Infections on Nervous System Flashcards

1
Q

Reminder: unique features of brain/spinal cord:
–________: protects from organisms, but also restricts immune system access
–________: with inflammation -> swelling & neurologic damage

A

Blood brain barrier

Rigid skull/vertebral canal

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2
Q

Leptomeningeal inflammation =

Encephalitis/cerebritis/myelitis (spinal cord) or Brain abscess =
A

Meningitis

Parenchymal inflammation

( When meninges and brain tissue are affected: meningoencephalitis)

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3
Q

Subdural or epidural inflammation =

A

Subdural/epidural empyemas

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4
Q

Routes of infection in the brain

A
  • Hematogeneous spread: Arterial spread = Retrograde venous spread from Anastomotic connections between face veins & cerebral circulation or 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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5
Q

Neurotropism ie special affinity for brain

What are some mechanisms?

A
  1. Viral specific Rs on brain
  2. Capsule proteisn adhere to meninges and have antiphogocytic properties
  3. Viral spread along nerves
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6
Q

Viral specific receptors on brain cells: what are two examples?

A

Poliovirus for motor neurons of anterior horns of spinal cord

Mumps virus for ependymal cells lining ventricles

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7
Q

Group B streptococci, E. coli subtypes modality of entering brain

A

Capsule proteins that adhere to meninges and possess antiphagocytic properties

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8
Q

Herpes simplex virus, Rabies, Varicella zoster virus enter brain:

A

Viral spread along nerves

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9
Q

Headache, photophobia, stiff neck (nuchal rigidity), clouded consciousness, fever

A

Meningitis

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10
Q

Hyperacute (<24 hrs) meningtis; see sparse inflammation, numerous organisms, congestion

A

– Meningococcal meningitis

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11
Q

Acute (2-7 days) - most common infection in CNS

A

– Usually bacterial
– Usually results from hematogeneous spread

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12
Q

Subacute/chronic (> 1 week)

A

– Tuberculosis, syphilis (often brain parenchyma also affected)

– Lymphocytes, plasma cells, macrophages appear in exudate

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13
Q

much less fulminant than bacterial meningitis & less severe symptoms

– Summer & early fall
– Lymphocytic infiltrate in meninges

A

“Aseptic” (usually viral) -

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14
Q

What do we see on histology of acute bacterial meningitis

A

exudate present, numerous PMNS, leukocytes in the subarachnoid spce

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15
Q

Complications of bacterial meningitis

A

Brain infarcts, secondary vasculitis, phlebitis may occur and cause infart of underlying brain tissue

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16
Q

Aseptic meningitis causitive organsims:

A

Arboviruses or Enterovirus (most common) :Echovirus and Coxsackie

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17
Q
  • Circumscribed focus of infection
  • Clinical S/S: focal deficits, raised intracranial pressure
  • Usually bacterial or fungal origin
A

Parenchynal infections: BRAIN ABSCESSES

–liquifactive necrosis

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18
Q

Cause of brain abcess in immunocompetent host

A

Step and staph

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19
Q

Brain abcesses are caused by what pathogens in immunocompromised hosts?

A

Toxo, Listeria, gram neg bacilli, myco, fungi

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20
Q

DEscribe a brain abcess histologically

A

center is necrotic and thre are inflammatory cells and fibrous capsule

*we also see giant cell; granulomatous and early fibrous wall

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21
Q

Inflammation of brain
• Spinal cord-myelitis
• Meninges and brain-meningoencephalitis

• May be bacterial, viral, or fungal in origin

A

examples of parenchymal infections: encephalitis

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22
Q

Causes of bacterial mengioencephalitis

A

• Tuberculosis

  • Syphilis
  • Lyme disease
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23
Q

Cause of TB

A

Mycobacterium tuberculosis

  • CNS involvement in 10-15%
  • HIV infection is risk factor
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24
Q

Most common form of TB in CNS

What do we see in CSF levels?

A

Meningoencephalitis

CSF: elevated pressure & protein, decreased glucose, lymphocytic pleocytosis

 Cultures for AFB are positive in 50% t**hus PCR for TB now** always performed
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25
Q

Sigs and symptoms of TB meningioencephalitis are simular to other meningitis; what do we see in the meninges?

A

Meninges contain lymphocytes, macrophages, granulomas with extension into underlying brain

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26
Q

Describe findings on scan and grossly in pt infected with TB mengioencephalitis

A

Gross; see exudate located in base of brain

scan see enhancement of meninges over brain base

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27
Q

Describe histological findings in pt with TB meningioencephalitis

A

Leptomeningeal vessels with arteritis; Hydrocephalus and infarcts may occur secondary to vessel occlusion

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28
Q

oh myyyy, what is this mean?

A

AFB + stain seen in pts with TB

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29
Q
  • Mass lesion with central necrotic core of caseation, surrounded by fibroblasts, epithelioid histiocytes, giant cells & lymphocytes
  • AFB are present in necrosis
A

Tuberculoma

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30
Q

Describe what you see on pathology of caseous necrosis in TB

A

see caseous necrosis with granulomatous inflammation

there are epitheliod histiocytes surrounding lesion

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31
Q

Spondylitis (Pott’s disease)

  • Granulomatous process involves vertebral bodies & discs
  • Causes epidural abscess
  • Cord compression, vertebral collapse

Epidural extension of the granulomatous inflammation

A

Tuberculosis osteomyelitis

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32
Q

• General paresis (paretic neurosyphilis) • Meningovascular • Tabes dorsalis

these are all possible progressions of what?

A

untreated Treponema pallidum: devos into neurosyphillis = tertiary syphillis

33
Q

Describe what you see in general paresis caused by neurosyphillis

A
  • Gradual impairment of cognition/attention
  • Meningo-encephalitis:Thickened meninges and atrophic brain ad meningeal & parenchymal perivascular lymphocytes, plasma cells, & microglia
34
Q

Meningovascular type Chronic meningitis and multifocal arteritis from tertiary syphillis:

Located at:

causes:

A
  • Severe at base of brain
  • Causes infarcts & hydrocephalus
35
Q

What do we see on histology in meningovasculr type chornic meningitis from tertiary syphillis?

A
  • 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
36
Q

Location of damage from Tabes Dorsalis

A

• Chronic inflammation in dorsal roots & ganglia with loss of neurons and associated degeneration of posterior columns (axons & myelin)

37
Q

• ‘Lightening pains’ or paraesthesias in affected roots, eventual loss of position/vibration sense; shuffling broad-based gait

A

Tabes dorsalis: d/t chronic inflammation in degen of posterior columns

38
Q

• General features: perivascular lymphocytes, microglial nodules, neuronophagia

A

Viral meningo-encephalitis

39
Q

Organisms responsible for viral (meningo)encephalitis

A
  • Arboviral encephalitis
  • Herpes virus infections (Herpes simplex 1, Herpes simplex 2, Cytomegalovirus, Varicella-zoster)
  • Human immunodeficiency virus
  • Progressive multifocal leukoencephalopathy (PML)
40
Q

What are these little buggers?

What disease are they associated with?

What else on histology would we expect to see?

A

Microglial nodules seen in viral ifnection!

will also see perivascular and parenchymal lymphocytic infiltration

41
Q

Whats going on with these buggers?

A

Neuronophagia: see remnant of neuronal cell body getting eaten up by inflammatory cells

42
Q
  • Most common cause of sporadic acute viral encephalitis in temperate climates
  • Headache, fever, mood, memory, behavior abnormalities, drowsiness, coma
  • MRI- focal abnormalities in frontal or temporal lobes
A

Herpes virus infection in CNS

43
Q

Pt comes in with headache, fever and drowsiness. Partner says they ahve been behaving different and struggling to remember things. You suspect encephalitis and below are the CSF labs:

Lymphocitic pleocytosis

Elevated protein

Increased pressure

What is your Dx and how do you confirm?

A

HSV-1 infection in CNS

Dx via PCR for HSV1

44
Q

What part of brain do HSV1 infections LOOOVE

A

frontal and temporal regions

45
Q

What do we see grossly in HSV1 encephalitis?

A

very hemorrhagic process with congestion, swelling, hemorragic necrosis of TEMPORAL lobes, cingulate, orbital cortex

46
Q

Where would you see these little nugglets?

A

Cowdry type A = intranuclear viral inclusion seen in HSV1 encephalitis

on the left is necrotizing hemorrhagic inflammation

47
Q

When would you see HSV2 CNS infections?

A
  • Herpes simplex virus type 2
  • Meningitis in neonates passing through birth canal in mother with active HSV2 infection
48
Q

• Commonest opportunist viral infection in AIDS patient that causes Subacute encephalitis

A

Cytomegalovirus

49
Q

What do we see on histology in pt with CMV infection?

A

Microglial nodules and viral inclusions-may be either intranuclear or intracytoplasmic

50
Q

Reactivation of latent virus residing in sensory ganglia:Vesicles in dermatome distribution followed by scar and pain

A

Varicella Zoster:

Dorsal root ganglia or sensory cranial nerve ganglia have lymphocytes, sometimes necrosis

51
Q

Important cause of epidemic encephalitis

Generalized neurological deficits (seizures, confusion, stupor, delirium, coma) & focal signs

A

Arboviral meningoencephalitis : west nile, venezuelan, St.Louis, California

*PCR is key for id of specific virus

52
Q

HIV - ________virus, retrovirus
•_______ are most common cell infected in CNS by HIV

•______ is a major target of HIV infection

A

RNA

Microglia

CNS

53
Q

Types of CNS involvement seen in HIV infected pts

A
  • HIV meningitis
  • HIV encephalitis/leukoencephalopathy

• Vacuolar myelopathy

54
Q

Present in > 75% of autopsied HIV patients

Clinical S/S (AIDS dementia complex) Cognitive and behavioral deterioration, eventually dementia, ataxia & tremor

Slight diffuse atrophy

A

HIV encephalitis/leukoencephalopathy

55
Q

What is the classic lesion seen in HIV encephalitis/leukoencephalopathy

A

microglial nodule containing multinucleated microglial cells (contain HIV virus)

• Also perivascular lymphocytes, patchy demyelination and astrocytosis

56
Q
  • 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
A

Progressive multifocal leukoencephalopathy

57
Q

You note small gray areas of focal necrosis on a brain specimen

on staining, your preceptor points out irregular poorly defined areas of demylenation

A

Progressive multifocal leukoencephalopathy

58
Q

Where would you see oligodendrocyte inclusions?

What else would you see?

A

Progressive multifocal leukoencephalopathy

*Enlarged oligodendrocyte nuclei immunostained for JC virus, at edge of area of early myelin loss

59
Q

ommonly occur in immunocompromised hosts (and occasionally in immunocompetent hosts):

A

FUNGAL (meningo)encephalitis

• Candida, Mucor, Aspergillus, Cryptococcus, Histoplasma, Coccidiodes, Blastomyces

60
Q

Patterns of disease seen in Fungal (meningo)encephalitis

A
  • Chronic meningitis
  • Parenchymal invasion (encephalitis)
  • Vasculitis (especially Aspergillus and Mucor) • Cause hemorrhagic infarcts
61
Q

What would you expect to see on an MRI of pt with Aspergillis brain infection

A

multiple focal areas of necrosis

62
Q

What do you see on histology of pt with Aspergillus brain infection?

A

Necrosis with inflammation, Vessel wall lined with fungal hyphae of aspergillus

63
Q

Affects lungs first usually & spreads hematogeneously to brain

Most often in immunosuppressed patients but may occur in immunocompetent hosts

Organism found in soil and bird excreta

A

Cryptococcus neoformans

64
Q

What are the main forms of cryptococcosis brain infectoins?

A

Main forms:
– Meningitis with or without brain parenchymal cysts (encephalitis)

– Abscesses (Cryptococcomas)

65
Q

What is CSF like in Cryptococcosis infection?

A

lymphocytes, high protein, normal or reduced glucose,

Assay for presence of Cryptococcal antigen is more sensitive

– India ink stains allows identification of organism (by negative staining of capsule)

: on the right is Organisms are single round yeast forms surrounded by capsule

66
Q

What does a gross specimen with crytococcal meningoencephalitis look like?

A

thickened meninges particularly over the sulci

Multiple intraparenchymal “cysts” Also called “soap bubbles” (secondary to gelatinous capsular material)

Occur in 50% of cases in addition to meningeal involvement

67
Q

Histological finding of cryptococcal meningitis

A

Also called “soap bubbles”

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

68
Q
  • Single-cell organisms
  • Infection occurs in immunocompetent and immunosuppressed (where the infection is more severe)

• Cause **meningoencephalitis or abscesses **

A

Parasites

• Amoeba

  • Plasmodium (Malaria)
  • Toxoplasma
  • Trypanosoma (Sleeping sickness)

• Cysticercus (Taenia solium)

69
Q
  • 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)
  • Congenital disease
  • Transmission to fetus if infection occurs during pregnancy
A

Toxoplasma gondii - protozoa

70
Q
  • Important infection in immunocompromised hosts, esp. AIDS patients
  • Most common cause of mass lesions in CNS in AIDS patients
  • Uncommon in healthy adults
A

Toxoplasma gondii - protozoa

71
Q

What do we see on histology in pt with toxoplasmosis?

A

organism w/in pseudocysts as well as lying free

72
Q

Epidural and subdural empyemas

  • Usually ___________
  • Local extension of infectious proces
A

bacterial (staph or strep commonly)

73
Q

Causes of epidural and subdural empyema

A
  • From frontal or mastoid sinusitis
  • Otitis media
  • Trauma
  • Osteomyelitis
  • Surgical procedure
74
Q
  • Disease may be inherited or idiopathic but also transmissible
  • Types of disease: Idiopathic, inherited, transmissible
A

Prion disease (transmissible spongiform encephalopathy)

75
Q

MOst common form of idiopathic prion disease

A

• Sporadic Creutzfeldt-Jakob disease (CJD) – most common form (also has iaotrogenic form you get when from growth hormone or corneal tranpslant

76
Q

What agent is responsible for prion disease, what conformation is it in?

A

PrPsc = abnormal disease causing form of protein, has an abnormal ß-pleated sheet (a type of amyloid) conformation

77
Q

Prion diesase does not contain _______ and is resistant to usual methods of denaturation (i.e., formalin fixation

A

nucleic acid

78
Q

Normal function and physciology of prion protein

A

PrPc = normal prion protein

Physiological function uncertain but likely participates in signaling pathways

Membrane sialoglycoprotein located on Gene (PRNP) on chr. 20

Normal prion protein is normally found in brain (neurons) and selected other organs

79
Q

Describe pathology of BSE and varient CJD

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