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Neuro Block 2 - KJ > Intro to Meningitis > Flashcards

Intro to Meningitis Flashcards

1
Q

What are meningitis symptoms?

A

-Fever (less likely in older people), headache, nuchal rigidity (30% cases), photophobia, rash upper respiratory symptoms, anorexia, nausea, vomiting, diarrhea, altered mental state

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2
Q

Where does meningitis develop? Why?

A

Subarachnoid space

-It lacks antibody & complement production required for phagocytosis

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3
Q

What are infectious agents associated with meningitis? What test can help you distinguish between these?

A
  • Viral (most common, least serious)
  • Bacteria
  • Mycobacteria
  • Fungi
  • Protozoa
  • CSF!!
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4
Q

What is unique in the CSF of Fungi and Tuberculosis?

A

-Protein levels elevated & more lymphocytes than PMNs for Fungi and Tuberculosis

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5
Q

Describe aseptic meningitis syndrome:

A
  • Often viral, but might be noninfectious
  • Fever, headache & photophobia (less neck stiffness and altered mental status)
  • Incidence highest during first year of life
  • CSF increase in lymphocytes and monocytes, slight increase in protein and normal glucose
  • Supportive therapy & recover on own –> can be fatal in neonatal period
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6
Q

What are 85% of viral meningitis associated with?

A

Enterovirus

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7
Q

What types of viruses are Enteroviruses?

A

RNA

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8
Q

What can cause Acute meningitis?

A 
Common:
-Enteroviruses (Coxsackieviruses, Echoviruses, and human enteroviruses 68-71)
-Herpes simplex virus 2
-Arthropod-borne viruses
-HIV
Less Common:
-Varicella-Zoster
-EBV
-Lymphocytic chorimeningitis virus
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9
Q

Tell me about Enteroviruses/Picornavirus (Coxsackie, ECHO virus, polio):

A

(+) ssRNA

  • Often in Summer or Fall
  • “Pico” for small, “RNA”
  • Transmitted oral, fecal or respiratory
  • Capsid symmetry: Icosahedral
  • No envelope (naked)
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10
Q

Tell me about Septic Meningitis:

A
  • Bacteria
  • Fever, stiff neck, irritability, neurologic dysfunction
  • Acute onset and progression
  • Meningeal inflamm. associated with inflammatory exudate in CSF containing many PMNs, increased protein, and decreased glucose
  • Life-threatening and requires prompt empiric therapy prior to lumbar puncture
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11
Q

What treatment should you use for bacterial meningitis?

A

Immediate, empiric –> Ceftriaxone (3rd gen. cephalosporin)

  • Prophylactic treatment of household and those exposed to oral secretions
  • There could be a risk of other agents causing it so use: Vancomycin (MRSA), Acyclovir (HSV-2), Cefepime (Pseudomonase), Ampicillin (Listeria)
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12
Q

What are the three most common causes of bacterial meningitis?

A

Streptococcus pneumonia
Neisseria meningitis
Haemophilus influenza type b

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13
Q

What is the most common cause of bacterial meningitis in adults?

A

Streptococcus pneumonia

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14
Q

What is the most common cause of bacterial meningitis in 11-17 year olds?

A

Neisseria meningitis

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15
Q

Why should adults over 65 years be vaccinated for Streptococcus pneumonia?

A

-Their risk is 10X higher than other adults to get the bacteria

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16
Q

What is GBS most common in?

A

Infants!

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17
Q

How do the 3 most common bacteria cause infection?

A
  1. Mucosal colonization at nasopharynx
  2. Invasion and multiplication in bloodstream
    3, 4. Cross blood brain barrier and egress into CSF
  3. Release of inflammatory cytokines in CSF by astrocytes and microglia
  4. Increased permeability of BBB
  5. Diapedesis of leukocytes into CSF
  6. Edema and increased intracranial pressure
  7. Neonatal injury including hearing loss (CN VIII)
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18
Q

What virulence factors do N. meningitis and H. influenzae have?

A

All of them! (Gram - bacteria)

  • Capsule
  • IgA protease
  • Pili
  • Endotoxin
  • Outer membrane proteins
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19
Q

What virulence factors do Streptococcus pneumoniae have?

A

Capsule & IgA protease

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20
Q

What is LPS and what does it do?

A

Endotoxin shed from outsell membrane of gram neg. bacteria
-LPS activates macrophages leading to release of NO (hypotension, shock) and IL-1 (fever), and can activate disseminated intravascular coagulation leading to purpuric skin rash

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21
Q

What is unique about Neisseria meningitides endotoxin?

A

It is called LOS (lipooligosaccharide) which mimics brain sphingolipids so recognized as self by the body.

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22
Q

What do pili do?

A

Allow colonization of nasopharynx

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23
Q

What does IgA protease do?

A

It cleaves IgA facilitating colonization of mucosa

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24
Q

What is the importance of the capsule?

A

It is composed of acidic polysaccharides and protects from phagocytosis by PMN granulocytes

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25
Q

What are the properties of Neisseria meningitis?

A

Meningococcal Meningitis

  • Gram -, diplococcus,
  • 13 Serogroups, vaccine covers 4
  • Virulence factors include = pili, IgA protease, capsule, and endotoxin
  • Outbreaks in later winter and early spring –> associated with overcrowding (dorms)
  • Transmits through resp. droplets
  • Has LOS
26
Q

What is the treatment for N. meningitis?

A

Ceftriaxone

27
Q

What is the significance of LOS with Neisseria meningitis?

A

LOS leads to thrombocytopenia, which is associated with disseminate intravascular coagulation leading to hemorrhagic skin rash.

28
Q

What are the properties of Streptococcus pneumonia?

A

Gram +, diplococci, lancet shape

  • Transmitted through resp. droplets
  • Meningitis is secondary to paranasal sinusitis and otitis media
  • Most common cause in people > 2 months
  • If prev. on antibiotic -> higher risk of having a resistant strain and can predict based off of serotype especially 19A-resistant S. pneumonia -> treat with Vancomycin
  • Heptavalent protein-conjugate vaccine
  • Not in long chains
  • Looks like 2 connected dots (purple)
29
Q

What are the properties of Hemophilus influenza type b?

A

Gram -, “Coccoid” rod

  • Occurs in unvaccinated infants & young children
  • Virulence factors: pili, outer membrane proteins, IgA protease and endotoxin
  • Infection can be followed by hearing loss
  • Prevention with Hib vaccine - B capsular polysaccharide
  • Chocolate agar with factors V (NAD+) and X (hematin)
30
Q

______ are important virulence factors in the pathogenesis of bacterial meningitis.

A

Polysaccharide capsules

31
Q

What are TORCH infections?

A

Perinatal infections

  • More serious fetal complications
  • Most concerned about Group B strep
  • Mild maternal morbidity, but serious fetal consequences
  • Meningitis: Group B strep, E. coli, Listeria
32
Q

What does TORCH include?

A

Toxoplasmosis, Other (syphilis, varicella-zoster, parvovirus B19), Rubella, Cytomegalovirus (CMV), and herpes infections (HSV-2)

33
Q

What is the name of Group B streptococus (Lancefield group B antigen)?

A

Streptococcus agalactiae

34
Q

Tell me about Strept. agalactiae:

A
  • GI and genitourinary tract flora
  • Vertical transmission to infant (utero or vaginal delivery)
  • Adult disease in immunocompromised individuals is increasing
  • Sepsis, pneumonia and meningitis
  • SIgn. racial disparity - twice as common in African American infants
  • Pregnant women screened with 25% as carriers and given Penicillin G as prophylactic
  • Bacitracin resistance, catalase negative, cAMP reaction (synergistic hemolysis of red blood cells by phospholipase of GBS and B-hemolysin of S. aureus)
35
Q

What are the properties of Escherichia coli K1?

A

Gram -, rod

  • Enteric organism (intestines), bacteremia, and transcellular permeation of BBB
  • LPS
  • K1 capsular polysaccharide prevents fusion with lysosome
  • If expressing beta-lactamase empiric coverage with ceftriaxone may not be sufficient -add carbepenem
36
Q

What can cause chronic meningitis?

A

Gradual onset - over weeks

  • Spirochetes (motile bacteria that is difficult to culture): Treponema palladium - Syphillis Leptospira, and Borrelia burgdoreferi - Lyme disease
  • Mycobacterium tuberculosis
  • Fungi (Cryptococcus neoformans, Cocidiodes and Candida)
  • Immunocompromised individuals - esp. HIV/AIDs
37
Q

What are the properties of mycobacterium tuberculosis?

A

Bacilli/rod

  • 25% of cases of milliary TB have meningeal involvement
  • Gradual onset beginning with a generalized illness
  • Where high incidence of TB mostly 0-4 year olds affected, where low incidence mostly adults affected
  • Acid fast bacilli stain (Ziehl-Neelsen) and culture
38
Q

What are the treatments/prevention for mycobacterium TB meningitis?

A

Rifampin, Isoniazid, Pyrazinamide & Ethambutol

-BCG vaccine

39
Q

What is the mechanism of Pyrazinamide?

A

Unknown

40
Q

What is the mechanism of Ethambutol?

A

CELL WALL INHIB - Inhibits cell wall synthesis by binding arabinosyl transferase

41
Q

What is the mechanism of Rifampin?

A

Inhibits DNA-dependent RNA polymerase induces the formation of drug-metabolizing enzymes including cytochrome P450

42
Q

What is the mechanism of Isoniazid?

A

CELL WALL INHIB - Inhibits mycelia acids (component of mycobacterial cell wall) Acetylation by liver varies genetically and fast acetylators may need higher dose

43
Q

What can cause fungal meningitis in immunocompromised individuals?

A

Cryptococcus neoformans

-Inhaled as spores

44
Q

What are the properties of Cryptococcus neoformans?

A
  • Has capsule around it as a virulence factor
  • Stained with india ink or latex agglutination test
  • Common in Africa
45
Q

What is used to treat Cryptococcus neoformans - meningitis?

A

Liposomal Amphotericin + Flucytosine
(until culture is negative)
-Followed by Fluconazole

46
Q

What is the mechanism of Amphotericin B?

A

Binds ergosterol, creating holes in fungi membrane allowing leakage of electrolytes

47
Q

What is the spectrum and distribution of amphotericin B?

A

Broad spectrum - invasive systemic fungal infections in immunocompromised patients, active against yeast and molds
Distribution - Liposomal crosses BBB

48
Q

What are the adverse effects of Amphotericin B?

A

TOXIC because it binds cholesterol. Decrease renal blood flow and can lead to permanent destruction of basement membrane.

49
Q

Resistance associated with Amphotericin B?

A

It’s RARE - happens via decreased ergosterol in membrane

50
Q

What is the mechanism of Flucytosine (5-FC)?

A

Nucleic acid synthesis inhibitor

-Antimetabolite selectively taken up and converted to 5-fluorouracil in fungi, interfering with DNA and RNA synthesis

51
Q

What is the spectrum of Flucytosine (5-FC)?

A

Narrow - yeast (not dimorphic or molds) - Candida Albicans and Cryptococcus

52
Q

What is the distribution of Flucytosine (5-FC)?

A

Oral, penetrates CNS

53
Q

What is the toxicity of Flucytosine (5-FC)?

A

Bone marrow suppression - follow patient’s cell counts closely!

54
Q

What resistance develops against Flucytosine (5-FC)?

A

Loss of converting enzyme or transporters - co-treat with amphotericin B to minimize development of resistance and to inc. uptake

55
Q

What organisms cause a lung infection that spreads to the brain and becomes meningitis?

A

TB & Cryptococcus neoformans

56
Q

What are the Azoles?

A

Fluconazole (CNS), Itraconazole, Voriconazole (CNS)

57
Q

What is the mechanism of Azoles?

A

Binds to fungal P450 enzyme and blocks production of ergosterol

58
Q

What is the spectrum of Azoles?

A

Systemic mycoses (dimorphic fungi) and yeast

59
Q

What is the distribution and toxicity of Azoles?

A

Dist - Orally available but substrate for efflux pump in brain
Toxicity - Drug-drug interactions, hepatotoxicity, neurotoxicity, alters hormone synthesis - avoid during pregnancy

60
Q

What resistance can develop against Azoles?

A

Altered cytochrome P450, Up-regulation of efflux transporters

Neuro Block 2 - KJ (14 decks)

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