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83 Cards in this Set
- Front
- Back
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What are the physical barriers shielding the CNS from infection?
What are the consequences of this? |
Bones of the skull and spine, the dura, the ia and arachnoid
Infectious are often contained in spaces between these anatomic structures |
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Where is an epidural abscess located?
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Between the bone and the dura
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Where is a subdural abscess located?
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Between the dura and arachnoid
Empyema |
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Where is leptomeningitis/meningitis located?
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In the CSF between the pia and arachnoid
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Where is encephalitis or cerebral abscess located?
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Between the pia in the brain parenchyma
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Describe intracranial epidural abscess
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-Relatively frequent
-Associated with overlying infection of cranial bones -Commonly due to direct extension from infected frontal or mastoid sinuses or osetomyelitis of skull |
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Describe spinal epidural abscess
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-Usually from direct extension from overlying skin infections, osteomyelitis of spinal vertebrae, pleural empyema, subphrenic or perinephric abscess
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What is usually the organism responsible for spinal epidural abscess?
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Staphylococcus (60% of cases)
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What are the symptoms of spinal epidural abscess?
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-Severe back pain
-Malaise -Fever -Neck stiffness -Headache Complications can include: -Spinal cord compression as a result of vascular thrombosis -Infarction and irreversible paraplegia |
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What is empyema?
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Subdural infection
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Describe subdural infections
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-Accumulation of pus within a potential space between dura and arachnoid
-Relatively rate -Dure to direct extension from infections of paranasal sinuses or skull and fractures of skull |
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What are the symptoms of subdural infections? Complications?
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-Local pain
-Tendernous -Fever -Chills -Headache -Neck stiffness Complications include: -Thrombophlebitis that may lead to superficial cerebral infarction and seizures |
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What is usually the organism responsible for subdural infections?
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Streptococcus
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Describe treatment of subdural infections
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-Difficult to treat
-High mortality |
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Describe meningitis/leptomeningitis
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-Infection of the subarachnoid space
-Due to hematogenous or direct invasion by organisms resulting from surgery, trauma, or CNS malformation -Most often due to bacteria or viruses -Fungi and parasites may also cause disease |
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Why do bacteria love CSF?
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-Physiologic salt concentrations
-Protein for growth -Glucose for energy -CSF is inadequate in fighting infection |
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What is the most important factor in absolute attack rate and host susceptibility for meningitis?
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Age
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What is the most common cause of meningitis in neonates?
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Group B streptococci
E. coli |
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What is the most common cause of meningitis in infants and children?
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Haemophilus influenza
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What is the most common cause of meningitis in adolescents and young adults?
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Neisseria meningitidis
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What is the most common cause of meningitis in the elderly?
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-Streptococcus pneumoniae
-Listeria monocytogenes |
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What are the general pathologic features of bacterial meningitis?
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Early: Leptomeningeal congestion, abundant neutrophils, intracellular bacteria
Few days: Purulent material, first cuffing blood vessels in cerebral sulci, later covering cortex, increasing proportion of mononuclear chronic inflammatory cells, fibrin exudate, ventricular dilatation as CSF outflow obstructed, cerebral swelling as a result of edema Later: Purulent ventricular exudate, vascular thrombosis with focal cerebral infarction Final: Thickenng of leptomeninges, chronic hydrocephalus |
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What are the complications of leptomeningitis?
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-Hydrocephalus
-Subdural effusion -Cystic loculation of subarachnoid fluid -Cranial nerve damage, especially deafness -Focal neurological deficits -Psychomotor retardation |
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Describe brain abscesses
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-Rare
-Due to contiguous spread (most commonly from sinusitis, otitis, mastoiditis) or from blood-borne infection (vegetative endocarditis, pulmonary disease, especially bronchiectasis, IV drug use, congenital heart disease) -Abscesses are often multiple -Often in MCA territory and have predilection for the gray/white junction |
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What are the most common causitive organisms for brain abscesses?
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Streptococci and Staphylococci
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What are the stages of cerebral abscess formation?
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-Early cerebritis (1-3 days): Acute inflammation and edema
-Late cerebritis (4-9 days): Central necrosis with peripheral invasion of macrophages and fibroblasts -Early capsule formation (10-13 days): Proliferation of capillaries and, fibroblasts and laying down collagen fibrils. Brain has poor supply of fibroblasts, derived from blood vessel adventitia Late Capsule Formation (14 days and later): Fibrotic capsule surrounded by edematous gliotic brain tissue |
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What are the symptoms and signs of cerebral abscess formation?
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-Most common in 1st-3rd decade of life
-Related to mass size and location and to degree of edema, not infection -Fever uncommon, -Headache, nausea, vomiting and seizures common -Sudden deterioration suggests internal herniation or rupture into ventricle |
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What is the treatment for cerebral abscess?
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-Surgical drainage or excision
-Systemic and sometimes local antibiotics |
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Who do cerebral fungal infections develop in?
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-May occur in previously healthy individuals
-Most often develop as opportunistic infection in patients with lowered resistance -This can be due to: -Diabetes -Ketoacidosis -Leukemia -Lymphoma -Other malignant processes -Prolonged use of antibiotics -Corticosteroids -Cytotoxic and immunosuppresive drugs -AIDS |
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What do cerebral fungal infections produce?
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-Meningitis
-Cerebritis -Cerebral abscess -Stroke-like syndrome |
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What are the common cerebral mycoses and their morphologies?
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Aspergillus - Septate hyphae
Rhizopus - Nonseptate hyphae Candida - Budding yeast Cryptococcus - Budding yeast, encapsulated *Cryptococcus can be in either opportunistic or previously healthy individuals* |
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What are the more unusual cerebral mycoses, their morphologies, and their locations?
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Coccidioides - Large yeast with endospores - In previously healthy individuals in the Southwest
Histoplasma - Budding yeast - in previously healthy individuals in the Ohio and Central Mississippi River Valleys Blastomyces - Budding yeast - in previously healthy individuals |
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Describe parasitic infections of the CNS
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-Relatively uncommon in USA
-Probability of exposure increases with travel to endemic areas -acanthamoeba, Naegleria, Trypanosoma and Toxoplasma cause diffuse meningoencephalitis, cerebral malaria (Plasmodium falciparum) lodges in capillaries resulting in petechial hemorrhages and angiitis Larger parasites obstructer larger blood vessels and/or migrate into the cerebral parenchyma |
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How does one acquire toxoplasma gondii?
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Eating raw or poorly cooked meat
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How many people have toxoplasma gondii?
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About 25-50% of adults have been infected
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What are the symptoms of toxoplasma gondii in an immunocompetent host?
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-Transient parasitemia
-Lymphadenopathy -May be entirely symptom free |
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What part of the toxoplasma gondii life cycle is in the human?
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The bradycyst - dormant stage
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How does toxoplasma gondii cause problems in immunocompromised individuals?
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Encysts organisms in the brain reactivate and give rise to toxoplasma encephalitis
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Describe the gross pathology of toxoplasma infection
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-Tends to be localized around ventricles in the basal ganglia and thalasmus and at the junction of gray and white matter where it may cause focal abscesses
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Describe the microscopic pathology of toxoplasma infection
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-Encephalitis is initially characterized by scattered microglial nodules within which toxoplasma cysts are frequently found
-Small foci of infection will eventually evolve into abscesses with: -A central necrotic zone containing few identifiable organisms -An intermediate zone with vascular congestion, neutrophilic infiltration and numerous tachyzoites -Peripherally, a zone with relatively litte inflammation but numerous encysted organisms |
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How common is congenital toxoplasmosis?
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Affects 1/1000 birtchs in the US
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Describe congenital toxoplasmosis
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-The fetus is infected via the placenta during maternal infection
-The earlier the infection the worse the consequences -Affected infants are often premature with jaundice, enlarged spleen and liver, chorioretinitis, micriphtalmus -Microscopically there is necrotizing cerebritis, diffusely scattered foci of coagulatuve necrosis follwed by calcification, meningeal inflammatory exudate. Hydrocephaly may occur as a result of periaqueductal inflammation, repair, and aqueductal stenosis |
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What are the stereotyped reactions in viral encephalitides?
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1. Infiltration by inflammatory cells
2. Hyperplasia and Proliferation of Microglia 3. Neuronophagia 4. Microglial nodules and gliomesenchymal nodules 5. Astrocytic proliferation 6. Intracellular inclusion bodies 7. Neuronal changes 8. Necrosis |
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Describe the infiltration by inflammatory cells in viral encephalitis
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This is usually the most conspicuous histologic abnormality. Perivascular and parenchymal mononuclear cell infiltrate, including lymphocytes, plasma cells, and macrophages is the most characteristic feature of viral infection
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Describe the hyperplasia and proliferation of microglia in viral encephalitis
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Seen throughout the brain and particularly in th ecortex and basal ganglia. The microglia hypertrophy to form "Rod cells" and these subsequently acquire long and slightly convoluted nuclei. They are most active in and around destroyed tissue where many become converted to lipid phagocytes (foam cells)
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Describe neuronophagia in viral encephalitis
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This refers to phagocytosis of an injured neuron by a dense mass of hypertrophied microglia often obscuring the dead cell. Hoever, in acute infections such as in polio, PMNs are the cells involved in neurophagia
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Describe astrocytic proliferation in viral encephalitis
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In acute encphalitis, enlarged astrocytes with plump cytoplasm are usually restricted to regions of tissue destruction. However, in certain subacute forms, there may be considerable astrocytosis
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Describe microglial nodules and gliomesenchymal nodules in viral encephalitis
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Often used synonymously to describe clusters of hypertrophied microglia admixed with other mononuclear cells not specifically related to nerve cells and occurring mainly in the white matter. Some of these clusters may contain as many as one hundred nuclei. It should be remembered that both neuronophagia and the microglial nodules, although frequently observed in viral encephalitidies, are by no means specific since both phenomena can occur in hypoxic brain damage.
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Describe intracellular inclusion bodies in viral encephalitis
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These are important and may be diagnostic of a specific viral infection. However, not all intracellular inclusions are caused by viruses. They may be found in neurons or/and glial cells. They may be intranuclear or intracytoplasmic or both. Intranuclear inclusions known as Cowdry type A are frequently seen in herpes encephalitis, cytomegalovirus infection and subacute sclerosing panencephalitis. The Cowdry type A inclusion is an eosinophilic oval or spherical mass with a clear halo surrounding it. Intracytoplasmic inclusions are characteristically seen in rabies, especially in Purkinje cells and pyramidal cells of the hippocampus. Both intracytoplasmic and intranuclear inclusions are seem in SSPE and CMV.
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Describe neuronal changes in viral encephalitis
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Acute degeneration of neurons such as chromatolysis, eosinophilia of cytoplasm, and pyknosis of nuclei can occur but are by no means characteristic unless there is actual necrosis of the nerve cells associated with neuronophagia
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Describe necrosis in viral encephalitis
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This may range from selective necrosis of one neuronal cell element (eg motor nerve cells in polio) to frank hemorrhagic infarctions of one or more lobes (eg herpes simplex encephalitis). Sometimes necrosis is scattered throughout the brain and form cavities (eg equine encephalitis)
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Describe the CNS effects of poliomyelitis
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The polio virus selectively destroys the motor neurons of the spinal cord and vbrain stem to cause flaccid, asymmetric weakness of the muscles innervated by the affected motor units
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What is the incubation period of rabies
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It is variable and dependent on retrograde axonal transport of the virus from the site of the bite wound along peripheral nerves into the CNS (usually 1-3 months)
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What is the pathognomonic pathologic finding in rabies?
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Negri body. They are most numerous in the pyramidal layer of hippocampus and Purkinje cells. They are well-defined, rounded, acidophilic, intracytoplasmic inclusions about 5-10nm.
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What is common amongst arboviruses?
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They are RNA viruses and are transmitted from host to host by insects
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Where does Western equine encephalitis occur?
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Over most of the US to the West of the Appalachian Mountains and in Southern Canada
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Where does Eastern equine encephalitis occur?
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Predominantly along the Eastern Seaboard.
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Compare Eastern and Western equine encephalitis
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Eastern has a high mortality rate (~75%) while the Western rate is ~10%
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What is the most important cause of fatal sporadic viral disease?
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Herpes simplex
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What are the clinical symptoms and signs of herpes simplex encephalitis?
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-Starts with fever and headaches
-Seizures are common -Nuchal rigidity may present -Progessive mental deficits, confusion and personality changes |
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What are the pathological findings of herpes simplex encephalitis?
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-Intense meningitis
-Necrotic, inflammatory, or hemorrhagic lesions -Predilection for frontal and temporal lobes -Intranuclear inclusions, Cowdry type A -Perivascular inflammation |
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Describe varicella-zoster
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-Viral disease that produces inflammatory lesions in the dorsal root ganglia clinically associated with pain and a skin eruption in the distribution of the ganglia
-Infection due to reactivation of latent varicella-zoster originally acquired as childhood chicken pox -There is a lymphocytic infiltrate in the ganglia of the spinal CN roots -Rarely, VZ may cause an acute encephalitis, particularly after involvement of CN roots |
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What is the leading opportunistic viral pathogen in AIDS?
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CMV
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Describe the pathologic features of CMV
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-Gross appearance of the mind is deceptively normal
-Microscopically there are scattered microglial nodules and large CMV infected cells containing both intranuclear and cytoplasmmic inclusion bodies |
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What are the most common sites of CMV infection?
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Basal ganglia, Diencephalon, and brain stem - possibly reflecting adjacent spread from ependyma that is particularly susceptible to CMV infection
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Describe congenital CMV
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-Fetal infections occur via transplacental transmission and result in still birth and prematurity
-The cerebrum is affected by a granulomatous encephalitis with extensive subependymal calcification -Hydrocephalus, hydranencephaly, microcephaly, cerebellar hypoplasia, or other developmental defects may be found |
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What is a common result of subclinical congenital CMV?
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Deafness
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Describe the primary neurologic effects of HIV
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-AIDS dementia affects ~30% of people with AIDS
-Many patients gradually develop mental deterioration and variable degrees of motor devilities that culminate in dementia, mutism and quadriparesis -HIV encephalopathy may result from primary HIV infection of the brain |
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Describe the gross neuropathology of HIV infection
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-In the early stages of HIV encephalopathy, brain may appear grossly unremarkable
-As disease progresses atrophy develop -Thre may be some attenuation of the white matter, particularly of the cerebral hemisphere |
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Describe the microscopic neuropathology of HIV infection
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-Reactive microglial cells are present throughout the gray and white matter
-They occasionally aggregate into cellular clusters with reactive astrocytes to form microglial nodules -Peculiar multinucleate cells with numerous small, dark nuclei and granular eosinophilic cytoplasm is a hallmark of HIV infection -These can be found in microglial nodules, perivascularly, or scattered through the brain parenchyma -There is a diffuse, mild gliosis -Nonspecific white matter changes such as foci of demyelination and vacuolar change occur -Cerebral calcificiation is common in pediatric AIDS |
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What viral infections are common in AIDS?
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CMV and PMV (progressive multifocal leukoencephalopathy)
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Describe progressive multifocal leukoencephalopathy
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-Progressive neurologic illness
-Caused by JC virus, a papovavirus -Second most frequent viral infection in AIDS (after CMV) |
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Describe the gross pathology of PML
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-Multiple areas of gray discoloration of white matter that consists of lesions measuring several mm to lesions that coalesce to form large zones of softening
-Lesions are found throughout the CNS wherever white matter is represented -They may also be found in the lower levels of the cortex and in the basal ganglia |
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Describe the microscopic pathology of PML
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Three cardinal features of the whit ematter lesions:
1) Abnormal oligodendrocytes with glass, purple intranuclear inclusions found predominantly at the periphery of the lesions 2) Bizarre astrocytes with large, hyperchromatic, irregular nuclei 3) Demyelination associated with a variable degree of inflammatory infiltration made up predominantly of macrophages. Immunocytochemical and ultrastuctural demonstration of the present of papovavirus confirms the diagnosis of PML |
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Describe primary CNS lymphoma
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-A rare disease accounting for 1-1.5% of all primary brain tumors
-One of the most common primary brain tumors as a result of the AIDS epidemic -Entity is the second most frequent CNS mass lesion in adults with AIDS -Most frequent mass lesion in children with AIDS |
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Describe prions
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-Proteins, no DNA or RNA
-Insensitive to physical or chemical treatments that inactivate all known viruses -Formalin fixation does not destroy infectivity -Clorox, formic acid, and stringent autoclaving can destroy it |
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Describe the pathological changes of prions
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-Limited to the CNS
-Characterized by: -Cytoplasmic vacuolization (status spongiosis) -Astrocytosis -Neuronal loss |
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Describe Kuru
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-Endemic to New Guinea
-Transmitted by ritualistic cannibalism of deceased family members -Cerebellar ataxia and later dementia predominate the clinical picture |
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Describe the pathology of Kuru
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Gross pathology:
-Closely resembles CJD "acute spongiform encephalopathy" -Atrophy of the vermis and flocculonodular lobe of cerebellum Microscopic Pathology: -Loss of Purkinje and granular cells -The presence of many "kuru" amyloid plaques |
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Describe Creutzfeldt-Jakob disease and its clinical presentation
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-Rare, subacute disease of late adulthood
Clinically presents with: -Progressive dementia (55-70yo, typical age of onset) -Focal neurologic deficits (eg cortical blindness, aphasia) -Evidence of cerebellar, pyramidal, extrapyramidal and gray matter involvment -By 6 months dementia is profound and myoclonic jerking is evident as the individual becomes vegetative, mute, and bedfast |
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Describe the pathology of Creutzfeldt-Jakob Disease
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-Widespread microcystic appearance of the gray matter (status spongiosis)
-Eventual neuronal loss -Astrocytosis out or proportion to neuronal loss -Absence of inflammatory infiltrates |
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Describe Gerstmann-Straussler (Scheinker) Syndrome
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-Familial disorder characterized by slowly progressive cerebellar ataxia
-Spinal tract signs, later dementia -Kuru-like plaques and spongy changes |
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Describe the clinical presentation and pathology of New varient CJD
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Clinical
-Mainly affects young people (19-39) in the UK -Presenting symptoms include behavioral changes, ataxia, dysesthesias -Insidious onset, prolonged course Pathology -Prominent "florid" plaques -Distinguishing PrP-Sc protein banding pattern on Western blot analysis which resembles that seen in bovine spongiform encephalopathy |
