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CNS infections - Neuro Flashcards

1
Q

CNS infections

A

Caused By: bacteria, viruses, fungi, parasites, prions
-enter body via: GI, respiratory, skin (bite)
-Replication begins in original tissue
-Reach CNS by: blood, peripheral nerves, Bone (open fracture or infected mastoid or sinuses
Uncommon because of-Reticuloendothelial systems remove bacteria and viruses from the blood, Cellular and humoral immune responses, Blood-brain barrier

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2
Q

How do they get in?

A
  • Infecting endothelial cells of cerebral blood vessels (encephalitis viruses)
  • Penetrating the blood-CSF barrier in meninges or choroid plexus (many bacteria)
  • Occluding small cerebral blood vessels with infected emboli from the blood (brain abscess organisms)
  • Once in, the CSF has about 1/500th the amount of antibody as blood and few WBCs
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3
Q

CNS hallmark

A

-Inflammation of the meninges or brain
-Inflammatory cells may be present in
• Meninges
• Perivascular spaces
• Within brain parenchyma
The signs and symptoms of a CNS infection depend on the site of the infection - not the organism.

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4
Q

Time Course

A

-The organism determines mainly the time course and severity
•Viruses - hours to 1 day
•Aerobic bacteria - hours to a few days
•Anaerobic bacteria, tuberculosis, fungi - few days to weeks
•Parasites and T. pallidum (syphilis) - weeks to years

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5
Q

Labs

A
  • WBC and ESR usually elevated
  • CSF is key
  • Usually obtain 4 tubes (varied amounts, 8-15 ml total in adults)
  • Glucose and protein
  • Bacterial culture, gram stain, TB, fungal cultures if suspected
  • Cell count and differential
  • Bacterial antigen tests, CRP
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6
Q

Bacterial Meningitis

A
  • Early symptoms are non-specific
  • Blood brain barrier
  • Invasive diagnostic testing
  • Skull and spine are enclosed spaces
  • Inflammation is poorly tolerated in the CNS
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7
Q

Aseptic Meningitis

A 
Meningeal inflammation without bacteria
•   Non-infectious causes
	•  Medications
	•  Rheumatologic disorders
	•  Immunizations
•   Infectious causes
	•  Tuberculosis, mycoplasma, rickettsia, fungi, viruses
•   Most common cause is viral infection
	•  Enteroviruses are > 80% of aseptic meningitis
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8
Q

Common Pathogens in Adult Patients: Bacterial Meningitis

A 
Streptococcus pneumoniae - 71%
Neisseria meningitidis - 12%
Listeria monocytogenes - 4%
Haemophilus influenzae - 6%
Group B streptococcus - 7%
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9
Q

Diagnosing Meningitis

A
  • History
    • Fever, stiff neck, altered mental status, headache, N&V
  • Physical Examination
    • Fever, nuchal rigidity, Kernig’s, Brudzinski’s
  • Lumbar Puncture
    • CT before LP
    • Interpretation of results
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10
Q

How do we diagnose CNS infection?

A
  • Lumbar puncture needed to analyze CSF
    • Invasive testing to obtain cerebrospinal fluid
    • Elevated white cells with meningeal irritation
  • Can we predict bacterial disease?
    • Risk of bacterial meningitis vs. aseptic meningitis
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11
Q

LP contraindication

A 
Delay LP if patient has:
evidence of brain shift
	Papilledema
	New onset seizures
	Focal neurologic signs
	Signs of space occupying lesions
	Moderate to severe impairment of mental status
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12
Q

Tx

A

Adults age =50 or other risk for listeria

-Ceftriaxone 2g IV or Cefotaxime 2 g IV plus, Vancomycin 1g IV plus Ampicillin 2g IV

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13
Q

Viral Meningitis

A
  • Enteroviruses (echoviruses and Coxsackie viruses) most common
  • HSV type 2, mumps virus, lymphocytic choriomeningitis, and HIV less common
  • CSF
    • Pleocytosis - lymphocyte predominant (neutrophils in 1st day)
    • Mildly elevated or normal protein, normal glucose
    • Negative gram stain
  • Treatment: symptomatic (analgesics, antiemetics); acyclovir for HSV
  • Course: Generally well in 1-2 weeks
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14
Q

Spirochete Meningitis

A
  • Organisms: Borrelia burgdorferi (CNS Lyme Disease), T. pallidum (neurosyphilis)
  • May cause a acute, and sometimes chronic meningitis
  • Course
    • Headaches
    • CNS palsies (esp. Bell palsy in CNS Lyme)
    • Brain infarctions (meningovascular syphilis)
    • Years later: low-grade encephalitis (general paresis or CNS Lyme)
  • CSF: Lymphocytic pleocytosis, elevated protein, normal glucose
  • Treatment: High dose penicillin or ceftriaxone for several weeks
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15
Q

TB and Fungal Meningitis

A

• Subacute onset - days to weeks
• Generally seen in patients who are: malnourished, debilitated, immunosuppressed
• Less than 50% will have active pulmonary infection
• CSF: Culture, Special tests for TB, Antigen for Cryptococcus neoformans, Serologic tests for fungi
• Treatment of TB: Rifampin + isoniazid + pyrazinamide + streptomycin or ethambutol for 2
months, then rifampin + isoniazid for 7 months, depending on sensitivities
• Dexamethazone if patent is comatose or severe neuro deficits
• Fungal: Broad spectrum triazole or liposomal Amphotericin B
• Mortality 20-50%

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16
Q

Encephalitis

A
  • Etiology: virus reaching brain by hematogenous route
    * Arboviruses (West Nile virus most common in US) require tick or mosquito vector)
    * Late spring to early fall
    * HSV Type 1 most common sporadic cause (latent)
    * Other: spirochetes, parasites, CMV, VZV, adenovirus
  • Pathophys: Neuronal necrosis and lysis of glial cells, then cerebral edema
17
Q

Encephalitis - signs and sxs

A

Acute encephalitis is a febrile illness characterized by the abrupt onset of headache and mental obtundation
•Seizures (generalized or focal), hyperreflexia, Babinski sign
•Hemiparesis, aphasia, ataxia, limb tremors, cortical blindness
•West Nile: 10% get myelitis like polio

18
Q

Encephalitis - work up

A
  • EEG: Abnormal - diffuse bilat slowing, occ seizures
  • CSF: Opening pressure nl or sl elevatd; WBC 5-several hundred, lymphocyte predominant; glucose nl, protein elevated, viral cultures neg
  • CT/MRI: nl early, then edema; then necrosis/hemorrhage
  • Diagnosis usually by PCR or serologic tests; HSV by CSF; PCR (detecting the HSV viral DNA which leaks into the CSF)
19
Q

Encephalitis - Management

A

Excellent symptomatic care
• Seizures - anticonvulsants
• Elevated intracranial pressure (ICP) - hyperventilation, mannitol
• Steroid controversial
• HSV - acyclovir early significantly improves outcome
• Rehabilitation for cognitive impairment and focal neurologic signs

20
Q

Encephalitis - prognosis

A

infectious agent dependent
• Excellent - Mumps, Venezuelan equine encephalitis
• Reasonable (2-15% mortality) - West Nile, western equine, St. Louis, California
• But up to 25% dementia, seizures, focal neurologic deficits
• Poor (20-40% mortality) - eastern equine, Japanese B, Murray Valley; HSV w/acyclovir 20% mortality and 55% left with neurologic sequelae
• Fatal - Rabies

21
Q

Brain Abscess

A

Viruses cause diffuse brain infections … but bacteria, fungi, and parasites cause localized brain disease
•Pathophysiology
•Direct extension (mastoiditis, sinusitis)
•Infections following open fracture or craniotomy
•Metastasis carried by blood from elsewhere
•Localized encephalitis, then focal softening, necrosis, and inflammation
•Fibroblasts proliferate at edges forming capsule wall
•Edema surrounds the lesion
•If bacterial or fungal, slowly expands and lethal if untreated

22
Q

Brain Abscess - Etiology

A
  • Anaerobic bacteria (anaerobic streptococci, Bacteroides fragilis) more than 50%
  • Occasionally multiple bacteria
  • If post trauma - Staphylococcus aureus
23
Q

Brain abscess - Sxs

A

Symptoms from localized brain infections typically are subacute in onset and produce symptoms from increased intracranial pressure and their location in the brain.
• Headache, lethargy, intermittent fever, focal or generalized seizures
• Focal neurologic signs dependent on location (frontal cortex -hemiparesis; occipital - homonymous visual defects)
• Expansion causes worsening increased ICP signs and ultimately herniation or rupture into ventricles - both fatal

24
Q

Brain Abscess - work up

A
  • CT and MRI essential
  • EEG - often abnormal, localized slowing in area of abscess
  • LP - rarely helpful and potentially dangerous
25
Q

Brain Abscess - Management

A
  • Antibiotic therapy + surgical drainage
  • Antibiotics - broad spectrum, anaerobic and aerobic coverage
    * Cefotaxime or ceftriaxone + metronidazole or chloramphenicol until culture and sensitivities
    * IV abx x 6-8 weeks
  • Mannitol for cerebral edema; steroid controversial
  • Rehabilitation for sequelae
26
Q

Brain Abscess - prognosis

A
  • Mortality - 30-65%
  • Neurologic sequelae - 50%
    • Seizures
    • Focal neurologic deficits
27
Q

Prion Diseases

A

• Prion - protein normally made by neurons that is somehow misfolded into an abnormal infectious particle — no DNA or RNA
• Not killed by formalin, ethanol, or boiling; can be destroyed by autoclaving
• Categories
• Creutzfeldt-Jakob disease (CJD) most common, 1/1,000,000 per year
• Gerstmann–Sträussler–Scheinker syndrome (GSS)
• Fatal familial insomnia
• Kuru
Transmission of a prion infectious disease may occur through inoculation via infected human cornea, dura, pituitary, or surgical instruments OR it may be hereditary as in familial CJD, GSS, and faltal familial insomnia.
-Rare cases of a variant of CJD (vCJD) appear to be transmitted from infected cattle with bovine spongiform encephalopathy (mad cow disease) - incidence falling due to feed changes

28
Q

Prion Diseases - presentation

A
  • Subacute to chronic progressive dementia, fatal over 6 months to 2 years
  • No fever, no increased WBC
  • CSF normal on standard tests because no immune response
29
Q

Prion Diseases - work up

A
  • Diagnosis difficult - suspect in this add presentation
    • Prion present in CSF, brain, pituitary, and peripheral nerves innervating cornea and dura
    • Not present in saliva, urine, sweat, or stool (isolation of patient unnecessary)
    • Blood considered infectious, but not likely

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