Central Nervous (awesome) Sauce

Question 1

In all cases of CNS disease, what do we need to do?

Answer 1

Remove the spinal cord! Even though clinical signs may be referable ONLY to the brain

Question 2

In small animals, how can we expose the spinal cord?

Answer 2

Dorsal laminectomy with bone rongeurs; Then remove by holding dura mater w/forceps and sectioning spinal roots as close to intervertebral foramina as possible (so basic…)

Question 3

On PM examination of the nervous system, what do we need to do with the brain and spinal cord before sectioning and submitting for histopath?

Answer 3

Immerse in formalin and fix for 5-7 days!

Question 4

What 2 protoplasmic properties are highly developed in neurons?

Answer 4

Irritability: generation of an impulse Conductivity: ability to transmit such an impulse from one location to another

Question 5

What are neuroglia and how can they be classified?

Answer 5

Maintenance (support, protection, cleanup) cells of the neuronal microenvironment MACROglia: astrocytes and oligodendrocytes MICROglia: gitter cells (globular/swollen after phagocytosis of debris from injury) *immunosurveillance/regulation, repair*

Question 6

Gliosis, perivascular cuffing (like that seen in Distemper on histo) indicates migration of inflammatory cells from where to where? Why?

Answer 6

From parenchyma–>vasculature Glial cells are phagocytic, so they’re responding to neuropil injury

Question 7

Astrocytes in the nervous system are analogous to what cell type?

Answer 7

Fibroblasts! They also proliferate/repair in response to injury

Question 8

Main distinction between Wallerian-type degeneration and Neuronal cell injury leading to axonal degeneration? (The 2 types of Degeneration that look awfully similar…)

Answer 8

Wallerian axons can potentially regenerate, depending on the damage; Whereas neuronal cell injury leading to axonal degeneration could be a result of an etiological agent TARGETING the neuron and the neuron will eventually die

Question 9

Term given to large fluid filled cavities in the brain (Not just ^CSF in ventricles, but also ^CSF in parenchyma*)

Answer 9

Hydranencephaly

Question 10

Term given for small fluid filled cavities in the brain

Answer 10

Porencephaly

Question 11

What viruses can lead to hydranencephaly/porencephaly?

Answer 11

Akabane Bluetongue Rift Valley Wesselsbron Pestiviruses

Question 12

Cerebellar hypoplasia may be the result of in utero OR peri-natal viral infection of ________ in kittens and _______ in calves.

Answer 12

Feline Panleukopenia (aka Feline Parvovirus; Parvoviridae–>protoparvovirus) BVD (Flavi–>Pestivirus)

Question 13

How do we distinguish Spina Bifida from Spina Bifida Occulta?

Answer 13

SB: defective closure of bony encasement of spinal cord - visually apparent SBO: can’t see this from the outside- need palpation

Question 14

Ingestion of locoweeds cause what?

Answer 14

Acquired form of mannosidosis The locoweeds contain potent inhibitors of alpha-mannosidase (which breaks down CHOs)

Question 15

Name the 3 traumatic injuries discussed in lecture in order of increasing severity…. GO!

Answer 15

Concussion
Contusion
Laceration

Question 16

What are 2 sources of sulfur toxicity that can result in polioencephalomalacia?

Answer 16

1) high sulfate concentrations in drinking water 2) ingestion of sulfate accumulating plants

Question 17

Thiamine deficiency is an important cause of what encephalopathy?

Answer 17

Polioencephalomalacia (Areas of softening in the grey matter that represent necrosis)

Question 18

Salt poisoning or water deprivation can lead to what encephalopathy?

Answer 18

Polioencephalomalacia

Question 19

Sheep with thiamine-responsive PEM may display what clinical sign?

Answer 19

Opisthotonus (“star-gazing”) And signs similar to those of CEREBELLAR DZ!

Question 20

Feline Ischemic Encephalopathy (FIE) resulting in cerebral infarction is usually a result of what parasitic migration?

Answer 20

Cuterebra via nasal passages thru piriform plate

Question 21

What term do we use to describe the breakdown/lysis of cytoplasmic Nissl bodies?

Answer 21

• *Chromatolysis**
• indicates neuronal cell injury*

Question 22

What’s the most suitable description for neurons that demonstrate cytoplasmic eosinophilia (red/pink cytoplasm), nuclear pyknosis (darkly-stained nucleus), or karyolysis?

Answer 22

Energy-deprivation change
may be result of ischemia, hypoglycemia, etc..

Question 23

What are we looking at?

Answer 23

Satellitosis

Question 24

What is this?

Answer 24

Neuronophagia
“neuronophagic nodules”
undergoing necrosis and being invaded by phagocytic cells

Question 25

Hepatic Encephalopathy in a Steer: What do we call this? what does the morphology represent, especially on the boundary of grey/white matter?

Answer 25

**Status Spongiosus;** Myelin!

Question 26

*Rut*-*roh*... Cerebellum of this dog is indicating what? what do the vacuolations suggest?

Answer 26

Distemper :( Family: **Paramyxoviridae** Genus: **Morbillivirus** *vacuoles suggest demyelination and perivascular cuffing*

Question 27

What do we call this? What cell is reacting?

Answer 27

**Astrogliosis** *Reactive (gemistocytic) astrocytes; homogenous, eosinophilic - nuclei become eccentric*

Question 28

* *Cerebellar white matter from K9 w/Distemper** * What cardinal tings are supporting this diagnosis?*

Answer 28

Perivascular cuffing, Eosinophilic intracytoplasmic inclusion bodies within neuroglia, and status spongiosus

Question 29

A variant of this disease is indicated with contaminated BSE meat. Describe the abnormalities...

Answer 29

**Creutzfeldt**-**Jakob** Dz (**CJD**) vacuolation, increased cellularity (GLIOSIS), and spongiform change

Question 30

What do we call these *"foamy macrophages"* seen in this lamb with Focal Symmetric Encephalomalacia (FSE)?

Answer 30

**Glitter cells aka Activated Microglial Cells** *"git 'er done!"*

Question 31

This congenital microencephaly in a newborn donkey is the result of what...

Answer 31

Prosencephalic Hypoplasia

Question 32

Microencephaly in a newborn donkey, resulting from prosencephalic hypoplasia, is pictured. If we saw this lesion in a ***calf***, what would we suspect the etiological agent to be? What about if we saw this in ***piglets***?

Answer 32

Calf: in utero infection w/ **BVD** Piglet: in utero infection w/ **Classical Swine Fever** *(remember: both of these are **Pestiviruses*** *belonging to the family **Flaviviridae****)*

Question 33

Cerebral edema can result in gyral herniation. What happened here?

Answer 33

Parahippocampal gyri herniated under the tentorium cerebelli

Question 34

Main lesion we would see in polioencephalomalacia?

Answer 34

Neuronal cerebral cortical necrosis \**note: in this case, we do NOT fix; we section the brain FRESH and look for the lesions: areas of palor in grey matter (may be subtle)*

Question 35

What diagnostic tool can we use for detecting SPECIFICALLY thiamine-responsive PEM?

Answer 35

Wood's Lamp

Question 36

Because hypernatremia is chemotactic for neurons, what may accompany polioencephalomalacia in pigs (or poultry) suffering from salt poisoning?

Answer 36

perivascular and meningeal eosinophilic infiltration

Question 37

Thiamine deficiency can also occur in carnivores, resulting in polioencephalomalacia, but how is it different in these animals compared to herbivores?

Answer 37

Lesions tend to be bilaterally symmetrical and specific to grey matter of the **brain stem** (as opposed to cerebral cortex in herbies) \***Chastek Paralysis**\* *ALSO: has more to do with diet...* *diets containing fish as primary ingredient=high in thiaminase; diets based entirely in cooked meat=thiamine deficient (cats may demonstrate VENTROflexion)*

Question 38

This transverse section of brain stem thru the pons demonstrates what?

Answer 38

necrosis of the **caudal colliculi** seen in B1-deficiency among *carnivores \*this has been in the NAVLE\**

Question 39

This was a case of alkaloid toxicity in a steer. We know that Severe Liver Dz can lead to neurological signs... but HOW?

Answer 39

toxins in the blood (ammonia) --\> hyperammonemia --\> microcavitation in the white matter --\> myelin edema --\> splitting of myelin sheath (esp at interface of white/grey matter) --\> head pressing, mentation abnormalities, circling...

Question 40

Lambs with **good BCS** may demonstrate this type of lesion. What would the MDx be and what is it associated with?

Answer 40

* *Focal Symmetrical Encephalomalacia** * throughout brain stem and basal nuclei* associated with the **epsilon toxin** produced by *C.perfringens (type D)*

Question 41

Ingestion of moldy feed (corn) contaminated with the fungus, *Fusarium verticillioides (F.moniliforme/F.proliferatum)* can result in this lesion. **MDx?** what is the lesion actually associated with?

Answer 41

Equine Leukoencephalomalacia It's actually associated with the mycotoxin: **Fumonisin** **B1**

Question 42

Also known as "Chewing Dz of Horses," muscles of prehension, mastication, and deglutition are characteristically dysfunctional as a result of the **Repin** toxin from ingesting *Centaurea* Solstitialis (Yellow Star Thistle/Russian Knapweed). What is the MDx and what is the damage incurred?

Answer 42

**_Nigropallidal Encephalomalacia_** MDx: bilaterally symmetric foci of liquefactive necrosis within the *midbrain* (substantia nigra and nucleus pallidus) **oxidative** damage to **dopaminergic** neurons bc glutathione is depleted \*usu die from starvation, dehydration, or aspiration pneumonia\*

Question 43

**Nigropallidal Encephalomalacia** the lesions pictured *here* are specifically where?

Answer 43

globus pallidus (part of the basal nuclei)

Question 44

Pig: meningoencephalitis, ependymitis, and ventriculitis (the abscesses around the ventricles) Et?

Answer 44

*E.coli*

Question 45

This important etiological agent of feedlot cattle is also indicated in **myocarditis** and **fibrinopneumonia**... What is it? How do we describe this nastiness?

Answer 45

*Histophilus somni* _fibrino-suppurative, hemorrhagic, and necrotizing meningoencephalitis_ (TEME) is **NOT** bilaterally symmetric **NOR** does it discriminate between grey and white matter *focal areas of hemorrhage seem to follow blood vessels*

Question 46

Focal areas of suppurative inflammation like this are HIGHLY indicative of what etiological agent? How do we confirm the diagnosis?

Answer 46

***Listeria monocytogenes*** these nasty beezies (not to be confused with Ashley Judd) are gram positive, so we gram stain

Question 47

Typically, when we think of bacterial infections, we think of neutrophilic infiltrate and when we think of viral infections, we think of lymphoplasmacytic infiltrate... This is an exception. **MDx? Et?** **Predilection site(s)?**

Answer 47

Polioencephalomyelitis EEEV (Togaviridae--\>alphavirus) brain stem/***grey*** ***matter** perivascular cuffing, degeneration on histo*

Question 48

Dz in horses characterized by ataxia, paresis, paralysis (esp of bladder); vasculitis leads to thrombosis and infarction **MDx? Et?**

Answer 48

Hemorrhagic and ischemic myeloencephalitis EHV-1 (same agent that causes respiratory dz)

Question 49

Bovine necrotizing meningo**encephalitis** is caused by \_\_\_\_\_\_\_; whereas Bovine meningo***encephalomyelitis*** is cause by \_\_\_\_\_\_\_\_.

Answer 49

BHV-5; BHV-1 (IBR) \**usually affecting young cattle, 5-18 mo*\*

Question 50

Eosinophilic intracytoplasmic inclusions bodies of this pathogen have a strong attraction to the urinary tract epithelium seen here

Answer 50

K9 Distemper Virus

Question 51

K9 Distemper can also result in these lesions when they attack enamelblasts. What is this lesion found in survivors?

Answer 51

enamel hypoplasia

Question 52

Thrombosis in a venule: this is pretty characteristic of *H.somni* in association with thrombotic meningoencephalitis (TME). what is **this** **MDx** exactly?

Answer 52

Fibrinonecrotizing vasculitis and thrombosis *remember, it likes the venules*

Question 53

What is this **cerebellar** histo slide from a dog with *distemper* exhibiting?

Answer 53

Demyelination

Question 54

Whats a good **MDx** for this piece of cerebellum from a Distemper dog?

Answer 54

Lymphocytic meningoencephalitis *primarily affects glia (astrocytes) and white matter (esp oligodendrocytes)*

Question 55

Serositis, fluid accumulation in the abdominal cavity, and varying degrees of pyogranulomatous inflammation are associated with which form of FIP?

Answer 55

Effusive (wet)

Question 56

Leptomeningitis, chorioependymitis, focal encephalomyelitis, and ophthalmitis are associated with which for of FIP?

Answer 56

**Non-effusive form**

Question 57

On histology, **what cells** might we see in the manifestation of the *dry* form of **FIP?**

Answer 57

mix of neutrophils, lymphocytes, plasma cells, and histiocytes