Neuropath- Part 5

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  1. Inflammation is characterized by increased ___________ with leakage of __________, often accompanied by ______________.
    vascular permeability; plasma; WBCs migrating to the perivascular space
  2. Inflammation of the grey matter of the brain.
  3. Inflammation of the white matter of the brain.
  4. Inflammation of the spinal cord.
  5. Inflammation of the peripheral nerve.
  6. Inflammation of a nerve root.
  7. Suppurative exudate contains ____________; it occurs due to __________; there may be accompanying ___________.
    neutrophils; bacterial infection; tissue necrosis
  8. Non-suppurative exudate contains __(2)__; it occurs due to... (3)
    lymphocytes and histiocytes; viral infections, immune-mediated processes, or certain parasitic diseases.
  9. Granulomatous exudate is __________ of ___________; occurs in the CNS due to __(2)__.
    focal accumulations; macrophages; mycoses and some bacteria
  10. Eosinophilic exudate occurs with ___________.
    parasitic infections
  11. Fibrinous exudate reflects a ___________ insult, which may suggest certain _____________.
    severe vascular; infectious agents
  12. _____________ are the accumulation of cells in the perivascular space and may be the result of __________.
    Perivascular cuffs; cellular efflux or influx
  13. Infiltrating cells associated with perivascular cuffs include... (4)
    lymphocytes/plasma cells, eosinophils, monocytes.
  14. Cellular efflux results in perivascular cuffs when _________ attempt to move back into circulation, but this process is compromised b/c of their ____________, therefore they accumulate in the perivascular space.
    gitter cells; extreme cytoplasmic engorgement
  15. Why is a spinal tap diagnostic for CNS inflammation but not localizing of the lesion?
    perivascular space communicates with the subarachnoid space; therefore, cells accumulating in perivascular space can get into the CSF
  16. The specialized lymphatic vessels lining the dural sinuses drain to the ______________, where immune responses can be primed.
    deep cervical lymph nodes
  17. What are risks associated with having the potential to initiate and maintain immune/inflammatory responses in the CNS? (2)
    cells lost may not be replaceable, CNS contains privileged antigens that may initiate autoimmune reactions
  18. Tissue-specific antigens are sequestered in the CNS during _____________; inappropriate presentation of these antigens to the immune system can result in _____________.
    T cell maturation; immune-mediated neurologic disease
  19. How does the CNS support inflammatory responses and avoid undue damage in the process? (3)
    restrict antigen presentation in the CNS by limiting MHC I and II expression, Tregs suppress inflammatory responses, cells are resistant to cytotoxic compounds released by I cells
  20. __(2)__ of the CNS are invisible to the immune system due to their poor expression of MHC.
    Neurons and somewhat oligodendrocytes
  21. MHC I may be induced in __(2)__.
    astrocytes and oligodendrocytes
  22. MHC II may be induced in _________.
  23. __(2)__ are the major APC of the NS.
    Endothelial cells and CNS macrophages
  24. __(2)__ are a good place for intracellular infectious agents to persist in the CNS.
    Neurons and oligodendrocytes (invisible to the CNS b/c do not express MHC)
  25. What is the most common route of infection for CNS inflammation?
  26. Infectious organisms localize wherever __________ is high and __________ is small, such as in the... (4)
    vascular density; vessel caliber; leptomeninges, choroid plexus, subependyma, grey-white junctions
  27. Factors affecting distribution of infectious agents. (2)
    size of particles, tropism for specific vascular beds
  28. Neural distribution of infectious agents occurs by ___________; 2 examples of agents that use this methods include...
    retrograde axonal transport; rabies, listeria
  29. Direct extension of infectious agents from surrounding structures occurs near the __________ and extension from the _____________.
    nasal turbinates; otitis meda/interna
  30. 2 ways bacterial infection is spread.
    hematogenous and direct extension
  31. Suppurative meningitis is secondary to  ____________; it is generally a disease of _____________ animals, which as those with __(2)__.
    septicemia; young, immunocompromised; FTPI or SCID
  32. With suppurative meningitis, _______ infectious particles are __________ aggregated by antibody and ___________ distributed in circulation to ____________.
    small; minimally; widely; multiple organ systems
  33. Organ systems commonly affected by suppurative meningitis include... (3)
    synovial membranes (polyarthritis), serosal membranes (serosal petechia), kidneys, and CNS
  34. A CNS lesion associated with suppurative meningitis is ______________; exudate is __(2)__.
    cloudiness of the meninges; bacterial or sterile (bacteria have been cleared)
  35. ____________ associated with suppurative meningitis occurs due to increased intracranial pressure, which is exacerbated by periventricular encephalitis and/or choroiditis, which directly ____________.
    White matter edema; obstruct CSF flow
  36. With meningoencephalitis, seeding of the CNS structures is by __________ particles that are __________ distributed in circulation; there is __________ of antibody aggregation.
    moderately-sized; sporadically; a greater degree
  37. The primary site of infection is more/less readily defined with meningoencephalitis than with suppurative meningitis.
  38. Extension of meningoencephalitis to involve the brain is facilitated by ________________.
    capillary embolization/ venous thrombosis
  39. With meningoencephalitis, the agent may have a tropism for __________, thus promoting __(3)__.
    brain endothelial cells; vasculitis, thrombosis, and infarction
  40. Infectious agent of bovines that has a tropism for brain endothelial cells.
    Histophilus somni
  41. With CNS abscess formation, _______ infectious particles are ___________ distributed in circulation; this may reflect the addition of ________ to the emboli.
    large; sporadically; fibrin
  42. The primary site of infection with CNS abscess formation is often the ___________ due to ____________.
    endocardium; bacterial endocarditis
  43. With CNS abscessation, infection does not spread beyond the ___________, which is ________ by _________.
    devitalized tissue; walled off; fibrous astrocytosis
  44. With a brain abscess, the thin fibrous capsule may _______ with ________, leading to... (3)
    break; head trauma; reactivation of infection, edema, and death.
  45. _____________ may represent a sequel to bacterial meningoencephalitis.
    Meningeal abscessation
  46. What are the 3 syndromes associated with Listeria monocytogenes?
    abortion, septicemia, encephalitis
  47. ____________ permits overgrowth of Listeria, which enters branches of the _________ when eaten.
    Inadequate fermentation of silage; trigeminal nerve (defects in oral mucosa, exposed dental pulp)
  48. Ascension of Listeria organisms from the __________ to the brainstem occurs via ____________, inciting __________.
    trigeminal n.; retrograde axonal transport; encephalitis
  49. Brainstem lesions associated with Listeriosis are ______________, __________ formation, and _____________.
    lymphocytic meningoencephalitis; parenchymal microabscess; lymphocytic perivascular cuffing
  50. What are the 2 requirements for a cell type to support viral replication?
    target cell must express the appropriate surface receptors, target cell must be able to provide the appropriate intracellular metabolic environment
  51. With hematogenous viral spread to the CNS, viral particles are carried by __________ across the BBB, where they infect ___________; this is followed by direct infection of the ___________ and are shed in _______ to spread to the rest of the NS.
    leukocytes; endothelial cells; choroid plexus epithelium; CSF
  52. What is required to create successful infection with retrograde axonal transport of viral particles?
    some type of amplification post-inoculation
  53. A virus that can infect neural cells under natural conditions.
    neurotropic virus
  54. Virus that is capable of entering the CNS from peripheral sites.
    neuroinvasive virus
  55. Virus that is capable of spreading through CNS and thus causing disease.
    neurovirulent virus
  56. A neurotropic virus with a low degree of neuroinvasiveness but a high degree of neurovirulence. [specific pathogen]
    herpes simplex virus (always enter PNS but rarely enters the CNS...when it does, it replicates like crazy and causes disease)
  57. A neurotropic virus with a high degree of neuroinvasiveness and neurovirulence.
    rabies virus
  58. Increased __(2)__ is observed in neonates because... (3)
    neuroinvasiveness and neurovirulence; biological barriers are not fully formed, not fully immune competent, cell proliferation/tissue development ideal for viral replication.
  59. Viral gene infection resulting in death of the host cell.
    cytopathic/lytic infection
  60. ______________ typifies persistent infection; ______________ is characteristic of latent infection.
    Low-level viral gene expression; no viral expression for extended periods of time
  61. RNA viruses replicating in the cytoplasm cannot undergo ____________.
  62. What is the result of toxic effects of viral genes at low level expression?
    sustained cell viability with loss of luxury functions, such as myelin production---> clinical neurologic disease with demyelination
  63. Cytopathic infection leads to _____________; therefore, ___________ is a continuum; the precise relationship is defined by _________.
    persistent non-ctopathic infection; latent infection; host factors (age, immune status)
  64. Viruses that exhibit non-cytopathic infection in differentiated cells, but exhibit cytopathic infection in dividing cells.
    radiomimetic viruses
  65. Cytopathic/lytic viral infection may result in __(2)__.
    direct or indirect damage on CNS cells
  66. Describe how cytopathic viral infection can lead to indirect damage of the CNS.
    highly inflammatory lesions resulting in extensive demyelination and productive infection of microglia; release of large amounts of antiviral antibody
  67. Highly inflammatory lesions due to viral infection result in the production of _________, which enhances microglial activation and __________, which can lead to ___________;
    IFNγ; MHC II expression; demyelination
  68. Vascular lesions associated with viral infection can lead to __(4)__; the mechanism of damage involves... (2)
    CNS edema, hemorrhage, thrombosis, and infarction; infection of vessel wall and deposition of immune complexes in the vessels.
  69. General features of virus infected tissues. (3)
    non-suppurative perivascular infiltrates, necrosis of specific cell types, inclusion bodies
  70. Viral clearance is ________-mediated; clearance is correlated to a _________ activity and can occur without _____________.
    T cell; cytolytic; destruction of infected neurons
  71. Accumulations of viral protein or mucoprotein in the nucleus or cytoplasm of target cells.
    viral inclusion bodies
  72. Derivative of nucleoli and arise to supplement nucleolar function to support the increased metabolic demand placed upon cells by virus replication.
    nuclear bodies
  73. CDV is caused by a __________ and it is a __________ disease; the extent of tissue destruction mediated by virus gene expression is a reflection of __(2)__.
    paramyxovirus; multisystemic; host age and immune status
  74. With CDV, initial virus replication is in ________ tissues of the __________, which leads to ________ with seeding of ________ of the body; virus replication results in __________.
    lymphoid; respiratory tract; primary viremia; lymphoid tissues; secondary viremia
  75. In what cells does CDV replicate?
    tissues with cell proliferation or cells with a high degree of metabolic activity (radiomimetic)
  76. What is the key to viral shedding with CDV?
    infection of epithelial tissues- bronchiolar, intestinal, cutaneous, urinary, odontogenic
  77. ___________ is the common cause of presenting clinical signs of CDV.
    Secondary bacterial infection (esp. respiratory and GI)
  78. 3 types of clinically evident CDV CNS infections.
    acute encephalopathy, subacute encephalitis, delayed onset encephalitis
  79. Acute encephalopathy associated with CDV is a ______________; it occurs in _________ animals that lack _________ from _________.
    neuronal lytic infection; animals < 4weeks old; protective immunity from colostrum
  80. Describe the appearance of acute encephalopathy associated with CDV. (4)
    rapid death, minimal structural evidence of infection, viral antigen is ubiquitous, inclusion bodies are RARE
  81. Subacute encephalitis caused by CDV is a ____________; it occurs in __________ animals that have a __________ but are ___________.
    glial lytic infection; animals > 4 weeks old; mature immune system; immunologically naive to CDV
  82. With subacute encephalitis caused by CDV, progression of virus through nervous tissue is ___________, and as a result, infection of ___________ is apparent, clinically apparent CNS involvement may develop, including __(3)__.
    protracted; non-neuronal; periventricular demyelination, glial inclusions, astrocytic syncytia
  83. How does CDV cause periventricular demyelination?
    oligodendrogial damage and loss of metabolic support by astrocytes--> demyelinating encephalitis
  84. Delayed onset encephalitis caused by CDV is known as __________; what are the 2 theories of pathogenesis?
    old dog encephalitis; viral persistence in neurons and reactivation, causing direct host cell damage; cumulative insults due to virus persisting in neurons and constant low level expression, leading to structural damage
  85. What features of old dog encephalitis are relatively constant? (2)
    no prior clinical evidence of CDV, but antiviral antibody titers in serum and CSF are high
  86. Lesions of old dog encephalitis are characterized by... (4)
    neuronal degeneration and necrosis, +/- intranuclear inclusion bodies, lymphoplasmacytic perivascular cuffs, gliosis
  87. Rabies virus infection results in ________________ with formation of ____________.
    neuronal degeneration and necrosis; Negri inclusion bodies
  88. Rabies virus initial viral replication is at the site of _________; prior to the completion of this stage, ___________ may suppress __________.
    entry; passive immunity; viral spread
  89. If point of entry of Rabies is by aerosol, initial replication takes place in ____________; if by bite wound, initial replication is in ___________ and ___________.
    neuroepithelial cells of nasal mucosa; muscle cells and cells of the sensory spinal apparatus
  90. After initial viral replication of rabies, virus enters ______________ and ascends to the associated _________ by ____________ transport; this allows the virus to be _______________.
    peripheral sensory nerve; paraspinal ganglion; retrograde axoplasmic transport; shielding from immune surveillance
  91. How does rabies virus get to the mandibular salivary gland for viral shedding?
    axoplasmic transport carries virus to peripheral tissues from the CNS; goes o sensory ganglion of CN5 to mandibular salivary gland (also goes to mammary gland and gravid uterus)
  92. What makes up the clinically observed incubation time/eclipse phase of rabies infection?
    viral replication at site of entry through transport to peripheral tissues from CNS
  93. Describe the onset of clinical signs associated with rabies infection. (3)
    weakness or paralysis, difficulty swallowing due to laryngeal paralysis, death occurs when virulent strains reach the brain
  94. Location of viral inclusion Negri bodies in carnivores and herbivores.
    carnivores: hippocampus, herbivores: Purkinje cells
  95. Les virulent strains of rabies virus will be stalled due to their tendency to _____________; this can lead to ________ restriction and _________ rabies; with this, there is decreased __(2)__.
    incite a substantial inflammatory response; spinal cord; paralytic; formation of inclusion bodies and likelihood of salivary shedding
  96. What is "post-vaccinal rabies"?
    we cannot be assured that a modified live vaccine approved for use in one species will be safe in another; modified live vaccine can lead to paralytic rabies
  97. How is rabies diagnosed? (4)
    immunofluorescence staining for viral antigen, inclusion bodies in hippocampus, histopath, RT-PCR of viral RNA
  98. Equine herpes myeloencephalitis is a _________ infection of ___________; it is caused by ____________.
    lytic; vascular endothelium; equine herpesvirus 1 subtype 1 (abortagenic strain)
  99. Equine herpesvirus 1 subtype 1 has a tropism for ____________ of ____________; infection of these cells results in ___________ with ___________.
    endothelial cells; spinal cord white matter; vasculitis; hemorrhage
  100. Grossly, what does equine herpes myeloencephalitis look like?
    diffuse red triangular foci of hemorrhage in spinal cord white matter, Wallerian degeneration
  101. Diagnosis of equine herpes myeloencephalitis is by...
    gross and histopathology
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Neuropath- Part 5
2015-10-13 01:25:13
vetmed neuropath

vetmed neuropath
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