Mid Sem. Flashcards
What are some health issues associated with acidosis?
Rumenitis Metabolic acidosis Laminitis Liver abscess Pneumonia Death
Describe the impact of acidosis on the rumen?
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.
What are some methods for controlling acidosis?
- 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).
What are some indirect indicators of acidosis?
Scouring - colour, consistency, smell, umdigested materials, bubbles.
Reduced milk fat, feed intake. LWG, cud chewing, laminitis
How do you treat acidosis?
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.
What are some general management recommendations for acidosis?
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
Describe the energy requirements of a lactating cow?
Glucose requirement increases 250%
Amino acid requirement increases 200%
What are the energy requirements of a pregnant cow?
Foetal placental requirement represents 45% of the maternal glucose and 72% of the maternal AA supply.
What is fatty liver disease?
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.
High body condition in dairy herds increases the risk of….
Metritis Ketosis Milk fever Cystic ovaries All reduce conception rate and increase days open. Poor fertility.
Why are high body condition score cows at greater risk?
Lower dry matter intake due to decreased room
Greater negative energy balance
Greater risk of metabolic issues
What are the clinical signs of ketosis?
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.
What are the critical thresholds for risk of clinical ketosis?
Prepartum - NEFA 0.29mEq/L
Postpartum - NEFA 0.57mEq/L, BHB 10mg/dL
What are the clinical signs of preg tox?
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
What are the sub clinical signs of preg tox?
Elevated BHB conc
Low glucose conc
Liver is yellow with fine mottled appearance
Plentiful abdominal fat although animal emaciated
Very little content in rumen
Why do sheep show depression in preg tox?
Under conditions of ketosis, glucose consumption is decreased in the cortex and cerebellum by about 10% per mM of plasma ketone bodies.
Nutritional disorders and pathology may arise from the presence of contaminants within feedstuffs. Discuss the major factors contributing to contamination of feedstuffs with mycotoxins.
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.
Identify the major effects of mycotoxins in the health and production of animals.
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.
How can contamination of feeds with mycotoxins be prevented?
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).
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.
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.
Describe the physiology of ruminal acidosis, explaining why we see changes in pH, lactate concentrations and osmolality.
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
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.
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.
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.
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
Average plasma BHB levels of 1.8mmol/L is…..
Elevated
Average serum D-lactate levels of 0.5mmol/L and blood pH of 7.3 are ….
Normal
Plasma Ca of 2.2mmol/L is …..
Low
Normal 2.8-3.2mmol/L
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.
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).
List three major antinutritional factors associated with concentrates and roughages.
Lectins: grains, legumes
Phytates: cereal grains
Tannins: Lucerne, ryegrass
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).
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)
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.
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.
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.
Describe the signs that indicate a cervid/camelid is suffering from thiamine deficiency.
Also known as polioencephalomalacia. Depression Seizures Blindness Hyperaesthesia Sudden death
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.
What is the antidote to cyanide poisoning?
Sodium thiosulphate
What is the antidote to nitrate/nitrite toxicity in cattle?
Methylene blue
Which is more toxic, the nitrate or nitrite ion?
Nitrite.
What does the nitrite ion do?
Convert haemoglobin to methaemoglobin.
True or false, diets rich in readily fermentable CHOs increase nitrite production in ruminants
True
Also increases its conversion to ammonia
Of the spleen, bile, urine and liver, which would be the best to test for toxins?
Liver
Oleandrin, cyanide, pyrrolizidine alkaloids.
List domestic animals in descending order according to their susceptibility to aflatoxins.
Cattle > sheep > pig > chicken
What are the major targets of Cyanobacteria?
Hepatotoxic
Neurotoxic
Cardiotoxic
What is the major toxic effect of hydrogen cyanide?
Inhibition of mitochondrial respiration.
True or false, cardiac glycosides stimulate parasympathetic discharge.
True.
What toxin comes from the castor oil plant?
Ricin
Which species is highly susceptible to zearalenone toxicity?
Porcine
What is the major organ responsible for detoxification in the body?
Liver
Zearalenone is ……
Non-steroidal oestrogenic compound.
Glucosinolates are defined as……
Goitrogens
Degraded to thiocyanites in rumen, interfere with iodine absorption.
What is one of the most com one aflatoxins?
Aspergillus
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
In acute cases of poisoning, activated charcoal acts to reduce absorption of the substance by;
Binding to poison molecules.
Which toxins are produced by Fusarium?
Deoxynivalenol
T2
Zearalanone
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.
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.
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.
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.
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.
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.
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.
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.
