Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology 3 > Neuro 3 - inflammation > Flashcards

Neuro 3 - inflammation Flashcards

1
Q

encephalitis

A

inflammation of the brain (doesn’t distinguish between gray and white matter involvement and therefore implies involvement of both compartments)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

polioencephalitis

A

inflammation of gray matter of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

leukoencephalitis

A

inflammation of white matter of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

myelitis

A

inflammation of the spinal cord (poliomyelitis/leukomyelitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

encephalomyelitis

A

inflammation of the brain/spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

meningitis

A

inflammation of the meninges (in general usage, implies involvement of leptomeninges)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

meningoencephalitis

A

inflammation of the meninges and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

choroiditis

A

inflammation of the choroid plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

neuritis

A

inflammation of a peripheral nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

polyneuritis

A

inflammation of multiple peripheral nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

radiculoneuritis

A

inflammation of a nerve root

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

suppurative exudate

A
  • neutrophils
  • bacterial infection
  • may accompany tissue necrosis
  • rarely neutrophilic exudates in viral infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

non-suppurative exudate

A
  • lymphocytes +/- plasma cells, histiocytes

- viral infections, autoimmune conditions, certain protozoal/parasitic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

granulomatous exudate

A
  • focal accumulations of histiocytic cells
  • mycoses (may be pyogranulomatous)
  • certain bacteria (myco), protozoa, metazoa
  • idiopathic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

eosinophilic exudate

A
  • certain parasitic infections
  • may represent species-specific responses to certain categories of non-infectious disease
  • porcine salt poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fibrinous exudate

A
  • reflects severe vascular insult which may suggest certain infectious agents (chlamydia, FIP)
  • rare to just see this in the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do you see in non-suppurative meningitis

A
  • mostly lymphocytes, monocytes

- some histiocytes, neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what do you see in suppurative meningitis

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pleocytosis

A

migration of leukocytes (especially neutrophils) across the BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

perivascular cuffs

A
  • general term for describing the accumulation of cells in the perivascular area of medium to small sized veins (space of virchow-robin) and may be the result of cellular efflux or influx
  • infiltrating cells: lymphocytes/plasma cells, eosinophils, monocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what can the route of CNS infection affect

A
  • distribution of lesions

- progression of clinical signs (depends on location)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

portals of infection into the CNS

A
  • hematogenous (most common)
  • neural (viral diseases)
  • direct extension from surrounding structures (trauma, abscess)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hematogenous route of infection

A
  • sites seeded (wherever vascular density is high and vessel caliber is small): leptomeninges, choroid plexus, ependyma, neural parenchyma
  • agents: bacteria, viruses, fungi, parasites, protozoa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

neural route of infection

A
  • retrograde axonal transport (rabies, human herpes-1)

- ascending neuritis from oral cavity (listeriosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

direct extension from surrounding structures route of infection

A
  • nasal turbinates (cryptococcosis)

- extension from otitis media/interna (actinomyces pyogenes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

once bacteria enter CNS through blood, what happens

A

multiple and induce the release of proinflammatory and toxic compounds, which lead to pleocytosis and increased BBB permeability –> bacterial meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is suppurative meningitis +/- choroiditis

A
  • secondary to generalized bacteremia (septicemia)
  • generally disease of young immunocompromised animals (FPT, e coli, strep)
  • primary infection site may be difficult to find (hematogenous dissemination) –> synovial membranes, serosal membranes, kidneys, meninges, CNS lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

lesions in suppurative meningitis +/- choroiditis

A
  • cloudiness of meninges (dependent portions)
  • when meninges are grossly altered by inflammatory exudate, process is generally suppurative (neutrophils, bacteria, exudate may be sterile)
  • secondary changes (brain swelling/edema, secondary hydrocephalus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

meningoencephalitis

A
  • similar pathogenesis as meningitis
  • seeding of CNS structures by bacterial emboli (increased particle size) –> pasteurella, actinobacillus, coliforms, histophilus
  • primary site of infection may be more readily defined
  • extension to involve brain facilitated by capillary embolization/venous thrombosis
30
Q

abscess formation

A
  • hematogenous seeding –> often associated with larger septic emboli (endocarditis, strep)
  • arterial embolization at cerebral gray-white junction and thalamus results in infarction
  • infection does not spread beyond the devitalized tissue, and that tissue is walled off by fibrillary astrocytes
31
Q

meningeal abscessation

A

may represent a sequel to bacterial meningoencephalitis

32
Q

thromboembolic meningoencephalitis

A
  • bacterial disease of cattle caused by histophilus somni
  • localization in vessels of CNS –> multifocal vasculitis, thrombosis, malacia
  • lesions of other organ systems (infection of endothelium, bacteria in macrophages)
  • thrombosis in CNS –> malacia, hemorrhage
33
Q

what is listeriosis and pathogenesis

A
  • short gram + rod associated with abortion, septicemia, encephalitis
  • inadequate fermentation of silage
  • enters rami of trigeminal nerve from buccal mucosa, erupting teeth, exposed dental pulp (ascending neuritis)
  • ascention to brainstem where encephalitis develops
34
Q

brainstem lesions of listeriosis

A
  • gross: meningeal congestion, turbid CSF, pinpoint yellow to red soft parenchymal foci
  • microscopic: non-suppurative meningitis/perivacular cuffing, parenchymal microabscesses
  • macroscopic hemorrhage, edema
35
Q

what do you see with granulomatous meningoencephalitis

A
  • center of necrosis
  • surrounded by macrophages and lymphocytes
  • can be caused by mycobacterium
36
Q

hematogenous route of CNS viral infection

A
  • virus carried by leukocytes across BBB

- virus infects endothelial cells followed by direct extension into neuropil

37
Q

extension along nerve processes of CNS viral infection

A
  • rabies, herpes
  • retrograde axoplasmic transport from peripheral sites to paraspinal ganglia and ultimately the brainstem or spinal cord
38
Q

direct virus-induced damage to CNS

A

-lytic infection: fulminant viral gene expression –> death of host cell
-persistent infection: low-level viral gene expression
-latent infection: no gene expression
(lytic –> PI –> latent)

39
Q

viruses causing lytic infection of neurons or glia regardless of host age (7)

A
  • canine distemper (neurons, astrocytes)
  • pseudorabies (neurons, glia)
  • herpex (neurons)
  • rabies (n)
  • polio (n)
  • EEE/WEE/VEE (n)
  • west nile (n)
40
Q

viruses causing lyic infection of CNS cell types in fetuses or neonates (5)

A
  • feline parvo
  • canine herpes
  • BVD
  • akabane
  • hog cholera
41
Q

indirect viruses and CNS damage - induction of immunomediated response

A
  • ex) caprine arthritis, FIV, HIV
  • immunopathogenic mechanisms: infection of microglia by lentivirus
  • highly inflammatory lesion –> demyelination with sparing of neurons
  • productive infection of microglia, T lymphocyte interaction with macrophages (cytokines), antiviral antibodies
42
Q

indirect viruses and CNS damage - induction of vascular lesions

A
  • may result in CNS edema, hemorrhage, thrombosis, infarction
  • may affect systemic vasculature (CNS included), or lesion may be prominently on CNS
  • damage may be from lytic virus infection of vessel wall (herpes)
  • damage to vessel may be immune mediated (malignant catarrhal fever, FIP)
  • may reflect endothelial damage and infection of neural cells when hematogenous route used (hendra virus, nipah virus, west nile)
43
Q

general microscopic features of virus-infected tissues

A
  • non-suppurative meningeal and/or parenchymal perivascular infiltrates (non-suppurative meningoencephalitis) –> lymphocytes, plasma cells
  • necrosis of specific cell types
  • viral inclusion bodies
44
Q

what are viral inclusion bodies

A
  • accumulations of virus protein or nucleoprotein in the nucleus or cytoplasm
  • formation of novel intranuclear structures
  • nuclear bodies are derived from nucleoli and arise to supplement nucleolar function
  • virus infection may induce these structures to support the increased metabolic demand placed upon cells by virus replication
45
Q

4 things you see microscopically in virus-infected tissues

A
  • lymphocytic perivascular cuff in CNS
  • neuronal degeneration and necrosis
  • stellitosis and neuroniophagia
  • viral inclusion bodies (intranuclear, intracytoplasmic)
46
Q

canine distemper virus info

A
  • paramyxoviral multisystemic disease
  • clinical signs may be referable to primary viral or secondary bacterial infection of resp or GI tract
  • replication within CNS is very age-related
47
Q

canine distemper pathogenesis steps

A
  • initial replication in lymphoid tissue of upper respiratory tract (tonsils)
  • viremia with seeding of lymphoid tissues of body (second viremia)
  • virus replication within other tissues (lymphoid tissue, bronchiolar epithelium, intestinal/gastric, cutaneous, urinary, odontogenic, nervous tissue)
48
Q

things that CDV causes (list 3)

A
  • acute encephalopathy/acute encephalitis
  • subacute encephalitis (most common)
  • delayed onset encephalitis (old dog encephalitis - neuronal viral persistence)
49
Q

acute encephalitis in CDV

A
  • neuronal lytic infection
  • infection of young dogs without protective immunity from colostrum
  • neurons of these animals support high-level virus replication
  • rapid spread through CNS neurons –> rapid death
  • +/- structural evidence of CNS infection
50
Q

subacute encephalitis in CDV

A
  • glial lytic infection
  • as CNS matures, neuronal support of virus replication declines –> infection of glia most apparent, progression through neuropil is protracted
  • infection of non-neuronal tissues (systemic signs may be cause of death)
  • white matter lesions in cerebellum, pons, mesencephalon, medulla, spinal cord
  • lesions tend to be periventricular
51
Q

lesions in CDV subacute encephalitis

A
  • loss of myelin (astrocyte infection –> oligodendrocytes degenerate, variable inflammation, glial intranuclear inclusions, astrocyte fusion, malacia)
  • CNS infection may be subclinical (virus persists in neurons)
52
Q

what is rabies

A

rhabdoviral disease of nervous system in which virus infection of neurons results in neuronal degeneration and necrosis with formation of viral inclusion bodies

53
Q

rabies pathogenesis

A
  • virus introduced to host with initial viral replication at site of entry
  • virus enters peripheral sensory nerve ending and ascends to associated ganglion (paravertebral/dorsal spinal) by retrograde axoplasmic transport
  • spread to spinal cord and ascension within the cord using axoplasmic transporter
  • axoplasmic transport of virus occurs as virus ascends spinal cord, infecting new populations of neurons
  • fatality as virulent strains reach brain
54
Q

how route of rabies entry affects replication and amplification

A
  • aerosol: replication in neuroepithelial calls of nasal nuclsa
  • bite: amplification in muscle cells and cells of sensory spindle apparatus
55
Q

rabies in horse v cow

A
  • horse: brain affected more

- cow: spinal cord affected more

56
Q

histopath of rabies

A
  • lymphocytic perivascular cuff in CNS and ganglioneurotis
  • neuronal degeneration
  • negri bodies
57
Q

equine herpesvirus 1 subtype 1 info

A
  • abortogenic strain
  • encephalitogenic variants: propensity to cause CNS signs is function of tropism for endothelial cells of vessels of spinal cord white matter
58
Q

insult in equine herpes

A
  • viral lytic infection of endothelial cells and immune complex formation –> necrotizing vasulitis with hemorrhage
  • lesions anywhere in CNS, mostly present in spinal cord and brainstem white matter
  • mononuclear cells may accumulate in or around affected vessels
59
Q

signifiance of changes in equine herpes

A
  • resultant white matter ischemia
  • wallerian degeneration
  • longest fiber tracts will accumulate greatest number of hits –> posterior paresis
60
Q

histopath of equine herpes

A
  • involvement of cerebrospinal ganglia
  • intranuclear inclusions NOT observed
  • IHC will demonstrate viral antigen
61
Q

FIP

A
  • coronavirus infection of cats –> multisystemic necrotizing vascular disease
  • affects vessels associated with choroid, meninges, ependyma
62
Q

systemic mycoses

A
  • hematogenous dissemination of fungal yeast forms results in seeding of leptomeninges (histoplasma, blasto, coccidio, crypto)
  • type of inflammatory exudate may vary (granulomatous, pyogranulomatous, negligible)
63
Q

opportunistic fungi

A
  • debilitation or immunosuppression results in tissue invasion
  • septic thromboemboli and mycelial forms which invade vessel walls result in infarctive lesions
  • agents: aspergillus, mucor, rhizopus, candida
64
Q

cryptococcus neoformans info

A
  • cats especially
  • entry may be hematogenous or by direct entension from nasal cavity
  • most frequently encountered CNS mycosis, 50% exhibit CNS symptoms
  • pathogenic variants have thick mucopolysaccharide capsule
65
Q

CNS lesions in cryptococcus

A
  • solid masses of organisms with minimal inflammatory response
  • grossly this is unapparent or see cloudy leptomeninges +/- hemorrhage
66
Q

protozoal infection overview

A
  • DH and IH
  • infection of DH is intestinal, often asymptomatic, sexual reproduction with shedding of infective oocysts
  • infection of IH may be symptomatic, asexual replication within vascular endohelium
  • replication within tissue parenchymal cells with encystment
  • some degree of immunocompromise generally required
67
Q

examples of protozoal infections (4)

A
  • toxoplasma gondii
  • neosporum caninum
  • sarcocystis neurona
  • encephalitozoon cuniculi
68
Q

equine protozoal myeloencephalitis (EPM)

A
  • sarcocystis neurona
  • DH: opossum, IH: raccoon
  • lesion: perivascular cuffs of lymphocytes/macrophages/multinucleated giant cells, eosinophils with edema, wallerian degeneration with malacia
  • organisms may be associated with lesions, free, or encysted
  • atrophy of peripheral nerves and corresponding musculature
69
Q

toxoplasmosis info

A
  • toxoplasma gondii
  • DH: cat - IH: mouse, mole, squirrel, etc (humans)
  • 1/3 involve CNS symptoms
  • immune suppression predisposes to infection
  • lesions: malacic foci, pseudocysts, histiocytic inflammation, granulomas
70
Q

metazoan parasites - aberrant migration

A
  • parasitic or verminous encephalomyelitis
  • aberrant migration through or encystment in CNS by parasite that is normally localized to other tissues of affected host
  • strongylus vulgaris, taenia solium, cuterebra
71
Q

metazoan parasites - aberrant host

A
  • parasitic or verminous encephalomyelitis
  • migration through CNS by parasite not normally encountered in affected host
  • parelaphostrongylus tenius (normal = deer, larval migrans in goats, sheep, camelids)
  • baylisascaris procyonis (normal = raccoon, larval migrans in dogs)
72
Q

parelaphostrongylus tenius

A
  • normal = deer, larval migrans goats, sheep camelids
  • moose circling in water
  • meningeal worm

Pathology 3 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions