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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
What is the characterstic **microscopic pathology** of viral encephalitis?
* Perivascular and parenchymal lymphocytic infiltrate * Microglial nodules
26
What happened if you see: * Remnant of a neuronal cell body w/inflammatory cells
**Neuronophagia**
27
What is the **most common cause of sporadic acute viral encephalitis in temperate climates**?
**HSV-1**
28
**HSV-1** in the CNS * Clinical S/S: * MRI: * CSF:
* **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
What are the **gross & microscopic changes** in acute herpes simplex encephalitis?
* **Gross:** * congestion * swelling * hemorrhagic necrosis of temporal lobes, insula, cingulate gyri, orbital cortex * **Microscopic:** * Necrotizing hemorrhagic inflammation * Intranuclear viral inclusion * Cowdry type A
30
When will HSV-2 be seen in the CNS?
Meningitis in neonates passing through birth canal in mother with active HSV2 infection
31
When will CMV be seen in the CNS?
* Commonest opportunist viral infection in **AIDS** patients * **Subacute encephalitis** * Microglial nodules * Cytomegalic cells contain viral inclusions * intranuclear or intracytoplasmic
32
When will *Varicella Zoster* virus be seen in the CNS?
* 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
What is an important cause of epidemic encephalitis?
**Arbovirus**
34
**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?
* **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
**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?
* 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
When does HIV meningitis present?
Presents during acute flu-like illness at time of seroconversion
37
What is the presentation of HIV encephalitis/leukoencephalopathy?
* 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
Progressive Multifocal Leukoencephalopathy (PML) * Which patients are vunerable? * What are the causative organisms? * Which virus is most common?
* 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
What are the pathological changes of PML?
* Small foci of gray discoloration in white matter * Irregular poorly defined areas of demyelination * Elarged oligodendrocyte nuclei * Oligodendrocyte inclusion
40
* In which patient population does fungi (menigo)encephalitis usually occur? * What are the patterns of damage?
* 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
What are the pathological changes seen with **Aspergillus** brain infection?
* Multiple foci of hemorrhagic necrosis * Brain necrosis with inflammation
42
**Cryptococcosis** * Causative organism: * Site of infection: * Who usually gets infected? * Source:
* *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
**Cyptococcosis** * Main forms: * CSF:
* **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
What is the gross change in cryptococcal meninges?
thickened meninges particularly **over the sulci**
45
What are the pathological changes seen in **cryptococcal menigoencephalitis**?
* **Multiple intraparenchymal “cysts”** * Also called “**soap bubbles**” (secondary to gelatinous capsular material) * Occur in 50% of cases in addition to meningeal involvement
46
What can be seen on microscopy in **cryptococcal meningitis**?
* Organisms are **single round yeast forms** surrounded by **capsule** (clear space around organism) * Usually minimal inflammatory reaction
47
**Parasites of the CNS** * Single or multicellular? * Who is the typical patient population? * What can they cause?
* Single-cell organisms * Infection occurs in immunocompetent and immunosuppressed (where the infection is more severe) * Cause meningoencephalitis or abscesses
48
List the parasites of the CNS (5):
1. Amoeba 2. Plasmodium (Malaria) 3. Toxoplasma 4. Trypanosoma (Sleeping sickness) 5. Cysticercus (Taenia solium)
49
What is the most common cause of mass lesions in CNS in AIDS patients?
***Toxoplasma gondii***
50
***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?
* **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
What can be seen in cerebral toxoplasmosis?
Multiple localized necrotic lesions
52
Epidural and subdural empyemas * Are usually caused by .... * What are they an extension of?
* **Usually bacterial** (staph or strep commonly) * **Local extension of infectious process** * Frontal or mastoid sinusitis * Otitis media * Trauma * Osteomyelitis * Surgical procedure
53
What is **transmissible spongiform encephalopathy** caused by?
**Prions**
54
What are the types of Prion disease?
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
Describe how a **defective prion protein** leads to prion disease:
* **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
Describe the role of the **normal prion protein:**
* **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
What is the BSE epidemic and what did it result in?
* 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
What is the **most common clinical presentation of prion disease**?
**Creutzfeldt-Jakob disease** (CJD)
59
**Creutzfeldt-Jakob Disease (CJD)** * Clinical Features * EEG * MRI * CSF * Treatment * Prognosis
* **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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