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107 Cards in this Set
- Front
- Back
Describe the different stages of clinical signs in hypoCa |
Stage 1: usually not seen - Brief excitement - Tetany and hypersensitivity - Muscle tremors of head and limbs - Animals disinclined to move - Teeth grinding - Bellowing, open mouth breathing and tonguing - HL muscle tremors - ataxia - Normal/slightly increased temperature Stage 2: - Sternal recumbency, unable to rise, depressed - Head turned into flank "S" bend in neck - Dry muzzle - Low rectal temperatures - GI stasis - HR: 60 - 80bpm - Low venous pressure - "expiratory groans" Stage 3: - Lateral recumbency +/- coma - Rectal temperature low - CO worsens - Rapid pulse, heart sounds faint - Severe bloat |
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What differences in clinical signs would you expect if concurrent hypoMg compared to hypoCa alone? |
If concurrent hypoMg, tetany and hyperaesthesia are present beyond stage 1 HR and RR much more intense |
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How is hypoCa diagnosed? |
Clinical signs and response to treatment Take pre-treatment blood to confirm serum Ca concentrations and check concentrations of other minerals e.g. hypoMg |
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What serum Ca level will cause problems e.g. cow down syndrome? |
0.5 - 2mM |
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What is treatment for hypoCa? |
Give Ca borogluconate IV slowly to effect; monitor HR at all stages Administer another bag Ca salts SC to reduce risk of relapse Another bag in 4 - 6hrs NSAIDs (IV) for muscle soreness
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If diagnosis of hypoCa is correct what signs/changes would you expect to see? |
Belching Muscle tremors Increased amplitude and pressure of pulse Increased heart sound intensity Defaecation and urination Sweat beads on muzzle and lacrimation starts |
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Are P and Mg necessary for treatment of hypoCa? |
No - most animals are hyperMg and serum P levels usually return to normal after Ca administration |
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What is the prognosis for hypoCa? |
Good if responds to initial treatment 60% cases stand shortly after treatment; further 15% stand in 2hrs Poor prognosis if inhalational pneumonia |
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If an animal does not respond in 8 - 12hrs of treatment, what should you do? |
Re-evaluate and check diagnosis May require re-treatment |
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How common are relapses of hypoCa following treatment? |
Common - of the cows responding to initial treatment 25 - 30% relapse within 24 - 48hrs |
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How can hypoCa relapses be prevented? |
Drench cow with oral Ca chloride e.g. Calcoral Gel® for 2 - 3days after initial treatment Do not milk the cow right out (48hrs) Don't allow calf unlimited access |
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How should a cow be managed that remains down after treatment for hypoCa? |
Ensure access to feed and water Provide non-slip bedding Sit in sternal not lateral recumbency |
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How is the risk of hypoCa minimised on a herd level? |
Balanced transition (springer) ration |
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Why should a transition diet be fed? |
1) Introduce concentrates to diet and adapt rumen microflora before calling to reduce risk of acidosis 2) Encourage bone calcium mobilisation, reducing milk fever risk in periparturient period |
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What is the aims of the transition cow diet? |
To induce mild metabolic acidosis to increase Ca mobilisation from bone and enhances Ca absorption from intestine Goal = induce mild metabolic acidosis to reduce risk of hypoCa |
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What are the basic principles of when/how long to feed transition diet? |
Feed transition diet for 21days before calving Feed for at least 10 - 14days Do not feed for >21days (increases milk fever risk again) |
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What should the DCAD (dietary cation anion difference) be in the springer cow transition diet? |
Negative DCAD (+5 to -5meq/100g DM) |
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What is the DCAD of lactating cows? |
Positive (+25 to +30 meq/100g DM) |
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What is the goal of positive DCAD in lactating cow ration? |
To neutralise acids from rumen fermentation and systemic metabolism |
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True or false: almost all forage rations result in positive DCAD |
True |
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What will diets high in K and Na result in? |
Positive DCAD - metabolic alkalosis - alkaline environment within bone cells reduces osteoclast activity - decreases Ca mobilisation from bone |
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Explain how negative DCAD reduces milk fever |
Negative DCAD - mild metabolic acidosis - increases osteoclast activity which increases Ca mobilisation from bone; increases Ca absorption from GIT |
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True or false: lucerne and kikuyu diets are low in K so suited to springer cow transition diet |
False - lucerne and kikuyu are high in K and result in positive DCAD Remember: almost all forage rations result in positive DCAD |
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When is monitoring DCAD with urine pH of use? |
Only useful when anionic salts are used and DCAD is negative Measure 3 - 7days after changing the ration |
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What is the target urine pH for Holesteins and Jerseys when using anionic salts and DCAD is negative? |
Jerseys = 5.8 - 6.3 pH Holsteins = 6.2 - 6.8 pH |
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What minerals will affect milk fever risk independent of DCAD? |
Ca Mg P |
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Why are minerals (Ca, Mg, P) not included in DCAD equation? |
Because they impact milk fever independent of DCAD |
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What is the recommended % Ca in the pre-calving ration? |
Keep Ca to 0.4 - 0.6% DM in pre-calving ration |
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What should the concentration of Mg be in the diet before calving i.e. pre-calving ration? |
Mg concentration in diet should be at least 0.45% of DM before calving |
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What is better at increasing Mg concentration in the blood, MgO or MgSO4? |
MgO |
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What P concentration should be fed in pre-calving ration? |
<0.4% |
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What causes grass tetany? |
HypoMg - associated with low serum Mg2+ levels |
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What groups of animals does hypoMg occur commonly? |
Lactating cows Young calves fed whole milk |
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What 2 forms of Mg are present in serum? |
1) Protein bound 2) Free and ionised |
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What % of Mg is found in bone compared to soft tissue? |
70% in bone - unavailable 30% in soft tissue - critical for bodily function |
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What will lead to development of hypoMg |
Lactating cows lose large quantities of Mg through milk. When intake is insufficient, hypoMg will occur |
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What is the pathogenesis of hypoMg? |
Mg is required for oxidative phosphorylation and the metabolism of CHO, lipids, proteins and nucleic acids Role in maintenance of normal RMP of nervous tissue, bone formation and ATP reactions Low Mg: Ca ratios potentiate acetylcholine release - muscle tetany |
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What are the 5 contributing factors of hypoMg? |
1) Diet 2) Season 3) P and Ca 4) Animal/individual 5) Environment |
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What dietary factors will contribute to hypoMg? |
1) High K intakes (decreases Mg absorption from GIT) 2) High CP intake, high rumen NH3 and low fermentable CHO (decrease Mg availability) 3) High lipid/fatty acid concentration (react with Mg to form Mg soaps - unavailable) 4) High rumen pH (reduce solubility of Mg in rumen) |
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What dietary supplement can be added to ration to increase Mg absorption and retention? |
Ionophores |
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What seasonal changes increase risk of hypoMg? |
Winter calving cows at greatest risk - cold, lush pastures low in soluble CHO, high in N and fats Also have increased demand for Ca and Mg in milk at this time Cows absorb less Ca from pasture during winter when grasses are immature |
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How do Ca and P contribute to hypoMg? |
Low rumen P concentrations impairs Mg absorption Low serum Ca levels may lead to development of grass tetany |
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What animal factors can contribute to hypoMg? |
1) Age - decreased absorption Mg with age 2) Breed (angus and angus X) 3) High milk production - loss of Mg in milk; concentration of Mg in colostrum is 2 - 3times more than milk (increased immediate demand following calving) |
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What environmental factors contribute to hypoMg? |
Environmental stressors at critical time may also trigger grass tetany in lactating cows - Exposure to bad weather, wind and rain - Sudden change feed quality/quantity - Low temperatures - Mustering/moving - Transport esp. last 6 weeks of pregnancy |
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What are the acute clinical signs of hypoMg? |
Stop grazing Very alert - twitching of ears/muzzle Animals may gallop wild in frenzy or charge Progression to staggering, lateral recumbency with frantic paddling and convulsions Opisthotonus Nystagmus Champing of jaws and clicking eyelids Head arches, mouth frothing Temp 41C, sweating Increased HR/RR Death 30 - 60min |
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What is mortality rate of hypoMg? |
High Death usually 30 - 60mins of onset of clinical signs |
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What signs may be seen in sub-acute phase of hypoMg? |
Gradual onset with stress increasing risk Slight inappetence Wild facial expression, exaggerated limb movements Difficult to drive Spasmodic/frequent urination and defaecatio Milk yield and ruminal movements decrease Blinking and clicking of eyelids when approached Fine muscle tremors Excitement causes convulsions Animals may recover spontaneously or progress to recumbency |
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What are chronic signs of hypoMg? |
Vague signs - dullness Ill-thrift Indifferent appetite |
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How is hypoMg diagnosed? |
1) Often on clinical signs 2) Pre-treatment bloods to assess Mg and Ca levels 3) Necropsy - collect samples - Serum (cardiac puncture) - CSF - Urine (up to 12hrs after death) - Enucleated intact eye for aqueous or vitreous humour (up to 48hrs after death if temp. <23C)
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Explain replacement therapy for hypoMg? |
Mg hypophosphate IV given slowly; monitor heart throughout treatment Or 5% Mg sulphate (Magnesate) diluted in 1L of saline and given IV (off label) Give Mg-Ca combination if suspect animal is also hypoCa
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Mg toxicity during treatment for hypoMg will result in death through what mechanism? |
Respiratory failure - Mg salts are toxic and can cause respiratory failure when given IV so need to give slowly and monitor heart throughout treatment |
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How long after replacement treatment for hypoMg should you see clinical improvement? |
3 - 5hrs |
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What do you need to warn owners of following treatment for hypoMg? |
Cow may die during convulsion even after treatment Relapses are common within 3 - 6hrs |
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What should be given to minimise relapses of hypoMg? |
Give MgSO4 SC or "Cal-Jet Oral®" PO Provide legume hay |
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If a cow is seen having convulsions due to hypoMg, what should be done? |
Sedation therapy - IV chloral hydrate Put into sternal recumbency |
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How can hypoMg be prevented? |
1) Supplementation Mg oxide contains highest concentration of Mg however Mg sulphate (epsom salts) are more available for absorption It takes 2 - 3days before stock are protected 2) Management |
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What is the daily requirement of Mg for cattle? |
30 - 40g/hd/day Cows need continuous supply of Mg because of high turn over |
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List methods of Mg supplementation |
Loose lick Mg treated hay Mg added to grain mix Medicated water troughs (need to be sole water source) Mg bullets - expensive but provide 80 -90d protection; give >1week before high risk period Mg blocks - high cost, all cows may not use |
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What management strategies can be employed to prevent hypoMg? |
- Avoid grazing cattle on new grass until it is 4 - 6inches tall (mature grass) - Graze mixed legume-grass pastures (>20% clover) and feed legume hay; if no legume hay available, feed any hay, straw or silage will reduce rumen flow rates and increase absorption of Mg and Ca - ID high risk paddocks and graze with low risk stock (i.e. not early lactating cows) - Feed Mg supplement - Provide shelter - Avoid calving older cows in winter and manage older fat cows in separate high risk group - Mg fertiliser and dolomitic limestone can be applied to soil to increase Mg concentration in plants - Dusting pastures with MgO increases Mg intake but often not cost effective |
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What causes ketosis? |
Multifactorial disorder of energy metabolism where breakdown products of fat metabolism accumulate in body fluids |
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What is ketosis characterised by? |
Hypoglycaemia Ketonaemia Ketonuria |
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When does ketosis usually occur? |
In the first 6 weeks of lactation Can affect a large proportion of the cows in early lactation in a herd |
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What cows are at most risk of ketosis? |
Dairy cows in early lactation |
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What are the risk factors for ketosis? |
Periparturient period (<60days post calving) Increased age (peak incidence 3rd - 6th lactation) Increased milk production Low E, high protein diets Obesity at calving Occasionally prepartum - twin bearing cows on low E diets are at increased risk |
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In terms of affect on production, what is associated with ketosis? |
Reduced milk production Reduced reproductive efficiency |
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What is the pathogenesis of ketosis? |
Ruminants rely on gluconeogenesis to maintain glucose homeostasis, in late pregnancy and early lactation, cows are often in a negative energy balance (low propionate and amino acids) - mobilisation of NEFAs from adipose tissue is stimulates by low glucose, low insulin and high lipolytic hormones - NEFAs either enter ketogenic pathway (ketogenesis) with oxidation to ketone bodies in liver, or esterification pathway with hepatic conversion to TG favouring fatty liver development NEFAs that enter ketogenic pathway predisposes to development of clinical ketosis
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What 2 pathways can NEFAs enter? |
1) Ketogenic pathway (ketogenesis) - oxidation to ketone bodies in liver 2) Esterification pathway - hepatic conversion to TG favouring development of fatty liver |
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What determines whether ketogenesis or esterification of NEFAs occurs? |
Glucose - low glucose (propionate) favours ketogenesis |
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What are the 3 categories of ketosis? |
1) Alimentary ketosis 2) Primary underfeeding ketosis 3) Secondary underfeeding ketosis |
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In alimentary ketosis, what is the cause? What should be checked in this case? |
Excessive intake of butyrate in silages and possible inappetence Need to check the diet |
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What causes primary underfeeding ketosis? |
Poor BCS and poor quality feeds means there is limited gluconeogenesis Low dietary CP is associated with decreased fermentation rates in rumen and DMI Need to check diet to ensure adequate CP
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What causes secondary underfeeding ketosis? What should be checked in this case? |
Caused by a decrease in voluntary feed intake due to underlining disease e.g. acidosis on herd scale Need to check lactating cow and transition cow diet for explanations of underlying disease |
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What are the 2 forms of ketosis? |
1) Wasting form 2) Nervous form |
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What clinical signs occur with the wasting form of ketosis? |
Depression Reduced feed intake - may still eat hay Decreased milk production Normal temperature, HR, RR Poor rumen contractions May be able to smell acetone on breath |
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What changes on clinical pathology occur in ketosis? |
- Hypoglycaemia - Ketonaemia - Ketonuria +/- elevated liver enzymes |
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What are the aims of treatment for ketosis? |
Restore blood glucose levels Correct clinical signs of ketosis |
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What is the replacement therapy for ketosis? |
Propionate precursors PO e.g. propylene glycol +/- IV glucose therapy |
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What can be given for hormonal/supportive therapy of ketosis? |
- Corticosteroids - commonly used - Anabolic steroids - Protamine Zn insulin - B group Vitamins - Digestive tract stimulants e.g. Clanobutin sodium |
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How do corticosteroids treat ketosis? |
Cause decreased peripheral utilisation of glucose in muscle and fat and increased Acetyl CoA utilisation - repartitioning of glucose rather than gluconeogenesis Cause hyperglycaemia within 24hrs of administration; 40mg dexamethasone sodium phosphate can produce hyperglycaemia in ketotic animals for 4 - 6days |
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How do anabolic steroid treat ketosis? |
Decrease blood ketone levels and stimulate appetite |
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Why are B group vitamins used in treatment of ketosis? |
Niacin increases blood glucose and decreases blood ketones |
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How does insulin therapy (Protamine Zn Insulin) treat ketosis? |
- Promotes cellular uptake of glucose - Suppresses fatty acid metabolism - Stimulates hepatic gluconeogenesis |
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How should ketosis be prevented? |
- Avoid poor-quality silages that may contain large amounts of butyrate esp. in immediate postpartum risk period - Manage BCS: > 3.5/5 greatly increases risk of ketosis - Ensure concentrate: forage ratio of 55 - 65: 45 - 35 in early lactating cow diets with NSC ~36% - Feed good transition diet and high quality forages to early lactating dairy cows - Limit protein concentrations to 16 - 18% - Ensure dietary vitamins/minerals are adequate - ID at risk animals early (weekly milk ketone tests) - Ionophores e.g. Monensin increases propionate % by modifying rumen flora |
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What BCS increases risk of ketosis? |
>3.5/5 |
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What should the concentrate: forage ratio be to prevent ketosis in early lactating cows? |
55 - 65: 45 - 35 in early lactating cow diets with NSC ~36% |
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What should protein concentrations be kept to in early lactating cow ration to avoid ketosis? |
16 - 18% |
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True or false: monensin reduces the risk of ketosis |
True - increases propionate % by modifying rumen flora |
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Define "downer cow syndrome" |
Paresis of unknown origin that affects 3 - 5% of cows in herd, most commonly first week after calving |
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What cows are most prone to downer cow syndrome? |
High producing dairy cows are most prone |
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What are the clinical signs of downer cow syndrome? |
BAR Appetite and thirst normal Temp and vital signs normal Unable to stand following treatment for milk fever Most will stand in few days provided good care Occasionally may see bizarre nervous signs (paddling, lateral recumbency) and death in a few days |
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What clinical pathology changes occur with downer cow syndrome? |
Increased serum and AST levels Serum P and K levels may be subnormal |
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What is the treatment for downer cow syndrome? |
Provide feed and water and good bedding on non-slip surface Roll animal from side to side every few hours Fluid and electrolyte therapy as required +/- NSAIDs |
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What is the prognosis for downer cow syndrome? |
Depends on mental state (depression or anorexia) The longer the animal down, the poorer the prognosis |
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What causes ephemeral fever? |
Rhabdovirus from blood of clinically affected animals |
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When/how long will a cow with ephemeral fever be infective? |
An animal is infective from later part of incubation period to day 4 after the fever has subsided |
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True or false: vectors have a role in spreading ephemeral fever |
True - spread via insect vectors e.g. mosquitos |
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Where is ephemeral fever endemic? |
Northern Australia (epizootic in southern Australia) |
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When is ephemeral fever most common? |
Over summer (mosquito vectors) |
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What is the incubation period of ephemeral fever? |
2 - 10days |
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What are the clinical signs of ephemeral fever? |
THINK FLU: - Shivering - Lameness - Prostration - Adult animals more severely affected than calves - Sudden onset - Pyrexia (40 - 42C) sometimes with a morning remission - Increased HR, RR - Decreased rumen sounds - Head shaking - Shivering, muscle trembling, weakness - Slobbering, mucous discharge from nose - Watery discharge from eyes - Profound anorexia - Usually severe constipation (occasionally diarrhoea) - Drop in milk production - Enlargement of peripheral LN - Occasionally joint enlargement +/- hypoCa |
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True or false: calves are more severely affected than adult animals by ephemeral fever |
False - calves are least affected; adult animals (esp. fat cows and bulls) are worst affected |
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In a dairy farm, what group of cows are at most risk? |
High producing cows |
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Progression of clinical signs of ephemeral fever leads to what? |
Lameness Weakness (day 2) Downer cows |
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How is ephemeral fever diagnosed? |
Paired blood samples - serum neutralisation Examine blood CBC (blood clots poorly in febrile stage) |
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List differential diagnosis for ephemeral fever |
Botulism HypoCa Pneumonia Traumatic reticulitis |
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How is ephemeral fever treated? |
NSAIDs IVFT Treat concurrent hypoCa Good nursing of downer cows - food, water, bedding |
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Is vaccination against ephemeral fever available in Australia? |
Yes: 2 doses given 2 - 4wk intervals to give immunity for 12mths from 6mths of age; yearly booster vaccination is recommended |