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Bacterial Meningitis Flashcards

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1
Q

Definition of meningitis

A

inflammation of the meninges (pia, arachnoid and dura mater)

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2
Q

how is meningitis practically defined?

A

abnormal number of WBCs– anything greater than 10 cells/mm cubed in CSF (but age dependent and person to person dependent)

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3
Q

meningitis is ofen (but not always) associated with what in terms of protein and glucose?

A

high protein (dead cells/proteinateous material/inflammatory proteins) and low glucose (protein material jams the active glucose transporters that pump glucose into the CSF, while glucose continues to diffuse out) in the CSF

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4
Q

why is it so dangerous to get an infection within the meninges?

A

the meninges are supposed to be a sterile site, so there are no inflammatory cells present to protect it

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5
Q

what inflammatory cells are most prevalent in viral meningitis? bacterial? fungal? parasitic?

A

viral: lymphocytic pleocytosis
bacterial (aka pyogenic– pus forming): PMN pleocytosis
fungal: lymphocytic pleocytosis
parasitic: eosinophilic pleocytosis

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6
Q

4 characteristics of viral meningitis

A

1) lymphocytic meningitis
2) bacterial cultures are negative
3) seasonality (late spring-fall = peak period in n hemishpere)
4) exposures to people with viral meningitis

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7
Q

Major viral causes of meningitis (5)

A
  1. enteroviruses
  2. Herpes virus
  3. HIV
  4. West Nile, Eastern equine, Western equine (arboviruses)
  5. Lymphochoriomeningitis (LCM) virus – board favorite though very rare!
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8
Q

aseptic meningitis– what is it and what is the cause?

A

when the meninges are inflammed and it’s not caused by pyogenic (pus forming) bacteria
Causes:
viruses, medications (NSAIDS, TMP-SMX), auto-immune dsorders (lupus), or oncologic causes (metastatic cancer)

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9
Q

symptoms you expect to see with Bacterial meningitis (6)

A
  1. headache
  2. fever
  3. photophobia
  4. nick stiffness (“meningisimus”)
  5. Positive Kernig’s and/or Brudzinski’s sign (kids 1-12 who can’t really express neck stiffness but have the musculature to resist movement)
  6. later confusion, stupor, coma
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10
Q

Brudzinki’s neck sign

A

tests for meningisimus (neck stiffness) by bending the head (think B from the name for brain) forward. It’s positive if the child brings their legs up to compensate for the pain

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11
Q

signo de kernig

A

tests for meningisimus (neck stiffness) by bending the knee (think K from the name for knee) toward the chest and then straightening the leg. It’s positive if the child curls in their head to compensate for the pain

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12
Q

Bacterial meningitis is usually community or hospital acquired?

A

generally community acquired

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13
Q

nosocomial

A

non-community acquired (aka hospital acquired) infection

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14
Q

normal path of bacterial infection in meningitis?

A

normally hematogenous spread (bacteria colonizes nasopharynx, invades tissue, gets into the blood stream and then into the CSF)

sometimes trauma that causes leaks in the CSF or a sinus infection in children can cause direct extension

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15
Q 
ypical laboratory findings for bacterial meningitis:
opening pressure
WBC count
%PMNs
Prot:
Glucose:
CSF to serum glucose ratio
gram stain
culture
A

opening pressure: elevated to 200-500 mm H20
WBC count: VERY HIGH (1000-5000) (viral would be closer to 50)
%PMNs: 80% (viral would see lymphocytes, not PMNs)
Prot: high! 100-500 (n < 30)
Glucose: low! <40 mg/dl
CSF to serum glucose ratio: .4
gram stain: positive 60-90%
culture: 70-85%, but sometimes just bacteremia (in blood) but not in csf

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16
Q

why do most cases of meningitis present with low glucose and high protein?

A

protein is high bc cells are dying– lots of extra proteinatious material, and inflammatory proteins in CSF. These proteins get into the active glucose transporters which fall apart– glucose can’t get into csf anymore, but glucose is passively diffusing out —> low glucose in csf

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17
Q

what predictors are used to determine if the meningitis is bacterial? (5)

A
  1. positive gram stain
  2. csf protein > 80 mg/dl
  3. peripheral ANC (absolute neutrophil count) > 10,000 cells/mm cubed
  4. seizure at/before presentation
  5. CSF ANC > 1000 cells/mm cubed
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18
Q

pathophysiology of bacterial meningitis (4 components)

A
  1. alterations of BBB (blood brain barrier)
  2. cerebral edema, both vasogenic and cytotoxic
  3. Increased intracranial P (ICP)
  4. decreased perfusion P (Cerebral perfusion P = MAP-ICP)
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19
Q

3 mediators of cerebral inflammation in bacterial meningitis

A
  1. bacterial components
  2. inflammatory mediators
  3. host cellular response
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20
Q

bacterial mediators of inflammation in bacterial meningitis (3)

A
  1. capsule
  2. cell wall
  3. LPS
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21
Q

Inflammatory mediators of bacterial meningitis (5)

A
  1. TNF
  2. IL 1 and 6
  3. Platelet-activating factor
  4. Prostaglandins
  5. Complement factors
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22
Q

Host cell mediators of inflammation in meningitis (3)

A
  1. PMNs
  2. CNS macrophages
  3. Endothelial cells
23
Q

the successful invasion by bacteria of the CNS and establishment of infection/meningitis requires: (4 steps)

A
  1. colonization of mucosa (gen nasopharynx)
  2. invasion of IV space
  3. cross BBB
  4. survival/replication in CSF
24
Q

most common causes of bacterial meningitis

A 
LEGSNH
listeria monocytogenes
E (E coli-- which is not one of the common causes, but is a less common cause)
Group B strep (streptococcus agalactiae)
Streptococcus pneumoniae
Nisseria meningitidis
Haemophpilus influenzae
25
Q

Less common causes of bacterial meningitis

A

Klebsiella, E coli, Serratia, Psudomas, Salmonella, Nosocomial (40% cases among adults), Spirochetal: lyme disease (borrelia burgdorfen) and syphilis (treponema pallidium)

26
Q 
what's the cause?
12 month old child
lethargy
fever
large red, flat facial rash that appeared 1-2 days prior
LOC
tachycardic
RR and BP normal
only arouses upon noxious stimuli
depressed mental status on neuro exam

Prior H/O:
ear infection 1 mo ago, txt w/abx

no H/O vaccines

A

Haemophilus influenza type B (HIB)– accounted for 70% of all cases of bacterial meningitis in childrel

27
Q

HIB -

size, gram stain, defining capsule characteristics

A

small
gram neg
typeable (has a capsule) with PRP (polyribitol ribose phosphate)

*there are other forms of HI that are nontypeable (nocapsule)– immunity probably strain dependent (recurrent colonization/infection)

28
Q

clinical spectrum of Haemophilus influenzae (5)

A
  1. Mucosal disease
  2. otitis media, sinusitis (often non-typeable)
  3. pneumonia (oftennon-typeable)
  4. epiglottitis
  5. metastatic foci (usually typeable type B)– septic arthritis, meningitis

*immunity probably strain dependent (recurrent colonization/infection)

29
Q

Immunity to HIB

A

Anti-PRP (capsule component) Abs activate comp and opsonic activity

maternal anti-PRP AB wanes at 6-24 months —> kids start getting sick

30
Q

The HIB vaccine contains what and achieved what?

A

contains PRP-conjugate, it decreased nasopharyngeal colonization (“carriage”) and invasion, so herd immunity!

31
Q 
HIB
source:
spread to host:
adhesion to host:
invasion/spread within host:
escape from host defenses:
damage to host/manifestations:
A

HIB
source: humans, mostly children

spread to host: nasal secretions

adhesion to host: pili, other

invasion/spread within host: Nasopharynx (NP) colonization —> otitis, pneumonia, epiglottitis and/or invasion of blood, replication, invasion of CSF/other metastatic site

escape from host defenses: mostly via capsule

damage to host/manifestations: otitis, pneumonia, epiglotittis, cellulitis, bateremia, meningitis, osteomyelitis, or arthritis

32
Q

post HIB vaccination, the median age for meningitis changed from 15 mo to ____ and the two main causes of bact. meningitis became

A

25 yo

S. pneumoniae and N, meningitidis

33
Q

what is the cause?
18 m/o
HO high fever and ear infection 2 days prior (though generally well looking)

fever high in spite of Abx admin
less active/listless
vomiting

A

Strep pneumoniae

34
Q

strep pneumoniae:
gram stain/shape
capsule?

A

gram positive diplococci

encapsulated (w/over 90 serotypes)

35
Q 
Streptococcus pneumoniae
source:
spread to host:
adhesion to host:
invasion/spread within host:
escape from host defense:
damage to host/manifestations:
A

Streptococcus pneumoniae
source: humans (mostly other kids), nonhuman primates/horses

spread to host: nasal secretions

adhesion to host: PAF receptor, pili, other

invasion/spread within host: NP colonization —> otitis, pneumonia, invasion of blood stream, replication, CSF invasion/other metastatic sites (joints/bones)

escape from host defense: thick polysac. capsule (like HIB)

damage to host/manifestations: otitis, pneumonia, bacteremia, meningitis (high mortality and morbidity!)

36
Q

Streptococcus pneumonia generally affects people of what age? when?

A

very young and the elderly (who get it from their grandkids)

seasonal colonization– highest mid winter

37
Q

6 things that make you more susceptible to strep pneumonia

A
  1. asplenia
  2. hypogammaglobulinemia
  3. proteinuric conditions
  4. multiple myeloma
  5. diabetes
  6. chronic disease in general
38
Q

what mediates the intense inflammation associated with strep pneumonia?

A

cell wall components and pneumolysin

39
Q

is there a vaccine for pneumococcus (strep pneumoniae)?

A

yes–

  1. conjugate vaccine, 13 valent for kids and adults– very expensive- not in most dvping countries
  2. polysac vaccine (23 valent- adults)
40
Q 
What is the cause:
college student
NK PMH
felt "cold"
left eye was painful/draining fluid (conjuctivitis/infection of the eye)
LOC
fever
tachycardic
low BP
high RR
diffuse non-blanching rash (petechiae) on extremities
coalescence of joints
poor perfusion to extremities, slow cap refill
no detectable meningismus
A

Neisseria meningitidis Group C

41
Q

Neisseria meningitidis
gram stain and shape?
encapsulated?
who does it affect?

A

Neisseria meningitidis:
gram neg doplococci (adjacent sides are flat)
encapsulated
leading cause of meningitis in children/young adults and epidemic in colleges, military bases and subsaharan africa

42
Q

clinical spectrum of invasive meningococcal disease associated with neisseria meningitidis (4)

A
  1. bacteremia (aka meningococcemia) w/ and w/out meningitis
  2. meningoencephalitis
  3. meningitis with and w/out documented bacteremia
  4. shock syndrome can dominate (hypotension, DIC (disseminated IV coagulopathy), Waterhouse-Fredericksen syndrome (bilateral adrenal hemorrhage with purpura fulminans)
43
Q

Waterhouse-Fredericksen syndrome

A

bilateral adrenal hemorrhage with purpura fulimans

a possible shock syndrome response to Neiserria meningitidis that can lead to death due to non-func kidneys

44
Q

risk factors for Neisseria Meningitidis (4)

A

dry-arid conditions
crowding
carriage
complement deficiency (terminal components C5-9)– with this deficiency, one is more likely to get it but less likely to die

45
Q 
Txt issues assoc with Neisseria meningitis (meningococcal)
timeframe:
Abx:
mortality (2):
morbidity (2):
controversial features (4):
A

speed is essential
most strains highly susceptible to penicillin (PCN) but resitance emerging
2 causes of mortality (CNS herniation or shock)
2 types of morbidity: CNS vs other organ failure (skin, renal, cardiac from shock)
controversial: role of steroids, activated prot C, plasmaphareisis, anti-LPS modalities

46
Q 
Summary Neisseria meningitidis (meningococcal)
source:
spread to host:
adhesion to host:
invasion/spread within host
escape from host defenses:
damage to host/manifestations
A

source: humans

spread to host: nasal secretions

adhesion to host: pili, other

invasion/spread within host: NP colonization can lead to conjunctivitis, pneumonia and/or invasion of bloodstream, replication, invasion of CSF or just remain in bloodstream

escape from host defenses: capsule, surface prots (fHbp, PorA) to evade complement

damage to host/manifestations: conjunctivitis, pneumonia, bacteremia, meningitis, purpura fulminans (PF- hemorrhagic condition), Waterhouse-Fredericksen (hemorrhaging to adrenals), petechiae

47
Q 
cause of meningitis?
21 day old
fussy
low grade temp
suddenly grey, unresponsive
bulging fontanelle
A

Group B strep (streptococcus agalactiae)

48
Q 
Group B strep/ streptococcus agalactiae
gram stain/shape
lancefield grp
different serotypes?
surface prot ags?
A 
Gram pos diplococci
encapsulated
Lancefield group B (beta hemolytic)
many serotypes
has surface prot Ags
49
Q

clinical manifestations of group be strep (strep agalactiae)

A 
puerperal sepsis (bacterial infection contracted by women during childbirth or miscarriage)
septicemia and meningitis in neonates and infants  65 with underlying medical conditions
50
Q

sources of group b strep (strep agalactiae):

A 
principal reservoir = GI tract
Gu colonization (risk factors = gender, race, age, frequency of sexual intercourse, diabetes)
vaginal colonization (vertical transmission to newborns)
51
Q

risk factors for vert. transmission of grp b strep (strep agalactiae)

A

maternal colonization (bacteruria = marker of heavy colonization and maybe lower immunity?)
ROM (rupture of membane) or delivery 38 degrees C
amnionitis
ROM (rupture of membrane) > 18 hrs

52
Q

2 types of group B strep (strep agalactiae)

A

early onset disease and late onset disease

53
Q 
Description of early onset Group B strep:
timing:
manifestations
meningeal signs:
prevention:
A

timing: within few hours of birth
manifestations: lethargy, poor feeding, hypothermia, grunting, hypotension, apnea, and overwhelming disease (pneumonia, CNS invasion, sepsis)

meningeal signs: no specific signs

prevention: with peripartum prophylaxis (PPP) to GBS+ mothers

54
Q

The utility of steroids in treating bacterial meningitis

A

Steroids given to adults and (now) children in treating meningitis caused by Hib and Strep. pneumoniae

    However, according to slide 62, the use of steroids in treating meningococcal disease remains controversial
    Being on steroids = a risk factor for meningitis by Listeria monocytogenes

Microbiology (11 decks)

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