Viral Cns Infection

Front 1

1. What is the most common portal of entry for viral meningitis? (other routs?)
2. How can the BBB be breached?

**No fibroblasts or lymphatics in the CNS
Bacterial meningitis is worse and faster

Back 1

1. Hmatogenous (peripheral NS (rabies, HSV) & directly via trauma)
2. replication/transcytosis through endothelial cells, migration of infected cells into CNS, infection through areas where BBB is incomplete like choroid plexus

Front 2

Terms:
1. Inflammatory process in the subarachnoid space involving the leptomeninges and the CSF
2. Increased number of WBCs in the CSF
3. normal WBC count in the CSF?
4. What is a parenchymal infection of brain, almost always accompanied by meningitis: Wide spectrum of clinical and pathologic findings, depending in part upon the etiologic agent

Back 2

1. Meningitis
2. Pleocytosis
3. 0-5
4. Viral encephalitis

Front 3

Causors of aseptic meningitis:
– Mumps
– Enteroviruses (ECHO and Coxsackie viruses, poliovirus)
– EBV
– HSV, type 2
– LCMV

Back 3

• Arthropod-borne
– St. Louis Encephalitis (SLE) virus
– West Nile Virus
– California Encephalitis virus
– Western (WEE), Eastern (EEE), and Venezuelan
(VEE) Equine Encephalitis viruses
– Japanese B Encephalitis Virus
– Murray Valley Fever Virus
– Tickborne Encephalitis Virus
Causes Headache, fever, chills, nausea, vomiting
• Rapid development of neurologic deficits with
some focal signs

Front 4

1. What is a key distinguishing feature between septic and aseptic meningitis?
2. What is the 1st sx of aseptic meningitis?
3. What are glucose levels (raised, low, normal) in viral encaphilitis?
4. A potential space that is continuous w/ surface of the brain, inflammation around there from the penetrative vessels cause the space to become inflamed

Back 4

1. Aseptic- normal glucose
2. Pain w/ lateral gaze
3. Normal (some PMN on day 1 or 2 but becomes rapidly lymphocytic)
4. Vircho' Robin space

Front 5

1. Key pathology characterstics for Viral encephalitis
2. Where does encephalitis localize for HSV-1?
3. what is the most sensitive dx tool for 2?

Back 5

1. parenchymal mononuclear cell infiltrates; glial nodules; neuronophagia, variable degrees of necrosis
2. Temporal lobe- destroys blood vessels, causes clots and necrosis
3. PCR of CSF

Front 6

Name it:
– Most common sporadic encephalitis
– Spread to the brain may be from either primary or
recurrent infections
– Most commonly presents with headache, alterations in mood, memory, or behavior, focal seizures
– May progress rapidly. If untreated has a high mortality, and a high rate of sequelae

Back 6

HSV-1

Front 7

What causes:
– Neonatal encephalitis
• Develops in up to 50% of babies delivered vaginally by women with active primary lesions
– Hemmorhagic encephalitis in AIDS patients

Back 7

HSV-2

Front 8

What causes:
– Acute encephalomyelitis in the setting of immunocompromised patient
– Sharply circumcised lesions with demyelination and necrosis
– Inclusions

Back 8

Herpes varicella Zoster Virus

Front 9

What causes:
• In Utero Infection
– Periventricular necrosis, microcephaly, calcifications
• Encephalitis in immunocompromised patients
– is the most common opportunistic infection in AIDS patients
– Subacute encephalitis
– Subependymal and ependymal regions
– Necrotizing and hemmorhagic ventriculoencephalitis
– Inclusions

Back 9

Cytomegalovirus

Front 10

1. How is poliomyelitis spread?

Back 10

1. Lymphohematogenously - but must get through blood to cause Sx

Front 11

What:
• Initially presents as aseptic meningitis
• Some patient progress to paralytic disease
• Flaccid paralysis with muscle wasting and hyporeflexia
2. What can occur years after having the above?
3. Cells infected by above?
4. What cell type helps distinguish this from other viral infections?

Back 11

Poliomyelitis
2. Progessive polio syndrome
3. Anterior horn cells and motor nucleus
4. PMNs - due to the large amount of necrosis

Front 12

1. What type of inclusion does rabies form? (inflammation?)
2. What does pediatric HIV infection lead to
3. Does HIV replicate in neurons?
4. What type of infiltrating cells in HIV encephalitis?

Back 12

1. Negri body (very little)
2. Microcephaly & mental retardation
3. No- but causes diffuse cortical atrophy- loss of myelin
4. Glial and macrophage giant cells & mononuclear cells

Front 13

HIV: Invasion of the CNS occurs early, disease occurs late
HIV Subacute Encephalitis:
Associated with AIDS-related dementia
• Frequent, 20-50% of patients with
immunodeficiency
• Slowly progressive disease with cognitive and mood disturbances
• Full fledged dementia

Back 13

Chronic Encephalitis - SSPE
• Grey and white matter
• Necrosis of neurons
• Loss of neurons with accompanying gliosis
• Perivascular lymphocytic infiltrate
• Intranuclear and intracytoplasmic inclusions

Front 14

1. When phase does HIV enter the CNS?
2. What stage does disease occur in?
3. Vacuolar degeneration of the posterior and lateral columns with destruction of myelin, resembles subacute combined degeneration• Vacuoles appear in the myelin lamellae which are subsequently stripped away by
macrophages

Back 14

1. Acute phase
2. Crisis stage
3. Vacuolar myelopathy - abnormal utilization of B12 suspected

Front 15

1. what causes Progressive multifocal leukoencephalopathy?
2. Key finding that is not present?
3. What cell types are infected with 1?

Back 15

1. JC virus (usu. no headache or fever)
2. Headache or fever- multifocal lesions
3. Oligodendrocytes are productively infected (intranuclear inclusions), astrocytes are non-productively infected (bizarre tumor looking cell)

Front 16

What is:
Progressive neurologic syndrome with onset between 5-15 years of age
• Usually male, rural setting
• Behavioral abnormalities, motor impairment, myoclonic seizures
• History of measles prior to age 2
• Variable but uniformly fatal course

Back 16

Subacute sclerosing pan encephalopathy - thought to be an assemply defect - there is a M protein defect

Front 17

1. How do you diagnose SSPE?
2. What causes:
• Rare sporadic dementia, even rarer inherited
form
• Clinical Presentation
– Age over 40 except in iatrogenic or BSE associated cases
– Progressive demenita
– Myoclonus
– Highly abnormal EEG
– Average course about 1 year

Back 17

1. CSF (elevated IgG & local synthesis of anti-measles Ab in CNS), EEG w/ burst suppression pattern, no CT finding
2. Creutzfeldt-Jakob Disease- accidentally transferred in corneal grafts, dural grafts, growth hormone therapy

Front 18

What are the 2:
• Inherited diseases with mutations in PrP gene
• Autosomal mode of inheritance

Back 18

GSS, FFI

Front 19

1. Disease associated w/ – M129cis/D178N (aspartate to asparagine) ,Neuronal loss and gliosis in thalmus, less spongioform change
2. Disease associated w/ P102L (proline to leucine) Clinical course starts with cerebellar ataxia, progresses more slowly than CJD; Pathology similar to CJD but with more plaques

Back 19

1. FFI
2. GSS