Bacterial meningitis Flashcards

1
Q

What is meningitis?

A

acute inflammation of the meninges, causes include bacteria, viruses and fungus

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2
Q

How would you describe Neisseria meningitis?

A

gram negative diplococcus, divided based on capsular group

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3
Q

What’s the importance of capsular groups shifting?

A

leaves a gap and there’s a selection pressure there when there’s a shift

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4
Q

Where does it initially colonise?

A

Nasopharynx

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5
Q

What factors affect carriage?

A

age, behaviour, and population

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6
Q

How is it transmitted?

A

Via aerosol droplets

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7
Q

Why is nasopharyngeal colonisation such a big problem?

A

affects mucociliary pathway (capsule prevents organism from getting trapped in mucus), colonisation resistance can occur, produces lactoferrin binding protein b which can neutralize the body’s innate defenses

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8
Q

What is carriage facilitated by?

A

a downregulation or loss of capsule expression

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9
Q

What are some virulence factors used to attach to URT epithelia?

A

capsule used to stop itself from getting trapped in Mucociliary pathway, type 4 pili to attach to post epithelia. In order to attach will reduce expression of capsule and upregulate expression of tfp, in some cases it’ll create a biofilm for long term carrier state in URT

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10
Q
  1. Describe a virulence factor that helps Nm survive in blood
A

The expression of a polysaccharide capsule - Most NM capsules inhibit opsonophagocytosis through charge (heavily charged layer which pushes away phagocytic cells) & the capsule serotype B is identical to NCAM so mimics host and doesn’t use charge

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11
Q
  1. Explain what happens when Nm enters blood from URT
A

eventual host cell damage following immune system activation (blebbing of cell wall) and uncontrolled growth in blood may lead to meningococcal septicaemia

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12
Q
  1. In order to cross BBB and enter CNS what must Nm do?
A

adhere to brain endothelial cell, tight junction depletion and paracellular movement may occur

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13
Q

Why does CNS injury result from migration across BBB?

A

results from endotoxin production and host inflammatory response

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14
Q

What’s the difference in symptoms of bacterial meningitis and meningococcal septicaemia?

A

both may experience a non-blanching rash and an altered mental status. Photophobia is not experienced in MS

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15
Q

What are some signs of shock?

A

tachycardia, difficulty breathing, leg pain, cold hands/feet. Altered mental state, poor urine output

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16
Q

What is the vaccination schedule for meningococcal disease?

A

8 weeks (men B), 16 weeks (menB), 12 months (HiB/MenC + MenB booster), 14 -25 years (Men ACWY)

17
Q

How is Bacterial meningitis treated?

A

if 3months+ then IV ceftriaxone but if less than 2 months then cefotaxime + amoxicillin or ampicillin

18
Q

What are the 2 predominant bacterial causes?

A

N.meningitidis and S.pneumoniae

19
Q

Describe the microbiology of pneumococci

A

gram positive coccus, non-motile. Has polysaccharide capsule (90 serotypes)

20
Q

What virulence factors does Sp produces and what are their purpose?

A

all aim to avoid immune response. Neuraminidase reduces viscosity of mucous and IgA protease cleaves IgA

21
Q

Sp is normally found where in the URT?

A

nasal cavity, nasopharynx, pharynx

22
Q

How does Sp survive in the blood?

A

charge effect of polysaccharide capsule prevents phagocytosis, massive activation of host cell complement and coagulation systems, host cell mediated damage and pneumolysin (pore forming toxin) assists BBB crossing. Neutrophil recruitment within the CNS leads to neurological sequelae

23
Q

Describe pneumococcal vaccination schedule

A

12 weeks (PCV 13), 12 months (PCV 13 booster), 65 (PPV) and 65+ inactivated flu vaccine (annual)

24
Q
  1. Infection with seasonal influenza can increase risk of CAP. True or false?
A

True

25
Q

How many serotypes of Sp do the PCV vaccine and the PPV vaccine have?

A

PCV has 13 and PPV has 23