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Neurology > Neuroinfectious Diseases > Flashcards

Neuroinfectious Diseases Flashcards

1
Q

Meningitis general

A

Defined as inflammation of the meninges

Leptomeninges (arachnoid and pia - these are more common) vs pachymeninges (dural inflammation)

White cells in CSF are always present in meningitis, except in systemic leukopenia

Presentation: HA, neck stiffness, fever if infectious

Many causes: Bacteria, virus, fungi, parasites, chemicals, blood, cancer

Note: Arachnoid and dura are technically not part of CNS (except in optic nerve)

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2
Q

Meningitis CSF profile

A

Differs by cause

Bacterial: Mainly PMNs, High protein, Low glucose, Positive gram stain 60-70%

Viral: Mainly lymphs, High protein, Normal glucose, Negative gram stain

Fungal and mycobacterial: Mainly lymphs, High protein, Low glucose, Negative gram stain

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3
Q

Complications of meningitis

A

CN issues (they run in subarachnoid) - CN 8 (deafness) associated with H Flu

Stroke (inflammation of circle of willis)

Death (cerebral edema or sepsis)

Coma/seizure

Adrenal infarction (N. meningitides)

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4
Q

Approach to meningitis

A

Things to consider doing:

1) BCx
2) LP - cell count w/diff, protein, gluc, cx
3) ABx**
4) Steroids
5) CT? Not needed if normal neuro exam and not immunosuppressed. Mass effect secondary to cerebral edema is what we worry about before an LP (this would cause herniation). We would see neuro signs though.

Random Note: Papilledema is not a contraindication to LP. Not always a great indication of increased ICP bc it takes a couple of days to develop it.

Give ABx ASAP. Everyone gets Ceftriaxone + vancomycin and maybe ampicillin (older, babies, immunocompromise)

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5
Q

Meningitis signs

A

Meningeal signs:

1) Neck pain elicited by flexion-extension, not side-to-side movement
2) Kernig sign - neck pain when patients knee is passively extended with the hip flexed at 90 degrees
3) Brudzinski sign - Patient flexes knee and hips when the neck is passively flexed while supine

HA (worsening and persistent)

Many of the signs and symptoms of meningitis are due to the immune response to it so people who are immunocompromised may not have any symptoms

Note: CNS has very poor immune surveillance (We have the BBB so we never really needed good immune surveillance in the CNS). We can have abscess with no fever or signs or anything. Whenever CNS needs help, BBB must break down then it’s TOO MUCH HELP.

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6
Q

Encephalitis general

A

1 = viral. #1 viral = HSV1

Defined as infection of the brain parenchyma itself

May be diffuse or focal

Presents with fever, HA and personality or mental status changes. Seizures and focal deficits commonly seen too. These personality and seizure features are due to its propensity for the temporal lobe (behavior and memory changes too)

Tends to be fatal

Few days prodrome/behavioral changes

However, 90% of encephalitis is not from HSV1

33% of encephalitis are AI-mediated. #1 = NMDA. #2 = Anti-hu (small cell lung)

Ovarian teratoma with a bit of nervous system tissue - immune system attacks it. This is NMDA

Tx = steroids, Rituxumab, IVIG, remove teratoma/germ cell tumors

Therapy aims to prevent antibodies from entering CNS

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7
Q

Myelitis

A

Defined as infection of the spinal cord. 3 patterns.

1) Transverse myelitis - disease at one or more segments with dysfunction below that level. #1 cause is demyelinating, AI. Can also be VZV. Everything can be explained by single lesion - inflammation at single segment
2) Slowly progressive spastic paraparesis - diffuse process. No real findings on MRI. Always r/o B12 deficiency. Non-localizing but progressive UMN dysfunction. Can’t find 1 single level. #1 is HIV or HTLV1 (caribbean)
3) Acute flaccid paralysis (AHC infection). Asymmetric LMN dysfunction - #1 = polio. Can be west nile, enterovirus D68, colorado, west coast

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8
Q

Polyradiculitis

A

Defined as infection of the nerve roots as they exit the spinal cord

Presents with shooting radicular pain, usually with weakness in the muscles supplied by the roots as well.

May mimic GBS except CSF is quite different

Consider Lyme or leptomeningeal carcinomatosis

GBS has sensory AND motor involvement. 3-4d feet tingling symmetric ascending paralysis. By 28d patient should be improving. This is a disease of nerve roots that are demyelinating. Chunks of myelin fall into CSF (increased protein). MRI might show enhancement of nerve roots.

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9
Q

How do bacteria gain access to the nervous system?

A

3 ways

1) Hematogenous spread - bacteremia, embolization of infected tissue
2) Direct extension - ears, sinuses, skull, penetrating trauma
3) Iatrogenic source - ventricular shunts, surgical, LP

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10
Q

Causes of bacterial meningitis

A

Neonates

1) GBS
2) E Coli
3) Listeria

Children and Adults

1) Meningococcal meningitis
2) Pneumococcal meningitis

Older adults and immune suppressed

1) Gram negatives
2) Listeria
3) Pneumococcal

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11
Q

Clues for S. pneumo meningitis

A

Associated with otitis media, sinusitis, skull fx. More frequent in alcoholics

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12
Q

Clues for N. meningidities meningitis

A

Can occur with meningococcemia, causing a rash and adrenal crisis

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13
Q

Clues for H flu meningitis

A

Unvaccinated children with nasosinal infections

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14
Q

Clues for Listeria meningitis

A

Elderly and immunocompromised

Rare listeria rhombencephalitis mimics other brainstem encephalitis (GAM, Bickerstaffs etc)

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15
Q

Treatment of bacterial meningitis - general

A

Antibiotics should be empiric at first then changed to specific one based on cultures

All patients should get a 3rd generation cephalosporin

Immunocompromised, young (less than 12w) and old (more than 50) should get ampicillin

Vanc in any patient with outside entry to CSF (skull fx, post NSGY), also in immunocompromised and in areas with high resistance of pneumococcus to PCN

Ceftazidime for gram neg coverage in immunocompromised patients

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16
Q

Specific treatment of various bacterial sources of meningitis

A

1) S.pneumo - PCN sensitive gets PCN-G. PCN resistant gets CTX
2) N.mening - PCNG, ppx close contacts
3) HFlu - PCNG
4) Listeria - Ampicillin and gentamicin
5) Others - should always consult local hospital resistance charts for proper coverage

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17
Q

Bacterial brain abscess general

A

Aerobes account for 67%. Strep milleri is 50% (sinuses, dental), S.aureus 25% (think trauma/surgery), Gram negative bacilli 25%

Anaerobes account for 33%. Associated with pulmonary and otitic sources. Bacteroides, Fusobacterium, Clostridium.

Not uncommon to find mixed flora

Generally presents as a subacute illness. Fever due to systemic infection but only seen in 50%. HA in 50-70%. Seizures in 30-40%, usually partial. Focal deficits based on location of lesion. Signs and symptoms of high ICP may be there.

May NOT have classic systemic signs and symptoms

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18
Q

Diagnosing an intracranial abscess

A

Elevated WBC in about half

LP should be avoided as 20-30% will deteriorate and usually only helps with dx with an associated ventriculitis or meningitis

MRI with gad is in the imaging of choice

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19
Q

Intracranial abscess treatment

A

Combined NRSGY and medical approach

ABx are given for 4-6w. Classic regimen is PCN-G + chloramphenicol. Modern is Cefotaxime + metronidazole. Consider vanc in postop/trauma.

AEDs should be considered. Up to 90% of survivors develop epilepsy.

Steroids reserved for increased ICP

20
Q

Mycobacterial infections - TB

A

Caused by myco TB and rarely M. bovis

1% of TB cases involve the CNS. TB meningitis, tuberculoma, Pott’s disease.

one third of world’s population is infected with TB. 4000 cases of TB meningitis occur in the US every year.

May occur during primary infection or reactivation, spreading to the CNS hematogenously.

21
Q

Spirochetal infections - neurosyphilis

A

Caused by T.pallidum

Five CNS syndromes:

1) Acute syphilitic meningitis
2) Cerebrovascular syphilis
3) Tabes Dorsalis
4) General paresis
5) Gummatous neurosyphilis

Tx involves high dose IV PCN-G

22
Q

Viral meningitis

A

Most common cause of acute asceptic meningitis

Usually consists of an acute, benign monophasic illness which is self-limited

Usually remits in 7-10d

Similar symptoms as bacterial meningitis but less intense.

  • fever, HA, nuchal rigidity
  • cranial neuropathies and ICP elevations are not expected in contrast to bacterial**
  • Alteration of consciousness, seizures, focal neuro signs suggest coexistent encephalitis
23
Q

Viral meningitis etiologies

A

1) Enterovirus - 85-95%. Echovirus, coxsackie
2) Arboviruses - flavivirus, reovirus, bunyavirus
3) Herpesviruses - HSV2 way more common than HSV1
4) HIV - acute seroconversion. HIV can get into CSF at this time. Look for HIV if you also see things like LAD
5) Mumps
6) Lymphocytic choriomeningitis virus (LCM)

Note: HIV doesn’t infect neurons. It targets microglia and neuronal damage is caused by cytokine-mediated processes

24
Q

Viral encephalitis etiologies

A

Herpes viruses - HSV1, HSV2 in neonates, VZV, EBV, CMV, HHV6, Herpes B

Paramyxoviruses - Measles (SSPE), Rubella, Mumps, Nipah, Hendra

Retroviruses - HIV, HTLV1

Papovaviruses - JC

Arboviruses - Alphaviruses (EEE, WEE, VEE), flavivirus (WNV, St Louis, Japanese), Reovirus (colorado tick), Bunyaviruses (LaCrosse)

Rhabdoviruses

25
Q

HSV1 viral encephalitis

A

Usually temporal lobe

Can cause encephalitis, meningitis, or myelitis

Most common cause of sporadic, fatal encephalitis in the USA

Accounts for 10% of encephalitis

Causes a focal encephalitis with predilection for inferior frontal and medial temporal lobes

Mortality 70% untreated. 20% with rapid treatment (acyclovir)

Even with treatment, 70% of survivors develop permanent deficits

Most cases are probably due to reactivation of latent infection in trigeminal ganglia

26
Q

Viral myelitis - polio

A

Incubation period 7-14d

8% develop meningitis

1% develop acute flaccid paralysis - asymmetric and develops over 3-5d

CSF with early PMNs then lymphocytes, elevated protein

PCR is available

Last WT case in USA 1979

Vaccine: Sabin is live attenuated. Salk is whole killed

27
Q

Viral ganglionitis - VZV

A

Herpes zoster begins with radicular pain followed in 3-4d by a painful vesicular rash in a dermatomal distribution. Most common is T5-12.

CN in 15% - zoster ophthalmicus, Ramsay-Hunt

CSF lymphocytic pleocytosis

Rash lasts 10-14d

Pain typically lasts 4-6w

May get post-herpetic neuralgia 1m after shingles

Tx for neuropathic pain: Gabapentin and pregabalin work on presynaptic VGCCs. TCAs (like nortriptyline, anticholinergic side effects). Duloxetine.

28
Q

HIV related neurologic disease

A

Caused mainly by HIV - AIDS dementia complex, HIV vascular myelopathy, HIV neuropathy, HIV myopathy

Caused by immunosuppression - progressive multifocal leukoencephalopathy, cryptococcal meningitis, cerebral toxoplasmosis, primary CNS lymphoma

Caused by antiretrovirals - myopathy from AZT and some D drugs, neuropathy

29
Q

CNS fungal syndromes

A

1) subacute to chronic meningitis - CSF usually demonstrates elevated opening pressure, lymphocytic pleocytosis, elevated protein and decreased glucose. Eosinophils should suggest C. Immitus and neutrophils should suggest Aspergillus or Mucor (for these 2 hyphae invade the brain).
2) Encephalitis
3) Abscesses
4) Cerebral infarctions

30
Q

Cryptococcus neoformans (fungal infections)

A

The most common cause of fungal meningitis

C.neoformans is a ubiquitous organism and enters the body via inhalation. It is a true yeast.

Most common presentation is a subacute meningitis

Can also present with focal deficits and seizures from abscess formation (cryptococcoma), either micro or large

Diagnosis can be rapid with the latex antigen agglutination test

Classically, the dx is made by staining capsule with india ink

Tx with amphotericin B plus flucytosine followed by fluconazole

Send the crypto antigen (quick, sensitive, specific)

31
Q

Fungal infections - aspergillus

A

Organism is transmitted by inhalation

It can cause a hypersensitivity pneumonia

CNS disease occurs in the immunosuppressed and mainly manifests as a brain abscess, parenchymal granuloma or a vasculitis by direct vessel wall invasion. Particularly affects the posterior circulation. Reports of cord compression from thoracic epidural disease exist.

Treatment with amphotericin followed by itraconazole

32
Q

Zygomycetes rhizopus (Mucor)

A

Diabetes and acidosis are risk factors in addition to the usual ones

Infects via paranasal sinuses causing a destructive rhino-orbital-cerebral invasion invading through bone and via vascular channels producing local destruction and infarction. Can cause cavernous sinus thrombosis.

Black discharge from the nose is a clue. Nonseptate hyphae are seen on pathology.

Treatment is with radical surgical debridement and amphotericin B

33
Q

parasitic infections - neurocysticercosis

A

Caused by Taenia Solium, the pork tapeworm

Most common cause of seizures in tropical countries!

Humans acquire the tapeworm by eating pig meat that has a cyst containing the scolex. The tapeworm then sets up shop in the human host and produces proglotids which are excreted in the stool. These hosts are asymptomatic.

Neurocysticercosis is caused by fecal-oral transmission of the eggs in the proglotid which then hatch to form larvae which invade the intestinal wall and hematogenously spread to the brain where cysts are formed. This is why even people who never eat pork can acquire the infection.

Seizures are the most common sign.

Calcified lesions causing seizures are not treated with cysticidal therapy as this is simply an old scar

The therapy for active disease is praziquantel or albendozol, and surgical resection of a dominant lesion if it is causing ICP issues.

“1 pig 2 people”

34
Q

Cerebral malaria - parasitic infections

A

Defined as malaria with unexplained unconsciousness lasting more than 30 minutes

Caused by Plasmodium falciparum and very rarely P. vivax. Occurs in 0.5-1% of patients with P.falciparum

Pathogenesis related to increased cytoadherence of the infected RBC leading to stasis in small cerebral arterioles

Cerebral symptoms start with seizures, acute delirium or coma. Also, focal neuro deficits can be seen from infarctions.

CSF is basically normal which helps exclude other causes of acute febrile encephalopathies.

The diagnostic test of choice is peripheral blood smear looking for the schizont-infected RBCs. The sensitivity is low for each specimen so three should be negative before dx is excluded.

Mortality without treatment is 100%

Treatment is quinine IV then PO. Resistance to chloroquine is widespread.

Best treatment is prevention with chemoprophylaxis usually with mefloquine.

35
Q

Toxoplasmosis - protozoal infections

A

1) Primary infection
Generally asymptomatic

10-20% have fever, LAD and a rash

Rarely can present as a meningoencephalitis with CSF pleocytosis. Glucose is normal.

Ocular infection can occur with primary infection as a focal necrotizing retinal vasculitis

2) Reactivation
Seen almost exclusively in immunocompromised patients, esp HIV when CD4 below 200.

Presents as a mass lesion with HA and focal deficits

On CT/MRI has a ring enhancement

Treated with sulfadiazine and pyrimethamine

ppx with TMP/SMX

“First ocular then brain”

36
Q

Acute Disseminated Encephalomyelitis (ADEM)

A

Acute, uniphasic syndrome probably caused by immune-mediated inflammatory demyelination

Often associated with immunization, vaccination, or postviral illness

Can be postinfectious complication in 1 in 400 - 1 in 2000 people with measles, 1 in 600 mumps, 1 in 10000 varicella, and 1 in 20000 rubella patients.

Can also be after diphtheria (tetanus), pertussis, and rubella

Multiple neuro signs and symptoms reflecting compromise of brainstem, spinal cord, cerebrum, optic nerves, and cerebellum. Symptoms appear suddenly 1-3w after the infection and can include HA, nausea, vomit, confusion, and can progress to obtundation and coma.

Patients can also have hemiparesis, hemisensory compromise, ataxia**, optic neuritis, transverse myelitis, seizures, myoclonus, and memory loss. When ADEM follows mumps the disease usually presents with cerebellar ataxia

37
Q

ADEM pathophys

A

Probably T-cell mediated autoimmune disease targeting myelin/oligodendrocyte antigens, possible myelin basic protein.

Viral infection causing subsequent downreg of CD4 positive suppressor T cells, activating myelin-reactive T-helper cells has been implicated

38
Q

ADEM pathology

A

Perivenular inflammatory myelinopathy with engorgement of veins in the white matter of the brain. There is perivascular edema with significant mononuclear infiltration, primarily lymphocytes and macrophages.

Primary findings is pervenular demyelination with relative sparing of axons.

39
Q

ADEM diagnosis

A

Primarily focuses on clinical presentation of a uniphasic illness.

CSF findings can be abnormal but are not specific (mononuclear pleocytosis, mildly high protein)

MRI shows hyperintense white matter, T2 weighted signals and enhancement on T1 weighted images. Lesions vary in size bc of significant associated edema. Lesions described are rather extensive and symmetric or asymmetric and more often located in peripheral subcortical cerebral white matter.

Lesions in the thalamus are more often described in ADEM than MS and can be a useful finding

To differentiate from MS - ADEM has clear timeline of feeling well for a few weeks following a viral illness

40
Q

Prognosis in ADEM

A

pretty good.

25% will subsequently relapse though. If so, suspect MS

41
Q

Treatment of ADEM

A

Management is supportive and symptomatic

Controversy over IVIG and plasmapheresis

If severe, maintain fluid and lyte balance, avoid pneumonia, UTI, and decubitus ulcers

IV steroids shorten duration

42
Q

Argyl Robertson pupils

A

Small pupils that constrict when focusing but fail to constrict when exposed to bright light (accommodate but do not react)

Tabes Dorsalis

43
Q

Confirming diagnosis of Tabes Dorsalis

A

LP for VDRL

CSF shows:
Elevated protein up to 200, lymphocytic pleocytosis less than 400, CSF VDRL positivity and elevated IgG synthesis

44
Q

Tabes Dorsalis clinical features

A

10-20y after infection

1) hyporeflexia
2) Sensory impairment
3) Pupillary changes
4) Cranial neuropathy
5) Dementia or psych symptoms
6) Positive Romberg
7) Intermittent pain of arms and legs
8) Ataxia
9) Gait disturbance
10) Loss of position sense
11) Impaired vibratory and position sense
12) Lancinating pain
13) Bowel dysfunction/bladder dysfunction

45
Q

Treating neurosyphilis

A

IV penicillin G

If allergic, Doxy BID for 28d then ceftriaxone qd for 14d

46
Q

Tests to confirm toxo

A

Serum IgM and IgG titers for Toxo gondii

LP to evaluate for PCR of T gondii

47
Q

Imaging CNS lymphoma vs Toxo

A

CNS lymphoma - single ring enhancing lesion

Toxo - multiple ring enhancing lesions

Neurology (14 decks)

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