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Nervous System > P- Infections of the CNS > Flashcards

P- Infections of the CNS Flashcards

1
Q

What are the routes by which infectious agents can gain access to the nervous system?

A
  1. Hematogenous spread
  2. direct implantation- in the setting of trauma or congenital CNS malformation
  3. Local extension - infection of middle ear and sinuses
  4. Invasion via peripheral nerves- rabies, HSV
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2
Q

What 2 factors influence the development of infections within the CNS?

A
  1. integrity of the normal host defenses
    - skull fracture or meningeal tear may let low virulence organisms to gain access to parenchyma
  2. nature of the infectious agent
    - highly virulent
    - rabies and HSV1 via peripheral nerves
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3
Q

In some instances infections become generalized, as in the case of ______________.
Others tend to be more localized, as is the case of ____________ or _________________.

A

Generalized:
-acute bacterial infections of leptomeninges

Focal:

  • abscesses by pyogenic bacteria
  • agents like poliovirus that affect neuronal subpopulations in a selective manner
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4
Q

In acute bacterial meningitis, how do most bacteria reach the CNS?
What organisms are most common in neonates?
Older children/adults?
Young adults/epidemic meningitis?
Following trauma/neurosurgery?

A

bacterial most often reach the CNS via the bloodstream often after colonizing the nasopharynx

  1. Neonates
    - E. coli
    - Group B strep
  2. Young children/adults
    - strep pneumo
  3. Young adults/epidemics
    - N. menigitidis
  4. Trauma/surgery
    - S. aureus
    - Gram neg rods
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5
Q

What is the morphology of fatal acute bacterial meningitis?

How does it differ depending on the cause of the infection?

A
  1. Meninges are congested with variable amounts of creamy opaque exudate
    - Strep pneumo - over the cerebral convexities
    - H. flu- basilar
  2. Vascular congestion
  3. swollen brain due to edema [vasogenic and cytotoxic]
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6
Q

What is the microscopic appearance of acute bacterial meningitis?

A
  1. characterized by neutrophils and fibrin in the acute phase
  2. inflammation can spread into the venticular cavities but do not infect the parenchyma
  3. bacteria seen on smears of the exudate
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7
Q

What are the clinical features of acute leptomeningitis?

A
  1. headache, increased ICP [mass effect]
  2. fever
  3. stiff neck
  4. altered mental status
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8
Q

What does the CSF show for an acute bacterial meningitis?

A
  1. high protein
  2. low glucose
    - increased anaerobic metabolism
    - impaired transport of glucose into CSF
    - glycolytic activity of neutrophils
  3. increased neutrophils [pleocytosis]
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9
Q

What are brain abscesses?
What are the most common infecting organisms?
How do they spread into the brain?

A

collections of pus in the brain associated with liquifactive necrosis

Common organisms:

  1. S. aureus
  2. S. pneumococcus
  3. anaerobic organisms

Spread into the brain by:

  1. hematogenous spread [endocarditis, lung abscesses, bronchiectasis]
  2. contiguous spread from sinusitis/otitis media
  3. direct implantation in trauma
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10
Q

Where are brain abscesses most likely to develop?

A

they are most common in the cerebral hemispheres

  • solitary or multiple
  • temporal and frontal lobe [if infections of the middle ear]
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11
Q

Describe the progression/formation of an abscess.

A
  1. lesion softens –>liquifies
  2. cavity fills with yellow-gray pus
  3. over several weeks the abscess is demarcated from the surrounding brain by fibroblasts and collagen/granulation tissue
  4. the surrounding brain is edematous, congested and contain reactive astrocytes w/ perivascular inflammatory cells
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12
Q

What are the clinical features associated with brain abscesses?

A
  1. fever
  2. increased intracranial pressure
  3. variable focal deficits
  4. enhancement on CT/MRI
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13
Q

Describe the CSF contents for a bacterial brain abscess.

A
  1. less neutrophils than acute bacterial meningitis
  2. mild increase in protein
  3. normal glucose
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14
Q

What are complications of brain abscesses?

A
  1. brain herniation
  2. rupture of the abscess into ventricle/subarachnoid space

*need to drain the abscess bc it is avascular so drugs won’t get to it

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15
Q

What effects does TB have on the brain?
How does it spread to the brain?
Where is the initial lesion?

A

TB can cause encephalitis and/or meningitis.

It is almost always caused by hematogenous spread from an organism from a primary pulmonary infection

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16
Q

Describe the gross appearance of a tuberculoma.

What is the histology?

A

Gross:

  1. small, single or multiple firm nodules
  2. large, irregular nodule with central area of caseous necrosis

Histological:

  1. aggregates of epithelioid histiocytes
  2. giant cells
  3. areas of necrosis with acid-fast bacilli
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17
Q

What happens if a tuberculoma ruptures into the subarachnoid space?

A

It can cause tuberculous meningitis

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18
Q

What are the 2 ways TB meningitis can occur?

A
  1. rupture of tuberculoma into the subarachnoid space

2. direct hematogenous seeding of the meninges or choroid plexus

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19
Q

Describe the gross appearance of TB meningitis.

What are histiological features?

A

Gross

  1. thick opacified exudate at the base of the brain [around optic chiasm]
  2. hydrocephalus
  3. vasculitis with 2ndary infarct

Histological:

  1. granulomatous inflammation [histiocytes, giant cells]
  2. caseous necrosis
  3. vasculitis
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20
Q

Who are most affected by fungal infections?
What fungal infection is associated with diabetes?
Which fungal infection is associated with neutropenia?

A

Most fungal infections occur in immunocompromised patients

  • Aspergillis occurs in patients with neutropenia
  • Mucor infection in diabetics
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21
Q

What is the most common fungal CNS infection in AIDS patients?
How does it present?
How do most of these infections usually begin?

A

Crypto is the most common fungal infection of the CNS in AIDS patients and usually presents as meningitis.

The primary infection is respiratory.

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22
Q

How does the morphology of meningitis differ for crypto from other types of meningitis?

A

It has scant inflammatory response.

Examination of the brain will not show exudate but it will look “shiny and slippery” from the mucopolysaccharides

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23
Q

What is found in the subarachnoid space for crypto meningitis?
What would you see in the parenchyma?

A

Subarachnoid
1. budding yeasts with abundant mucoid capsules

Parenchymal
1. soap bubble lesions - usually in the corpus striatum because of the lenticulostriate arteries

24
Q

How is crytococcus meningitis diagnosed?

A

detection of crypto antigen in the CSF

25
Q

What are the 2 types of angioinvasive fungal infections?

A
  1. Aspergillis

2. phycomycetes [mucor, rhizopus, absidia]

26
Q

How does the morphology of mucormycosis and aspergillis differ from other fungal meningitis?

A
  1. invasion of the blood vessels–>inflammation and thrombosis
  2. parenchymal hemorrhagic necrosis
27
Q

What parasitic infections cause CNS problems in immunocompetent hosts?

A
  1. plasmodium
  2. cysticercosis
  3. malaria
28
Q

Toxoplasma gondii is a protozoan that can produce systemic and CNS infection.
Who is most likely to be infected by T. gondii?

A
  1. neonates

2. patients with AIDS/immunocompromised

29
Q

What is the route of infection and manifestation of primary systemic infection in t. gondii?

A

Both are uknown.

It is well documented however that T. gondii is a reactivation of latent infection

30
Q

How does T. gondii infection of the brain present?

A

It is a mass lesion in the gray matter.

There are multiple distinct masses so the patient will present with focal symptoms

31
Q

Describe the histology of an untreated T. gondii lesion.

A
  1. necrosis
  2. variably developed mononuclear infiltrate
  3. pseudocysts [collection of organisms within cells]
    4 tachyzoites- cresent shaped extracellular organisms
32
Q

How is toxoplasmosis diagnosed?

A
  1. PCR of CSF specimen

2. brain biopsy [not much of a role anymore]

33
Q

How is cysticercosis transmitted?
How does it affect the brain?
What areas of the brain tend to be affected?

A

Infection follows the ingestion of food or water contaminated with feces that have eggs of T. solium.

  1. eggs hatch to oncospheres
  2. onchospheres disseminate to CNS
  3. develop into encysted larval forms cysticerci

It affects any area of the brain including the ventricles and can cause:

  • focal deficits
  • hydrocephalus
  • seizures
34
Q

What is the most common type of GENERALIZED brain parenchymal infection?

A

Viral infection

35
Q

In terms of viral infections ___________ selectively infects neurons, while _____________ selectively infects oligodendroglial cells

A

Rabies–> only neurons

JC virus in progressive multifocal leukoencephalopathy

36
Q

Which 2 viruses are most likely to infect and immunocompetent host?

A
  1. HSV1

2. arbovirus [west nile, st. louis]

37
Q

What is the term for infection of the grey matter of the brain and spinal cord?
White matter?

A

Grey:

  • brain = polioencephalitis
  • cord = poliomyelitis

White

  • brain = leukoencephalopathy
  • cord = leukomyelitis
38
Q

What are the three main morphological features of viral encephalitis?

A
  1. perivascular inflammation [[mononuclear cells-lymphocytes, plasma cells, macrophages]
  2. microglial nodules [sometimes associated with neutrophagia-the phagocytosis of neurons in grey matter]
  3. inclusion bodies
    - intranuclear in HSV, CMV, varicella
    - intracytoplasmic in rabies [negri] and PML
39
Q

What histological changes are seen with arbovirus infection?
What areas of the brain are most affected by:
1. st. louis virus
2. WNV

A
  1. perivascular inflammation
  2. microglial nodules
  3. NO INCLUSIONS
  4. involvement of grey and white matter and meninges

St. Louis - substantia nigra and thalamus
WNV- substantia nigra and/or spinal motor injury difficult to differentiate from poliomyelitis

40
Q

What does infection by enterovirus cause?

A

Classic poliomyelitis-

  • loss off lower motor neurons in the spinal grey
  • perivascular inflammation, microglial nodules, NO inclusions
41
Q

What is the most common type of sporadic encephalitis in the US?
What areas of the brain does it have proclivity for?
What is the presentation?
What are the histological features?

A

HSV-1 which tends to infect the frontal/temporal lobes where it produces necrotizing, hemorrhagic encephalitis.

Histology:

  1. perivascular mononuclear inflammation
  2. microglial nodues
  3. smudgy nuclear inclusions in infected glial cells and neurons
42
Q

How is HSV1 detected as a cause of encephalitis?

How is it treated?

A

PCR analysis of the CSF

[but can also do immunohistochemistry, viral culture, EM]

Treat with antivirals like acyclovir

43
Q

What is the cause of PML?
Who is mainly infected?
What cells of the CNS are preferentially targeted?

A

PML is caused by JC virus [a DNA papovavirus].

It usually infects immunocompromised as a reactivation of infection acquired earlier in life.

JC virus targets oligodendroglial cells causing degeneration and demyelination

44
Q

What is seen grossly and microscopically for PML?

A

Grossly:

  • randomly distributed small lesions of demyelination
  • especially at grey/white junction

Histologically

  1. inclusion-bearing oligodendroglial cells
  2. demyelination
  3. cytologically atypical reactive astrocytes
45
Q

What will the CSF show for PML?

What is necessary for diagnosis?

A

CSF is normal so you must do PCR analysis to identify JC virus-related nucleic acid sequences

46
Q

What causes neurological diseases in AIDS patients?

A
  1. opportunistic infections
  2. HIV virus itself
    - aseptic meningitis
    - HIV1 encephalitis [subacute AIDS encephalitis]
47
Q

What does HIV-1 encephalitis/subacute AIDS encephalitis cause?
Describe the clinical presentation

A

AIDS-dementia complex

  • late stages of HIV infection
  • memory loss
  • cognitive impairment
  • motor disturbances
  • most common cause of young adult dementia worldwide
  • improves with HAART
48
Q

Describe the 4 major morphological changes that occur with HIV-1 encephalitis [gross and histologic]

A

Gross:

  1. brain atrophy with enlarged ventricles
  2. vacuolar myelopathy [vacuolar change in lateral and dorsal columns of the spinal cord like B12 deficiency]

Histologic:

  1. central white and deep grey myelin pallor, perivascular inflammation, microglial nodules
  2. multinucleated giant cells
  3. spinal cord involvement
49
Q

What is thought to play a critical role in the pathogenesis of HIV-1 encephalitis?

A

HIV-infected macrophages:

  1. allow HIV to get into CNS
  2. develop subsequent brain damage via cytokines, chemokines, cytotoxic viral proteins
50
Q

HIV-1 encephalitis can cause vacuolar myelopathy. How does this condition present?

A

It is a condition characterized by myelin breakdown and vacuolar change in the lateral and dorsal columns.

It will present like a vitamin B12 deficiency

51
Q

What causes spongiform encephalopathies?

What is seen microscopically?

A

prion proteins cause them and you will see microscopic vacuoles in the neuronal cell bodies and processes

52
Q

What are the 3 ways a spongiform encephalopathy can arise?

Which is most common?

A
  1. sporadic- most common
  2. transmitted person-to-person
  3. inherited [autosomal dominant]- 15%
53
Q

Describe the structure of a normal and mutated prion.

Why does the mutation cause problems?

A

It does NOT have DNA, RNA and is not a virus. It is just a normal protein in the mammalian nervous system that can reek havoc if it gets misfolded.

Normal = PRPc = multiple a-helical structures
Mutated = PRPsc [scapie] = b-pleated sheets

B-pleated sheets allow PRPsc to form amyloid deposits

54
Q

What are infectious prions resistant to many agents that normally sterilize?

A

They lack nucleic acid so a lot of the viral targets are ineffective [like UV, autoclaving, disinfectants]

55
Q

How can CJD be genetically transmitted?

A

a mutant gene that encodes an inherently unstable PRPc is much more likely to undergo “spontaneous” conformational change to PRPsc

56
Q

What is seen microscopically for sporadic CJD?

A
  1. vacuoles in neuronal cell bodies and surrounding neuropil
  2. neuronal loss
  3. gliosis [astrocytic]
  4. NO inflammatory infiltrates
57
Q

Describe the clinical presentation of sporadic CJD. How does it differ from variant CJD?

A

Sporadic:

  • peak in 7th decade
  • rapidly progressing dementia [wks to months]
  • ataxia, startle myoclonus
  • cortical blindness

vCJD:

  • acquired from ingestion of tissue from cattle with bovine spongiform encephalopathy
  • younger
  • progresses more slowly
  • behavior and psychiatric disturbances

Nervous System (32 decks)

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