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Neuropathology > Infections Diseases in the Nervous System > Flashcards

Infections Diseases in the Nervous System Flashcards

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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

Study These Flashcards
A

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

21
Q

Chronic meningitis

pathology

Study These Flashcards
A

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

22
Q

Chronic meningitis

CSF findings

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

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

25
Empyema and abscesses Def/main patterns
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
Empyemas and abscesses Clinical syndromes result from…
1. infection/inflammatory process: fever, malaise, etc. 2. mass effect: headache, increased intracranial pressure 3. localizing signs, if brain parenchyma is involved: e.g., seizures, focal deficits 4. CSF findings may be minimal if lesion does not involve CSF pathways, and lumbar puncture may be contraindicated because of ↑ ICP.
27
Empyemas and abscesses Pathogenesis Predisposing factors
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
Empyemas and abscesses Organisms/pathology
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
Empyemas and abscesses Complications include
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
Empyemas and abscesses tx
May require drainage or surgical removal of lesion
31
Acute viral encephalitis def
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
Acute viral encephalitis Clinical presentation
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
Herpes Zoster Agent/preferential site of involvement
Varicella-Zoster | Trigeminal or DRG, with pain, dermatomal distribution of vesicular rash
34
Acute poliomyelitis Agent/preferential site of involvement
Poliovirus | Anterior horn cell destruction leads to lower motor neuron paralysis
35
Acute (meningo)encephalitis acute necrotizing Agent/preferential site of involvement
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
Acute (meningo)encephalitis Epidemic, seasonal Agent/preferential site of involvement
Arboviruses | Deep gray nuclei, cortex; syndromes are variable; often transmitted by arthropod bites
37
Acute (meningo)encephalitis Rabies Agent/preferential site of involvement
Rabies virus | Brainstem (cytoplasmic viral aggregates – Negri bodies – in infected cells); usually lethal
38
Acute viral encephalitis dx
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
Acute viral encephalitis pathogenesis
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
Chronic (“slow”) viral encephalitis Def/clinical findings
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
Chronic (“slow”) viral encephalitis Examples
AIDS dementia PML: progressive multifocal leukoencephalopathy SSPE: subacute sclerosing panencephalitis TSP: tropical spastic paraparesis
42
Chronic (“slow”) viral encephalitis Agent/special features AIDS dementia
HIV Brain atrophy Demyelination Encephalitis with monocytes and giant cells
43
Chronic (“slow”) viral encephalitis Agent/special features PML
Papovavirus (JC strain) Infection and destruction of oligodendrocytes → progressive demyelination, usually in immunocompromised host
44
Chronic (“slow”) viral encephalitis Agent/special features SSPE
Measles Virus Diffuse brain involvement, children/adolescents, ? related to unusually early primary measles infection (this disease is very rare)
45
Chronic (“slow”) viral encephalitis Agent/special features TSP (tropical spastic paraparesis)
HTLV-1 Progressive spastic leg weakness & sensory loss due to involvement of lower spinal cord; endemic or common in particular geographic areas
46
Chronic (“slow”) viral encephalitis Non-viral agents
Non-viral agents can also occasionally cause slowly progressive conditions such as syphilis (paretic neurosyphilis or tabes dorsalis) or borrelia (neuroborreliosis: Lyme disease).
47
HIV infection Neurologic syndromes
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
HIV Opportunistic CNS infections
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
HIV Other risk complications include…
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

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