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Learning Objectives: Infectious Diseases of the CNS

1. Define the following:

a. meningitis Infection of the leptomeninges (arachnoid and pia)b. brain abscess staph or other bacteria, in circumscribed area in brainc. cerebritis inflammation of cerebrum

d. encephalitis inflammation of cerebrum (viral)e. myelitis inflamed spinal cord

2. List three symptoms or signs of acute meningitis. Acute onset (hours), fever, lethargy, headache,altered mental status, neck stiffness3. Define the CSF profile, and list three complications of acute bacterial meningitis. Increasedpressure, decreaded glucose, increased protein, numerous PMNs. Can get cerebral edema,hydrocephalus, cranial nerve palsy, seizures, death.

4. For acute viral meningitis, define the CSF profile, and indicate the likely clinical outcome.Increased lymphocytes in CSF, normal or slightly high pressure, normal or slightly high protein,

normal glucose. Usually benign, resolves on its own without sequelae.

5. For chronic meningitis, list the typical symptoms, the two most common etiological agents, in theU.S., and define the typical CSF profile. Headache, fever, stiff neck, mental status change, cranialnerve deficits. CSF has high pressure, high protein, low glucose, mononuclear cells. Two most commonare Tuberculosis and Cryptococcus. Two less common are Syphilis and Lyme disease. The meningitis isgenerally associated with infection somewhere else in the body.

6. List the three classic forms of neurosyphilis in adults and their common symptoms.Meningovascular SyphillisSubacute, chronic meningitis with lymphocytes, plasma cells, andmacrophages. Vessels get fibrotic and eventually occlude causing infarctions. Meninges get fibrosed.

General Paresischronic meningoencephalitis with brain atrophy, neuronal loss, and gliosis. Vesselschange and can infarct. Progressive mental and physical decline is seen. Dementia and personalitychanges.

Tabes Dorsalismyelopathy of the posterior columns of spinal cords, causing pain, ataxia, urinaryincontinence, loss of deep tendon reflexes, impaired vibration sense in lower extremities (position sensetoo) but motor functions are ok.7. For acute encephalitis/encephalomyelitis, list three major symptoms, four main pathologic features, andthree etiologic agents. Symptoms inclue altered mental status, seizures, and fever, developing overhours to days. Pathology includes neuronophagia (microglia eat infected neurons), microglial nodules,astrocytosis, edema of brain, and mononuclear cell infiltration. Sometimes tissue necrosi occurs.Someitmes viral inclusions. Some causes are Herpes virus (HSV 1), Rabies virus, Polio virus, West NileVirus, Arboviruses (eastern & western equine encephalitis, st. louis encephalitis, west nile encephalitis).

8. Define what a Negri body is. Inclusion seen in rabies infection, sharply defined, rounded or oval,eosinophilic cytoplasmic inclusion usually seen in pyramidal cells of hippocampus or in cortex or in

purkinje cells of cerebellum.

9. Define the tropism of the polio virus in the CNS. First multiplies in oropharynx, spreads to smallintestine, infrequently spreads to CNS where it selectively infects motor neurons in spinal cord andbrainstem (rarely cortex). You see in anterior horn of spinal cord inflammatory infiltration by lymphocytes,or if necrotizing, neutrophils and macrophages. Motor neurons die and are eaten with microglial nodulesformed. Also seen in motor cranial nerve nuclei and sometimes (rarely) in motor cortex areas. Grossvisible atrophy of anterior spinal nerves.

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10. For West Nile virus, indicate the method of spread to humans, the usual severity of the infection, andtypical pathological findings. Animal reservoirs are birds and horses, and virus gets to humans throughmosquito bite. Usual infection is mild or flu-like. About 1 in 150 people gets severe neurologic symptoms,with viral encephalitis typical pathology. Treatment is only supportive.

11. For subacute encephalitis, list two etiologic agents and be able to define the typical clinical settingsand pathologic findings. Subacute Sclerosing PanencephalitisSSPEhappens in children/adolescents5-15 years after a measles episode. Starts with behavioral problems, then in a few months seizures andmotor problems, then later progression to coma and death. CSF shows IgG against measles virus, andbiopsy shows perivascular inflammation, astrocytosis, neuronophagia, eosinophilic inclusion of viralnucleocspsids.

Progressive Multifocal LeukoenccephalopathyPMLcaused by polyoma virus called the JC virus, seenin immunosuppression, mostly in AIDS. Presents with visual deficits, personality changes, dementia,motor deficits. MRI shows multifocal lesions in white matter, widespread. No mass effect. Death withinmonths without antiviral treatment. Softening, crumbling, discoloration of hemispheric white matter. Onstaining, demyelination , oligodendroglia with inclusions and marginated chromatin.

12. For postinfectious encephalitis, define the usual clinical setting, the typical symptoms, and majorpathological findings. Occurs just as patient is recovering from measles/mumps/varicella/rabies

vaccination. Symptoms are high fever, headache, vomiting, convulsions, coma, focal signs. Pathology isdemyelination of white matter and some mononuclear iniltrate. Immune attack on myelin somehow.Recovery brings remyelination.

13. List three opportunistic infections affecting the CNS in AIDS. Cytomegalovirus, Toxoplasmagondii, JC Virus (PML).

14. List two conditions thought to be due to infection of the CNS by HIV. HANDHIV AssociatedNeurocognitive Disorder, and HIVEHIV Encephalitis.

15. List three forms of human spongiform encephalopathy.III. Kuru, Creutzfeldt-Jakob Disease (CJD),and Gerstmann-Straussler Syndrome (GSS).

16. List three ways a person can acquire a spongiform encephalopathy. Contact with infected tissue byeating or touching it; Genetic inheritance of autosomal dominant form (GSS); sporadic disease (CJD)17. Explain how spongiform encephalopathies differ from viral encephalitis in terms of:

a. How they are acquired. Eating or touch infected tissue; inheritance; mutationb. Latency from exposure to symptoms very long latency with SE (months to years)

unlike most viruses. But death happens quickly after onset, whereas viral encephalitis is generally benign.c. Resistance of the infectious agent to sterilizing techniques still active after formalin

fixation