10-14 L1-2 CNS infections Flashcards

(31 cards)

1
Q

What are some cardial mainfestations suggesting CNS infection?

A
  • Fever
  • HEadache
  • Aleration of mental status
  • Focal neurological signs
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2
Q

Discribe the difference between

Acute vs Chronic infections

A
  • Acute: rapid or sudden (a couple of hours)
    • clinical presentation maybe be quite dramatic or fulminate
  • Chronic: slower (several days or months)
    • clinical presentation may not be as dramatic or fulminate.
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3
Q

Encephalitis

vs

Meningitis

A
  • Encephalitis: inflammation of the brain (‘brain fever’)
  • **Meningitis: **inflammation of any or all o fhte meninges of the brain & spinal cord, usually caused by a bacterial infection.
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4
Q

Postinfectious syndromes

A
  • Usually begins as another infeciton (many times sub-clinical or not soncidered to be noteworthy)
  • Infection maybe in CNS
  • Presumed to be immunologically-mediated
    • GBS (guillain barre syndrome)
    • Post-infection encephalomyelities
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5
Q

Prions

A
  • Unconventional infection
  • chronic (years to decades)
  • usually no fevers
  • high mortality
    • Kuru, CJD, PML, nvCJD
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6
Q

What CSF values are different in adults than infants (or premature infants)

A
  • Neutrophils
    • adults: 0
    • infants: 60
  • Proteins
    • adults: 30
    • infants: 90
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7
Q

What is the CNS infection entity that causes the most sensation?

What is at risk for involvement with the disease mentioned above?

A
  • Meningitis (especially acute, bacterial meningitis)
  • When meninges inflamed, anything passing thorugh them is at risk for involvement
    • blood vessels feeding the cerebral cortex
    • Nerves exiting the brain (cranial nerves, especially those at the base of the brainstem)
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8
Q

Meningitis epidemiology

  • <1 month old
  • Toddler
  • Teenagers
  • >19 yrs old
A
  • <1 month old: Group B strep
  • Toddler: Streptococcus pneumoniae
  • Teenagers: meningitis
  • >19: streptococcus pneumonia
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9
Q

The vaccination that dramatically changed the survival rate of 1-23 month old, b/t 1986 adn 1995 was against what virus?

A

Hib

(haemophilus influenzae b)

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10
Q

Streptococcus pneumoniae

  • morphology
  • blood culture
  • aviasion of immune system
  • transmission
A
  • morphology: G+, diplococcus (typically found in lancet-shaped pairs)
  • blood culture: Alpha-hemolytic
  • **aviasion of immune system: **
    • polysaccharide capsule (avoid phagocytosis)
    • Pneumolysin (cytoctoxic for phagocytic cells)
    • IgA protease
  • transmission: spread by airborn droplet and direct contact with secretions
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11
Q

Streptococcus agalactiae

Group B Streptococcus

  • morphology
  • blood culture
  • aviasion of immune system
  • transmission
A
  • morphology: FAcultative G+ coccus
  • blood culture: Beta-hemolytic
  • aviasion of immune system:
    • adherence to vaginal and intestinal epithelium, placental membranes, BBB
    • Pili
    • Polysaccharide encapsulated (not major): inhibits complement deposition
  • transmission: puerperal sepsis in newbrons (spread by direct contact)
    • Preventable process: vaccinate the mom!
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12
Q

Haemophilus influenzae (Hib)

  • morphology
  • aviasion of immune system
  • specious found in:
  • transmission
A
  • morphology: Facultative, G- coccobacillary organism, noo-motile (encapsulated(sm polysaccharide capsule)
  • aviasion of immune system: pili, epithelial adherence, IgA protease
  • specious found in: exlusively humans
  • transmission: sread via airbone droplets and direct conteat with csecretions
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13
Q

Neisseria Meningititdis

  • morphology
  • aviasion of immune system
  • Seortype production
A
  • morphology: G-, diplococcus, polysaccharide capsule, fastidious growth
  • aviasion of immune system: Pili, IgA protease, terminal complement deficiences pre-dispose
  • serotype production: A, B, C, W-135, and Y
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14
Q

Escherichia coli

  • Morphology:
  • aviason from immune system
  • member of what
A
  • Morphology: G-, Facultative bacillus, rapidly growing and ferment lgucose
  • Aviason from immune system: Pili, LPS, Exotoxins
  • Member of the Enterobacteriaceae
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15
Q

Listeria monocytogenes

  • Morphology
  • Hemolysis
  • Aviasion from immune system
  • Transmission
A
  • Morphology: Facultative anerobic, G+, non-spore-forming bacillus, Motile with tumbling motilitys
  • Hemolysis: Beta-hemolytic
  • Aviasion from immune system: intracellular invasion, use listerolysin O to escape the phagosome and the cellular movement using acting polymerization
  • Transmision: cold enrichment, via food
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16
Q

Mycobacterium tuberculosis

  • Morphology
  • Cell composition
A
  • Morphology: acid fast bacillus (tubercle bacillus) Slow growing
  • Meningitis is a form of extrapulmonary TB, typically chronic, may or may not occur in face of immunocompromise
  • Cell composition: cell wall characteristics with mycoloic acids and lipoarabinomannas (LAMs)
17
Q

What are common antitubercular treatment?

A
  • INH (Isonizaid) and PZA (pyrizinamide) reach CSF concentraitons equal to blood concentrations
  • Rifampin penetrates BBB also to a lesser degree (in also increases cYP450)
18
Q

INH (isoniazid)

MOA

A

inhibition of mycolic acid synthesis (cell wall)

19
Q

Riampin

MOA

A

DNA dependent RNA polymerase

20
Q

PZA (pyrizinamide)

MOA

A

Mechanism of action is unknown

21
Q

Cryptococcus neoformans

  • Morphology
  • Aviasion of immune system
  • Transmission
  • Population most effected
A
  • Morphology: not dimorphic fungus (always in yeast phase),
    • polysaccharide capsule (antiphagocytic): Glucoronoxy lomannan (aslo immunomodulateory suppressive)
  • Aviasion of immune system: Intracellular phagocyte survival (melanin)
  • Transmission: aerosolized/inhaled fungi from environmental source (breating it in)
  • Population most effected: Immunocompromised (AIDS!)
22
Q

How do you treat pt with fungal infection?

A
  • Antifungal therapies amide at fungal cell membrane componenets (erostersols) not found in mammalian cells
  • Azole antifungals target sterol synthesis
  • Amphtericin B binds to ergosterol and likely through steric hindrance causes membrane permeability to increase.
  • Fluocytosin: cnoncompetitive inhibitor of thymidilate sythetase
23
Q

How do you treate an AIDS pt vs a non-AIDS pt?

A
  • AIDS: induction w/a_mphotericin B+/- fluocytosine for 4 weeks,_
    • followed by a consolidation phase of fluconazole (which may be life-long depending upon underlying immune compromise)
  • Non-AIDS cases: Amphotericin B+ flyocytosine for 2 weeks
24
Q

Whats the most commonc cause of aseptic meningitis ‘virus meningitis’?

  • Transmission
  • Treament
A

Enteroviruses

  • sm ss + sense RNA viruses (picornaviruses) in a naked icosahenral capsid
  • spread by the fecal oral route and have a summer-Fall seasonality in temperate climates
  • Include polioviruses, coxsackieviruses, echoviruses, parechoviruses, and others simply designated enteroviruses
  • Treatment: supportive care
25
How is **lymphocytic choriomeningitis virus** transmited what disease does it cause?
* Arenea virus family * singlestranded RNA * _Predilection for rodents_ * parasites of rodents with high species specificity _Mus domesticus and Mus musculus_ * Worldwide * human infection only demonstrated in Europe and Americas * Autumn occurrenece (due to rodent seasonlaiyt) * _Aseptic meningitis._
26
What virus causes the highest morbidity and mortality? Is this virus treatable? (MOA)
Herpes simplex yes, high dose IV acyclovir MOA: activated by viral thymidine kinase to become a competitve inhibitor of viral DNA polymerase by blocking deoxyguanosine uptake.
27
What is the most common US mosquito borne encephalitidies? Treatment?
West nile and St. Louis are the most common treatment: supportive care
28
How is rabies spread?
* Rhabdovirus * NEg sense, single stranded RNA virus * Rod or bullet shaped * helical nucleocapsid * liporotein envelope * Affects all mammals * **Retrograde axonal spread** * **spread via bites and infected oral secretions and organ transplant**
29
What is the cause of Meningo-encephalitis?
Listeriosis
30
How are Toxoplasmosis acquired? How is it diagnosed?
* consumption of raw meat (beef, pork, lamb) * Diagnosis * serologic testing IgG and IgM (though IgM less reliabel methodology) * Direct tissue bipsy (for definitive diagnosis) * PCR
31
How do you treat toxoplasmosis: Chorioretinitis & encephalitis?
* Chorioretinitis (3-4 weeks) * Pyrimethamine, sulfadiazine, leukovorine and corticosteroids * Encephalitis (4-6 weeks) * Pyrimethamine, sulfadiazine, leukovorine and corticosteroids (steroids are controversial)