Bacterial Meningitis Flashcards

1
Q

What is meningitis?

A

Acute inflammation of the meninges around the brain typically as a result of an infective cause originating (usually) in the blood

  • Bacterial
  • Fungal
  • Viral
  • Aseptic? (no discernable cause)
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2
Q

What does the BBB do

A

Its a specialist structure of endothelial cells within the blood suppl of the cns which prevent entry of bacteria and toxins into the cns

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3
Q

What is the meninges?

A

A protective membrane found under the skull and around the brain.

The meninges is made up of the dura, the arachnoid and the Pia Mater

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4
Q

How common is bacterial meningitis

A

Annual incidence (developed countries): 2-5 / 100,000 population

2011/12
1355 (57.4%) meningococcal
340 (14.4%) pneumococcal meningitis

2017/18
755 cases meningococcal disease
(is on the decline)

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5
Q

Which bacterial organism causes meningococcal meningitis

A

Neisseria meningitidis

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6
Q

What are the characteristics of Neisseria meningitidis

A

Gram negative diplococcus - unusual

Inhabitant of nasopharynx
Serology based on capsular polysaccharide used to avoid the host immune system, excess outer membrane protein which will illicit immune response away from the bacterial cell and LPS

Causative agent of meningococcal meningitis

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7
Q

How do we differentiate between the at least 12 types of NM

A

Divided based on distinct capsular groups
At least 12 types identified
B, C, W, Y most common in UK (historically)
A, B, C account for 90% disease on global scale
However, the importance of the capsular groups is always shifting due to vaccination strategies

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8
Q

Is NM only found in ill patients?

A

No, Nm resides in the URT of healthy individuals

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9
Q

How does NM colonise the host

A

Nasopharyngeal carriage (10-25% of people do)
Age - a major factor
Behaviour (e.g.) key age group is students
Population

Transmission via aerosol droplets

Nasopharyngeal colonisation
represents a significant challenge

Mucociliary pathway - capsule prevents it being caught in it
Nitric oxide
Colonisation resistance
Lactoferrin

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10
Q

Who is most likely to carry meningococcal bacterium

A

Late teens, early 20s. Increases up to this point from childhood and decreases afer this point

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11
Q

Vhich virulence factors does NM use to adhere to host cells

A

Carridge in the healthy host occurs before infection. To cause disease the capsule expression is down regulated and the pilli expression is increased (it may also create a biofilm)

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12
Q

In some cases Nm enters the blood. How does it survive?

A

Survival in blood is dependant on the presence of certain virulence factors

A critical virulence factor for survival in the blood is the expression of a polysaccharide capsule

Most Nm Capsules inhibit opsonophagocytosis through charge (they repel host immune response cells (phagocytes))

Capsule serotype B mimics host so evades the immune response (identical to NCAM) - it doesn’t work through charge repulsion

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13
Q

What is the issue of Nm colonising the blood

A

Eventual host cell damage following immune system activation (Blebbing of cell wall - triggers the immune response in areas away from the viable cell)

Uncontrolled growth in the blood may lead to meningococcal septicaemia

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14
Q

What happens to allow NM to move across the BBB

A

Presence of bacteria in the host blood supply (surviving in it’s capsule) leads to adherence to brain endothelial cells required for BBB crossing (pili). This leads to tight junction depletion and paracellular movement of the bacteria may occur

CNS injury results from endotoxin production and host inflammatory response following migration of PMNs across BBB

Infection of meninges by Nm is meningococcal meningitis

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15
Q

What are the key symptoms of meningitis

A

Non blanching rash due to damage to capilliaries (not always present)
stiff neck
altered mental state (confusion, delirium, impaired conciousness)
bulging fontanelle (only relevent in <2y)
photophobia (not seen in meningococcal septicaemia)

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16
Q

What are the signs of septic shock

A

Tachycardia; difficulty breathing; leg pain; cold hands/feet; altered mental state; poor urine output

17
Q

What is the vaccine schedule for meningitis

A
8 weeks 
MenB vaccine (Bexsero) 

16 weeks
MenB vaccine

12 months
HiB/Men C vaccine (Menitorix)
MenB booster (Bexsero)

14 years (school year 9). Eligible up to 25y
Men ACWY Vaccine (Nimenrix/Menveo)
18
Q

SInce its introduction in 1999, what impact has the menC vaccine had on case numbers

A

95% decline in menC cases. However, due to selection pressures, other capsule types will increase in prevelence

19
Q

Which patient group does menB particlarly affect

A

0-5yrs. Carriage is highest in adolescence but most invasive infection occurs in very young children

20
Q

What is the nice guidance surrounding the treatment of bacterial meningitis

A

Transfer to secondary care as a 999 emergency

Secondary Care: Prompt antibiotic treatment!!
Suspected bacterial meningitis
3m+: Immediate intravenous ceftriaxone
7d confirmed meningococcal
14d confirmed Sp
<3m: Cefotaxime plus amoxicillin or ampicillin

21
Q

What is the public health role of the pharmacist surrounding bacterial meningitis

A

Awareness of symptoms
Public education
Awareness of vaccination schedule

22
Q

Name a second bacterium which can cause meningitis

A

Streptococcus pneumoniae. A cause of pneumococcal meningitis (and community acquired pneumonia)

23
Q

What is the microbiology of pneumococci

A

Gram positive coccus

Non motile

Polysaccharide capsule
>90 serotypes reported

Generates other virulence factors to avoid immune response

  • Neuraminidases (reduce viscosity of mucous) Less likely to be trapped in mucousiliary pathway
  • IgA protease – cleaves immunoglobulin A which is something which usually amkes up 90% of the humoral response in the upper respiratory tract.

Normal inhabitant of URT
Nasal cavity
Nasopharynx (10%)
Pharynx

24
Q

How does strep pneumo. survive in the blood

A

Survival in the blood is again linked to virulence factor production

Polysaccharide capsule
-Charge effect prevents phagocytosis

Massive activation of host cell complement and coagulation systems - pneumolysin production. This initiates an inflammatory response which damages the hosts epithelial cells allowing the bacteria to slip through BBB gaps

Host cell mediated damage and pneumolysin assists BBB crossing

Neutrophil recruitment within the CNS leads to neurological sequelae

25
Q

Who are mostly affected by pneumococcal meningitis

A

5yo and under usually. Not the difference between this and community aquired pneumonia

26
Q

What is the vaccine schedule for pneumococcal infections

A
12 weeks
Pneumococcal vaccine (PCV)
12 months (Booster)
Pneumococcal vaccine (PCV)

Eligible paediatric groups
Live attenuated flu vaccine / annual

65 years
Pneumococcal vaccine (PPV) polysaccaride vaccine

65 years +*
Inactivated Flu vaccine (annual)

27
Q

How has the vaccnation strategy affected the epidemiology of pneumococcal infections

A

Reduced invasive pneumococcal infections by c. 80%

Name of vaccine - Prevenar 13 (pneumococcal conjugate vaccine - PCV)

13 valent conjugate vaccine used in <2 yo - more effective

1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, 23F

Increase in invasive disease due to non vaccine serotypes occurring!!

Pneumococcal polysaccharide vaccine (PPV) - isn’t very effective in children so isn’t used. is used in 65+s

23 serotypes