Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

19 Cards in this Set

  • Front
  • Back
Microbial access to CNS
-Only direct route
-Most common route
-Different possible route for spinal abcess
-Only direct route is the olfactory epithelium. Also potential rare innoculation from trauma or surgery

-Most common route is hematogenous spread

-Spine epidural space has lymphatics that are a possible route for production of spinal abcess
Cellular and anatomic tropisms
-3 viral cellular tropisms
-1 viral anatomic tropism
-Poliomyelitis: anterior horn motor neurons
-PML (JC virus): oligodendrocytes
- HIV: microglia

-Herpes encephalitis: temporal lobe
CSF diagnosity utility
-2 sites of infection that will show in CSF
-Lumbar puncture CSF can be cultured
-Can reveal infections in subarachnoid space or leptomeninges
Hydrocephalus as a complication
-Impairs CSF resorbtion in arachnoid villi. Can follow chronic meningitis

-Leads to dilation of ventricular system rostral to the obstruction; confined CSF can act as a mass lesion
-Caused by compression from abcess, mass, hemmorrhage or caused by ventricular inflammation.
2 big predisposing host characteristics to CNS infection
-Diabetes mellitus
Process naming according to tissue
-Brain parencyhma
-Spinal cord
-Ventricular System
Process naming according to tissue
-Encephalitis (viral) / Cerebritis (bacterial/fungal)
-Ventriculitis (often extension of meningitis or parenchymal abcess)
3 Types of Meningitis
1. Acute bacterial meningitis
2. Acute Viral meningitis
3. Chronic menigitis (tuberculous, cryptococcal)
Features of Chronic Tuberculous meningitis
-Area of the brain involved
-CT scan
-Infects leptomeninges, opacification is most prominent over the brain stem--> frequent cranial nerve involvement.

-Granulomatous inflammation seen with giant cells and acid fast bacilli

-Tuberculomas mimic tumors on CT

-Hydrocephalus from inflammation, cerebral infarction from inflammatory obstruction of blood vessels.
Brain abcess
-Pathogenic cause
-Commonly caused by bacteria; also fungi or parasites

-Progresses from untreated cerebritis to suppuration to encapsulation

-Cause mass effect, edema, and /or increased ICP
Acute Viral Encephalitis
-Typical agents
-General histologic features
-Arborviruses, HSV, rabies, CMV, polio

-perivascular/parenchymal lymphocytic infiltrate
-scattered glial (microglial) nodules
-neuronophagia (ex: polio)
-intranuclear (ex: herpes) or intracytoplasmic (ex: rabies) viral inclusion bodies
Acute Bacterial Meningitis
-4 most common agents
-Site of invasion
-Inflammation response
-Potential cortical involvement
-E. Coli, H. Influenzae. N. meningitides, and pneumococcus
-Invades leptomeningeal space
-Purulent exudate with PMN's initially accumulates around vessels and in sulci. Reaches confluence.
-Can involve superficial cortex by extending into the virchow robin spaces of penetrating vessels
-Fibrosis during healing can lead to hydrocephalus
Viral Meningitis
-5 main viruses
Usually self limiting, with minimal complications

-ECHO, Coxsacki, mumps, HSV-II, and EBV, but the agent is rarely identified

-Lympoctyic infiltrate
HIV direct effects
-Cells infected
-Infects microglia and macrophages

-Atrophy/neuron loss. Multifocal glial nodules: microglia, macrophages, and multinucleated giant cells. Nodules associated with foci of necrosis and astrogliosis. Seen in deep white matter > deep gray matter > cortex. Clinical syndrome is HIV-1 associated cognitive/motor complex.

-Diffuse damage to white matter with little inflammation. Myelin loss and reactive astrogliosis. Clinical syndrome is HIV-1 associated cognitive/motor complex.
Spongiform Encephalopathies
-Epidemiology and Symptoms
-Middle aged acute dementia followed by jerks. Very specific EEG pattern

-Spongiform grey matter; vacuolization in neuropil; loss of organelles in dendrites

-Clinical phenotypes correlate with polymorphisms at codon 129 of the prion gene
HIV Direct Effects
-Vacuolar Myelopathy
Vacuolar Myelopathy
-Macrophage vacuoles seen in posterior and lateral columns of thoracic spinal cord. Indicates myelin damage. Non-specific for HIV. Clinical syndrome is HIV-1 associated myopathy
HIV Direct Effects
-Lymphocytic Meningitis
-Leptomeninges infiltrated with lymphocytes
-Occurs within 2 weeks of HIV seroconversion
-Clinical syndrome is viral meningitis
Fungal Infections
-Patient population
-Spread to CNS
-Pathology caused
Parasitic Infections
-Patient population