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IDMM > CNS infections > Flashcards

CNS infections Flashcards

1
Q

What are the possible causes of meningitis?

A

Bacteria: S. pneumo, N. meningitidis, GBS, H. influenzae, Listeria

Viral: Enterovirus (95%), Herpesvirus (VZV, HSV)

Fungal: Coccidiodes immitis, Crytococcus neoformans (immune compromise ONLY)

Mycobacterium tuberculosis

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2
Q

What are the possible routes of entry for a pathogen into the CNS?

A

Blood–>CSF (meningitis)

Blood–>brain (encephalitis)

Local invasion (bacteria)

Nerve invasion (VSZ, HSV)

Direct inoculation (surgery)

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3
Q

What is the prevalence of bacterial and viral meningitis?

A

Viral: 11-27/100 000

Bacterial: 3/ 100 000 **viral is 4-8 times more common

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4
Q

What pathogens are more likely to cause neonatal meningitis vs. paediatric or adult meningitis?

A

Neonatal: GBS is most likely (can be caused by others too)

Paeds + adult: S. pneumo, N. meningitidis are most common. Others can cause it too.

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5
Q

What is the basic pathophysiology of meningitis?

A

Pathogen causes inflammation in the CSF–> hydrocephalus–> increased intracranial pressure–> decreased cerebral perfusion

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6
Q

What is Kernig’s sign, Brudzinski’s sign and jolt accentuation?

A

Kernig’s sign: supine patient, hips flexed at 90 degrees, when you try and extend the knees there is pain/resistance.

Brudzinsky’s sign: passive flexion of the neck causes flexion of the hips +/- knees

Jolt accentuation: ask the patient to rotate head side to side (shake head “no”) 2-3 times per second. If the headache worsens this is a positive sign.

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7
Q

What time is year is more likely for a case of viral meningitis? Bacterial?

A

Viral: summer/fall

Bacterial: no seasonality

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8
Q

What kind of meningitis gives a rash? What kind of rash is it classically?

A

Menningicoccal meninigitis: petechial rash on the limbs, advances to purpura.

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9
Q

When/where would you see fungal meningitis?

A

Coccidiodes immitis: in the southwest US. 1% of infections progress to this.

Cryptococcus neoformans: occurs in immune deficient hosts.

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10
Q

When/where would you see tuberculous meningitis?

A

In areas with a high prevalence of TB. Most are associated with TB infection elsewhere or miliary TB, but this may not always be detectable

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11
Q

What are indications for doing a CT before doing a lumbar puncture?

A

-if there is neurological involvement, or history of neurological problems, or high intracranial pressure (papilledema)

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12
Q

What are the signs and symptoms of meningitis? What is the classic triad? Can viral and bacterial meningitis be differentiated based on S/S?

A

Classic triad: nucal rigidity, altered mental status, fever.

Symptoms: headache, photophobia, nausea, rash, lethargy

Signs: kernig’s, brudzinski’s, jolt accentuation

**viral and bacterial cannot be differentiated based on symptoms, but viral meningitis tends to be milder**

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13
Q

What is the empiric therapy for meningitis?

A

ceftriaxone + vancomycin +/- ampicillin +/- dexamethasone

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14
Q

What are the CSF characteristics of viral and bacterial meningitis? (cell #, WBC differential, protein, glucose, Gram stain, culture, PCR)

A
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15
Q

What are the basic principles of diagnosis and treatment in meningitis? (flowchart..)

A
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16
Q

How to differentiate between meningitis and encephalitis?

A

Since encephalitis is inflammation of the brain parenchyma, abnormalities in brain function will definitely be present (e..g mental status, sensor deficits, change in behaviour or personality).

17
Q

Define meningitis, encephalitis, and meniogoencephalitis

A

Meningitis: inflammation of the meninges

Encephalitis: inflammation of the brain parenchyma

Meningoencephalitis: inflammation of both

18
Q

What are the causes of encephalitis?

A

Infectious

viral

  • infectious (_HSV, _VZV, CMV, EBV, enterovirus, measles, arboviruses, mumps, rubella, polio, rabies, west nile)
  • post-infectious encephalitis (Acute disseminated encephalomyelitis)

non-viral

  • bacterial (syphillis, TB, Borellia (ticks))
  • fungal (cryptococcus, toxoplasmosis in immunecompromised)
  • Parasitic (African trypanosomiasis, Naegleria fowleri–>ameoba that lives in warm, fresh water)

Non- infectious

  • tumours
  • vasculitis
  • drug-induced
  • trauma
  • auto-immune (Lupus, Behcets)
  • etc..
19
Q

What encephalitis pathogens do the following point to:

  • Bats
  • Birds
  • Cats
  • Mosquitos
  • Ticks
  • Unpasteurized milk
A

Bats: rabies
Birds: west nile

Cats: toxoplasmosis

Mosquitos: west nile, other arboviruses, plasmodium
Ticks: Borellia (lyme disease)
Unpasteurized milk: Brucella, Listeria monocytogenes

20
Q

In a patient with suspected infectious encephalitis, what questions are important in the history? Why?

A

Travel history (e.g. Africa -> plasmodium, African trypanosomiasis)

Sexual history (syphillis)

Animal/Insect exposures (bats, cats, birds, insects)

Unpasteurized food (unpasteurized milk products)

Season of the year (seasonality of some agents)

Age (west nile)

Vaccination history (measle, mumps, VZV)

21
Q

Mnemonic for encephalitis differential

A

HE’S LATIN AMERICAN

Herpesviridae

Enteroviridae (esp. polio)

Slow viruses (JC virus, prions)

Syphillis

Legionella/Lyme disease/Lymphocytic meningoencephalitis

Aspergillus

Toxoplasmosis

Intracranial pressure

Neisseria meningitidis

Arboviridae

Measles/Mumps/Mycobacterium TB/Mucor

E. coli

Rabies/Rubella

Idiopathic

Cryptoccocus/Candida

Abscess

Neoplasm/Neurocysticercosis

22
Q

What is ADEM?

A

Acute desseminated encephalomyelitis

  • Immune mediated
  • usually happens post viral infection
23
Q

What is the general pathophysiology of encephalitis?

A

Inflammation of the brain parenchyma. Can be necrotizing, can cause hemorrhage, can destroy neurons and cause brain damage.

24
Q

Clinical manifestations of encephalitis. Can infectious and non-infectious be distinguished based on the symptoms?

A
  • Fever
  • Headache
  • Cognitive dysfunction (speech, memory, behaviour, personality, confusion, agitation, unresponsiveness)
  • Seizures
  • +/- rash

Cannot distinguish infectious from non-infectious based on clinical manifestations alone.

25
Q

On the physical exam of a patient with encephalitis, what do the following indicate:

  • flaccid paralysis –>encephalitis?
  • tremors (eyelids, tongue, lips, extremities)
  • hydrophobia, aerophobia, pharyngeal spasm
  • vesicular rash
A
  • flaccid paralysis –>encephalitis–> west nile
  • tremors (eyelids, tongue, lips, extremities)–> west nile
  • hydrophobia, aerophobia, pharyngeal spasm–>rabies
  • vesicular rash–>VZV
26
Q

Diagnostic approach to encephalitis

A
  • S/S
  • Physical exam
  • LP with CSF analysis (including PCR, culture)
  • Serology
  • MRI (temporal lobe inflammation typical of HSV)
27
Q

Treatment of HSV encephalitis

A

acyclovir

28
Q

What is a brain abscess? How does it occur? What are predisposing factors?

A

A focal, encapsulated collection of suppurative fluid. Local or hematogenous spread of a pathogen.

There are usually one of more predisposing factors:

  • immunesuppresion
  • chronic cardiopulmonary conditions (e.g. congenital heart abnormalities)
  • penetrating head trauma
  • local infection (osteomyelitis, otitis media, sinusitis)
  • distant infection
29
Q

What are the causative agents of brain abscess in an immuncompetent and immunocompromised host?

A

Immunocompetent: polymicrobial (Strep anginosus, Anaerobes, S. aureus)

Immunocompromised: parasite (toxoplasmosis), fungal (crytptococcus neoformans, mycobacterial (TB))

30
Q

What are the clinical manifestations of brain abscess?

A

headache localized to side of abscess

fever

focal neurologic deficit (depending on location in brain)

mental status changes

seizures

nausea

nuchal rigidity (sometimes)

31
Q

Diagnostic approach to brain abscess

A
  • S/S
  • Physical exam
  • CBC may have elevated WBC
  • CT/MRI
  • LP is contraindicated because of focal headache and focal neurological involvement
32
Q

What is the treatment for a brain abscess?

A
  • aspiration of abscess
  • empiric antibiotics (ceftriaxone +metronidazole +/- vancomycin OR meropenem +/- vancomycin)
  • glucocorticoids if swelling (dexamethasone
33
Q

How common are brain abscesses?

A

Not common! Only 0.3-1.5/100 000 people per year

34
Q

What is an epidural abscess? How common is it?

A

A focal collection of suppurative fluid in the epidural space (outside the dura, between the dura and the bone).

Classified as intracranial and spinal (9x more common)

Very uncommon (2-25/100 000 hospital admissions)

35
Q

What are the risk factors for epidural abscess?

A
  1. Epidural manipulation (catheter in obstetrics, paraspinal injections)
  2. Contiguous bony or soft tissue infections
  3. bacteremia
  4. trauma
36
Q

What are the main pathogens involved in epidural abscesses?

A

S. aureus (63%)

gram negative bacilli (16%)

streptococci (9%)

37
Q

What is the general pathophysiology of a spinal epidural abscess?

A
  • the abscess compresses the spinal cord, cuts off blood supply.
  • bacterial toxins mediate inflammation
38
Q

What is the clinical presentation of an epidural abscess?

A

Classic triad:

  • fever
  • back pain
  • neurological deficits
39
Q

What is the diagnostic approach to an epidural abcess?

A
  • S/S: the triad
  • physical exam
  • diagnostic imaging (MRI is best, then CT, then Xray)
  • Analysis of abcess fluid
  • Empric antibiotic treatment (ceftriaxone +metronidazole + vancomycin)
  • Surgical decompression and drainage

IDMM (33 decks)

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