Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Human Microbial Diseases Block 1 > Neisseria > Flashcards

Neisseria Flashcards

1
Q

What is the shape of Neisseria?

A

Diplococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Are Neisseria gram negative or gram positive?

A

Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percentage similarity do N. gonorrhoeae and N. meningitidis have?

A

80-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does N. meningitidis colonise?

A

The human upper respiratory tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does N. gonorrhoeae infect?

A

Primarily infects the urogenital epithelia but can also cause pharyngitis and conjunctivitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can N. gonorrhoea lead to?

A
  • Epididymitis
  • Cervicitis
  • Endometriosis
  • PID
  • In rare cases can have disseminated gonococcal infection (DGI), arthritis and endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What percentage of men have asymptomatic N. gonorrhoeae infections?

A

10-15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What Neisseria has a capsule?

A

N. meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the key virulence factor of N. meningitidis?

A

Endotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is meningitis?

A

Inflammation of the meninges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the signs and symptoms of meningococcal meningitis?

A
  • Vomiting
  • Excruciating intense headache due to escalated CSF pressure
  • Confusion
  • Drowsiness
  • Fever
  • Sensitivity to light
  • May get a skin rash
  • Eventually the neck stiffens as nerves along the spine become increasingly irritated
  • Convulsions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can meningococcemia progress towards?

A
  • Septic shock
  • Purpura fulminans
  • Acute systemic inflammatory response
  • Intravascular coagulation
  • Tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mortality of meningococcal sepsis?

A

40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What percentage of patients with meningococcal sepsis will have severe sequelae?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the infection pathway of Neisseria meningitidis

A
  • Inhalation of respiratory droplets
  • Nasopharyngeal colonisation
  • Epithelial cell invasion
  • Survival in blood
  • Bacteraemia leading to septicaemia or meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the natural habitat of N. meningitidis?

A

Human nasopharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is N. meningitidis transmitted?

A

From person to person by aerosol droplets or direct contact with contaminated fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the carriage of N. meningitidis

A
  • 10-35% carriage -> some university students up to 55%
  • The human nasopharynx is the sole ecological niche and carrier isolates show extensive genetic diversity as compared with hyper-invasive lineages
  • Horizontal gene exchange and recombinant events during residence in the human nasopharynx result in antigenic diversity
  • Carriage offers some immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the molecular interactions between N. meningitidis and its human host

A
  • The mucus in the nasopharynx is poorly nutritive but rich in microbiota -> competitive niche
  • Meningococci survive by expressing capsule, lipooligosaccharide, the MtrCDE efflux pump and factors that capture nutrients
  • N. meningitidis also express 2 families of polymorphic toxins -> MafB and CdiA
  • For an unknown reason, meningococci cross the epithelial layer and enter the bloodstream
  • In the bloodstream bacteria adhere to the vascular wall and form microcolonies
  • Adhesive bacteria proliferate and induce an active signalling that leads to better adhesion and opening of the vascular barrier, vessel leakage and massive thrombrosis
20
Q

How do we protect against meningitis?

A

Antibody directed towards capsule play a major role in protection against meningitis and form the basis of the vaccination and typing strategy

21
Q

What serogroup of N. meningitidis isn’t antigenic?

A

Serogroup B -> molecular mimicry

22
Q

What serogroups of N. meningitidis cause life threatening disease?

A
  • A
  • B
  • CW-135
  • X
  • Y
  • Z
23
Q

Can capsular switching occur in N. meningitidis?

A

Yes

24
Q

What are serogroups based on?

A

The composition of the capsular polysaccharide

25
Q

What is LOS?

A
  • LPS but without the O antigen
  • Endotoxin
  • Major antigenic and immunogenic component of pathogenic Neisseria
26
Q

What does LOS cause?

A
  • Induces and immune cascade
  • Produces a lot of cytokines
  • Can lead to endotoxic shock
27
Q

What is the main adhesion protein of Neisseria?

A

Pili

28
Q

What do pili target?

A
  • Epithelial cells
  • Endothelial cells
  • RBCs
29
Q

Describe the adhesion of Neisseria

A
  • Pili enable the organisms to ‘twitch’
  • Pili traverse the capsule and act as adhesins
  • The integral outer membrane adhesins (OM), Opa and Opc, also mediate interactions with specific host-cell receptors
  • LOS may interfere with the adhesion functions of OM proteins, but can also contribute to cellular interactions by interacting with various cellular receptors
30
Q

How do meningococci survive in serum?

A
  • Neisseria uptake nutrients and iron from extracellular environment
  • Pathogenic N. meningitidis are capsulated which is anti-phagocytic and the sialic acid on group B capsules inhibits complement deposition
  • Several mechanisms to resist intracellular oxidative killing -> e.g. catalase and superoxide dismutase
  • Meningococci avoid complement killing by antigenic variation and complement resistance
31
Q

How do meningococci evade the immune system?

A
  • A signature property of the pathogenic Neisseria is their ability to modulate their surface antigen very fast
  • Pilin antigenic variation is mediated by gene conversion
  • The PilE protein contains a highly conserved N-terminal domain and a variable C-terminal domain (antigenicity)
  • The variable region is the result of non-reciprocal transfer of DNA from 1 of many silent partial pilS loci to the single pilE expression
  • Extensive surface variation also poses a substantial problem in developing effective vaccines
32
Q

How does antigenic variation occur in Neisseria?

A

Free exchange between genes (gene conversion) both within and between the genomes of Neisseria sp.

33
Q

Why is Neisserial DNA in the environment?

A

Arises by autolysis and by an identified type IV secretion system that actively transports DNA out of the cell

34
Q

Describe the epidemiology of meningitis

A
  • Meningococcal disease mainly affects children
  • Most disease in Europe and USA is caused by serogroup B and C whereas group A is responsible for most cases worldwide
  • The highest incidence of disease occurs in the tropics in the meningitis belt
  • Peaks occur in winter months in industrially developed countries
35
Q

What are the symptoms of Neisseria gonorrhoeae?

A
  • Discharge from the genitals

- Burning when peeing

36
Q

What can disseminated gonococcal disease lead to?

A
  • Endocarditis
  • Arthritis
  • Pelvic inflammatory disease
37
Q

What occurs in pelvic inflammatory disease?

A
  • Abnormal vaginal discharge
  • Bleeding between your periods, or having heavier periods than normal
  • Pain in lower part of your abdomen
  • Uncomfortable or painful sex
  • Pain or difficulty wen urinating
  • Fever
  • Can cause abscesses, scarring and damage to your reproductive organs
  • Can cause pelvic pain, infertility and ectopic pregnancies
38
Q

Give an overview of the Neisseria gonorrhoeae infection

A
  • Adherence to urogenital epithelium
  • Competition with resident microbiota, nutrient acquisition and microcolony formation
  • Colonisation and invasion of epithelium
  • Release of peptidoglycans, LOS and outer membrane vesicles
  • Cytokine, chemokine and inflammatory TF activation
  • Peptidoglycans, LOS and OMVs cause NOD and TLR activation on epithelial cells, macrophages and dendritic cells
  • HBP causes activation of TIFA-dependent innate immunity in epithelial cells and macrophages
  • Influx of neutrophils -> adherence and phagocytosis of N. gonorrhoeae
  • A neutrophil-rich purulent exudate facilitates transmission
39
Q

How does N. gonorrhoeae modulate the immune system?

A
  • Prevents deposition of complement
  • Prevents opsonisation
  • Modulates activity of macrophages, dendritic cells and neutrophils -> modulates apoptosis
  • Immunosuppressive
  • Modulates T cell function
40
Q

Describe the epidemiology of N. gonorrhoeae

A
  • Gonorrhoea mainly affects people in their 20s
  • Increasing incidence in the UK
  • Increase transmission of HIV
41
Q

How is meningococcal disease diagnosed?

A
  • Often diagnosed on the signs and symptoms
  • CSF and blood samples
  • Gram stains and microscopy to look for gram negative diplococci
  • Culture takes too long
  • PCR
  • Detection of soluble bacterial polysaccharides in CSF by latex agglutination
42
Q

How is gonococcal disease diagnosed?

A
  • Direct examination of exudates in genitourinary medical (GUM) clinics
  • Endocervical, cervical, anal and eye swabs
  • Urines
  • Gram stain and microscopy
  • Nucleic amplification tests
  • QRT PCR
  • Old fashioned culture methods
43
Q

How is meningococcal disease treated?

A
  • IV antibiotics -> benzyl penicillin or amoxicillin, third generation cephalosporins
  • Maintenance therapy for shock
  • Vasoactive treatments -> e.g. IV adrenaline
  • Steroids
  • Experimental therapies, such as anti-cytokine and anti-endotoxin have been investigated
44
Q

How is gonococcal disease treated?

A
  • First line treatments now extended spectrum

- Duel treatments are now recommended

45
Q

What is the biggest issue for the meningococcal vaccine?

A

Surface variation poses a big problem in vaccine development

46
Q

How was the Bexsero B vaccine developed?

A

Reverse vaccinology

47
Q

What is the future of treating gonorrhoea?

A
  • LpxC inhibitors
  • Molecules mimicking host defensins
  • Host defense proteins
  • NanoCapc

Human Microbial Diseases Block 1 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions