CNS Flashcards

1
Q

The Central Nervous system is made up of?

A

the brain and the spinal chord

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2
Q

The ___________ of the CNS is a significant deterrent to its routine examination in the course of a necropsy. If there is no indication that the patient suffered from neurological trauma/issues, pathologists will ?

A

The inaccessibility of the CNS is a significant deterrent to its routine examination in the course of a necropsy

Not even examine

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3
Q

The ______ _____ should be removed in all cases of CNS disease, even though clinical signs may be referable only to the brain

A

The spinal cord should be removed in all cases of CNS disease, even though clinical signs may be referable only to the brain

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4
Q

What tool is pictured here?

A

Head vise
Used to steady the head when removing the brain.

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5
Q

What tool is pictured here?

A

Band saw
Used to separate and remove spinal column from large animals.

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6
Q

Removal of the brain and spinal cord of rabies suspect animals needs to be performed only by ________ and ________ with caution and using appropriate _____. The same careful approach is taken when doing autopsies of suspected _______ ________ suspected individuals (e.g., _____ ______ _______).

A

Removal of the brain and spinal cord of rabies suspect animals needs to be performed only by pathologists and technicians with caution and using appropriate personal protective equipment (PPE). The same careful approach is taken when doing autopsies of transmissible encephalopathy suspected individuals (e.g., mad cow disease).

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7
Q

What is pictured below?

A

Perform Dorsal laminectomy to expose the spinal cord, dog
- Remove skin on dorsom of animals
- Remove epaxial animals
- Do this to expose vertebral arches –> dorsal laminectomy
- Start to pull and cut bone without damaging spine underneath.

In this particular case, this was a case of IVDD –> degeneration of disk, protrusion of nucleus corpuscles –> focal compression of spinal chord. Focal compression = softer due to malacia which is actually necrosis.

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8
Q

“In small animals the spinal cord can be exposed by performing a ________ ________ with bone _______ → then the spinal cord is removed by holding the ______ _____ with forceps and sectioning the spinal roots as close to the ________ _______ as possible”…

A

“In small animals the spinal cord can be exposed by performing a dorsal laminectomy with bone rongeurs → then the spinal cord is removed by holding the dura matter with forceps and sectioning the spinal roots as close to the intervertebral foramina as possible”…

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9
Q

What is pictured below?

A

In large animals, we have to isolate the vertebral column. Must take everything else in order to do this. Cut in segments and then pass through band saw. Can not cut through chord, but cut through the edge so that way you can remove it later.

Severe trauma resulted in fraction of vertebra. Rupture of spinal cord and areas of epidural and subdural hemorrhage.

Mid sagittal section of the vertebral column to expose the spinal cord.

Young horse, Cornell’s files

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10
Q

What is pictured below?

A

Brain, dog, partially covered by the
dura mater, McGavin’s

Dura mater contains more connective tissue. It is the outside meningeal layer.
- In the cranium, it is usually attached to the endostium of the bone. You must section with scissors the meninges in there to see the brain.

Pia mater –> close to parenchyma of brain
Arachnoid –> layer in between
Dura Mater –> thickest meningial layer

CSF produced in ventricles of the brain circulates in the ventricles of the brain and central canals of spinal cord but also in the subarachnoid space.

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11
Q

What can be seen here?

A

Knowledge of the basic functional anatomy of the
brain is quite useful since there are several degenerative, toxic and inflammatory diseases that induce lesions in specific areas.

Cerebral hemispheres
Cerebral cortex

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12
Q

Label this diagram accordingly

A
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13
Q

Label this diagram accordingly

A
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14
Q

The brainstem is divided into?
Rostral = __________
mid brain = __________
pons = __________
caudal = __________ ________

A

Cranial, medial, caudal
Rostral = diencephalon
Mesencephalon = mid brain
Metencephalon = pons
Medulla oblongata = caudal

Lateral ventricles in the cerebrum
Third ventricle in the thalamus
Ventricular system is connected through mesencephalic aqueduct with the 4th ventricle int he cerebellum. This connects with the central canal of the spinal cord.

Corpus callosum = white structure

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15
Q

POST MORTEM EXAMINATION OF THE NERVOUS SYSTEM
❑ Brain should be examined for abnormalities in _____, ___________, _________, _________ and/or meningeal ______ (presence of _________).
❑ The entire brain and spinal cord should be immersed in _______ and fixed for ___-____ days. Why is this done?
❑ Once fixed for this period of time the brain and the spinal cord can be _________ to be submitted to the histopathology laboratory for tissue processing and microscopic slide preparation. How big are these sections?
❑ During trimming, the brain is sectioned _________ and sequentially at ______ intervals and closely examined to detect any gross abnormalities (areas of _______, _________, _______ etc.).

A

POST MORTEM EXAMINATION OF THE NERVOUS SYSTEM
❑ Brain should be examined for abnormalities in size, malformations, dissymmetry, swelling and/or meningeal opacity (presence of exudates).
❑ The entire brain and spinal cord should be immersed in formalin and fixed for 5-7 days or even 10 days. If section immediately –> artifacts –> make evaluation difficult.
❑ Once fixed for this period of time the brain and the spinal cord can be sectioned to be submitted to the histopathology laboratory for tissue processing and microscopic slide preparation.
- Normally sections are small, but the brain is the exception.
❑ During trimming the brain is sectioned transversely and sequentially at short intervals and closely examined to detect any gross abnormalities (areas of discoloration, softening, cavitation etc.).

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16
Q

Label this graph accordingly.

A

Sign-Time Graph: Useful to determine then etiology of neurological disease according to the progression and severity of clinical signs

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17
Q

________ and ____ cells (neuroglia = “neural glue”)

A

Neurons and glial cells (neuroglia = “neural glue”)
Glia comes from the greek word = glue B/c they pull everything together in the brain and spinal chord. E.g. astrocytes, oligodendrocytes (CNS; octopus shape; provides myelin sheath to multiple axons), schwann cells (Only provide myelin sheath to one axon; PNS)

Apendymal cells are considered by some apart of the glia. Line the ventricles and cells of spinal chord. Not true epithelial cells

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18
Q

Label this image accordingly.

A
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19
Q

The neurons are the __________ cells of the nervous system in which two protoplasmic properties are highly
developed: ________ (generation of an impulse) and ________ (ability to transmit such an impulse from one locality to another).

A

The neurons are the functional cells of the nervous system in which two protoplasmic properties are highly
developed: irritability (generation of an impulse) and conductivity (ability to transmit such an impulse from one locality to another).

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20
Q

Neurons can be located _______ within the CNS or _____ or ______ within the PNS

A

Neurons can be located entirely within the CNS or entirely or partially within the PNS

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21
Q

What are the functions of microglia?

A

They are the phagocytic cells; get rid of debris.
Detect presence of tumor cells
Very difficult to see.
- When activated, they become bigger and easier to recognize; Look like a foamy macrophage. These are the gitter cells
Bean shape nuclei

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22
Q

What are gitter cells?

A
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23
Q

The blood brain barrier has a protective function for the neuronal microenvironment → ________ control of substances moving from the ______. Protects nerve cells from some potential _____ and __________.
These protective barriers are:
1. ______ junctions of endothelium
2. __________ membrane of endothelial cells
3. __________ end feet

A

The blood brain barrier has a protective function for the neuronal microenvironment →tighter control of substances moving from the blood. Protects nerve cells from some potential toxins and pathogens.
These protective barriers are:
1. Tight junctions of endothelium
2. Basement membrane of endothelial cells
3. Astrocyte end feet

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24
Q

T/F: Some Antibiotics can cross the blood brain barrier

A

True

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25
Q

What can be seen in the image below?

A

Neurons & Glial cells,
Ventral grey horn of SC, horse

Bluish material –> Nissl bodies that are aggregates of RER and ribosomes. In cases of degeneration, an early change = cytoplasm becomes swollen and lysis of the nissel substance.

Special stains can be used to show Nissel bodies.

Arrow with solid arm = astrocytes
Arrow with dashed arm = microglial cells

Arrow head = Oligodendrocytes = clear cytoplasm.

Very little CT in brain and spinal chord, which is why it is gelatinous in consistency.

Pink material in brain is called? Neuropile. Eosinophillic material in between cells composed of cytoplasmic projections of neurons and glial cells.

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26
Q

Because of the unique population of cells present within the nervous system the language use to describe pathologic changes is somewhat different to the one use in other systems.

A
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27
Q

What can be seen here?

A

One of the earliest changes you will see in a neuron undergoing degeneration

Chromatolysis – Breakdown (lysis) of cytoplasmic Nissl bodies
(aggregates of RER and free polyribosomes). Indicates neuronal cell injury.
Other neuronal changes include “satellitosis” and “neuronophagia”

Bluish aggregates: these are the Nissl bodies. This is normal.

One on the bottom = swollen, showing chromatolysis

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28
Q

What can be seen in the image below?

A

Normal cortex, H&E
Bigger cells with bluish cytoplasm = neurons
Nuclei around are glial cells
Material in between = neuropile
Tubular looking things = capillaries

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29
Q

What can be seen in the image below?

A

Ischemic neurons, H&E
Lack of Oxygen in area –> degenerate –> die
- Characteristic morphology
- Some neurons are normal (round, prominent nucleoli)
- Others change–>called ischemic neurons. Cytoplasm appears to have shrunken. Nucleus becomes smaller, pyknotic (dark stained), brightly eosinophilic cytoplasm.
- Energy deprivation change as well. E.g. hypoglycemia –> seizures –> die. Brain of this individual –> ischemic change.

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30
Q

Ischemic cell change: Affected neurons are ________ and exhibit cytoplasmic ___________ (___-___ cytoplasm), nuclear _______ (________-stained) nucleus , or ________. The name “energy-deprivation change” has been proposed as more suitable for this change since it may be the result of ______, _________ etc., (Summers et al., 1995)

A

Ischemic cell change: Affected neurons are shrunken and exhibit cytoplasmic eosinophilia (red-pink cytoplasm), nuclear pyknosis (darkly-stained) nucleus , or karyolysis. The name “energy-deprivation change” has been proposed as more suitable for this change since it may be the result of
ischemia, hypoglycemia etc., (Summers et al., 1995)

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31
Q
A

Satellitosis/ Neuronophagia
Early degenerative changes
Top left –> neurons are relatively normal. Slightly shrunken. But you do see increased # of satellite cells around neuron (little dots). Eventually, this neuron can die.
bottom image: neuronophagic nodule –> cytoplasm shrunken, pignotic. Nuclei are odd shaped. Neuron is dead. Some cells surrounding neuron are microglial cells that are phagocytizing the dead neuron.

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32
Q

What can be seen in the image below?
What condition is this animal suffering from?
Can this be seen in the grey matter or white matter?

A

“Status Spongiosus” (spongiform change)
Brain, Hepatic encephalopathy, Steer, AVC, HE
Found in white matter or gray matter
Looks like a sponge; can be found in cases of encephalopathy and distemper

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33
Q

What can be seen in the image below?

A

“Status Spongiosus” (spongiform change)
Cerebellum, dog –Canine distemper,
Texas A&M

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34
Q
A

Gliosis, perivascular cuffing
in any kind of inflammatory condition in brain or spinal chord –> accumulation of inflammatory cells –> perivascular cuffing
E.g. glial cells, nuclei, miosis, and status spongiousus (usually associated with splitting of myelin sheath –> glial cells, or demyelination or swelling and vacuolization of glial cells and neurons

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35
Q
A

Astrogliosis with formation of reactive (gemistocytic)
astrocytes

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36
Q
A

Dog, canine distemper –cerebellar white matter: status spongiosus,
perivascular cuffing, inclusion bodies.

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37
Q
A

Gliosis, spongiform change, neuronal loss, HE
Creutzfeldt-Jakob disease (CJD)

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38
Q
A

Gitter cells (foamy macrophages): active macrophages that
phagocytize necrotic debris within the brain/ spinal cord,
HE section, case of Focal Symmetric Encephalomalacia (FSE),
Lamb, Atlantic Veterinary College (AVC), OI.

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39
Q

Label the different axon types below

A

See below

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40
Q

The following is a list of different types of CNS injuries:
1. Congenital abnormalities
- _______, ________
- ________ _____
2. Lysosomal Storage Diseases can be?
3. Increased intracranial ______, cerebral ______ and _____
4. ________ Injuries
5. __________ conditions (including metabolic, nutritional and toxic causes)
6. _________ conditions
7. _________ Diseases

A
  1. Congenital abnormalities
    - Cerebrum, cerebellum
    - Spinal cord
  2. Lysosomal Storage Diseases
    - Inherited
    - Induced (acquired)
  3. Increased intracranial pressure, cerebral swelling and edema
  4. Traumatic Injuries
  5. Degenerative conditions (including metabolic, nutritional and toxic causes)
  6. Inflammatory conditions
  7. Neoplastic Diseases
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41
Q

Congenital abnormalities are relatively common in _______ animals.
❑ May be ________ or the result of exposure to _________.
❑ __________, except for viruses, act mainly during the
first _____ of the pregnancy, during __________.
❑ Viruses may cause malformations over a ______
period.

A

Congenital abnormalities are relatively common in domestic animals.
❑ May be inherited or the result of exposure to
teratogens.
❑ Teratogens, except for viruses, act mainly during the
first third of the pregnancy, during organogenesis.
❑ Viruses may cause malformations over a wider
period.

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42
Q

What can be seen in this image below?

Newborn donkey, TAMU

A

Congenital abnormalities
Newborn donkey – Microencephaly (in this case the result of prosencephalic hypoplasia), TAMU

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43
Q

What can be seen in this image below?
If this were a calf, what may have caused this?
If this were a piglet, what may have caused this?

Newborn donkey, TAMU

A

Newborn donkey – Microencephaly (in this case due to prosencephalic hypoplasia – he most rostral portions of the brain are underdeveloped), TAMU.

In calves it may be the result of in utero infection with BVD virus.
In piglets, in utero infection with classical swine fever virus can induce this lesion.

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44
Q

Within the brain and spinal chord, we have the ventricular system in which we have the presence of CSF.
The CSF circulates within the ventricles and within the central canal of the spinal cord. The canal goes to the end of the spinal cord and carries CSF.
Lateral ventricles are found in the cerebral hemispheres.
The ventricles communicate with the third ventricle, ventral to the lateral ventricles. The third ventricle is located around the intraforamic region.

CSF flow path: Third ventricle –> mesencephalic aqueduct of the mid brain –> fourth ventricle (located underneath the cerebellum, on top of the medulla oblongata) –> central canal.
- CSF escapes through the lateral apperatures located near the fourth ventricle. Enter the subarachnoidal space and circulate on surface of the brain.

  • CSF function: produced by the choroid plexuses; to serve as a protective caution against traumatic brain injury.
A

See notes.

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45
Q

What can be seen in the image below?

List the causes of this condition.

A

 Hydrocephalus: Increase in CSF (cerebrospinal fluid) volume.
- It can be internal (most common, CSF fluid accumulates within the ventricles) or external (CSF fluid accumulates in the arachnoid space); also compensatory or obstructive.
Compensatory: CSF ↑ to take up the space where parenchyma has been destroyed, failed to developed or both.
Obstructive: aqueductal atresia or stenosis (mesencephalic aqueduct) → can be pre-natal (congenital) or post-natal (e.g.: secondary to inflammation)

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46
Q

What condition is the dog pictured below suffering from?
What are two common signs of hydrocephaly?

A

Condition: Hydrocephalus

Domed-shaped head (due to megalencephaly) and
ventrolateral strabismus, boxer puppy.

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47
Q

The most critical component of the pathway of CSF circulation is the __________ ___________ of
the __________, and is the most common site of malformations that result in __________ hydrocephalus.

A

The most critical component of the pathway of CSF circulation is the mesencephalic aqueduct of
the midbrain, and is the most common site of malformations that result in obstructive hydrocephalus.

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48
Q

What is pictured below?

A

Depression, dementia, seizures, blindness, exophthalmos and ventrolateral strabismus (deviation
of the eyes) are common manifestations of hydrocephalus in puppies.

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49
Q

Below is a picture of a brain from a hydrocephalus puppy.

You can clearly see extreme _____ of ventricles and ______ of cerebrocortical tissue

A

Extreme dilation of ventricles and thinning of cerebrocortical tissue

Dorsal view of the exposed brain of a puppy with hydrocephalus

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50
Q

HYDRANENCEPHALY, PORENCEPHALY
❑ Formation of fluid filled cavities in the brain → __________ (small cavities) and ___________ (large cavities).
❑ Usually occurs in ______ during gestation → cavitations result from destruction of immature _________ or due to ________ injury
❑ In contrast to hydrocephalus, the cranium is ______ malformed and CSF accumulates _______ the lateral ventricles and the _________ parenchyma.
❑ In hydranencephaly there can be complete or almost complete absence of the _________ __________, leaving only membranous _____ filled with CSF and enclosed by the ___________. Cavitations occur secondary to _________.
❑ Viruses → ________ virus, __________ virus, ______ _______ _____ virus and ________ virus, or __________, such as ________ _______ _______ virus and ________ disease virus can lead to these abnormalities

A

HYDRANENCEPHALY, PORENCEPHALY
❑ Formation of fluid filled cavities in the brain → porencephaly (small cavities) and hydranencephaly (large cavities).
❑ Usually occurs in utero during gestation → cavitations result from destruction of immature neuroblasts or due to vascular injury
❑ In contrast to hydrocephalus the cranium is not malformed and CSF accumulates within the lateral ventricles and the cavitated parenchyma.
❑ In hydranencephaly there can be complete or almost complete absence of the cerebral hemispheres, leaving only membranous sacs filled with CSFand enclosed by the leptomeninges. Cavitations occur secondary to necrosis.
❑ Viruses → Akabane virus, Bluetongue virus, Rift Valley fever virus and Wesselsbron virus, or pestiviruses, such as Bovine viral diarrhea virus and Border disease virus can lead to these abnormalities

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51
Q
A

Cerebellar hypoplasia, dog, AVC.

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52
Q
A

Cerebellar hypoplasia, kitten.
Left: normal, Cornell

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53
Q
A

Cerebellar hypoplasia, kitten, Dr.
King’s Show & Tell

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54
Q

Cerebellar hypoplasia
- May be the result of a ______ developmental defect/
____________
- May be the result of ___-_____ or ____-____ ___ infection:
- Cats: ___________ ___________ virus infection
- Calves: ______ virus infection.
- Affected animals present signs of cerebellar dysfunction: ________ ataxia characterized by ______ ____ (wide) base gait, ______ ataxia and intention _____ more pronounced in the head when the animal attempts __________ or __________.

A

Cerebellar hypoplasia
 May be the result of a primary developmental defect/
malformation
 May be the result of in-utero or peri-natal viral infection:
 Cats: Feline panleukopenia virus infection
 Calves: BVD virus infection.
Affected animals present signs of cerebellar dysfunction: symmetric
ataxia characterized by hypermetric broad (wide) base gait, truncal
ataxia and intention tremor more pronounced in the head when the
animal attempts drinking or eating…

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55
Q
A

Spina Bifida: Defective closure of
bony encasement of the spinal cord.

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56
Q

What is pictured below?

A

Diagram of Spina Bifida.

Spina bifida occulta –> skin covering anomaly so you do not see it from the outside.

Top diagram: dorsal arch with transverse processes = normal
In spina Bifida = lack of development of arch, no protection on dorsal surface of the spinal chord. Transverse processes appear soft.
Skin can sometimes be open and can see the meninges on the top.

Bottom diagram:
Meningocele = fluid from CSF can accumulate –> herniation of meninges.
Myelomeningiocele = Herniation of meninges and the CSF but also herniation of the spinal chord.

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57
Q

Lysosomal storage diseases
 In these diseases, which affect animals and humans, _________ cell types, including neurons, are unable to eliminate normal ___________ of their metabolism because of some biochemical defect. Eventually leads to cell _________ and _________.
 Most lysosomal storage diseases are _________, __________ determined ______ disorders.
 A few of these conditions however are acquired through exposure to __________ substances that inhibit specific lysosomal activities (e.g., ___-_________ →consumption of locoweeds in sheep, cattle and horses).

A

Lysosomal storage diseases
 In these diseases, which affect animals and humans, various cell types, including neurons, are unable to eliminate normal by-products of their metabolism because of some biochemical defect. Eventually leads to cell degeneration and death.
 Most lysosomal storage diseases are progressive, genetically determined (inherited) fatal disorders.
 A few of these conditions however are acquired through exposure to neurotoxic substances that inhibit specific lysosomal activities (e.g., α-mannosidosis →consumption of locoweeds in sheep, cattle and horses).

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58
Q

In lysosomal storage disease a normal or abnormal __________ substance accumulates because of __________ or _________ defects in metabolism, packaging, transport or secretion of these substances. e.g. , of lysosomal storage diseases
→ ?

A

In lysosomal storage disease a normal or abnormal endogenous substance accumulates because of
genetic or acquired defects in metabolism, packaging, transport or secretion of these substances.
e.g. , of lysosomal storage diseases
→ gangliosidosis globoid cell leukodystrophy, ceroid lipofuscinosis, mannosidosis etc..

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59
Q

List some examples of lysosomal storage disease

A

GAG Me Now, Christine
 Gangliosidosis
 Globoid cell leukodystrophy
 Alpha and Beta Mannosidosis
 Mucopolysaccharidosis
 Ceroid –lipofuscinosis
 Niemann-Pick disease

Present with neuro changes
Histo changes in cerebral cortex, cerebellum (swollen, cytoplasm appears to be foamy due to substrate; microvacuoles?).

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60
Q
A

Lysosomal storage disease

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61
Q

What condition does this breed of sheep typically suffer from here in the states? What are the clinical signs associated?

A

Ceroid lipofuscinosis, Rambouillet sheep.
Seen in dogs, cats, and sheep.
More often reported in sheep. Several breeds here in the states can be affected.

When comparing the left and right brain: Cerebellum looks similar in size so can assume it is sheep of similar age and size.
Left: normal brain. normal cerebral hemispheres; can see gyra and sulci.
Right: cerebrocortical atrophy. Prominent cerebral cortical atrophy. Gyra appears to be narrowed and sulci appear wider.

Clinical signs: Progressive ataxia, clinical signs of CNS disease, depression, wandering around, recumbent, eventually die/euthanized etc.

Sheep suffer from lysosomal storage disease. Substrate –> degeneration

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62
Q
A

Ceroid lipofuscinosis in sheep. Cerebrocortical atrophy. TAMU (Dr. R. Storts, Rambouillet sheep. Also reported in South Hampshire, Borderdale and other breeds of sheep). Nubian goats may also have this inherited defect.

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63
Q

6 month old Salers calf.
Presented with progressive neuro signs, normal at birth –> ataxic, lethargic, intention tremors –> indicated central involvement. Eventually euthanized.
Pathologists were suspecting to see cerebral atrophy on necropsy, however grossly, the cerebellum appeared normal.

What do you think this Salers calf suffered from?

A

On histo: foamy, vacuolization –> Diagnosed with Mannosidosis
Purkinje cells were swollen, vacuolated cytoplasm –> sign of lysosomal storage disease.
Salers calfs are prone to develop alpha and beta mannisidosis.
Some labs will test for the enzyme missing in lysosomes, in this case mannosidase which breaks down the sugar? Mannose sugar. Accumulation of this sugar.

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64
Q

What plant is pictured below? Describe what happens as a result of ingesting this plant.

Seen in ______, _____ and _____.
Ingestion of “__________”: genera ________ and _________ cause an acquired form of _______ → contains potent inhibitors (_______) of ________-_________ (enzyme that breaks down the carbohydrates that forms _______)

A

Seen in sheep, cattle and horses.
Ingestion of “locoweeds”: genera Astragalus and Oxytropis cause an acquired form of mannosidosis → contains potent inhibitors (swainsonite) of alpha-mannosidas (enzyme that breaks down the carbohydrates that forms mannose)

Locoweeds contain swainosonine, a phytotoxin that is harmful to livestock.

Locoweeds from Colorado and Utah, web images. Potent inhibitors of the alpha-mannosidase enzyme (causes Alpha-mannosidosis).
Clinical Disease in sheep, cattle and
horses

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65
Q

Locoweeds contain?

A
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66
Q

What can be seen in the image below?

A

Increased Intracranial pressure: Associated cerebral swelling and edema.
 There is only a narrow space separating the brain and the dura matter. The dura matter and the skull are unyielding structures that only allow a small increase in volume of the intracranial contents without increasing intracranial pressure

Edema: may have very low amt of protein and therefore not stain. See presence of spongiform change: vacuolization. Perivascular spaces are also distended. Life threatening condition –> distention of respiratory centers –> death

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67
Q

What is the Significance of cerebral edema?

 Severe → ____-threatening
 Leads to increased _________ pressure- ________- _______ (hypoxia)- _____- ______
 Brain wet, ______, swollen, _______ gyri, soft
 Cerebellar _______ or gyral ________ may occur (two changes we can see grossly)

A

 Severe → life threatening
 Leads to increased intracranial pressure- compression- ischemia (hypoxia)- edema- necrosis
 Brain wet, soggy, swollen, flattened gyri, soft
 Cerebellar coning or gyral herniation may occur (two changes we can see grossly)

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68
Q
  1. What condition is this feline patient suffering from?
  2. White arrow = ____ located here
    When remove head, we section at this _____. Normally when look at foramen magnum, should only see _________. In a case of cerebrally edema –> bran _____ –> no room –> pressure –> part of ______ protrudes underneath the ______ ________ (part of the dura mater that is present between the more dorsal portion of the _______ and the _______ portion of the cerebral hemisphere).
A
  1. Cerebellar coning
  2. White arrow = C1 located here
    When remove head, we section at this joint. Normally when look at foramen magnum, should only see brainstem. In case of cerebrally edema –> bran swells –> no room –> pressure –> part of cerebellum protrudes underneath the tentorum cerebelli (part of the dura mater that is present between the more dorsal portion of the cerebellum and the caudal portion of the cerebral hemisphere). This is cerebellar coning
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69
Q
A

Foramen magnum with the condyle
Cerebellar coning, cat
Due to coning –> part of cerebellum protruding

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70
Q

What can be seen in the image below?

A

Horse, cerebral edema resulted in gyral herniation (herniation of parahippocampal gyri under the tentorium cerebelli).

Occipital lobe looks abnormal - why? B/ in this case part of the parahypocampal gyrae was pushed underneath tentorum so we have both protrusion of cerebellum but also part of cerebral hemisphere underwent changes resulting in this.

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71
Q
A

Concussion,
Contusion, Laceration

B/c animals have 4 legs, they are less prone to these type of head injuries. Also they have smaller sized brains so that makes them less prone.

Movement of the brain due to trauma –> injury

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72
Q

A concussion is defined as a __________ loss of __________ due to trauma.

A

A concussion is defined as a temporary loss of consciousness due to trauma

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73
Q

A contusion is defined as a _________ loss of consciousness in addition to the presence of ________ and ________ of the brain which is more _______ than a concussion.

A

A contusion is defined as a temporary loss of consciousness in addition to the presence of bleeding and bruising of the brain which is more severe than just concussion

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74
Q

Laceration –> part of the _______ of the brain

A

Laceration –> part of the parenchyma of the brain

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75
Q

Define coup and countercoup injuries.

A

Brain Injury: Coup & Countercoup lesions

If you hit head in car accident can have a Coup & Countercoup injury. Meninges hold brain but the trauma, the rostral portio of rbain hits the frontal portion –> coup injury.

Counter coup: brain moves forwad and can produce trearing of meninges in the back of the head and then it bounces back to hit counter part of the head. Lesion may be more prominent in the back of the head. In any kind of brain injury, this shaking of the brain will disrupt biochemical environment –> loss of consciousness –> Severe sequalae.

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76
Q

Boxers eventually develop..

A

Chronic Traumatic Encephalopathy (CTE); Boxer’s encephalopathy (dementia pugilistica) – presence of “neurofibrillary tangles”

77
Q

Soccer plays

A

soccer ball is very hard when properly inflated. Some players develop chronic encephalopathy due to this.
Can only hit the ball with their head after 11 years of age.

78
Q
A

HBC presents with head trauma
–> fracture of cranium in some cases
In horses –> basilar fracture. Horses that fall backwards may present with immediate neuro signs. Can collapse, etc. If do post mortem, you will find a lesion pictured above.

Floor of cranium where there is the sphenoid bone (vascular portion of oscippital bone forming floor of cranium). You can have fracture around this joint in here resulting in traumatic damage to the base of the brain. Damage to brain stem, meninges, parenchymal damage, etc.

79
Q

Different kinds of severeity of traumatic injury. If servere can lead to…

A
  1. Meningial hemorrhage
  2. subdural hemorrhage under dura mater
  3. parenchymal hemorrhage
80
Q
A

CSM: cervical stenotic myopathy
- can produce focal compression of spinal chord
- young horses, dog breeds: rottweilers, great danes
- E.g, of traumatic spinal injury
- focal ischemic injury –> trauma
Traumatic Spinal Cord Injury
 Like in traumatic brain injury,
it may also be the result of
external (extrinsic) or internal (intrinsic) causes.
 Examples of intrinsic spinal
cord injuries are injuries
associated with intervertebral disk disease, vertebral abscesses or cervical stenotic myelopathy (Wobbler disease).

81
Q

List the Degenerative diseases of the CNS (include metabolic, nutritional and toxic diseases)

A

 Polioencephalomalacia (cattle, sheep, pigs, carnivores)
 Focal symmetric encephalomalacia (Clostridium perfringens type D
enterotoxemia, lambs)
 Edema Disease (Enterotoxemic colibacillosis) of pigs → Shiga-like
toxin induces angiopathy/ vasculitis: edema (Cerebrospinal angiopathy of swine).
 Hepatic encephalopathy
- severe liver disease –> neuro signs
 Equine leukoencephalomalacia
 Equine nigropallidal encephalomalacia
 Age-related degenerative myelopathy of German Shepherds
 Equine neuroaxonal dystrophy/ equine degenerative
myeloencephalopathy – may be related to Vitamin E deficiency

Lesions are primarly degenerative,l NOT inflammatory

82
Q

List the Causes of polioencephalomalacia

 Primarily ________ deficiency
 ________ toxicity
 High ______ concentrations in drinking water
 Ingestion of _______ accumulating plants
 ______ toxicity
- can produce ____ problems
- can also produce lesions in the ______ and ________ nerves
- can also produce polioencephalomalacia
 _____ poisoning/ water ______

this condition primarily effects the ____ matter of the brain

A

 Primarily Thiamine deficiency
 Sulfur toxicity
 High sulfate concentrations in drinking water
 Ingestion of sulfate accumulating plants
 Lead toxicity
- can produce GI problems
- can also produce lesions in the brain and peripheral nerves
- can also produce polioencephalomalacia
 Salt poisoning/ water deprivation

polio = gray matter
this condition primarily effects the gray matter of the brain

83
Q
A

Opisthotonus –Sheep with thiamine-responsive PEM
Opisthotonus: Marked dorsal extension of the head and neck
(in an arching position) accompanied by rigid extension of the limbs.

Pathogenesis is unclear. We know Vitamin B1 is very important for brain development (myelin, phospholipids). Ruminants can produce thiamine they need due ot bacterai in rumebn but in many cases, ruminal flora problem –>
Bacteria produce thiaminase –> thiamine deficiency –> polioencephalomalacia

Sheep and cattle are affected at a very young age (up to 6 months of age).

These animals may develop ataxia, fepression, dorsal extension of head and neck –> extension of limbs, backward bending of the head and vertebral column.

84
Q
A

Opisthotonus- Lamb, PEM

Also become blind very quickly and in a few days will die.

When die, present like this. Not specific to encephalomalacia
Stargazing

Dorsal medial deviation of straism. Eyes point medially which is characteristic of this condition
DDx: sulfur

85
Q
A

Lamb, polioencephalomalacia, U of Missouri, Noah’s Arkive.
Yellowish areas of discoloration (malacia) in the cerebral cortex
close to the longitudinal fissure

In order to confirm diagnosis and look at brain closely.
Cut brain when fresh and look for lesions. Subtle, very difficult to find.
Look at difference bet. white and grey matter. On surface of brain you can see paler/yellower discoloration of gray matter –> unclear demaraction of white and grey matter

86
Q
A

Cross section of cerebral hemisphere
Polioencephalomalacia, calf, Texas A&M.
Yellowish discoloration of the cortical grey matter

Called thiamine responsive because animal may respond with thiamine so treat other animals with thiamine to treat iwht possibility of thiamine deficiency;.

87
Q
A

Cross section of cerebral hemisphere
Polioencephalomalacia, calf, Texas A&M.
Yellowish discoloration of the cortical grey matter

Called thiamine responsive because animal may respond with thiamine so treat other animals with thiamine to treat iwht possibility of thiamine deficiency;. Other DDx is sulfur toxicity. underground water may have high levels of sulfur –> send to lab to check sulfur levels. Lead toxicity is another DDx: old batteries, machine oil leaking –> exposure

88
Q
A

Use UV light to see affected areas confined to cerebral cortex. Also seen in brain stem. UV lamp only works with thiamine affected areas not thrombotoci meningoencephalitis associated with histophilius somni. EVen if see necrosis grossly, UV won’t work. May be associated with pigment associated with thiamine deficiency

89
Q

Polioencephalomalacia may be a

A

Incidental finding
Polioencephalomalacia, cow, chronic lesions

Chronic case
sgnificant atrop y of gray matter of cerebral hemispheres, whichis very rare

90
Q
A

Salt poisoning/ water deprivation occurs primarily in pigs and poultry,
occasionally in ruminants
–> polioencephalomalacia

More common cause in poultry and swine.
Feed is more salty for swine

Water –> frozen during winter

91
Q

Farmer was using fries from mcdonalds and giving them in the feed. The pigs loved it but in the winter several of the pigs developed neuro signs

A

Polioencephalomalacia – Pig, cerebral cortex

Lesions primarily confined ot this part of the brain
Evaportaon of neuropile (swpongiform change)
increased cellularity
Increased inflammatory cells
these larger cells thatn are bluer are neurons.
some appear reddish and larger –> ishcemic damage

92
Q
A

eosinophilic cytoplasm, darker nuclei, shrunken

Polioencephalomalacia, pig AVC, OI

93
Q
A

Salt poisoning/ water deprivation: Occurs primarily in pigs and poultry, occasionally in ruminants
In addition to polioencephalomalacia, perivascular and meningeal eosinophilic infiltration occurs occasionally.

94
Q

What condition is this dog suffering from below?

A

Chastek paralysis: foxes, mink, cats, dogs

Thiamine deficiency is also reported in cats, dogs and farmed wild carnivores (mink
and foxes).

Causes:
Diets containing fish as the primary ingredient contain high levels of thiaminase (destroys thiamine).
Diets based entirely in cooked meat are thiamine deficient and also may produce the disease…

Mix fish in diet containig thiaminase producing bacteria –> thiamaine deficiency

95
Q
A

Lesions primarily in gray matter of brain stem

Fox, Chastek paralysis Cornell Files. In carnivores, lesions of
polioencephalomalacia have a different distribution than those in
ruminants

96
Q

These histological samples were taken from a patient suffering from Chastek paralysis. This condition affects which parts of the brain in carnivores?

A

Fox, Chastek’paralysis – lesions in brain stem and hippocampus,
Atlantic Veterinary College, Canada

Ischemic neurons

97
Q
A

Transverse sections of the brain stem through the pons.
Dog, Texas A&M: Necrosis of caudal colliculi

In caudal colliculi –> look here b/c may see characteristic lesions aka areas of cavitation

Cats with thiamine deficiency: cats roll into a ring with ventral flextion of head and stay that way

cats and dogs: associated with pure meat diet

98
Q

Animals with severe (congenital or acquired) liver disease may develop __________ signs (worst after feeding) and ________/_______ change of the ______ matter (___________ of myelin sheaths)

Damage in liver –> accumulation of toxins e.g. ___________, ________ chain FA, and _______ –> accumulate in ______ –> damage brain –> neuro signs

A

Degenerative conditions.. Toxic/ metabolic etiology…
Hepatic encephalopathy, Steer, AVC case.
Animals with severe (congenital or acquired) liver disease may develop neurologic
signs (worst after feeding) and polymicrocavitation/ spongiform change of the white matter (ballooning of myelin sheaths) .
Pathogenesis?…
Hyperammonemia, short-chain fatty acids and mercaptans…

Damage in liver –> accumlation of toxins e.g. ammonium, short chain FA, and mercaptans –> accumulate in blood –> damage brain –> neuro signs

relisten

99
Q
  1. Based on the gross and histological images, what did the sheep in the top right-hand image die from?
  2. Does this condition only affect sheep?
  3. What microbial agent is this condition associated with?
  4. Describe a typical patient’s behavior on presentation.
  5. What are the typical clinical signs?
  6. What is the pathogenesis?
A
  1. Focal symmetric encephalopathy (FSE)
  2. Happens in sheep, usually young sheep.
  3. Associated with clostridium perfringens type D. This is the causative agent of enterotoxemia in sheep; Type D–> acute hemorrhagic enteritis in lambs.
  4. People say there is a wide range of presentations of this disease.
    - Some animals may not have enteric lesions but present with neuro signs and eventually die.
    - Neuro effects associated with epsilon toxin produced by clostridium that produce damage to blood vessels, especially in basal nuclei and there is where we will have lesions of FSE.
  5. Neuro signs, opisthotonus, seizures –> Can die in just a few hours
  6. Brain: endothelial junctions in capillaries –> pathogenic edema –> damage in basal ganglia, containing umn. Lesions of FSE found here. Degenerative, necrotic changes, areas of congestion and hemorrhage
100
Q

You are presented with a sheep that died due to, what the owner describes as, Neuro signs, opisthotonus, and has had several seizures over the past few days. You are performing a necropsy and find this when you open the brain. Based on the clinical history and gross examination:
1. What is your preliminary Dx?
2. What is the etiologic agent?
3. What is your morphological Dx?
4. What is important to note about the morphological characteristics of this brain?

A

Lamb, Texas A&M,
1. Dx: FSE
2. Etiologic Agent: Clostridium perfringens type. D - Epsilon toxin
3. Multifocal, bilaterally symmetric encephalomalacia

Areas of softening
4. Lesions that are asymmetric in brain suspect infectious etiology. If symmetric it is probably a toxin of some sort, in this case clostridum type D

101
Q

You are a barn aid on a horse ranch when you notice that several of your horses are ataxic, depressed, head pressing, wandering aimlessly, and are walking into the sides of their stalls. You notify the barn owner, and you both decide to thoroughly examine barn when you come across a stack of moldy corn. Based on the clinical signs:
1. What is your preliminary Dx?
2. What is the etiologic agent?
3. What happens as a result of this condition? What are the clinical signs?
4. What are the main species affected?

A
  1. Equine (Mycotoxic) Leukoencephalomalacia aka Moldy Corn Toxicity
    - Cause: Ingestion of moldy feed, specially corn and corn by-products
  2. fungus Fusarium verticillioides (F. moniliforme ) and/ or F. proliferatum (Fumonisin B1)
  3. Produces severe neuro disease
    ataxia, depression, head pressing, wandering aimlessly, blindness potentially
  4. Imp condition in horses; horses of all ages affected
102
Q

You are a barn aid on a horse ranch when you notice that several of your horses are ataxic, depressed, head pressing, wandering aimlessly, and are walking into the sides of their stalls. You notify the barn owner, and you both decide to thoroughly examine barn when you come across a stack of moldy corn. Based on the clinical signs and the gross image presented to you below:
1. What is your preliminary Dx?
2. Describe what you see in the image below.
3. The damage seen below is confined to what areas of the brain?

A
  1. Moldy corn toxicity in a Horse (Noah’s Archive) → Equine (Mycotoxic) Leukoencephalomalacia
  2. areas of cavitation, depression, malacia/necrosis
  3. Primarily confined to the white matter.
103
Q
  1. What is the name of the plant pictured below?
  2. What condition does this plant cause? What species is affected?
  3. What happens as a result of this condition?
  4. What is the toxic principle?
  5. What do these animals ultimately die from?
A
  1. Centaurea Solstitialis (“yellow star thistle”). Northern and Central California, also Oregon
  2. Nigropallidal Encephalomalacia (Chewing Disease of Horses, Centaurea poisoning) → 3. Dysfunction (dystonia) of muscles of prehension, mastication and
    deglutition -innervated by motor fibers of CNs V, VII and XII.
  3. Repin is the toxic principle → Glutathione depletion → results in oxidative damage, mitochondrial dysfunction and neuronal cell death.
  4. Die from starvation, dehydration or aspiration pneumonia
104
Q

What flower is pictured below?

A

Centaurea repens: “Russian Knapweed”,
Colorado, Utah

105
Q

What condition is pictured below?

A

Dx: Centaurea repens: “Russian Knapweed”,
Colorado, Utah

Bilaterally symmetric foci of liquefactive necrosis within the substantia nigra (located in mesencephalon - mid brain) , Horse, UCDavis.

Affected horses exhibit idle drowsiness and are unable to grasp food or drink water. Purposeless
chewing motions are apparent. Horses die of starvation, dehydration or aspiration pneumonia.

106
Q
A

Nigropallidal encephalomalacia, Horse, UCDavis.
Bilaterally symmetric lesions located in the globus
pallidus (part of the basal nuclei)-Blue stars.

Basal nuclei forms portion of basolateral floor
Star = globus pallidus
Areas of malacia
usually symmetric, maybe asymmetric

107
Q

Inflammatory conditions of the CNS are often caused by?

A

infectious agents and are the most important cause of
neuropathology in domestic animals

108
Q

What are the routes of infection of inflammatory conditions?

A

 Haematogenous (bacteremia,viremia,embolic)
 Direct extension e.g. sinusitis, otitis media
 Neurogenic e.g., rabies via axonal transport, listeria can reach the brain stem via
trigeminal nerve, tetanus toxin

109
Q

ANy kind of bacteremia can result in?

A

systemic infection and meningitis or meningioencephalitis

110
Q

List the conditions that result in inflammation?

A

 Bacterial Diseases
 Viral Diseases
 Parasitic infections
 Prion Diseases (Transmissible encephalopathies)
 Miscellaneous infections (rickettsial and fungal
diseases that primarily affect other tissues and
systems).

111
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A
  1. Suppurative meningitis
  2. Bacterial infection of the CNS
  3. Look for brain swelling.
    In cases of cerebral edema, if the brain is swollen, you can have cerebral ?, swelling of hyper?. culling?
    - The gyra of the brain are going to be wider and also more flattened due to presence of edema.
    - Hyperemia of meningial blood vessels, making them very prominent.
    - The sulci in the gyra are covered with cloudy fluid, which may contain suppurative exudate, fibrin. This makes this condition very easy to recognize.
112
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Ventral view of the brain
1. suppurative meningitis
2. Bacterial infection of the CNS
3. May only see hyperemia on dorsal surface. Always turn to look at the dorsal surface, because exudate will fall to ventral surface due to gravity.

Foal brain, neonatal meningitis, meningioencephalitis

113
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Leptomeningitis; when we take out the brain, we take it out without the dura mater, whihc is still attached ot the cranium. Here we are looking at the dura matter which collapsed on top?

If we see something like this, MDx: suppurative meningioencephalitis but also fibrinosuppurative could be used here too

114
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Pig brain
1. suppurative meningitis, Etiological agent: Streptococcus suis; E.coli can also cause this as well.
2. Bacterial
3. Hyperemia, in sulci there is a cloudy gray material that represents the presence of fibrin mixed with neutrophils.
- Very common in farm animals
- Manifestation of neonatal bacteremia and sepsis
- Evidence of policephaltiis, peritoniitis, pleuritis, also polynephritis, polysynovitis, etc. b/c it is a systemic condition so in addition to affecting meninges, will have lesions in other places.

115
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A
  1. Pig, meningo-encephalitis and ependymitis (also ventriculitis),
    E. coli
  2. Invade parenchyma = meningioencephalitis. Many times will involve chorid plexus and also involve the pendymal surface. Can prpduce what people call ependymitis and also periventriculitis.
    - In a pig, this is a more chronic severe bacterial infection of the brain whre there is clear formation of abscesses in the parenchyma. In serial sections, you can see the laterla ventricus appears to be markedly dilated which is abnormal in the sense that the ventricle should not be so large.
    - Serial sections of brain –> want to be parallel so you should usually see some degree of symmetry. But here, you can see that there is asymmetric dilatation of the lateral ventricle.
    - Inflammatory cells and necrotic cellular debris present will obstruct mes. aqueduct, so communicationbetween laterla and third ventrical, third and fourth –> accumulation of CSF –> obstruct communication?

Pigs with UR infection –> eustachitis –> middle ear infection aka otitis media
- happens in babies too
- these cases in pigs are more diffiuclt b/c

116
Q

_________ ________ is an important
cause of disease in feedlot cattle

A

Histophilus somni

117
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A
  1. Thrombotic Meningoencephalitis (TME,
    TEME) – Histophilus somni
  2. Fibrino-suppurative, hemorrhagic and necrotizing meningoencephalitis
  3. Hemorrhagic and necrotic lesions
    - Can also see cloudiness of fluid within the sulci.
    - Neutrophils in fibrinous fluid
118
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Multifocal areas of hemorrhage, necrosis

119
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Multifocal areas of hemorrhage, necrosis

9-months old Angus Steer, Case 2, Conference 1, 2012, WSC,
JPC.

120
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

Thrombotic meningoencephalitis, H. somni, Steer, AVC

Hypercellularity of the meninges

121
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A

TME, fibrinonecrotizing vasculitis and thrombosis, brain,
Atlantic Veterinary College

Thrombus in the middle containing necrotic debris

122
Q

Listeriosis
 Sporadic in adult ______ & ______
 Etiologic Agent: ?
 _______/____ erupt.
 Silage; ______ feed –> lesions in _____ cavity –> infected; Root of infection will be through the ________ nerve, aka a ________ type of infectious condition.
 ________ to brainstem via _______ nerve, speficially the ______ of ________ nerve.

A

Listeriosis
 Sporadic in adult sheep & cattle
 Etiologic Agent: Listeria monocytogenes
 Peridontitis/tooth erupt.
 Silage; rough feed –> lesions in oral cavity –> infected; Root of infection will be through the trigeminal nerve, aka a neurogenic type of infectious condition.
 Retrograde to brainstem via
trigeminal nerve, speficially the nuclei of trigeminal nerve.

123
Q

What clinical signs are seen in a cow or sheep suffering from Listeriosis?

A

Circling, head tilt, facial paralysis (VII); involve nuclei of this cranial nerve, drooling saliva (V),
death with a few days

May also cause abortion/septicemia/conjunctivitis

124
Q

How do you confirm a patient has/died of listeriosis?

A

Histopath. Will see:
Areas of necrosis, malacia, or inflammation can be seen grossly.

125
Q

What else can you do to confirm listeriosis?

A

Can do immunohistochemistry/culture

126
Q
A

Cow, Listeria monocytogenes – medullary
abscess, Cornell Files

127
Q
A

Cluster of neurons of Cranial Nerve 7 are affected by this.
- Hypercellularity
- Perivascular cuffing results because cells follow blood vessels

128
Q
A

Sheep, microabscess, medulla oblongata, Listeriosis, Cornell Files.

129
Q
A
130
Q
A

Listeria is a gram + bacteria. All blue = listeria

will be found in microabscesses in the brain stem

131
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
  4. This etiologic agent primarily targets?
A
  1. Equine encephalomyelitis
  2. Viral induced inflammatory diseases
  3. polioencephalomyelitis; Sometimes you may not see anything grossly in viral conditions, but especially eastern equine enceph is more severe and tehrefore may see areas of hemorrhage and necrosis. Virus targets primarily the gray matter whihc is why it is polio. The lesions are also going to be more prominent.

Horse: Eastern virus encephalomyelitis,
Prominent lesions in the brain stem
Equine encephalomyelitis:
Eastern, Western and Venezuelan
encephalomyelitis viruses →
family Togaviridae, genus
Alphavirus (vector-born diseases
– mosquitos)

Primarily see outbreaks of Eastern and Western outbreaks in atlantic region of NA.

132
Q
  1. What condition is pictured below?
  2. What type of CNS infection is this?
  3. What are you looking for grossly?
A
  1. Equine encephalomyelitis
  2. Viral induced inflammatory diseases
  3. polioencephalomyelitis; Sometimes you may not see anything grossly in viral conditions, but especially eastern equine enceph is more severe and tehrefore may see areas of hemorrhage and necrosis. Virus targets primarily the gray matter whihc is why it is polio. The lesions are also goingx to be more prominent.

Horse: Eastern virus encephalomyelitis,
Prominent lesions in the brain stem
Equine encephalomyelitis:
Eastern, Western and Venezuelan
encephalomyelitis viruses →
family Togaviridae, genus
Alphavirus (vector-born diseases
– mosquitos)

Primarily see outbreaks of Eastern and Western outbreaks in atlantic region of NA.

133
Q

These are photos of histological samples taken from a horse that died of equine viral encephalitis. Based on this condition:

  1. What are the typical clinical signs associated with EVE?
  2. What do you typically see on histology?
A

Equine Viral encephalitis

Clinical signs: depressed, head-pressing which is a manifestation of headaches sometiemes, aimless wandering, and then become ataxic, recumbent, eventually die

Perivascular cuffing

This is a picture of gray matter. Can see increased numbers of glial cells around degenerating neurons and neurophagic neurons

134
Q

What is the most common inflammatory cell seen in a viral infection?

A

Lymphocytes and plasma cells

135
Q
  1. The horse pictured below is most likely suffering what from viral infection?
  2. What is the etiologic agent?
  3. What are the most common clinical signs?
  4. This virus primarily targets?
A
  1. Herpesvirus myeloencephalitis
  2. EHV-1
  3. Ataxia, bladder paralysis (dribbling urine)
  4. primarily target nerve tissue –> sever myeloencephalitis or encephalomyelitis
    - Preferred term is myeloencephalitis.
    - The lesions are more significant and more severe in spinal chord.
136
Q

Bovine herpesvirus encephalitis
- Outbreaks of disease may occur in _______ cattle (___-___ months of age)
- Bovine necrotizing meningioencephalitis caused by ____-___
- Bovine meningioencephalomyelitis caused by _____-__ (infectious bovine rhio)

A

Bovine herpesvirus encephalitis
- Outbreaks of disease may occur in young cattle (5-18 months of age)
- Bovine necrotizing meningioencephalitis caused by BHV-5
- Bovine meningioencephalomyelitis caused by BHV-1 (infectious bovine rhio)

137
Q

Canine herpesviral encephalitis is an _____, highly ____ disease of _______ (after the age of ___ weeks are _______ to an infection).

A

Canine herpesviral encephalitis is an acute, highly fatal disease of neonates (puppies after the age of 3 weeks are resistant to an infection).

138
Q
A

Rabies

139
Q
A

Rabies

140
Q

__________ disseminate rabies, because they bite other animals.

A

Carnivores disseminate rabies, because they bite other animals.

141
Q

What is the loocalization of the rabies virus?

A

Localization of rabies virus varies between species.
in carnivores the prominent lesions are going to be located in the lymbic system, so in the hippocampus. Hippocampus of dogs and carnivores was the predilected location to send for diagnositc confirmaton. Now you are supposed to send the entire brain for testing.

Adaptve mechanism of virus becuase limbic and hippocampus is important in animal behavior. Lesions result in increased aggression, so these animals are more aggresive and bite other animals. protective mechanism of vorus = theory

142
Q

Lesions in salivary glands -> infected –> saliva will contain virus so when aniamls die the virus is present within the saliva. Adaptations that the virus has in order to increase ? in environment.

A
143
Q
A

Inflammation in cattle is surprisingly minimal

Section of cerebellum.
Basically no inflamamtion, only a bit of perivascular cuffing in 1 blood vessel (on right image)

144
Q
A

Neurons morphlogically normal, even though infected with rabies.

Can see small eosinophillic IB in cytoplasm

145
Q
A

In the past, the Finding of Negri
bodies was crucial for the post-mortem diagnosis of rabies
Negri bodies in Purkinje cells, steer – CL Davis slide collection,
picture, OI.

146
Q
A

Negri body, TEM

Amorphous matrix of viral proteins.

In the past, negri bodies were used for diagnosis a lot but between 15-30% of animals with rabies may not have negri bodies.
need to do IHC, Immunofluorescent test

147
Q

Canine Distemper Virus is a __________ virus, meaning it will affect multiple systems.
Patient can present with ______ clinical signs, ______ issues, and/or ____ disease –> neuro signs a few ______ post systemic signs. These signs can be very severe, so the virus will enter the brain and target ________ and _______ cells. It will also target the ____________ –> vacuolation of white matter in many cases.
Clinical Signs: ______ nose, _________ exudate, _______, _______, __________.

A

Canine Distemper Virus
Is a Pancytotropic virus, meaning it will affect multiple systems.
Can present with respiratory clinical signs, intestinal issues, and/or CNS disease –> neuro signs a few weeks post systemic signs. These signs can be very severe, so the virus will enter the brain and target astrocytes and microglial cells. It will also target the oligodendrocytes –> vacuolation of white matter in many cases. Runny nose, suppurative exudate, fever, depression, conjunctivitis.

148
Q
  1. What can be seen on histology?
A
  1. Vacuolization, See the presence of eosinophilic inclusion bodies in cytoplasm of the effected epithelium. Also affects urothelium –> sections of urinary bladder present IC eosinophillic IB, occasioanlly these IB can be in nuclei.
149
Q

1.

A
  1. Distemper also targets enamoblasts.
    Areas of brownish discoloration in the root of the teeth is very characteristic of distemper. This is a NAVLE question.

Will affect different kinds of animals, including wildlife and ferrets, raccoons, skunks.

  1. Foot pad is not as common. Marked thickening of the footpads.
150
Q

Canine distemper virus primarily targets _________ and ________ cells. Can also damage oligodendrocytes –> __________ changes in _______ matter –> __________.

Inclusion bodies can be found in the __________.

A

Canine distemper virus primarily targets astrocytes and microglial cells. Can also damage oligodendrocytes –> spongiform changes in white matter –> vacuolization.

Inclusion bodies can be found in the cytoplasm.

When look at brain of patient with neuro signs: depression, seizures, tremors, these aimals may have spongiform changei in white matter, especially cerebellum (status spongiosus). Assocaited with intramyelin edema due to direct damage ot oligodendrocytes by this virus.

151
Q

nn

A

Canine Distemper, dog, TAMU. Intranuclear inclusions in
astrocytes from cerebellar white matter

typical inflamamtory changes: Perivascular cuffing, encephalitis, encephalomyelitis, meningoencephalitis.

vVAcuolation in white matter assocaited with targeting oligodendrocytes whihc represents primarily intramyelin edema, and to dome degreee demyelination.

Very often in CDV –> infection of astrocytes –> these are the second biggest cells after neurons int he brain.

152
Q

FIP will produce ________ effusion in young cats –> _______ abdomen.
- When open them up, a lot of _______ fluid (______). May see ________ _______ on surface of visceral organs.
- Some of these animals may develop the dry form/________ form of FIP –> lesions in the _____ occurs in this form aka Pyogranulomatous meningoencephalitis. –> Leptomeningitis, choroid?, chorioependymitis.
- Histo: Cross section of brain with FIP –> discoloration, discoloration edges of ventricles due to _________ (inflamation of ________ ________ and ependyma).

A

FIP will produce peritoneal effusions in young cats –> Distended abdomen.
- When open them up, a lot of fibrinous fluid (cloudy). May see fibrinous plaques on surface of visceral organs.
- Some of these animals may develop the dry form/noneffusive form of FIP. Lesions in the brain occurs in this form. Pyogranulomatous meningoencephalitis. –> Leptomeningitis, choroid?, chorioependymitis.
- Histo: Cross section of brain with FIP –> discoloration, irregular edges of ventricles due to choriopendymitis (inflamation of choroid plexus and ependyma).

FIP is an important cause of pyogranulomatous encephlalitis in cats. Inflammation of chorodi plexus and ventricles too

153
Q

What can be seen in the image below?

A

FIP (dry form), pyogranulomatous or
granulomatous (non-suppurative) meningo-encephalitis, around ventricles

MQ, lymphocytes, some neutrophils scattered through.

154
Q

What can be seen in the image below?

A

Cat, FIP, acquired hydrocephalus

Inflammation, destruction of ventricles. Clogging of the mesencephalic aqueduct due to debris in CSF –> acquired hydrocephalus.

Asymmetry in ventricles is clearly seen.

Sometimes in these cases of FIP, with neuro disease, we freeze the brain so it will become solid, cross-section in band saw, to get a better sense of its symmetry and prevent CSF from escaping and ventricles from collapsing.

155
Q

 Caprine Arthritis Encephalitis (CAE) [Visna] syndrome:
- ___________ disease is seen primarily in young ____, mostly ___-___months of age.
- Caused by a ________, and is transmitted to goat _____ through _______, ____ and _______ contact with infected dams.
- Clinical signs in kids include: (2?).; (3?) occur in adult goats.
- The CNS lesion – mainly in the _______ brain stem and ________ ________ - is a demyelinating encephalomyelitis.

When goats have both Visna and Maedi –> ovine progressive pneumonia (OPP) [“Maedi-visna is also known as ovine progressive pneumonia (OPP).” ]

“Caprine arthritis-encephalitis (CAE) and maedi-visna (MV) are persistent lentivirus infections of goats and sheep. They are often grouped together as the small ruminant lentiviruses (SRLVs). Maedi-visna is also known as ovine progressive pneumonia (OPP).”

A

 Caprine Arthritis Encephalitis (CAE) syndrome:
- Neurological disease is seen primarily in young kids, mostly 2-4 months of age.
- Caused by a lentivirus and transmitted to goat kids through colostrum, milk and direct contact with infected dams.
- Clinical signs include: paresis, posterior paralysis.
- Arthritis/bursitis, pneumonitis and mastitis occur in adult goats.
- The CNS lesion – mainly in the caudal brain stem and spinal cord - is a demyelinating encephalomyelitis.

156
Q

Lentivirus produces Ovine Progressive Pneumonia. This condition is also referred to as Maeidi.
- This same virus produces a neurological condition called Visna, a lymphoid meningoencephalitis in sheep. ???

closely related to that causing Maeidi (Ovine Progressive Pneumonia → Lymphoid Interstitial Pneumonia).
“In both conditions (CAE andVisna) an immune-mediated etiology is
suspected”

A

“Caprine arthritis-encephalitis (CAE) and maedi-visna (MV) are persistent lentivirus infections of goats and sheep. They are often grouped together as the small ruminant lentiviruses (SRLVs). Maedi-visna is also known as ovine progressive pneumonia (OPP).”

157
Q

Equine Protozoal Myeloencephalitis/ Encephalomyelitis (EPM) is the most common disease in horses; Very prevalent in the states: _______, ___________. Results in _________ or ________ neurologic deficits.
- more severe lesions are confined to the _______ ________.
- Clinical Signs: Sudden or gradual onset of _______ limb paresis and ataxia
- Is a result of malformation in ________ vertebrae that compress the spinal cord.
- _________ signs seen in younger horses.
Etiologic Agent: Caused by infection with ________ _______. DNA tests have demonstrated that this microbe is identical to _________ _________, a protozoal parasite for which the opossum is the definitive host (sexual stages within the GI tract).

A

Equine Protozoal Myeloencephalitis/ Encephalomyelitis (EPM) is the most common disease in horses; Very prevalent in the states: Texas, California. Reults in multifocal or asymmetric neurologic deficits.
- more severe lesions are confined to the spinal chord.
- Clinical Signs: Sudden or gradual onset of pelvic limb paresis and ataxia
- Is a result of malformation in cervical vertebrae that compress the spinal cord.
- Neuro signs seen in younger horses.
Etiologic Agent: Caused by infection with Sarcocystis neurona. DNA tests have demonstrated that S. Neurona is identical to Sarcocystis falcatula, a protozoal parasite for which the opossum is the definitive host (sexual stages within the GI tract).

158
Q

Horses are an _______, or ______ _____, host of Sarcocystis neurona. Gets infected during ingestion of feed contaminated with infected _________ present in the feed of the oppossum.
Lesions in the horse with this condition are primarily confined to the ?

A

Horses are an aberrant, or dead end, host of Sarcocystis neurona. Gets infected during ingestion of feed contaminated with infected sprozoites present in the feed of the oppossum.
Lesions in the horse with this condition are primarily confined to the brain stem and spinal cord.

159
Q

Dx: EPM
▪ In the horse the organism replicates in the _____ rather than in ______.
▪ Asymmetry of clinical signs help to differentiate this disease from _______
syndrome and ________ myeloencephalitis (usually symmetric or mildly asymmetric).
- Pathologists perform ______ examinations of brain, especially the brain ____ and _____ _______.
- Multifocal areas of discoloration = areas of _________ and _______. Confined to both the ______ and ________ matter.
- Not completely _______ for EPM. Equine herpesvirus produces areas of _______ and ________ throughout spinal chord and brainstem, so gross examination not _______.

A

▪ In the horse the organism replicates in the CNS rather than in muscle.
▪ Asymmetry of clinical signs help to differentiate this disease from wobbler
syndrome and herpesvirus myeloencephalitis (usually symmetric or mildly asymmetric).
- Pathologists perform serial examinations of brain, especially the brain stem and spinal cord.
- Multifocal areas of discoloration = areas of hemorrhage and necrosis. Confined to both the white and gray matter.
- Not completely diagnostic for EPM. Equine herpesvirus produces areas of malacia and hemorrhage throughout spinal chord and brainstem, so gross examination not definitive.

▪ The Horse my be an aberrant host which gets infected after accidental
ingestion of sporocysts shed in opossum feces or feed contaminated by
dead birds (intermediate hosts).

160
Q

In cases of EPM, you will see on gross examination:
__________, _________ distributed areas of _______ and _______ within the spinal cord. Many lesions are confined to _____ matter but some are in the ______ matter.

A

In cases of EPM, you will see on gross examination:
Multifocal, randomly distributed areas of hemorrhage and malacia within the spinal cord. Many lesions are confined to gray matter but some are in the white matter.

161
Q

Animal presented with neurological signs, lameness, etc but the clinicians decided that the animal may have been Wobbler’s syndrome rather than EPM so they treated with corticosteroids. After the treatment, the horse became worse because the protozoa produced more lesions and was then euthanized. Lesions found on necropsy. This is a classical case.
Produces foci of necrosis, nonsuppurative myeloencephalitis.

Signs of Inflammation on histo:?

A

Horse, EPM, inflammatory changes in
brain and spinal cord

Perivascular cuffing
Glial cells
Vacuolization
Axonal degeneration

162
Q

Below is an image of a histological slide of a sample taken from a patient that died from S. neurona. What can be seen below?

A

Characteristic lesion:
Nuclear debris due to necrosis
Presence of bradyzoites
Form rosettes very characteristic within cytoplasm of neurons

Very hard to find
Focus of gliosis and intralesional protozoa (S. neurona), horse, TAMU

163
Q
A

Horse, Sarcocystis neurona bradyzoites, brain stem. Texas A&M
University, OI.

164
Q

Halicephalobus gingivalis (formerly called ?) and ________ _______ larvae migration are the most common cause of verminous encephalomyelitis in the horse.

In _______, we see this more commonly.
SV = will produce _______ and ________ of the ___________ _________ artery (verminous thrombosis in horses).

SV –> enter the _______ –> can migrate via aberrant migration and go anywhere by chance. Happens occasionally and sometimes the nematodes will produce ____________ in horses. Lesions are not characteristic, but see foci of _________ and ___________ in white matter.

Halicephalobus gingivalis = _____ ranging, present in ________. Nematode can get in through ________ –> enter brain

A

Halicephalobus gingivalis (formerly called H. deletrix) and Strongylus vulgaris larvae migration are
the most common cause of verminous encephalomyelitis in the horse.

In horses, we see this more commonly.
SV = will produce vasculitis and thrombosis of the cranial mesenteric artery (verminous thrombosis in horses).

SV –> enter the colon –> can migrate via aberrant migration and go anywhere by chance. Happens occasionally and sometimes the nematodes will produce meningoencephalitis in horses. Lesions are not characteristic, but see foci of hemorrhage and necrosis in white matter.

Halicephalobus gingivalis = free ranging, present in environment. Nematode can get in through laceration –> enter brain

Cerebrospinal nematodiasis, horse, Dr. Storts,
TAMU.

165
Q
  1. Based on the histological image below, what condition is this horse suffering from?
  2. How is this condition typically diagnosed?
  3. What does this condition sometimes do?
A
  1. Cerbrospinal nematodiasis, horse, aberrant migration of Strongylus vulgaris larvae.
  2. Dx via histology
  3. Sometimes: Produces nodular granulomatous lesions within the gums.
166
Q

?

A

Very characteristic
Cat, non-suppurative encephalitis, Toxoplasma gondii, Noah’s
Arkive. Cysts containing bradyzoites

do not induce a very prominent inflammatory response, so inflammation may be minimal

167
Q

Transmissible Spongiform Encephalopathies (TSEs).
- Believe to be caused by a _____, an abnormal isoform (_____) of the host ____ protein (___). Conformational changes in this abnormal isoform renders it resistant to protease ________ → accumulates within neurons causing ___________ and ________ neurological disease –> Disease of human and animals:
A. TSE’s in animals are: ____ ____ disease
B. TSEs in humans are:
1. ________ _______ disease (____D)
- Happens _______ in people. 1 in a _______
- Accelerated form of ________. People in their __s/__s develop clinical signs and die in just a few weeks or months.
2. ________ _______ _______ (FFI)
3. ______
- Dx first in papa new guinea.
- native communities here, one of the things they do is to eat the ______ of the ancestors after death b/c it frees the ______ of the ancestors and get some of the wisdom of the ancestors. Outbreaks of neuro disease, fatal. Associated primarily with tremors, weakness, etc.
4. _______-________-______ Disease (GSS).

A

Transmissible Spongiform Encephalopathies (TSEs).
- Believe to be caused by a prion, an abnormal isoform (PrPSc) of the host prion protein (PrP). Conformational changes in this abnormal isoform renders it resistant to protease degradation → accumulates within neurons causing progressive and fatal neurological disease
- Disease of human and animals.
- TSE’s in animals are: Mad cow disease
- TSEs in humans are:
1. Creutzfeldt-Jakob disease (CDJ)
- - Happens sporadically in people. 1/million
- Accelerated form of alzehimers. People in their 50s/60s develop clinical signs and die in just a few weeks or months.
2. Familial Fatal Insomnia (FFI)
3. Kuru
- Dx first in papa new guinea.
- native communities here, one of the things they do is to eat the brain of the ancestors after death b/c it frees the spirit of the ancestors and get some of the wisdom of the ancestors. Outbreaks of neuro disease, fatal. Associated primarily with tremors, weakness, etc.
4. Gertsmann- Straussler-Scheinker Disease (GSS).

168
Q
  1. Other than mad cow disease, name four other examples of TSE’s in animals.
  2. Outbreaks of mad cow are associated with?
  3. What condition is the cow suffering from below? How long is the incubation period?
  4. What are the clinical signs of this condition?
  5. Lesions of this condition are typically found in?
A
  1. In animals TSEs include: Scrapie in sheep, feline spongiform encephalopathy in cats, mink spongiform encephalopathy, chronic wasting disease (CWD) in deer, elk and moose, and BSE.
  2. Feeding of bone and meat meal containing material from scrapie infected sheep.
  3. BSE; BSE has a long incubation period (2-8
    years).
  4. Clinical signs in BSE include aggression,
    incoordination, abnormal posture,
    hypermetria, progressive weakness, ↓
    milk production and emaciation.
  5. Lesions are commonly found in the obex (marked in red below). This is the dorsal part of the brain stem is where neurons are vacuolated and diagnostic of bovine spongiform encephalopathy. Also present in other areas as well.
169
Q

The BSE agent has been identified in the neural tissue (______, ______ ______, ______, ______, ______) and lymphoid tissue (______, bone ________, and GALT in the ______ intestine→ SRM, specific risk material).

Practically no ________ or ______ in these cases.

In canada you must dispose of tissues of exposed animal, by ______ or ________ in a separate way.

BSE, neuronal _______, brain stem, HE, AFIP.

A

The BSE agent has been identified in the neural tissue (brain, spinal cord, nerves, ganglia, eyes) and lymphoid tissue (tonsils, bone marrow, and GALT in the small intestine→ SRM, specific risk material).

Practically no inflammation or gliosis in these cases.
In canada you must dispose of tissues of exposed animal, by burning or biodigested in a separate way.

BSE, neuronal vacuolation,
brain stem, HE, AFIP.

170
Q

What condition is this sheep suffering from?

A

Fleece self-inflicted damage caused by pruritus, sheep with
Scrapie. Signs: Ataxia, weight loss, behavioral changes, gait abnormalities and scratching
and rubbing against fixed objects…

Animal is very itchy, scratching on fence posts

171
Q

What condition is this deer suffering from?

A

Deer with CWD – web image.
In Canada the disease has been reported in
Saskatchewan and Alberta.
Animals have poor BCS, coat is in bad shape, lose fear of human contact. Do not consume.
Human implications? –> people who hunt

172
Q

Rickettsial diseases:
A. Rocky mountain spotted fever (RMSF), Clinically important in the _____.
→ Etiology: __________ _________.
- The disease is characterized by _________ in the brain.

B. Canine Ehrlichiosis
→ Etiology: _______ ________
- Causes a non-________ meningitis/ meningo-encephalitis.

A

Rickettsial diseases:
Rocky mountain spotted fever (RMSF), Clinically important in the dog.
→ Etiology: Rickettsia rickettsi. The disease is characterized by vasculitis in the brain.
Canine Ehrlichiosis → Ehrlichia canis, causes a non- suppurative meningitis/ meningo-encephalitis.

173
Q

Several fungi can produce systemic infections in animals –> ______________.

___________ is technically the only fungal organism that is in the position to produce lesions in the brain. Characteristic lesions in the ______ cavity, __________ sinuses, and then travels and invades ________ in the brain.

___________ capsule –> gelatinous, mucoid appearance on histo. ________ lesions containing mucoid material

A

Several fungi can produce systemic infections in animals –> meningoencephalitis.

Cryptococcus is techncially the only fungal organism that is in the position to produce lesions in the brain. Characteristic lesions i the nasal cavity, paranasal sinuses, and then travels and invades meninges in the brain.

Polysaccharide capsule –> gelatinous, mucoid appearance on histo. CAvitated lesions containing mucoid material

Cat, Cryptoccocus neoformans (cryptococcal meningo-encephalitis)
Viscous mucoid exudate mucopolysaccharide capsule of the yeasts.

174
Q

?

A

Cat, Cryptococcosis,
brain

Lesions are translucent, mucoid appearance.

175
Q
A

Cat, cryptococcosis
Noah’s Archives

176
Q

??

A

Cryptococcosis, Histo, HE and Mucicarmin
stain

Inflammatory response may be minimal, subtle.

Characteristic yeast found in brain, surrounded by halos, where the mucopolysaccharide capsule is. red = capsule, used Mus stian

Areas of mysosi, nonsuppurative type of exudate.

177
Q

Primary Neoplasms seen in brain:
 Meningiomas
 Astrocytomas
 Oligodendrogliomas
 Choroid plexus papillomas
 Ependymomas
 Medulloblastomas
 Neuroblastomas

A

More likely to see in small animals

Arise from cells normally found in brain and spinal chord.
Most are benign, but sometimes can be malignant.

MAOC

MEN MAC Oli

178
Q

Secondary (metastatic) Neoplasms arise somewhere else and metastasize to the brain:
 Hemangiosarcoma (very common in dogs)
 Mammary adenocarcinoma
 Pulmonary carcinomas
 Lymphosarcoma
 Melanoma

A

??

179
Q
A

Cat, Adult, Meningioma, occipital lobe,
Texas A&M

Present on surface of the brain = meninges = meningioma

180
Q
A

Cat, meningioma, Noah’s
Archives

Producing significant compression of the brain.
If meningioma not treated –> benign tumor of meninges –> lead to death

181
Q
A

Cat, Malignant meningioma

182
Q
A

Dog, Texas A&M, Malignant meningioma -invasion of bone and nasal cavity

Can not tell if it is meningioma or tumor arising from nasal cavity (carcinoma) that metastasized to the brain.

183
Q
A

Dog, Texas A&M, Choroid plexus papilloma
- Arising from the choroid plexus of lateral ventricle.
- If lesion was similar but infilatrating parenchyma, would be called choroid pledxus carcinoma

184
Q
A

Dog, Astrocytoma, intraventricular
hemorrhage, AVC
Swelling, asymmetry of brain.
Tumor arised from parenchyma and invaded ventricles. –> hemorrhage

185
Q
A

Glioblastoma, 18m-old Boston Terrier,
Texas A&M
Arise from glial cells

186
Q
A

Dog, Medulloblastoma, Cerebellar
hemisphere, AVC
Dogs and calfs
Arise from cerebellum
Younger dog presented with unilateral central signs.
Composed of primitive neurons

187
Q
A

Dog, female, Metastatic mammary
carcinoma, Texas A&M

188
Q
A

Dog, Texas A&M, metastatic hemangiosarcoma
Arise from endothelial cells
multifocal, cavitating lesions containing blood –> metastatic hemangiosarcoma

189
Q
A

Cat, metastatic hemangiosarcoma Noah’s Archives
multifocal nodular cavitating lesions containing blood (appears dark because was fixed) –>