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Neuro Block 2 > Meningitis > Flashcards

Meningitis Flashcards

1
Q

In what area does meningitis occur?

A

subarachnoid space

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2
Q

What sorts of immune response are packing in the subarachnoid space?

A

antibody and complement production = no phagocytosis

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3
Q

What are the typical clinical symptoms for meningitis?

A

fever (but less likely in older individuals)

headache

nuchal rigidity

photophobia

rash

URI symotoms

nausea

vomiting

maybe seizures and altered mental status

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4
Q

What test can be used to differentiate between bacterial and viral (and other) types of meningitis?

A

CSF analysis - WBC

bacteria will have more PMNs

viral will have more lymphocytes

both will have elevated protein, but bacterial will have DECREASED GLUCOSE

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5
Q

Is aseptic meningitis syndrome usually viral or bacterial?

A

viral - can also be noninfectious like with some drugs

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6
Q

What is the treatment for aseptic meningitis syndrome?

A

supportive therapy - most recover on their own but it can be fatal in the neonatal period

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7
Q

Do you need to do PCR confirmation of the organism in aseptic meningitis?

A

not really

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8
Q

What group of viruses are the vast magority of viral meningitis cases associated with?

A

enteroviruses

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9
Q

What are some examples of enteroviruses?

A

coxscadkieivruses

echoviruses

human enteroviruses 68-71

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10
Q

Besides enteroviruses, what are some viruses that have been associated with viral meningitis?

A

HSV 2

HIV

VZV

EBV

Arthropod-born viruses

Lymphocytic choriomenginitis virus

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11
Q

What is the risk factor for lymphocytic choriomeningitis virus?

A

exposure to rodents

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12
Q

What type of viruses are enteroviruses?

A

picornaviruses

small

single stranded + sense RNA

icosahedral

naked

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13
Q

How are enteroviruses transmitted? WHen in the year?

A

fecal oral

usually late summer and fall

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14
Q

Which has more neck stiffness, viral or bacterial meningitis?

A

bacterial

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15
Q

Which has a more acute onset, viral or bacterial meningitis?

A

bacterial

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16
Q

What is the go-to drug for bacterial meningitis empiric treatment?

A

ceftriazone (3rd generation cephalosporin)

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17
Q

What drug should you add if MRS or resistant strep?

HSV?

Pseudomonas or AIDS?

Listeria?

A

MRSA = vanco

HSV = acyclovir

Pseudomonas = cefepime

Listeria = ampicillin

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18
Q

What is the concern with using Ceftraxone? Why is it utilized for CNS infections>

A

It’s broad spectrum, so the issue is C. diff, but bacterial meningitis is life threatening, so it’s worth it

Particulalry useful in the CNS because it has less of an inhibitory effect on GABA release than other beta-lactams, so the risk of seizure is lower

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19
Q

What is the pimarily mechanism of action for ceftriaxone?

A

It blocks the transpeptidation of peptidoglycan, thus inhibiting cell wall synthesis

binds to the penicillin binding proteins on transpeptidase

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20
Q

What is the main mechanism of action for vancomycin?

A

blocks the translygosylation of peptidoglyan by binding to NAM and NAG - cell wall inhibitor

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21
Q

What is the spectrum for ceftriaxone? How does resistance develop?

A

It’s used for streptococci and more serious gram negative infections

can cross the blood brain barrier

Resistance thorugh beta-lactamases and alteration of the PBP binding site

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22
Q

What are the three most common bacteria causing meningitis? For adults? FOr 11-12 yr olds?

A

Streptococcus pneumonia (adults)

Neisseria meningiditis (11-17 yr olds)

Haemophilus influenza type B

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23
Q

Where does the initial bacterial infection with H. influenza, N. meningiditis, or S. pneumonia occur?

A

typically in the nasopharynx

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24
Q

What are the 5 main virulence factors that play importnant roles in bacterial meningitis?

A

the capsule (neisseria, haemophilus and streptococcus)

IgA protease (Neisseria, Haemophilus, strep)

Pili for adhesion (neisseria an dhaemophilus)

Endotoxin (neisseria and haemophilus)

Outer membrane proteins (Neisseris and Haemophilus)

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25
Q

The LPS of Niesseris meningitidis is structured slightly differently. WHat is the significance of this and what is it called?

A

It’s called LOS and it looks like sphingolipids, so it’s recognized as self

26
Q

What occurs with LPS endotoxin shedding?

A

It activates macrophages to release NO, causing hypotension and shock. Also IL-1, for fever.

May lead to disseminated itnravascular coagulation = purpuric skin rash

27
Q

What are neisseria meningiditis outbreaks associated with?

A

overcrowding in the dorms, especially during late winter or early spring

28
Q

How is Neisseria meningiditis transmitted?

A

respiratory

29
Q

How many serogroups of neisseria meningiditis are covered by the meningococcal meningitis?

A

4 out of 13

30
Q

What shape is streptococcus pneumonia?

A

gram positive diplococci in a lancet shape

31
Q

In pneunococcal meningitis, what can you give prior to antibiotic treatment to reduce hearing loss and other neurological sequelae in adults?

A

dexamethasone

32
Q

What is hte most common cuase of bacterial meningitis in individuals over 2 years of age?

A

streptococcus pneumoniae

33
Q

What does hemophilus influenza b look like on histology?

A

a gram negative “coccoid” rod

34
Q

What is the vaccine for Haemophilus influenza b meningitis?

A

the Hib vaccine

(a B capsular polysaccharide)

35
Q

What can hemophilus influenza type b infections be followed by?

A

hearing loss

36
Q

What are the 3 more common bacterial imeningitis causes in patients under 2 months old?

A

Group B streptococcus

Listeria monocytogenes

Escherichia coli

37
Q

WHy is the risk of infection from the most common causes be lowe rin infants?

A

maternal immunity

38
Q

What is another name for group B streptococcus?

A

streptococcus agalactiae

(lancefield group B antigen)

39
Q

Where is Group B strep normally found and how do infants get it?

A

GI and GU tract flora

infants get it through vertical transmission either in utero or during vaginal delivery

40
Q

How do we avoid transmission of Group B strep to infants in the US?

A

We screen pregnant women and give penicillin G as prophylactic treatment before birth

41
Q

What is the CAMP reaction that comes with grou B strep and staph aureus?

A

a synergistic hemolysis of RBCs by phospholipases from gruop B strep and the betal-hemolysins of Staph aureus

42
Q

What does listeria monocytogenes look like on histology?

A

gram positive rod

itnracellular pathogen

43
Q

With listeria monocytogenes, you don’t really get neck stiffness, but you do get___

A

diarrhea

44
Q

How is listeria monocytogenes transmitted? How does this relate to advice given to pregnant women?

A

consumption of contaminated food

this is why pregnant women aren’t suposed to drink unpasteruized milks, cheese, or deli meats

45
Q

For Listeria, ____ induces phagocytosis by epitherlial cells of the GI tract, while phospholipase and _____ allow excape from the vacuole

A

Internalin induces phagocytosis by epithelial cells of the GI track, and phospholipase and listeriolysin O allow escape from vacuole

46
Q

What protein facilitates speudopod spread between adjacent cells for listeria?

A

actin tails

47
Q

What polysaccharide in the capsule of E. coli prevents fusion with the lysosome?

A

K1 capsular polysaccharide

48
Q

IF the E coli strain is expression a beta lactamase, what should you add to the ceftriazone?

A

a carbapenem

49
Q

What are some common bacterial causes of CHRONIC meningitis?

A

mycobacterium tuberculosis

Borrelia burgdorferi

Treponema pallidum

Syphillis Leptospira

50
Q

What are some common fungal causes of chronic meningitis?

A

crytococcus neoformans

coccidioides

candida

51
Q

What percentage of miliary TB will have meningeal involvement?

A

25%

52
Q

What is the treatment for mycobacterium tuberculosis infection? Why does it take so many drugs?

A

RIPE

Isoniazid to inhibit mycolic acid (acetylation by liver - fast acetylators will require higher dose)

RIfampin - inhibits RNA polymerase

Ethambutol - binds to arabinosyl transferase to inhibit cell wall synthesis

pyrazinamide - unknown mechanism

Takes 4 because mycobacterium develop immunity quickly - less likely to be able to do it against 4 at once

53
Q

How is crytococcus neoformans transmitted?

A

inhaled as spores, dissmeinated hematogenously to CNS in immunocompromised individuals

54
Q

What stains/tests are needed to diagnose crytococcus?

A

india ink stain

latex agglutination test

55
Q

Where in the world is crytococcus neoformans most common?

A

africa

56
Q

What is the treatment for crytococcus meningitis?

A

amphotericin and flucytosine until culture negative

followed by fluconazole for 3-12 months or rest of life in immune compromise

57
Q

How does amphotericin B work? Why is it highly toxic? How does it get to the BBB? Spectrum? Resistance?

A

It binds ergosterol to create holds in fungal membrane

Broad spectrum against systemic fungal infections - yeasts and molds

The liposomal form can cross the BBB

It’s toxic because it binds patient’s cholesterol and decreases renal blood flow, potentially causing permanent destruction of basement membrane

Resistance is rare, but reduced ergosterol in membrane

58
Q

How does flucytosine work? Spectrum? Toxicity? Resistance?

A

It’s an antimetabolite that is selectively taken up by fungi and converted to 5-FU to interfere with DNA and RNA synthesis

Narrow spectrum - yeast only, like candida albicans and cryptococcus

Toxic because of bone marrow suppression

Resistance is thorugh loss of converting enzymes or transporters - cotreat with amphotericin B

59
Q

How do the azoles like fluconazole work?

A

they bind the fungal p-450 enzyme to block production of ergosterol

spectrum - dimorphic fungi and yeast

Toxicity - drug-drug interactions, hepatotosicity, neurotoxicity, alters hormone synthesis so AVOID during pregnancy

Resistance is thorugh altered cytochrome p450 and efflux transporters

60
Q

What type of agar can hemophilus influenza b grow on?

A

chocolate agar, but not blood agar

Neuro Block 2 (19 decks)

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