User:Bbyrudown?/sandbox

Scenario
During a routine fertility visit you are asked to examine 2 calves (one steer and one heifer, approximately 150 kg) which have been down for several days. Both animals are bright and alert, eating and defecating. Both were unable to stand and had been down for several days. The steer had significant swelling of both hind limbs. The amount of swelling made it impossible to palpate the bones of the limbs or flex and extend the legs. The heifer calf had crepitus palpable in one hind leg.

You have a full schedule of visits today, so you elect to collect blood and have asked the farm manager for farm records including ration fed to calves and any recent changes. Blood work on the steer reveals the following findings:

The calves are fed the following diet: 1.5kg Barley grain 1.5kg DDG (dried distiller’s grain) Unknown amount of Oaten Hay (you estimate the maximum must be 1.5kg, as this comes to a total feed intake of 3% of bodyweight (2.8% of bodyweight as DM). 50g of RT50 (specifications are not supplied, but you are informed by the client this is a trace element (not macromineral) and monensin additive. You discover components of RT50 to be Co, Cu, I, Mn, Se, Zn, vit. A, B, E (from the students summary doc)

The client has been feeding his calves this ration for 6 months having changed from using a traditional calf rearer pellet on the basis that the new ration is less expensive. The calves are in an outside paddock with minimal grass present and rely solely on the ration to meet nutritional and energy demands Chemistry Results are as follows

Questions

1. What are your differential diagnoses for recumbent weaner stock based on this presentation and clinical history?

Clinical findings Interpretation Down / recumbent for several days Metabolic Hypocalcemia: Lack of calcium in the diet Low Ca intake Low Vit D intake Low dietary Mg 9cofactor by PTH messengers) Acid:base (dec pH= inc PTH activity) High phosphorous in diet= dec renal phosphorylation of 25-dihydroxyvitamin D (Vit D required absorption of Ca++ from gut) Older age Breed: Jerseys more susceptible in regards to lactating cows Inc dietary fat Hypophosphatemia Bright-eyed downer Chronic P deficiency= chronic rickettsia & osteomalacia in calves Acute P deficiency= metabolic disorder Hypocalcemia → PTH increases → phosphorous losses from kidneys and salivary glands -ve energy balance Increase glucose demand by tissues Decrease DMI (decrease diet palatability, increase anionic salt, increased fibre content) Hypomg (also leading to hypoCa) GI absorption inhibited by high dietary K or protein and low sodium Demands on tissue requirements and renal excretion Infectious causes Botulism No: not flaccid paralysis Tetanus No: the absence of rigidity and spasms & not generalized (only bilateral in one and unilateral in the other) Bovine ephemeral fever (3d sickness) No: no evidence of fever, not 3d since down for 7d, CSx & environment don’t match Downer cows Neuropathies: femoral nn., sciatic nn. Ischaemic myonecrosis: CK and AST elevated, usually affects hamstring m. group (AST less sensitive indicator of compartment syndrome.- Secondary? MSK injury Joint luxation Fractures: Inc risk with inadequate dietary Ca++/ Ca:P ration or Cu deficiency (Cu component for collagen production → suppressed osteoblastic activity → osteoporosis → fractures)/ nutritional sec hyperPT/ prolonged feeding of DCAD diet (to milkers)

Steer - Bilateral hind limb swelling (impalpable bones or unable to flex/extend) (due to fractures & haematomas) Fractures: Inc risk with inadequate dietary Ca++/ Ca:P ration or Cu deficiency (Cu component for collagen production → suppressed osteoblastic activity → osteoporosis → fractures)/ nutritional sec hyperPT/ prolonged feeding of DCAD diet (to milkers) Hematomas Traumatic (from fractures) Vascular defect Swelling: Inflammation Protein loss (dec intake, increase a loss from GIT/renal)

Heifer - Unilateral HL crepitus OA- pseudocrepitus Tenosynovitis Spondylitis (spine and large joints) Joint luxation - pseudocrepitus Fracture (where close to the femoral head) Pathognomic Bony crepitus - gritting sensation transmitted to the palpating fingers by the contact of the broken bone ends on each other.

Elevated CK Rhabdomyolysis

Tentative diagnosis: Pathological fracture associated with nutritional metabolic bone disease (prolonged dietary imbalance ⇒ low dietary P and Ca +/- VitD, Mg)

2. What about the diet, physical examination, post mortem findings and clinical pathology allows you formulate a tentative diagnosis for this cracking case. Including additional testing or parameters to evaluate to reach a definitive diagnosis.

Diet

1.5kg Barley grain:

1.5kg DDG (Dried Distiller’s Grain)

Unknown amount of Oaten Hay (you estimate the maximum must be 1.5kg, as this comes to a total feed intake of 3% of bodyweight (2.8% of bodyweight as DM). ((is oat hay the same as oaten hay??)) Oat hay:

50g of RT50 (specifications are not supplied, but you are informed by the client this is a trace element (not macromineral) and monensin additive. Components of RT50 to be Co, Cu, I, Mn, Se, Zn, vit. A, B, E

Physical Examination BAR Eating, defecating Unable to stand (down for several days → downer cow) Steer: significant swelling of both hindlimbs Impossible to palpate bones or flex/extend the legs Heifer: crepitus in one hindlimb

Post-mortem Findings

Fractured vertebrae, with hemorrhage in spinal cord

Comminuted fracture of the femur Clinical Pathology Normal AST Mild increase in CK → Skeletal muscle disease/damage, HypoT, autoimmune disease, exertional disorders

PCV + TPP normal Fibrinogen normal

3. What are your recommendations to treat current cases and to prevent further cases from occurring. Include the aetiology of the disease process and advice to the client. We need to take the food and perform a ration analysis Once the analysis is performed we need to reformulate the ration and supplements to meet the nutritional requirements

Mild metabolic acidosis induced by diets with negative DCAB > increased production of vitamin D3 per unit of increase of PTH (due to upregulation) > target tissues are more sensitive to PTH and 1,25(OH)2D3 > increased calcium mobilisation from bone → E.g. Diet treated with HCl drops urine + blood pH à more mobilisation (and excretion) of Ca Fractures: Inc risk with inadequate dietary Ca++/ Ca:P ratio or Cu deficiency (Cu component for collagen production → suppressed osteoblastic activity → osteoporosis → fractures)/ nutritional sec hyperPT/ prolonged feeding of DCAD diet (to milkers)

Aetiology of disease has been written in varsha/rav section

PTH Mechanism -       Increase plasma calcium -       Regulates bone calcium mobilisation when there is a decline in blood Ca through increase osteoclastic activity (mobilises Ca from bone) -       Enhances renal tubular reabsorption of Ca -        Stimulates hydroxylation of 25-hydroxyvitamin D by the kidney to form 1,25(OH)2D3 (activates vitamin D in within the kidney) -       High dietary phosphorus inhibits renal activation of VitD -       Vitamin D regulate the production of calcium transport proteins within GIT and enterocytes -       Factors affecting PTH secretion -       Hypomagnesemia – ­ risk of hypoCa -       This can blunt the effects of hypocalcaemia response -       Low calcium diets – -       Low Ca > ­ PTH receptor receptiveness > PTH secretion > osteoclastic bone resorption > renal production of 1,25(OH)2D3 > increases bone Ca efflux > intestines are ready to absorb Ca efficiently should it become available