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BOD 3 > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

The outermost layer of the meninges

A

Dura
“pachymeninges”

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2
Q

send, stores, and receive electical and chemical signals
lots of different types
cell body, dendrytes, axons

A

neurons

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3
Q

local immune cells of the CNS

A

Microglia

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4
Q

Types of glial cells (supportive cells)

A

1) Microglia
2) Astrocytes
3) Oligodendrocytes

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5
Q

cells of the CNS that function for regulation, repair and support

A

astrocytes

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6
Q

cells of the CNS that produce myeline for insulation

A

oligodendrocytes

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7
Q

What does polio- root word mean

A

disease affecting the gray matter (neurons or stroma-neurpil)

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8
Q

What does the leuko- rootword mean

A

disease affecting the white matter

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9
Q

anterograde transport

A

moved towards the synapse

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10
Q

retrograde transport

A

moved away from the synapse (upwards)

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11
Q

in the spinal cord, the white matter is on the _______ while the grey matter is on the _______

A

inside; outside

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12
Q

layers of the meninges

A

1) Dura mater
2) Arachnoid
3) Pia mater

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13
Q

Which of the following cell types is local immune cell of CNS

A

Microglial cell

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14
Q

Encephalo-

A

brain

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15
Q

myelo-

A

spinal cord

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16
Q

polio-

A

greymatter

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17
Q

leuko-

A

white matter

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18
Q

gross softening of the brain (necrosis)

A

malacia

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19
Q

malacia

A

gross softening of the brain (necrosis)

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20
Q

What are the neuronal reactions to injury

A

1) Chromatolysis
2) Ischemic cell change (acute neuronal necrosis

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21
Q

degenerative change seen in cell body associated with axonal injury
swelling of nerve cell body (perikaryon) with dispersion (loss) of Nissl substance and peripheral displacement of the nucleus

A

Chromatolysis

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22
Q

Chromatolysis

A

-degenerative change seen in cell body associated with axonal injury
-swelling of nerve cell body (perikaryon) with dispersion (loss) of Nissl substance and peripheral displacement of the nucleus

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23
Q

Is Chromatolysis reversible ir irreversible

A

reversible degenerative change seen in cell body associated with axonal injury
-swelling of nerve cell body (perikaryon) with despiersion (loss of Nissl substance and peripheral displacement of the nucleus)

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24
Q

is acute neuronal necrosis reversible or irreversible

A

irreversible

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25
Q

What might lead to acute neuronal necrosis

A

1) Ischemia
2) Hypoxia
3) Hypoglycemia
4) Nutritional deficiency
5) Chemical intoxication
6) Excitatory toxicity - excessive sustained release or reduced clearance of excitotoxic neurotransmitters (e.g glutamate, aspartate)

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26
Q

excessive sustained release or reduced clearance of excitotoxic neurotransmitters (e.g glutamate, aspartate)

A

Excitatory toxicity

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27
Q

What do you see on histo after acute neuronal necrosis

A

shrunken and angular cell bodies with hypereosinophili cytoplasm and pyknotic nuclei

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28
Q

________________ cause swelling of the neuronal cell body with finely vacuolated cytoplasm

A

Lysosomal storage diseases- eg Locoweed

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29
Q

What is an example of a toxin that causes swelling of the neuronal cell body with finely vacuolated cytoplasm *lysosomal storage disease

A

Locoweed (swainsonine) toxicity

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30
Q

transmissible spongiform encephalopathy characterized by large discrete cytoplasmic vacuoles

A

neuronal vacuolization in prion diseases

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31
Q

prion diseases cause

A

transmissible spongiform encephalopathy characterized by large discrete cytoplasmic vacuoles

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32
Q

What is the aging pigment seen in aging neurons

A

Lipofuscin- no harmful effects
-orange-brown granular pigment

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33
Q

What causes Negri bodies (intracytoplasmic neuronal inclusion bodies)

A

Rabies virus

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34
Q

Are Negri bodies, seen in Rabies, intracytoplasmic or intranuclear?

A

Intracytoplasmic inclusion bodies

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35
Q

______________ bodies are _______________ inclusions seen in Rabies virus

A

Negri ; intracytoplasmic

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36
Q

Are herpes viral inclusion bodies intracytoplasmic or intranuclear?

A

intranuclear

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37
Q

Are Canine distemper viral inclusion bodies intracytoplasmic or intranuclear?

A

Both - intracytoplasmic and intranuclear

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38
Q

_________ virus only causes intranuclear inclusion bodies

A

Herpes virus

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39
Q

Why might injury to the cell body result in axonal changes

A

the axon is dependent on the neuronal cell body for delivery of nutrients and essential materials (neurofilaments) and removal of debris by active transport

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40
Q

the axon is dependent on the ____________ for delivery of nutrients and essential materials (neurofilaments) and removal of debris by active transport

A

neuronal cell body

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41
Q

Why might there be primary axonal injury

A

1) Trauma
2) Nutrient deficiencies (Vitamin E deficiency in horses)
3) Toxicoses
4) Inherited defects (ie axonopathies)

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42
Q

What are the progressive changes of axonal degeneration after injury

A

Swelling (spheroid) -> fragmentation -> removal by microglial cells (Gitter cells)

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43
Q

Cells that eat both the axon and myelin after axon injury/fragmentation. sit in digestion chambers

A

Gitter cells (microglial cells)

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44
Q

What is Wallerian degeneration*

A

degeneration of the axon and its myelin sheath distal to the site of focal injury (away from cell body). In the spinal cord, it occurs
1) Ascending tracts (tracts heading cranially towards the brain) cranial to the site of focal axon injury- dorsal funiculi and dorsolateral portion of lateral funiculi
2) Descending tracts (tracts heading further caudally towards the axon synapse) caudal to the site of axon injury- ventral funiculi and deep tracts of lateral funiculi

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45
Q

degeneration of the axon and its myelin sheath occurs _________ to the site of focal injury (away from cell body).

A

distal

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46
Q

What happens in the neuronal cell body survives following axonal injury

A

Regeneration from proximal stump can occur
Budding axon sprouts “neurites” can grow 2-4mm/day in pNS but much slower in the CNS
*Requires intact endoneurium and guiding influences of Schwann cells (PNS) or oligodendrocytes (CNS)

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47
Q

Schwann cells are in the

A

PNS

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48
Q

Oligodendrocytes are in the

A

CNS

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49
Q

What does the neuronal cell body need to grow new axons after injury

A

Requires intact endoneurium and guiding influences of Schwann cells (PNS) or oligodendrocytes (CNS)

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50
Q

What is the difference between Astrocytosis vs Astrogliosis

A

Astrocytosis is hyperplasia after injury
Astrogliosis is hypertrophy (increased number, size, and complexity of processes)

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51
Q

Gemistocyte

A

a reactive astrocyte with prominent eosinophilic cytoplasm (really large)

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52
Q

Alzheimer type II astrocytes

A

swollen ,degenerating astrocyte cells with clear cytoplasm and pale staining nuclei
-most often with renal or hepatic encephalopathy

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53
Q

When are Alzheimer type II astrocytes most commonly seen

A

with renal or hepatic encephalopathy

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54
Q

What are the two types of oligodendrocytes (CNS)

A

1) Interfascicular (white matter)- formation of maintenance of myelin in CNS
2) Perineuronal “satellite” cells (gray matter)- neuronal metabolism

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55
Q

myelinating cell of PNS

A

Schwann Cell

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56
Q

Satellitosis

A

hyperplasia of satellite cells in response to neurons in distress

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57
Q

T/F: if satellite cells die, the injury is irreversible and it leads to primary demyelination

A

true

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58
Q

T/F: Schwann cells have a limited capacity, compared to oligodendrocytes to remyelinate

A

False- oligodendrocytes are the cells whos damage is irreversible and leads to primary demyelination
*limited capacity compared to Schwann cells in PNS

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59
Q

degeneration/degradation of myelin sheath, with sparing of axon
-direct damage to myelin sheath or damage to myelin-producing cells (Schwann and oligodendrocytes)

A

primary demyelination
due to:
toxic (bromethalin), metabolic (hepatic encephalopathy), inherited enzymes defect in myelin metabolism, inflammatory/ immune mediated (canine distemper, caprine artheritis- encephalomyelitis)

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60
Q

what toxin might lead to primary demyelination

A

bromethalin

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61
Q

demyelination that is secondary to primary axonal injury (wallerian degeneration)
myelin depends on integrity of axon

A

Secondary demyelination

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62
Q

insufficient or absent myelin production
-in-utero pestivirus infections

A

Hypomyelination

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63
Q

formation of abnormal or unstable myelin leading to premature demyelination
-inherited leukodystrophies

A

Dysmyelination

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64
Q

Hypomyelinogenesis

A

insufficient or absent myelin production
-in-utero pestivirus infections

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65
Q

Dysmyelination

A

formation of abnormal or unstable myelin leading to premature demyelination
-inherited leukodystrophies

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66
Q

resident mononuclear phagocytes *resident macrophages of the CNS)

A

Microglial cells

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67
Q

Responses of microglial cells due to injury

A

1) Hypertrophy- activated macrophages with prominent cytoplasm- Rod cells
2) Hyperplasia: clusters of microglia in glial nodules- common with viral infections
3) Phagocytosis of: Lipid/myelin debris = Gitter cells and dead neurons (neuronophagia)

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68
Q

Rod cells

A

activated microglial cells (macrophages) with a prominent cytoplasm

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69
Q

Status spongiosis

A

spongy appearance of parenchyma (non-specific change) that can result from
-Postmortem artifact
-Intra-myelinic edema
-Loss of axons and/or myelin
-Vacuolation of neurons, glial cells, or their processes

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70
Q

How are small vs large CNS lesions healed

A

Small: proliferation of astrocytes/ processes
Large: astrocyte proliferation cannot occur leading to cavitation or cystic spaces

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71
Q

What are the types teratogens that can lead to congenital malformation of the nervous system

A

1) Physical agents: trauma, radiation
2) Nutritional factors (hypovitaminosis A -> optic nerve hypoplasia or congenital copper deficiency in lambs leads to white matter necrosis/ cavitation)
3) Toxins: eg steroidal alkaloid from veratrum californicum (skunk cabbage) in hseep at day 14 gestation -> synopthalia (failure of the 2 eye globes to separate and holoprosencephaly)
4) Virus e.g feline panleukopenia lead to cerebellar hypoplasia
or VBDV leads to cerebellar hypoplasia, hydranencephaly, porencephaly

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72
Q

Hypovitaminosis A during gestation leads to

A

optic nerve hypoplasia

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73
Q

Congenital copper deficiency in lambs leads to

A

Swayback
white matter necrossi and cavitation

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74
Q

Ingestion of Steroidal alkaloid from Veratrum californicum (skunk cabbage) at day 14 leads to________ in sheep

A

synopthalia (failure of the 2 eye globes to separate and holoprosencephaly

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75
Q

What what day of gestation does ingestion of Veratrum californicum (skunk cabbage) lead to synopthalia and holoprosencephaly in sheep

A

Day 14

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76
Q

Veratrum californicum **

A

Skunk cabbage that when ingested at day 14 of gestation in sheep leads to synopthalia and holoprosencephaly

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77
Q

Feline panleukopenia virus causes newborns to have

A

cerebellar hypoplasia

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78
Q

BVDV causes newborns to have

A

cerebellar hypoplasia
Hydrancephaly
Porencephaly

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79
Q

Synophthalmia

A

failure of the 2 eye globes to separate
-idiopathic
-veratrum californicum

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80
Q

Holoprosencephaly

A

where the two hemispheres of the brain do not separate
-idiopathic
-veratrum californicum

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81
Q

Most congenital malformations of the CNS occur immediately after birth or within the first week of life. When might they not

A

some may occur later in life (ie Lysosomal storage diseases)

*also some malformations are obvious externally while others require sectioning brain/spinal cord

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82
Q

Cranium bifidum

A

cranioschisis
-midline bony defect in the cranium
may be accompanied by
a) Meningocele (sac like protrusion of meninges through defect
b) Meingocephalocele (sac-like protrision of meninges and brain parenchyma through defect)

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83
Q

-midline bony defect in the cranium
may be accompanied by
a) Meningocele (sac like protrusion of meninges through defect
b) Meingocephalocele (sac-like protrision of meninges and brain parenchyma through defect)

A

Cranium bifidum (cranioschisis)

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84
Q

What might accompany Cranium bifidum

A

a) Meningocele (sac like protrusion of meninges through defect
b) Meingocephalocele (sac-like protrision of meninges and brain parenchyma through defect)

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85
Q

What are the different neural tube closure defects

A

1) Cranium bifidum (Cranioschisis)
2) Spina bifida

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86
Q

midline bony defect in vertebral column
usually involves lumbar, sacral or caudal vertebrae
ranging from failure of closure of vertebral arches (most common) to agenesis of vertebrae
may be accompanied by meningocele, meningomyelocele, or myelodysplasia

A

Spina bifida

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87
Q

What vertebrae does spina bifida most commonly affect

A

lumbar, sacral or caudal vertebrae

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88
Q

What may accompany spina bifida (midline bony defect in vertebral column leading to failure of vertebral arches to close or agenesis)

A

meningocele, meningomyelocele, or myelodysplasia

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89
Q

What results in interference with normal migration of neurons during development

A

genetic defects

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90
Q

What is Lissencephaly

A

agyria- cerebrum has smooth surface without gyri and sulci
due to a genetic defect resulting in interference of normal migration of neurons during development

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91
Q

What causes Lissencephaly

A

agyria- cerebrum has smooth surface without gyri and sulci
due to a genetic defect resulting in interference of normal migration of neurons during development

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92
Q

You see a rat with a smooth brain upon necropsy. You are thinking lissencephaly (agyri). What is significant?

A

Lissencephaly is genetic defect resulting in interference with normal migration of neurons during development leading to no gyri and sulci

Rats, Mice, and Rabbits normally have a smooth brain so this is not signficiant

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93
Q

formation of fluid filled cavities in brain reuslting from destruction of immature neuroblasts preventing appropriate migration and development
-usually occurs in utero

A

Encephaloclastic defects

a) Porencephaly: smaller cavities in cerebral hemispheres

b) Hydranencephaly: more severe destructive event resulting in massive cerebrocortical necrosis (gray and/whte matter) with almost complete loss of pre-existing tissue -> compensatory expansion of the lateral ventricles

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94
Q

Porencephaly

A

smaller fluid-filled cavities in cerebral hemispheres resulting from destruction of immature neuroblasts preventing appropriate migration and development, usually in utero

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95
Q

Hydranencephaly

A

more severe destructive event resulting in massive cerebrocortical necrosis (gray and/whte matter) with almost complete loss of pre-existing tissue -> compensatory expansion of the lateral ventricles

due to destruction of immature neuroblasts preventing appropriate migration and development

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96
Q

Encephaloclastic defects

A

formation of fluid filled cavities in brain reuslting from destruction of immature neuroblasts preventing appropriate migration and development
-usually occurs in utero

can be Porencephaly or Hydranencephaly

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97
Q

Encephaloclastic defects are often associated with

A

utero viral infections (eg. BVDV, bluetongue virus, Border disease virus)

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98
Q

You see several lambs from a flock of sheep in Germany were aborted or stillborn with several neuromuscular congenital malformations. You note porencephaly and arthrogryposis. What are some potential causes

A

Schmallenberg Virus *

Other possible causes:
Akabane Virus
Cache Valley Virus
Bluetongue Virus

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99
Q

What are the fetal teratogenic effects of feline panleukopenia virus (parvovirus)

A

Cerebellar hypoplasia, dysplasia
Purkinje cell loss
Hydranencephaly

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100
Q

What are the fetal teratogenic effects of Classical Swine Fever Virus (Pestivirus)

A

Dysmyelinogenesis, cerebellar hypoplasia

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101
Q

What are the fetal teratogenic effects of BVDV

A

Hydrocephalus, cerebellar hypo- and aplasia, prosencephaly in calves; hypomyelination ,orencephaly in lambs

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102
Q

excessive accumulation of cerebrospinal fluid leading to expansion of ventricular system +/- Subarachnoid spaces

A

Hydrocephalus

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103
Q

What is the most common congenital malformation in Vet med

A

Hydrocephalus

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104
Q

With hydrocephalus there is excessive accumulation of CSF leading to expansion of the

A

ventricular system +/- subarachnoid spaces

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105
Q

What are the different types of Hydrocephalus

A

1) Non-communicating (most common): fluid within ventricular system, obstruction anterior to lateral apertures of 4th ventricle and (mesencephalic aqueduct)

2) Communicating (rare): excess fluid in ventricular system and subarachnoid spaces leading to malformation of arachnoid villi

3) Hydrocephalus Ex vacuo: loss of brain tissue (eg hydranencephaly) leading to dilation of ventricular system

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106
Q

What is the most common site of obstruction in non-communicating hydrocephalus *

A

Mesencephalic aqueduct

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107
Q

Hydrocephalus Ex vacuo

A

loss of brain tissue (eg hydranencephaly) leading to dilation of ventricular system

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108
Q

What are the sequelae to hydrocephalus

A

1) dilation of ventricles- secondary compression atrophy of white matter
2) May have flattened gyri and shallow sulci
3) Possible herniation through foramen magnum (depending on how rapid obstruction occurs)

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109
Q

What breeds is congenital hydrocephalus most common in

A

toy and bracycephalic breeds of dogs
and
calves

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110
Q

Congenital hydrocephalus is most commonly a malformation of the _____________ **

A

mesencephalic aqueduct

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111
Q

congenital hydrocephalus

A

associated with enlargement of cranium (doming) and open fontanelles
most commonly a malformation of mesencephalic aqueduct
most common in toy and brachycephalic breeds and calves

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112
Q

How might an animal get acquired hydrocephalus

A

obstruction of CSF flow due to inflammation, neoplasia or other compressive lesions
-location varies

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113
Q

obstruction of CSF flow due to inflammation, neoplasia or other compressive lesions
-location varies

A

acquired hydrocephalus

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114
Q

abnormal dilation of central canal of spinal cord

A

hydromyelia

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115
Q

What is the most appropriate term for dilation of the ventricular system secondary to an encephaloclastic defect such as hydranencephaly

A

non-communicating hydrocephalus

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116
Q

Hydromyelia

A

abnormal dilation of central canal of spinal cord
-most are congenital (genetic or infectious)
-acquired are rare (similar causes to acquired hydrocephalus)

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117
Q

which of the following locations of stenosis is most commonly found in congenital hydrocephalus

A

Mesencephalic aqueduct

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118
Q

Syringomyelia

A

cystic fluid filled tubular cavity (syrinx) within the spinal cord that is not lined by ependyma
-congenital or acquired (rupture of ependyma with secondary cavitation)
Dogs and calves; Weimaraner and CKCS -associated with Chiari-like malformation)

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119
Q

cystic fluid filled tubular cavity (syrinx) within the spinal cord that is not lined by ependyma

A

Syringomyelia

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120
Q

What breeds is syringomyelia most common in

A

Dogs and calves; Weimaraner and CKCS -associated with Chiari-like malformation)

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121
Q

Syringomyelia can be congenital or acquired. How might it be acquired

A

rupture of the ependyma with secondary cavitation leads to a cystic lfuid-filled tubular cavity (syrinx) within the spinal cord

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122
Q

What will you see microscopically in a patient with cerebellar hypoplasia

A

the cerebellum is decreased in size but microscopically you will see decreased Purkinje cells and granular layer cells- destruction of mitotically active external granular cells

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123
Q

What are the causes of cerebellar hypoplasia

A

1) Viral infections: parvoviruses (feline panleukopenia and canine parvovirsu) or Pestiviruses (BVDV at fetal 100-150 days gestation or classical swine fever, or border disease virus)

2) Inherited genetic defect

3) Toxins: piglets from sows treated with organophsophate insecticide during second half of gestation

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124
Q

piglets from sows treated with organophsophate insecticide during second half of gestation will develop

A

cerebellar hypoplasia

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125
Q

At what time frame of gestation do fetal infections of BVDV result in cerebellar hypoplasia

A

between days 100-150

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126
Q

What is cerebellar cortical abiotrophy (CCA)

A

the lack of vital, nutritive substance necessary for normal cell lifespan
-premature degeneration/ necrosis and loss of Purkinje cells and granular layer cells (cerebullum can be smaller or normal size)
-Intrinsic metabolic defect susepcted (most autosomal recessive)
early onset and progressive (but not as borth) -> cerebllar ataxia with head tremor, truncal ataxia, symmetrical hypermetria, spasticity and broad-based stnace

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127
Q

-premature degeneration/ necrosis and loss of Purkinje cells and granular layer cells (cerebullum can be smaller or normal size)
-Intrinsic metabolic defect susepcted (most autosomal recessive)

A

Cerebellar cortical abiotrophy (CCA)

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128
Q

How do you differentiate cerebellar hypoplasia from cerebellar cortical abiotrophy *

A

CCA is early onset and progressive (NOT present at birth)

cerebellar ataxia with head tremor, truncal ataxia, symmetrical hypermetria, spasticity and broad-based stanace

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129
Q

CCA is inherited in the breeds_______

A

dogs (Airdale, border collie, gorden setter

horses (arabian*, gotland pony

cattle (holstein, hereford, angus)

sheep (merine, coriedale)

pigs (Yorkshire)

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130
Q

What breeds get Chiari-like malformations

A

Cavalier King Charles Spaniel

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131
Q

What is Chiari-like malformation

A

when there is a mismatch between the caudal fossa volume and the brain parenchyma mass leading to caudal herniation of cerebellar vermis and brainstem into the foramen magnum
leading to
-Alteration in CSF flow between intracranial and spinal compartments and reduced craniospinal compliance can lead to springomyelia
common in CKCS

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132
Q

when there is a mismatch between the caudal fossa volume and the brain parenchyma mass leading to caudal herniation of cerebellar vermis and brainstem into the foramen magnum
leading to
-Alteration in CSF flow between intracranial and spinal compartments and reduced craniospinal compliance can lead to springomyelia
common in CKCS

A

Chiari-like malformation

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133
Q

what leads to syringomyelia in CKCS that hav chiari-like malformation

A

when they have chairi-like malformation there is a mismatch between caudal fossa volume and brain parenchyma mass leading to caudal herniation of cerebllar vermis and brainstem into foramen magnum

this creates alteration in CSF flow between intracrnail and spinal compartments and the reduced craniospinal compliances leads to syringomyelia

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134
Q

most biochemical defects are

A

lysosomal storage diseases
usually autosomal recessive (homozygotes manifest disease, heterozygotes are phenotypically normal by 50% have norma enzume activity

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135
Q

Do homozygotes or heterozygotes get lysosomal storage diseases

A

it is autosomal recessive
often gene dose dependent

homozygotes- manifest disease while heterozygotes are phenotypically normal but have 50% of normal enzyme activity

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136
Q

What do you see histologically of patients with lysosomal storage diseases

A

neurons +/- other cell types such as glial cells, macrophages, hepatocytes, renal tubular epithelium) with finely vacuolated cytoplasm

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137
Q

Ceroid lipofuscinosis

A

clinical signs are usually seen 1-2 years of age
widespread sotrage: moost severe/damaging to neurons of cerebral cortex, retina, and cerebellar Purkinje cells
leading to dementia blindness, ataxia
Atrophied regions may have brown tinge
*Only storage disease with gross lesions

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138
Q

What is the only storage disease with gross lesions

A

Ceroid lipofuscinosis
-atrophied regions may be brown tingue

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139
Q

widespread storage to severe/damaging to neurons of cerebral cortex, retina and cerebllar Purkinje cells
leaves atrophied regions with brown tingue *

A

Ceroid lipofuscinosis

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140
Q

When are the clincial signs of Ceroid lipofuscinosis apparent

A

typically 1-2 years of age

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141
Q

What plants do you see acquired/ induced storage disease due to Swainsonine toxicity

A

Astragalus and Oxytropis (locoweeds)

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142
Q

What happens when sheep, cattle, and horses eat Astragalus and Oxytropis (locoweeds)

A

1) Indolizidine alkaloid: inhibitor of a-mannosidase enzyme
2) get microscopic lesions idenditcal to genetic alpha-mannosidosis (finely vacuolated cytoplasm)
3)Storage disease

*Can be transfered to the fetus if pregnant animals consume it

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143
Q

T/F: if animal eats Astragalus and Oxytropis (locoweeds), the storage disease can be transferred to the fetus

A

True

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144
Q

you have a 6yo MN greyhound with peracute (sudden) onset of disorientation behavior changes and head pressing
Clinicalsigns after initial onset have no progressed and possibly improved over time. What is ths likely

A

Stroke or Neoplasia

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145
Q

What is the typical clinical presentation of cerebrovascular disease (stroke)

A

peracute/acute onset of neuro signs (usually indicating a focal lesion) which typically do not progress and may ablate with time

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146
Q

the outcome of thrombosis and infarction to nervous system depends on

A

-Type and size of obstructed vessel
-Rapidly of onset of ischemia (gradual to sudden obstruction)
-Vulnerability of the area of brain or spinal cord to hypoxia
(Neurons > Oligodendrocytes > astorcytes > microglia > vascular endothelial cells

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147
Q

What are the susceptibility levels of different cells in the CNS to hypoxia

A

Neurons > Oligodendrocytes > Astrocytes > Microglia > Vascular endothelial cells

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148
Q

What are the two different types of infarcts to the nervous system *

A

1) Ischemic infarcts: Thrombus or Thromboembolism leading to well circumscribed area of tan to yellow discolaration and softening (malacia), gray matter more susceptible, with chronicity- cavitation (if large region of injury)

2) Hemorrhagic infarct: vascular damage/ rupture leading to leakage of RBCs (venous thrombosis)
gross lesion: regional area of parenchymal hemorrhage

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149
Q

What gross lesion will you see with ischemic infarcts to the nervous system*

A

Thrombus or Thromboembolism leading to well circumscribed area of tan to yellow discolaration and softening (malacia), gray matter more susceptible, with chronicity- cavitation (if large region of injury)

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150
Q

What gross lesion will you see with a hemorrhagic infarct to the nervous system *

A

vascular damage/ rupture leading to leakage of RBCs (venous thrombosis)
gross lesion: regional area of parenchymal hemorrhage

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151
Q

Is gray or white matter more susceptible to ischemic infarcts

A

gray matter- more vasculature and susceptible cells (neurons)

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152
Q

Ischemic infarcts are due to _____________ while hemorrhagic infarcts are due to ___________

A

vascular (artery/arterioles) obstruction- thrombus or thromboembolism

Vascular damage/ rupture leading to leakage of RBCs (venous thrombosis

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153
Q

Why might a dog get atherosclerosis

A

secondary to hypothyroidism

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154
Q

you see multifocal acute hemorrhages on a canine brain. What might be the cause

A

Septicemia
Neoplasia

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155
Q

common in dogs
peracute (usually lateralized) spinal signs without pain
exact mechanism is unknown but herniation herniation of degenerative disk material (nucleus pulposus) Hansen type I -> vasculature -> occlusive emboli -> ischemic injury

A

Fibrocartilaginous emboli

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156
Q

Fibrocartilaginous emboli

A

common in dogs
peracute (usually lateralized) spinal signs without pain
exact mechanism is unknown but herniation herniation of degenerative disk material (nucleus pulposus) Hansen type I -> vasculature -> occlusive emboli -> ischemic injury

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157
Q

Although unknown, why might a dog get fibrocartilaginous emboli

A

herniation of degenerative disk material (nucleus pulposus) Hansen type I -> vasculature -> occlusive emboli -> ischemic injury

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158
Q

excess fluid accumulation in the CNS parenchyma
can be associated with most CNS disease processes

A

Edema

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159
Q

What are the types of cerebral edema

A

1) Vasogenic: most common type, due to increased vascular permeability -> extracellular fluid accumulation. White matter is most affected (spongiosis)
common causes- neoplasia, inflammation, trauma, and some toxic/metabolic conditions

2) Cytotoxic Edema: altered cellular metabolism -> intracellular fluid accumulation
Low O2 -> interference with ATP dependent Na/K pump in cell membrane leading to swelling of neurons, glial and endothelial cells (gray and white matter)
common causes are hypoxia, neoplasia, toxic/ metabolic conditions (ie salt poisoning in pigs, hepatic encephalopathy)

3) Interstitial edema (hydrostatic): accumulation of fluid in the periventricular white matter associated with increased ventricular pressure (hydrocephalus or hydromyelia)

4) Hypo-osmotic edema: osmotic imbalances associated with water intoxication

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160
Q

What is the most common type of cerebral edema

A

Vasogenic edema

most common type, due to increased vascular permeability -> extracellular fluid accumulation. White matter is most affected (spongiosis)
common causes- neoplasia, inflammation, trauma, and some toxic/metabolic conditions

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161
Q

How does vasogenic edema occur *

A

increased vascular permeability leading to extracellular fluid accumulation
white matter is most affected (spongiosis)

cause: neoplasia, inflammation, trauma

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162
Q

How does cytotoxic edema occur*

A

altered cellular metabolism -> intracellular fluid accumulation
Low O2 -> interference with ATP dependent Na/K pump in cell membrane leading to swelling of neurons, glial and endothelial cells (gray and white matter)
common causes are hypoxia*, neoplasia, toxic/ metabolic conditions (ie salt poisoning in pigs, hepatic encephalopathy)

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163
Q

How does hypo-osmotic edema occur

A

osmotic imbalances associated with water intoxication

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164
Q

How does interstitial edema occur

A

(hydrostatic): accumulation of fluid in the periventricular white matter associated with increased ventricular pressure (hydrocephalus or hydromyelia)

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165
Q

What gross lesions do you see with CNS edema

A

-flattened gyri and shallow sulci
-clear, watery fluid in leptomeninges
-posterior shifting of brain (herniation through foramen magnum)
-White matter may be soft, wet, pale yellow

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166
Q

edema may cause

A

herniation
1) through the foramen magnum (foramenal herniation)
2) Under tentorium cerebelli (transtentorial herniation)
3) Under the falx cerebri (falcine herniation)
4) Through defect in skull (eg. fracture) calvarial herniation

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167
Q

Clostridium perfringens type D (epsilon) may cause ____________ in sheep

A

focal symmetrical (hemorrhagic) encephalomalacia (internal capsule)

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168
Q

What causes focal symmetrical (hemorrhagic) encephalomalacia (internal capsule) in sheep

A

Clostridium perfringens type D (epsilon)

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169
Q

As the brain swells it can herniate. What are common locations for this to occur

A

1) through the foramen magnum (foramenal herniation of cerebellar vermis)
2) Under tentorium cerebelli (transtentorial herniation)
3) Under the falx cerebri (falcine herniation)
4) Through defect in skull (eg. fracture) calvarial herniation

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170
Q

caudal displacement of the parahippocampal gyri caused by sudden swelling of the brain from severe blunt trauma to head

A

transtentoral herniation

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171
Q

forces that are external to the body (HBC, kicks to head, falls ,gunshot wounds, bites)

A

external injury

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172
Q

what might be cause of intrinsic physical disturbances to the nervous system

A

disc extrusion,vertebral abscesses, neoplasia, congenital malformations causing compression

173
Q

primary traumatic injuries

A

from the direct trauma (fractures, hemorrhage, edema, and direct injury to the parenchyma from forces acting on the brain
(acceleration/deceleration and rotational forces)

174
Q

How do acceleration/deceleration forces differ from rotational forces in context of traumatic brain injuries

A

Acceleration/deceleration- superficial gray matter (hemorrhages, contusion, and tearing of neuronal tissue)

Rotational forces- deeper white matter (causing concussive injuries and axonal damage)

175
Q

What is second injury to trauma

A

series of events that can lead to continued injury to the neurons/glial cells
Major mediators- oxygen free radicles, excitatory amino acids, nitric oxide

176
Q

series of events that can lead to continued injury to the neurons/glial cells
Major mediators- oxygen free radicles, excitatory amino acids, nitric oxide

A

What is second injury to trauma

177
Q

What is seen in acceleration/ deceleration trauma

A

Acceleration/deceleration- superficial gray matter (hemorrhages, contusion, and tearing of neuronal tissue)

178
Q

What is seen in rotational trauma

A

Rotational forces- deeper white matter (causing concussive injuries and axonal damage)

179
Q

diffuse but transient brain injury associated with temporary loss of consciousness
typically no gross lesions
uncommon in animals

A

Concussion

180
Q

focal brain injury which may (but not usually) results in unconsciousness
usually a grossly detectible, superficial area of brain hemorrhage
often associated with skull fracture

A

Contusion

181
Q

How does concussion differ from contusion

A

Concussion: diffuse but transient brain injury associated with temporary loss of consciousness
typically no gross lesions
uncommon in animals

Contusion: focal brain injury which may (but not usually) results in unconsciousness
usually a grossly detectible, superficial area of brain hemorrhage
often associated with skull fracture

182
Q

Coup contusion

A

the inside of the cranial vault strikes the stationary brain at the point of impact

183
Q

Contrecoup contusion

A

lesion occurs on the opposite side due to stretching and tearing of vessels or the brain struck by inside of cranial vault, on opposite side from blow, where there is reduced CSF buffer present

184
Q

How does Coup differ from contrecoup

A

Coup: the inside of the cranial vault strikes the stationary brain at the point of impact

Contrecoup:

185
Q

What is the most common place you see hemorrhage following cranial trauma? **

A

The subarachnoid space

186
Q

What are the causes of brain hemorrhage

A

1) Trauma
2) DIC
3) Damage to vessels/ vasculitis (viruses, septicemia, immune complex, neoplasia, parasites)

187
Q

What fractures are common with horses that rear over backwards

A

fracture of basisphenoid bone
displaced bone lacerates large vessels at the base of the brain
hemorrhage becomes the dominant lesion

188
Q

Fracture of what bone in horses leads to laceration of large vessels at the base of the brain leading to hemorrhage *

A

basisphenoid bone

189
Q

The extradural space is greatest in the

A

cervical vertebral column, cranial thoracic, and caudal lumbar region

spinal cord compression is less likely

190
Q

There is a lower risk of intervertebral disc extrusion at the

A

intercapital ligaments (T2-T10)

191
Q

What does T2- T10 have a lower risk of intervertebral disc extrusion

A

intercapital ligaments (T2-T10)

192
Q

What might lead to contusion to the spinal cord

A

Focal hemorrhage associated with fracture, luxation, subluxation, or disc herniation

193
Q

What might lead to compression of the spinal cord *

A

extramedullary pressures (disc herniation, vertebral/ meningeal neoplasia, vertebral fracture/ subluxation, vertebral malformation

194
Q

What is seen microscopically with spinal cord trauma*

A

hemorrhage (more prominent in gray matter)
axonal/myelin degeneration at site of compression
degeneration of axon and myelin sheath distal to site of injury (Wallerian degeneration)

195
Q

Acute spinal cord compression

A

1) sudden direct impact to spinal cord (contusion)
2) Hypoxia caused by direct injury to vessels leading to hemorrhage or thrombosis
compression of vessels without vascular injury (blood stasis)
release of local neurotransmitters (norepinephrine) -> vasospasm and vasoconstriction

ex: Hansen type I intervertebral disc extrusion

196
Q

acute extrusion of nucleus pulposus through annulus fibrosus and into the canal
-usually associated with “chondroid” degeneration/metaplasia of nucleous pulposus
genetically programmed and starts early (6months)
Chondrodystrophic breeds

A

Hansen type I disc extrusion, leads to acute compression (contusion)

197
Q

Hansen type I disc extrusion

A

acute extrusion of nucleus pulposus through annulus fibrosus and into the canal
-usually associated with “chondroid” degeneration/metaplasia of nucleous pulposus
genetically programmed and starts early (6months)
Chondrodystrophic breeds

198
Q

chronic spinal cord compression that is slowly developing
Low grade hypoxia due to compression of vessels leading to reduced perfusion, vascular stasis, and increased hydrostatic pressure leading to edema

A

Hansen type II intervertebral disc protusion
or
cervical vertebral stenotic myelopathy

199
Q

bulging of disc material into the vertebral canal associated with fibrous degeneration of annulus (usually around 8-10 years of age)
More common in non-chondrodystrophic dogs

A

Hansen type II disc protrusion

200
Q

Hansen type II disc protrusion

A

bulging of disc material into the vertebral canal associated with fibrous degeneration of annulus (usually around 8-10 years of age)
More common in non-chondrodystrophic dogs

201
Q

acute and chronic spinal cord compression can lead to

A

ascending/ descending hemorrhagic myelomalacia
more common in type I IVDD
12-24 hours after injury

202
Q

high-velocity-low volume disc extrusion

A

acute non-compressive nucleus pulpsosus extrusion

203
Q

What is Wobbler’s syndrome

A

cervical vertebral stenotic myelopathy

204
Q

What can be the causes of Wobbler’s Syndrome

A

Cervical Vertebral Stenotic myelopathy caused by:
1) Osseous (young adults) where vertebral malformations often associated with degeneration of facet joint (osteochondrosis dissecans)
can be complicated/ exacerbated by hypertrophy of ligamentum flavum or synovial cysts

2) Disc-associated in adult dogs born with congenital vertebral canal stenosis: prone to cord compression because smaller extradural space with secondary hypertrophy of dorsal longitudinal ligament and annulus fibrosis
C5-C6 and C6-C7

205
Q

What is the osseous form of cervical vertebral stenotic myelopathy

A

Cervical Vertebral Stenotic myelopathy caused by:
1) Osseous (young adults) where vertebral malformations often associated with degeneration of facet joint (osteochondrosis dissecans)
can be complicated/ exacerbated by hypertrophy of ligamentum flavum or synovial cysts

206
Q

What causes the osseous form cervical vertebral stenotic myelopathy

A

vertebral malformation -degeneration of facet joints (osteochondrossis dissecans)

207
Q

What is the difference between static vs dynamic Wobbler’s syndrome in horses

A

Static >1 year of age - compression regardless of neck position (C5-C6 and C6-C7)

Dynamic (typically 8-18 months): flexed neck: C3-C4 and C4-C5

208
Q

Glioma

A

neoplasia of glial cell origin
most common type of primary intra-axial CNS neoplasia in dogs and cats (dogs more frequent)
major types:
Astrocytoma
Oligodendroglioma
Undefined glioma (both phenotypes in high proportions >30-40%)

209
Q

What is an undefined glioma

A

when there is both phenotypes (astrocytoma and oligodendroglioma) at high proportions >30-40%

210
Q

What CNS neoplasia are brachycephalic breeds predisposed for

A

Astrocytoma
Oligodendroglioma

211
Q

Where are astrocytomas most commonly located in

A

temporal and piriform lobes

212
Q

What is the gross appearance of astrocytomas *

A

firm and tan-gray with indistinct boundaries
high grade tumors have more distinct mass with hemorrhage and necrosis

213
Q

What is the gross appearance of oligodendroglioma *

A

well-demarcated with gelatinous or mucoid texture

214
Q

Where are oligodendrogliomas typically located

A

Cerebrum- olfactory bulbs and front, temporoal, and piriform lobes

215
Q

How do you diagnose gliomas

A

immunohistochem
A) Glial fibrillary acidic protein (GFAP) for cytoplasm of astrocytes
B) Oligodendrocyte lineage transcription factor 2 (Olig2) - labels nucleus of all gliomas
C) 2,3’ cyclic nucleotide 3’- phosphodiesterase (CNPase): fairly specific of oligodendroglioma (cytoplasmic)

216
Q

Where are choroid plexus tumors located *

A

Ventnricular location
-Hydrocephalus: obstructive or increased CSF production

217
Q

Choroidplexus can lead to

A

Hydrocephalus: obstructive or increased CSF production

218
Q

How do you classify choroid plexus tumors

A

Papilloma
Atypical papilloma
Carcinoma

219
Q

Where are Ependymoma located*

A

ventricular system (lateral and third most common) or extraventricular

lead to obstructive (acquired) hydrocephalus

220
Q

What is sequela of ependymoma

A

lead to obstructive (acquired) hydrocephalus

221
Q

What are the classification of Ependymoma

A

1) Ependymoma
2) Anaplastic (malignant_ ependymoma

222
Q

What is the most common primary CNS tumor of cats and dogs*

A

Meningioma

223
Q

what are the common sites for meningioma in dogs and cats

A

Dogs: frontal lobes and olfactory lobes

Cats: usually solitary (can have multiple) and supratentoral; associated with tela choridea of third ventricle

*extra neuronal metastasis is rate

224
Q

What are the gross lesions of meningioma

A

extra-axial, well circumscribed +/- secondary pressure necrosis of parenchyma
commonly amenable to surgical excision

225
Q

Meningiomas are (intra/extra) axial

A

extra axial

226
Q

neoplasm derived from neuronal precursor cells in olfactory mucosa
in the caudal aspect of nasal cavity

A

Olfactory neuroblastoma
(Esthesioneuroblastoma)

227
Q

Esthesioneuroblastoma

A

Olfactory neuroblastoma
neoplasm derived from neuronal precursor cells in olfactory mucosa
in the caudal aspect of nasal cavity

228
Q

Olfactory neuroblastoma

A

Esthesioneuroblastoma
neoplasm derived from neuronal precursor cells in olfactory mucosa
in the caudal aspect of nasal cavity

229
Q

Neoplasm of undifferentiated cells of cerebellum
often congenital (calves and young dogs)
originate from external granular cell layer

A

Medullobastoma

(a primitive neuroectodermal tumor- PNET)

230
Q

Where do Medulloblastomas originate from

A

a primitive neuroectodermal tumor- PNET
Neoplasm of undifferentiated cells of cerebellum
often congenital (calves and young dogs)
originate from external granular cell layer

231
Q

Spinal Nephroblastoma *

A

thoracolumbar spinal cord tumor of young dogs
Between T10-L2
Young <1 year
2 cell populations (embryonic blastemal cells and epithelial cells)

232
Q

Where does spinal nephroblastoma typically occur *

A

T10-L2 in young dogs (<1yr)

thoracolumbar spinal cord tumor of young dogs

233
Q

What age of dog does spinal nephroblastoma typically affect *

A

T10-L2 in young dogs (<1yr)

thoracolumbar spinal cord tumor of young dogs

234
Q

What are the cells of origins of nerve sheath tumors

A

1) Schwannoma- Schwann cells
2) Neurofibroma- fibroblasts
3) Perineurioma- perineural cells
4) Malignant nerve sheath tumor

235
Q

What are the common sites of nerve sheath tumors in dogs, cattle, horses, and cats

A

Dog:
brachial plexus&raquo_space; lumbosacral plexus
distal peripheral nerves/skin
trigeminal (most common cranial nerve)

Cattle:
Multicentric (Neurofubromatosis): ANS, heart, mediastinum, 8th cranial nerve, intercostal nerves, brachial plexus

Horses/Cats: Skin

236
Q

What do nerve sheath tumors look like grossly

A

nodular subcutaneous mass or thickening of nerves
fusion with adjacent nerves

237
Q

What is the most common spinal cord tumor and second most common intracranial tumor in cats

A

Multicentric lymphoma

238
Q

Leukocytic tumors (lymphoma) in canine and feline are mostly (B or T cell)

A

T cell lymphoma (90%)

239
Q

What causes lymphoma in cattle **

A

Bovine leukemia virus associated (intradural and extramedullary in caudal equina)

240
Q

Where in the nervous system is bovine leukemia virus associated with *

A

intradural and extramedullary in caudal equina

241
Q

What is Cholesteatoma

A

a tumor like lesion that is common in 15-20% of old horses
suspected chronic intermittent hemorrhage or congestion/edema of choroid plexus
usually incidental (unless large)

242
Q

a tumor like lesion that is common in 15-20% of old horses
suspected chronic intermittent hemorrhage or congestion/edema of choroid plexus
usually incidental (unless large)

A

Cholesteatoma

243
Q

A cholesteatoma in older horses is thought to be due to _________________ of the _____________

A

chronic intermittent hemorrhage or congestion/edema of choroid plexus

244
Q

Secondary tumors of the CNS are ________ common than primary tumors

A

less

245
Q

How might an animal get secondary tumors of the CNS

A

1) Direct extension:
a) bony tumors of cranium or vertebrae (osteoma, osteosarcoma, osteochondrosarcoma, multiple myeloma)
b) Carcinomas of nasal and paranasal sinuses
c) Ocular tumor

2) Hematogenous metastasis: mammary and pulmonary tumors, melanoma, hemangiosarcoma, and multicentric lymphoma

246
Q

What tumors might spread hematogenously to the CNS

A

Hematogenous metastasis: mammary and pulmonary tumors, melanoma, hemangiosarcoma, and multicentric lymphoma

247
Q

What tumors might spread via direct extension to the CNS

A

a) bony tumors of cranium or vertebrae (osteoma, osteosarcoma, osteochondrosarcoma, multiple myeloma)
b) Carcinomas of nasal and paranasal sinuses
c) Ocular tumor

248
Q

What is the blood brain barrier

A

tight junctions between capillary endothelial cells

*inflammation can readily develop in the brain and spinal cord
-cytokines or local mast cells products (eg histamine) -> increase permeability of vascular endothelium

249
Q

What will a dog with multilobular osteochondrosarcoma look like

A

a large lump on they head

250
Q

how might the capillary endothelial cells become leaky

A

-cytokines or local mast cells products (eg histamine) -> increase permeability of vascular endothelium

251
Q

Once CNS infection occurs __________

A

it tends to persist
-drainage of exudate from CSF is poor (lack of lymphatic vessels in CNS)
-diffucult to treat because of poor penetration of blood brain barrier by drugs

252
Q

Why does CNS infection typically persist

A

-drainage of exudate from CSF is poor (lack of lymphatic vessels in CNS)
-difficult to treat because of poor penetration of blood brain barrier by drugs
-No fibroblasts to wall off the area

253
Q

Many agents have no neurotropism and you really only see brain involvement with systemic infection but what are some agents that are neurotropic

A

Rabies- neurons of grey mater
Prions- medulla
Listeria monocytogenes- Pons and medulla

254
Q

Rabies targets neurons of (white/grey) matter

A

grey matter

255
Q

Most viruses target the (white/grey) matter

A

grey matter

256
Q

Where do you sample for prions disease

A

obex of the medulla (dorsal motor nucleus of the vagas nerve)

257
Q

inflammation of the brain

A

encephalitis

258
Q

inflammation of the spinal cord

A

myelitis

259
Q

inflammation of the pia-arachnoid *

A

leptomeningitis

260
Q

inflammation of the dura mater*

A

pachymeningitis

261
Q

pachymeningitis

A

inflammation of the dura mater

262
Q

inflammation of the ependyma

A

ependymitis

263
Q

inflammation of the choroid plexus

A

choroiditis

264
Q

inflammation of the ventricles

A

ventriculitis

265
Q

What are the different routes of CNS infection *

A

1) Direct extension/implantation- penetrating trauma (stab wound, gun shot, skull fracture), middle/inner ear infections, nasal cavity/sinus infections through the cribriform plate along olfactory nerve, osteomyelitis, neoplasia
2) Hematogenous- localization within capillary beds of meninges or choroid plexus (eg. neonatal septicemia)
3) Via peripheral nerves (retrograde axonal transport) via axoplasmic flow from PNS to CNS (rabies virus and Listeria monocytogenes)
4) Leukocyte trafficking- macrophages or lymphocytes containing microbes during their transit through CNS (retroviruses)

266
Q

What virus infects the ventricles of the brain

A

FIP- feline infectious peritionitis virus

267
Q

How might the CNS get infected through direct extension

A

1) penetrating trauma (stab wound, gun shot, skull fracture), 2) middle/inner ear infections
3) nasal cavity/sinus infections through the cribriform plate along olfactory nerve
4) osteomyelitis
5) neoplasia

268
Q

How might a sheep get a frontal lobe abscess from direct extension from the nasal cavity

A

Oestrus ovus (nasal bot)

or dehorning

269
Q

What is the most common route of CNS infection

A

Hematogenous- localization within capillary beds of meninges or choroid plexus (eg. neonatal septicemia)

270
Q

What are examples of pathogens that infect the CNS via retrograde axonal transport

A

Via peripheral nerves (retrograde axonal transport) via axoplasmic flow from PNS to CNS (rabies virus and Listeria monocytogenes)

271
Q

What is a common site to see CNS infection through hematogenous spread

A

pituitary abscess

272
Q

you have several piglets (5-8 weeks), some sudden deaths that are all paddling.
some develop neurologic abnormalties, swollen joints or cutaneous lesions- incoordination, tremors, lateral recumbency, padlding, and opisthonos. Upon necropsy you see suppurative meningitis. What might have causes this

A

Major causes of meningitis in pigs (as part of polyserotis)
1) Steptococcus suis
2) Glasseurella parasios (Glasser’s disease)
3) Mycoplasma hyorhinis (does not cause meningitis)
4) Other gram negative septicemia (e.g Salmonella)

273
Q

What are major causes of meningitis in pigs (as part of polyserositis)

A

Major causes of meningitis in pigs (as part of polyserotis)
1) Steptococcus suis
2) Glasseurella parasios (Glasser’s disease)
3) Mycoplasma hyorhinis (does not cause meningitis)
4) Other gram negative septicemia (e.g Salmonella)

274
Q

Meningitis is most often ____ *

A

part of systemic bacterial infection (septicemia)
also can result from direct extension (ie. fractures, otitis, sinusitis)

a common finding in neonatal septicemia

275
Q

What are the gross lesions of meningitis *

A

*Opaque leptomeninges (look at ventral aspect of brain)
+/- thickening of choroid plexus and roughening of ependymal surface
+/- other lesions of septic animals - peritonitis, pericarditis, endophthalmitis, polyarthritis

276
Q

Why do you need to look at the ventral aspect of the brain when necropsy of an animal with menigitis *

A

*Opaque leptomeninges (look at ventral aspect of brain)

277
Q

What is the possible causes of bovine neonatal septicemia that can lead to CNS infection

A

*Coliforms
Strep
Pasteurella
Salmonella
Klebsiella
Staphyococcus
Actinpbacillus equi (foals)

278
Q

Where in the nervous system do you typically see empyema

A

epidural
-vertebral canal (tail docking or other traumatic injuries
-cranium (secondary to infection following skull fracture

279
Q

Oestrus ovis infection in sheep can lead to *

A

direct extension through cribiform plate to cause a frontal abscess of the brain

280
Q

What can thermal injury from dehorning result in?

A

frontal abscess

281
Q

What can inner ear infection result in

A

cerebellopontine abscesses from direct extension from adjacent tissues

282
Q

What are common isolates of bacterial abscesses to nervous system

A

Trueperella pyogenes
Streptococcus
Pasteurella

283
Q

What might cause chronic cerebral abscess in sheep

A

Corynebacterium pseudotuberculosis

284
Q

Direct extension of bacteria from middle/inner ear can lead to

A

cerebellopontine abscess (look at the ears/ typanic bullae

285
Q

What is the most common cause of middle/inner ear infections in cattle leading to cerebellopontine abscess *

A

Mycoplasma bovis

286
Q

_____________ in the middle/inner ear of cattle can lead to __________ via direct extension *

A

Mycoplasma bovis ; cerebellopontine abscess

287
Q

you have a circling adult ewe, depressed, right sided head tilt, stumbling/circling to the right, right sided facial paresis, several animals affected. What might be the differential

A

Listeria monocytogenes

or
Inner ear infection

288
Q

Listeria monocytogenes is associated with *

A

spoiled silage

289
Q

What is the pathogenesis of Listeria monocytogenes *

A

1) Spoiled silage
2) Oral wound allows bacterial invasion of mucosa
3) Bacteria invade trigeminal (other nerves possible)
4) Travel to brainstem via axons (retrograde)
5) Gross lesions typically absent but causes microabscesses in brainstem (pons and medulla)

290
Q

What are the typical gross lesions you see with Listeria monocytogenes infection *

A

Gross lesions typically absent but causes microabscesses in brainstem (pons and medulla)

291
Q

How do you diagnose Listeria monocytogenes

A

culture, IHC, Gram stain

292
Q

What will you see on histology of animal with Listeria *

A

**microabscesses in brainstem (pons and medulla)

293
Q

What nerve does listeria invade

A

tirgeminal and travels to the brainstem via axons (retrograde)

294
Q

What is the pathogenesis of Histophilus somni

A

1) Normal genital and nasal flora of cattle and sheep
2) Respiratory tract -> septicemia
3) Thrombotic meningoencephalitis (and lesions in other tissues such as bronchopneumonia and myocarditis)

295
Q

How does Histophilus somni cause multifocal hemorrhages and necrosis (malacia) *

A

Septicemia leads to thrombotic meningoencephalitis

gross lesions: multifocal hemorrhages and necrosis (malacia)- brain and spinal cord

Primary histological lesion
-Vasculitis -> thrombosis +/- infarcts with gram positive bacteria within thrombi and vessel walls

296
Q

What lesions do you see with Histophilus somni infection

A

gross lesions: multifocal hemorrhages and necrosis (malacia)- brain and spinal cord

Primary histological lesion
-Vasculitis -> thrombosis +/- infarcts with gram positive bacteria within thrombi and vessel walls

297
Q

What is the primary lesion you see with Histophilus somni

A

multifocal hemorrhages and necrosis (malacia)- brain and spinal cord caused by thrombotic and vasculitis

298
Q

What causes focal symmetrical encephalomalacia

A

Clostridium perfringens type D
epsilon toxin

299
Q

What is the pathogenesis of Clostridium type D leading focal symmetrical encephalomalacia (FSE) *

A

1) Food animals eat lots of highly fermented carbs
2) Overgrowth of Clostridium perfringes type D producing epsilon toxin
3) Degeneration of vascular endothelial tight junctions
4) Swelling and rupture of perivascular astrocyte processes
5) Leakage of fluid and increased intracerebral pressure
6) Parenchymal necrosis

300
Q

How does epsilon toxin cause focal symmetrical encephalomalacia

A

1) Degeneration of vascular endothelial tight junctions
2) Swelling and rupture of perivascular astrocyte processes
3) Leakage of fluid and increased intracerebral pressure
4) Parenchymal necrosis

Sheep: thalamus, cerebellar peduncles,internal capsule with acute protein rich perivascular edema

Goats: can be acute or chronic fibrinohemorrhagic colitis)

301
Q

What is the pathogenesis of botulism (limber neck)

A

1) Clostridium botulinum (type A, B or C) in soul
2) Botulinum toxin blocks the release of acetylcholine, inhibiting contraction
3) Flaccid paralysis
4) Diaphragm -> death

*NO gross or microscopic lesions

302
Q

What lesions do you see with botulism

A

no gross of microscopic lesions

diagnosis: history plus toxin detection in clinical samples collected for lab analysis
(intestinal contents, serum, liver)

303
Q

What is the pathogenesis of tetanus (lockjaw)

A

1) Clostridium tetani toxin
2) Motor end plate, blocks release of glycine (inhibitory neurotransmitter)
3) Symptoms: stiffness of jaw, severe muscle spasms, sweating, fever, stiffness of abdominal muscles, difficulty swallowing

*No gross of microscopic lesions

304
Q

What lesions do you see with tetanus

A

No gross of microscopic lesions

305
Q

What is the mechanism of action of tetanus toxin?

A

binds to the motor end and blocks the release of glycine (inhibitory neurotransmitter)
leading to rigid paralysis (lockjaw, severe muscle spasms, fever, sweating)

306
Q

you have a 10yo gelding that is ataxic, fever, and depression, headpressing, muscle fasciculations, hind limb weakness, progression to parlaysis, convulsions and death

prior to death, CSF showed mononuclear pleocytosis with predominance of lymphocytes

upon necropsy, grey matter is affected, neuronal necrosis, glial nodules, and non-suppurative perivascular cuffs.

What might be the cause

A

Viral infections of the CNS in horses

1) West Nile Virus
2) Equine Encephalitis Virus (Eastern- neutrophils), Western, and Venezuelan encephalitis
3) Equine herpesvirus -1 (myeloencephalopathy)- primarily causes vasculitis (does not specifically target gray matter)
4) Rabies virus

307
Q

What are the different viral infections of the CNS in the horse

A

1) West Nile Virus
2) Equine Encephalitis Virus (Eastern- neutrophils), Western, and Venezuelan encephalitis
3) Equine herpesvirus -1 (myeloencephalopathy)- primarily causes vasculitis (does not specifically target gray matter)
4) Rabies virus

308
Q

Eastern Equine Encephalitis virus causes

A

neutrophilic infiltration- dies fast enough where neutrophils do not go away)

309
Q

How does Equine herpesvirus-1 cause myeloencephalopathy

A

primary causes vasculitis (does not specifically target gray matter)

310
Q

What are important viral infections of the CNS in dog

A

1) Canine distemper *
2) Rabies virus
3) Canine adenovirus- vascultis
4) Canine herpesvirus-1

311
Q

What are characteristic lesions of viral infections of the nervous system *

A

usually no gross lesions

Histopathology: lesions most prominent in the gray matter (polioencephalitis)
1) Nonsuppurative inflamamtion (lymphocytes and plasma cells) - perivascular cuffs, mild meningitis)
2) Gliosis/ glial nodules
3) Injury to neurons (chromatolysis and necrosis) with neurophagia

other viral associated lesions: demyelination (immune destruction), meningitis/ventriculitis (FIP)

viral inclusion bodies

312
Q

When might you see intracytoplasmic negri bodies

A

Rabies virus

313
Q

when might you see both intracytoplasmic and intranuclear inclusion bodies

A

Canine distemper virus

314
Q

What kind of inclusion bodies do you see with pseudorabies

A

it is a herpesvirus so you will see intranuclear

315
Q

What virus can cause ventriculitis

A

feline infectious peritionitis virus

316
Q

What viruses can cause demyelination through immune destruction or viral infection of oligodendrocytes

A

Canine distemper virus or small ruminant lentiviruses (caprine arthritis- encephalitis virus and vesna)

317
Q

What are important viral infections of the CNS in cats

A

1) FIP
2) Rabies virus

318
Q

What are the important viral infections of the CNS in cattle

A

1) Bovine herpesvirus-5 (and less commonly BHV-1)
2) Malignant catarrhal fever (MCF)- vasculitis
3) Rabies virus
4) West Nile Virus

319
Q

What are the important viral infections of the CNS in sheep/goats

A

1) Lentivirus (Caprine arthritis- encephalitis virus in goats, visna in sheep)
2) Rabies virus
3) West NIle Virus

320
Q

What causes granulomatous/ pyogranulomatous inflammation focused on meninges and ventricular system

A

Feline Infectious Peritonitis virus

321
Q

Feline Infectious Peritonitis virus causes

A

granulomatous/ pyogranulomatous inflammation focused on meninges and ventricular system

322
Q

Which of the following is the primary histologic lesion seen with locoweed toxicity?

Neurons with large discrete intracytoplasmic vacuoles

Neurons with finely vacuolated cytoplasm

Acute neuronal necrosis

Lipofuscin accumulation in the cytoplasm of neurons

A

Neurons with finely vacuolated cytoplasm

323
Q

Which of the following conditions exhibits autofluorescence of the neuropil when examined under a black light?

A

Polioencephalomalacia

324
Q

Which of the following is a cause of polioencephalomalacia in ruminants?
A) Thiamine deficiency
B) Sulfur deficiency
C) Moldy corn poisoning
D) Selenium toxicity

A

A) Thiamine deficiency

325
Q

Which of the following is a cause of cerebellar aplasia or hypoplasia in pigs?

A

Classical swine fever

326
Q

What lesion is shown in the nucleus pulposus of the image and what type of intervertebral disc disease would this patient be predisposed to develop?

A

Chondroid degeneration/metaplasia; Hansen type I disc extrusion

327
Q

What is the most common location of stenosis with congenital hydrocephalus?

A

Mesencephalic aqueduct

328
Q

Which of the following would cause an ischemic infarct (and not a hemorrhagic infarct)?

A) Thrombus of an artery
B) Thrombus of a vein
C) Traumatic rupture of a blood vessel
D) Vasculitis leading to leakage of RBCs

A

A) Thrombus of an artery

329
Q

What type of hydrocephalus can occur following in utero destruction of the cerebrocortical parenchyma (i.e., hydranencephaly)

A

Hydrocephalus ex vacuo

330
Q

exposure to organic and inorganic compounds- pesticides, heavy metals, plants, microbial products, etc.

A

Intoxication

331
Q

inadequate levels of minerals, vitamins, metabolites

A

deficiency

332
Q

What are the clinical features of toxic/ metabolic CNS disease

A

peracute to acute (headpressing, disorientation, recumbency, tonic-clonic seizures, partial seizures)

age is not a generalized feature- certain toxins/deficiencies do express predilections

commonly an outbreak

333
Q

Know this: Toxic and Metabolic Diseases are of often (bilateral/unilateral) and (symmetrical/asymmetrical) *

A

Bilateral and Symmetrical

334
Q

True/False: Toxic and Metabolic Disease of the CNS target specific anatomic areas and cell types of the CNS *

A

true
it is dependent on vascular geography and concentration of receptors

335
Q

Why do toxic and metabolic diseases of the CNS target specific anatomic areas and cell types of the central nervous system *

A

1) Vascular geography
2) Concentration of receptors

336
Q

What are the major patterns of toxic/metabolic disease

A

1) Malacia (softening- common pathway) +/- hemorrhage
2) Selective necrosis- neurons, axons, myelin
3) Spongiform state (status spongiosis- irregular cavities within the neuropil secondary to neuronal loss

337
Q

irregular cavities within the neuropil secondary to neuronal loss

A

Spongiform state (status spongiosis-

338
Q

What are the 4 causes polioencephalomalacia in large animals *

A

1) Sulfur toxicity
2) Thiamine deficiency
3) Water deprivation encephalopathy
4) Lead toxicity

339
Q

Polioencephalomalacia in large animals

A

cerebrocortical necrosis (CCN) to the cerebral cortex- basal/thalamic nuclei, colliculi, and cerebellar cortex
caused by:
1) Sulfur toxicity
2) Thiamine deficiency
3) Water deprivation encephalopathy
4) Lead toxicity

Diagnosis: postmortem: gross and histological findings

340
Q

What does sulfur toxicity in large animals lead to *

A

Polioencephalomalacia

341
Q

What does thiamin (B1) deficiency in large animals lead to

A

Polioencephalomalacia

342
Q

What is the pathogenesis of sulfur toxicity in ruminants

A

1) Sulfur ingested in excess (feed or water)
2) Rumen microbes produce excess hydrogen sulfied (H2S) where it accumulates in ruminal gas cap and
3) soluble hydrosulfide anions accumulate in ruminal fluid and diffuse across the rumen wall
3) H2S decreases mitochondrial respiration- inhibits cytochrome oxidases *
4) Brain has a high demand for oxygen, glucose, and energy metabolites and leads to neuronal dysfunction, degneration, and necrosis
5) Polioencephalomalacia

343
Q

What do the soluble hydrosulfide anions (H2S gas) that accumulate in ruminal fluid due in cattle with sulfur toxicity **

A

they diffuse across the rumen wall and decrease mitochondrial respiration via inhibiting cytochrome oxidases
causing neuronal dysfunction, degeneration, and necrosis

344
Q

How does sulfur toxicity cause polioencephalomalacia *

A

H2S diffuses across rumen wall decrease mitochondrial respiration via inhibiting cytochrome oxidases
causing neuronal dysfunction, degeneration, and necrosis

345
Q

What is the pathogenesis of thiamin deficiency in cattle *

A

1) High carbohydrate diets lead to overgrowth of thiaminase producing bacteria (Cl. sprogenes and Bacillus thiaminoolyticus) or grazing of thiaminase containing plants (Bracken fern, Nardoo) or Amprolium
2) Insufficient thiamine leads to neuronal dysfunction, degeneration, and necrosis

346
Q

a vitamin that is a crucial cofactor for glucose metabolism and glial-neuronal membrane interactions

A

Thiamin (B1)

347
Q

What diet causes cattle to develop a thiamin deficiency *

A

High carbohydrate diet-
overgrowth of thiaminase producing bacteria (Cl. sprogenes and Bacillus thiaminoolyticus) or grazing of thiaminase containing plants (Bracken fern, Nardoo) or Amprolium

348
Q

How might cattle get thiamin deficiency *

A

1)High carbohydrate diet-
overgrowth of thiaminase producing bacteria (Cl. sprogenes and Bacillus thiaminoolyticus) *
2) Thiaminase containing plants (Bracken fern, Nardoo)
3) Amprolium

349
Q

What are gross findings of polioencephalomalacia in large animals

A

1) Gyri are flattened
2) Sulci are less sistinct
3) Multifocal to coalescing yellow foci (necrosis)
4) Cerebellar hemorrhage suggestive of herniation
5) Deep laminar necrosis resulting in perisulci cystic cavities ***
6) Tan to yellow discolored cortex with shrunken to absent grey matter

350
Q

Deep laminar necrosis resulting in perisulci cystic cavities is seen in_________ **

A

polioencephalomalacia in large animals

351
Q

What tool on necropsy floor can you use to diagnose polioencephalomalacia **

A

UV/Woods lamp

*autofluorescent of the necrotic areas
when neurons die they release lipofuscin and the macrophages pick that up

352
Q

What do you see on histology in large animals with polioencephalomalacia *

A

1) Spongy change (edematous)
2) Neuronal necrosis- band like “Pseudo laminar” ***
3) Gliosis- reactive astrocytes, increased microglia
4) Vascular proliferation
5) Infiltration of the neuropil by macrophages with phagocytic ability “Gitter cells”

353
Q

How does neuronal necrosis with polioencephalomalacia present itself on histology **

A

In a band like “pseudolaminar” form

354
Q

How do carnivores get thiamin

A

through dietary intake
ruminants have bacteria to rpduce it

355
Q

How is the topography of thiamin deficiency in carnivores different from ruminants *

A

In carnivores: caudal colliculi, medial vestibular nuclei and lateral geniculate bodies (often hemorrhagic) *

356
Q

What are the etiologies of thiamin deficiency in carnivores *

A

1) Starvation (cats)
2) Raw fish
3) Thiamin inactivation - thiamin levels are measured and addressed in commerical dog foods

357
Q

What are the most commonly affected regions in thiamin deficiency in carnivores *

A

caudal colliculi, medial vestibular nuclei and lateral geniculate bodies (often hemorrhagic)

Bilateral and symmetrical

358
Q

How are water deprivation encephalopathies caused

A

1) Pigs fed a high salt ration
2) occurs in other animals as a result of water deprivation. arid environments, broken water pipes, frozen water, neglect

*Pathogenesis revolves around osmotic gradients between the blood stream and CNS

*PEM/CCN lesions

359
Q

What species is salt toxicity common in? *

A

Pigs

360
Q

What is the pathogenesis of salt toxicity (common in pigs) *

A

1) Water intake restriction in pigs being fed a high salt diet
2) Blood becomes hypernatremia
3) Following osmotic gradient, fluid from brain moves into vessels
4) Brain becomes dehydrated
5) Equilibration of NaCl between plasma and extracellular space if the CNS is slow
6) Development of PEM is unclear but not hypothesized to be secondary to compression and anorexia

*When water is provided the blood becomes hypotonic in comparison to the brain. Excess fluid from blood moves into the dehydrated brain

361
Q

What lesions do you see on necropsy of an animal with salt toxicity

A

Gross: Tonsillar Cerebellar Herniation

Histologic: Perivascular infiltrate of eosinophils is essentially pathognomonic

362
Q

Water Toxicity

A

Causes PEM/CCN
excess water consumption following deprivation following the osmotic gradient, IV fluid moves into brain

Similar necropsy findings but eosinophilic perivascular infiltrates are not a feature

363
Q

Salt toxicity has similar necropsy findings from water toxicity. What is not seen in water toxicity but is seen in salt toxicity

A

Eosinophilic perivascular infiltrates on histology

364
Q

Lead toxicity

A

Causes PEM/CN
young animals: milk substitutes, paint, plumbing, batteries
birds: leadshot, fishing, coin

oxidative stress leads to erythrocytic and vascular damage-> generating edema

can occur with other heavy metals

365
Q

What causes Equine Nigropallidalencephalomalacia *

A

Ingestion of the yellow star thistle or Russian knapweed

-dry summer pastures
-chronic exposure, acute onset of disease

*Repin is suspected toxic compound

366
Q

What plants cause Nigropallidalencephalomalacia *

A

Yellow Star Thistle (Centaurea solstitalis)

Russian Knapweed (C. repens)

367
Q

What is Equine Nigropallidalencephalomalacia *

A

caused by Yellow Star Thistle or Russian knapweed (dry summer pastures and chronic exposure with acute onset)

Signs: Abnormal tongue movement, difficulty with prehension, swallowing, and drinking

Gross/Histologic lesions- bilaterally symmetrical malacia of substantia nigra and globus pallidus effecting conscious proprioception and movement

*Pseudolaminar necrosis is not a feature

368
Q

What causes Equine Leukoencephalomalacia

A

Mycotoxic (Moldy corn disease) producing Fumoninsin B1*
acute onset with chronic exposure

369
Q

What is the pathogenesis of Moldy Corn Disease *

A

1) Ingestion of moldy corn contamined with Fusarium moniliforme
2) Fumonisin B1 causes vascular damage selectively in the white matter with secondary encephalomalacia
3) Bilateral asymmetrical, centrum semiovale, corona radiata

*Leukoencephalomalacia
may also cause concurrent hepatic necrosis

370
Q

Fumoninsin B1 *

A

produced by Fusarium moniliforme that grows in moldy corn

causes vascular damage selectively in the white matter with secondary encephalomalacia

Causes Equine Leukoencephalomalacia

371
Q

What lesions do Fumoninsin B1 from Fusarium moniliforme cause

A

Bilateral asymmetrical * damage to the centrum semiovale and corona radiata
(occasionally in the brainstem and cerebellar white matter) via vascular damage to white matter with secondary encephalomalacia

Equine Leukoencephalomalacia

372
Q

What are the general characterisics of degenerative disease

A

1) Selective degeneration and loss of cells or cell components
2) Bilaterally symmetric
3) Individual animals

373
Q

How are degenerative diseases named?

A

by their main cellular target and/or lesion patterns

374
Q

What are major patterns with degenerative disease

A

-Loss of neurons, axons and/or myelin. compare with normal animal, swollen axons (primary axonal pathology)
-Pallor of white matter
-Spongy state
-Intracellular storage: most easily recognizable, accumulatio of abnormal material, malacia

375
Q

Degeneration of neurons is often

A

degeneration and loss of neurons in a specific anatomic structure
often polyphasic

can lead to anterograde or retrograde axonal lesions

376
Q

What is one of the most common and important degenerative diseases (neuronal)

A

Motor Neuronal Diseases
-Hereditary Canine Spinal Muscular Atrophy
-Bovine Motor Neuron Disease with neurofilamentous accumulation

Clinical: weakness of limb, spinal and head muscles with progressive atrophy and eventual paresis and paralysis

376
Q

Spongiform Encephalopathies

A

Transmissible degenerative diseases
1) TSEs
2) Prions

Normal prion protein exposed to scrapie related protein (abnormally conformed prior protein) serves as a template to influence a geometric conformation change in exposed animal

Disease examples: BSE, FSE, Scrapie, SWD, Creutzfeldt-Jakobs Disease, fatal insomnia

377
Q

What is the pathogenesis of Spongiform Encephalopathies *

A

Normal prion protein exposed to scrapie related protein (abnormally conformed prior protein) serves as a template to influence a geometric conformation change in exposed animal

378
Q

What are the clinical signs of Spongiform Encephalopathies

A

slowly progressive deteriration
long incubation period (years) -> disease of adult animals
almost always fatal
changes in behavioral or temperament
progressive ataxia (+ other neurologic signs) and weight loss

379
Q

Where do you submit samples for prion diseases/ chronic wasting disease *

A

Medulla oblongata - obex

380
Q

What is the etiology of equine degenerative myeloencephalopathy *

A

hereditary defect that predisposed to pathology related to environmental or nutritional factors

-Vitamin E deficiency has been demonstrated **

381
Q

Equine Degenerative myeloencephalopathy *

A

occurs sporadically in many breeds

hereditary defect that predisposed to pathology related to environmental or nutritional factors
Vitamin E deficiency

Clinical: onset at around 6 months, ataxia and tetraparesis

Pathology: Dystrophic axons and neuronal degernation, lipofiscin accumulation in endothelial cells, neurons, and macrophages in affected nuclei

382
Q

Does normally the dry or wet form of FIP affect the CNS and eyes

A

dry form

383
Q

FIP causes:

A

granulomatous and exudative ventriculitis and periventricular encephalitis

obstructive lesion with secondary hydroencephalus

384
Q

Does canine distemper virus cause grey or white matter lesions

A

BOTH
grey matter- similar to other viruses

but also white matter (more common)- causing demyelination (primary)

385
Q

Distemper causes

A

1) White matter lesions -primary demyelination leading to spongy changes that can progress to necrosis
2) Intranuclear and intracytoplasmic inclusion bodies

386
Q

Post-vaccinal distemper

A

occurs 1-2 weeks after vaccination
aggressive behavior, progressive ataxia, paresis and death within a few days

*Disseminated lesions in gray matter

associated with MLV

387
Q

old dog encephalitis

A

rare manifestation- thought to be subclinical persistent infection of canine distemper infections

lesions in gray and white matter of forebrain (including demyelination)

388
Q

What age does caprine arthritis encephalitis virus typically affect

A

2-4 month old kids

389
Q

What is the pathology of small ruminant lentiviruses like CAEV and Visna *

A

Demyelinating leukoencephalomyelitis

CAEV: 2-4 month old kids
Visna: sheep >2 years old

390
Q

What age of visna typically affect sheep

A

usually older animals >2 years

391
Q

What might cause demyelinating leukoencephalomyelitis in small ruminants

A

Caprine arthritis encephalitis virus or visna

392
Q

10 yo MC cat with several week history of sneezing, nasal discharge and firm swelling over bridge of nose. 2 day history of depression, disorientation, and seizures.
What additional diagnostic tests would you perform?

A

Advanced imaging to rule out some sort of mass

Cytology

393
Q

Fungal and algae infections of the CNS

A

mostly isolated occurences and often opportunisitc infection in immunocompromised animals

pathogenesis:
1) mostly hematogenous (systemic) - Blastomyces dermatitidis
2) Extension from nasal cavity- Cryptococcus sp.- direct extension through the cribiform plate

Gross legions: regions of parenchymas discoloration or a mass like lesion

Histopathology: granulomatous to pyogranulomatous inflammation with organisms histologically

394
Q

What lesions do you see with fungal and algae infections of the CNS

A

Gross legions: regions of parenchymas discoloration or a mass like lesion

Histopathology: granulomatous to pyogranulomatous inflammation with organisms histologically

395
Q

How does Cryptococcus sp. typically infect the CNS

A

through direct extension through the cribiform plate

396
Q

How does Blastomyces dermatitidis typically infect the CNS

A

mostly hematogenous (systemic)

397
Q

How does fungi and algae infect CNS

A

1) mostly hematogenous (systemic) - Blastomyces dermatitidis
2) Extension from nasal cavity- Cryptococcus sp.- direct extension through the cribiform plate

398
Q

What is the pathogenesis of Feline Cryptococcosis

A

1) Inhalation into nasal cavity
2) Invasion through cribiform plate or along olfactory nerve
3) Meningoencephalitis - granulomatous to pyogranulomatous inflammation with regions of parenchymal discoloration in a mass like lesion

399
Q

You have a 3yo QH mare with chronic history of gait abnormalities (ataxia, knuckling, crossing over) and progressive unilateral muscle atrophy of right pelvic limb
Upon CSF you see eosinophilic pleocytosis. What might have caused this?

A

EPM
Infarction
EHV-1
Parasite

400
Q

Equine protozoal myeloencephalitis (EPM)

A

Asymmetrical foci of hemorrhage and malacia caused by Sarcocystis neurona

have a distribution of lesion- typically the spinal cord +/- brainstem
predilection for cervical and lumbar intumescences

401
Q

What causes Equine Protozoal Myeloencephalitis

A

Sarcocystic neurona

402
Q

What protozoa has a predilection for the CNS of horses

A

Sarcocystic neurona - asymmetrical foci of hemorrhage and malacia

403
Q

What gross lesions are seen with Equine protozoal myeloencephalitis (EPM) *

A

asymmetrical foci of hemorrhage and malacia

404
Q

What protozoa cause CNS signs due to sludging of parasitized erythrocytes in the cerebral capillaries

A

Babesia sp infection in cattle, dogs and horses

Trypanosoma sp in cattle

405
Q

What lesions are seen with protozoal infections of the NS *

A

Gross: random regions of parenchymal discolaration and malacia

Histo: Pyogranulomatous/ granulomatous inflammation +/- eosinophils in a random pattern (asymmetrical)
Necrosis
see organisms histologically

406
Q

What protozoa cause midterm abortion in cattle

A

Neospora caninum

407
Q

Neospora caninum affct what two species

A

Dogs- young dogs infected in-utero leading to polyradiculoneuritis, polymyositis, and meningoencephalomyeltis

Cattle- abortion (midterm) with lesions in the fetus of encephalitis, myositis/myocarditis

408
Q

How are dogs typically infected with Neospora caninum

A

in-utero

cause polyradiculoneuritis, polymyositis, and meningoencephalomyeltis

409
Q

What is the typical signalment of dogs with neospora caninum

A

young puppies (infected in utero) with weakness progressing to paralysis

410
Q

What lesions are seen in Neospora caninum infection of puppies *

A

1) Polyradiculoneuritis - inflammation of multiple nerves and spinal nerve roots
2) Polymyositis- inflammation of multiple muscles
3) Meningoencephalomyelitis

*Granulomatous and eosinophilic encephalitis

411
Q

you have a 2.5 yo female llama from indiana with a two week history of dragging the left pelvic limb. the clinical signs progressed to ataxia and tetraparesis with loss of superficial pain in the pelvic limbs.
bright and alert with normal appetite
CSF- elevated protein content and an increased white blood cell count with a predominance of eosinohphils. What classes of organisms would you suspect

A

Parasite - Parelaphostrongylus tenuis

412
Q

What lesions do you see with cattle with neospora caninum

A

Abortion (midterm)
lesions: encephalitis and myositis/myocarditis of the fetus

413
Q

Parelaphostrongylus tenuis

A

Meningeal worm

Definitive host: White tailed deer- typically no clinical signs (reside in subdural space)

Camelids: ingest infected mollusks (intermediate host) which result in aberrant migration in the CNS parenchyma

*Granulomatous and/or eosinophilic inflammation with linear tracts of hemorrhage and necrosiss
can see organisms (larva or adults)

414
Q

What lesions do you see with parasitic infections of the CNS*

A

Granulomatous and/or eosinophilic inflammation with linear tracts of hemorrhage and necrosiss
can see organisms (larva or adults)

415
Q

What species do you typically see Parelaphostrongylus tenuis in

A

Camelids- ingest infected mollusks (intermediate host) which results in aberrant migration in the CNS parenchyma

416
Q

insect larvae live in nasal cavity of sheep and penetrate the cribriform plate

A

Oestrus ovis

417
Q

insect that affects the spinal cord of cattle

A

Hypodermis bovis

418
Q

insect that causes feline ischemic encephalopathy

A

Cuterebra sp.

419
Q

What does Cuterebra cause

A

feline ischemic encephalopathy- regionally extensive encephalomalacia with cuterebra larva

420
Q

Cestode infection of the CNS*

A

Adults (intestine of final host)- larva can infect CNS of intermediate host*

Pathology: Single or multiple cysts (space occupying mass)*

Coenurus cerebralis (Taenia multiceps- dogs) sheep

Cysticercus cellulosae (Taenia solium- humans) pigs and dogs

421
Q

What are the different types of canine meningoencephalitis of unknown origin (MUO) *

A

1) Granulomatous meningoencephalitis (GME)
2) Necrotizing meningoencephalitis (NME)
3) Necrotizing leukoencephalitis (NLE)

422
Q

What is canine meningoencephalitis of unknown origin (MUO) *know this to memory

A

1) Granulomatous meningoencephalitis (GME) - angiocentric granulomatous inflammation of white matter

2) Necrotizing meningoencephalitis (NME)

3) Necrotizing leukoencephalitis (NLE)- gross large asymmetric malacic foci confined to deep white matter

immune mediated mechanism?

Most cases in young adults (6 months to 3 years)

usually multifocal disease

423
Q

What age of dog does MUO typically affect

A

young adult dogs (6 months to 3 years)

424
Q

Is MUO focal or multifocal disease? *

A

Multifocal disease

425
Q

Coonhound paralysis

A

polyradiculoneuritis in dogs that affects spinal nerve roots/ peripheral nerves

ascending paresis- paralysis of limbs

suspected immune mediated reaction suspected (hypersensitivity to raccoon saliva)

426
Q

polyneuritis equi

A

neuritis of the cauda equina

autoimmune or post infectious?

see swollen nerves with adhesions (can see cranial nerve involvement)

chronic progressive tail and sphincter paralysis, urinary incontinence, fecal retention, perineal paresthesia/ analagesia

427
Q

Beagle pain syndrome *

A

Steroid-responsive meningitis arteritis that occurs in young adult dogs

acute fever, neutrophilia, neck pain

see subarachnoid hemorrhage in the brainstem/cervical spinal cord

Histologically: meningitis and necrotizing arteritis

428
Q
A

BOD 3 (5 decks)

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