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Neisseria meningitis


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What is the microscopic appearance of Neisseria?
gram-negative diplococci (ususally seen in pairs)
What diseases does Neisseria cause?
N. meningitis --> attacks CNS
[CNS irritation --> irritable]

N. gonorrhea --> attacks mucosal epithelium to cause sexually transmitted disease

True or false:
Neisseria are aerobic, gram-negative diplocci which appear in pairs and have a "kidney bean" appearance

Makes sense they are aerobic b/c normally found in upper respiratory tract and alimentary tract

What are the two pathogenic species of Neisseria that only naturally infect humans.
(1) Neisseria meningitis
(2) Neisseria gonorrhoea
where does N. meningitis commonly colonize?
How many serogroups of meningococcus are there (based on capsular polysaccharide structureal differences)
13 serogroups of meningococcus
what % of young adults have asymptomatic carriage of Neisseria meningitis?
Name 3 methods of N. meningitis transmission?
(1) during or through close contact
(2) directly from person to person
(3) droplet spread of nasopharyngeal secretions

Which N. meningitis serogroups are predominant in North America?

Which one is most common in Canada?

B, C and Y

Canada --> mainly serogroup C

U.S. --> Y is now a factor

Incidence of N. meningitis in Canada is ______ cases per 100,000 population
1.64 cases per 100,000 population.

FYI: the incidence has remained steady over past years

Which serogroups commonly cause meningitis?
A, B, C, Y, W-135 and X

(remember abc wxy)

Which serogroup is endemic and has caused sporadic cases and outbreaks in Canada & the U.S.

..some studies have shown it to be associated with high rates of mortality & morbidity

serogroup C

[note that serogroup Y is now associated with meningitis in the U.S.]

compare the capsular features of N. meningitidis and N. gonorrhoeae
N. meningitidis clinically important strains are ENCAPSULATED & rarely have plasmids

N. gonorrhoeae strains have no capsule (NO CAPSULE biosynthetic genes), but do HAVE PLASMIDS

Name 3 factors important in meningococcal virulence:
(1) genome plasticity
(2) horizontal DNA exchange
(3) phase and/or antigenic variation

Meningococci colonize the upper respiratory tract. How do they get into the submucosa?

What tissue do they damage while entering the submucosa?

They are internalized by NON-ciliated mucosal cells.

While entering the submucosa, they damage the ciliated epithelium through direct action of lipooligosaccharide

After entering the submucosa (via the non-ciliated mucosal cells), invasive meningococci spread to the bloodstream. From here, what are the 2 possible fates?
(1) undergo SLOW multiplication --> MENINGITIS (N. meningitidis infects subarachnoid space).

(2) RAPID multiplication --> MENINGOCOCCEMIA causes symptoms before local sites become infected
(ie. multiplication is so rapid that inflammation has not resulted. Can be fatal --> apoptosis, necrosis).

What is meningococcemia and what does it cause?
Meningococcemia is an acute & potentially life-threatening infection of the bloodstream. It causes fulminant (sudden) meningococcal septicemia (systemic inflammatory response to an infection)
After penetrating host defenses, SLOW bacterial multiplication can cause what?
most common: LOCAL infection of meninges (meningitis)

- joints (arthritis)
- pericardium (pericarditis)

After penetrating host defenses, RAPID bacterial multiplication can cause what?
- petechiae, pupura
- disseminated intravascular coagulation (DIC) [blood clotting] --> especially seen in Gram-Negative septicemias
- bleeding in adrenals
- shock

Name 5 Neisseria meningitidis antigenic outer membrane structures:
(1) Opacity proteins: Opa and Opc (adhesion)
(2) Porin proteins: PorA or PorB
(3) Lipooligosaccharide (endotoxin)
(4) Pili
(5) Capsule (13 serogroups)

What are the 4 stages of N. meningitidis infection?
(1) colonize nasopharyngeal epithelium
(2) septicemia --> intravascular invasion
(3) entry & breakdown of blood brain barrier endothelium
(4) tissue & meningeal infiltration

Which capsular polysaccharides are associated with invasive disease?

How does the capsule promote transmission, spread and survival?

A B C Y and W-135

Capsule is antiphagocytic if IgG and IgM levels are depressed and antibactericidal

What are two of Neisseria meningitidis's major outer membrane proteins?

What do they do?

PorA and PorB

They activate immune cells and induce formation of bacterial antibodies. [vaccines based on PorA?]

What is frustrated phagocytosis?
If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues
what are the two virulence factors that bind to CD46 and CD66 and heparan sulfate proteoglycan receptors [what is the term for these]
(1) PILI are major adhesins that first target host receptor CD46

(2) The opacity associated proteins Opa and Opc bind to integrins on the host cell

Binding of pili & Opa / Opc (virulence factors) stimulates what?
engulfment of meningococci by epithelial cells --> meningococci cross the mucosal epthelium through phagocytic vacuoles.

Rarely, N. meningitidis penetrates mucosa & gains access to bloodstream causing system disease

Name a N. meningitidis virulence factor that depresses mucosal immunity
IgA Protease - enzyme that cleaves IgA in half & depresses mucosal immunity
Name two other virulence factors that N. meningitidis uses:
(1) Iron extraction - Neisseria can extract iron from human transferrin via a non-energy requiring mechanism (ie. they get iron in the restricted environment)

(2) Lipooligosaccharide is an endotoxin.

What are the two potential routes LOS endotoxin can take in a N. meningitidis infection?
(1) host cell cytokine production
- inflammatory cytokines
- IL1B, 6, 8 and 10

(2) Alternate complement pathway

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