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Neurology > Infectious Diseases of the Nervous System Pathology > Flashcards

Infectious Diseases of the Nervous System Pathology Flashcards

1
Q

How does infection manifest in the brain?

A
  • Hematogeneous spread
    • Arterial spread
    • Retrograde venous spread
      • Anastomotic connections between face veins & cerebral circulation
      • Paravertebral venous plexus, Batson
  • Local extension – air sinuses, infected tooth
  • Neural Route (Extension from PNS to CNS)
  • Direct implantation – trauma, iatrogenic
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2
Q

What is neurotropism?

A

A special affinity for nervous tissue

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3
Q

What are the mechanisms for neurotropism?

A
  • Viral specific receptors on brain cells
    • Poliovirus for motor neurons of anterior horns of spinal cord
    • Mumps virus for ependymal cells lining ventricles
  • Capsule proteins that adhere to meninges and possess antiphagocytic properties
    • Group B streptococci, E. coli subtypes
  • Viral spread along nerves
    • Herpes simplex virus
    • Rabies
    • Varicella zoster virus
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4
Q

Meningitis

Clinical signs/symptoms

A
  • headache
  • photophobia
  • stiff neck (nuchal rigidity)
  • clouded consciousness
  • fever
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5
Q

Meningitis

Clinical subtypes (4)

A
  • Hyperacute (<24 hrs)
    • Meningococcal meningitis
    • Sparse inflammation, numerous organisms, congestion
  • Acute (2-7 days) -most common infection in CNS
    • Usually bacterial
    • Usually results from hematogeneous spread
  • Subacute/chronic (> 1 week)
    • Tuberculosis, syphilis (often brain parenchyma also affected)
    • Lymphocytes, plasma cells, macrophages appear in exudate
  • “Aseptic” (usually viral) - much less fulminant than bacterial meningitis & less severe symptoms
    • Summer & early fall
    • Lymphocytic infiltrate in meninges
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6
Q

What can be seen grossly if there is acute meningitis?

A

layer of exudate under the meninges

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7
Q

What will be seen micropscopically in acute bacterial meningitis?

A

Exudate present, numerous polymorphonuclear
leukocytes, in subarachnoid space

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8
Q

What are complications of bacterial meningitis?

A
  • Brain infarcts
  • Phlebitis
    • may cause infarction of underlying brain tissue
  • 2° vasculitis
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9
Q

What causes aseptic meningitis?

A
  • Arboviruses
  • Enterovirus (most common)
    • Echovirus
    • Coxsackie
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10
Q

Parenchymal infections: Brain Abscesses

  • Definition:
  • Clinical Signs & Symptoms:
A
  • Definition: Circumscribed focus of infection
  • Clinical S/S:
    • focal deficits
    • raised intracranial pressure
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11
Q

What are the usual causes of brain abscesses?

A

Bacterial or fungal

  • Immunocompetent host:
    1. Strep
    2. Staph
  • Immunocompromised host:
    1. Toxoplasma
    2. Nocardia
    3. Listeria
    4. Gram neg bacilli
    5. Mycobacteria
  • •Fungi
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12
Q
  • What is encephalitis?
  • What are the causes?
A
  • Inflammation of brain
    • Spinal cord-myelitis
    • Meninges and brain-meningoencephalitis
  • **Causes: **
    • Bacterial meningoencephalitis
      • Tuberculosis
      • Syphilis
      • Lyme disease
    • Viral meningoencephalitis
    • Fungal meningoencephalitis
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13
Q

What is the most common form of tuberculosis in the brain?

A

Meningoencephalitis

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14
Q

What is a risk factor for TB in the brain?

A

HIV

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15
Q

Menigoencephalitis

  • CSF:
  • S/S:
  • Meninges contain:
A
  • CSF: elevated pressure & protein, decreased glucose, lymphocytic pleocytosis
    • Cultures for AFB are positive in 50%
    • PCR for TB now always performed
  • S/S: headache, lethargy, confusion, vomiting
  • Meninges contain:
    • lymphocytes
    • macrophages
    • granulomas with extension into underlying brain
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16
Q

Where is TB of the brain usually found?

A

Exudate, primarily over the base of brain

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17
Q

What is a tuberculoma?

A
  • Mass lesion with central necrotic core of caseation, surrounded by fibroblasts, epithelioid histiocytes, giant cells & lymphocytes
  • Acid-fast bacilli (AFB) are present in necrosis
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18
Q

What is the result of TB osteomyelitis?

A

Spondylitis (Pott’s disease)

  • Granulomatous process involves vertebral bodies & discs
  • Causes epidural abscess
  • Cord compression, vertebral collapse
  • Epidural extension of the granulomatous inflammation
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19
Q

What stage of Syphilis affects the CNS?

A

Tertiary

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20
Q
  • When does the tertiary stage of Syphilis manifest?
  • How does it manifest?
A
  • Typically manifests months/yrs after inital infection
    • 10% of patients
  • Major forms:
    • General paresis (paretic neurosyphilis)
    • Meningovascular
    • Tabes dorsalis
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21
Q

Describe general paresis (paretic syphilis):

A
  • Gradual impairment of cognition/attention
  • Meningo-encephalitis:
    • Thickened meninges and atrophic brain
    • Meningeal & parenchymal perivascular lymphocytes, plasma cells, & microglia
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22
Q

Describe the menigovascular type of syphilis:

A

Chronic meningitis & multifocal arteritis

  • Severe at base of brain
  • Causes infarcts & hydrocephalus
  • Meningeal & arterial/arteriolar lymphocytes & plasma cells with collagenous thickening of wall and eventual occlusion
  • Often focal neurologic deficits due to vascular compromise secondary to arteritis
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23
Q

Tabes Dorsalis

  • Definition
  • Clinical S/S
A
  • Chronic inflammation in dorsal roots & ganglia with loss of neurons and associated degeneration of posterior columns (axons & myelin)
  • Clinical S/S:
    • “lightening pains” or paraesthesias in affected roots
    • eventual loss of position/vibration sense
    • shuffling broad-based gait
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24
Q

Viral (menigo)encephalitis

  • General Features:
  • Specific Organisms:
A
  • General features: perivascular lymphocytes, microglial nodules, neuronophagia
  • Specific organisms
    • Arboviral encephalitis
    • Herpes virus infections (Herpes simplex 1, Herpes simplex 2, Cytomegalovirus, Varicella-zoster)
    • HIV
    • Progressive multifocal leukoencephalopathy (PML)
25
Q

What is the characterstic microscopic pathology of viral encephalitis?

A
  • Perivascular and parenchymal lymphocytic infiltrate
  • Microglial nodules
26
Q

What happened if you see:

  • Remnant of a neuronal cell body w/inflammatory cells
A

Neuronophagia

27
Q

What is the most common cause of sporadic acute viral encephalitis in temperate climates?

A

HSV-1

28
Q

HSV-1 in the CNS

  • Clinical S/S:
  • MRI:
  • CSF:
A
  • Clinical S/S:
    • Headache, fever, mood, memory, behavior abnormalities, drowsiness, coma
  • MRI:
    • focal abnormalities in frontal or temporal lobes
  • CSF:
    • Increased pressure
    • Lymphocytic pleocytosis
    • Elevated protein
    • PCR for HSV1 DNA
29
Q

What are the gross & microscopic changes in acute herpes simplex encephalitis?

A
  • Gross:
    • congestion
    • swelling
    • hemorrhagic necrosis of temporal lobes, insula, cingulate gyri, orbital cortex
  • Microscopic:
    • Necrotizing hemorrhagic inflammation
    • Intranuclear viral inclusion
      • Cowdry type A
30
Q

When will HSV-2 be seen in the CNS?

A

Meningitis in neonates passing through birth canal in mother with active HSV2 infection

31
Q

When will CMV be seen in the CNS?

A
  • Commonest opportunist viral infection in AIDS patients
  • Subacute encephalitis
    • Microglial nodules
    • Cytomegalic cells contain viral inclusions
      • intranuclear or intracytoplasmic
32
Q

When will Varicella Zoster virus be seen in the CNS?

A
  • Reactivation of latent virus residing in sensory ganglia
  • Vesicles in dermatome distribution
  • Followed by scar and pain
  • Dorsal root ganglia or sensory cranial nerve ganglia have lymphocytes, sometimes necrosis
33
Q

What is an important cause of epidemic encephalitis?

A

Arbovirus

34
Q

Arboviral meningoencephalitis

  • What are the clinical s/s?
  • What are the specific types important in the US?
  • What is important for identification of the virus?
A
  • Generalized neurological deficits (seizures, confusion, stupor, delirium, coma) & focal signs
  • Specific types important in U.S.
    • West Nile
    • Eastern, western equine
    • Venezuelan
    • St. Louis
    • California
  • PCR important for id of specific virus
35
Q

HIV in the CNS

  • What type of virus is HIV?
  • What is the most commonly affected cell?
  • What is a major target of HIV infection?
  • What are the different types of involvement of HIV?
A
  • RNA virus, retrovirus
  • Microglia are most common cell infected in CNS by HIV
  • CNS is a major target of HIV infection
  • Types of involvement
    • HIV meningitis
    • HIV encephalitis/leukoencephalopathy
    • Vacuolar myelopathy
36
Q

When does HIV meningitis present?

A

Presents during acute flu-like illness at time of seroconversion

37
Q

What is the presentation of HIV encephalitis/leukoencephalopathy?

A
  • Present in > 75% of autopsied HIV patients
  • Clinical S/S (AIDS dementia complex):
    • Cognitive and behavioral deterioration
    • eventually dementia
    • ataxia & tremor
  • Slight diffuse atrophy
  • Classic lesion – microglial nodule containing multinucleated microglial cells (contain HIV virus)
    • Also perivascular lymphocytes, patchy demyelination and astrocytosis
38
Q

Progressive Multifocal Leukoencephalopathy (PML)

  • Which patients are vunerable?
  • What are the causative organisms?
  • Which virus is most common?
A
  • Occurs in immunosuppressed hosts (often AIDS patients)
  • Caused by JC virus, polyomavirus, infects oligodendrocytes
  • Most have serologic evidence of prior JC virus infection by adolescence
    • JC virus is re-activated with immunosuppression
39
Q

What are the pathological changes of PML?

A
  • Small foci of gray discoloration in white matter
  • Irregular poorly defined areas of demyelination
  • Elarged oligodendrocyte nuclei
  • Oligodendrocyte inclusion
40
Q
  • In which patient population does fungi (menigo)encephalitis usually occur?
  • What are the patterns of damage?
A
  • Commonly occur in immunocompromised hosts (and occasionally in immunocompetent hosts):
    • Candida, Mucor, Aspergillus, Cryptococcus, Histoplasma, Coccidiodes, Blastomyces
  • Patterns of damage
    • Chronic meningitis
    • Parenchymal invasion (encephalitis)
    • Vasculitis (especially Aspergillus and Mucor)
      • Cause hemorrhagic infarcts
41
Q

What are the pathological changes seen with Aspergillus brain infection?

A
  • Multiple foci of hemorrhagic necrosis
  • Brain necrosis with inflammation
42
Q

Cryptococcosis

  • Causative organism:
  • Site of infection:
  • Who usually gets infected?
  • Source:
A
  • Cryptococcus neoformans
  • Affects lungs first usually & **spreads hematogeneously **to brain
  • Most often in immunosuppressed patients
    • may occur in immunocompetenthosts
  • Organism found in soil and bird excreta
43
Q

Cyptococcosis

  • Main forms:
  • CSF:
A
  • Main forms:
    • Meningitis with or without brain parenchymal cysts (encephalitis)
    • Abscesses (Cryptococcomas)
  • CSF: lymphocytes, high protein, normal or reduced glucose
    • India ink stains allows identification of organism (by negative staining of capsule)
    • Assay for presence of Cryptococcal antigen is more sensitive
44
Q

What is the gross change in cryptococcal meninges?

A

thickened meninges particularly over the sulci

45
Q

What are the pathological changes seen in cryptococcal menigoencephalitis?

A
  • Multiple intraparenchymal “cysts”
    • Also called “soap bubbles” (secondary to gelatinous capsular material)
  • Occur in 50% of cases in addition to meningeal involvement
46
Q

What can be seen on microscopy in cryptococcal meningitis?

A
  • Organisms are single round yeast forms surrounded by capsule (clear space around organism)
  • Usually minimal inflammatory reaction
47
Q

Parasites of the CNS

  • Single or multicellular?
  • Who is the typical patient population?
  • What can they cause?
A
  • Single-cell organisms
  • Infection occurs in immunocompetent and immunosuppressed (where the infection is more severe)
  • Cause meningoencephalitis or abscesses
48
Q

List the parasites of the CNS (5):

A
  1. Amoeba
  2. Plasmodium (Malaria)
  3. Toxoplasma
  4. Trypanosoma (Sleeping sickness)
  5. Cysticercus (Taenia solium)
49
Q

What is the most common cause of mass lesions in CNS in AIDS patients?

A

Toxoplasma gondii

50
Q

Toxoplasma gondii

  • Man is ________ host
    • Cat is ________ host
  • Infection is secondary to ingestion of ___________ ____ or _____________ _____ from another intermediate host
  • What can happen if there is tranfer to the fetus during pregancy?
  • Which population is at risk for this infection?
A
  • Man is intermediate host
    • Cat is definitive host
  • Infection secondary to ingestion of contaminated food (cat feces) or raw/undercooked meat from another intermediate host (sheep, pig)
  • Tranfer during pregnancy ⇒ Congenital disease
  • Important infection in immunocompromised hosts, esp. AIDS patients
    • Uncommon in healthy adults
51
Q

What can be seen in cerebral toxoplasmosis?

A

Multiple localized necrotic lesions

52
Q

Epidural and subdural empyemas

  • Are usually caused by ….
  • What are they an extension of?
A
  • Usually bacterial (staph or strep commonly)
  • Local extension of infectious process
    • Frontal or mastoid sinusitis
    • Otitis media
    • Trauma
    • Osteomyelitis
    • Surgical procedure
53
Q

What is transmissible spongiform encephalopathy caused by?

A

Prions

54
Q

What are the types of Prion disease?

A
  1. Idiopathic
    • Sporadic Creutzfeldt-Jakob disease (CJD) –most common form
    • Inherited (15%): several forms of familial disease
  2. Acquired
    • Iatrogenic CJD (growth hormone, corneal transplant, etc.)
    • Dietary
      • Kuru (Papua, New Guinea)
      • New-variant CJD (vCJD) - linked to “mad-cow” disease
55
Q

Describe how a defective prion protein leads to prion disease:

A
  • Infectious agent is abnormal form of prion protein
  • PrPsc= abnormal disease causing form of protein, has an abnormal ß-pleated sheet conformation
    • a type of amyloid
    • Does not contain nucleic acid
    • Resistant to usual methods of denaturation (i.e., formalin fixation)
56
Q

Describe the role of the normal prion protein:

A
  • PrPc = normal prion protein
    • Physiological function uncertain but likely participates in signaling pathways
    • Membrane sialoglycoprotein
    • Gene (PRNP) on chr. 20
    • Normal prion protein is normally found in brain (neurons) and selected other organs
57
Q

What is the BSE epidemic and what did it result in?

A
  • BSE epidemic
    • Diets contained feed from scrapie infected sheep
    • Spread by addition of infected cow tissues to cattle feed
    • Ban on feeding ruminant-derived protein to ruminants (1988)
  • Ban on cattle offal in human food (1989)
  • Coincidence of vCJD and BSE in time and space
    • Similarity in biological strain phenotypes of vCJD and BSE
58
Q

What is the most common clinical presentation of prion disease?

A

Creutzfeldt-Jakob disease (CJD)

59
Q

Creutzfeldt-Jakob Disease (CJD)

  • Clinical Features
  • EEG
  • MRI
  • CSF
  • Treatment
  • Prognosis
A
  • Clinical features
    • Rapidly progressive dementia
    • Often cerebellar signs (ataxia)
    • Myoclonic jerking
    • Mean survival is 7 mos.
  • EEG – triphasicwaves at 1-2 sec intervals
  • MRI – often increased signal in basal ganglia
  • CSF usually normal
  • No effective treatment at present
  • Death occurs w/in one year

Neurology (26 decks)

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