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Production Diseases - Coggle Diagram

- - - - Ionised Ca = 1-1.5 mmol/l
      - Cation- more ionised in an acidic environement
      - Bound to albumin
  - - - Sheep + beef cows
      - Heavily pregnant
      - Not eating
        
        Hypocalcaemia exacerbated by metabolic alkalosis due to rumen stasis
      - Occurs a an outbreak
    - - Dairy cows + goats
      - Failure to rapidly mobilize Ca from bone
        
        Mobilization Determined by
        
        pH of body fluids
        
        age of animal
        
        effectiveness of parathyroid hormone
        
        PTH responds to low Ca++ levels
        
        Stimulations conversion of cholecalciferol -> Vit D*
        
        Stimulates osteooclasts
        
        Stimulates kidney reabsorption of Ca ++in exchange for phosphorus.
        
        ⚠ Fed High Ca in dry period -> Calcitonin release -> inhibition of osteoclastic activity. Sudden drop in Ca levels at the start of lactation -> refractory 48-72h before PTH activity
        
        Metabolic alkalosis -> change in morphology of PTH Rs -> PTH is ineffective
        
        ✔ Prevent this by feeding anionic salts during the dry period to induce a mild metabolic acidosis
        
        Mg needed to saturate the binding site of Adenyl cyclase complex for proper functioning of PTH receptor
        
        thyroid activity (calcitonin)
        
        Calcitonin reacts to high blood Ca++ levels
        
        Inhibitis intestinal Ca ++uptake
        
        Stimulates urinary loss of Ca ++
        
        Stimulates osteoblasts, inhibits osteoclasts
        
        kidney activity (Vit D)
        
        *Vit D increases intestinal uptake of Ca ++
      - Failure to rapidly absorb Ca from the GIT
        
        Uptake determined by
        
        Rumeno-intestinal movements
        
        pH of rumen
        
        Mineral levels of the ration
        
        Effectiveness of 1:25(OH)2 D3
      - Small amount of available Ca vs amount required for milk production - Ca loss in milk is not hormonally regulated - continues despite deficiencies
    - - Metabolic Alkalosis
        
        Ax
        
        Diet high in Na / K / rumen degradable protein
        
        Secretion of colostrum (acidic)
        
        Rumen hypomotility (reduced VFA absorption)
        
        LDA
        
        Effect
        
        Bone refractory to effect of PTH (Change in morphology)
        
        Prevention
        
        Feed diet high in Cl and S during the transitional period to indice a slight metabolic acidosis
        
        Monitor urine pH - should be 6-6.8
      - Rumen Alkalosis
        
        Ca salts become INSOLUBLE -> trapped in rumen
      - Reduced DMI for 12-16h -> Rumen stasis + Reduced Ca intake
        
        Oestrus
        
        Bad weather
        
        Transport (stress)
        
        Disease: mastitis/metritis/LDA/rumen acidosis
      - Ration
        
        High Ca intake during dry period, refractory period seen @ start of lactation
        
        not seen in sheep, lower Ca intake during dry period ➡⬆milk fever
        
        Defective mobilization of Ca from bone due to fewer PTH Rs in bone
        
        Pasture irrigated with slurry -> High K
        
        Pasture low in Ca- Kikuyu, Barely, Oats
        
        Diet low in Mg /Vit D
        
        Plants containing oxalates -> bind Ca
      - High producing
        
        Channel
        
        Saanen
        
        Ewes with twins / triplets
      - Older animals
        
        Reduced intestinal absorption of Ca ++
        
        Decreased production and response to Vit D3
        
        Fewer osteoclasts to respond to PTH
      - Hypomagnasaemia
        
        Mg co-factor in PTH & Vit D action
        
        Mg plays a role in Ca release from ER of muscle cells
        
        ⬇ Mg = ⬆ Milk fever
      - Stress: "Transport Disease"
        
        Adrenalin -> reduced appetite -> decreased Ca absorption
        
        Chronic stress -> cortisol -> ⬆osteoclastic activity +⬇ Ca absorption -> depleted Ca stores
      - Disease
        
        Kidney Disease -> Ca loss + reduced Ca absorption due to ⬇ Vit D production (unresponsive hypocalcaemia)
        
        PKD : Ca -> intracellular compartment
      - Overfat animals in last half of lactation / dry period
  - - - dry muzzle
      - cyanosis and tachycardia
      - upright hock, a swaying gait, particularly in sheep, difficulty in rising and walking; gradual loss of anal tone and swallowing reflex.
      - excited and hypersensitive. light muscle tremors of head and limbs.
      - rumen atony/stasis
    - - Sternal recumbency with neck in s-curve (‘torticollis’) / directed towards lateral flank (milk fever position) Sheep often initially present recumbent with the hind limbs stretched backwards
      - Mydriasis
      - Semi coma 1-3h after going down
        
        cold extremities/limbs
        
        poorly audible heart: stroke volume (SV) decreases due to negative inotropic effect, tachycardia as animal tries to compensate
        
        shallow respiration due to alkalosis and paretic respiratory muscles
      - Flaccid paralysis, hard, bulging of perineal area due to loss of muscle tone - mucus covered faeces.
    - - rumen content runs out of the nose - due to oesophageal reflux
      - loss of muscle tone (flaccid paresis)
      - subnormal temperature
      - tympany
      - coma
    - - Dystocia due to poor uterine contractions (in cases that occur prepartum such as sheep and beef cows)
      - Retained placenta
      - Muscle necrosis/muscle injuries
      - Hip dislocation
      - Aspiration pneumonia
  - - - 💡Metabolic Alkalosis -> ⬇ Ionised Ca in the presence of normal / increased Ca
  - - - paralysis
    - - 3 days stiff sickness
      - botulism
      - cerebral theileriosis
      - Pulpy kidney
      - haemonchosis etc
  - - - Parity
      - Previous history of milk fever (50% recurrance)
      - Time from initial recumbency to treatment
      - Body Condition of the animal
      - Serum Ca ++and Mg + level before initial treatment
      - Haematocrit before initial treatment
    - - Slow jugular IV admin using a flutter valve and 18G needle
        
        Calcium borogluconate 40% solution or Norcal 40 MP ®
        
        pH 3: corrects metabolic alkalosis and gets rumen working again, ⬆ PTH stimulatory effects due to receptors regaining normal shape (high pH changed PTH receptor morphology)
        
        MFC ® (milk fever compound) or Norcal PMD ®
        
        Less Ca and contains Mg (protects the heart), Phosphate + glucose
        
        Preferred Tx for 🐑🐐, safer for farmer to administer (less Ca)
      - Monitor for arrythmias / Bradycardia- stop admin at the first sign of arrythmia / 80 bpm with normal strength of cardiac contractions
      - Nursing Care
        
        Remove calf / lamb after feeding sufficient colostrum
        
        Prop up to prevent aspiration
        
        Regularly move from side to side and massage legs if not up after an hour.
        
        If recumbent for more than 48 hours use a hip sling or bovijack to help the animal to stand
        
        Provide shade
    - - ⬆ Audibility and strength of cardiac contractions
      - Cow starts to shiver
      - Shows interest in her surroundings
      - urinates / defaecates / eructates
      - sweats from the muzzle
      - Attempts to rise within 20-40 minutes, or within an hour in the case of sheep.
    - - Hypophosphataemia: react slowly to Ca Tx
        
        Oral / IV Phosphate
      - Hypomagnasaemia
        
        SC MgCl / MgSO4
      - Rumen stasis
        
        Warm water / vinegar and physically massage rumen
      - Hypolalaemia
        
        KCl slowly IV / oral if rumen is functional
  - - - phosphoric acid PO
      - 100 ml 1% HCl IV or 30 ml 10% HCl orally (dairy cows)
  - - - Don't graze heavily pregnant ewes carrying multiples on green pasture
    - - Keep dry cow ration low in Ca
        
        Additives added to normal ration to bind Ca, then removed at parturition -> ensure responsive Ca absorption system at parturition
        
        Zeolite A (NaAlSilicate)
        
        Calcigard
      - 🌟Acidify the steam up diet (3w b4 parturition)
        
        Increased Ca++ & ⬆ PTH action
        
        ⬆ Cl + S (Anionic Salts), ⬇ K +Na: DCAD must be reduced to -100 - 200meq/kg
        DCAD increased to 225 meq/kg after partus - Fresh Cow Ration
        
        🙈 Anionic Salts are unpalatable, must be added to a palatable concentrate
        
        HCL (BIO-CHLOR’, ‘NUTRI-CHLOR) can replace some of he anionic salts - doesn't affect palatability
        
        Calculating DCAB
        
        Converting % to milliequivalence
        
        (0.15Ca + 0.15Mg + Na + K) – (Cl + 0.6S + 0.5P)
        
        If DCAB <200 meq/kg, can add anionic salts to decrease to 0 mEq/kg
        
        If DCAB >200 mEq/kg, switch Lucerne, fertilized hay -> mielie silage (lower in K)
        
        Monitoring Diet
        
        Spot tests - urine must be between 6-6.8
        
        If Mg low, add 25g Mg / cow
        
        ⚠ Overdose of Anionic Salts -> Metabolic Acidosis
- - - - High yielding lactating dairy cows / goats, esp over 3rd lactation
      - 3rd - 6th week lactation
    - - Secondary Type 1 Ketosis: Accumulation of Ketones due to anorexia resulting from disease
      - Primary Type 1 Ketosis: NEB -> Oxaloacetate Deficiency
        
        Glucose loss in milk continues despite cow's nutritional state
        
        Excess production of ketone bodies due to insufficient oxaloacetate
        
        Low glucose -> Low Insulin -> Hormone sensitive lipase -> breakdown of fat -> NEFA -> Acetyl CoA -> Ketone Bodies
    - - Insufficient glucose to the brain
        
        Anorexia
    - - Ketonaemia
      - Ketouria
      - Hypoglycaemia
    - - 50% recover spontaneously, mortalities are rare - more of a production loss
    - - deficiency of cobalt and phosphorus
        
        Needed for formation of Vit B12: Co-factor for proprionate to enter CAC
      - stress -> ⬇ DMI
      - lack of exercise
      - silage
      - type of diet
        
        High protein diets
        
        ⬆ Butyrate
        
        Energy needed to excrete N
        
        Rapid change from dry cow to lactation diet
        
        ⬆ Acetic, butyric, ⬇propionic
        
        Grass, maize silage
      - change of diet
      - Cannot physically eat enough during early lactation - depend on fat stores. ⬇ Rumen size and activity peripartum
      - high milk production
      - genetic
    - - 🌟post-partum beta-hydroxybutyrate (BHB)
        
        15 cows / does sampled in the first few days post-partum
        
        1 Subclinical
        
        1.2 = Clinical
      - Urine Ketone Test
    - - Steam Up Diet: good quality silage, hay concentrate- rumen papillae need 5w to adapt to energy rich lactation ration
      - Monensin + Ionophores ->⬆ Propionic Acid Production
    - - Propylene glycol
      - Glucocorticoids
      - Monensin
      - Dextrose
  - - - Fatty infiltration of the liver
    - - Peripartum (vs 3rd = 6th week of lactation with Type 1)
      - High producing dairy cows
      - Late pregnancy in ewes / does carrying multiples
      - Good / excessive BCS
    - - Often leads to death / exaggerated response to common PP diseases
    - - Poor reproduction -> long lactation
      - Flush feeding of sheep
      - Obesity
      - Poor pre-partem diet
      - Pre / postpartem stress
    - - Animal overfed before partus -> ⬆ glucose -> ⬆ insulin
      - Constant high insulin -> Hormone sensitive lipase develops insulin resistance
      - Hormone sensitive lipase becomes oversensitive to other hormonal stimuli - "Adipose sensitivity"
      - Sudden rapid breakdown of fat -> NEFA to liver
        
        Normal Glucose: NEFA to mitochondria (Enzyme CPT1) ( -> Acetyl CoA -> gluconeogenesis / ketogenesis
      - ⬆ Glucose: Citrate overflows from mitochondria to cytoplasm ->⬆ Malonyl CoA
      - Malonyl CoA inhibits CPT1 -> NEFA cannot enter mitochondria
      - NEFA is esterified with glycerol -> macrovesicles in hepatocyte cytoplasm
    - - Increased peripartem conditions + poor response to tX
        
        Mastitis
        
        Metritiis
        
        Displaced abomasum
        
        Ketosis
        
        Lameness
        
        RFM
      - Decreased breeding efficiency (NEFA toxic to oocyte)
      - Many cows BCS >3.5, other <2
    - - Hiistology of liver: 60% of liver volume occupied with fat droplets
      - ⬆ Serum NEFA, bilirubin and AST
      - ⬇ Serum glucose, cholesterol, albumin, magnesium, insulin, WCC.
      - Herd Surveilance
        
        Serum samples of multiparous cows/does for NEFA @ 2-14 days prepartum of 5-15 animals
        
        0.3mEq/l = At Risk
        
        Number foetuses (US)
        
        BCS
    - - Tx frustrating and unrewarding, rather prevent
      - Constantly monitor NEFA for early ID
        
        Clinical Ketosis
        
        Electrolytes
        
        Appetite stmulants
      - Exercise
    - - Reduce stress
      - Emergency C section in mutiparous ewes
      - Good diet management
        
        Condition score mid lactation and adapt diet to manipulate weight before drying off: Must enter dry period @ 3 / 3.5
        
        RBST in last 100d of lactation to prevent obesisty
        
        Daily exercise of dry cows
        
        3: keep her in this condition throughout fry period
        
        Fatten up thin cows before drying off
        
        BCS must not change by more than 1 in dry period
      - Add propylene gycol to fresh cow ration to reduce NEFA
      - Add chromium to reduce insulin resistance
  - - - 70% Acetate (Ketogenic)
        
        Small amount enters the CAC as Acetyl CoA if oxaloacetate is available
        
        Most -> fat synthesis
        
        Animal in a catabolic state -> ketone bodies
        
        Enter the CAC if oxaloacetate is available
        
        Oxidized for E in heart, kidney, skeletal muscle, lactating mammary glands NOT Brain
        
        Oxaloacetate not available: excess Acetyl CoA -> ketone bodies
      - 20% Propionates
        
        Glucogenic: can enter the CAC direclty and form glucose
      - 10% Butyrate (Ketogenic)
        
        Triglycerides
        
        Ketone Bodies
    - - Absorption of sugars / starches from intestine
      - Metabolised from propionic acid
      - Metabolised from Acetyl CoA
  - - - Metabolic acidosis
      - Hypocalcaemia
      - Hypokalaemia
      - Hypoglycaemia
      - Uraemia
- - - - Gradual onset over 3-4 days
      - Inappetance
      - Drop in milk yield
      - Wild facial expression
      - Wide open eyes and rolling of the eyes (dairy goats)
      - Exaggerated limb movements (hyperesthesia)
      - Opisthotonos (dairy goats)
      - Frequent urination and defecation
      - Teeth grinding and extension of the head and neck (goats)
      - Unsteady, wide - stanced gait (ataxia)
      - Tetany and seizures
      - Animals may recover spontaneously or progress to recumbency
      - Relapses and subsequent coma may occur following treatment.
- - - - ⚠ Fed High Ca in dry period -> Calcitonin release -> inhibition of osteoclastic activity. Sudden drop in Ca levels at the start of lactation -> refractory 48-72h before PTH activity
    - - More free Ca and primes PTH receptors