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Neuropathology > Infections Diseases in the Nervous System > Flashcards

Infections Diseases in the Nervous System Flashcards

1
Q

Characteristic syndromes

Pattern of infection/typical agents

Bony coverings

A

Pattern of Infection
Osteomyelitis

Typical agents
Bacteria, fungi

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2
Q

Characteristic syndromes

Pattern of infection/typical agents

Meninges

A

Epidural/subdural empyema
Bacteria, fungi

Meningitis (leptomeningitis):

Acute purulent - Bacteria, fungi
Aspetic, Viral - Viruses, chemical agents, cancer,
Subacute/chronic - Some bacteria or fungi, viruses
Granulomatous - TB, syphilis, fungi, sarcoidosis

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3
Q

Characteristic syndromes

Pattern of infection/typical agents

Parenchyma

A

Cerebritis (Abscess)
Bacteria, fungi, parasites

Encephalitis
Bacteria, fungi, viruses, protozoa

Demyelinating encephalitis
 Some viruses (papovavirus)

Infectious vasculitis
Bacteria, fungi

Spongiform encephalopathies
Prion agents

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4
Q

Meningoencephalitis/myelitis/encephalomyelitis

def

A

MENINGOENCEPHALITIS: diffuse meningeal and parenchymal process

MYELITIS: localized to spinal cord, often immune-mediated process

ENCEPHALOMYELITIS: usually viral or immune-mediated process involving gray and white matter throughout nervous system

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5
Q

Routes of infection to the CNS

A

BLOODSTREAM (hematogenous) - most common route
DIRECT IMPLANTATION - traumatic or iatrogenic (surgical)
LOCAL EXTENSION - e.g., from skull, sinuses, middle ear
AXONAL TRANSPORT - used by some viruses
CSF PATHWAYS – often important means of dissemination

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6
Q

Pathogenesis of NS infections

Important immunologic and vascular considerations

A
  • Brain lacks lymphatics and formed lymphoid tissues. * Lymphocytes and monocytes normally circulate through CNS in small numbers.
  • Microglial cells serve as resident CNS macrophages and may enlarge or proliferate in response to CNS injury. Macrophages also come from blood-borne monocytes.
  • Blood-brain barrier may hinder access to CNS by therapeutic drugs.
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7
Q

Manifestations of infections

list

A
  • DIRECT TISSUE DAMAGE - may produce irreversible deficits
  • INFLAMMATORY EDEMA - mass effect, increased intracranial pressure
  • INVOLVEMENT OF BLOOD SUPPLY – ischemia/thrombosis —> infarction/hemorrhage
  • TOXIC EFFECTS - substances produced by infectious agent causing tissue damage or dysfunction
  • IMMUNOLOGIC DAMAGE - both direct and “innocent bystander” damage
  • COMMENSALISM - infectious agent persists in host with or without significant tissue damage and symptoms
  • NEOPLASTIC TRANSFORMATION - e.g., EBV is involved in pathogenesis of primary CNS lymphoma in HIV patients
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8
Q

Acute purulent leptomeningitis

def

A

acute infection in subarachnoid space caused by virulent bacteria, fungi, some protozoans

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9
Q

Acute purulent leptomeningitis

Acute manifestations include

A
  • non-specific, systemic: fever, nausea/vomiting, irritability, lethargy
  • signs of meningeal irritation (meningismus): nuchal rigidity, Brudzinski sign (passive flexion of neck → flexion of hip and knee), Kernig sign (starting from flexed knee/thigh, extension of knee is resisted)
  • direct CNS involvement: headache, photophobia, alteration of consciousness, seizures, focal localizing signs
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10
Q

Acute purulent leptomeningitis

Basic pathology

A

acute inflammation (neutrophils) in subarachnoid space: presence can be ascertained by examining CSF

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11
Q

Acute purulent leptomeningitis

CSF findings

A 
elevated pressure (200-500mm H2O) 
elevated protein (> 50mg/dl)
decreased glucose (often < 40mg/dl) 
leukocytosis (predominantly PMN’s) 
organism may be detectible by Gram stain or culture
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12
Q

Acute purulent leptomeningitis

Spectrum of organisms

A

spectrum of organisms causing acute purulent leptomeningitis varies with age and clinical circumstances, but common agents include:

a. bacteria: Streptococci, Staphylococci, Hemophilus, Neisseria, Gram negative rods, Listeria, anaerobes
b. fungi: immunosuppressed patients: Aspergillus, Candida, Mucor environmental exposure: Coccidioides, Histoplasma
c. other: Toxoplasma, ameba

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13
Q

Acute purulent leptomeningitis

Pathogenic sequence

A

primary colonization/infection elsewhere in body →
dissemination to CNS, usually hematogenous → infection of meninges → acute inflammatory response in SA space → consequences: brain swelling, focal damage,spread, etc. → outcome

NOTE: The inflammatory and overall response to infection may be modified by the immune status of the patient, the virulence of organism, effects of treatment, etc.

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14
Q

Acute purulent leptomeningitis

dx

A

Acute purulent leptomeningitis requires prompt diagnosis and treatment to prevent irreversible brain damage and optimize outcome.

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15
Q

Acute lymphocytic (viral, “aseptic”) meningitis

Def/causes

A

Definition: acute, usually self-limiting viral infection in subarachnoid space characterized by lymphocytic inflammation; syndrome is produced by

a. viral agents: common, includes common viruses causing upper respiratory or upper GI infections
b. some less virulent bacteria or other agents
c. non-infectious agents (cancer cells—“leptomeningeal carcinomatosis”, chemicals/drugs–“chemical meningitis”) can produce similar syndrome

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16
Q

Acute lymphocytic (viral, “aseptic”) meningitis

Clinical findings

A

Syndrome includes fever, headache, signs of meningeal irritation, lethargy, and rash but is milder than acute purulent leptomeningitis and usually does not result in significant alteration of consciousness.

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17
Q

Acute lymphocytic (viral, “aseptic”) meningitis

CSF findings

A

Elevated protein (mild)
Normal glucose
Leukocytosis (very early: a few PMNs, later: mostly lymphocytes)

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18
Q

Acute lymphocytic (viral, “aseptic”) meningitis

Clinical course

A

Clinical course is usually self-limited and mild with full recovery; although the syndrome is common, the diagnosis is often missed.

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19
Q

Chronic meningitis

def

A

chronic inflammatory process in leptomeninges due to relatively indolent/persistent agent (e.g., TB, meningovascular syphilis; sarcoidosis, some low-grade tumors, some foreign substances cause a similar picture)

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20
Q

Chronic meningitis

Clinical sx

A

Syndrome: often non-specific/non-localizing, slowly evolving (+/- headache, +/- stiff neck, low-grade fever, seizures, cognitive dysfunction)

21
Q

Chronic meningitis

pathology

A

commonly “basal meningitis”, with mononuclear inflammation, fibrosis, +/- granulomas (depends on agent), most prominent at base of brain

22
Q

Chronic meningitis

CSF findings

A

elevated pressure or blockage of CSF flow
elevated protein (100-200mg/dl or even higher with CSF flow blockage)
decreased glucose (less dramatic than in acute purulent meningitis)
leukocytosis (predominantly lymphocytes, monocytes)
agent (organism, tumor cell, etc.) may be detectible

23
Q

Chronic meningitis

pathophysiology

A

chronic inflammation in subarachnoid space leads to effects: progressive meningeal fibrosis, vasculitis, root/parenchymal involvement

consequences: hydrocephalus (non-obstructive),
↑ ICP, infarcts, focal deficits, cognitive decline

24
Q

Chronic meningitis

dx

A

Chronic meningitis can be very difficult to diagnose due to the relatively indolent chronic course and often non-localizing findings.

25
Q

Empyema and abscesses

Def/main patterns

A

Definition: acute/chronic localized purulent or necrotizing infections due to destructive bacteria, fungi, or other organisms fall into two main patterns:

  1. subdural/epidural empyema
  2. brain parenchymal abscess (“cerebritis”)
26
Q

Empyemas and abscesses

Clinical syndromes result from…

A
  1. infection/inflammatory process: fever, malaise, etc. 2. mass effect: headache, increased intracranial pressure
  2. localizing signs, if brain parenchyma is involved: e.g., seizures, focal deficits
  3. CSF findings may be minimal if lesion does not involve CSF pathways, and lumbar puncture may be contraindicated because of ↑ ICP.
27
Q

Empyemas and abscesses

Pathogenesis

Predisposing factors

A

a. infection elsewhere (especially osteomyelitis, dental infection, sinusitis, otitis media, endocarditis, congenital heart disease)
b. trauma to skull or spine, including surgery
c. presence of foreign body (catheter, gauze pad, bullet fragment, etc.)

28
Q

Empyemas and abscesses

Organisms/pathology

A

organisms: bacteria, fungi, others
pathology: localized area of tissue damage and acute/chronic inflammation surrounded by reactive layer; brain parenchyma may show prominent edema.

29
Q

Empyemas and abscesses

Complications include

A

mass effect may lead to increased ICP and herniation

abscess may rupture into ventricles or disseminate in subarachnoid space as acute purulent leptomeningitis

infection can spread to other organs or become systemic (sepsis)

focal permanent neurologic deficits may develop.

30
Q

Empyemas and abscesses

tx

A

May require drainage or surgical removal of lesion

31
Q

Acute viral encephalitis

def

A

Definition: acute viral infection of brain parenchyma +/- meninges

  1. most viral infections display tissue tropism, i.e., a particular virus infects a particular cell type: requires specialized cell surface receptors
  2. infections may be lytic or non-lytic to infected cell
32
Q

Acute viral encephalitis

Clinical presentation

A

Syndrome: prodrome of infection involving nervous system (fever, headache, malaise, etc.) followed by acute onset of neurologic symptoms including seizures, focal deficits, and alteration of consciousness: the specific syndrome varies with virus and specific location of infection

33
Q

Herpes Zoster

Agent/preferential site of involvement

A

Varicella-Zoster

Trigeminal or DRG, with pain, dermatomal distribution of vesicular rash

34
Q

Acute poliomyelitis

Agent/preferential site of involvement

A

Poliovirus

Anterior horn cell destruction leads to lower motor neuron paralysis

35
Q

Acute (meningo)encephalitis

acute necrotizing

Agent/preferential site of involvement

A

Herpes Simplex I
Medial temporal lobes (cowdry type A nuclear viral inclusions in infected cells)

CMV
Periventricular tissues (cytomegalic cells) occurs as congenital infection (recall TORCH syndrome) and in immunocompromised hosts
36
Q

Acute (meningo)encephalitis

Epidemic, seasonal

Agent/preferential site of involvement

A

Arboviruses

Deep gray nuclei, cortex; syndromes are variable; often transmitted by arthropod bites

37
Q

Acute (meningo)encephalitis

Rabies

Agent/preferential site of involvement

A

Rabies virus

Brainstem (cytoplasmic viral aggregates – Negri bodies – in infected cells); usually lethal

38
Q

Acute viral encephalitis

dx

A
  1. high index of suspicion based on history and exam
  2. CSF exam shows
    protein: mild-moderate increase
    glucose: normal
    leukocytosis: +/- PMN’s (early acute phase)
    lymphocytes (50-500/ul)
    NOTE: more destructive infections show more dramatic changes.
  3. electroencephalography (EEG): may help to localize lesion
  4. imaging studies (CT, MRI): help to localize and characterize lesion
  5. serology, culture, or PCR assay for specific virus, based on index of suspicion
39
Q

Acute viral encephalitis

pathogenesis

A
  1. infection of host with transport of virus to CNS.
    * hematogenous
    * some viruses use axonal transport
  2. host response cells: lymphocytes, plasma cells microglial cell proliferation is prominent edema and vascular response tissue or cellular (neuronal) necrosis
  3. outcome depends of virulence of virus, availability of appropriate anti- virals, degree of tissue damage, etc.
40
Q

Chronic (“slow”) viral encephalitis

Def/clinical findings

A

Definition: progressive viral infection, with prolonged incubation following initial exposure, insidious onset, slow progression of symptoms, due to conventional viral agents: NOTE: prion diseases are not included in this category

Syndrome: usually slowly progressive dementia or neurologic syndrome.

41
Q

Chronic (“slow”) viral encephalitis

Examples

A

AIDS dementia

PML: progressive multifocal leukoencephalopathy

SSPE: subacute sclerosing panencephalitis

TSP: tropical spastic paraparesis

42
Q

Chronic (“slow”) viral encephalitis

Agent/special features

AIDS dementia

A

HIV

Brain atrophy

Demyelination

Encephalitis with monocytes and giant cells

43
Q

Chronic (“slow”) viral encephalitis

Agent/special features

PML

A

Papovavirus (JC strain)

Infection and destruction of oligodendrocytes → progressive demyelination, usually in immunocompromised host

44
Q

Chronic (“slow”) viral encephalitis

Agent/special features

SSPE

A

Measles Virus

Diffuse brain involvement, children/adolescents, ? related to unusually early primary measles infection (this disease is very rare)

45
Q

Chronic (“slow”) viral encephalitis

Agent/special features

TSP (tropical spastic paraparesis)

A

HTLV-1

Progressive spastic leg weakness & sensory loss due to involvement of lower spinal cord; endemic or common in particular geographic areas

46
Q

Chronic (“slow”) viral encephalitis

Non-viral agents

A

Non-viral agents can also occasionally cause slowly progressive conditions such as syphilis (paretic neurosyphilis or tabes dorsalis) or borrelia (neuroborreliosis: Lyme disease).

47
Q

HIV infection

Neurologic syndromes

A
  1. acute lymphocytic meningitis: often during primary infection.
  2. chronic HIV encephalitis with progressive dementia (AIDS dementia)
  3. vacuolar myelopathy: uncommon degeneration of posterior and lateral columns in spinal cord in patients with chronic AIDS resembles subacute combined degeneration seen in vitamin B 12 deficiency.
  4. peripheral neuropathy (various types)
  5. inflammatory myopathy (polymyositis-like)
48
Q

HIV

Opportunistic CNS infections

A

Opportunistic CNS infections related to immunodeficiency common in poorly controlled HIV infection include

  1. Toxoplasma cerebritis
  2. PML
  3. CMV encephalitis
  4. Cryptococcus meningitis
49
Q

HIV

Other risk complications include…

A
  1. risk of developing primary CNS lymphoma
  2. drug toxicity to neuromuscular system from anti-retroviral drugs.
  3. Treatment of HIV sometimes results in an acute encephalitic syndrome due to return of immunologic function (immune reconstitution inflammatory syndrome –IRIS), often triggered by residual infections such as PML or Toxoplasma

Neuropathology (29 decks)

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