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Neurosciences > Week 5: infectious diseases of the CNS (Commins and Landolph) > Flashcards

Week 5: infectious diseases of the CNS (Commins and Landolph) Flashcards

1
Q

List three symptoms or signs of acute meningitis.

A
  1. fever
  2. headache
  3. altered mental status
  4. lethargy
  5. signs of meningeal irritation, e.g. neck stiffness
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2
Q

List 3 complications of acute bacterial meningitis

A
  • edema of the brain
  • arteritis and phlebitis result in vascular thrombosis
  • hemorrhagic necrosis due to arterial or venous occlusion
  • pus accumulation at base of brain and in sulci, bathing cranial nerves, can result in permanent functional disturbances such as ocular palsies and deafness
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3
Q

What is the likely clinical outcome of acute viral meningitis and what type of inflammatory cells would you see? Where would they be located?

A
  • self limited
  • benigh
  • resolves without sequelae
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4
Q

What is the clinical signs/symptoms of chronic meningitis? List the most common etiological agents, and one common long term sequelae. What type of inflammatory response would you see in histology?

A
  • symptoms: fever headache, stiff neck, mental status change, cranial nerve deficits,
  • causes: TB and cryptococcus (in US)
  • generally no sequelae
  • histology: epitheliod histiocytes and giant cells surrounded by lymphocytes in TB, granulomatous response in cryptococcus also that is similar to TB
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5
Q

How does acute bacterial meningitis differ from a bacterial abscess in terms of clinical presentation?

A

Clincal:
-headache and fever
-confusion, possible aphasia, IV drug use
-mild papilledema
Other:
-abscesses require dead brain tissue to get a start, often associated with endocarditis causing emboli
-most cerebral abscesses present as masses
-abscess has a contrast enhancing ring on imaging

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6
Q

For acute viral encephalitis/encephalomyelitis, list 3 major symptoms, 4 main pathologic features, and 3 etiologic agents.

A

Symptoms
-tropism
-latency
-headache, fever, mental status change,
Path features
-perivascular lymphocytes
-microglial activation with microglial nodules
-neuronophagia (activated microglia and PMNs and lymphocytes surround sick and dying neuron)
Viral agents: HIV, CMV, HSV, arboviruses, polio, rabies

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7
Q

What is a Negri body?

A
  • viral inclusion (preference for Purkinje cell) in Rabies

- sharply defined, oval, eosinophic cytoplasmic inclusions

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8
Q

Is aspergillus an opportunistic infection? why does it appear as multiple soft areas with red brown discoloration on gross examination of an affected brain?

A
  • Affects immunosuppressed, esp transplant patients
  • necrosis and acute inflammation
  • affinity for blood vessels-destroys and has surrounding hemorrhage and necrosis
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9
Q

Is cystercercosis an opportunistic infection? How does a human get it? what is a typical symptom?

A

=pork tapeworm

  • not opportunistic
  • from eating ova from recalling contaminated water or food
  • symptoms: seizures, mass effects, obstruction of CSF, periventricular cystic lesions,
  • cysts usually found in gray mater, meninges, or ventricular system
  • illicit inflammatory reaction, develop granulation tissue, infection may become symptomatic when parasite dies
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10
Q

Define tropism of the polio virus in the CNS

A
  • acute stage: infiltrates anterior horns of the spinal corn

- selectively infects motor neurons in spinal cord and brain stem, rarely in cortex

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11
Q

How do people contract an arbovirus? Although variable, what are the 3 most typical histopathological features seen in the brain at autopsy of someone who dies of an arbo virus encephalitis? List 2 etiologic agents of subacute or chronic viral encephalitis.

A
  • virus alternates between mammalian or avian host and an insect vector
  • pathology: affects gray matter, no viral inclusions, looks like nonspecific acute viral encephalitis
  • causes of subacute/chronic viral encephalitis: measles, JC virus causing PML, HTLV, HIV,
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12
Q

How has effective antiretroviral treatment modified the natural history of HIV int rems of patient longevity, incidence of opportunistic infections, prevalence, and severity of neurocognitive dysfunction?

A
  • greatly reduced opportunistic infections

- milder neurocognitive problems

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13
Q

What is HIV encephalitis? What is it look like histologically?

A
  • HIV infects the brain directly via migration of infected monocytes, passes no to microglia
  • inflammatory mediators and neurotoxic viral proteins cause white matter and neuronal damage
  • histology: multinucleate giant cells, microglial nodules
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14
Q

What are the gross and histopathologic features of PML and how are they caused by the tropism of JC virus?

A
  • multifocal areas of softening, discoloration, and crumbling of white matter
  • staining for myelin with Luxol blue shows destruction of myelin
  • infected oligodendroglial enlarged with inclusions
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15
Q

List 3 opportunistic infections affecting the CNS in AIDS.

A

-CMV, toxoplasmosis, PML, mycobcteria

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16
Q

List 3 major ways a person can get a human spongiform encephalopathy.

A
  • transmitted through ingestion
  • inoculation of infected tissue
  • familial, e.g. sporadic CJD
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17
Q

Why do you not see much inflammation on histologic exam of a brain with a spongiform encephalopathy?

A

-there is no infectious agent involved

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18
Q

Explain how spongiform encephalopathies differ from viral encephalitis in terms of: how they are acquired, latency, causative agents.

A
  • caused by prions, misfiled protein

- long incubation periods but rapidly progression dementia

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19
Q

What are pathways in which pathogens spread to the CNS?

A
  1. Direct:
    - craniotomy and skull fracture: staph aureus and enterbacteraceae
    - via surgical shunt: S. epidermidis
  2. Neural (via axon transport): tetanus, rabies,
  3. olfactory: HSV, Naegleria fowleri
  4. Hematogenous: H. influenzae, S. pneumonaiae, Neisseria meningitidis, TB, fungi, rickettsiae, enteroviruses, arboviruses, HIV, plasmodium, tapeworm embryos
20
Q

Define meningitis.

A

A diffuse infection by bacteria, fungi, viruses, resulting in an inflammation of the pia-arachnoid meninges

21
Q

What pathogens are commonly responsible for bacterial meningitis in neonates? in childhood? in adults?

A
  • neonates: E coli, group B strep, Listeria (10% of cases, 50% of meningitis deaths)
  • post natal: H influenzae
  • adults: Neisseria meningitidis, Strep pneumoniae (epidemic)
22
Q

What are the causes of viral meningitis?

A

-enteroviruses, mumps, lymphocytic chorio meningitis, other/unknown

23
Q

What are the clinical manifestations of meningitis?

A
  • headache, fever, nuchal rigidity (neck stiffness on passive forward flexion)
  • Flexion of neck may cause reflex flexion of legs (brudzinski sign) and limit flexion of the knee (Kernig sign)
  • reduced consciousness, seizures in children
  • bacterial w/ bus around base of brain: CN palsies, CSF obstruction, hydrocephalus, vasculitis w/ brain infarct, multifocal neuro deficits
24
Q

What provides the most important diagnostic information for meningitis?

A
  • examination of CSF
  • acute bacterial infections: PMN cell response and reduction of CSF glucose
  • viral: modest mononuclear cell response, possible elevated CSF protein, CSF sugar normal or mildly decreased
  • Cryptococci: india ink, can see capsule
25
Q

What is the treatment for meningitis? What is the mortality rate?

A
  • treat with antimicrobial agents that cross BBB for bacterial meningitis
  • mortality for acute bacterial meningitis is 15%, with pneumonococcal meningitis, 30%
  • viral: symptomatic treatment only, disease is self limited
26
Q

Define abscess.

A

a focus of purulent infection, usually due to bacteria

27
Q

What is the etiology of brain abscesses?

A
  • contiguous focus of infection (ears, teeth, sinus) or by hematogenous spread from distant focus of infection of lungs or heart, particularly chronic purulent pulmonary disease, subacute bacterial endocarditis, cyanotic congenital heart disease
  • many brain abscess have mixed bacteria: mostly Streptococci, Staph aureus, Enterobacteria, and bacterioides are seen
28
Q

What is the pathogenesis of brain abscesses?

A

-thought to result from bacterial seeding of already devitalized tissue

29
Q

What are the clinical manifestations of brain abscesses?

A
  • primarily: headache, focal signs, seizures. often no fever. might be insidious
  • if focal signs present: CT or MRI done, abscess identified by hypo dense area (pus) surrounded by enhancing area representing neovascularization and edema around fibrous abscess wall
  • CSF usually sterile, bacteria diagnosis can be made only by culturing aspirate of abscess cavity
30
Q

What is the treatment for brain abscesses?

A

-treat with multiple antibiotics if poorly defined area of cerebritis is found
-if encapsulation present: IND, then determine specific bacteria
spinal epidural and cerebral or spinal subdural abscesses are surgical emergencies
-spinal epidural: rapid course, segmental pain along nerve roots, paresthesias below abscess, then irreversible paraplegia
-subdural: spread rapidly over wide area, causes septic thrombosis of bridging veins, hemiplegia, seizures

31
Q

Define encephalitis.

A

An inflammation of the brain, usually due to viruses tha produce wide spread intracellular infections

32
Q

What is the etiology of encephalitis?

A
  • many different viruses: enteroviruses, mumps, lymphocytic choriomeningitis–>mild
  • life threatening: HSV and arboviruses
  • rabies, but less common
33
Q

what are the clinical manifestations of HSV-1 encephalitis in a non neonate?

A

-focal signs over 1-2 weeks, headache and fever, hallucinations and bizarre behavior, focal seizures and hemiparesis, aphasia

34
Q

What are the clinical manifestations of arbovirus infections that cause encephalitis?

A

-more diffuse and acute disease, rapid depression of consciousness, greater frequency of generalized seizures, multi focal signs, may localize to temporal areas sometimes, producing signs similar to those of HSV encephalitis

35
Q

What are the CSF findings in acute encephalitis?

A
  • RBCs frequently found due to necrotizing pathology
  • elevated CSF protein, normal CSF sugar
  • PCR tests for HSV are sensitive
  • virus specific IGM present in spinal fluid for arboviruses
36
Q

In addition to CSF fluid examination, what else is useful in diagnosing HSV encephalitis?

A
  • EEG: periodic spikes and slow waves often localize to the infected temporal lobe
  • CT: shows attenuated area if medial temporal lobes, sometimes a mass effect
  • definitive diagnosis requires brain biopsy, look for inclusion bodies and stain for HSV antigens
37
Q

What is the treatment of encephalitis?

A
  • HSV: anti-viral therapy, acyclovir
  • some prevented by vaccines or controlled by reducing mosquito population
  • supportive care
38
Q

What is the progression of disease of secondary syphilis, caused by Treponema pallidum?

A

-1.5-3 months: mild meningitis
-3-5 years: acute meningovascular inflammatory disease leading to stroke
8-10 years: progressive dementia
10-20 yrs: chronic arachnoiditis involving posterior roots of spinal cord
-vasculitis, parenchymal involvement, chronic arachnoidnitis

39
Q

What is the progression of disease of Lyme borreliosis caused by Borrelia burgdorferi?

A
  • mild meningitis and facial palsy after initial rash and systemic symptoms
  • 1-9 months later: subacute or recurrent meningitis, encephalitis, cranial nerve palsies, peripheral neuropathies
40
Q

What is the CNS involvement in HIV infections?

A
  • acute meningitis, demyelinating polyneuritis (Guillain-Barre syndrome) occasionally occurs at time of zero-conversion
  • long seropositive period: recurrent meningitis and motor neuropathies
  • AIDS demential, myelopathy, painful sensory neuropathy frequent in later years
41
Q

-What is progressive multifocal leukoencephalopathy (PML) caused by?

A
  • JC virus, papovavirus
  • immunodeficient patients: subacute or chronic demyelinating disease of the brain with multi focal signs, leading to death in <6 months
42
Q

What is Rubella virus associated with after congenital infection?

A

-chronic encephalitis

43
Q

How do prions cause CJD?

A
  • prions are misfolded proteins that aggregate into amyloid rods and is secreted
  • accumulates for years(~30yrs)
44
Q

What are the parasites that produce acute encephalopathy or meningitis?

A
  • malaria (plasmodium falciparum)-cerebral malaria
  • amebiasis-ameobas
  • trichinosis-caused by trinella spirals or park tapeworm
45
Q

What parasitic infections that produce chronic neurological disease?

A
  • African trypanosomiasis: sleeping disease
  • chronic cerebral granulomas: schistosoma japonicum
  • abscesses by toxoplasma gondii in immunodef
  • cystocercosis caused by larval from of taenia solium
46
Q

What is the neuro disease caused by measles virus?

A
  • subacute sclerosing panencephalitis (SSPE)

- progressive dementia with myoclonus years after measles

47
Q

What are the CSF findings of septic meningitis, aseptic (viruses), and aseptic (fungi)?

A

bacterial: PMNs, >100mg/dl protein, <45-85 glucose
normal: 15-45 protein, 45-85 glucose

Neurosciences (59 decks)

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