Ruminant Neurology 2 Flashcards
Histophilus somni
- pathogenesis of neuro disease
- organism characteristics
- spectrum of diseases
- 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
Histophilus somni
Neurologic signs, regions affected
Fever, depression, anorexia, ataxia
Conscious proprioceptive deficits
Stumbling
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Brainstem
Cerebellum
Histophilus somni
Clinical pathology
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
Histophilus somni
Virulence factors, consequences? tissues affected?
Induce apoptosis of endothelial cells
Expose subendothelial collagen
Thrombus formation
Tissues most affected: brainstem, spinal cord,
synovial membranes, pleura, lungs
Histophilus somni
Epidemiology
- who gets it, when?
Beef cattle
Feed lots, pasture
Seroconversion occurs early after entry into lot (co-mingling, transport, feed change)
Histophilus somni
Necropsy
Disseminated, multifocal hemorrhages
Infarctions
Brainstem, spinal cord, cerebral cortex
Histophilus somni
- prevention and treatment principles
Examine often
Treat early
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Sensitive to many antibiotics:
Oxytetracycline
Penicillin
Ampicillin
Others – tulathromycin, ceftiofur, florfenicol
Salt Poisoning
- types
- prevention
- signs
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
Salt Poisoning
- pathogenesis
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
Salt Poisoning - risk factor for calves
improperly mixed electrolyte solutions
Salt Poisoning
Diagnosis
Blood sodium level >160 mEq/L
CSF sodium level
Salt Poisoning
Treatment
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
Vitamin A Deficiency
- where is found?
- metabolism considerations?
- who gets this? why?
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!
Vitamin A Deficiency
- immune, pasture, feed management, bloat factors?
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)
Vitamin A Deficiency
- eye and other tissue requirements
Eye requirements: rhodopsin (retina), outer retinal layers, optic foramen growth
Other tissue requirements: osteoblast/osteoclasts, epithelium, reproductive tissues
Vitamin A Deficiency
Signs – Calves and Adults
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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Vitamin A Deficiency
Concomitant secondary diseases
Nutritional deficiencies, parasitism, pneumonia
Vitamin A Deficiency
Eye observations
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
Vitamin A Deficiency
Differentiate from?
Salt poisoning, lead poisoning → PLRs usually normal
Vitamin A Deficiency
- Diagnosis, treatment, prevention
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
Lead Poisoning
- what does it cause in ruminants?
- why does it happen in ruminants?
- what about horses - what do we see with them?
Ruminants – acute encephalopathy; blindness,
ataxia, depression
Ruminants – propensity to ingest lead; availability
of lead containing materials
Horses – chronic polyneuropathy; weight loss,
dysphagia, secondary pneumonia
Lead Poisoning
Diagnosis
Examine environment & feed
Lead levels in blood (collect heparinized blood; EDTA chelates, messes up test result), rumen, tissues
Hemogram– RBC abnormalities
Lead Poisoning
- treatment
Treatment – remove source, empty rumen
Magnesium sulfate (GIT)
Calcium, disodium EDTA
Thiamine
Supportive care
