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Central Nervous System Pathology > CNS Infections > Flashcards

CNS Infections Flashcards

1
Q

Host response to Bacteria

A
  • Elicits neutrophilic & pyogenic response

Labs:

  • Neutrophils
  • Decreased CSF glucose
  • gram stain/culture to ID causative organism

Complications:

  • Death: herniation secondary to cerebral edmea
  • Hydrocephalus
  • Hearing Loss
  • Seizures
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2
Q

Host response to Viruses

A
  • generally elicits lymphocytes and activate microglials (the resident macrophages in the nervous system).

Labs:

  • Lymphocytes
  • Normal CSF glucose
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3
Q

Host response to Mycobacteria & Fungi

A
  • elicit granulomas, which is an aggregation of epithelioid histiocytes with multi-nucleated giant cells.

Labs:

  • Lymphocytes
  • Decreased CSF glucose
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4
Q

Host response to Treponemal organisms, especially syphilis:

A
  • elicits a special granuloma called a gumma
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5
Q

Routes of CNS Infection

A
  1. Hematogenous (most important):
    - Arterial: Heart (esp cardiac valves) & Lungs
    – Venous: Centripetal spread from veins
    of face
  2. Local extension (more chronic)
  3. Direct innoculation
    – Traumatic: Open head injury
    – Iatrogenic: Lumbar puncture; Surgery
  4. Retrograde spread from peripheral nervous
    system (PNS)
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6
Q

Meningitis

  • general definition
  • classic clinical symptoms
  • Dx
A

Inflammation of Leptomeninges (Arachnoid and pia matter) and CSF

Classic Triad:

  1. Headache
  2. Nuchal Rigidity
  3. Fever
    - Photophobia
    - Vomiting
    - Altered Mental Status

Dx: Lumbar Puncture (sample CSF) btw L4 & L5 (level of iliac crest)
- DO NOT PIERCE THE PIA MATER

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7
Q

Meningitis + Brain involvement

A

Encephalitis/Cerebritis

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8
Q

Meningitis + Spinal Cord

A

Myelitis

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9
Q

Meningitis + Spinal Nerve Roots

A

Radiculitis

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10
Q

Acute Pyogenic Meningitis

A
  • Leptomeninges infected by pus (PMN)-eliciting bacteria
  • Systemic Sx: Fever, chills,, anorexia, vomiting
    – Neurologic: Headache, photophobia, irritability, loss of consciousness, stiff neck
    – Infection progresses rapidly (septicemia)
    – Rapid/early diagnosis essential for
    patient salvage
CSF findings:
– ­Increased Opening pressure (lumbar tap)
– ­ Increased CSF cells (mostly PMNs)
– ­ Increased CSF protein
– Large decrease in CSF glucose
Causative agent:
Microscopy:
– Gram stain (bacteria)
– India ink prep (Cryptococcus)
 Serology:
– Antibodies against specific
microbial antigens
 Culture:
– Provides material for antibiotic
sensitivity studies
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11
Q

Waterhouse-Friderichsen syndrome

A
  • Acute Primary Adrenal Insufficiency due to adrenal septic hemorrhagic necrosis, with skin petechiae and systemic collapse

Associated with:

  • Neisseria meningitidis
  • Septicemia
  • DIC
  • Endotoxic shock
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12
Q

Common causative agents of Acute Pyogenic Meningitis in Neonates

A 
- – Group B streptococcus
– E. coli and other GNRs
– Listeria monocytogenes
- H. influenza
- Staphylococcus aureus
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13
Q

Common causative agents of Acute Pyogenic Meningitis in Children

A
  • Streptococcus pneumoniiae (pneumococcus)
    – Hemophilus infflluenzae type b
    • Among uniimmuniized: Neisseria meningitidis (meningococcus)
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14
Q

Common causative agents of Acute Pyogenic Meningitis in Adults

A
  • S. pneumoniae: All ages, sporadic
    – N. meningitides (meniingococcus): Young adults, epidemiic in crowded living conditions
    – Gram negative rods (E.. coli, Klebsiella, Pseudomonas)
    – L. monocytogenes
  • S.. aureus
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15
Q

Acute Aseptic Meningitis

A
  • “Aseptic”: No organism by Gram stain or
    (bacterial) culture of CSF
  • usually Viral: esp. Enteroviruses (70 serotypes): Polio, echo, coxsackieviruses
    – Less fulminant than acute pyogenic meningitis; w/ Spontaneous remission
CSF findings
– Normal to ­increased opening pressure
– ­mosttlly lymphocytes
– ­Increased protein
– NORMAL GLUCOSE
- Viral identification:  Serum Titer
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16
Q

Brain Abscess

  • Definition
  • causative organisms
  • Dx
A
  • Localized pus-forming infection of brain parenchyma
  • Multiple sources of infection: Hematogenous (cardiac, pulmonary); Local extension (oro-sino-naso-facial)

Common organisms in Immunocompetents:
- Staphylococcal and streptococcal bacteria
– Anaerobiic and microaerophilic species

Common organisms in Immunocompromised:

  • Toxoplasma gondi
  • Nocardia asteroides
  • L. monocytogenes
  • Gram negative bacteria, mycobacteria, fungi

Diagnosed by imaging and biopsy with culture:
– Potentially fatal without treatment
– Treated with surgery and antibiotics

Lumbar puncture rarely warranted; Contraindicated with ­ ICP
– CSF findings: Increased Openiing pressure; PMNs or lymphocytes, increased Protein; NORMAL GLUCOSE
- Negative cultures

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17
Q

Brain Abscess Morphology

A

Gross
- Early cerebritis (First 1-3 weeks): Hyperemic softened focus
– Development of purulent abscess: Suppurative cavity with fibrous capsule and surrounding
edema; Often based at gray-white
cortical junction

Microscopic:
– Central core of suppurative liquefactive necrosis
– Intermediate zone of proliferating granulation tissue (reticulin stain positive) –> Only instance of intracerebral fibrous proliferation, where fibroblasts are derived from granulation tissue blood vessel walls
– Outer ring of gliotic edematous brain

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18
Q

Subdural Empyema

A
  • Pus-formiing infection between dura and
    arachnoid, from Spread of skull/sinus infection
    – Organiized by fibroblasts from dura
    – Complication: Thrombophlebitis of dural
    venous sinus or bridging veins with cerebral
    venous thrombosis
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19
Q

Epidural Abscess

A
  • Pus forming infection between bone (skull,
    vertebra) and outer dural surface, Spreading from osteomyelitis or sinusitis
    – Spinal epidural abscess may compress spinal cord –> Surgical emergency requiring decompression/drainage
20
Q

Chronic Bacterial Meningoencephalittis

A
  1. Mycobacterial Infections
  2. Neurosyphilis
    3. Neuroboreliosis (Lyme Disease)
21
Q

CNS Mycobacterial Infections

A

Mycobacterium tuberculosis may infect meninges, parenchyma, spinal vertebrae (Pott Disease)

  • CSF findings: increased cells (mostly lymphocytes); increased protein; Normal or slightly elevated gllucose
  • Acid-fast bacteria on microscopy
  • M. tuberculosis on culture
  • Gross: cheesy caseating material at the base of the brain
  • Histo: typical granuloma with multi-nucleated giant cells, central caseation, and epithelioid histiocytes

M. avium-intracellulare may infect immunocompromised

22
Q

Neurosyphilis

A

Treponema pallidum may spread to meninges
- Early: limited to meninges
– Asymptomatic: CSF findings: Normal to ­ cells (lymphocytes); increased protein; NORMAL GLUCOSE
– Symptomatic: Aseptic meningitis presentation
- Secondary Dormant phase
- Late (tertiary) Phase:
- Meningovascular Syphillis: Involvement limited to CNS mesodermally-derived tissues (meninges + arteries); Meningeal gummas
- Parenchymatous Neurosyphillis: Involves mesoderm + neuroectoderm
- General Paresis of the Insane
- Tabes Dorsales: infection of dorsal roots & sensory ganglia of spinal nerves; result in Charcot Joint (loss of pain sensation)

23
Q

Gumma

A
  • Granulomatous tissue reaction of syphilis
  • like a granuloma, there is Necrosis, but with preservation of tissue reticulin
    – Plasma cells prominent
    – Occurs in meninges, including dura; May extend into brain cortex from meninges
    – May occur in brain parenchyma in late tertiary syphilis
24
Q

Neuroborreliosis

A
  • CNS infection by spirochete Borelia burgdorfi; Transmitted by Ixodes ticks

    Lyme disease
    – Multisystem disorder involving skin, cardiovascular
    system, joints, PNS, CNS with Variable manifestations: Aseptic meningitis, CN VII palsy, peripheral neuropathy,
    encephalopathy
    – Histo: Microglial activation (rod cells), granulomas, vasculitis
25
Q

Viral Meningoencephalitis

A
  • Def: Viral infection of meninges and brain parenchyma

All have:
– Perivascular and parenchymal mononuclear cell infiltrates; MICROGLIAL NODULE FORMATION, i.e., lymphocytes, plasma cells, monoctyes, macrophages, and microglia
– Microglial cell actiivation: Microglia transform into ROD CELLS
– Neuronophagia: Neuronal death and phagocytosis
– Gliosis

26
Q

Viral tropism

A
  • Targetiing of specific cell types or CNS regions by specific viruses

CNS cell types:
– Poliovirus: Motor neurons of spinal cord
and brainstem; anterior horns
– JC virus: targets Oligodendrocytes
– VZV, HSV-1 &2: Ganglion cells of dorsal root and cranial nerve ganglia

CNS regions:
– HSV-1: Medial temporal/inferior frontal lobes
– CMV: Subventricular region

27
Q

Latent Viruses

A

– Dormant viral persistence in specific CNS cell types
- VZV
- HSV-1,2
- Measles (SSPE)

28
Q

Transplacental passage of Viruses

A

“toRCH”

  • Rubella
  • CMV
  • HSV-2
29
Q

HSV-1 CNS Infection

A 
– Important cause of sporadic viral
encephalitis
– Involves CNS on primary infection
(lips, face) or by reactivation from
trigeminal (CN V) ganglion
– Targets:  Medial temporal lobe, limbic
regions
– Necrotizing, hemorrhagic infection with Intranuclear viral inclusions in
neurons and glia
30
Q

HSV-2 CNS Infection

A 
Adults
- Retrograde spread to CNS from
sacral dorsal root ganglia
- Aseptic meningitis in healthy adults
 Necrotiziing encephalitis in immunocompromised

Neonates
- Acquired during birth through vaginal canal with primary HSV-2 infection, or transplacentally
- Necrotizing encephalitis

31
Q

VZV CNS Infection

A 
– Childhood viral exanthem (Varicella)
- Latency established in dorsal root and
trigeminal ganglia
– Reactivation after many years with
anterograde axonal transport to skin
in dermatome distribution:  Herpes zoster (shingles)

– With primary infection or reactivation,
VZV may travel retrograde to spinal
cord/brain, especially in immunosuppressed, causing Encephalitis, Myeloradiculitis, or CNS vascular infection
– Micro: intranuclear inclusions in neurons
and glia

32
Q

CMV CNS Infection

A

− Intrauterine infection
• Targets periventricular regions with severe necrosis → periventricular calcification, microcephaly, CNS malformations
− Infection in immunosuppressed
• Encephalitis
• Retinitis
• Myeloradiculitis
− Cellular enlargement with prominent intranuclear (± cytoplasmic) inclusions in neurons, glia, endothelial cells

33
Q

Arbovirus CNS Infection

A

Arbovirus = ARthropod BOrne (commonly mosquitos, rarely ticks)
− Important causes of epidemic viral encephalitis
− Viruses endemic in birds and small mammals
• Transmitted by insects to horses and humans as incidental hosts
• Names reflect geographic distribution, insect vector, or incidental host
• West Nile virus: Birds normal reservoir; May cause meningoencephalitis when transmitted by mosquitoes to human as incidental host
• Incidence of human encephalitis coincides with season of vector (mosquito) activity, e.g., Summer through early fall

34
Q

CNS Poliovirus Infections

A

− Enteroviruses that infect gut and spread to blood
− A few strains can invade CNS from blood
• Neurovirulence
• Produce aseptic meningitis picture ± acute myelitis
− In myelitis, virus targets motor neurons of spinal cord (anterior horn cells) and brainstem
• Flaccid areflexic paralysis major clinical manifestation
• Respiratory muscle involvement may be fatal
− Vaccination has reduced world-wide incidence

35
Q

CNS Rabies Virus Infection

A

• Virus endemic in small mammals (Dogs, bats, wild animals) transmitted to human by bite of infected animal
− Virus inoculated at bite site
− Travels retrograde through axons of PNS to reach CNS
• Time to disease onset reflects bite distance from CNS
• Fulminant encephalitis
− Negri bodies: Neuronal cytoplasmic inclusions that are round or oval, pink; Seen best in Purkinje cells and hippocampal pyramidal neurons

36
Q

Subacute Sclerosing Panencephalitis (SSPE)

A

− Rare complication of early-age (<2 years) measles infection
− Non-productive (= i.e. no viral replication) CNS latency of altered measles virus after primary infection
− Onset of progressive behavior, cognitive, motor disturbances months to years after initial measles infection
− Encephalitis with widespread neuronal and white matter destruction
• Intranuclear inclusions in neurons, oligodendrocytes

37
Q

Progressive Multifocal Leukoencephalopathy (PML)

A

− Reactivation during a period of immunocompromise of latent JC polyomavirus infection acquired earlier in life
• Primary JC virus infection asymptomatic
• Latency in lymphocytes, kidney

− JC virus infects glia on reactivation
• Oligodendrocyte involvement → myelin loss
• Astrocyte involvement → enlarged bizarre astrocyte nuclei
− Progressive neurologic syndrome due to CNS white matter destruction
• Multiple foci of secondary demyelination in cerebral, cerebellar, brainstem white matter
• Viral intranuclear inclusions in oligodendrocyte nuclei

38
Q

CNS HIV Infection

A

• HIV may directly infect CNS early or late
− Early/seroconversion: Aseptic meningitis
− Late: Subacute meningoencephalitis: Direct HIV infection of cerebral microglia and macrophages (→ multinucleated giant cells) ± Infection of astrocytes, endothelial cells; Neurons destroyed by cytokines, blood-brain barrier failure
- results in Clinical dementia, motor disturbances, seizures

  • Direct CNS infection by HIV: More commonly seen in pediatric HIV/AIDS
  • Opportunistic CNS infections and malignancies: More commonly seen in adult HIV/AIDS
39
Q

CNS Rickettsial Infection

A
  • e.g., Rocky Mountain Spotted fever; Typhus
    − Unicellular organisms between viruses and bacteria
    • Possess cell walls, antibiotic-sensitive (like bacteria)
    • Live and reproduce only inside host cells (like viruses)
    − Spread by insect vectors: Ticks, lice, mites

− Infection of CNS vascular endothelium → Vasculitis, hemorrhage, thrombosis, infarction

40
Q

Fungal Meningoencephalitis

A

• Fungal infection of meninges ± brain parenchyma
− Associated with immunocompromise
− Hematogenous dissemination or local extension of extracranial (pulmonary, sinonasal) infection to CNS
− Common organisms: Candida albicans, Aspergillus fumigatus, Mucor species, Cryptococcus neoformans

Three infection patterns

  1. Chronic meningitis: Cryptococcus
  2. Septic vasculitis: Aspergillus, Mucor
  3. Parenchymal invasion: Candida, Cryptococcus
  • Inflammatory response granulomatous or minimal
  • Cryptococcus may elicit little inflammatory response to large organism burden
41
Q

Parasitic Meningoencephalitis

- CNS protozoan (unicellular) parasitic diseases

A

− Malaria, amebiasis, trypanosomiasis, toxoplasmosis

− Cerebral toxoplasmosis: Meningocerebral infection by Toxoplasma gondii
• Cat definitive T. gondii host
­ Sexual stage of parasite reproduction
• Human intermediate host
­ Acquires disease from food tainted by oocyst-containing cat feces →
­ GI cyst digestion and liberation of tachyzoites → tachyzoites infect GI macrophages → hematogenous and lymphatic dissemination of tachyzoites → CNS invasion

42
Q

Parasitic Meningoencephalitis

- CNS metazoan (multicellular) parasitic diseases

A

− Cysticercosis, echinococcosis
− Neurocysticercosis: Larvae of Tenia solium (pork tapeworm) encyst in human CNS
• Human (definitive host) ingests eggs meant for pig (intermediate host); Human functions as dead-end intermediate host

43
Q

CNS Toxoplasmosis

A

Two forms of CNS toxoplasmosis
− Intrauterine/neonatal infection (“ToRCH”)
− Primary/reactivation CNS infection in immunocompromised

Intrauterine infection
− Transplacental passage of tachyzoites during primary maternal infection
− Fetal meningoencephalitis: Targets subpial and subventricular regions; Widespread gray and white matter destruction
• Diffuse (contrast with subventricular [in CMV]) brain calcification, hydrocephalus, CNS malformations

CNS toxoplasmosis in immunosuppresion
− Toxoplasmosis abscess most common mass lesion in brain of AIDS patient
− Ring-enhancing cerebral abscess(es) gray/white cortical junction, deep gray matter
• ± Meningitis, vasculitis, retinitis
− Free tachyzoites and encysted bradyzoites on microscopy

44
Q

Transmissible Spongiform Encephalopathies: Infectious proteins
- Prion Disease

A

− Normal neuronal protein PrPc converted from usual alpha-helix isoform to beta-pleated sheet PrPsc
• Single aberrant molecule of PrPsc serves as template for conversion of other PrPc molecules (Cascade effect)
• PrPsc resistant to usual cellular degradation mechanisms and normal techniques of sterilization and tissue fixation
• Aberrant PrPsc in brain may arise spontaneously: Inherited amino acid substitutions in polypeptide sequence predispose PrPc to abnormal folding
• PrPsc accumulates in brain tissue
• Neuronal cell bodies and axons acquire vacuoles (spongiform change)
• Aberrant PrPsc does not contain nucleic acid (No DNA or RNA)

45
Q

Creutzfeldt-Jacob disease (CJD)

A
  • Rapidly progressive (weeks to few months) dementia with myoclonic jerks (myo = muscle + clonus = rapidly alternating contraction and relaxation)
  • Fatal in < 1 year
  • Widespread neuronal loss, gliosis, and spongiform change in brain gray matter
  • No inflammatory response
Variant CJD (vCJD)
•	BSE crossing species barrier from infected cattle to humans ingesting BSE-infected beef

Central Nervous System Pathology (15 decks)

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