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Meningitis Flashcards

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1
Q

Define meningitis.

A

-Inflammation of meninges (3 membranes enveloping brain & spinal cord
-Can be caused by infection by bacteria, viruses, & protozoa - other causes = cancer, inflammatory diseases & drugs

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2
Q

Define encephalitis.

A

-Inflammation of brain
-Severity = variable
-Causes - most common= viral (HSV) & microorganisms e.g., parasites - other causes = autoimmune diseases & certain meds

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3
Q

What makes up the CNS?

A

CNS = brain + spinal cord

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4
Q

What is CSF?

A

-Clear fluid
-In subarachnoid space & ventricular system
-Around & inside brain & spinal cord
-Cushions the brain
-Can sample ‘easily’ - can be painful = lumbar puncture

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5
Q

What may cause infection of CNS?

A

-Often come from bloodstream = haematogenous - bacteraemia (infections of blood)
-Severe trauma - to head, spine
–> but CNS = normally sterile & has good physical protection - BUT poor immune protection!!!

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6
Q

What are the meninges?

A

3 membranes enveloping CNS
-Dura mater
-Arachnoid mater
-Pia mater

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7
Q

In simple terms - what is meningitis?

A

Inflammation of meninges - due to infection

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8
Q

What is the blood-brain barrier?

A

Separation of circulating blood & CSF in CNS

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9
Q

Where is the blood-brain barrier & what is it composed of?

A

= selective barrier between cerebral capillary blood & brain tissue/interstitial fluid in brain - high permeability
–> formed by:
-Capillary endothelial cells
-Basement memb
-Astrocytes
-Tight junctions between endo cells

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10
Q

Where is the blood-CSF barrier & what is it composed of?

A

= interface between blood & CSF
–> formed by:
= choroid plexus endothelial cells & tight junctions that linking them & the arachnoid membrane (envelopes brain)
(choroid plexus - secretes/produced CSF)

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11
Q

Compare BBB VS BCSFB?

A
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12
Q

Role of the endothelial cells in BBB?

A

Restrict diffusion microscopic objects e.g., bacteria & large or hydrophilic molecules into brain & CSF

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13
Q

How does meningitis occur in terms of BBB?

A

Bacteraemia, systemic invasion - crossing BBB/blood-CSF barrier

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14
Q

3 different pathogenic causes of meningitis?

A

-Bacterial = often most severe
-Viral
-Fungal

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15
Q

What are the 2 outcomes - comparing use of or no use of antibiotics for meningitis?

A

-Without antibiotics = high mortality rate
-With antibiotics = risk of neurological disorders

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16
Q

Why can serious neurological damage occur in meningitis?

A

Due to inflammation

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17
Q

What are the common causative organisms for meningitis in:
-Neonates
-Infants/children/adults
-Immunosuppressed

A

Bold = most common

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18
Q

Symptoms of meningitis?

A

-Fever – temp >38oC
-Physical signs Mental status – reduced consciousness
-Neurological deficits – vision, hearing & memory
-Seizures
-Headache
-Photophobia
-Nausea & vomiting
-Rash
-Nuchal rigidity
-Kernig’s sign
-Brudzinski’s sign = elicited when patient is in supine position & = +ve when passive flexion of neck causes spontaneous flexion of hips & knees
-Purpuric rash

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19
Q

What is Nuchal rigidity?

A

“stiff neck”
= the pathognomonic sign of men­ingeal irritation & is present when neck resists passive flexion

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20
Q

What is Kernig’s sign?

A

= elicited when patient is in the supine position - hip is flexed to 90 degrees BUT knee cannot be fully extended; attempts to passively extend knee cause pain when meningeal irritation is present

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21
Q

What is Brudzinski’s sign?

A

= elicited when patient is in supine position & = +ve when flexion of neck causes spontaneous flexion of hips & knees

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22
Q

What is a purpuric rash?

A

Rash that does not fade under pressure - non-blanching rash - i.e., put glass on top & press down = sign of meningococcal septicaemia - septicaemia also has high fatality rate

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23
Q

Name the common pathogens involved in meningitis?

A

-Streptococcus pneumoniae
-Group B Streptococcus
-Neisseria meningitidis
-Haemophilus influenzae
-Listeria monocytogenes
-Escherichia coli

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24
Q

What is the gram stain & shape of Streptococcus pneumoniae?

A

Gram +ve
Cocci (round) - often diplococci

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25
Q

What is the gram stain & shape of Group B Streptococcus?

A

Gram +ve
Coccus (round) - tends to form chains

26
Q

What is the gram stain & shape of Neisseria meningitidis?

A

Gram -ve
Cocci (round) - diplococci!

27
Q

What is the gram stain & shape of Haemophilus influenzae?

A

Gram -ve
Bacillus (rod shaped)

28
Q

What is the gram stain & shape of Listeria monocytogenes?

A

Gram +ve
Bacillus (rod shaped)

29
Q

What is the gram stain & shape of Escherichia coli?

A

Gram -ve
Bacillus (rod shaped)

30
Q

Name the bacteria causing meningitis seen in newborns.

A

-Group B Streptococcus
-S. pneumoniae
-L. monocytogenes
-E. coli

31
Q

Name the bacteria causing meningitis seen in babies & young children.

A

-S. pneumoniae
-N. meningitidis
-H. influenzae
-Group B Streptococcus
-M. tuberculosis

32
Q

Name the bacteria causing meningitis seen in teens & young adults.

A

-N. meningitidis
-S. pneumoniae

33
Q

Name the bacteria causing meningitis seen in older adults.

A

-S. pneumoniae
-N. meningitidis
-H. influenzae
-Group B Streptococcus
-L. monocytogenes

34
Q

Role of the BBB in protection?

A

Protects brain & meningeal spaces from bacterial invasion -> due to specialised endo cells & tight intercellular junctions

35
Q

Describe the interaction of Neisseria meningitidis with the BBB?

A

Enters meninges by a variety of routes:
-Traverse through endo cells of BBB (endo cells on blood capillary)
–> pili bind - rearrange actin cytoskeleton - so that microvilli-like structures form - then N. meningitidis engulfed into cell within vacuole
-Degrade tight junctions - enables crossing of endo barrier (of BBB)
-Trojan horse strategy = as N. meningitidis = encapsulated - so if are engulfed by e.g., neutrophil (phagocyte) - will survive within - as capsule protects from phagocytosis (& so destruction - can also prevent engulfment from start) –> so neutrophil infiltration occurs - neutrophils move across BBB - endo cells = enter meninges - containing N. meningitidis –> can occur due to damage to endo cells of BBB - allows passage & also due to inflammatory response causing damage -> attracts neutrophils
–> may be many N. meningitidis within the neutrophil

~ Bacteria carried across BBB by infiltrating phagocytes

36
Q

Describe the pathogenicity of bacteria in meningitis.

A

Bacteria require access to meninges to cause meningitis
Invasion of bacteria into the subarachnoid space results in inflammation of the meninges.

  1. Bacteria e.g., N. meningitidis in bloodstream
  2. N. meningitidis cross BBB - endo cell layer by various mechanisms
  3. Movement of N. meningitidis across BBB - causes damage to endo cells - host cell/tissue damage
    = release of DAMPs (PAMPs also being released by bacteria)
  4. DAMPs & PAMPs bind to PRRs = causes release of pro-inf cytokines - inflamm response targeted to CEREBRAL VASCULATURE
  5. Pro-inf cytokines lead to inflamm response -> get immune cell infiltration into meninges - & some immune cells (in low numbers) are already found here
    -PAMPs recognised before DAMPs production = activates resident immune cells e.g., microglia, macrophages, astrocytes & pericytes
    -Then recruit more immune cells
  6. Neutrophil infiltration due to inflamm response -> allows for trojan horse mode of crossing BBB for N. meningitidis (due to capsule preventing phagocytosis) = more DAMPs & PAMPs = more inflamm response
    -Consequence of host response (resident imm cells + recruiting imm cells) = activates a fibrinolytic & coagulation cascade***
    -Neutrophils produce reactive O2 species (destroy pathogens) & release NETs (= netosis - cell death) - damage to host cells too!

*Fluid movement across BBB into the space due to inflamm response = increased intracranial pressure
*Fluid accumulation in brain intracellular or extracellular spaces causes -> cerebral oedema (brain swelling)
Inflamm induces clotting ** = walls of microvs = leads to neuronal ischaemia (lack of blood supply) = so lack of O2 supply to brain tissue = cerebral hypoxia -> so some cell death due to this
–> this clotting causes inc ICP & oedema (?)

-Over time blood-brain barrier breaks down - inc in permeability -> due to damage -> more infiltration of bacteria & immune cells
-Get inflamm of arachnoid & pia mater

-MMP inc = matrix metalloproteinases -> degrade tight junctions
-NO inc - nitric oxide = causes vasodilation = dec BP

-Bacteria cross blood-CSF barrier & BBB(?)

37
Q

Differentiate between all the types of BBBs & blood-CSF barriers.

A
38
Q

Which region of the brain is most susceptible to damage due to meningitis?

A

Hippocampus - regulates beh, gait, sensory elements = shown within clinical signs

39
Q

Describe Neisseria meningitidis.

A

-“The Meningococcus”
-Gram -ve
-Diplococcus (intracellular)
-Encapsulated (= virulence factor)
-Humans = only known reservoir
-High levels of asymptomatic carriage in throat
~20 % of which ~10 % may be non-pathogenic (non-capsulate)
-Crosses nasopharyngeal mucosa -> bloodstream***

40
Q

What are some of the pathogenicity factors of Neisseria meningitidis? (pathogenicity = ability of pathogen to cause disease)

A

-Type IV pilus involved in mucosal colonisation = main means of meningococcal adhesion to host cells (= important in colonisation - so = important virulence factor)
–> pilus-mediated adhesion causes microvilli-like structures to form at these sites of interaction
–> these “microvilli” = cause internalisation of N. meningitidis
*-> so these pili cause reorganising of actin cytoskeleton - so that microvilli-like structure form (= protrusions) & then enter host cell by engulfing into intracellular vacuoles
-Polysaccharide capsule helps avoid phagocytosis –> not all have this
-Major toxin: lipo-oligosaccharide (LOS) endotoxin

41
Q

What is meant by serotypes of Neisseria meningitidis?

A

= distinct variation within a the N. meningitidis species

42
Q

What are 6 serotypes of Neisseria Meningitidis - causing most cases of meningitis worldwide?

A

A, B, C, W, X, Y
(are 13 in total)

43
Q

What is NMEC?

A

Neonatal Meningitis E. coli

44
Q

What type of meningitis is NMEC most responsible for & why?

A

-Gram -ve meningitis in neonates
–> due to perinatal transfer from mother to child - as this bacteria resides in GI tract

45
Q

Mortality rates from NMEC?

A

40% fatality rates

46
Q

How common is neonatal bacterial meningitis in general in UK?

A

250-300 cases per year

47
Q

Describe the pathophysiology of NMEC (neonatal meningitis E. coli).

A

-Crosses BBB via trojan horse approach (as NMEC = encapsulated by K1 capsule - so survive in phagocytes), or cross BBB by traversing across endo cells = damages - this method involves pili adhering to host cell & microvilli-like structures (like N. meningitidis) - so bacteria move across in vacuole
-IbeA domain on bacteria = binds to receptors of endo cells of BBB - for invasion = as this also causes actin rearrangement - for invasion of bacteria
-OMPA = adhesins also involved
-CNF-1 = toxin released by bacteria - assists with invasion

*Image shows pili related invasion method -> with Ca2+ inc & actin rearrangement - eventually leading to invasion of bacteria

-Same immune response as N. meningitidis

48
Q

Give some of the pathogenicity factors of NMEC.

A

*Adhesins
-OmpA (= Outer Memb Prots)
-S-fimbriae - bind sialic acid of human cell-surface glycoproteins (type 1 pili)

*Immune evasion
-K1 Capsule (antiphagocytic)

*Iron acquisition
-Ent(erobactin)

*Invasion factors
-IbeA (receptor-binding)

*Toxins
Cytotoxic necrotising factor (CNF-1)

49
Q

What are the diagnostics (techniques of diagnosis) for possible meningitis?

A

-Urgency: diagnosis of meningitis is a medical emergency
-Samples must be processed without delay
-Results must be reported back to ward immediately to guide antibiotic therapy

50
Q

What is the name of the method to sample CSF?

A

Lumbar puncture

51
Q

What is involved in a lumbar puncture?

A

-Needle inserted between lower vertebrae - where spinal cord has ended
-Needle pierces lining of spinal column
-Often take 3 samples

Spinal needle safely inserted into subarachnoid space at L3-4 or L4-5 interspace, as this is well below termination of spinal cord in most patients

52
Q

What are the processing steps carried out on a CSF sample?

A
  1. Appearance
  2. Cell count
  3. Centrifugation
  4. Gram stain
  5. Culture
  6. Further tests
53
Q

What can be determined by assessing the appearance of CSF?

A

= Rapid indication of problems

-Normal = clear fluid/colourless
(Bacterial meningitis = cloudy & turbid, BUT viral = clear, and fungal = clear or cloudy an tuberculosis men = opaque & if left to settle forms fibrin web)
-Turbidity – WBCs = possibly other cells seen by microscopy
-Red staining (RBCs) - stroke/haemorrhage - subarachnoid haemmorhage

54
Q

What does processing of CSF - the cell count show in meninigitis?

A

-In bacterial meningitis = will be high levels of leukocytes in CSF

*Total no.s & types of:
-WBCs
-RBCs
–> then ratio of no. RBCs:WBCs

-Bacterial = elevated WBCs >100 cell/µL (primarily polymorphonuclear leukocytes (>90%))
-Viral = elevated (50 – 1000 cells/µL, primarily lymphocytes, can be PMN early on)
-Fungal WBC = elevated (10 – 500 cells/µL)
-TB men WBC = elevated (10 – 1000 cells/µL, early PMNs then mononuclear)

-Normally WBC count is LOW:
Children/adults = <5mm(cubed)
Neonates = <20mm(cubed)

-Bacterial meningitis WBC = higher count of polymorphonuclear lymphocytes - often is 1000mm(cubed) in later stages

55
Q

How to detect pathogen in meningitis?

A

GRAM STAINING = very fast & high sensitivity

*Microscopy - but in some cases may be high no. of polymorph. lymphocytes but bacteria not visible
-Culture CSF samples - as may be small numbers of bacteria - so is easier to identify them
*ELISA - antigen detection - capsules = highly antigenic
*PCR gives rapid diagnosis of:
-Alternative to antigen testing
-Confirmation of Gram staining
-Specific primers e.g., for Neisseria
-Broad-range/universal primers

–> but in early stages of meningitis & if have already treated with antibiotics as a precaution = harder = fewer bacteria
-Presence of capsules = helps with ID

56
Q

How to detect fungi & parasitic meningitis?

A

-Microscopy
-Culture?
-Antigen detection - ELISA?
-PCR

57
Q

How is bacterial meningitis treated?

A

-ASAP treatment outweighs need for microbiological diagnosis
–> i.e., strong suspicion of meningitis – treatment begins before CSF sample taken
-High dose intramuscular OR IV - benzylpenicillin given at earliest opportunity (under 16’s)

*High dose (IV) 3rd generation cephalosporins
Ceftriaxone OR Cefotaxime OR Broad spectrum activity VS Gram +ves & Gram -ves
Penetrate well into CSF

-Antibiotic susceptibility test results may modify treatment
-Household/“kissing” contacts may be given prophylactic antibiotics
-TB/cryptococcal meningitis need long-term treatment with specialised anti-tubercular/anti-fungal agents

58
Q

What are some of the various meningitis vaccines?

A

-Meningitis B vaccine = MenB - protects against meningococcal group B bacteria
-6-in-1 vaccine - aka DTaP/IPV/Hib/Hep Bvaccine = protection against diphtheria,tetanus,whooping cough, hepatitis B, polio& Haemophilus influenzae type b (Hib)
-Pneumococcal vaccine
-Hib/Men C vaccine = protects against meningococcal group C bacteria
-Meningitis ACWY vaccine (Uni?) = protects against meningococcal groups A, C, W & Y –> for 14 yos & people up to 25 (if never had vaccine containing MenC)

59
Q

What are some of the common viral meningitis pathogens?

A
60
Q

How is acute viral meningitis treated?

A

-Most cases = primarily asymptomatic - treatment includes analgesics, antipyretics, & antiemetics
-Oral or IV acyclovir may = beneficial for meningitis caused by HSV-1 or -2 & in severe EBV or VZV infection
(Data concerning treatment of HSV, EBV, & VZV meningitis = v. limited)

Microbiology (6 decks)

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