, rod-shaped
165
why do black pigmented anaerobes appear black on blood agar
they store oxidised iron which is black
166
what is the morphology and staining of fusobacterium
LONG Rod shaped spindle-shaped bacilli, Gram negative
167
where would we find Eubacterium and Bifidobacterium
isolated from abdominal infections POST oral/ genital trauma.
168
what relevance does Fusobacterium Nucleate have to cancer
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
describe the general structure and staining of actinomyces
filamentous sometimes branched gram positive with uneven staining
170
which bacteria is most found in actinomycosis
A. Israeli 70%
171
what would A.Meyeri cause
brain abscess
172
what type of bacteria are likely to cause brain abscess
A. Meyeri
173
name 2 type of actinomycetes found in caries
A. odontolyticus A. gerencseriae
174
how do we grow actinomyces and what does it appear as
'molar colonies' will grow in an anaerobic brain heart infusion broth due to them being fastidious and facultatively anaerobic
175
how many species of actinomyces are there
21
176
where are actinomyces found
mouth, gut and vagina commensals
177
what is Actinomycosis
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
where do most actinomycosis occur
55-65% cervicofacial
179
what type of pus do we get from actinomycosis
'sulphur pus' yellow
180
what does actinomycosis look like histologically (3)
Locules of pus and filametous gram positive bacteria surrounded by fibrous eosinic amorphous club shaped material surrounded by dense sheets of neutrophils
181
how does an Actinomycosis abscess defend itself (2)
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
what disease is associate with Splendore-Hoeppli Phenomenon
Actinomycosis
183
what are the virulence factors of actinomyces
induction of chronic inflammation walling off from defences slow growth as large aggregates in a matrix
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what is treatment for actinomycosis
Surgical removal/drainage 6-8 week course of penicillin, amoxicillin o tetracycline
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what is the structure of candida
Trimorphic blastopore (yeast) - circles Pseudohyphae - short chains Hyphae (chlamydospores) - long chains
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what agar can we use for growth of Candida
Sabouraud’s dextrose medium SAB - straw colour doesnt row bacteria, Candida. Albicans grows white colones
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what is chromatic agar used for
growth of multiple fungi, differentiating by enzyme
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compare the 3 forms of Candida Albicans
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
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what is the main fungus and bacteria to cause infective endoarditis
S. Aureus C. Albicans
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What is Candidosis
Systemic infection of Candida Albicans 50% fatal
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What is Candidosis
Infection/Colonisation of Candida Albicans on skin/mucosa Systemic infection of Candida Albicans is uncommon but 50% fatal
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what causes chronic Atrophic Candidosis
Dentures
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what causes chronic hyperplastic candidosis
smoking
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what causes acute pseudomembranous Candidosis
Trush/HIV
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what causes Erythromatus Candidosis
Red patches = HIV
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give 4 pre-disposing factors of Candidosis
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
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which type of form is more dangerous in fungi
yeast forms = commensals Hyphae = Pathogenic
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what pH favour hyphae/Yeast
under 6 = yeast over 6 = hyphae
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how do candida albicans attach to epithelium
Agglutinin-Like Sequence (ALS) 8 family members, ALS3 appears to be most important for adhesion to cells – only expressed by hyphae
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how do hyphae invaginate into epithelium
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
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what is candidolysin
A pore forming toxin that kills human cells and also initiates an immune response
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what is SAP
secreted Aspartyl Proteases secreted by the tip of Hyphal Penetration
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what are 2 mechanicams important for hyphal penetration
SAP - Secreted Aspartyl Proteases Candidolysin
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what is the most common cause of hospital-acquired-related death in the US (even greater than MRSA !)
systematic Candidiasis 50% mortality
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why can we use zebra fish ethically and biologically (2)
they are not classed as animals and their endothelium is flourescent
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how does candida cause death
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
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how do we treat candidiosis
Fluconazole - antifungals removal of predisposing factors
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describe the structure and gram stain of spirochetes
gram negative very thin spiral shaped rods
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how do spirocheates move
internal flagella
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how are different spirochetes identified
Identification by Sequence analysis of 16s rRNA gene which is well conserved due to need for function
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what and where are axial filaments found
found in the periplasmic space of spirochaetes internal flagella
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how many people have candida albicans
40-60% have candida albicans in their mouth
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what is wild type fungus
mixture of yeast forms and hyphae forms
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what would happen if the internal flagella were removed from spirochaetes
this would lead to the spiral shape going and the bacteria becoming straight non-motile
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do spirocheates have LPS?
no
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what are the three major spirocheates that cause clinical problems
Leptospira = Weil's disease Leptospirosis Borella = Lyme Disease, Relapsing fever Treponema = Syphilis, ANUG, Periodontitis
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what are zoonotic infections
They have an animal reservoir of infection that can under certain circumstances infect humans via a zoonotic vector
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what bacteria causes Lyme's Disease
Borrelia burgdorferi - zoonotic, tics
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how can we view Borrelia burgdorferi
EM or darkfield microscopy
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how does lymes disease spread
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
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what symptoms is specific to lymes disease
Bulls eye rash
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what happens if a patient goes undetected with lymes disease
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
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how do we treat lymes disease
doxycycline 100 mg twice per day or 200 mg once per day 3 weeks Borrelia burgdorferi
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how can we prevent Lymes disease
wear long clothes DEET repellents vaccination (pulled due to antivaxx movement)
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what is the main virulence factor of Borrelia burgdorferi
motility
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how does Borrelia burgdorferi survive in low iron levels
Copes with low-iron levels by using Manganese instead of iron as an enzyme co-factor
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what is Borrellia Recurrentis and what does it cause and how
Spirochaete recurrent fever of 3-10 episodes due to genetic variation of surface protein
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what causes Wiels Disease
"Leptospira interrogans
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describe the shape of Leptospira interrogans
very thin, coiled spirochaete Two terminal Periplasmic flagella
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where would we find "Leptospira interrogans
stagnant water near dog/rat colonies as in their urine
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what is Leptospirosis
infection of
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what are the symptoms of Leptosperosis and what can it lead to
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
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what are most symptoms of Leptosperosis due to
damaged blood vessels
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How do we reduce cases of Leptospirosis and Wiels Disease
Rodent control Doxycycline Avoid swimming in infected rivers
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why do patients with Leproperosis get red eyes
Haemorrhage in Aqueous humour of eye due to damaged blood vessels
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how do we treat necrotising ulcerative gingivitis
metronidazole or Hydrogen peroxide washes deep removal of plaque and bacteria
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what causes ANUG
acute necrotising ulcerative gingivitis Treponema Vincentii , Rods and fusobacterium (fuso-spirocheatal complex)
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what are the red complex bacteria
Porphyromonas gingivalis Tannerella forsythia Treponema denticola
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describe the structure of T. Denticola
spirochete, gram negative, anaerobic
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what are T. Denticola's virulence factors
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
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compare narrow and broad spectrum antibiotics
narrow only aerobic/anaerobic or only gram positive/negative broad can be negative AND positive or aerobic AND anaerobic
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what is selective toxicity
where a drug has a high affinity and toxicity to bacteria but low toxicity to human cells
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the larger to theraputic index...
the safer the drug is for use
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ideal characteristics of an antimicrobrial
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
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what three ways can we classify anti-biotics
by chemical structure e.g. β-lactam ring by target site according to whether they are bactericidal (kill) or bacteriostatic (inhibit growth)
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how can we test the efficacy of an anti-biotic (2)
disc plates on agar lquid MIC/MBC testing
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explain MIC MBC testing
MIC = minimal inhibitory concentration MBC = minimum bactericidal concentration Standardised [bacteria] + different [drug] MBC usually higher than MIC
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what are the main targets for antibiotics
Cell wall - peptidoglycan Protein synthesis - ribosomes or enzymes unique to bacteria Metabolic pathways DNA Membranes Enzymes
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what is antibiotic resistance
an organism that is not inhibited or killed by an antibacterial agent at concentrations of the drug achievable in the body after normal dosage.
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give three ways of spread of antibiotic resistance
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
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what mechanisms might cause an antibiotic to no longer work (4)
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
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how can we gain a blood sample for testing infections
needle aspiration
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what organisms are likely to be found in pharyngitis
Streptococcus pyogenes: beta haemolytic, Coagulase -ve, Lancefield Group A EBV (glandular fever is virus with no medication)
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what type of bacteria are likely in a dental abscess
Viridans group streptococci Anaerobes Gram negative rods
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what is the centor criteria
set of criteria to determine if a sore throat is of viral or bacterial origin
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what are the set of centor criteria (CENT)
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).
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what determins if the antibiotic can penetrate the site (2)
the pH of the site - abscess/infection is low pH weather the drug is lipid soluble
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why is infective endocarditis hard to treat (3)
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
give an example of intrinsic resistance
Naturally resistant pseudomonas is naturally resistant to penicillin
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give some ways of finding if an antibiotic is effective
sensitivity testing with discs breakpoint testing tube dilution
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explain how we can find the MIC of an antibiotic
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
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what are the major 2 determinants of effectiveness of an antibiotic
the concentration at the binding sites the time that the antibiotic remains on these binding sites to allow sufficient inhibition of metabolic processes
262
compare concentration and time dependant killing
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
give a few ways that horizontal gene transfer can occur
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
what is the structure of herpes virus (3)
Icosahedral capsid surrounding dsDNA Virus tegument glycoproteins on outside very important for specificity e.g. binding to oral mucosa
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what are the three alpha-herpese viruses
Type 1 Herpes Simplex Virus Type 2 Herpes Simplex Virus Varicella-Zoster Virus (VZV)
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what are the 3 beta-herpes viruses
Cytomegalovirus (HCMV) Human Herpesvirus 6 Human Herpesvirus 7
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what are the 2 gamma-herpes viruses
B-lymphocytes Epstein-Barr virus (EBV) Human Herpesvirus 8 (important in HIV)
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what mucosa does HHV-1 and HHV-2 affect and why does this occur
1 = oral mucosa 2 = genital and oral due to cross contamination due to different tegument glycoproteins on outside
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what are the two stages of herpes viruses
infection reactivation
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what are the two stages of HHV-1 (3)
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)
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what can cause secondary herpes simplex re-activation
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
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of those infected with primary herpes infection, how many are symptomatic and what would they present with
1-10% are symptomatic herpetic gingivostomatitis
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what is the incubation, duration and symptoms of herpatic gingivostomatitis
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
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how could we diagnose gingivostomatitis genetically and histologically
genetically = PCR histologically = ballooning of epithelial cells due to intraepithelial vesicles
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how do we treat herpatic gingivostomatitis (3)
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.
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what is added to cordysol toothpaste apart from flouride
CHX
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how does Acyclovir work (4)
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
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What is herpes Labialis and what are its clinical features
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
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what is management of Herpes Labialis
5% Acyclovir cream prophylactic acyclovir very rare - only in immunocompromised patients or if patients are having very frequent problems
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what are the effects of using prophylactic Acyclovir for Herpes 1
reduces duration of cold sores reduces pain Reduces re-occurance by 50%
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what is herpatic whitlow and how can we prevent it
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
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what is HSV encephalitis and what does it effect
swelling of frontal lobes of brains in 1 in 500,000 patients Usually only people >50 years (HSV-1) and neonates (HSV-2) affected
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what is the mortality and recovery rate of HSV encephalitis
70% - 80% mortality if untreated Of survivors, only 3% return to normal
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how might we tell if an adult has HSV encephalitis
headaches change in behaviour over a few days history of HSV infection
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what are the two stages of VZV
varicella = chicken pox = primary infection Zoster = shingles = secondary infection
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at what age do 70% of shingles cases occur
>50
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what 4 factors lead to increased chances of developing shingles in the future
Age (70% >50yrs) Stress Illness Immunosuppression
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explain the progression of a shingles belt
blisters of epithelial balooning cells intracellular vesicles turns to rash release and heal contagious throughout
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what are the three phases of oral herpes zoster
Pre-herpetic neuralgia Rash Post-herpetic neuralgia
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what is oral herpes zoster
infection of VZV along the trigeminal nerves from the trigeminal ganglion
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explain pre-herpetic oral zoster
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
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if a patient has sound teeth but is complaining of tooth ache in a lower or upper reigon, what might this be
oral zoster pre-herpatic symptoms
293
explain the rash of oral zoster virus
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
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which division of the trigeminal ganglion is oral zoster most likely to have severe implications
opthalmic divison: glaucoma, cataract, double vision and scaring of the cornea = shingles of the eye send to hospital immediately
295
how do we manage oral zoster
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
what is post-herpetic neuralgia of oral zoster
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
how do we treat post-herpetic oral zoster
Treat pain with tricyclic anti-depressants and neuropathic pain drugs
298
how many patients with shingles will get post-herpetic neuralgia
10%
299
what is EBV
Epstein Barr virus affecting B cells beta-herpes virus depending on the local environment, can cause 4 different diseases
300
depending on the local environment, can cause 4 different diseases. what are they
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
where does EBV initiate and then where does it remain latent
Primary infection EBV replicates in oro-pharyngeal epithelial cells but then establishes latency in B- lymphocytes.
302
how many people have EBV
95%
303
what are symptoms of symptomatic EBV
Symptoms include sore throat, swollen cervical lymph nodes and mild fever, Petichae on palate (red spots)
304
a young patient has a sore throat, cervicale lymphadenopathy and petechiae. what are they likely to have
Infectious mononucleosis (Oral) from EBV
305
where is Burkitts syndrome prelevent and what is it
b cell carcinoma caused by EBV found in tropical Africa at elevations below 1500 metres where malaria is present
306
how do we treat burkitts syndrome and why is this not usually done
cyclophosphamide (chemo) relatively cheap but not available where this disease is prelevent: tropical Africa at elevations below 1500 metres where malaria is present
307
a child, recently migrated from tropical Africa, has a very swollen jaw/face and is generally ill. what are they likely to have
Burkitts syndrome B cell carcinoma caused by EBV
308
how does Burkitt's syndrome often present
usually forms a bone tumour on the mandible
309
where is nasopharyngeal cancer related to EBV and why
japand due to high soya eating
310
how might cytomegalovirus present
Glandular fever-like illness Salivary gland swelling rarely causes illness in healthy individuals
311
what might CMV cause in immunocompromised patients
Large ragged oral mucosal ulcers Salivary gland swelling Retinitis
312
what is the cause of kapsosis sarcoma in AIDs patients
HSV-8
313
what does HSV-8 cause
usually has no effect in very immunocompromised patients (AIDS) the patient will get Kapsosi's Sarcoma = very large, red swollen gingiva
314
what is HIV
human immunodeficiency virus causes depletion of host immune system resulting in AIDs
315
what is HIV
human immunodeficiency virus causes depletion of host immune system resulting in AIDs type of lentivirus - slow growing retrovirus
316
what is AIDs
Acquired Immune Deficiency Syndrome
317
give 5 ways HIV is transferred
sexual contact blood contamination placental carriage to uterus breast milk infected blood products e.g. meat
318
what are, and compare breifly, the two types of HIV
HIV 1 = more common, more symptomatic and more easily tranferred HIV 2 = less pathogenic and less easily tranferred, localised to western africa
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why does HIV mutate readily
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
what do M, O and N stand for e.g. HIV-1m
m = main/pandemic n = new o = outlier e.g. confined to cameroon
321
describe the structure of HIV (5)
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
what are the major two glycoproteins on HIV
gp120 and gp41 (begin as one protein but then cut in two by a proteas)
323
explain how HIV binds to cells, and which cells
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
how might someone be naturally immune to HIV
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
how many people are immune to HIV and how
2-14% europeans (caucasian) , and 15% of Icelandic mutatin in CCR5 gene that is used by HIV to attach via gp41
326
after binding, how does HIV proliferate
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
after binding, how does HIV proliferate
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
what is the most important post-translational modification with HIV
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
explain the virus variation during HIV infection
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
explain the course of HIV infection
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
what are some AIDs defining illnesses
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
what is cryptosporidum
chronic diarrhea aids defining
332
what is toxoplasma gondii
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
why should pregnnat women not handle cats
prengnancy = immunocompromised more suseptable to toxoplasmosis caused by the common parasite toxoplasma gondii found in cat litter and blood
334
what would the mouth of a pt with HBV look like
hairy, striated leukoplakia on tongue
335
give 4 oral representations of AIDS
hairy, striated leukoplakia - HBV oral candidiasis - thrush erythematous candidosis - red markings gingival erythema
336
why does HIV treatment rely on compliance (2)
drugs have a short half life so must take regularly have to take in combination so multiple drugs
337
name some targets for HIV treatment
protease inhibitors (no gp120 and gp41) Reverse transcriptase inhibitors (no DNA) CCD5 entry inhibitors (no co-receptor)
338
what are NNRTI and NRTI
(non) nucleoside reverse transcriptase inhibitors main tx for HIV
339
how do NRTIs work
nucleoside reverse transcriptase inhibitors similar shape to a nucleotide implemented into growing nucleotide chain terminates the chain = no DNA formation
340
what is HAART
highly-active anti-retroviral treatment
341
what are zidovudine (AZT), lamivudine (3TC), emtricatabaine (FTC), stavudine (d4T)
NRTIs for HIV tx
342
what are Ritonavir, Indinavir (IDV), Fos-amprenavir (FPV) and what are there side effects
protease inhibitors lipodystrophy- fat loss from legs, fat gain-pot belly
343
a pt is on treatment for HIV and also has a pot belly and thin legs. what are they taking
protease inhibitors e.g. ritonavir
344
which NRTI do we use less now
AZT - zidovudine headaches and nausea, anaemia, neutropenia
345
what can be a side effect of NNRTIs
Stevens Johnson Syndrome: a severe disorder of mucous membranes teratogenecity
346
what is Stevens Johnson Syndrome and what causes it
severe disorder of mucous membranes following flu like symptoms caused by drugs e.g. Carbamazapine, NNRTIS for HIV and Phenytoin
347
how can we prevent dental contamination with HIV
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
what is PEP
post exposure prophylaxis
349
if we get a needlestick with a pt possibly have HIV what do we do
PEP < 72 hours test at 3 months where virus would be at its highest
350
how do we test for HIV
ELISA or PCR