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166 Cards in this Set
- Front
- Back
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What is different with a small ruminant neuro exam as opposed to small animal?
How about a large animal? |
NOTHING! Same thing
Large animal neuro exam is close to the same but more difficult (also no postural reflexes done-wanna wheelbarrel a cow?) |
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What are two common neuro diseases with ruminants?
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Polienchephalomaclacia (forebrain)
Listeria (brainstem) |
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What are the three functional areas of the brain that we deal with when localizing lesions in the brain?
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Forebrain (dienceph)
Cerebellum Brain stem (mesenceph, pons, medulla) |
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Where would you localize a lesion if you saw these CS:
altered mentation behavioral changes contralateral visual and postural deficits ipsilateral circling seizures |
Forebrain
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Where would you localize the lesion if you saw a dorsomedial strabismus and the eye can be moved out of position
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Diffese forebrain disease
Also CN, muscle, or vestibular problem but the eye is more fixed with this |
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If you were localizing CS to a neuro location, where would you localize an animal with dysphagia?
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Forebrain
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Case Localization: Cow that appears dull. When she moves, she bumps into the walls. She has no menace and appears to have dysphagia
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Diffuse Forebrain Disease
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What are four general categories you would think of for Forebrain disease differential diagnoses?
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Metabolic (hepatic encheph)
**Toxic/Nutritional (polioencheph, Pb poison, salt intox, NPN poison) Infectious (bacterial, viral, prion, protozoal, parasitic) Trauma |
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What differentials might you think of if you have focal forebrain disease?
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*Infectious (bacterial, viral, prion, protozoal, parasitic)
Trauma These things can also cause diffuse forebrain disease |
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What are the clinical forms of rabies
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Cerebral (furious)
Brainstem (dumb) Spinal cord (paralytic) -ascending |
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What is the most common form of rabies seen in ruminants?
What will be the typical CS? |
Cerebral (furious)
Salivation Aggressiveness Abnormal vocalization HOWEVER-consider choke! Death within 14d onset CS |
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How will you diagnose rabies?
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positive IFA results on fresh brain
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What are 2 causes of cerebrocoticonecrosis in ruminants?
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Thiamine responsive polioenchephalomalacia
Sulfur induced poliencephalomalacia Salt/water intoxication Pb poisoning Listeria DOES NOT cause diffuse forebrain disease |
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What might be some precipitating causes of policencephalomalacia?
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High CHO feeds/lush pastures, braken fern ingesion (thiamine def)
Drought conditions (increased sulfur content of water for those seeking deeper water sources) |
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What factor can affect sulfide levels
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Rumen pH - High CHO diet effect rumen flora (influences distribution of sulfide between fluid and gas phase)
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What is the pathogenesis of polioencephalomalacia?
What about Pb poisoning pathogenesis? |
Disturbance in cellular energy metabolism leads to laminar cortical necrosis
Pb poisoning same as PEM pathogenesis |
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Diagnosis of polioencephalomalacia?
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Presumptive based on CS and hx
Response to thiamine supp (evidence of altered thiamine metabolism) Autofluorescence of cortical tissue Measure sulfur content of feed and water |
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How can you treat polioencephalomalacia?
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Administer thiamine
Supportive care Prognosis good if not recumbent |
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What pattern of histologic lesions in a PEM case would suggest sulfur induced disease?
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Subcortical necrosis
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What are sources on the farm that can lead to Pb poisoning?
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Motor oil
Machinery grease Batteries |
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What is the most common form of rabies seen in ruminants?
What will be the typical CS? |
Cerebral (furious)
Salivation Aggressiveness Abnormal vocalization HOWEVER-consider choke! Death within 14d onset CS |
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How will you diagnose rabies?
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positive IFA results on fresh brain
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What are 2 causes of cerebrocorticonecrosis in ruminants?
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Thiamine responsive polioenchephalomalacia
Sulfur induced poliencephalomalacia Salt/water intoxication Pb poisoning Listeria DOES NOT cause diffuse forebrain disease |
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What might be some precipitating causes of policencephalomalacia?
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High CHO feeds/lush pastures, braken fern ingesion (thiamine def)
Drought conditions (increased sulfur content of water for those seeking deeper water sources) |
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What factor can affect sulfide levels in the cow?
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Rumen pH - High CHO diet effect rumen flora (influences distribution of sulfide between fluid and gas phase)
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What is the pathogenesis of polioencephalomalacia?
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Disturbance in cellular energy metabolism leads to laminar cortical necrosis
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Diagnosis of polioencephalomalacia?
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Presumptive based on CS and hx
Response to thiamine supp (evidence of altered thiamine metabolism) Autofluorescence of cortical tissue Measure sulfur content of feed and water |
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How can you treat polioencephalomalacia?
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Administer thiamine
Supportive care Prognosis good if not recumbent |
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What pattern of histologic lesions in a PEM case would suggest sulfur induced disease?
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Subcortical necrosis
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What are sources on the farm that can lead to Pb poisoning?
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Motor oil
Machinery grease Batteries |
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Diffuse forebrain disease differentials
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PEM
Pb poisoning Salt intoxication Rabies and TEME not forebrain specific |
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How can you fix Pb poisoning?
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Remove source
Chelation therapy Thiamine |
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What causes salt intoxication?
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Water deprivation followed by unrestricted drinking
shifts in serum osmolality --> shifts in intracellular water --> cellular edema --> corical laminar necrosis and edema |
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Case: Herd with signs of diffuse forebrain disease. Also see colic, fluid filled rumen, diarrhea, cardiac arrhythmias, hemoglobinuria, fever. CSF sodium concentration to serum sodium concentration >1.
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Salt intoxication
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TEME =
What is the cause? |
Thromboembolic meningoencephalitis
Histophilis somni |
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Case: Herd that has been at the feedlot for 4wks now and is showing signs of respiratory dz and some polyarthritis.There is low morbidity but high mortality. They have a fever and progressing CNS signs of forebrain, cerebellum, and brainstem. CSF analysis yields neutrophilic pleocytosis.
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Thromboembolic meningoencephalitis
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What are potential causes of focal forebrain disease
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Brain abscess/encephalitis
Trauma |
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What is a potential sequelae of forebrain disease
(don't say death or euthanasia because that is not the answer :P) |
brain herniation with compression of brainstem
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What are two unique signs of ruminant forebrain disease as opposed to small animal forebrain disease?
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Dorsomedial Strabsimus (diffuse)
Dysphagia |
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T/F: Listeria is a differential for forebrain disease
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FALSE!!!!!!!
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Case: Calf with incoordination, absent menace, vestibular signs, and NO weakness. The incoordination can be described as ataxic gain with hypermetria. She has a wide based stance and an intention tremor
Localization? |
Cerebellum
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What can cause congenital cerebellar hypoplasia?
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BVD --> fetus exposed during day 100-200 days of gestations
destroys germinal layer of cerebellum |
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What are two infectious differentials for cerebellar disease
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TEME
Scrapie |
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How can you diagnose cerebellar hypoplasia caused by BVD?
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positive presuckle viral titer
known exposure of dam to virus during gestation |
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Case: Sheep 2-5yrs old begin showing cerebellar signs and pruritis. What are you worried about?
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Scrapie
REPORTABLE |
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Signs of Brain Stem Disease include
a. CN 1 and 2 deficit b. Paresis, postural rxn deficits c. Heightened altertness |
b. Paresis, postural rxn deficits
ALSO: CN 3-12 deficit, Depression of consciousness |
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Case: Goat with ataxia. He is falling, rolling, and circling. He has a head tilt along with a strabismus and nystagmus. Localization?
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Vestibular Disease
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T/F: You will see Horner's syndrome associated with peripheral nerve disease in ruminants
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False
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Which things below are associated with central vestibular disease?
a. Depression b. Paresis c. Vertical nystagmus |
A, B, & C (ALL OF THE ABOVE)
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What are your ddx for peripheral vestibular disease?
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Otitis media/interna
Trauma |
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How is a ruminant different than a small animal with respect to how they get otitis media/interna?
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Ruminants normally get hematogenous spread or ascending infection from respiratory system that result in otitis media/interna
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What is your top differential when you have central vestibular disease?
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LISTERIA, LISTERIA, LISTERIA
could also see brain abscess, rabies, parasitic encephalitis, TEME, or trauma |
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T/F: Listeria is typically a disease of the young
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False- typically a disease of adults
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What is the pathogenesis of Listeria?
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Organism enters mucous membranes of head --> migrate up CN5 --> enter brainstem
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What is the most useful anetmortem test used to diagnose Listeria (other than hx & CS)
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CSF analysis
marked mononuclear to mixed pleocytoisis |
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How can you treat Listeria?
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Penicillins, Sulfonamide, Tetracyclines, or Ampicillin
Supportive care |
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What is the natural progression of a neurologic lesion going from least severe to most severe?
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Loss of:
1. proprioception 2. voluntary movement 3. superficial pain 4. deep pain |
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Case: 2 month old kids with progressive UMN signs. They have fever, tachypnea, and some chronic arthritis
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CAE
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What are ways to prevent CAE?
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Separate kids from dam
Heat treat colostrum and milk Maintain a closed herd Serologic monitoring |
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Case: 4wk growing kids present with pelvic limb ataxia and paresis. The signs are LNM in character and some have progressed to tetraplegia
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Enzootic ataxia
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What is enzootic ataxia due to?
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Copper deficiency
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Does a cow have a closed or open orbit?
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Closed
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What motor blocks should you perform in an ophtho exam in a ruminant
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MOTOR
Eyelid - Auriculopalpebral (CN 7) Glode - Peterson block and Retrobulbar block (CN 3, 4, and 6) |
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What is the general rule of thumb with lidocaine blocks in terms of amounts to give?
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15-20 ml Large ruminants
8 ml small ruminants |
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Explain how to perform a Peterson Block
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posterior angle of junction of zygomatic arch and supraorbital process
concavity of needle pointed posteriorly Advance needle medially and slightly ventrally (3-4inches in in large and 2-3 in small) |
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What are some risks of orbital blocks (if you can name all 5 you are a superstar!)
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Globe proptosis
Globe penetration Optic nerve damage Orbital hemorrhage Sudden Death |
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Where does your ophtho exam begin and where does it end (general terms)
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Begin with Anterior segment
End with Posterior segment (after dilation) |
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What are four general parts/things of the ruminant fundus
What are the species differences of cattle, sheep, and goats? |
Holangiotic
Bergmeisters papilla Fibrous tapetum Stars of Winslow Cattle - retinal vessels vitread to nerve fiber layer and elliptical optic disk Sheep - kidney shaped optic disk Goat - more major venules, rounder optic disk surrounded by ring of pigment |
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What is special about a camelid fundus?
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Atapetal
Elliptical, darker optic disk |
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What teratogen can cause cyclopia, anophthalmia and/or synophthalmia
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Veratrum californicum eaten on day 14 of gestation
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What is esotropia?
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Convergent strabismus
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What are three eyelid problems that are commonly seen in ruminants
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Entropion
Blepharitis Neoplasia |
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How would you diagnose infectious keratitis?
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Species
CS cytology/ culture |
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What is the most common agent associated with infectious keratoconjunctivitis in sheep?
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Chlamydophila spp
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What 6 things should you consider when an animal has diarrhea?
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Age of animal
Onset, severity, and duration Number of animals affected CS other than diarrhea Diet Introduction of new animals |
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What is the most common cause of transient diarrhea in ruminants?
When does it occur |
Simple indigestion
Occurs following an abrupt dietary change as a result of alteration in rumen flora |
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Case: Multiple cows with decrease in appetite, decreased milk production, rumen hypomolitiy, mild bloat, watery diarrhea. Producer notes that they just had to change the feed recently
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Simple indigestion
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What causes BVD?
Hows is it characterized? |
a pestivirus
biotype: cytopathic vs noncytopathic genetic lineage: type 1 vs type 2 |
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T/F: You can get BVD even when vaccinated
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True-a lot of antigenic diversity
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Explain the difference between non-cytopathic and cytopathic BVD
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Non-cytopathic --> does not cause visible degen. lesions to cells grown in culture
Cytopathic -->causes visible degen lesions in cells grown in culture |
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How do you differentiate between strains of BVD (type 1 vs type 2)
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Serology
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How does the BVD virus spread?
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direct contact with secretions or viremic animals-->virus taken up by RE cells in LN and spleen --> replicates in lymphocytes and macrophages-->colonize GI/reps/repro and shed for up to 10d
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What is the hallmark CS of BVD?
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mucosal erosions
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Why is BVD so important?
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Economic loss associated with secondary complications and not diarrhea
IMMUNOSUPPRESION! (transient leukopenia and lymphopenia = decreased resistance to infection) Hemorrhage (thrombocytopenia) Fetal Disease and Death |
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1. What happens to cow during the first 100d of gestation if infected with BVD?
2. What can happen to the fetus exposed during 60-180d to BVD? 3. What can happen to the fetus when exposed before 125d? 4. Exposure after 180d? |
1. Abortions: Fetus resorbs, cow returns to estrus
2. Cerebellar hypoplasia/other congenital probs 3. Born persistently infected and shed for whole life 4. Normal seropositive calf |
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T/F: A persistently infected calf comes from a persistently infected cow
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False
However-A persistently infected cow will give birth to a persistently infected calf |
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KNOW BVD CHART (time when problems occur)
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Go look it up now or you might forget!
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How can you diagnose acute BVD?
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CS (mucosal erosions)
Serology - 4 fold increase in ab titer over 4 weks (differentiate bw type 1 and type 2) Virus isolation from buffy coat Fluorescent ab test Immunoperoxidase tests PCR (not on vaccinated) Necropsy |
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How can you diagnose persistently infected BVD calves?
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VI: 2 pos test at least 3-4wks apart
Suspect when seroneg cattle or cattle with low titers are ID after vaccination or known exposure--however usefulness is limited Biopsy of skin/ear-stain for BVD into the root sheath epith and hair bulb |
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What is the best way to treat BVD
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Nothing specific (supportive, abx)
Cull PI calves Most will recover |
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What is a problem with MLV vaccination for BVD?
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transient immunosuppresion and viremia that can cause abortion
GOOD=long-lasting immunity and inexpensive |
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What is the pathogenesis of mucosal disease?
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Specific form of BVD
Fetus exposed to a NON-CYTOPATHIC strain in utero <125d and becomes PI. Calf is then later exposed to a CYTOPATHIC strain = severe cytopathic lesions = death |
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T/F: A calf can be born with mucosal disease
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False-acquire later in life
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You see a severe leukopenia and lymphopenia. What is your top differential?
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BVD
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What is the likely cause of winter dysentery and what evidence supports it?
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Coronavirus
Coronavirus like particles in feces Rising titers following clinical cases Coronavirus antigen in cyrpts Coronavius isolated from feces |
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Case: High morbidity in your herd--> acute/profuse/transient diarrhea that is dark or bloody. Decreased milk production by about 50%. No fever.
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Winter Dysentery
usually resolves in 3d |
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T/F: Presence of Salmonella is higher in beef than in dairy
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False-greater presence in dairy
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How can you diagnose a chronic clinical case of Salmonella
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repeated fecal cultures or by serologic testing
Boards: can culture milk filter |
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What is an important chronic enteritis that can affect all ruminants?
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Johne's Disease (Paratuberculosis)
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What is the etiology of Johne's Disease?
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Mycobacterium avium subsp paratuberculosis
bacterium colonizes ileum, cecum, and ileocecal LN -->spread proximally and distally in GI tract and surrounding L |
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When are animals infected with Johne's Disease?
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during first months of life
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T/F: Johne;s disease can spread via MPs to the mammary gland and uterus and can be shed in colostrum, milk, and feces
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True
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What is the incubation time of Johne's disease?
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1.5-2 yrs
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T/F: If only one or two cows on a farm show CS of Johne's disease, you can assume that those cows are the extent of the problem
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False-iceberg disease!
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What is the hallmark CS of Johne's disease?
What is the hallmark of clinical disease tests in ruminants? |
Progressive weight loss with good appetite
Effortless diarrhea Severe hypoablubminemia (<2 really suggestive) |
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What are some pathological lesions with Johne's disease
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Thickened ileum
Thickened intestines Acid fast organisms in ileum Giant cells common |
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What would you do to control Johne's disease?
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treatment is not recommended-Slaughter or euthanize ASAP
Can control by minimizing exposure of newborns to M. paraTB Test and cull program REPORTABLE in most states |
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T/F: small ruminants can show anemias with Johne's disease
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True
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What has been considered the gold standard to diagnosis for Johne's disease?
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Fecal culture but it isn't without problems-results take about 4 months and can get false neg.
History and CS help! |
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What is an important chronic enteritis that can affect all ruminants?
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Johne's Disease (Paratuberculosis)
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What is the etiology of Johne's Disease?
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Mycobacterium avium subsp paratuberculosis
bacterium colonizes ileum, cecum, and ileocecal LN -->spread proximally and distally in GI tract and surrounding LN |
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Besides Fecal Culture for Johne's Disease, what other tests can you run
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Acid fast stains of fresh feces show clumps of bacilli (quick but only suggestive of)
Nucelic acid probes and PCR (2mo) Serology: ELISA-false neg fairly common AGID good specificity (for clinical cases-not monitoring) Johnin tests |
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When are animals infected with Johne's Disease?
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during first months of life
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T/F: Johne's disease can spread via MPs to the mammary gland and uterus and can be shed in colostrum, milk, and feces
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True
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What is the incubation time of Johne's disease?
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1.5-2 yrs
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T/F: If only one or two cows on a farm show CS of Johne's disease, you can assume that those cows are the extent of the problem
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False-iceberg disease!
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What is the hallmark CS of Johne's disease?
What is the hallmark of clinical disease tests abnormalities in ruminants? |
Progressive weight loss with good appetite
Effortless diarrhea Severe hypoablubminemia (<2 really suggestive) |
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T/F: small ruminants can show anemias with Johne's disease
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True
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Other than veratrum californicum, what are two other "teratogens" that can cause orbital/retrobulbar disease
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Maternal vitamin A deficiency
BVD |
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What is generally the underlying cause of glaucoma in ruminants?
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uveitis
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Name the three common agents associated with cattle infectious keratoconjunctivitis?
What about the one with goats? |
Cattle: Moraxella bovis, Mycoplasma spp, IBR
Goat: Mycoplasma spp |
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How does moraxella bovis cause disease and how does it spread?
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UV light induces conversion from smooth to rough type-->Attaches to corneal epithelium
Spread-direct contact fomites vectors (face fly) |
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What is a good prevention method for moraxella bovis?
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Fly control
Isolate affected Protect from UV light Vaccine may reduce symptoms |
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Case: Sheep with conjunctivitis, chemosis and stromal vascularization OU. She also has concurrent polyarthritis. What agent is at the top of your list?
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Chlamydiophila
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What form of Chlamydiophila is the infectious form, has extracellular survival, and is insensitive to abx?
a. Elementary body b. Reticulate body |
Elementary body
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With bacterial keratoconjunctivitis, what abx are most organisms sensitive to?
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Tetracyclines
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T/F: Infectious Bovine Rhinotacheitis causes conjunctivitis and keratitis along with ulceration
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False: NO ulceration
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What is the most common ocular tumor of cattle and the second most common overall tumor of cattle?
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OSCC-Ocular Squamous Cell Carcinoma
First is LSA |
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What are some risk factors (increase incidence) for OSCC
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Older age
Decreased pigment around eye High UV exposure |
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What is the most common location for OSCC tumor?
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bulbar conjunctiva and cornea (75%) with 90% of that being at the lateral limbus
the rest is eyelids, 3rd eyelid and palpebral conjunctiva |
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What is the basic behavior of OSCC tumors?
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Metastasize late (more likely with eyelids)
Locally aggressive |
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What are some causes of bovine uveitis?
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Secondary to keratoconjunctivitis
Neonatal septicemia Septicemia Systemic infection LSA Traumatic Idiopathic |
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Name one cause of cataracts in cattle?
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Congenital
In utero exposure to BVD Acquired: secondary to uveitis, toxic, traumatic |
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Name three congenital lesions of the ocular fundus
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Hyaloid vascular remnants
Coloboma Retinal dysplasia |
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Causes of chorioretinitis?
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systemic infections (BVD, rabies, bluetongue, scrapie, psuedorabies, toxo, etc)
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Case: Toggenburg goat with vision deficits, vascular attenuation, optic nerve palor, and tapetal hyperreflectivity
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Retinal degeneration
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T/F: Hypovitaminosis A eye lesions (retinal degen/constriction of optic n) can be reversed with a proper diet
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True
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Name one cause of optic neuritis and one cause of central/cortical blindness
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Optic neuritis: male fern poisoning, BVD, causes of chorioretinitis
Central/Cortical blindness: Pb poisoning, polioencephalomalacia, ketosis, scrapie, etc |
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Where does 90% of lameness originate in bovines (location)
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Foot
90% of that is rear foot 90% of rear foot is in lateral claw |
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What are two principles of a lameness exam
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Observe at rest
Observe walking |
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Second most common reason for culling cattle?
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Lameness
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What is the easiest way to trim and look at feet?
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Tilt table
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What disease process is is one of the most common causes of dairy lameness and when are you most likely going to see it?
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Sole ulcers
First 60d of lactation |
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Name 4 factors that contribute to sole ulcers
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Claw length
Claw concavity Weight bearing Environment |
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What are the goals of treatment with sole ulcers?
How do you treat? |
Decrease severity of lameness
Decrease granulation tissue prolif. Prevent infection of deep structures Ensure other rear lateral claw not affected Institute control measures Treat with corrective trimming and block on unaffected claw |
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What is the most common type of laminitis seen in cattle?
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Subclinical and chronic
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What is a main feature of chronic laminitis?
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Claws become long and misshapen
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What are predisposing factors for subsolar abscess?
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Anything that softens the hoof
Excessively worn soles Foreign body |
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Treatment of a subsolar abscess?
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All undermined horn must be pared away leaving no areas for dirt accumulation (drain pus)
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What can cause herd outbreaks of pedal bone fracture?
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Fluorosis
Pedal bone fractures in general are most often cause by trauma |
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How do you treat a pedal bone fracture?
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Block on unaffected claw and stabilize for >8wks
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What causes corns?
How do you treat? |
Heavy older cattle getting chronic irritation on loading
Surgical excision only if lame |
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Where does a vertical wall crack usually occur?
Treatment? |
At site of greatest concussive impact and lameness occurs when crack reaches coronary band or pinches corium
Treat with dremmel or acrylic if extensive |
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Where does a horizontal wall crack usually occur?
Treat? |
Near toe (assoc with hard dry horn)
Treat by removing crack or repair with acrylic |
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What is a predisposing factor for overgrown hooves?
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Housed on concrete
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What can cause scissor claws?
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subclinical laminitis
chronic laminitis overgrown hooves genetic component |
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What is a common cause of lameness in DAIRY cattle?
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Digital dermatitis (Hairy heel warts) due to spirochete bacteria
also sole ulcers |
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What are the risk factors for digital dermatitis (hairy heel wart)?
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Large herd, purchased cows
Grooved concrete floor with high moisture Shared hoof trimming equip |
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What is the proposed etiology of digital dermatitis?
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Treponema (boards)
other one is serpens |
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Case: Young dairy cow with a very painful well demarcated ulcerative lesion confined to the plantar aspect of the digit.
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Hairy heel wart
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What is a good treatment for hairy heel wart?
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Oxytetracycline spray covering area entirely
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How can you control hairy heel wart?
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Oral biotin
Prevent cattle from standing in moisture Disinfect hoof trimming equip Individual spraying of hind feet |
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What is the pathophysiology of foot rot?
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Most common in BEEF cattle
Bacteria invade through damaged skin (trauma or water softened interdigital area) --> infection |
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What is the treatment for foot rot?
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May not require any treatment-dry feet out
Can wrap feet with topical abx (parenteral) with oxytet. |
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What is the most common cause of sheep foot rot?
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Dichelobacter nodosus
See rapid onset of moderate to severe lameness in MULTIPLE sheep Sheep will kneel to graze |
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How do you treat foot rot in sheep
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Historically-Pare feet first
Foot bath with zinc sulfate Systemic abx Now = systemic abx and no paring |
