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MICROBIOLOGY II > Lecture 8 - Neisseria > Flashcards

Lecture 8 - Neisseria Flashcards

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1
Q

Where does neisseria sp. fall in phylogenetic tree

A

Beta proteobacteria

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2
Q

What 3 genus’s fall under neisseriaceae

A

Neisseria, eikenella, kingella

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3
Q

What are 4 key neisseriaceae species

A

N. Gonorrheae (neisseria)
N, meningitidis (neisseria)
E,corrodens (eikenella)
K.kingae (kingella)

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4
Q

Eikenalla and kingella are pleomorphic. What does this mean

A

Variability in shape, sizeand staining

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5
Q

Describe eikenella and kingella characteristics

A

Gram negative
Colonies oropharnyx / URT
Opportunistic pathogens

Can get eikenella from human bite e.g. In wards - cause deep seated bone infections

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6
Q

Describe neisseria sp. structure membrane

A 
Non motile 
Gram negative 
LOS 
Thin PG layer 
OMPs
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7
Q

What is diplococcus

A

Flat side which is division plane

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8
Q

What is size of neisseria sp.

A

0.6-1um

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9
Q

neisseria sp. are fastidious. What do they need

A

AA, purines/pyramadines, Vitamins. Al require cysteine as aa

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10
Q

What temp do neisseria sp. grow in

A

35-37deg c

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11
Q

What us unique about oxygen/co2 requirement for neisseria sp.

A

AEROBIC but capnophilic - like bit of co2 approx 5%

Grow with bit of co2

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12
Q

Describe neisseria sp. charactersists in terms of oxidase/catalase production

A

Oxidase positive
Catalase positive - get rid of hydrogen peroxide prude water and oxygen. 3% H2o2 drop on and if bubbles then catalase positive
Produce acid from sugars (oxidative- use to speciate between neisseria sp. )

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13
Q

What sugars can meningitis and gonoccos process or not

A

Meningococcus - both glucose and Maltose get acid

Gono- only glucose

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14
Q

Describe for both neisseria sp. whether they are commensel, what epilthelial they target, whether they are invasive or not, a
And whether it is purulent.

A

Commensal - meningococcus (approx 10%) in nasopharynx but never carry gonococcal
Target epithelial - meningococcus attack nasopharynx and gonococous genital tract

Invasive - meningococcus very invasive, gonococcus not very invasive

Purulent - both purulent

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15
Q

How can neisseria sp. attach

A

Pili which travel through plasma membrane

Tip have adhesion molecule pil c - name of one of protein domains

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16
Q

Where does Pil C bind in our cells

A

Bind CD46 receptor on cells to attach and invade

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17
Q

What part of pilE is constant and which part varies

A

N eteminus constant 5’ end

C terminus highly variable ( from 3’ end )

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18
Q

What is phase variation and where does it occur

A

Pili - turn things on and off - can vary the antigen

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19
Q

What does endotoxin not have if it is LOS not LPS

A

Lacks O antigen
So small but deadly LOS

Only has lipid A anchored inmemrbane and core sugars

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20
Q

Which part is toxic is LOS

A

LIPID A

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21
Q

What can bacteria cover themselves in to look like human cells and how much does neiserria have

A

Sialic acid

Neiserria low sialic acid - MORE INFECTIVE, EASIER TO KILL

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22
Q

What does sialic acid protect bacteria from

A

Serum factors e,g, complement cascade which is most important defence against neisssria

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23
Q

What does neisseria release to act as a decoy for immune system

A

Release LOS in blebs during division (outer membrane blebs released as “microparticles”

If deploy complement on blebs mother cell still alive and not killed.

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24
Q

What do the micro particles from neisseria cause

Study These Flashcards
A

As leave organism cause GENERALISED INFLAMMATION ALL OVER BODY - deadly as general

25
What Momps (major outer membrane proteins) are present on n. Meningitidis
There are I-V with decreasing molecular weight I to III are porins IV is RMP - reduction modifiable proteins V is opa - when it is expressed colonies are white (opacity)
26
What do porins inhibit
Inhibit phagosome maturation (stop lysosomal fusion) so sit inside cell
27
RMP are found where
Only found within pathogenic neisseria Marker of disease Immunogenic - immune response against them
28
What do 3 opa proteins do
Mediate TIGHT binding - phase variation here. E.g. 1 and 2 on 3 off etc. (Pili mediate some binding) Two Hypervariable domains - massively variable. Point mutations massively variable we don't have antibodies against then
29
What does HS and CEA stand for after OPA
What opa bind to Hs - bind to heparan sulphate - sugar chains that hang off proteins. By binding to this can interact also with extracellular matrix (all cells stuck to). Can also interact with integrins - across cell membrane and touch Extracellular world and send signal in cell. CAN STIMUAKTE CELL TO CHANGE CYTOSKELETON TO EAT MICROBE SO IT CAN BE TRANSFERRED SOMEWHRE ELSE. OPA CEA . Same principal as heparan sulphate binds CEA adhesion molecules and stimulate own uptake
30
Of neiserria hasn't got _ (major virulence factor) then it is aparhogenic
Capsule
31
IMPORTANT WHAT ARE THE SEROGROUPS OF NEISSERIA AND WHAT IT IS BASED ON.
A,B,C,Y,W135 based on capsule
32
What modified sugars are the serogroups based on? | IMPORTANT
Serogroup A - based on N-acetylmannosamine-1-phosphate | Serogroup B,C,Y,W135 - sialic acid
33
What do we use to generate vaccine response | IMPORTANT
The serogroup sugars
34
What is one way of capsular variation occurring
Horizontal DNA transfer
35
What element do bacteria struggle to obtain but neiserria is very good at
Iron Neisseria good at wrestling iron from proteins
36
What two proteins carry and hold iron and what does neisseria do
Transferrin and lactoferrin Bind these proteins so iron limitation jot an issue Also have haemoglobin binding proteins
37
How to neisseria attach
Via pili for initial attachment then opa for tight binding Can sit and divide now attached Then get extension of pseudopodia - endocytosis Internalise cell and can see dividing diplococcus. LOS essential to stimulate cells to change membrane and start internalisation
38
Why does neisseria want to be endocytosed
More chance of being disseminated around the body | Just want to survive
39
What does transcytosis do for neisseria
Get eaten one end and spat out other end so can get into blood vessel Even though have to deal with immune system can cause disease
40
What is host defence against neisseria
Innate - mucocilariy escalator and antimicrobial effectors (defensins, lysozyme, lactoferrin In respiratory epithelium Adaptive - secretory IgA pumped out into respiratory epithelium. If igA there get meningococcus make proteases to chop it up to make it less affected, COMPLEMENT (most important as once inside)
41
When does mothers IgG run out for babies
6+ months Sensitive to meningitidis
42
What are the antibodies formed against for meningitis
Formed from exposure to relatives e,g, n.lactamica and other bugs with similar capsules e.h. Ecoli k1 and bacillus pumilis People carry n meningitis
43
What key deficiencies lead to neisseria etc infections
Complement E.g, alternative pathway - lose factor B, D ( needed to form c3 convertase), properdin (prolong c3 convertase activity) Classical and lectin and alternative pathway C3 factors H and I - pyogenic infections e.g, meningitidis Membrane attack complex MAC C5,6,7,8,9 severe neisseria infections
44
What is dangerous about losing C3 factors H and I
Turn C3 convertase off | If lose this then use up all C3 available in blood so can no longer activate complement
45
How can neisseria EVADE complement
Neisseria porin recruit Factor H and I which inactivate C3 convertase of alternative pathway By decorating themselves with complement protective factors can turn off complement. Recruit c4bp (binding protein) and Factor I to PILUS. get reduced C3 convertase form lectin pathway.
46
What does it mean by n meningitidis being a commensal and obligate human pathogen q
Commensal found living on body | OBLIGATE - won't cause disease elsewhere
47
What does itis at the end of a word mean
Inflammation
48
Meningitis is main cause of bacterial meningitis. Where is disease mostly found q
Under 5 yrs, teenagers, institutionalised people, people with complement deficiencies
49
What are risk factors
Smoking - breach epithelial barrier in some Age Previous flu Close living (halls) Highly polymorphic organism - change a lot Seasonal side - winter and spring (dry cold months)
50
What condition from this may or may not lead to meningitis
Bacteraeimia
51
Describe the different world countries and the associated serogroup
Subsuharan Africa - serogroup A Pilgrimages led to high dissemination of A,c,Y,W135 UK change over time Serogroup B after WWI AND II 1985 hyoerendimic b serogroup 1995 hyperendemic c serogroup (towards teenagers with high mortality rate)
52
What are clinical conditions of meningitidis
Bacteriaema - septeciamea, meningococcoaeamia - meningitis - pneumonia - initially fever and flu like symptoms, vomiting. (May resolve) - some may get classic rash but not everyone (80% of individuals)
53
Why is bacteria life threatening even if doesn't cause meningitis
- Bacterial division in blood - shock and intravascular coagulation - see bottom paragraph - release LOS - general systemic inflammation - los can activate complement ,PRR, coagulation pathways Massive pro inflammatory response - increased vascular permeability - loss of protein, fluid, and electrolytes - cardiac output falls, extravasculsf fluid accumulates (pulmonary oedema and respiratory failure - DEATH)
54
Describe meningitis infection and symptoms Nd mortality
Purulent infection lots of neutrohilis Symptoms - headache, fever, seizures, stiff neck, photophobia (often non specific especially in young) Rash in 50% of patients Mortality - without antibiotics 100% With 10% chance of death
55
How do you diangose in lab
Take CSF and gram stain (sensitive and specific) can see neutrophils and see organism inside Usually use PCR to pick organisms up
56
Describe men c vaccine positives
Reduced infection in immunised people by 90% Cases in other groups fell by 75% (herd immunity) Capsular polysaccharide conjugated to protein, T cell dependant immunogen
57
What does the tetravalant vaccine cover
A,c,y,w135 Capsular polysaccharide conjugated to protein Recommended for sub Saharan travel especially pilgrimage To Mecca
58
What is new vaccine against
Vaccine for serogroup B Targeted at all things used by organism to protect against complement e.g. Factor h binding protein, neisseria heparin binding Ag, nerissrial adhesin a , NZ vaccine strain Until recently wasn't vaccine for this - capsule is sialic acid (self Ag), no immune response. Not adopted by NHS
59
How can we manage
Early recognition Antibiotics - rapid - penicillins (b lactamases a problem) - cephalosporins Close contact receive prophylactic antibiotics Close kissing contact can increase risk by 1000 times.

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