Mid Sem. Flashcards
1
Q
What are some health issues associated with acidosis?
A
Rumenitis Metabolic acidosis Laminitis Liver abscess Pneumonia Death
2
Q
Describe the impact of acidosis on the rumen?
A
Most likely after rapid ingestion of starch or other readily fermentable CHO.
Conversion to glucose varies with grains and processing - higher energy and acidosis risk positively correlated.
Free glucose in rumen; certain bacteria become more competitive and produce lactate, other opportunistic microbes thrive and can release endotoxins or amides, increased osmolality of rumen contents can increase acid accumulation by reducing VFA and lactic acid absorption.
3
Q
What are some methods for controlling acidosis?
A
- Limit starch and glucose - control starch intake (source and type, regular feed intake, introduce slowly), dilute with roughage (saliva and decreased intake), Protozoa (can stabilise pH by engulfing starch.
- Control glycolysis and the controlling rate - anaerobic microbes thrive on free glucose in rumen which isn’t normally available, metabolic inhibitors can be administered to rumen to retard glycolysis and reduce acidosis.
- Controlling VFA and lactate production and utilisation - lactate users sensitive to low pH, lactate producers not. VFA rapidly absorbed but if production exceeds absorption then pH can fall without lactate. Ionophore use to limit lactate producers.
- Control ruminal pH - bases or buffers (bicarbonate), or feeds that produce these.
- Control ruminal osmolarity - normally 240-300mOsm/L, acidosis increases this and draws water from blood to rumen (swelling, decreased intake, liver abscess due to bacteria entering blood). Control by reducing minerals or increasing saliva.
- Acid absorption control - lactate and VFA absorbed passively and at greater rate when conc high, pH low and osmolality normal. In chronic cases; increased pH reduces acid absorption and stimulates lactate use.
- Control blood pH - bicarbonate major buffer, manipulating DCAD can influence (increased cations = increased pH).
- Control blood osmolarity - ruminal osmolarity increases with acidosis, hoof damage associated with increased blood vessel damage in hoof due to high blood pressure and histamine conc. Feed intake and salivation reduced (increased roughage and water intake, adequate cofactors for VFA metabolism).
4
Q
What are some indirect indicators of acidosis?
A
Scouring - colour, consistency, smell, umdigested materials, bubbles.
Reduced milk fat, feed intake. LWG, cud chewing, laminitis
5
Q
How do you treat acidosis?
A
Feed hay
If condition worsens drench with normal rumen fluid, sodium bicarbonate.
Vet attention for expensive animals - surgical removal of rumen contents and replacing with normal rumen fluid, IV fluids to prevent dehydration.
6
Q
What are some general management recommendations for acidosis?
A
Recognise weather can influence risk - cold increases intake, hot decreases fibre, rumination and salivation.
Ensure enough fibre - dairy >32%NDF, feedlot >30%
Introduce or change grain slowly
Don’t let feed troughs get empty
7
Q
Describe the energy requirements of a lactating cow?
A
Glucose requirement increases 250%
Amino acid requirement increases 200%
8
Q
What are the energy requirements of a pregnant cow?
A
Foetal placental requirement represents 45% of the maternal glucose and 72% of the maternal AA supply.
9
Q
What is fatty liver disease?
A
Occurs during first few weeks of lactation
Large amounts of NEFAs are delivered to the liver.
NEFA in liver can either be; esterfied into triglycerides, oxidised to CO2 and ketones.
Triglycerides accumulate in parenchyma of liver.
May be associated with ketosis.
10
Q
High body condition in dairy herds increases the risk of….
A
Metritis Ketosis Milk fever Cystic ovaries All reduce conception rate and increase days open. Poor fertility.
11
Q
Why are high body condition score cows at greater risk?
A
Lower dry matter intake due to decreased room
Greater negative energy balance
Greater risk of metabolic issues
12
Q
What are the clinical signs of ketosis?
A
Reduced appetite, milk production. Excess loss of body weight Neurological signs Hard dry faeces High serum conc of NEFA And ketone bodies, low conc of glucose.
13
Q
What are the critical thresholds for risk of clinical ketosis?
A
Prepartum - NEFA 0.29mEq/L
Postpartum - NEFA 0.57mEq/L, BHB 10mg/dL
14
Q
What are the clinical signs of preg tox?
A
Separated from rest of mob Lethargy Not eating Stiff gait Nervous system signs - tremors, blindness, stumbling Lying on side for 3-4days Death 3-4 days later
15
Q
What are the sub clinical signs of preg tox?
A
Elevated BHB conc
Low glucose conc
Liver is yellow with fine mottled appearance
Plentiful abdominal fat although animal emaciated
Very little content in rumen
16
Q
Why do sheep show depression in preg tox?
A
Under conditions of ketosis, glucose consumption is decreased in the cortex and cerebellum by about 10% per mM of plasma ketone bodies.
17
Q
Nutritional disorders and pathology may arise from the presence of contaminants within feedstuffs. Discuss the major factors contributing to contamination of feedstuffs with mycotoxins.
A
Mycotoxin is fungi, factors affecting fungal growth;
Plant stress caused by weather extremes, insect damage, inadequate storage practices, faulty feeding conditions.
Aflatoxins - temp 25-32dc, moisture >12-16%, humidity 85%, delayed harvest to increase maturity and decrease moisture may increase mould growth.
Fusarium - cool, wet conditions during growth, harvest and storage.
18
Q
Identify the major effects of mycotoxins in the health and production of animals.
A
Cause mycotoxicoses. Young are more susceptible.
Primary acute - hepatitis, haemorrhagic disease, epithelial necrosis, death.
Primary chronic - low toxin levels consumed over long period, decreased growth rate, repro efficiency, market quality.
Secondary - low level intake, increased susceptibility to inter current disease and infections, decreased immune processes.
Aflatoxins - severe liver damage (aflatoxin B1 metabolised to aflatoxin M1). GIT dysfunction, anaemia, jaundice, decreased repro and production.
Fusarium - trichothecenes - T2 inhibits protein synthesis, disrupting DNA and RNA synthesis. Irritation, haemorrhage and necrosis in GIT.
19
Q
How can contamination of feeds with mycotoxins be prevented?
A
Store feeds below recommended moisture levels.
Add propionic acid to stored grain, decreases mould as denatures mycotoxins.
UV irradiation deactivates mycotoxins prior to storage.
Heating denatures.
Ammoniation - ammonium hydroxide, gaseous ammonia, denatures mycotoxins (alkaline conditions).
20
Q
Called to provide advice to local feedlot. Cattle are off feed, loose light coloured faeces, rumen fluid samples are pH 4.8-5.5, lactate concentrations 5-50mmol/L. Describe whether you think the feedlot has an acute or subacute ruminal acidosis problem, include a description of each condition.
A
Acute ruminal acidosis - rumen pH <5, marked increase in ruminal acidity.
Sub acute/Chronic - pH <5.6, decreased feed intake, decreased production.
Other clinical signs; blood pH <7.35, diarrhoea, increased lactic acid conc (50-120mM), decreased VFA conc (<100mM), anorexia, variable feed intake, decreased milk production, lethargy.
Problem seems to be largely sub acute though there may be some acute cases due to pH4.8.
21
Q
Describe the physiology of ruminal acidosis, explaining why we see changes in pH, lactate concentrations and osmolality.
A
Acidosis is decrease in alkali content of body fluids relative to acid content. Can be caused by abrupt increase in intake of rapidly fermentable CHO (increased grain or fruit), increases VFA supply and lactate, decreases ruminal pH.
DIAGRAM
22
Q
The feedlot is feeding a ration consisting of 85% cereal grain and 15% corn silage, once daily. Discuss how changes could be made to feed type and management to limit the incidence of acidosis in future.
A
Feedlot ration should have >30%NDF.
Not enough fibre - increase length of corn silage, increased chew and saliva (buffer).
To much grain - decrease grain, increase fibre (decreases intake and rate).
Other options; use metabolic inhibitors that retard glycolysis (decrease acidosis), ionophores (decrease lactate production), bases/buffers (bicarbonate), DCAD ( increased cations, increased pH), ensure feed troughs don’t get empty.
23
Q
Ketosis in cattle and preg tox in sheep are similar conditions. Describe the metabolic causes of ketosis and preg tox, including a discussion on our understanding of why this occurs at a different physiological state for cattle compared to sheep.
A
Ketosis - 3-6weeks postpartum (peak lactation), demand for glucose outstrips gluconeogenesis (supply of glucose precursors insufficient to permit max production). Blood glucose conc and insulin conc is low. Extensive use of NEFAs for ketone synthesis, these enter the hepatic mitochondria.
Preg tox - last 4-6wks gestation, rapid increase in nutritional demands due to rapid foetal development. Decreased quality and quantity of feed. New green pasture; decreased DM, increased H2O. Extreme weather, worms. Hyperketonaemia and hypoglycaemia cause increased ketones and decreased blood glucose.
Occurs due to increased hepatic entry rates of beta-hydroxybutyrate, decreased glucose and insulin. Particularly when twin foetus present. BHB turnover rates are lower in late gestation than lactation, decreased ability to dispose ketones, increased hypoglycaemia by inhibiting hepatic glucose production. Increased negative energy balance by decreasing peripheral glucose uptake (increased ketones and lipolysis).
Sheep add 70% of final birth weight in last 6-8weeks.
DIAGRAM
24
Q
Average plasma BHB levels of 1.8mmol/L is…..
A
Elevated
25
Average serum D-lactate levels of 0.5mmol/L and blood pH of 7.3 are ....
Normal
26
Plasma Ca of 2.2mmol/L is .....
Low
| Normal 2.8-3.2mmol/L
27
Called by producer mid winter as he is loosing late gestation ewes at an alarming rate. Joined in February for 6weeks on basis of high weaning weight, BCS were excellent, early break of season, 50% bearing multiples, vaccinated, pasture growth slowed, clinical signs were listless and isolated, began supplementing with oats. What do you think the primary cause of mortality is? Are there any secondary conditions?
Primary cause is preg tox.
Secondary condition is hypocalcaemia.
Exacerbates preg tox as decreased plasma glucose, decreased endogenous glucose production.
HYPOCA DOESNT PROMOTE ONSET OF PREG TOX BUT WILL FACILIATE ITS DEVELOPMENT WHEN PRESENT IN COMBINATION WITH HYPERKETONAEMIA.
28
What would you recommend to a producer to decreases loses for preg tox? Both now and in the future.
Recommendations for current; treatment success often low, SC insulin (0.4 U/kg x 1day) and oral glucose precursor therapy with electrolytes (Ca, Na, K).
Prevention for future; maintain BCS 3/5, maintain appetite and energy intake, avoid handling in late gestation, ensure twinning ewes have adequate pasture (1500kg/ha high quality).
29
List three major antinutritional factors associated with concentrates and roughages.
Lectins: grains, legumes
Phytates: cereal grains
Tannins: Lucerne, ryegrass
30
Using examples, describe how and why some antinutritional factors can be either harmful or beneficial to the animal.
Tannins; either hydrolysable or condensed. CTs decrease nutrient utilisation by forming complexes with proteins in high concentrations for ruminants. Decrease feed intake, gut enzyme activity and therefore passage through wall. Low concentration of CTs can increase production; Ruminants can affect milk, wool, Ovulation rate and lambing %, decrease bloat risk, decrease internal parasites. CT-adverse to monogastrics, decrease growth, protein utilisation, damage GIT mucous, increase excretion of protein and essential AA. Decreased growth and egg production in poultry, also intestinal damage and death.
HTs. - conjugated in liver where its derivatives are hepatotoxic and nephrotoxic. Necrosis of liver and kidney leads to death.
Lectins; CHO binding proteins, bind to epithelial cells affecting cellular proliferation and turnover (increased shedding of brush border, cell loss and decreased enterocytes). Decreased absorption due to loss of surface area.
Phytates; chelate with mineral ions (making unavailable). Adding phytase increases digestibilty therefore increasing performance (piglets, broilers).
31
In crevid/new world camelid nutrition, which nutrients are the most at risk of being deficient?
Deer - copper
Crias - iron
NW camelids - vitamin D, thiamine.
HypoCa 3-4 weeks postpartum (peak lactation)
32
Describe the signs that indicate a cervid/camelid is suffering from copper deficiency.
Deer have increased requirements compared to other stock.
Steely coat, excess shedding
Uncoordination, joint abnormalities
Decreased growth, general ill thrift, decreased immunity, decreased velvet yields.
33
Describe the signs that indicate a cervid/camelid is suffering from iron deficiency.
Most common in Crias.
Decreased growth, chronic weight loss.
Non-regenerative microcytic hypochromic anaemia.
34
Describe the signs that indicate a cervid/camelid is suffering from vitamin D deficiency.
Thick hair coat and pigmentation to protect again solar radiation in high Andes.
Winter at low altitudes or high latitudes.
Decreased growth.
Reluctance to move, humped back stance.
Shifting leg lameness.
35
Describe the signs that indicate a cervid/camelid is suffering from thiamine deficiency.
```
Also known as polioencephalomalacia.
Depression
Seizures
Blindness
Hyperaesthesia
Sudden death
```
36
Describe the major considerations in the nutritional management of new world camelids to minimise health problems and enhance productivity.
Microbial population similar to ruminants
Increased VFA absorption, increased fermentation chamber pH.
Decreased particulate passage rate compared to ruminants.
Evolved to graze coarse, highly lignified material.
Vitamin A and E decrease when feeding hay.
BW first breeding 60%MW, growth should continue during preg.
Critical periods relate to physiological development of cria and annual production cycle. For parturition; demands on rapid foetal growth, onset of lactation, rebreeding (within 1 month).
Don't allow to become obese during non-productive period.
Wean 4-6months, feed levels at maintenance or slightly increased to regain BCS lost during lactation.
Obesity predisposes to hepatic lipidosis.
Underfeeding during late gestation increases risk of preg tox.
Excessively low nutrition during early/mid preg can cause embryonic death.
37
What is the antidote to cyanide poisoning?
Sodium thiosulphate
38
What is the antidote to nitrate/nitrite toxicity in cattle?
Methylene blue
39
Which is more toxic, the nitrate or nitrite ion?
Nitrite.
40
What does the nitrite ion do?
Convert haemoglobin to methaemoglobin.
41
True or false, diets rich in readily fermentable CHOs increase nitrite production in ruminants
True
| Also increases its conversion to ammonia
42
Of the spleen, bile, urine and liver, which would be the best to test for toxins?
Liver
| Oleandrin, cyanide, pyrrolizidine alkaloids.
43
List domestic animals in descending order according to their susceptibility to aflatoxins.
Cattle > sheep > pig > chicken
44
What are the major targets of Cyanobacteria?
Hepatotoxic
Neurotoxic
Cardiotoxic
45
What is the major toxic effect of hydrogen cyanide?
Inhibition of mitochondrial respiration.
46
True or false, cardiac glycosides stimulate parasympathetic discharge.
True.
47
What toxin comes from the castor oil plant?
Ricin
48
Which species is highly susceptible to zearalenone toxicity?
Porcine
49
What is the major organ responsible for detoxification in the body?
Liver
50
Zearalenone is ......
Non-steroidal oestrogenic compound.
51
Glucosinolates are defined as......
Goitrogens
| Degraded to thiocyanites in rumen, interfere with iodine absorption.
52
What is one of the most com one aflatoxins?
Aspergillus
53
True or false, phytase cleaves physic acid to release phosphorus and calcium.
True
| Depending on what it is bound to, may also be Mg, Zn, Fe, Cu
54
In acute cases of poisoning, activated charcoal acts to reduce absorption of the substance by;
Binding to poison molecules.
55
Which toxins are produced by Fusarium?
Deoxynivalenol
T2
Zearalanone
56
List four factors that affect susceptibility to pyrrolizidine alkaloid toxicity.
Previous exposure - more susceptible to relapse.
Species - small herbivores highly resistant.
Level of exposure
Age - young more susceptible.
57
Which species are most susceptible to pyrrolizidine alkaloid toxicity and why?
Pigs
Monogastrics and don't have necessary microorganisms to break down PA. Causes liver and kidney tissue to slowly be destroyed.
58
Under what circumstances are animals most commonly poisoned by pyrrolizidine alkaloid containing plants?
Lack of other available feed - hunger or more dominant animal takes feed
Boredom
Young animals - increased curiosity, decreased detoxification mechanisms
Toxins may be mixed in hay.
59
List 6 samples to be collected when investigating a potential plant poisoning of animals and provide specific reasons as to why these samples are useful.
Ingesta (rumen contents, SI, LI)- allows plant/seed identification, largest range of possible tests including cardiac glycosides, grayanotoxins, alkaloids, tannins, cyanids, ammonia, nitrate/nitrite.
Milk - can be collected form live animal, plant toxins.
Whole blood - live animals, can also get serum from this (nitrate/nitrite, alkaloids, oleandrin), cyanide.
Liver - oleandrin, cyanide, biopsy for pyrrolizidine alkaloids.
Ocular fluid - can be collected from animal dead for a while, nitrate.
Kidney (cortex) - oxalates, sodium fluoroacetate. Only way to test for these.
60
List the major clinical signs of acute nitrate/nitrite toxicity in ruminants.
```
Rapid, deep breathing
Irregular, weak pulse
Muscle weakness, spasms, tremors.
Coma and death
Brown mucous membranes
Abortion 3-7d post toxicity.
```
61
Explain how these clinical signs are related to the mode of action of nitrate/nitrite in ruminants.
Oxidised haemoglobin to methaemoglobin.
| O2 not carried, once meth conc is >75% O2 supply to tissues and vital organs is inadequate.
62
Describe the mechanisms of toxicity of cardiac glycosides.
Cardiac glycosides - induce direct cardiotoxicity and indirect vagaries nerve modulation. Done via inhibiting Na/K/ATPase pump. Increased K concentration in heart ECF and NA in ICF causes increased Ca release.
Ca sequestering mechanisms become insufficient and myocytes maintain tone when not desired leading to sustained contraction, decreased function and rhythm. Vagus nerve decreased AC pacemaker activity.
All cells in body affected however heart is lethal.
63
Describe the mechanisms of toxicity of cyanogenic glycosides.
Cyanide bound to sugars in plants. (Plants protected by two features; contained in cell vacuoles, presence of detoxifying enzymes).
Crushing/mastication release toxin from plant cell vacuoles and exposes them to catabolism by beta-glucosidase and hydroxynitrile lyase present in plant cell cytosol.
Beta- glucosidase and hydroxynitrile are present in rumen as well, pH 6.5-7 favours conversion of toxin to hydrogen cyanide (HCN).
Excess HCN inhibits cytochrome oxidase - blocks reduction of O2, required for cellular respiration, leading to cytotoxic hypoxia.
Myocardium tissue is most affected, cardiac failure and cerebral anoxia.
64
Define physically effective fibre and explain its effect on ruminant health.
Effective fibre length >1.5cm.
Fibre promotes chewing and rumination (also development of rumen muscular layer).
Not enough effective fibre leads to decreased chewing and saliva, decreased ruminal pH, increased acidosis risk.
Rumination stimulated by tactile means/pressure of coarse material 'Scratch factor' - abrades rumen surface and decreases keratinisation (papillae clump and decreased SA).
Fibre required for VFA production, also stimulates increased papillae.
65
Describe what happens to ruminal pH following a period of feed deprivation followed by refeeding. What are the risks to the animal and how can these be alleviated?
Refeeding can be via high intake of grain which increased risk of acidosis via decreased pH.
66
Outline the key reactions in acidosis in a ruminant.
High grain/fruit intake - abrupt increase in rapidly fermentable CHO - increased VFA, lactate - decreased ruminal pH.
DIAGRAM
Once osmolarity is greater than blood, it decreases passive transfer from the rumen.
67
Describe effective prevention strategies for ketosis, preg tox, and pasture bloat.
Preg tox; BCS 3/5, maintain appetite and energy intake, avoid handling in late gestation, ensure twins have at least 1500kg/ha of high quality pasture (can feed grain carefully).
Ketosis; avoid ketongenic feedstuffs (silage), feed conc in last few weeks of gestation (NDF 28-30%). Avoid over conditioning, particularly in late lactation and dry period. Additives to diet - niacin, Ca, sodium propionate, monensin from 2-3wks pre calving. Protected choline can be added to rumen - facilitates triglyceride export from liver. Management vs nutrition (shorter dry period means decreased time to replenish body stores).
Pasture bloat; avoid fast growing, clover dominated pastures, particularly newly sown. Increase fibre intake (feed grass hay daily), anti bloat medications (broken into fermentation modifiers, detergents and anti foaming agents) include anti bloat capsules, bloat blocks, water trough treatments, hay treatments (anti foaming agents), flank applications, spray oil on pasture. Introduce legumes gradually over several days (allow access for short periods-1hr), feed before grazing (silage, hay, mature pasture).
68
List the 6 common nutrition-related diseases found in sheep and/or cattle.
```
Acidosis
Pregnancy toxaemia
Ketosis
Hypocalcaemia
Hypomagnesemia
Bloat
```
69
An improved Lucerne/clover/ryegrass pasture produces 2800kg DM/ha/yr. If the pasture yields 11.0MJ/kg DM ME, how many DSE can be run on 450ha?
(2800 x 450 x 11)/(8.3 x 365)
| =4575DSE
70
Assume a cow consumes 2.5% DM on a body weight basis. What would be the daily ME (MJ/d) and CP intake (g/d) of a 470kg cow consuming a ration containing 11.5MJ ME/kg DM and 10.8% CP?
```
CP = 470 x 0.025 x 0.108 = 1.27kg/d = 1271g/d
ME = 470 x 0.025 x 11.5 = 135.13MJ/d
```
71
Explain what is meant by the term 'Scratch factor' in compiling rations for nutrients.
Effective fibre length
| Stimulates rumination and papillae growth.
72
If a 35kg wether is being fed 2% BW and the pellets have DM content of 90%, how much ME (MJ/d), CP (g/d) and ADF (g/d) does the sheep receive? Assume pellets are ME = 8.0MJ/kg DM, CP = 9%DM, ADF = 18%DM.
```
ME = 35 x 0.02 x 8 = 5.6MJ/d
CP = 35 x 0.02 x 0.09 = 0.063kg/d = 63g/d
ADF = 35 x 0.02 x 0.18 = 0.126kg/d = 1260g/d
```
73
Describe why and how nutrition can affect the immune system of animals.
Nutrition plays a critical role in immune response - specific nutrients can influence several, if not all aspects of immune response.
New born - colostrum for passive immunity (IgG). Increased Se can increase colostrum yield in ewes, increased iodine can decrease lamb serum antibodies. Increased vitamin A can decrease vit. E causing decreased lymphocyte function and retained foetal membranes.
Dams - decrease Se and Vit E can decrease neutrophil function.
DIAGRAM
74
Describe why and how the feeding of plant secondary metabolites may be useful in stimulating the immune system of animals.
Plant secondary metabolites are plant based immunomodulators that can stimulate or suppress components of the immune system.
Include; Alkaloids - increase natural killer cells (NKC) activity, antibody dependant cellular cytotoxicity. Seaweed can increase monocyte function due to antioxidants.
Beta-glucans - bacteria, fungi and plants. Act on several immune cell receptors resulting in innate and adaptive response. Induce humoral and cell mediated immunity. Antibiotic properties.
Curcumin - anti cancer, antioxidant, antiangiogenic, antiproliferative, pro-apoptotic.
Flavanoids - protein binding, active site interference, antioxidant. Target enzymes involved in immunosurveillance and inflammation.
Proanthocyanidins - condensed tannins, increase bypass protein causing increased immune response. Bactericidal (decrease intestinal parasites), decrease bloat as bind proteins in rumen, linked to regulation of activation of T and B lymphocytes, NKC, macrophages, gene expression, lymphocyte proliferation, antibody production, cytokines and cytotoxic substances. Increased resistance to GIT nematodes.
Resveratol - antimicrobial, chemopreventive, anticancer/proapoptic, antiinflammatory, antioxidant. Inhibits NF-kB in PMA, LPS or TNF-alpha-mediated macrophages, epithelial, jurkat, myeloid and dendritic cells.
Nutraceuticals - 'nutritional pharmaceuticals'.
75
What is the treatment for ruminants suffering enterotoxaemia?
Pulpy kidney.
No treatment, can vaccinate affected group to decrease further losses and put onto poor quality feed.
Caused by c. perfringens type D, proliferate due to rapid feed change to lush pasture.
76
Discuss the nutrient requirements of deer.
Diet formulation well established for white-tail deer, wapiti, red deer & reindeer/caribou.
Generally based on improved pastures and formulated rations for fully confined, higher production systems.
Species composition of diet strongly. influenced by seasonal availability.
Supplements to meet nutrient short-falls.
Cereal grain based supplements used extensively, hay preferred for wapiti.
Animals fed whole grain barley ad lib deposit excess fat so need to exercise caution.
77
How do you determine BW0.75?
Take BW and multiply 3 times.
Then square root the number twice, this gives metabolic body weight.
Can then use this number to times by the maintenance protein requirements (as an example) to give recommended protein ration.
Allows comparison between species
78
When are mineral deficiencies more likely?
When pasture is rapidly growing.
79
What are some common feed related disorders that affect deer?
Acidosis
| Ryegrass staggers - more common in wapiti, muscle tremors in neck, back and shoulder. Can die.
80
Describe the stomach situation in NW camelids.
Forestomach with 3 compartments.
Compartments 1 and 2 have 85-90% total stomach volume. Fermentation vats. Increased VFA absorption and higher fermentation chamber pH than rumen.
Microbial population similar to ruminants.
Still major gaps in knowledge.
81
Discuss the digestive efficiency of NW camelids?
Perform better on poor quality pasture than ruminants due to slower particulate passage rate (but faster fluid passage rate possibly due to large amount of saliva production). Evolved to graze on coarse, highly lignified material - obesity can be a problem in farmed animals.
82
Compare NW camelids to ruminants.
NW Camelids - higher blood glucose concentrations. Extreme hyperglycaemic response to minimal stress situations. Moderate insulin resistance which may account for higher susceptibility to hepatic lipidosis during periods of stress and decreased feed intake. Higher blood urea N conc. Llamas have lower rate of urea turnover and kidney excretion. Higher digestive coefficients when fed low or medium quality diets.
83
Discuss Cria nutrition.
Alpaca Crias - minimum 5.5kg birthweight, normal 7kg.
Llama crias - minimum 7kg birthweight, normal 9kg.
Hand feed colostrum 30mL hourly for 24hrs.
Cow, goat, or sheep colostrum can be used.
Milk from camelids has higher sugar content (6.5%) and lower fat (2.7%) than ruminants.
84
Discuss Hyperlipaemia/ketoacidosis is NW camelids.
Complex condition that can occur at any stage. Most likely in overweight animals in stressful situations (parturition, travel, shearing, teeth grinding).
Animals immediately become anorexic and show acute depression, ceased movement of C1, fat can be seen in blood sample.
Vital animals encouraged to eat anything possible (hand feed or drench), ingestion of fibre to help C1.
IV NSAIDs
Saline drip with 5% glucose solution if recumbent.
85
Describe lactic acidosis in NW camelids.
Similar to ruminants, affected animals are dehydrated, lethargic and depressed. Forestomach motility is decreased, diarrhoea may be present. C1 pH <5, accompanying metabolic acidosis and electrolyte disturbances. Respond well to fluids and alkalising agent therapy. Less grain required to induce the condition than in ruminants.
86
How many MJ/day ME does 1 DSE need?
8.3MJ/day ME
87
What is facial eczema?
Caused by fungus Pithomyces chartarum in perennial ryegrass pastures.
Spores release a mycotoxin-sporidesmin
Damages –liver, (particularly bile ducts), bladder & mammary gland
Causes a dramatic fall in milk production
Metabolic disturbances -ketosis
Photosensitisation of unpigmented skin, with severe pain
Surviving animals often suffer permanent liver damage, never fully recover & require culling
88
What is the signalment for facial eczema?
Shade seeking
Kicking, licking at flanks
Sudden decline in milk production
Redness and peeling of unpigmented skin
Sudden or unexplained deaths at calving
Increased incidence of ketosis at calving
By the time signs of FE are visible, liver damage has already been done
For every 1% of clinical cases there can be 20 -30% or more sub-clinical cases
89
When, where and why can you expect to see facial eczema?
Gippsland, Victoria & New Zealand
Late summer & autumn when periods of rain or high humidity occur in combination with high night-time minimum temperatures. Despite recent advances in weather forecasting, use of weather data to accurately predict FE danger periods has not been very successful
Germination is all-year round, but sporulation is very seasonal
There is no fixed beginning or end to the yearly FE danger period & it may extend more than 100 days
Onset of cold weather does not spell the end of a FE danger period
Fungus won’t germinate but spores are still there and may persist until May/June
Hills are worse than flats (not better as commonly believed)
Rain does not wash spores off pasture
90
What is the risk level for spore counts and facial eczema?
>20,000 spores/gram
91
How do you prevent facial eczema?
Zinc supplements
Prevents cell damage -forms an inactive complex with the toxin sporidesmin.
Zinc sulphate via drinking water
Zinc oxide via oral drench or feed supplements
Aim: maintain blood serum zinc level at 20 to 35 μmol/L
Need 20 mg elemental Zinc/kg bodyweight per day
Ensure Zinc Oxide is certified feed grade (containing no more than 200 mg/kg (0.02%) lead and 20 mg/kg (0.002%) cadmium)
Dose needs to be carefully calculated –too little, no protection, too much, risk zinc toxicity
Prevention dosing is safe up to 100 days –then monitoring zinc serum concentrations
92
Why are plants poisonous?
Defense mechanisms against attack by other animals/insect, or against microbial infections.
Competitive advantage
Disturbance of normal plant physiology.
93
What plant factors affect the level of toxicity?
Palatability - applying herbicides may temporarily increase palatability as it concentrates sugar in the leaves, unpalatable plants only eaten when other feed scarce, mixed with other palatable feeds or animals very hungry.
Stage of growth - toxin conc vary in different parts of plant at different stages of maturity. Nitrate in stems, CG and oxalates in young leaves, some have poisonous seeds.
94
What animal factors affect levels of toxicity?
Species - metabolism differs between ruminants, monogastrics and birds. Rumen microbes can detoxify (oxalates) some toxins or potentiate them (nitrate).
Age - young more susceptible (less effective detoxification, curiosity), older animals may experience toxin build up.
Degree of hunger
Boredom
Rank within group - dominant animals have first access to limited feed.
Intensity and length of exposure - acute (single exposure over short period), chronic (repeated over long period). Tolerance may develop if detoxification processes have time to develop.
Health Status - health are more likely to be able to detoxify.
Access to water - some toxins not released or absorbed until after water consumer.
Exposure - most pastures contain some level of potentially poisonous plants. Weedy hay has concentrated toxins.
95
Ture or false, concentrations in blood may not reflect dosage at site of action.
True
| Conc in blood may also reflect very poorly how much is being absorbed into cells.
96
Discuss the species difference in sheep and cattle exposed to oestrogen clover.
Sheep more sensitive and fertility impaired more severely.
Active form of plant oestrogen produced more actively by cows and occurs at higher blood conc than sheep eating the same clover.
Example of when high toxicant conc in blood may reflect poor metabolism and indirectly, relative tolerance to that toxicant.
97
What are some environmental factors affecting plant toxicity?
Season - some only poisonous at certain times of year (presence of fruit, flowers, seeds, young leaves). Annual plants.
Wilted or dried plants often just as toxic.
Seasonal conditions - drought, high rainfall, fire can influence growth and amount of toxin.
98
What are the plant associated factors of toxicity?
Soil - Se accumulating plants most toxic when growing in Se rich soils. Soils high in N predispose plants to develop large conc of nitrates and oxalates.
Fertilisers - can cause flush in growth, can increase amount of toxin in some plants.
99
What do you look for when suspecting poisoning?
Large number of animals affected - not all cases will exhibit signs though.
Area that group was in, change in management, time/season, weather.
Sudden death, struggling death, staggers, diarrhoea, hyperthermia, lameness, behavioural abnormalities, vomiting, skin lesions, acute or chronic signs, weight loss, repro performance.
100
Which toxin causes estrogenism? How do you treat it?
Zearalenone (fusarium mould)
Affects pigs, cattle, sheep, poultry.
Causes anoestrus, decreased conception rates, embryonic death, reduced egg production.
Also can be due to phytoestrogens in older varieties of sub clover - mainly affects sheep.
Treat by removing from affected feed or pasture. Practice appropriate grazing management (fertiliser usage, herbicides, improved pastures). Feed storage. Do not put hungry stock onto new growth or different pastures without feeding hay first.
101
What is the treatment for Cardiac glycoside poisoning?
Activated charcoal.
102
What is the treatment for cyanogenic glycoside poisoning?
Sodium thiosulphate (known as hypo) IV 500mg/kg
Cattle - 150g in 300ml water
Sheep - 60g in 60ml water
103
What is the treatment for fluroacetate poisoning?
Vinegar or ethanol
0.5ml/kg BW IM
Fluroacetate replaces acetate in CAC, prevents ATP being formed.
104
What is the treatment for ergot alkaloids?
No treatment
| Replace contaminated feed
105
What is the treatment for pyrrolizidine alkaloids?
No treatment, affected animals do recover.
| Significant scaring of liver and susceptible to relapse.
106
What is the treatment of oxalate poisoning?
25% Ca borogluconate solution IV or SC
Sheep - 50-100mL
Cattle - 300-500mL
Limewater orally to prevent further absorption.
107
Discuss why nitrate poisoning may occur
Accumulates in stems, higher conc in immature forage.
High soil N can lead to increased amounts in the plant.
During periods of drought soil nitrate can increase greatly, then when drought break nitrate uptake by plants increases, especially first week after rain.
Also boosted by low light (overcast, cold conditions), some herbicides, attack by insects, fungi or viruses, water stress.
Ruminants most likely to be poisoned if hungry and eat large amounts of hazardous feed rapidly - introduce slowly.
Crops - cereal grasses (oats - esp if very dark green, blue, stunted or frosted, millet, rye), corn (incl silage), sunflower, sorghum (incl silage). Lucerne hay also may have nitrate.
Hazardous plants contain >1.5% nitrate (KNO3) DM.
108
Can monogastrics be poisoned by nitrates? What about dogs and cats?
Monogastrics - yes, if nitrite formed by bacterial action (plant becomes wet for over 24hrs and gets significant bacterial growth).
Dogs and cats - yes, from excessive use in preservative in meat.
109
What are the clinical signs of nitrate poisoning in ruminants?
Death
If alive, rapid, deep breathing, irregular, weak pulse, muscle weakness, tremors and spasms. Coma, terminal convulsions.
Brown discolouration of mucous membranes.
Abortion 3-7days post poisoning if survive.
110
What is the treatment for nitrate poisoning?
2-4% solution methylene blue IV at 2-22mg/kg BW
Prevents oxidation of haemoglobin to methaemaglobin.
Relapse can occur if nitrate continues to be absorbed.
Meth blue not approved for use in food producing animals in Aus.
111
Discuss Nutritional Secondary Hyperparathyroidism in Horses.
Bighead.
Ca:P imbalance
Excess P hinder Ca absorption.
Seen in horses grazing tropical pastures - buffel, pangolin, setaria, kikuyu, green panic, guinea and signal grass. Oxalates >0.5%. Can also occur when large amounts of cereal grain concentrates fed - wheat bran, rice bran.
Signs - shifting lameness, tender joints, reluctance to move, stiff gait, mineral loss in bone (fractures) - only become obvious once disease has progressed beyond early stages.
Bony structures become enlarged to assist with strength as bone integrity is lost due to leached Ca. Cartilage disruption. Tearing of tendons and ligaments and weakening dental structures. Weight loss and poor body condition.
112
What is the treatment for NSH?
Ca:P 2:1
Mineral mix may be required or Ca supplementation.
2kg mix 1 part ground limestone (CaCO3) to 2 parts dicalcium phosphate (DCP) OR
1.4kg dolomite and 1.4kg DCP.
Prognosis good for older horses although lifelong skeletal problems may remain and compromised conformation.
113
What is fibre?
Polysaccharides resistant to hydrolysis by mammalian digestive enzymes.
Cellulose, hemicellulose, pectin and lignin.
114
What does fibre do?
Important for normal physiological function of GIT.
Feeds rumen microbes - VFA's (major energy source)
Regulates GIT motility.
Assists in regulation of ruminal pH.
Initiates correct rumen function in young animals.
Dependent on type and amount of dietary fibre.
115
Discuss ruminal lining papillae.
Increased surface area for VFA absorption.
Vary in appearance
Development stimulated by VFAs, particularly butyric acid.
Affected by; age, diet composition, quality of diet, fibre content and type, concentration and ratio of produced VFAs.
116
What is the link between fibre and saliva?
Fibre promotes chewing and rumination.
Healthy cows ruminate 40-50% of day, per cud a cow ruminates 50-70 times.
Rumination should be vigorous and aggressive.
Increased chewing increases saliva (pH8) which buffers ruminal pH.
Cows produce 180L of saliva per day with long fibre.
117
What is effective fibre length?
>1.5cm
118
Discuss rumen development and the scratch factor.
Depends on access to fibre & inoculation by rumen microbes
Rumen wall development depends on stimulation by VFA –need requisite bacteria & substrate (Fibre)
Milk vealers have an under developed rumen due to milk only diet
Rumination induced by sensors in the rumen wall, innervated by dorsal trunk of vagus nerve
Rumination stimulated by tactile means or pressure of coarse material –‘scratch’ factor
Probably responsible for inducing normal rumination
Lack of stimulation may be responsible for low rumination in animals on concentrate or pelleted diets
Related to both particle size & cell wall content of feedstuffs
Fibre promotes development of the muscular layer of the rumen
Rumen papillae proliferate in response to high concentrations of VFA
Papillae may clump together, actually reducing surface area & keratinise reducing VFA absorption
Some ‘scratch’ is needed to abrade the rumen surface to prevent keratinisation
119
What is inanition? How does it present?
Prolonged state of inappetence leading to exhaustion. Death either via starvation or secondary disease such as salmonellosis.
Primary and secondary inanition.
Major welfare risk and economic loss in live export and feedlots.
Presents as severe anorexia and weight loss. Hollow flanks, low BCS, minimal movement, difficult to pick the animals out from flock. Secondary inanition has limited weight loss.
First sign usually death.
120
What are the post mortem findings of inanition?
Rumen lacking feed material - liquid only content.
Thin, pale rumen wall lacking papillae, semi translucent. (primary only)
Decreased rumen size
Empty caudal GIT
Enlarged gall bladder
Absence of other major post-mortem indicators or primary cause of death (other than secondary inanition symptoms).
121
What are the proposed causes of inanition?
Voluntary refusal to eat, non-acceptance perhaps brought about be unfamiliar ration. Inhibition to eat due to dominant animals.
Inappetence due to secondary disease or failure to adapt to surroundings.
Complex neurohormonal systems surrounding drive to eat, unable to fully understand yet.
122
What factors affect inanition?
Animal factors - age, body fat, origin, neophobia.
Environmental factors - season, climate
Feed Factors - type, prior exposure, palatability.
Stressors - transport, time off feed, mixing with new animals.
Link between inappetance and large scale salmonellosis outbreaks.
123
Is live export fibre provision enough?
ADF 18-35%DM
Bottom end of scale is not enough.
No provision for max or min fibre length either.
124
What problems are seen when feeding pelleted feed?
Affects normal rumination
Decreased salivation and ruminal pH
Acidosis, rumenitis.
Bloat in cattle due to consumption of fines.
125
When does inanition develop and what is its treatment?
May commence in pre-export quarantine
During the sea voyage (16 to 21 days)
At the recipient feed lot in the Middle East
Existing management is ineffective: Corticosteroid administration (dexamethasone)
Electrolyte (Flopak4 in 1) and vitamin therapy (VitBs)
Current basis of inanition management once at sea & during the post-discharge period -roughage provision & attempted stress reduction
126
What is the role of fibre in inanition treatment?
Conflicting & sparse evidence leads to the variation in roughage provision to exported Australian sheep in foreign feedlots.
Post-discharge period range of 1-60 days Essential to encourage rapid & ongoing acceptance of feed on offer
Extended off-feed periods of 24-48 hours are likely immediately following unloading (discharge)
Rumen microbe populations & rumen motility decrease significantly within 12 hours if feed not provided
Most effective method to re-establish & maintain microbe populations, rumen fermentation & function is to provide roughage
127
Why will an animal collapse when suffering from bloat?
Pressure on diaphragm - can't breathe.
128
Discuss rumenotomy.
10cm incision in paralumbar fossa on left hand side of animal.
Allows gas and foam to be expelled in cases of bloat.
Administer 250-500ml antifoaming agent (vegetable oil, paraffin oil, conditioner, dishwashing detergent) through incision.
Wound care - stitch rumen wall to epithelial layer but leave incision open.
Try administering oil vie stomach tube first. Make sure you blow down tube and move it around to find pockets of gas and release them.
129
What are the signs of enterotoxaemia?
Sudden death with convulsions.
Bloody scouring
Incoordination, weakness and circling.
Haemorrhages under skin, heart and kidney.
Blood tinged pericardium fluid.
Presence of tags - soft, jelly like clots.
Kidneys dark and jelly like.
130
What are the risk factors for enterotoxaemia?
High level of starchy feed - easily digestible.
Slow movement of GIT
Sudden change to decreased fibre and increased CHO.
131
Why are mycotoxicoses difficult to recognise?
Biological action of toxin in host is delayed.
Diagnosis dependent on recognition of specific clinical signs which may or may not be present.
Toxin not uniformly distributed in environment or feedstuffs.
Detection methods not available but can test for in animal using immunoassays, thin layer chromatography or high-pressure liquid or gas chromatography.
Toxin unstable and short period of existence in animal.
132
Discuss aflatoxins.
```
Young more susceptible.
GIT dysfunction
Decreased productivity, feed utilisation and efficiency.
Anaemia and jaundice.
Liver damage.
Embryonic death. Teratogenicity.
Tumours.
```
133
What is lupinosis?
Significant cause of livestock deaths.
Occurs in summer and autumn.
Fungus that grows on green stems during winter and spring, toxin produced after plant dies when fungus adapts to being saprophyte.
Increased toxicity in stubbles after rain or in high humidity.
Stubbles can be toxic for months or years.
Sheep, cattle, goats, horses, pigs.
Weaners most commonly affected.
May develop secondary photosensitisation.
Liver damage, increases chances of prey fox in late preg ewes and cows.
Clinical changes mainly due to toxic hepatocyte injury.
134
What are the clinical signs of Lupinosis in sheep?
Acute - within 2 days of feeding stubble. Severe depression, icterus, lethargic, dead.
Post mortem shows jaundice on tissues, liver markedly swollen and yellow.
Chronic - (narrow leaf lupin) inappetance, loss of condition, lethargic, weak, stiff legged, hunched back, disorientation, no icterus or photosensitisation. Chronic Cu toxicity may be observed.
135
What are the clinical signs of lupinosis in cattle?
Common - late preg, recently calved cows in autumn - sudden deaths, abortion, icterus and photosensitisation.
Less common - ill thrift, some deaths, photosensitisation in following season.
136
How do you treat lupinosis?
Sheep - oral zinc dose >0.5g/d
| Protects liver against injury.
137
Discuss blue-green algae.
Cyanobacteria.
Present in water bodies, livestock poisonings uncommon but can occur. Ruminants more susceptible.
Need to ingest large amount in short period.
Dead and dying algae releases toxins into water.
Warm sunny weather, low turbidity, minimal turbulence and eutrophication increase bloom.
Signs of poisoning; sudden death near water, tremor, staggering, coma, icterus, ill thrift, photosensitisation.
Scum can clear quickly so may not be obvious in water source.
138
What is the treatment and prevention for blue green algae poisoning?
Remove stock to shaded area with ample, clean water. Good quality hay.
Can administer activated charcoal in singular cases.
Prevent by having clean water sources, surface barriers to keep shore free of algal scum (limited success).
Algaecides - copper suphate - don't allow access for 5-7d post treatment.
139
Disucss salt toxicity.
Excessive NaCl with limited water intake.
Pigs most susceptible, cattle, poultry and sheep relatively resistant.
Acute lethal dose 2.2g/kg BW in pigs, 6.0g/kg BW sheep.
Water intake reduced or abolished due to mechanical failure, overcrowding, unpalatable water, new surroundings, frozen water.
Recommended that drinking water should contain less than 0.5% salt for all species.
140
Discuss the signs and treatment of salt toxicity in pigs.
Early signs are rarely seen, increased thirst, scratching/itching, constipation.
Blindness, deaf, oblivious to surroundings, no eating or drinking, wander aimlessly, bump into objects, circle or pivot on single limb.
1-5 days limited water intake results in recurrent seizures at approx 7 minute intervals then struggling coma and death.
Treat with gradual reintroduction of water (if off water for over 24hrs), electrolytes in water, place pigs with nervous signs in darkened area with bedding to help prevent injuries.
141
What are the signs of salt toxicity in cattle?
Salivation, increased thirst, vomiting, abdominal pain, diarrhoea.
Ataxia, circling, blindness, seizures, partial paralysis.
Sometimes belligerent and aggressive, drag hind feet, knuckling of fetlock joint.
142
What are the sings of salt toxicity in poultry?
Increased thirst, laboured breathing, fluid discharge from beak, weakness, diarrhoea, leg paralysis.
143
What is the treatment for salt toxicity?
Remove offending feed or water.
Provide fresh water, small amounts at frequent intervals.
Water via stomach tube for severely effected.
Mortality rate is 50% regardless of treatment.
Small animals - slow administration of hypertonic dextrose or isotonic saline.
144
What are some prevention methods for salt toxicity?
Monitor salt conc in water - poisoning can be gradual due to evaporation of bore water in dams or troughs.
Frequent observation and maintenance of water systems.
Correctly balanced rations.
Show stock watering point when moving to new paddock.
145
What is fluorosis?
High fluorine content –artesian bore water
Maximum tolerable concentrations varies with species: 40 to 50 mg/L cattle, horses, 60 to 150 mg/L sheep, 200 mg/L for chickens
Chronic toxicity –small amounts over a long time period, cumulative effect
Protective mechanisms against fluorosis:
Excretion in urine, Deposition in bones & teeth, Loss of appetite when elimination ceilings are reached.
146
What are the signs of fluorosis?
No one definite diagnosis. Brown mottling, excessive erosion of teeth.
Hip lameness, stiffness of limbs, painful gait, unthriftiness, fractures
Visibly enlarged bones –mandible, sternum, metacarpals, metatarsals, exostosis, ankylosis
Excessive fluorine in blood, urine (need lab tests)
Mechanism –alters the molecular structure of hydroxyl-apatite, F-replaces the hydroxyl radical = ‘softer’ bone, less compact, more porous.
Similar signs to big head in horses however there is no effective treatment.
147
Discuss hypocalcaemia.
Lack of Ca. Occurs at/after calving, up to a week.
Massive demand on Ca for lactation, body is unable to immobilise enough and therefore inadequate Ca for muscle function.
Can be fatal.
148
What are some risk factors for hypocalcaemia?
Advancing age - clinical disease rare in heifers.
High oestrogens inhibit bone resorption.
High dietary phosphorous.
Breed - jerseys less likely to affected than Holsteins.
High dietary fat??
149
List the stages of clinical signs of hypocalcaemia.
1. Cow standing, brief excitement, tetany, hypersensitivity, muscle tremors, ataxia, anorexia, stiff gait.
2. Sternal recumbancy, depressed consciousness, head turned to flank, dry muzzle, skin and extremities cool, weak pulse, pupillary light reflex incomplete, ruminal stasis, constipation, tachycardia. S shaped neck.
3. Lateral recumbancy, comatose, flaccid, heart difficult to hear, bloat, death.
150
How do you treat hypocalcaemia?
IV Ca infusion (1g/45kg BW of Ca gluconate).
| SC Ca gluconate - need to back up with oral administration of Ca chloride or Ca propionate to reduce chance of relapse.
151
What steps can be implemented to manage hypocalcaemia?
Short term - Ca gel orally at calving, vitamin D injection 1wk before calving, monitor herd closely and treat early.
Long term - feed anionic salts to springers (MgSO4), limit Ca intake in dry period, feed ad lib hay to springers.
Dietary Ca should be 1-1.2%, P and Mg at 0.4%, sulphur 0.25-0.4%, Na 0.1%, K 1.0%, add chloride to balance dietary cation-anion difference (not above 0.8%).
152
Discuss hypomagnesaemia.
Grass tetany. Multi factorial; incorporates weather, pasture growth, dietary Mg, K, Na and protein. Tends to be seasonal in Autumn and Spring.
More common in older cows grazing lush grass dominant pasture.
Can be seen in calves (2-4months age) as milk is low in Mg.
High ruminal K concentration reduces Mg uptake.
153
What are the clinical signs of hypomagnesaemia tetany?
In coordination, hyperaethesia, tetany, tonic-clonic muscular spasms and convulsions, high case fatality rate without treatment. Aggression.
154
Discuss the treatment of hypomagnesaemia tetany.
MgCl2 or MgSO4 IV, SC or enema.
| IV Mg requires caution as Mg is muscle relaxant (causes heart to relax). SC and rectal safer.
155
Discuss short term prevention strategies for grass tetany.
Dietary supplementation with Mg - oxide, carbonate, sulfate, phosphate.
Pasture dusting, mix with molasses into hay, daily drenching, Mg rich pellets, reticulum bullets, top dress pasture (Mg fertiliser), supplement in drinking water.
156
What other measures can be implemented to prevent grass tetany?
Avoid grazing new, fresh pasture.
Avoid use of potash (K) fertiliser at high risk times.
Include legumes in seeder mix for crops (higher Mg levels).
Ensure adequate feed, shelter (particularly when cold).
Change calving season.
157
What is Mg important for?
Enzyme activator important for the control of nerve impulses.
Synthesis of RNA, DNA and proteins.
Regulates membrane channels.
Exictaiton - contraction coupling in skeletal muscle.
Requires regular diet input - absorbed from reticule-rumen via active transport.
Bone and tissue Mg unavailable.
158
The concentration of Mg in the ECF is dependent on?
GIT absorption
Tissue requirements (milk, foetus)
Excretion from the kidneys
Less than 1% of Mg in ECF, not regulated by specific hormones.
