Ruminant Neurology 2

Question 1

Histophilus somni
- pathogenesis of neuro disease
- organism characteristics
- spectrum of diseases

Answer 1

• ITEME/TEME (Infectious thromboembolic meningoencephalitis, Thromoembolic meningoencephalitis)
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   Septicemia fulminant neurologic disease
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   Gram-negative, pleomorphic bacterium
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   Multi-systemic disease:
• Neurologic
• Reproductive, urogenital
• Respiratory
• Mammary
• Musculoskeletal
• Eye, ear

Question 2

Histophilus somni
 Neurologic signs, regions affected

Answer 2

 Fever, depression, anorexia, ataxia
 Conscious proprioceptive deficits
 Stumbling
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 Brainstem
 Cerebellum

Question 3

Histophilus somni
 Clinical pathology

Answer 3

Neutropenia, left shift, toxic changes PMNs
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CSF:
 Hemorrhage, xanthochromia
 Increased nucleated cell (neutrophils)
 Increased protein
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Culture fluids, tissues
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Antibody titers

Question 4

Histophilus somni
 Virulence factors, consequences? tissues affected?

Answer 4

 Induce apoptosis of endothelial cells
 Expose subendothelial collagen
 Thrombus formation
 Tissues most affected: brainstem, spinal cord,
synovial membranes, pleura, lungs

Question 5

Histophilus somni
 Epidemiology
- who gets it, when?

Answer 5

 Beef cattle
 Feed lots, pasture
 Seroconversion occurs early after entry into lot (co-mingling, transport, feed change)

Question 6

Histophilus somni
 Necropsy

Answer 6

 Disseminated, multifocal hemorrhages
 Infarctions
 Brainstem, spinal cord, cerebral cortex

Question 7

Histophilus somni
- prevention and treatment principles

Answer 7

 Examine often
 Treat early
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Sensitive to many antibiotics:
 Oxytetracycline
 Penicillin
 Ampicillin
 Others – tulathromycin, ceftiofur, florfenicol

Question 8

Salt Poisoning
- types
- prevention
- signs

Answer 8

 Salt poisoning with or without water
deprivation
 Always provide free access to salt &
water
 Acute or chronic ingestion
 Signs: diarrhea (may be hemorrhagic),
brain signs

Question 9

Salt Poisoning
- pathogenesis

Answer 9

 Passive diffusion of sodium into the CNS
 Hyperosmolality
 Reduces energy-dependent sodium transport
mechanisms & glycolysis need to remove
sodium from cells
 Thirst centers respond, ingest water, expansion
of ECF
 Osmolar gradient – CNS
 CNS edema, ↑ intracranial pressure, acute
encephalopathy

Question 10

Salt Poisoning - risk factor for calves

Answer 10

improperly mixed electrolyte solutions

Question 11

Salt Poisoning
 Diagnosis

Answer 11

 Blood sodium level >160 mEq/L
 CSF sodium level

Question 12

Salt Poisoning
 Treatment

Answer 12

Difficult, depends on onset & signs
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Non-neurologic high sodium cases:
- Gradual reduction in sodium level by giving the following, oral or IV:
 Hypertonic solutions
 Isotonic solutions
 (Hypotonic solutions)
> ie. taper the concentration down over time

Question 13

Vitamin A Deficiency
- where is found?
- metabolism considerations?
- who gets this? why?

Answer 13

 Vitamin A (retinol) found in green plants
 Precursor carotenoids may be converted to
retinol by liver & intestinal mucosa
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Most affected are feedlot cattle:
 Growing, need more Vitamin A
 Limited access to succulent plants
 Vitamin A is labile in plants; depletes with storage
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 Cereal grains, beet pulp, cotton seed hulls > they need leafy greens!

Question 14

Vitamin A Deficiency
- immune, pasture, feed management, bloat factors?

Answer 14

 Immune response ↑ Vit. A demand
 Prolonged feeding on dry pastures
 Prolonged feeding non-corn dry feeds
 Feed stored at high temperature & humidity
 Chronic mineral oil use (eg. bloat cases)

Question 15

Vitamin A Deficiency
- eye and other tissue requirements

Answer 15

 Eye requirements: rhodopsin (retina), outer retinal layers, optic foramen growth
 Other tissue requirements: osteoblast/osteoclasts, epithelium, reproductive tissues

Question 16

Vitamin A Deficiency
 Signs – Calves and Adults

Answer 16

Signs – Calves
 Anorexia, ill-thrift, diarrhea, pneumonia, blindness
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Signs – Adults
 Ocular – blindness, strabismus, nystagmus,
exophthalmos, ↓PLRs, “star gazing”
 Diarrhea
 Intermittent tonic/clonic convulsions
 Seizures may cause death
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Question 17

Vitamin A Deficiency
 Concomitant secondary diseases

Answer 17

 Nutritional deficiencies, parasitism, pneumonia

Question 18

Vitamin A Deficiency
 Eye observations

Answer 18

Dilated, unresponsive pupils
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Papilledema:
 Optic nerve swelling, lose detail esp. dorsally
 Faded, gray, flat, smaller than normal
 Retinal vessels more tortuous, appear
obstructed
 May have retinal hemorrhages & detachment

Question 19

Vitamin A Deficiency
 Differentiate from?

Answer 19

 Salt poisoning, lead poisoning → PLRs usually normal

Question 20

Vitamin A Deficiency
- Diagnosis, treatment, prevention

Answer 20

Diagnosis
 CBC, profile – usually not helpful
 CSF – increase in nucleated cells & protein
 Measure Vitamin A & β carotene in blood, liver
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Treatment: parenteral & oral Vit. A
 Detect early, treat early – may regain vision
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Prevention
– exogenous stabilized Vitamin A in feed, including milk replacers

Question 21

Lead Poisoning
- what does it cause in ruminants?
- why does it happen in ruminants?
- what about horses - what do we see with them?

Answer 21

 Ruminants – acute encephalopathy; blindness,
ataxia, depression
 Ruminants – propensity to ingest lead; availability
of lead containing materials
 Horses – chronic polyneuropathy; weight loss,
dysphagia, secondary pneumonia

Question 22

Lead Poisoning
 Diagnosis

Answer 22

 Examine environment & feed
 Lead levels in blood (collect heparinized blood; EDTA chelates, messes up test result), rumen, tissues
 Hemogram– RBC abnormalities

Question 23

Lead Poisoning
- treatment

Answer 23

Treatment – remove source, empty rumen
 Magnesium sulfate (GIT)
 Calcium, disodium EDTA
 Thiamine
 Supportive care