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NMSP Exam 1 > Cerebrovascular Infections > Flashcards

Cerebrovascular Infections Flashcards

1
Q

Common causative agents for bacterial meningitis? (Acute)

  • Infants
  • Unvaxxed 2mo-2yo
  • Young adults
  • Older adults
A
  • Infants: E coli and GBS
  • Unvaxxed young: HiB
  • Young adults: Neisseria meningitidis
  • Older adults: Streptococcus pneumoniae and Listeria monocytogenes
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2
Q

Common causative agents for bacterial meningitis? (Chronic)

A

Mycobacterium tuberculosis

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3
Q

Common causative agents for viral meningitis?

A
  • Enterviruses
  • Influenza species
  • Lymphocytic choriomeningitis virus
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4
Q

Common causative agents for abscesses?

A

Streptococci and staphylococci

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5
Q

Common viral causative agents for encephalitis? (encephalitic syndromes)

A
  • HSV-1,2
  • CMV
  • HIV
  • JC Polyomavirus (progressive multifocal leukoencephalopathy)
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6
Q

What are 4 routes that CNS infections are spread?

A
  • Hematogenous (most common)
  • Direct implantation (trauma or congenital malformations like meningomyelocele)
  • Local extension (sinuses, teeth, etc)
  • PNS (viruses like rabies, herpes)
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7
Q

How often is there a complete exchange of CSF

A

Every 3-4 hours

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8
Q

How does TB invade CNS?

A

Seeding CSF from subepidural or submeningeal granulomas

Side note: There ARE lymphatics in epidural space, not in rest of CNS

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9
Q

How do HSV simplex and zoster invade CNS?

A

Produce latent infection of sensory ganglia, replicate in Schwann cells, ascend from periph to the CNS within sensory nerves

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10
Q

How does the rabies virus invade CNS?

A

Binds at or near ACh receptors at NMJ & ascends to the CNS via motor nerves

Side note: Do NOT need to get bit to get rabies

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11
Q

What are anatomic considerations with capillaries that are pertinent to CNS infections? (i.e. how to molecules move across)

What is something to note about immunoglobulins, complement, and antibiotics?

A
  • Caps do not have fenestrations, molecules move across foot processes mainly by active transport and lipid solubility
  • Blood brain barrier

Relative impermeability to immunoglobulins, complement, and antibiotics

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12
Q

What are the 5 main types of meningitis?

Examples of each

A
  • Meningoencephalitis
  • Chemical: Non-bacterial irritant in subarachnoid space like rupture of cyst
  • Acute pyogenic: Bacteria
  • Aseptic: Virus
  • Chronic: TB, spirochetes, Cryptococcus
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13
Q

What can accelerate cerebral edema in response to infection?

What can slow it down?

A

Accelerated by products released by both living bacteria and antibiotic-lysed bacteria

Slowed and reserved by corticosteroids

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14
Q

Symptoms of meningitis?

Specialty tests?

How long does disease process take?

A

Sx: H/A, meningeal irritation, high fever, confusion, coma

ST: Kernig, Brudzinski

Full syndrome usually develops within several days but could take a few hours with a fulminant course

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15
Q

Where on the brain does pneumococcal meningitis usually present?

A

Densest over convexities near sagittal sinus (sulci)

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16
Q

Where on the brain does H. flu meningitis usually present?

A

Basal location

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17
Q

What is focal cerebritis?

A

Inflammatory cells infiltrate walls of veins & extend into brain substance

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18
Q

What can phlebitis lead to?

A

Venous thrombosis & hemorrhagic infarction of underlying brain

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19
Q

What can leptomeningeal fibrosis lead to?

A

Hydrocephalus

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20
Q

What can pneumococcal meningitis lead to?

A

Chronic adhesive arachnoiditis

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21
Q

What are some complications of bacterial meningitis?

A
  • Seizures
  • Encephalitis
  • Hearing loss, blindness, paralysis
  • Fulminant esp w meningococcemia
  • Waterhouse-Friderichsen syndrome: Rash over body, hemorrhagic adrenals
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22
Q

What gram-stain and shape is N. meningitidis?

A

Gram - diplococci

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23
Q

What gram-stain and shape is S. pneumoniae?

A

Gram + diplococci

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24
Q

What gram-stain and shape is H. flu?

A

Gram - pleomorphic

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25
Q

What gram-stain and shape are S. aureus, S. epi, and streptococci?

A

Gram + cocci

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26
Q

What gram-stain and shape is E. coli?

A

Gram - bacilli

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27
Q

What features does bacteria in CSF have?

A
  • Cloudy or turbid
  • Inc neutrophils
  • Dec glucose
  • Inc protein
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28
Q

What features do viruses in CSF have?

A
  • Clear, colorless
  • Inc lymphocytes
  • Nml glucose
  • Moderate inc in protein
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29
Q

What are 7 things that inc risk for meningitis?

A
  • Age <5yo or >60yo
  • DM
  • Immunosuppression/HIV
  • Contiguous infection (sinusitis)
  • IVDU
  • Bacterial endocarditis
  • Sickle cell anemia
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30
Q

Common bacterial pathogen for acute meningitis is the pt has an immunocompromised state?

A
  • S. pneumoniae
  • N. meningitidis
  • L. monocytogenes
  • P. aeruginosa (CF pts)
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31
Q

Common bacterial pathogen for acute meningitis is the pt has a basilar skull fracture?

A
  • S. pneumonia
  • H. flu
  • Group A beta-hemolytic strep
32
Q

Common bacterial pathogen for acute meningitis is the pt has head trauma (post neurosurg)?

A
  • S. aureus (from skin)
  • S. epidermidis (from skin)
  • P. aeruginosa
33
Q

Common bacterial pathogen for acute meningitis is the pt has CSF shunt

A
  • S. aureus (from skin)
  • S. epidermidis (from skin)
  • P. aeruginosa
  • P. acnes
34
Q

What are sx of an abscess?

What does CSF show?

What are possible complications?

Tx?

A

Progressive focal neurological deficits w/ s&s of inc ICP

CSF: High WBC, high protein, normal glucose

Complications: Herniation, abscess rupture w ventriculitis or meningitis, venous sinus thrombosis (fatal)

Tx: Surgical drainage and abx

35
Q

What is a subdural empyema? What can it do to bridging vessels? What happens with dura?

A

Bacterial or fungal infection of skull bones or sinuses spread to subdural space (arachnoid and subarachnoid usually not affected)

  • Can cause thrombophlebitis of bridging vessels which can lead to infarct
  • Causes thickened dura
36
Q

What is an extradural abscess a/w? What can this cause? (emergency)

A

Usually a/w osteomyelitis

-Extradural abscess of the spine may cause cord compression (neurosurgical emergency)

37
Q

Clinical manifestations of N. meningitidis?

A

Rapidly progressive septicemia w fever, hypoTN, DIC, petechial and purpuric lesions

Waterhouse-Friderichsen syndrome:

  • Purpura fulminans: Hemorrhagic skin lesions which progress to gangrene in distal portions of limbs
  • Hemorrhagic infarct of adrenal glands
38
Q

Chronic meningitis:

  • Sx
  • CSF
  • How dx is made
  • Common pathogens
A
  • Sx: Fever, H/A, lethargy, confusion, N/V, stiff neck
  • CSF: Elevated protein, lymphocytes, low glucose
  • Dx is made if sx and CSF abnormalities persist or progress for a period of at least 4 weeks
  • TB, neuroborreliosis, neurosyphilis

Note: Though TB is bacterial, still has lymphocytic proliferation

39
Q

Chronic meningitis: Mycobacterium TB diffuse meningoencephalitis

What is the appearance? Where does is normally appear on the brain?

What is Obliterative endarteritis? What is a tuberculoma?

A
  • If it gets into subarachnoid space, becomes gelatinous or has fibrinous exudate
  • Predilection for base of the brain (arachnoiditis); obliterates cisterns & encases cranial nerves (hydrocephalus and CN sx)
  • Obliterative endarteritis: Inflamm infiltrates vessel walls; intimal thickening; arterial occlusion & infarct
  • Tuberculoma: Well-circumscribed intraparenchymal mass; central caseous necrosis; inactive lesions may calcify

Note: Always get a culture in addition to a smear

40
Q

Chronic meningitis: Borrelia burgdorferi

How do you get it?

What are some sx and what is the timeline?

What can this cross react with?

A
  • Neuroborreliosis (Lyme disease)
  • Neuro sx follow characteristic rash by ~4wks
  • CN palsies and peripheral neuropathies
  • CSF w antibodies
  • Abs can cross react w infection mono, RA, SLE, syphilis
41
Q

What are 3 disorders that treponema pallidum can cause?

A
  • Meningovascular neurosyphilis
  • Paretic neurosyphilis
  • Tabes dorsalis

Note: Pts often show mixed picture, most often combo of tabes dorsalis & paretic disease (aka taboparesis)

42
Q

How common is it for treponema pallidum to become neurosyphilis and what increases the risk?

A

Only about 10% of untreated pts develop

- HIV inc the risk d/t impaired cell-mediated immunity

43
Q

What part of the brain does meningovascular neurosyphilis affect? What 2 things does it do to the brain?

A

Chronic meningitis involving base of the brain (variable convexities & spinal leptomeninges)

  • Causes communicating hydrocephalus
  • Causes obliterative/Heubner endarteritis
44
Q

How quickly does paretic neurosyphilis set in and what mental defects are a/w it? What is a phrase a/w this?

What is granular ependymitis?

A

Insidious but progressive mental defects a/w mood alterations (delusions of grandeur) that end w severe dementia (aka general paresis of the insane)
- Perivascular iron deposits

Proliferation of subependymal glia under damaged ependymal lining (a/w communicating hydrocephalus)
- Granulations lose ability to reabsorb

45
Q

What is tabes dorsalis? What are some sx?

A

Damage to sensory nerves (loss of myelin and axons) in the dorsal roots

  • Impaired joint position sense & resultant ataxia
  • Loss of pain sensation
  • Joint damage (Charcot joints)
  • “Lightning pains”
  • Absence of DTRs
46
Q

Aseptic (Viral) meningoencephalitis

  • Clinical picture
  • Cause
  • CSF
  • Tx
A

Absence of recognizable organism in pt w meningeal irritation, fever, & alterations of consciousness w relatively acute onset

  • Often caused by enteroviruses
  • Less fulminant than pyogenic meningitis
  • CSF: Lymphocytes, mod inc in protein, glucose normal
  • Tx: Usually self-limiting; supportive care
47
Q

How do viruses reach CNS in meningitis and encephalitis?

A
  • Often hematogenous

- Reach CNS thru nerves (like olfactory & trigeminal)

48
Q

What are sx of west nile involving the spinal cord?

CSF?

A

Polio-like syndrome w paralysis

CSF: Initially shows neutrophilic pleocyotsis which rapidly converts to lymphocytes, protein elevated, glucose normal

49
Q

What are two things that histology might show w west nile in the spinal cord?

A

Neurophagia: Single-cell neuronal necrosis w phagocytosis of the debris

Microglial nodules: Small aggregates around foci of necrosis

50
Q

What are sx of HSV-1 encephalitis?

What is a feature of what it physically does to the brain?

Where does it most commonly act?

What type of inclusions can you see?

A

Alterations in mood. memory, behavior

Causes necrosis and hemorrhage in inferior and medial temporal lobes

Shows Cowdry Type A intranuclear viral inclusions in neurons and glia

51
Q

When do we see HSV-2 encephalitis?

What does is physically do to the brain?

A

in 50% of neonates born by vaginal delivery to women w active primary HSV

Acute hemorrhage and necrosis

52
Q

Where does herpes zoster stay during latent phase?

A

Sensory neurons of dorsal root or trigeminal ganglia

Reactivation limited to dermatome

53
Q

What is postherpatic neuralgia syndrome?

A

Persistent pain as well as painful sensation following nonpainful stimuli

54
Q

Who gest CMV infections?

Where does it localize?

A

Fetuses and immunosuppressed (HIV)

Localized in paraventricular subependymal regions

55
Q

What happens in utero with CMV infections?

A

Periventricular necrosis -> severe brain destruction -> microcephaly & periventricular calcification

56
Q

Where does poliomyelitis affect in the nerve roots? What does it cause?

A

Anterior horn motor neurons and causes flaccid paralysis w muscle wasting & hyporeflexia

May extend to posterior horns & occasionally produces cavitation

57
Q

What is post-polio syndrome?

A

Develops 25-35 years after resolution of inital illness; prgressive weakness w decreased muscle mass & pain

58
Q

How long does rabies incubate?

How does it travel from wound site into nervous system?

Sx?

Inclusion seen in rabies?

A

1-3 months depending on distance of wound to brain

Ascends along periph nerves from wound site

CNS excitability; violent motor responses, flaccid paralysis, resp center failure, hydrophobia

Inclusion: Negri bodies

59
Q

What happens in HIV aseptic meningitis during acute phase?

A

Perivascular inflammation & some myelin loss

60
Q

What happens in HIV aseptic meningitis during chronic phase?

A

Microglial nodules w multinucleated giant cells

61
Q

What happens to the white matter in HIV aseptic meningitis?

A

Loses myelin (pallor), axonal swelling, gliosis

62
Q

What is IRIS?

A

Immune reconstitution inflammatory syndrome: Paradoxical deterioration after starting antiviral therapy

63
Q

What is HAND?

A

HIV-Associated Neurocognitive Disorders: Mild to florid cognitive changes, persisting despite effective tx

64
Q

What is a cancer that HIV is associated with?

A

Primary CNS lymphoma (EBV + B-cell tumor)

65
Q

What virus causes progressive multifocal leukoencephalopathy?

What does it infect and what is the major effect of that?

Who does it mainly infect?

A

JC polyomavirus

Infects oligodendrocytes and causes demyelination of subcortical areas; dec number of axons

Infects immunocompromised individuals

66
Q

What pathogen causes subacute sclerosing panencephalitis (SSPE)?

What early childhood infection can cause this?

What are some sx>

A

Paramyxovirus

Causes cognitive decline, spasticity of limbs, seizures
- Widespread gliosis & myelin degeneration w viral inclusions and neurofibrillary tangles

Children or non-immunized adults that had prev measles (rubeola) infection

67
Q

What 4 species often cause fungal meningoencephalitis?

A

Candida albicans, mucor species, aspergillus fumigatus, cryptococcus neoformans

68
Q

Which fungal meningoencephalitis pathogen is a/w DM?

A

Mucormycosis

69
Q

Which fungal meningoencephalitis pathogens commonly cause vasculitis?

A

Mucormycosis & aspergillosis (sometimes candida)

70
Q

Which fungal meningoencephalitis are endemic?

A

Histoplasma capsulatum, coccidiodes immitis, blastomyces dermatitidis

71
Q

Which fungal meningoencephalitis pathogens cause parenchyma infections?

A

Candida and cryptococcus

72
Q

What is cryptococcus meningitis a/w?

A

AIDS

73
Q

Who does toxoplasmosis gondii affect?

Where in the brain does is affect?

Histology?

A

HIV or immunocompromised, pregnant

Causes brain abscesses located near the grey-white junction of cerebral cortex and deep grey nuclei; ring-enhancing lesions

Histo: Central foci of necrosis, petechial hemorrhages surrounded by inflam, vascular proliferation

Free tachyzoites & encysted bradyzoites???

74
Q

Name 6 prion diseases

What is the spongiform change in these?

A
  • CJD
  • Gerstmann-Straussler-Scheinker syndrome
  • Fatal familial insomnia
  • Kuru
  • Scrapie
  • Bovine spongiform encephalopathy

All rapidly progressive with prion protein PrP

Spongiform change is intracellular vacuoles in neurons and glia

75
Q

CJD

What brain changes do we see?

What is a unique sx?

A

So rapid (7mo survival) that there is little, if any, gross evidence of brain atrophy

Shows startle myoclonus

76
Q

What will the Kuru plaque in vCJD stain with?

A

+ Congo red and + PAS

77
Q

Survival time for fatal familial insomnia?

A

Less than 3 years

NMSP Exam 1 (9 decks)

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