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136 Cards in this Set
- Front
- Back
What is this disease? What is the probable cause of this disease? What clinical signs would an animal with this present with? |
Juvenile Pancreatic Atrophy Probably autoimmune but the exact cause is unknown Veracious appetite, voluminous feces |
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This is a histologic slide of Juvenile Pancreatic atrophy. This is most commonly seen in what breeds? |
German Shepherds |
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Describe what lesions are seen in this pancreas. What disease causes this? What triggers the formation of these lesions? |
Acute pancreatitis This is the autodigestion of the pancreas of an unknown trigger. Grossly, you see hemorrhage, edema and foci of chalky-white fat necrosis. |
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Describe what is seen in this histologic slide and what disease is most likely causing this. What would be seen on a CBC with this disease? |
Fibrinous, suppurative pancreatitis and widespread inflammation (seen in Acute pancreatitis) On a CBC, you would see increased liver enzymes due to the close proximity of the liver to the pancreas. |
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What are the 5 different vesicular stomatitis diseases? What species gets infected with each? |
1. Foot and mouth disease- All cloven footed animals 2. Vesicular stomatitis- Cattle, Horse, Swine 3. Swine Vesicular Disease- Swine 4. Vesicular Exanthema of swine- Swine 5. Seneca valley virus- Swine |
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Along with these lesions seen in this cow's tongue, the farm had a devastating outbreak where several cattle and pigs died with vesicles on the feet and snout, palate, and hypersalivation. What disease do you suspect? What do you say about the farms downwind from this farm? |
Foot and mouth disease This disease is extremely contagious and can spread in the direction of the prevailing wind very long distances. |
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How do sloughing lesions of foot and mouth disease originally begin? How do they progress? What symptoms are seen in sheep? How do you definitively diagnose this disease? |
The lesions start as small vesicles, grow together to form larger bullae and then they rupture to form sloughing lesions. Sheep have less of these symptoms and it is not as devastating as it is in cattle and pigs You have to have the lab perform a test in order to distinguish it between this disease and the other vesicular diseases. |
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Describe the difference between Noncytopathic and Cytopathic strains of BVD. |
Noncytopathic- no changes seen on histologic slide, you only get the phenotypic changes Cytopathic- cells look vacuolated and necrotic along with the phenotypic changes |
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How does an animal become infected with the "mucosal disease" form of this virus? What is one symptom of BVD that happens in very few other diseases and can help confirm the diagnosis of BVD? What other clinical signs are seen with Mucosal Disease? |
Immunotolerant cattle gets infected with the Cytopathic strain of BVD Hemorrhagic peyer's patches Ulcers on ventral tongue, esophagus, abomasum, small intestine, vasculitis |
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If you get infection of BVD with an animal that is pregnant, what can happen? |
Fetal abortion and mummification Congenital defects Late term abortion |
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If a cow is infected with BVD at time of breeding, will this animal typically breed? |
No |
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If you have an immunotolerant mom that infects the calf before 125 days of gestation, what is seen in the calf? If you get a late gestation infection? |
With early stage- the calf becomes consistently viremic for life With late stage- you get a normal calf that is just seropositive to BVD |
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If you get an infection of an immunocompetent, non pregnant cow, what types of scenarios can result? |
Sub-clinical infection *most common Pyrrexia, diarrhea, mild oral ulcers/erosion Hemorrhagic syndrome Lymphoid necrosis in peyer's patches- where cysts will replace the empty holes Immunosuppression Severe peracute BVD Clinical BVD |
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There are three different forms of malignant catarrhal fever in cattle. Name the three and what symptoms are associated with each? histologically, what do you see? |
Peracute- high fever, death in 1-3 days Head and eye *most common- corneal opacity, nervous system signs Intestinal form- photophobia, lacrimation, ulcers on tongue, rumen, esophagus Histologically, you see lymphocytic infiltration and vasculitis in the brain (resembles lymphoma) |
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What are the three papular somatides? |
Parapoxvirus infections Bovine papular stomatitis Contagious ecthyma (sore mough in sheep and goats) |
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These blisters are seen on the gums, roof of mouth and esophagus. What disease is this? What change histologically causes these lesions? |
Bovine Papular stomatitis Proliferation of epithelium |
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This type of lesion is seen in what type of dog? |
(Gingival hyperplasia) Seen in brachycephalic dogs |
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While most epuli are benign, this type of epulis is invasive. What is it called? How can it be treated? What is the prognosis? |
This is an acanthomatous epulis. This is the invasion of acanthomatous epithlium into the bone of the animal. You can treat this with radiation but, regrowth can occur. And, if this does regrow, it will regrow as a squamous cell carcinoma |
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The carcinoma seen here is most likely a what? This is most commonly seen in what species of animal? |
A squamous cell carcinoma, most likely found in a cat *This can metastasize to other locations |
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The image seen here is an image of? What kind of prognoses do these carry? |
This is an oral melanoma. 90% of these will metastasize to other areas in the body, they usually carry a poor prognosis |
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What is this an image of? What type of therapy should be done? |
These are benign, wart-like structures caused by canine oral papilloma virus These do not need to be treated, they will regress spontaneously as the immune system fights them off. |
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The black tarry blood seen in this ulcer can eventually lead to what? What predisposes a dog or cat to ulcers? |
Can eventually lead to melena 1. the presence of histamine producing mast cell tumors anywhere in the body 2. Zollinger-Ellison Syndrome- a gastrin secreting pancreatic cancer 3. Previous treatment with NSAIDS or steroids 4. Chronic renal disease |
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Ulcers of the pig stomach are found in what location of the stomach? Are these common? What clinical signs are associated with them? |
These are found in the nonglandular mucosa of the stomach These are very common in pigs but rarely do they cause death or they are rarely associated with any clinical signs |
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What is the cause of ulcers in the calf abomasum? |
If paired with ulcers in the mouth, think viral diseases. If alone, check to see if they were treated with antibiotics for longer than a week, as this predisposes the calf to this disease. |
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If you found ulcers in an adult horse GI tract, and the mucosa of the esophagus was thickened, what would that mean in terms of disease cause? What if it were a foal? |
Adult- incidental finding, especially prominent the more athletic the horse was Foal- they get these and then they will perforate, causing acute peritonitis. |
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What is the most common stomach cancer in dogs and cats? What prognosis does this disease carry? |
Gastric Adenocarcinomas These will metastasize widely, prognosis is quite poor |
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What is the most common stomach cancer in horses? What symptoms are associated with this cancer? What prognosis does this disease carry? |
Squamous cell carcinomas Weight loss and anorexia Very poor prognosis, most diagnoses are done at necropsy |
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What is the most common stomach cancer in cattle? What is the progression of this disease? |
Lymphosarcoma They are found in cattle that have been previously infected with bovine leukemia virus They can be infected with this virus at any age and then the cancer develops at 5-7 years of life |
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What damage to the small intestine is seen here? What virus commonly does this? |
Loss of crypt cells, atrophy of the villi Caused by parvovirus attacking rapidly dividing cells in the body. This then causes severe malabsorptive diarrhea |
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What is the cat's version of parvovirus? Where does this virus attack in the body? |
Panleukopenia Wipes out the bone marrow |
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How do you want to treat an animal with parvovirus? What is important to remember when looking for this virus grossly and histologically? |
Give antibiotics to prevent a secondary infection with an overgrowth of clostridia, this overgrowth can cause disease Both grossly and histologically, the disease is segmental. So, look at multiple sections of the intestine to find the lesions caused by this virus. |
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What disease is seen in these villi? What is the two different causes of this? What is seen on a CBC? |
This is lymphangectasia, where the central villi lymphatics are swollen This can be congenital, caused by not enough lymphatics to drain the villi or it can be acquired, caused by a blockage of the lymphatics in the villi On CBC, you will see hypoproteinemia |
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What are the 6 mechanisms of diarrhea? |
1. Altered motility- not well understood 2. Hypersecretion (ETEC) 3. Malabsorption 4. Maldigestion- ex. pancreatic exocrine insufficiency 5. Altered permeability and protein loss (Johne's, Lymphangectasia) 6. Infiltration of gastric mucosa |
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What mechanism of diarrhea is seen in this image? If this animal recovered in a few days, what virus most likely caused the diarrhea? |
Malabsorption caused by villous atrophy Coronavirus |
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These arrows are pointing to what? What mechanism of diarrhea can this cause? |
These are inclusion bodies in the gastric mucosa, as caused by canine distemper virus. This can cause malabsorption diarrhea although the main disease here is still respiratory related |
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What mechanism of diarrhea is represented in this picture? What can cause this? |
Infiltration of the gastric mucosa, eosinophilic gastroenteritis This can be caused by parasites, food allergies. But, if neither of these exist, it can be idiopathic too. |
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What lesion is seen in this image from a boxer? What mechanism of diarrhea does this cause? What would you see histologically? Treatment would involve what? |
This is histiocytic, ulcerative colitis, common in boxers. Treatment may be best by using antibiotics as it seems to have a better response than steroids |
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What are the 6 causes of neonatal diarrhea? |
E. Coli Rotavirus Coronavirus Cryptosporidia Coccidia Clostridia |
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Where is E. coli found in the digestive tract? What is the difference between a pathogenic and a nonpathogenic strain of E. coli? |
Found lining the epithelium in the small intestine Pathogenic strain has fimbriae that allow the attachment to the small intestine and can produce enterotoxins that produce disease |
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If you were looking to test for calf coronavirus in the small intestine, what sections of the small intestine would you want to test? What lesions would you expect to see? |
Sample the ileum and the colon, the duodenum won't have lesions in it You will see villous atrophy in the intestine |
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Describe the life cycle of cryptosporidia Histologically, what do you see? Clinically, how does this cause rapid death? |
The oocyst made is immediately infective, most maturation of the oocyst happens in the environment. These protozoa then rest on the surface of the cilia causing neonatal diarrhea. Histologically, you see the "little blue dots" Death is not often solely caused by cryptosporidia but is a part of death due to atrophy of the fat cells. |
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how can clostridium type C affect piglets? Gross lesions? |
It can cause neonatal diarrhea that will wipe out whole litters of piglets very quickly You can get grossly black, necrotic lesions of the jejunum and the ileum |
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What are the 5 bacteria species that cause enteric disease after the neonatal period? |
Salmonella Brachypsira Hyodysenteriae Lawsonia Intracellularis Mycobacterium Avium subsp. Paratuberculosis Clostridium Perfringens Type D |
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Salmonella has three different species and each of them affect different animals. What are those three and what animals do they affect? What gross lesions do you see with this bacteria? |
Dublin- calves Cholerasuis- swine Both cause focal random necrosis, enteritis Mucosal necrosis is dull/tan yellow appearance of the intestinal surface Typhurium- chronic intestinal salmonella in pigs The spiral colon can become necrotic due to a rectal stricture |
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Brachyspira hyodystenteria affects what age of piglets? What symptoms are seen? Where are the gross lesions seen in the body? |
Growing pigs 6-17 weeks of age Weight loss, anorexia, guant piglets, bloody diarrhea Affects the large intestine only |
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Lawsonia intracellularis causes what gross and histologic lesions? If you were to stain them, what shape would it take on? |
Gross lesions- proliferative, necrotizing enteritis causing thickened, corrugated enteritis Histologically- causes the crypts to proliferate like they're neoplastic if you stain them with silver stain, they are comma shaped organisms |
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What are the two diseases that cause an influx of macrophages in between the crypt cells? |
Johne's Disease Boxer colitis |
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What is the gross and histologic lesions caused by Johne's disease? |
Gross- small intestinal disease causing thickened and corrugated mucosa Histologic- causes the influx of macrophages in between crypt cells |
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What are the 5 things you want to look at a gross, unfixed brain for? |
1-Asymmetry
2- Leptomeninges, should be clear 3- Edema 4- Petechia/Ecchymoses 5- Large areas of hemorrhage |
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What are some things that can cause asymmetry in a fresh brain? |
Atrophy Hypo/Hyperplasia Hemorrhage |
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What causes the cloudiness appearance seen in this image? |
Inflammation of the leptomeninges This fluid exudate will move when pushed around the brain |
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Edema in the brain leads to what gross changes in the brain? |
Wet leptomeninges, flattened gyri, shallow sulci |
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What causes petecchia/eccymoses in the brain? What causes larger areas of hemorrhage? |
Small hemorrhages- septicemia Larger hemorrhages- trauma |
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Describe how and where rabies testing is done in MI If you send in a sample, what parts of the brain do you want to include? |
The MI department of health and human services does direct fluorescent antibody testing to test for rabies. Submitted brain must include sections of pons/rostral medulla along with the cerebrum. You must never freeze the sample. |
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How long is a brain in formalin before it is looked at? How do you section it? |
About a week Sectioned using a brain knife |
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What gross lesions do you look for and what do they indicate when looking at a formalin fixed brain section? |
Discoloration- nonspecific, can mean hyperemia, hemorhage, degeneration, necrosis and inflammation Malacia- softening, necrosis Cystic lesions- hydrocephalus |
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What is the general term for this condition in the brain? If it was of the grey matter, it would be what term? White matter? |
Malacia- the softening/necrosis of brain
Grey matter of the brain- encephalomalacia White matter of the brain- polioencephalomalacia (image) |
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If the discoloration of the brain or spinal cord is very dark brown or black, what process is likely to have happened? |
Hemorrhage |
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In order to formalin fix the spinal cord, what step must you do to insure proper fixation? |
Cut the dura mater to allow the penetration of the formalin |
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What is seen in this section of the spinal cord? |
Myelomalacia- softening of the spinal cord (the discoloration is non-specific) |
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Compression of the spinal cord can happen in what three ways |
1. vertebral lesions 2. disc disease 3. mass lesion |
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Define hydromyelia |
Dilation/distension of the central canal of the spinal cord |
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Define Syringomyelia |
Holes in the neuropil of the spinal cord |
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What sections of the spinal cord would you want to send in for testing? |
Depending on clinical and gross symptoms |
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What are some of the things you want to evaluate fresh and formalin fixed peripheral nerves for? |
Fresh- look on both sides and compare for symmetry, thickness/color Fixed- look for thickening (indicating inflammation, neoplasia), thinner (atrophy, degeneration), and discoloration (hemorrhage, degeneration, inflammation) |
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While regeneration of neurons is minimal, what nervous system is better at regeneration than the other? |
PNS nervous system is better at regeneration than the CNS |
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What are the three supporting cells of the CNS |
Astrocytes Oligodendrocytes Microglial cells |
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What are some of the primary injuries to a neuronal axon? |
Trauma Nutritional deficiencies Toxicoses Inherited defects |
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Define/describe wallerian degeneration |
The axon will degenerate distal to the axon injury In the spinal cord, the degeneration cranial to the site of injury will be in the ascending tracts and the degeneration in the caudal spinal cord will be in the descending tracts |
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What are the mechanisms of primary myelin sheath degeneration? |
Inflammatory/immune mediated- either by leukocyte enzymes or a specific immune response to myelin proteins Toxic/metabolite Inherited defect in metabolism Oligodendrocyte injury |
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What are the causes of secondary myelin sheath degeneration? What does this lead to? |
Ex. Wallerian degeneration (secondary to axon degeneration) Fragmentation of myelin leads to vacuolization of the neuropil, whichs termed "spongiosis", or a spongy appearance to the nervous tissue |
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What are the two ways spongiosis can occur?
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Fragmentation of myelin Edema |
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What is the most numerous cell type in the CNS? What are their functions? |
Astrocytes 1. Structural support 2. Detoxification 3. Maintain BBB 4. Inflammatory/immune- phagocytosis, antigen presentation, produce cytokines 5. Lay down glial processes to induce the formation of tight junctions (reperative cell) |
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Are infections properly walled off with just astrocyte function alone? |
No, tey lay down glial processes, not collagen so a junction tight enough to wall off infections is not created. |
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What is the function of an oligodendrocyte? |
In white matter- formation/maintenance of myelin in the CNS In grey matter- they're called "satellite cells" and they are responsible for neuronal metabolism |
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What is the function of a microglial cell? |
Resident macrophage of CNS |
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What are the three components of the blood-CNS barrier |
1. tight junction of endothelial cells 2. Basement membrane of capillaries 3. Astrocyte foot processes |
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What is true about the efficiency of the lymphatic vessels in the CNS? |
There is poor exudate drainage so, the CSF stays in the brain. This is why CSF can lead to a diagnosis of certain diseases |
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What is the ependymal epithelium? |
Epithelium lining the ventricular system in the brain and the central spinal canal |
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What is the Choroid plexus epithelium? What is its function? |
Tufts of epithelium in the lateral, 3rd and 4th ventricles They are responsible for making CSF |
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What is the function of the CSF? |
Deliver nutrients/remove wastes Shock absorber for the brain |
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Describe the CSF flow through the brain |
It flows through the lateral apertures of the 4th ventricles and into the subarachnoid spaces The fluid is then absorbed into the brain at the arachnoid villi, which are evaginations of the arachnoid into the dural venous sinuses on the convex brain |
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What are the three layers of the meninges? What is the function of the meninges? |
Dura mater- later that is closely associated to the skull periosteum Leptomeninges- the arachnoid and the pia mater Function is to protect the brain and spinal cord |
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Why do different congenital malformations of the nervous system develop at different ages in different species? Can multiple malformations happen? |
They develop at different times in different species because each species develops their nervous system at different rates Multiple malformations are possible because all of the nervous system components are closely connected |
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What are the two general causes of congenital malformations in the nervous system? |
Genetic errors Environmental |
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What are the two ways that genetic errors can occur which lead to congenital malformations of the nervous system? |
During gestation, a somatic mutation happens. You get one animal affected and its an isolated event Inherited from mom, a germ cell mutation, you get multiple animals affected |
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What are some examples of environmental causes of congenital malformations in the nervous system? |
Physical agent Nutrition Toxin Virus |
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Define Hydrocephalus: Differentiate between internal and external hydrocephalus. What does it mean if it is communicating? |
Hydrocephalus- the accumulation of too much CSF leading to the dilation of the ventricles Internal has no involvement of the subaracnoid space, external has subarachnoid space involvement Communicating comes secondary to extravascular obstruction, your subarachnoid spaces are involed. Noncommunicating, only the lateral ventricles or lateral and the 3rd ventricles are affected, the obstruction is only within the ventricles. |
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What is the difference between compensatory and obstructive hydrocephalus? |
Compensatory- ventricles expand because the nervous tissue parenchyma is lost Obstructive- Acquired- neoplasm/inflammation compresses the ventricle Developmental- malformations interfere with flow, most often a narrowing of the aqueduct |
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What defect is seen in this picture? What is the two causes of this? |
Cerebellar hypoplasia- Small cerebellum Caused by a viral infection, inherited/developmental genetic defect |
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What defect is seen in this picture? Histologically, what would you expect to see? What causes this? |
Cerebellar abiotrophy- Premature degeneration, loss of purkinje cells and granular layers Due to intrinsic metabolic defect |
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Biochemical defects of the nervous system are most often what type of disease? |
Lysosomal storage disease |
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How does the genotype of the lysosomal disease inherited influence the phenotype of the lysosomal activity? |
(autosomal recessive disease) AA- No/minimal measurable enzymatic activity Aa- 50% normal enzyme activity aa- fully functional This is called "Gene dose dependent" |
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How can you determine if an animal is a carrier for a lysosomal storage disease?
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Measure the level of enzymatic activity. If you're at about 50% of normal, you'd expect that animal to be a carrier. |
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How does lysosomal storage diseases lead to neuronal dysfunction? How do you classify these diseases? |
Dysfunction is due to the accumulation of uncatablized substrates in the neurons You classify them based on the biochemical nature of these substrates |
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How is the brain protected from trauma? |
1. Frontal sinuses 2. bone layers 3. meninges 4. CSF |
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What are the two pathogenic factors that lead to brain trauma? |
1. Distortion/tearing of the nervous tissue and blood vessels 2. Hypoxia, leading to neural ischemia |
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Where is spinal cord injury most likely to occur along the spine? Why is this so? |
Most likely to occur at the thoracic/lumbar area due to the smallest space between the cord and canal |
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What are the things that protect the spinal cord from injury? Why is T2-T10 less likely to have vertebral disc extrusion? |
Vertebral bodies Intervertebral discs Vertebral ligaments Fat Meninges CSF T2-T10 have intercapital ligaments making them stronger |
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What are the two ways that acute spinal cord compresion happen? Chronic? |
Acute- Physical force from direct tearing/shearing or hypoxia Chronic- Slowly forming direct physical injury to spinal cord or low-grade hypoxia due to blood vessel compression |
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Compare the lesions seen with acute v. chronic spinal cord compression |
Acute- hemorrhage/necrosis of the GREY matter Chronic- MYELIN/AXON degeneration of the WHITE matter. |
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What may acute spinal cord compression progress to? What is the pathogenesis of this? |
Hematomyelia Nervous tissue damage -> lipid peroxidation -> release of free radicals -> more tissue damage So you get necrosis cranial and caudal to the lesion |
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Compare a hansen type 1 disc extrusion with a hansen type 2 disc extrusion |
Type 1- acute injury, the nucleus pulposis extrudes into the canal. This is common in chondrodystrophic breeds where the degeneration happens less than a year of age and replaces it with fibrosis Type 2- Chronic compression, you get the bulging of discs in non chondrodystrophic breeds, you get the degeneration of nucleus fibrosis at 8-10 years of age |
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What is cervical vertebral stenotic myopathy? What pathogenic factors are at play? |
"Wobblers Syndrome" Genetic, conformational and nutritional all come into play In horses, you get both a developmental form (in young horses) and a acquired form (in older horses) |
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What are the three common causes of CNS hemorrhage? |
Trauma Vasculitis- bacterial/viral infections, pececchia/ecchymoses Parasite migration |
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What are some of the gross lesions associated with brain edema? |
Flattened gyri/shallow sulci Clear watery fluid in leptomeninges Posterior shifting of brain |
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What are the two mechanisms of brain edema? What are their causes? How do they lead to edema? |
Vasogenic (most common)- physical breakdown of tight junctions leading to EXTRAcellular accumulation of fluids. Caused by inflammation or trauma Cytotoxic (2nd most common)- Impairment of the Na/K pump leading to altered cellular mechanism and INTRAcellular accumulation. Caused by hypoxia or toxin/metabolic causes |
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Why is infarction uncommon in our animal species? |
There is abundant arteries supplying the brain Primary vasculature disease is rare in animals |
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Feline Ischemic encephalopathy is an infarction of what central nervous system structure? What is it's etiology? |
Infarction of cerebrum/brainstem in cats Uncertain etiology, maybe liked to cuterebra? |
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Ischemic Myelopathy is an infarction of what central nervous system structure? |
Spinal cord, in dogs |
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Fibrocartilagenous emboli are infarctions of what central nervous system structure? What is it's etiology? |
leptomeningeal blood vessels Possibly intervertebral disc origin but pathogenesis is controversial |
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What are the 4 general features of neuronal degeneration and necrosis? |
Slowly progressive clinical signs Lack of inflammatory response Primary effects on neurons No gross lesions |
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Define Myelomalacia |
Softening/necrosis of the spinal cord |
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What are the causes of neurodegenerative diseases? |
Toxicants Metabolic Disturbances Nutritional deficiencies/excesses Inherited/suspected inherited Infectious agents |
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Hyperammonemic encephalopathy is most commonly a disease of what system? What category of neurodenerative disease is it? |
Liver disease (most commonly) Can also be renal, or intestinal (in horses) Metabolic disturbances |
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Thiamine-responsive polioencephalmalacia is most commonly a disease of what species under what circumstances? What gross lesions are seen with this disease? What category of neurodenerative disease is it? |
Ruminants with increased concentrate diets Edema of the cerebrum, yellow discoloration of the grey matter Nutritional deficiencies/excess |
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Age related/degenerative myelopathy of some dog breeds is an example of what category of neurodegenerative disease?
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Inherited/suspected inherited |
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How is a prion disease suspected to work in the brain? What clinical signs are associated with them? Wat is the pathologic lesions seen in the brain? |
The prion has a PrPSPc gene that serves as a template to change the genes made by the host Affects only a few species Slow, progressive deterioration, long incubation period, usually fatal Noninflamatory, lesions in the brain, vacuolation of neurons |
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What are some of the specific prion diseases we deal with in animals? |
Scrapie- seen in seep, suffolk sheep mostly BSE- Great Britain, from feeding meat/bone meal concentrate vCJD- consumption of BSE and cattle meat CWD of deer |
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Define Encephalitis Myelitis Meningitis |
Encephalitis- inflammation of the brain Myelitis- of the spinal cord Meningitis- of the meninges (leptomeningitis is inflammation of the leptomeninges) |
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Define Astrocytosis Astrogliosis |
Astrocytosis- increased number of astrocytes in inflammation Astrogliosis- increased cytoplasmic processes |
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How does the immune system play a role in the diseases of the nervous system? |
Low level of CMI and low levels of immunoglobulins mean that when an infection can get in, it can spread rapidly and tends to persist for a long time |
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What are all of the routes of CNS infection? |
Via peripheral nerves Direct implantation from traumatic injuries Spread from surrounding tissues Hematogenous *most common |
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What are the lesions of a bacterial CNS infection |
Usually systemic Suppurative/fibrinopurulent meningitis or abscesses |
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What are the lesions of a viral CNS infection? |
Usually part of a systemic infection Some viruses have specific tropisms for CNS No gross lesions Nonsuppurative inflammation Demyelination, Viral inclusion bodies |
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What are the lesions of a fungal/mycotic linfection? |
Localization from a systemic infection, extension from surrounding tissues Lesion- granulomatous, pyogranulomatous inflammation |
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What are the lesions of a protozoal infection of the CNS? |
Some protozoa want to be in the nervous system, others come from a systemic infection Lesion- granulomatous, pyogranulomatous inflammation Ex. sarcocystic neurona (in horses) |
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What are the lesions of a parasitic/helminth infection of the CNS? |
Natural life cycle of some parasites involve the tracking throught he CNS Signs most likely to be worse in an aberrant host, rather than in the natural host Lesions- granulomatous/eosinophilic |
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What is an example of an unknown cause but a suspected immune-mediated pathogenesis disease of the CNS? Unknown cause and unknown pathogenesis? |
Cauda Equina Neuritis, in horses Granulomatous meningoencephalitis in dogs (GME) |
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Primary neoplasms of the brain are really only found in what species? What are the clinical signs of these attributed to? What is the one site of metastasis that could occur in the nervous system? |
Dogs and cats Compression/infiltration effects on a space-occupying mass brain- due to large blood flow |
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The most common brain tumor in a dog is a ? Are these benign or malignant? What are the two types? |
Glial cell tumor Malignant Astrocytoma (grey matter), Oligodendrioma (white matter) |
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The most common brain tumor in a cat is a ? Are these benign or malignant? |
Meningioma Most are benign- they would be easily cut out with surgery if you would want to perform that surgery |
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Pituitary adenomas are neosplasms of what? Associated with what disease? |
Pars intermedia Associated with Cushing's |
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PPID is a neoplasm of what species? |
Pars intermedia dysfunction Seen in older horses |
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Choleastoma are non-neoplastic findings in what species? |
Incidental findings in old horses |
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Peripheral nerve sheath tumors are of what cell origin? Are they benign or malignant? Most common in what species? |
Shwann cells origin Can be benign and malignant Most common in dogs |
