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Clinical Medicine > CNS infections > Flashcards

CNS infections Flashcards

1
Q

Types of CNS infections

A
  • meningitis: acute bacterial, aseptic, chronic
  • encephalitis
  • space occupying infectious lesions of CNS
  • prion diseases
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2
Q

Risk factors

A
  • immunosuppression: leukemia, HIV/AIDS, steroids, spleneectomy
  • cranial trauma: brain surgery, skull fx
  • peds: premature, perinatal complications
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3
Q

CNS infection organisms

A
  • bacteria
  • spirochetes
  • viruses
  • fungi
  • protozoa
  • prions (mad cow disease)
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4
Q

bacterial meningitis epidemiology

A
  • The age of the pt often suggest the likely etiologic organism
  • neonates (acquired during vaginal birth): stretococcus, group B, E.coli, listeria
  • 1 month to 4 yr: h. flu
  • 4 to 30 yr: neisseria meningitidis (meningococcal meningitis)
  • 30-65 yr: s. pneumo
  • over 65 yr: s. pneumo, GNR, listeria
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5
Q

Bacterial meningitis prevention

A
  • H.flu vaccine
  • strep pneumo vaccines
  • minningococcal vaccines
  • Rifampin (abx) for prophylaxis in contacts of those w/ meninogoccal infections
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6
Q

Bacterial meningitis transmission

A
  • exposure: birth canal and other routes
  • colonization: nasopharynx colonization
  • invasion: organism gains access and sustains itself in bloodstream
  • Bad bug breaches BBB
  • organism invades meninges, subarachnoid space and cerebrospinal fluid
  • once organism gains access the CSF is very vulnerable b/c the organism is in a protected area where there are few WBC
  • vein damage occurs causing proteins to seep in CSF
  • brain edema results from inflammation of meninges and CSF outflow
  • intracranial pressure rises and cerebral perfusion pressure drops
  • causes brain hypoxia, seizures, hydrocephalus, brain herniation, death
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7
Q

Bacterial meningitis clinical dx

MISSING ONE MORE SLIDE

A
  • neurologic emergency which evolves over hours or quicker
  • HA w/ nausea, vomting, anorexia
  • fever
  • stiff neck
  • malaise
  • rash: petechial rash
  • meningeal signs: nuchal ridigity (stiff neck), Brudzinski sign, Kernig sign
  • progression
  • change in mental status
  • LP reveals CSF abnormalities
  • LP contraindicated if elevated intracranial pressure (look for papilledema in eyes)
  • If ICP suspected: draw blood, start IV steroids and abx, get CT
  • No ICP do LP
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8
Q

CSF analysis

A
  • cell count
  • protein
  • glucose
  • opening pressure
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9
Q

Normal CSF analysis

A
  • cell count: 0-5 lymphocytes
  • protein: 15-45 mg/dl
  • glucose: 50-70% of blood glucose level
  • opening pressure: 70-180 mm H2O
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10
Q

Bacterial meningitis tx

A
  • must use bactericidal abx
  • causes cell lysis increased inflammatory meditors occur causing more problems
  • so give steroids to help with the abx
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11
Q

Bacterial CSF analysis

A
  • cloudy or grossly purulent
  • elevated protein: > 45mg/dL
  • low glucose: <40 mg/dL
  • high opening pressure
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12
Q

Viral meningitis/encephalitis

A
  • HA, fever, stiff neck, other nonspecific sx of viral infection
  • HSV, VZZ, enterovirus, HIV, CMV, equine encephalitis virus, WNV, St. Louis encephaltis
  • change in consciousness and localizing neurologic signs are rare in meninigits
  • encephalitis has more LOC changes and neurological signs
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13
Q

Viral CSF analsysis

A
  • Cell count: increased WBC (100-1000)
  • increased protein: >50 mg/dL
  • glucose: normal or slightly changed
  • opening pressure: normal to slightly elevated
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14
Q

Viral meningitis workup

A
  • CSF
  • CXR
  • TB skin test
  • syphilis/HIV serology
  • blood bacterial and viral cultures
  • PCR of virus from the CSF is becoming the test of choice due to it s sensitivity
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15
Q

Menigitis vs encecphalitis

A
  • menigitis: infection of meninges, normal cerebral function
  • encephalitis: infection of brain tissue itself, abnormalities in brain function (AMS, motor or sensory deficits, altered behavior, personality changes, speech or movement disorders)
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16
Q

Rabies encephalitis transmission

A
  • salivary transmission, usually via a bite from an infected animal
  • scratches, mucus membrane exposures with infected animals
  • recent cases show “casual contact” routes of infection
  • salivary exchange to health care workers
  • some cases linking to infected organ transplants
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17
Q

Rabies manifestations

A
  • tingling feeling at the site of inoculation
  • incubation period of 10 days to 1 year
  • acute viral syndrome with non-specific features
  • progresses to anxiety, agitation, delirum
  • spasms of the throat and frothing at the mouth at the sight of water, coma, and death
  • if pt has become symptomatic, death is nearly certain, even if treated
18
Q

Prophylaxis and tx of rabies

A
  • early prophylactic tx is needed to prevent death (when in doubt, treat)
  • in absence of early tx, virtually all cases are fatal
  • if pt presents w/ neurologic sx then supportive care only is given
  • prevention: vaccinate all pets and livestock
19
Q

West Nile virus

A
  • most affected are asymptomatic or mildly ill
  • if symptomatic, usually flu like sx
  • outdoor exposure at dawn or dusk increases risk for infection
  • other mosquito-borne viruses (St. Louis Western equine, Eastern equine) can also cause encephalitis
  • tx is supportive
20
Q

Chronic meningitis

A

-usually mycobacterial (TB) or fungal meningitis: can mimic viral
CSF findings: looks a lot like viral

21
Q

Chronic meningitis CSF findings

A
  • Cell count: increased WBC (100-1000)
  • protein: increased
  • glucose: decreased
  • opening pressure: moderately elevated
22
Q

Bacterial, chronic, and viral CSF finding

A
  • Bacterial: high neutrophils, low glucose, high protein, markedly elevated opening pressure
  • chronic: increased lymphocytes, low glucose, moderately elevated opening pressure
  • viral: increased lymphocytes, increased protein, increased glucose, normal opening pressure
23
Q

Manifestations of chronic meningitis

A
  • mild meningeal signs (stiff neck, HA)
  • disease evolves over a prolonged period, weeks or months
  • cranial nerve palsies
  • invasion into the brain
  • seizures
  • CSF rhinorrhea
  • chronic infections leads to arachnoid fibrosis, hydrocephalus, and underlying brain infarction
  • often fatal
24
Q

Chronic meningitis tx

A
  • culture is diagnostic
  • multiple drug therapy for meningeal tuberculosis
  • antifugal therapy for cryptococcal
  • fungal infections by direct extension from sinuses require debridement of involved areas and systemic antifungal therapy as dictated by antifungal susceptibility testing
25
Q

Cysticerocosis

A
  • causes by the larval from Taenia Solium, the pork tapeworm
  • transmission: obtained by eating the eggs of the tapeworm (not the larvae), associated w/ pica (dirt eating), poor handwashing, ingestion of T. solium eggs in contaminated water
26
Q

Neuro-cysticerosis

A
  • human is accidental intermediate host of the encysted larval form of the tapeworm
  • most sx due to cysticerci in the CNS
  • frequent causes of seizures in children
  • with very large infection, extensive brain swelling leads to herniation and death
  • in brain matter not just meninges
  • if they are not causing problems then just leave them alone
27
Q

Cysticercosis tx

A
  • antihelminthic drugs may agument sx due increased CNS inflammation that occurs as the larvae die
  • need to give steroids
  • may need seizure meds
  • albendazole or praziquantel are drugs of choice
  • treat only acute CNS disease
  • if you tx you end up w/ a lot of dead larvae and swelling and inflammation
28
Q

Toxoplasmosis

A
  • caused by parasite (toxoplasma gonii)
  • transmission:
    • ingesting raw beef
    • oral fecal contamination usually via ingestion of sporazoites from handling the litter of an infected cat
    • congential form: infected in utero through transplacental inoculation in the 3rd trimester
  • exposure while pregnant is bad for fetus (1st exposure only - if exposed prior not an issue)
29
Q

Toxoplasmosis disease manifestations

A
  • asymptomatic infection
  • respiratory disease
  • CNS infection: space occupying lesions, seizures, mental status changes, fever, focal neurologic defects
  • ocular infections
30
Q

Toxoplasmosis dx

A
  • serology IgM and IgG may be detected in CSF and serum
  • no culture commercially available
  • tissue biopsy demonstrates intracellular tachyzoites
  • MRI demonstartes RING ENHANCING LESIONS in the brain
31
Q

Toxoplamsosis tx

A
  • trimethoprim/sulfamethoxazole (septra/bactrim)

- long term prophylaxis may be needed for immunosuppressed pt

32
Q

Brain abscesses

A
  • caused by any number of bacteria, depending upon the cause of the infection
  • often seen as mixed infections of anaerobes and aerobes if oral/HENT primary source
  • GNR, s. aurea, coagulase negative staphlococci
  • fungi: cause disease by direct extension from sinuses
  • constant HA, stiff neck, possible focal neurological findings
33
Q

Brain abscess pathogenesis

A
  • infections start at non-CNS site and spread to CNS
  • may occur secondary to seeding by infected heart valve or other sources of sepsis
  • may occur by direct extension from abscessed teeth, otitis media, or sinus infection
  • may occur from peritoneal seeding
  • may occur from direct inoculation
34
Q

Brain abscess clinical manifestations

A
  • fever (low grade)
  • drowsiness
  • HA
  • focal neurological deficits
  • seizures
35
Q

Brain abscess course

A
  • indolent (slow) to fulminant (fast)
  • 75% have sx for 2 weeks or less
  • clinical picture: look for source
  • lung, ear, or sinus disease with signs of intracranial infection and seizures
36
Q

Brain abscess work up

A
  • CBC: typically normal WBC count
  • CT or MRI of the brain: localizes the abscess and determines the degree of capsule formation
  • LP is contraindicated
  • Aspiration of biopsy of abscess
37
Q

Diagnostic testing for CNS abscesses

A
  • MRI/CT scan show RING ENHANCING LESISONS
  • CSF exam may not be informative if the abscess does not communicate w/ the meningeal space
  • CT: guided FINE NEEDLE ASPIRATE of the abscess contents
38
Q

CNS abscesses tx

A
  • surgical drainage
  • abx therapy should be guided by susceptibility testing and gram stain morphology
  • intrathecal administration of drug may be required for adequate penetration into tissues
  • tx underlying cause of infection
39
Q

Brain abscess prognosis

A
  • 40-60% mortality rate
  • poor prognostic factors: delayed dx, ventricular rupture, fungal infection, coma, multiple and deep inoperable abscesses, inappropriate abx
40
Q

Prions

A
  • “protein infectious” causes
  • mode of infection unclear
  • “mad cow” disease is transmitted via eating infected nervous tissue
  • Kuru and Creutzfeldt-Jakob disease preceded mad cow disease
  • progressive encephalitis
  • no tx, bad prognoses

Clinical Medicine (19 decks)

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