Metabolic causes of neurological disease in ruminants

Question 1

Nervous ketosis (cattle) / pregnancy toxaemia (sheep)

Answer 1

• both secondary neuro conditions related to NEB
• increased ketones and decreased glucose = negative effects on brain function

Question 2

Pregnancy toxaemia

Answer 2

• sheep
• energy demands of foetus(es) in late gestation > energy obtained from diet
• often associated with temporary food deprivation or reduction in intakes
• primarily seen in ewes carrying twins/triplets in more intensive systems during last 2w of gestation

Question 3

Pregnancy toxaemia - clinical signs of early stages

Answer 3

• separation from group
• apparent blindness
• sheep seem alert but don’t want to move, even if dog present
• bump into obstacles and exhibit head pressing

Question 4

Pregnancy toxaemia - clinical signs of later stages

Answer 4

• marked drowsiness
• facial twitching, jaw champing, salivation
• deviations of head position
• star-gazing and ataxia
• seizures, marked drowsiness seen between seizures
• ketone breath

Question 5

Pregnancy toxaemia - clinical signs of final stages

Answer 5

• recumbency develops after 3-4d
• develops comatose state, typically lasts for 3-4d
• if foetal death occurs, ewe appears to recover but secondary toxaemia results in deterioration and death

Question 6

Pregnancy toxaemia tx

Answer 6

• parenteral glucose: 5-7g glucose IV 6-8x daily recommended, but 2-4x daily a more practical amount
• supportive IV fluids: Hartmann’s or saline
• oral propylene glycol: 100mL once daily, in milder cases can be very effective alone, more sustained increase in glucose
• supplement with calcium and potassium: increases success rate, potassium stimulates appetite and often associated with hypocalcaemia in sheep
• can consider inducing lambs if in early stages of dz: if don’t think ewe will survive the delay between induction and parturition (24h) C-sec can be considered

Question 7

Pregnancy toxaemia prevention and control

Answer 7

• when clinical cases occur carefully monitor rest of flock and treat affected animals immediately with oral glucose/propylene glycol/glycerol
• prevent by ensuring there’s a rising plane of nutrition in 2nd 1/2 of pregnancy: nutrition needs to be improving, may need to restrict in early pregnancy to achieve tis
• recommend scanning and feeding singles/twins/triplets separately if possible

Question 8

Nervous ketosis

Answer 8

• cattle
• uncommon presentation of ketosis
• likely due to isopropanol -> breakdown product of acetone
• hypoglycaemia also likely to contribute
• ketone bodies further exacerbate signs

Question 9

Nervous ketosis clinical signs

Answer 9

• sudden onset neurological signs occurring in short recurring bouts
• circling and aimless wandering
• crossing limbs and ataxia
• apparent blindness, walking into objects, head pressing
• hyperaesthesia
• mild tremors
• key ddx is BSE -> notifiable

Question 10

Nervous ketosis diagnosis and tx

Answer 10

• dx based on CS + blood BHB concentration >3.0mmol/l
• IV glucose (500ml of 50% solution), rapid improvement but is transient (only lasts 3-4h)
• oral propylene glycol, 300ml once daily for 5d
• glucocorticoids, best responses if given with glucose, probably due to glucose repartitioning, limited evidence basis for treating less severe cases of ketosis, tend to use if not responding to other tx
• control - transition management

Question 11

Cerebrocortical necrosis (CNN) (polioencephalomalacia)

Answer 11

• thiamine (vitB1) deficiency/inadequancy
  – high [thiaminases] formed in rumen (reason unknown)
  – destroy thiamine (produced by microbes)
  – increase pyruvate (thiamine important component of metabolic enzymes)
  – negative effect on glucose pathways -> damage to cerebral neurons
• sulphur induced CCN
  – diets high in sulphates
  – young cattle on feedlots (6-18m/o)
  – reported more in America but might see more of it in UK in the future

Question 12

CCN clinical presentation

Answer 12

• usually young, growing animals -> weaned lambs and calves most often
• typically a history of recent dietary change (~2w prior) -> disruption of rumen microflora
• CS start with sudden onset blindness, aimless wandering and circling, head pressing, star-gazing
• progress over 12-24h to lateral recumbency and opisthotonos
• death occurs in a few days in untreated animals

Question 13

CCN diagnosis

Answer 13

• history and CE
• ante-mortem definitive diagnosis not possible: response to thiamine tx = highly suggestive, sulphur induced CCN doesn’t respond to thiamine tx
• confirmed on PM: brain fluoresces under UV light
• ensure euthanasia of these animals is by pentobarb/somulose not shooting as this would destroy brain tissue and make dx impossible

Question 14

CCN ddx

Answer 14

• meningitis
• lead poisoning
• twin lamb dz / nervous ketosis
• vitamin A deficiency

Question 15

CCN tx and control

Answer 15

• thiamine tx: 10mg/kg, give slow IV initially, repeat every 3h up to 5 doses (IV or IM), use B1 products (multivitamins don’t have high enough [])
• supportive care: may also need dexamethasone (1mg/kg) if cerebral oedema
• prognosis is good if tx instigated early
• supplementation of diets with thiamine for ongoing control (3mg/kg dry matter, may need to be higher on some farms)
• ensure roughage in diet
• ensure sulphur content of diet is appropriate

Question 16

Swayback

Answer 16

• sheep and goats
• copper deficiency of ewes/does in mid-pregnancy
• 3 presentations: congenital cerebrospinal swayback, progressive spinal swayback, cerebral oedema

Question 17

Congenital cerebrospinal swayback

Answer 17

• Lambs born dead or weak and unable to stand
• Liveborn lambs are recumbent with spastic paralysis of all limbs
• Movement is uncoordinated and erratic

Question 18

Progressive spinal swayback

Answer 18

• Stiff staggering gait, hindlimb ataxia (swaying gait)
• Signs develop at 3-6 weeks of age
• Most common form

Question 19

Cerebral oedema (swayback)

Answer 19

• Reported in Wales only
• Similar signs to progressive spinal form but develops more quickly and progresses to death in 1-2 days

Question 20

Swayback diagnosis

Answer 20

• Diagnosis is usually based on history and clinical signs
• Blood copper not reflective of copper status because copper stored in the liver
  Liver biopsy is a better indicator
• Interpret results with care because animals may show clinical signs before liver/blood copper concentration very low
• Consider assessing copper status at flock level
• Treatment trial can be useful

Question 21

Swayback tx and prevention

Answer 21

• Treatment involves oral supplementation of copper
  –Severely affected lambs = poor prognosis
• Prevention is better
  – Ensure ewes/does have adequate copper supplementation in diet during mid pregnancy
  – Oral dosing
  – Slow release bolus
  – Injections
• Care with sheep -> susceptible to copper toxicity

Question 22

Vitamin A deficiency (hypovitaminosis A) primary deficiency

Answer 22

• associated with diets insufficient in vitamin A

Question 23

Vitamin A deficiency (hypovitaminosis A) secondary deficiency

Answer 23

• associated with chronic liver or enteric disease
• Failure of conversion of carotene to vit A

Question 24

Hypovitaminosis A main clinical signs

Answer 24

• Night blindness – earliest c/sign -> young adult animals
• Corneal keratinisation, mucoid ocular discharge, photophobia
• Skeletal muscle paralysis (weakness and ataxia that starts in hindlimbs) -> young animals
• Encephalopathy (convulsions) -> young animals
• Dry, brittle hooves and reduced reproductive performance -> adults

Question 25

Hypovitaminosis A tx and prevention

Answer 25

• Vitamin A supplementation at 440 IU/kg (10-20x maintenance requirement)
• Response to treatment is rapid
• Calves with encephalopathy typically resolve within 48hrs
• Blindness does not improve
• Ensure adequate dietary vitamin A
  – 40IU/kg is minimum daily requirement for all species
  – May need to be increased if pregnant/lactating

Question 26

Hypomagneseamia

Answer 26

= grass staggers / hypomagnesaemic tetany
- Common in cattle, occurs rarely in sheep
- Low serum magnesium
– Alterations in nerve impulses to muscles
- cattle don’t store magnesium so need regular intake daily to meet demands
- often just can’t eat enough grass to meet the demands of the calf

Question 27

Hypomagnesaemia clinical signs

Answer 27

• Acute form: hyperaesthesia, ataxia, collapse, seizures
• Subacute form: wild facial expression, hypermetric gait, muscle tremors, spasmodic urination and defecation
• May present as sudden death
  – Important ddx is anthrax (notifiable)

Question 28

Hypomagnesaemia diagnosis

Answer 28

• based on characteristic CS and history
• Typically seen in cows at pasture in Spring/Autumn with older suckling calves at foot
  – Lots of milk demand -> increased magnesium losses
  – Young, growing grass has lower magnesium content -> reduced magnesium consumption

Question 29

Hypomagnesaemia additional diagnostics

Answer 29

• Live animal = blood sample
  – Lithium heparin (green top) tube
  – External lab or in house analyser
  – Worth also testing for calcium and phosphorus at same time
• Dead animal = vitreous humor
  – Remains stable after death longer than serum/plasma concentration
  – Use 14G or 16G needle and aspirate with syringe
  – Do not sample aqueous humor – easily contaminated by iris tissue if deteriorating

Question 30

Hypomagnesaemia treatment

Answer 30

• Emergency!
• Sedate if seizuring (tail vein not jugular as could tip them over the edge)
• IV calcium with magnesium added
• SC magnesium

DO NOT GIVE WHOLE BOTTLE OF MAGNESIUM IV!!

Question 31

Hypomagnesaemia prevention and control

Answer 31

• Supplement diet with magnesium
  – Included in TMR or concentrates -> typically for dairy cows
  – Magnesium salts
• Graze suckled cows on lower risk pastures
• Consider calving earlier in winter/late autumn so cows are housed until calves are weaned (often not practical)

Question 32

Common methods of magnesium supplementation

Answer 32

• daily oral drenching: ensures each cow is dosed, but time consuming and need to catch cows daily
• top dressing pasture: straightforward and only needs doing once every 1-3y depending on pasture, but variable in individual cow consumption, need equipment for spreading salts
• magnesium in drinking water: easy to do, cost effective, but need to ensure alternate water sources are available, individual cow variations in consumption, needs checking daily for both water and Mg salt content in trough
• salt licks: easy to use, cost effective, but variability in individual cow consumption