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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

A

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

25
Q

What Momps (major outer membrane proteins) are present on n. Meningitidis

A

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
Q

What do porins inhibit

A

Inhibit phagosome maturation (stop lysosomal fusion) so sit inside cell

27
Q

RMP are found where

A

Only found within pathogenic neisseria
Marker of disease
Immunogenic - immune response against them

28
Q

What do 3 opa proteins do

A

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
Q

What does HS and CEA stand for after OPA

A

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
Q

Of neiserria hasn’t got _ (major virulence factor) then it is aparhogenic

A

Capsule

31
Q

IMPORTANT

WHAT ARE THE SEROGROUPS OF NEISSERIA AND WHAT IT IS BASED ON.

A

A,B,C,Y,W135 based on capsule

32
Q

What modified sugars are the serogroups based on?

IMPORTANT

A

Serogroup A - based on N-acetylmannosamine-1-phosphate

Serogroup B,C,Y,W135 - sialic acid

33
Q

What do we use to generate vaccine response

IMPORTANT

A

The serogroup sugars

34
Q

What is one way of capsular variation occurring

A

Horizontal DNA transfer

35
Q

What element do bacteria struggle to obtain but neiserria is very good at

A

Iron

Neisseria good at wrestling iron from proteins

36
Q

What two proteins carry and hold iron and what does neisseria do

A

Transferrin and lactoferrin
Bind these proteins so iron limitation jot an issue

Also have haemoglobin binding proteins

37
Q

How to neisseria attach

A

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
Q

Why does neisseria want to be endocytosed

A

More chance of being disseminated around the body

Just want to survive

39
Q

What does transcytosis do for neisseria

A

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
Q

What is host defence against neisseria

A

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
Q

When does mothers IgG run out for babies

A

6+ months

Sensitive to meningitidis

42
Q

What are the antibodies formed against for meningitis

A

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
Q

What key deficiencies lead to neisseria etc infections

A

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
Q

What is dangerous about losing C3 factors H and I

A

Turn C3 convertase off

If lose this then use up all C3 available in blood so can no longer activate complement

45
Q

How can neisseria EVADE complement

A

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
Q

What does it mean by n meningitidis being a commensal and obligate human pathogen q

A

Commensal found living on body

OBLIGATE - won’t cause disease elsewhere

47
Q

What does itis at the end of a word mean

A

Inflammation

48
Q

Meningitis is main cause of bacterial meningitis. Where is disease mostly found q

A

Under 5 yrs, teenagers, institutionalised people, people with complement deficiencies

49
Q

What are risk factors

A

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
Q

What condition from this may or may not lead to meningitis

A

Bacteraeimia

51
Q

Describe the different world countries and the associated serogroup

A

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
Q

What are clinical conditions of meningitidis

A

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
Q

Why is bacteria life threatening even if doesn’t cause meningitis

A
  • 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
Q

Describe meningitis infection and symptoms Nd mortality

A

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
Q

How do you diangose in lab

A

Take CSF and gram stain (sensitive and specific) can see neutrophils and see organism inside

Usually use PCR to pick organisms up

56
Q

Describe men c vaccine positives

A

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
Q

What does the tetravalant vaccine cover

A

A,c,y,w135
Capsular polysaccharide conjugated to protein
Recommended for sub Saharan travel especially pilgrimage
To Mecca

58
Q

What is new vaccine against

A

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
Q

How can we manage

A

Early recognition
Antibiotics - rapid
- penicillins (b lactamases a problem)
- cephalosporins

Close contact receive prophylactic antibiotics

Close kissing contact can increase risk by 1000 times.

MICROBIOLOGY II (9 decks)

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