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Bacterial meningitis Flashcards

1
Q

Why is bacterial meningitis associated with elevated protein levels?

A

BBB breakdown

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2
Q

Causative agents of bacterial meningitis: 0-3 months

A

GBS (S. agalactiae)
Listeria
Gram - enterics (E. coli, Klebsiella, Enterobacter, Salmonella)

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3
Q

Causative agents of bacterial meningitis: 3 months - 2 years

A

H. flu B
N. meningitidis
Strep pneumo

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4
Q

Causative agents of bacterial meningitis: 2-18 years

A

S. pneumo

N. meningitidis

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5
Q

Causative agents of bacterial meningitis: 18+

A 
S. pneumo
N. meningitidis
Listeria
HIB
Gram - enterics
Pseudomonas
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6
Q

Causative agents of bacterial meningitis: immunocompromised patients

A

Staph
Gram - enterics
Pseudomonas

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7
Q

MCC bacterial meningitis 0-3 months

A

GBS

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8
Q

MCC bacterial meningitis 3 months-adulthood

A

S. pneumo

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9
Q

Strep pyogenes has which Lancefield antigen?

A

Rhamnose-acetylglucosamine

GAS

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10
Q

Step agalactiae has which Lancefield antigen?

A

Rhamnose-glucosamine

GBS

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11
Q

What are capsular polysaccharides used for diagnostically?

A

Determining types of strep pneumo

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12
Q

What are streptococci biochemical reactions used for diagnostically?

A

Strep that don’t have Lancefield antigens or specific hemolysis patterns, like strep viridans

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13
Q

What is Lancefield antigen?

A

An antigenic carbohydrate found in cell walls of strep

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14
Q

MCC invasive disease in children, elderly, and immunocompromised?

A

Strep

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15
Q

Place the diseases caused by strep in order of case fatalities

A

Meningitis (30%) > Sepsis (20%) > Pneumonia (5%)

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16
Q

What type of pneumonia does strep cause?

A

Lobar

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17
Q

Where do strep initially adhere?

A

Nasopharyngeal epithelium

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18
Q

How does strep cause middle ear inflammation?

A

Cell wall components cause cytotoxicity of ciliated cochlear cells

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19
Q

List 3 ways in which strep can invade.

A
  1. Alter vascular permeability and get into blood [pneumonia + bacteremia]
  2. Go though endothelial cells transcellularly and get into blood
  3. Bind to cerebral endothelial cells and transmigrate to enter CSF [meningitis]
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20
Q

How does the capsule of strep confer anti-phagocytic properties?

A

Prevents binding of C3b

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21
Q

List the 7 virulence factors of strep

A
  1. Capsule
  2. Pili
  3. Cell wall components
  4. Choline binding protein
  5. Hemolysin
  6. Neuraminidase and IgA protease
  7. H2O2
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22
Q

Which components of strep cell wall are proinflammatory?

A

Techoic and lipotechoic acids containing peptidoglycan and phophorylcholine

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23
Q

Which virulence factor of strep is important in crossing the BBB to cause meningitis?

A

Choline binding protein

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24
Q

What is the function of the choline binding proteins?

A

Adhesion

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25
Q

What is the function of pneumolysin?

A

Lyse host cells and activate complement

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26
Q

What is the function of neuraminidase?

A

Invasion of host cells

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27
Q

What is the function of H2O2?

A

Bactericidal of competing organisms

Damage to host cells

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28
Q

Which strep pneumo vaccine is conjugated? What does this mean?

A

Prevnar - longer lasting immunity

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29
Q

Which type of molecules provide short-lived immunity? Memory?

A

Carbs

Proteins

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30
Q

Which S. pneumo vaccine is indicated for infants?

A

Prevnar

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31
Q

Which S. pneumo vaccine is indicated for asplenic patients?

A

Pneumovax

32
Q

Which S. pneumo vaccine has an amnestic response?

A

Prevnar

33
Q

Which S. pneumo vaccine is not effective in infants?

A

Pneumovax

34
Q

Which S. pneumo vaccine has more capsule types?

A

Pneumovax (23 vs 13)

35
Q

Morphology Strep vs. Neisseria

A

Strep = G+ diplococci, divide on a plane, capsule

Neisseria = G- diplococci, divide as diplococci, +/- capsule (meningitidis has capsule, gonorrhoeae doesn’t)

36
Q

Rates of N. gonorrhoeae vs. N. meningitidis

A

N. gonorrhoeae = high prevalence, low mortality, not present in absence of disease

N. meningitidis = low prevalence, high mortality, 5-30% carriage in persons without disease

37
Q

How are N. meningitidis spp typed?

A

Based on their capsular polysaccharides into A, B, C, Y, W135

38
Q

___% of patient with meningococcus die despite Abx

A

10-15%

39
Q

___% of surviving patients with meningococcus have long-term sequela, including:

A

10%

Lose arms or legs, deaf, mentally retarded, seizures, strokes, nervous system problems

40
Q

An 18 yo college students presents with nuchal rigidity, HA, fever. Which meningococcal serotypes do you expect?

A

B, C, Y

41
Q

Which meningococcal serotype is associated with meningitis epidemics? Where is this especially prominent?

A 
A
Subsaharan Africa ("Meningitis Belt")
42
Q

Describe the development of fulminant meningococcal meningitis

A

Abrupt onset neck stiffness, fever, chills, N/V
Mental status change within a few hours (apprehension, confusion, delerium, coma)
Petechia, purpuric rash
Pulmonary insufficiency within a few hours
Death

43
Q

What are the early signs of meningococcal meningitis? Late?

A

Neck/back stiffness, mental changes = early

Rash = late

44
Q

List the 4 virulence factors of N. meningitidis

A
  1. Capsule
  2. Pili
  3. Endotoxic LOS
  4. Phase variation
45
Q

What is the only known reservoir for meningococcus?

A

Human nasopharynx

46
Q

How is meningococcus spread?

A

Aspiration

47
Q

Which symptoms are unique to meningococcemia vs meningococcal meningitis?

A

Meningococcemia = diarrhea, cramps, spots/rash

Meningitis = photophobia, severe HA, stiff neck

48
Q

DOC meningococcemia vs. meningitis?

A

DOC for both is PCN

49
Q

Why do neither meningococcal vaccines cover group B?

A

It’s capsular polysaccharide is a polymer of sialic acid, which is not immunogenic to humans

50
Q

What are the big differences between menomune and menactra?

A

Menomune is unconjugated so has short-lived immunity; menactra is conjugated so has anamnestic response

Menomune is only given to high risk pt’s, cochlear transplant patients, and those traveling to subsaharan africa (group A epidemic); menactra is suggested for anyone 11-55 years old

51
Q

Which serogroups are covered by both menomune and menactra?

A

A, C, Y, W135

52
Q

Describe phase variation

A

N. meningitidis can turn genes on or off

ex. turning genes off so it can inavde then back on once in bloodstream

53
Q

Describe antigenic variation. Which N. meningitidis system uses this mechanism?

A

Changes in a gene leads to expression of a different form; pili - move silent loci into expression loci for antigenically different loci

54
Q

Why is Hib infection uncommon prior to 3 months of age?

A

Maternal antibodies

55
Q

What is the chief virulence factor of Hib? What is unique about it?

A

Capsule

Polysaccharide antigens are T cell independent so immunity is short-lived

56
Q

Describe the Hib vaccine. Who gets it?

A

Type b polysaccharide capsule (PRP) conjugated to diphtheria toxin
Infants 2-15 months

57
Q

Does the Hib vaccine offer anamnestic response?

A

Yes - conjugated to diphtheria protein

58
Q

___% of kids with Hib meningitis die. ___% develop severe sequela.

A

5% die

15-30% have neurological sequela

59
Q

Morphology of H. flu?

A

Gram - coccobacillus

60
Q

Morphology of Listeria?

A

Gram + rod

61
Q

Who gets Listerosis?

A

Infants, immunocompromised, pregnant women

62
Q

What do immunocompotent patients with Listerosis experience?

A

Mostly asymptomatic, can experience mild flu-like sx, occasionally diarrhea and abdominal pain

63
Q

What do infants, immunocompromised, pregnant women with Listerosis experience?

A

Meningitis and bacteremia

64
Q

How do neonates contract Listerosis?

A

Vaginal canal of mother

65
Q

What are the two human sources of Listeria?

A

Vagina and intestines

66
Q

Which two animal sources are associated with Listerosis?

A

Sheep and chickens

67
Q

What food sources are associated with Listerosis?

A

Raw veggies, dairy (soft cheeses), meat (sheep, chicken)

68
Q

Prognosis of intrauterine Listerosis?

A

Death

69
Q

What is the problem with decontaminating food suspected of harboring Listeria?

A

Listeria can be killed by pasteurization but may replicated during refrigeration, amplifying the bacterial load during storage

70
Q

What cell types does Listeria invade?

A

Macrophages and endothelial cells

71
Q

Describe the invasion scheme of Listeria

A
  1. Internalin binds to E-cadherin on epithelial cells
  2. Escapes phagolysosome via Listeriolysin O
  3. Polyermization of F-actin propels bug into adjacent cell
  4. Replicates
  5. Cell death
72
Q

What is the purpose of intracellular spread of Listeria?

A

Evades host immune system

73
Q

What is necessary to kill Listeria?

A

Cytokine activation of macrophages

74
Q

“Tumbling motility”

A

Listeria and trich

75
Q

Trimethoprim-sulfamethoxazole can prevent which two infections in AIDS patients?

A

Listerosis, pneumocystis

Neuro (5 decks)

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