-
What are some clinical symptoms of cerebral
cortex disease?
Change in mentation
+/- blindness
circling
-
What are some clinical symptoms of brain stem disease?
CN deficits
Circling
Head tilt
-
What are some clinical symptoms of cerebellar disease?
Intention tremors
Hypermetria / dysmetria
Incoordination
-
What are some clinical symptoms of spinal cord disease?
Ataxia
- Spinal reflexes (increased or decreased depending on
- location)
Paralysis / paresis
-
What are some clinical symptoms of peripheral nerve disease?
Muscle tone
Muscle atrophy
Paralysis / paresis
Absence of spinal reflexes
-
What are the common brain stem diseases in ruminants?
Listeriosis
- Otitis media / interna (M. bovis, P. multocida, H. somni, C
- pseudotuberculosis, T. pyogenes)
TEME (H. somni)
Brain or pituitary abscess
Meningeal worm (more often spinal cord)
-
What are the common brainstem diseases in pigs?
- Otitis media / interna (P. multocida, S. suis, H. suis, T.
- pyogenes)
-
What are the common cerebral diseases in ruminants?
Cerebrocortical necrosis (CCN)
TEME
Nervous ketosis
Nervous coccidosis (Eimeria)
Pregnancy toxemia
HypoMg
BSE
Scrapie
Rabies
VitA deficiency (prolonged storage of green plants
-
What are the common cerebellar diseases in ruminants?
Cerebellar hypoplasia (BVDV type 2)
-
What are the common spinal cord diseases in ruminants?
Tetanus
Enzootic ataxia
Meningeal worm
Lymphosarcoma
CAE
-
What are the common cerebral diseases in pigs?
Strep meningitis
Glasser’s (H. parasuis)
Edema disease (E. coli)
HyperNa
Pseudorabies
-
In which pigs are clinical symptoms of cortical disease
seen?
Nursery
-
What is the mechanism of polioencephalomalacia (CCN)?
Altered thiamine metabolism
-
What are some causes of CCN?
Pb poisoning
Lactic acidosis (e.g. grain overload)
HyperNa
Bracken fern toxicity
Sulfur intoxication
Amprolium intoxication
-
What is the normal pentose phosphate pathway?
- Glucose is used to make ATP by the rate limiting enzyme
- VitB1 dependent transketolase
- The ATP is used to maintain 3Na+/2K+ pumps on the cell
- membrane
Most affected are nervous tissue cells and RBCs
-
Where do ruminants normally get thiamine?
Rumen microbes
-
What does a CSF analysis of CCN in ruminants show?
Increased protein, monocytes (unless it’s a pig with hyperNa
-
What does a CSF analysis of a pig with hyperNa show?
Eosinophilia
-
What does gross pathology of CCN show?
Diffuse cerebral edema
Cerebellum pushed back to magnum foramen
Wood’s Lamp shows fluorescence in gray and white cerebral cortex
-
Why do ruminants get Pb poisoning?
Calves are curious, esp after weaning
May have mineral deficiency
-
What is the mechanism of Pb poisoning?
Pb binds sulfhydryl groups esp on RBCs
Pb inhibits PPP transketolase in RBCs
-
What are the clinical symptoms of Pb poisoning?
Cortical signs like bellowing, mania, seizures
Cortically blind
CCN
Mild anemia
Diarrhea
Death from respiratory paralysis
-
How is Pb poisoning dx?
Heparinized blood sample
Tissue samples (liver and kidney)
-
What is the txt for Pb poisoning?
Give thiamine
CaEDTA to chelate Pb in tissues, excreted by kidney
Cathartics e.g. MgSO4
Diazepam
-
What does an increase in rumen lactic acid cause, and why?
Rumenitis
Metabolic acidosis (if severe)
Dehydration (water is pulled into the rumen)
Bloat (CHOs are fermented)
Endotoxemia (no more g-)
CCN (no more thiamine)
Liver abscess (F. necrophorum gains access to the portal v.)
Caval syndrome (F. necrophorum causes lung abscesses and death)
-
How does lactic acidosis occur in a ruminant?
Ingestion of high CHO
The microflora shift to be more g+
Strep/ bovis proliferates
VFAs increase
Rumen pH decreases
G- bacteria and protozoa die
Lactobacillus proliferates
Lactic acid increases in the rumen
-
How is lactic acidosis dx?
Rumen pH <5.5
-
How is lactic acidosis tx?
Give thiamine
Transfaunate rumen
IVF of NaHCO3 + KCl or glucose
Systemic abx
NSAIDs (if kidneys ok)
-
Why do you need to give KCl to a ruminant with lactic
acidosis?
- HyperK likely, but increasing K will move H+ out of cells
- and out of tubules(?)
-
How can lactic acidosis be prevented?
Adapt animals to a high CHO diet
Put ionophores and NaHCO3 in feed
-
What are the clinical symptoms of hyperNa?
Change in mentation, central blindness, circling
Aggressive, excitable
Seizures
Dog sitting position (pigs)
-
How is hyperNa dx?
Serum increase in Na, hemoconcentration, pre renal azotemia, metabolic acidosis (anaerobic glycolysis)
CSF increase in protein, Na and monocytes (ruminants) or eosinophils (pigs)
-
What neurological conditions cause pigs to dog sit?
Rabies, hyperNa
-
What causes the CS of hyperNa?
- Increased electrolyte [], followed by heavy water drinking
- -> water drawn into ventricles
-
How is hyperNa tx?
Give IVF with higher [Na] than serum
Check every hour, adjust IVF accordingly
-
How is hyperNa related to CCN?
- The cells are dying, so they’re not performing PPP, so
- there’s less ATP available
-
How does amprolium cause CCN?
Incorrect mixing means [thiamine analogue] competes with thiamine on transketolase
-
How can amprolium toxicity be dx?
Hx
RBC transketolase activity
-
How is amprolium toxicity tx?
Give thiamine
-
How does bracken fern ingestion cause CCN?
Presence of thiaminases in plant
Also has oxidizing agents resulting in hemolysis and hematuria
-
How can bracken fern ingestion be dx?
Hematuria, bladder TCC
-
What causes bladder TCC?
Bovine papilloma virus, bracken fern ingestion
-
How does sulfur intoxication cause CCN?
Direct thiamine destruction
Sulfates converted to sulfide in the rumen (normally hydrogen sulfide)
Hydrogen sulfide inhibits cytochrome oxidase (electron transport chain) and transketolase enzyme
-
How is sulfur intoxication dx?
[Sulfur] in water or feed
Hx (smell)
-
How is sulfur toxicity tx?
Give thiamine, but unlikely to be successful
Supportive, IVF, transfaunation
Dexamethasone (reduce cerebral edema)
Mannitol (reduce cerebral edema)
-
What is the prognosis of CCN diseases?
Good except sulfur intoxication
-
Which pigs are affected by edema disease?
Weaned piglets
-
What is the mechanism for edema disease?
- E. coli adheres to gut via fimbria F18ab, producing a toxin
- that damages the vascular endothelium
-
What are the CS of edema disease?
Lesions include edema of the stomach, colon and eyelids
Cortical signs (edema and necrosis of cortex)
-
Which pigs are affected by Strep meningitis?
Weaned piglets
-
What are the CS of Strep meningitis?
Pneumonia
Polyserositis
Septicemia (signs on infection more common than neurological signs)
Incoordination
Stupor
Seizures
-
How is Strep meningitis tx?
Vaccination and antibiotics, but variably effective
-
How can Strep meningitis be prevented?
Vaccines (variably effective, zoonotic)
Not SEW
-
Which pigs are affected by Glasser’s disease?
Weaned piglets
-
What causes edema disease?
E. coli
-
What causes Strep meningitis?
Strep suis type II
-
What causes Glasser’s disease?
Haemophilus parasuis
-
What are the CS of Glasser’s disease?
Pneumonia
Polyserositis
Septicemia
…looks like Strep meningitis
-
How can Glasser’s disease be prevented?
Good vaccine
-
How is Glasser’s disease tx?
Abx
-
How can edema disease, Glasser’s and Strep meningitis be
differentiated on necropsy?
Edema disease has edema of stomach and eyelid
Fibrin on serosal surfaces if Step or Glasser’s
-
How can CNS diseases in nursery pigs be dx (e.g. Glasser’s,
edema disease, Strep meningitis, hyperNa)?
Culture (meninges for Step or Glasser’s, intestine for E. coli)
Histopathology (purulent meningitis for Strep or Glasser’s, eosinophils for hyperNa)
Serum analysis (eosinophils and hyperNa)
-
How does cerebellar hypoplasia occur?
Inherited or acquired (more common)
-
In which breeds is cerebellar hypoplasia inherited?
Hereford, Shorthorn, Angus, Holstein, Guernsey, Ayrshire
-
How is cerebellar hypoplasia acquired in cattle?
BVD in-utero infection
Blue tongue
-
How is cerebellar hypoplasia acquired in sheep?
Border disease
Blue tongue
-
What are the CS of cerebellar hypoplasia?
Spasticity
Dysmetria
Seizures maybe
Intention tremors
Incoordination
Normal intelligence
Viable
-
What diseases cause drooling in ruminants?
Rabies
CN VII dysfunction
Listeria
-
What can cause spinal cord disease in ruminants and pigs?
Clostridium tetani
-
Where is C. tetani found?
Soil and intestinal tract
-
How does an animal get infected with C. tetani?
- Wound is contaminated by soil spores, which vegetate and
- produce toxins
- Associated with parturition, retained fetal membranes,
- vaginal bruising, teeth eruption, castration, tail docking and shearing
-
What toxins are produced by C. tetani?
Tetanospasmin (binds inhibitory neurons in spinal cord)
Tetanolysin (causes tissue damage)
-
What are the CS of C. tetani infection?
Uninhibited muscle contractions
Sawhose stance, pump handle tail lock jaw
3rd eyelid prolapse
Bloat
Exaggerated response to sound
Sardonic grin
Death when diaphragm muscles are paralyzed
-
How can C. tetani infection be dx?
Can’t – the toxin is in the nerves, not the blood
-
How is tetanus tx?
PPG, neuromuscular relaxants like diazepam or MgSO4
Tetanus anti-toxin
Minimize neural input
-
How is tetanus prevented?
Vaccine with C. tetani + C. perfringens C and D
-
What are the characteristics of C. tetani?
G+ anaerobe
-
What is enzootic swayback?
Lambs born to chronically Cu deficient does have progressive posterior ataxia and weakness
-
What is the mechanism of enzootic swayback disease?
Cu required for myelin formation in the spinal cord
Hind limb -> front limb demyelination
-
What are the CS of enzootic swayback disease?
Observed progressive ataxia in lambs 0-6 months old
Maintenance of spinal reflexes
-
How is enzootic swayback disease tx?
Can’t reverse any of the neuro signs
PO Cu if mild
-
How is enzootic swayback disease prevented?
Cu supplementation of does
-
Which lymphosarcoma is BLV-associated?
Enzootic
-
What are the juvenile forms of lymphosarcoma?
Multicentric, thymic, cutaneous, enzootic
-
How is BLV spread?
Vertically (8%)
Colostrum or milk (8%)
Horizontal (majority)
Events: dehorning, ear tagging, tattooing, injections, vaccinations, rectal palpation, biting flies
-
How many animal are infected with BLV, and how many will
develop enzootic BLV lymphosarcoma?
>80% infected, <5% get lymphosarcoma
-
What kind of virus is BLV?
Retro (exposure = infected)
-
What organs are commonly affected by lymphosarcoma?
LNs, retrobulbar, uterus, spinal cord, abomasum
-
How is lymphosarcoma dx?
- Persistent lymphocytosis (2 samples 2 weeks apart, 20% sensitive)
- LN biopsy (best)
- BLV PCR / AGID / ELISA (only tells you exposure)
-
How is lymphosarcoma tx?
n/a – poor px
-
In which animals are vertebral or epidural abscesses seen?
Calves
Bacteremic animals (omphalophlebitis, endocarditis, liver abscess, pneumonia)
Working ruminants like bucking bulls
-
What agent usually causes vertebral or epidural abscesses?
T. pyogenes
-
What are the CS of vertebral or epidural abscesses?
Gradual onset of paresis and paralysis
Sudden vertebral fracture and paralysis
-
How can vertebral or epidural abscesses be dx?
CSF has neutrophils and macrophages, high protein
Radiographs very helpful
-
How are spinal cord diseases managed?
Dx to know the px
Treat the underlying disease
Pain management
Physiotherapy
Sling
Float tank
Beach balls
-
What are the 4 “m’s” of downer cows?
Musculoskeletal
Metabolic (hypoCa, hypoK)
Mastitis
Metritis
-
What does the radial n. supply?
Extends the elbow, carpus and digits of thoracic limb
Cutaneous sensation to lateral part of the leg
-
How does radial n. paralysis occur?
Prolonged recumbency
-
What is the txt for radial n. paralysis?
Bandage, splint, or cast the fetlock to avoid abrasion
Use deep soft bedding
Dexamethasone to stabilize the cell membrane and prevent inflammation
-
What happens when a cell membrane is damaged?
PLA2 breaks phospholipids down to arachidonic acid
- Arachidonic acid is broken down to thromboxanes,
- prostaglandins and prostacyclins (COX1, COX2) or leukotrienes (lipoxygenase)
-
Where do steroids inhibit inflammation?
Inhibits PLA2
-
Where do NSAIDs inhibit inflammation?
COX1 or COX2
-
What does the obturator n. supply?
Muscles that adduct the hip
-
When is obturator n. damage seen?
Dystocia from feto-pelvic disproportion pressure ischemia
-
How is obturator n. damage tx?
Put in stall with good footing
Hobble
Float tank
Corticosteroids and NSAIDs
-
What is the most common nerve injury in dairy cattle?
Sciatic n. damage
-
What causes sciatic n. damage?
Injecting the gluteal muscles
Pelvic fracture
Dystocia
-
What are the CS of sciatic n. damage?
- Dropped stifle, hip and hock
- Flexion of fetlock
-
What does the peroneal n. supply?
Flexor muscles of the hock
Extensor muscles of the digit
-
How is the peroneal n. damaged?
Exposed superficially distal to the stifle
Prolonged recumbence
-
What are the CS of peroneal n. damage?
Hyper-extension of the hock (looks super straight)
Flexion of the fetlock
-
What does the tibial n. supply?
Extensor muscles of the hock
Flexors of the digits
-
What causes tibial n. damage?
Irritating injections in the caudal leg (near stifle)
Dog or coyote bite
-
What are the CS of tibial n. damage?
Over-flexed hock
Extended fetlock and pastern
-
What nerve paralysis is seen in calves?
Femoral n. if pulled during dystocia from a posterior position
Secondary to injection site abscess
-
What does the femoral n. supply?
Quadriceps, so flexes hip
-
What are the CS of femoral n. damage?
Non weight bearing if severe
Muscle atrophy
Absence of patella reflex
-
How is peripheral n. damage tx?
NSAIDs
Corticosteroids
Good footing
Bandage the limb to prevent pressure sores
Float tank
Time (<14 days)
-
What does the sciatic n. supply?
Extensor muscles of the hip
Flexor muscles of the stifle and distal limb
-
What does the sciatic n. divide into?
Tibial and peroneal n.
-
What is botulism caused by?
Clostridium botulinum B, C, D
-
How do animals get botulism?
Ingest a pre-formed toxin from carcasses or rotting vegetation
Wound contamination
-
Which animals get botulism?
Animals with pica eating rotting carcasses or vegetation because of a mineral deficiency
-
What is the botulism toxin mechanism?
Inhibits release of Ach from pre-synaptic membrane
-
What are the CS of botulism?
Flaccid paralysis (progressive caudal to cranial, esp limbs, throat and jaws)
Normal sensation and mentation
Occurs in 1-4 days
Respiratory arrest
-
What is the px for botulism?
Few will recover in 3-4 weeks
-
How is botulism dx?
Find pre-formed toxin in the feed
-
How is botulism tx?
Symptomatic
-
How is botulism prevented?
Vaccination
-
What are the five freedoms according to the Brambell report and the OIE code for animal welfare?
Freedom from hunger, thirst and malnutrition
Freedom from physical and thermal discomfort
Freedom from pain, injury and disease
Freedom to express normal behavior
Freedom from fear and distress
-
What are the four principles of good welfare according to David Fraser?
Maintain basic health
Reduce pain and distress
Accommodate natural behaviors and affective states
Natural elements in the environment
-
What are some examples of the principles of Davis Fraser being upheld?
Maintain basic health: check BCS
Reduce pain and distress: check for disease and injury, low stress handling
Accommodate natural behaviors and affective states: watch herd interactions
Natural elements in the environment: tress, shade, water, salt
-
What are the two main emphases of standards to assess animal welfare?
Animal-based measures performance standards or outcome criteria
Practices that are prohibited
-
How do animals get sulfur intoxication?
High sulfate feed or water
-
What bacteria are commonly isolated from spinal cord abscesses?
Trueperella pyogenes most commonly isolated
Streptococcus (especially in pigs), Mycoplasma, Staphylococcus, and Corynebacterium have been reported
-
How are spinal cord abscesses tx?
Abx that penetrate BBB (macrolides, tetrayclines)
-
When do you see CS of botulism?
3-7 days after ingestion (pre-formed toxin)
-
What is the definition of a "natural" product?
- No officially regulated definition
- -look for USDA verification
- -minimally processed
- -no artificial ingredients
- -no preservatives
- No specific restriction on management
- practices during the life of the animal!
-
Describe the USDA label for natural beef cattle.
- No abx
- No hormone implants
- Vegetarian diet
- Maybe ionophores
- Don't need organic feed
- Affidavit = certification = "brand"
-
Describe the USDA label for certified organic beef cattle.
- No abx, ionophores, hormone implants
- Vegetarian organic diet only
- Cows are organically managed last 1/3 in-utero, and rest of lifeOrganic feed for >3 yearsAccess to pasture >120 days / year = 30% DMI
-
What are the requirements for selling organic milk?
Cows have been eating organic food for >1 year
-
What is a violation of organic feed of beef cattle?
- No drugs (e.g. hormones)
- No supplements or additives
- No plastic feed pellets
- No urea / manure
- No animal by-products
-
What are some of the allowed drugs in organic beef cattle?
- Disinfectants
- Aspirin
- Atropine
- Butorphanol
- Chlorhex
- Vaccines
- IVF
- Flunixin
- Iodine
- Glucose
- Oxytocin
- Lidocaine
- Xylazine
- Furosemide
- H2O2
- Mineral oil
-
What are the basics of how to run an organic beef program?
- Prevention is the key!
- -select appropriate breeds & types
- -provide balanced nutrition
- -appropriate housing for the species, clean environment
- -provide natural behavior, stress reduction & exercise
- -chose appropriate vaccination program
-
Which drugs are general accepted in organic beef cattle?
- natural
- -if synthetic must be specifically allowed
-
What is the approach for treating infectious disease without anti-microbials according to Dr. Karreman?
- -stimulation or modulation of the immune system via biologics
- -antibacterial phytotherapy
- -antioxidants
- -fluid therapy for rehydration need proper circulation
- -use of antiseptics for lavage & irrigation as needed
-
When do you see CS of C. tetani?
2-3 weeks after wound infection
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