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Flashcards in CNS Infection IV Deck (30)
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1
Q

symptoms of brain abscesses

A

– Rapid

– Headache, Changes in mental status, Generalized seizure

2
Q

predisposing condition and organisms if brain abscess is at frontal site

A
  • sinusitis and dental abscesses

- Streptococci, Bacteroides, S. aureus, Haemophilus spp.

3
Q

predisposing condition and organisms if brain abscess is at temporal site

A
  • otitis media and mastoiditis

- Streptococci, Bacteroides, Enterobacteriacea

4
Q

predisposing condition and organisms if brain abscess is at frontal, temporal, and parietal site

A
  • Trauma, Penetrating wound

- S. aureus, Clostridia

5
Q

predisposing condition and organisms if brain abscess is at multiple site

A
  • Infective endocarditis, Congenital Heart Disease, Lung abscess
  • S. aureus, Streptococci (viridans), Fusibacteria, Nocardia
6
Q

fungal brain abscesses

A
– Candida sp
– Aspergillus sp.
– Cryptococcus sp
– Histoplasma capsulatum 
– Blastomyces dermatitidis
7
Q

diagnosis of brain abscesses

A

– CT scan
– Hypodense centre
– Peripheral uniform ring
– Brain oedema

8
Q

clinical presentation of subdural and epidural empyema

A

headache

fever (higher than 39oC)

9
Q

etiology of subdural and epidural empyema

A
– Streptococci (25-45%)
– Staphylococci (10-15%)
– Enterobacteriacea (3-10%) 
– Anaerobic bacteria (33%) 
– Polymicrobial
10
Q

predisposing factor for subdural empyema

A

sinusitis (male to female: 3 to 1)

11
Q

how do you diagnose epidural empyema

A

MRI pachymeningeal enhancement, superficial area of diminished intensity

12
Q

what are prions

A

infectious proteins that are resistant to formaldehyde, dry heat, boiling, ethanol, and ionizing radiation

13
Q

disease of Prions

A

– Transmissible Spongiform Encephalopathies (TSE)

• Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, familial fatal insomnia, Kuru

14
Q

biology of prions

A

– Normal cellular glycoprotein: PrPc (↑ 􏰈 alpha helix, ↓ beta 􏰆􏰆􏰇􏰇helix)
– Infectious glycoprotein form: PrPsc (↓􏰈 alpha helix, ↑ 􏰆 beta helix)
– Aggregates in neurons (myeloid plaques)
– Spongy cerebrum (vacuoles in cortex & cerebellum)

15
Q

are most cases of prions sporadic or familial

A

sporadic

16
Q

how does on get prion diseases

A

eating undercooked beef

17
Q

clinical feature of prions

A

– Nonspecific prodromal symptoms (1/3 CJD patients): fatigue, sleep disturbance, weight loss, headache, malaise, and ill-defined pain

– Most higher cortical function deficits.
• Progress over weeks-months: profound dementia (memory loss, impaired judgment, 􏰅􏰅intellectual function

18
Q

how does one get Tania solium and what is a big symptom

A

uncooked pork

neurocystercosis

19
Q

what does negleria and acanthamoba lead to?

A

• Negleria
– primary amebic meningoencephalitis (PAM)
• Acanthamoba
– Granulomatous Amebic Encephalitis (GAE)

20
Q

what is the most common cause of brain abscess in immunocompromised people like AIDs patients

A

toxoplasmosis - toxoplasma gondii

multi ring lesions that involve the basal ganglia

21
Q

how long after exposure does it take to see symptoms to nagleria and how long till death?

A
  • 1 day to 1 week week after exposure –> symptoms

- death at 7-14 days for 97% of those infected

22
Q

what are symptoms of nagleria

A
  • Headache
  • Fever
  • Nausea, vomiting
  • Confusion
  • Rapidly worsen over 3‐7 days
23
Q

pathogenesis of nagleria

A

starts at the amoeba olfactory nerve –> migrates to olfactory bulbs –> feeds on nerve tissue –> necrosis and hemorrhaging –> migrates along nerve fibers –> enters the floor of the cranium via the cribriform plate and into the brain –> consume cells of the brain a amoebostome (a unique actin‐rich, sucking apparatus extended from its cell surface)

24
Q

treatment of nagleria

A

– Amphotercin B (only shown effective in vitro)

– Combined Miconozole, Sulfadiazine and Tetracycline shows “some” benefit

25
Q

who does acanthamoeba affect

A

people with compromised immune systems

26
Q

symptoms of acanthamoeba

A
  • headache, confusion
  • nausea, vomiting, fever
  • lethargy, stiff neck
  • focal neurologic deficits
  • signs of increased intracranial pressure
27
Q

treatment of acathamoeba and how many survive

A

Combined Miconozole, 5‐ fluorocytocine “some” benefit

almost 100% dies

28
Q

causes cerebral malaria

A

Plasmodium falciparum

29
Q

symptoms of plasmodium falciparum

A

unarousable coma which leads to death if left untreated

30
Q

used to treat neurocystercosis

A

Albendazole and praziquantel