Feeding the Dairy Cow

Have to Understand the Lactation Curve

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Lactation Curve Lactation curve Gradually increases following calving Peaks at 45-90 days in milk (DIM) Stage 1 is where most metabolic diseases occur.

Cures There are many “band aid” cures that will make the dairy producer feel better that they are doing something at the moment, but the real problem is solving the reason it occurs and “fixing it”

Critical Days 90-100 days Deliver a healthy calf No milk fever No retained placenta -8 wk 44 wk of lactation Increase DMI No fatty liver No displaced abom. No ketosis Limited loss of BCS No mastitis High peak production 6-8 wk -3 wk 90-100 days 10 wk High fertility No metritis Not all days are of equal importance in the life of a cow. Typically we separate the lactation into the dry period and the lactation phase. However, from a nutrition perspective, the critical days start about 3 week prior to calving and goes on until the cow is pregnant again 10-12 weeks after calving. The three things we expect of our cows are; (1) delivery of a healthy calf, (2) the highest peak production and (3) revovery of a high rate of fertility withing 60-70 days after calving. The usual problems usually interfereing with these objectives include:….

Managing Cow During Critical Days Early lactation Dry period -8 Dried-off Wk Far-off -4 Calving “Close up” -1 -2 -3 2 3 1 5 6 4 7 8 10 9 11 Energy balance - - - - - - + + + Successful insemination Bred Fat mobilization High forage diet High Conc. Diet Highest Req. Lowest Req. Calving stress Depressed Immune system Acute calcium demand Production & repro are set for the next 200- days Slow rise in DMI (rumen capacity) Lowest rumen capacity & 50% loss in absorption by papillae Severe drop in DMI

DMI is the Key Dry matter intake (DMI) General shape of curve is same as for milk Peak is later in lactation than milk curve

About Metabolic Disorders Metabolic disorders occur primarily in early lactation period of great stress and drastic changes in nutritional requirement Energy metabolism (ketosis, fatty liver, rumen acidosis) Minerals and vitamin metabolism (milk fever, metritis, udder edema, retained placenta)

About Metabolic Disorders Metabolic disorders are correlated with each other: A cow with milk fever is 4 x more likely to also suffer from retained placenta and 16 x more likely to develop ketosis than a cow with no milk fever. Early detection and prevention is far better than treatment

DMI Dry matter intake Factors used to estimate DMI: body weight milk production fat test days in milk

Overview of Metabolic Disorders in Dairy Cattle

Metabolic Disorders Energy-Related Disorders 1- Fatty Liver Syndrome 2- Ketosis (Acetonemia) 3- Rumen Acidosis 4- Laminitis (Locomotion Score) 5- Displaced Abomasum 6- Milk Fat Depression Minerals & Vitamins-Related Disorders 1- Hypocalcemia (Milk Fever) 2- Udder edema 3- Retained Placenta

Disorders Related to Mineral Metabolism 1 - Hypocalcemia (Milk Fever)

Hypocalcemia and milk fever Most cows suffer from (sub-clinical) hypocalcemia in early lacation Clinical hypocalcemia or milk fever is a misnomer: cows do not have a “fever”, but rather are “paralyzed.” The disease has a low heritability, but has a genetic component as Jerseys and Swedish red have a higher incidence than other breeds.

Hypocalcemia and milk fever The disease is related to age and occurs more in third lactation than second or first lactation. Cows having milk fever once are apt to repeat More than about 5-8 % incidence in a herd is cause for concern If you find milk fever in dry cows, there is a problem with your mineral balance of Ca:P

Prevention Calcium levels during Close-up period Check forage levels? DCAD level – negative 20 (neg 17 -23) Urine pH 5.5 to 6.0 during the close up time Use palatable sources to lower DCAD Soy-clor, Bio-clor, Molasses Anionic Salts - less palatable

Disorders Related to Mineral Metabolism 2 - Retained Placenta

Retained Placenta Overview Retention of placental membrane for more than 12 hours after calving *(twins do not count) Often time this condition is due to bacterial infections, but it might also have a nutritional component Deficiency of selenium and vitamin E and imbalance of Calcium may be implicated in increased incidences of retained placenta

Prevention Provide 2400 – 2500 IU Vitamin E during close up Provide selenium in combination with vitamin E Monitor forage Calcium levels This can sneak up on you!

Disorders Related to Energy Metabolism 3 - Ketosis

Glucose secretion in milk (as lactose): Ketosis or Acetonemia Insufficient glucose is the source of ketosis or acetonemia: Blood concentration of glucose drops from 50 mg/100 ml to < 25-30 mg/100 ml Signals cow to digest body fat! Body reserve: 0 g Glucose lost in feces: ~0 g/d Intake during Dry period: ~0 g/d Lactation: ~0 g/d Glucose secretion in milk (as lactose): 2.kg/d (for 35 kg/d of milk)

Ketosis Occurs 2 to 4 weeks after calving (peak incidence is about 3 week) Affect most high producing cows (sub-clinically) in early lactation Detection: Urine - Ketostik

Ketosis “Typical” ketone (acetone) smell in the breath; Lack of appetite, especially for grain associated with drop in milk yield; Decreased rumen mobility and production of “dry feces” Loss of weight, gaunt appearance, and dullness Symptoms:

Ketosis - Prevention Avoid excessive fatness at calving (proper BCS) < 4.25 Smooth dietary transition between dry cow ration and early lactation ration Close-up ration should contain same feeds with anions and Niacin No Bicarb Gradual change in forage types Gradual change in amount of concentrates

Disorders Related to Energy Metabolism 4 - Fatty Liver

Lower Intake at Calving Means Increased Fat Mobilization (Blood NEFA) 5 10 15 20 25 Dry Matter Intake Kg/day Weeks relative to calving -1 -2 1 2 3 200 400 600 800 1000 Non-Esterified Fatty Acids um/l 300% Increased fat mobilization 30 -35% intake depression Grummer, 1993

Excess Fat Mobilization Means “Liver Problem” Triglycerides Adipose tissue NEFA FFA Liver Energy Triglyceride Low blood glucose Low insulin ++ TG-r-LP Storage Fatty liver Ketones Uptake of NEFA by the liver is proportional to NEFA in the blood (Bell, 1979). Export of triglyceride from the liver occurs at a very slow rate in ruminants compared to many other animal species. Because of the slow rate of export of triglycerides from the liver, once fatty liver has developed, it will persist for an extended period of time. Depletion usually commences wht the cow reaches positive energy balance and may take several weeks until completion. FFA Milk fat (Triglycerides) Glycerol Energy TG-r-LP Ketones Key: NEFA = Non-Esterified Fatty Acids FFA = Free fatty acids TG-r-LP = Triglyceride-rich-lipoproteins or Very Low Density Lipoprotein (VLDL)

Ketosis - Prevention Supplementation with niacin Niacin supplementation (6-12g/d) seem to work best when forage and grain are fed separately (greatest fluctuation of glucose, insulin, NEFA and ketones in the blood.)

Band Aid = Metabolic Switch Propylene glycol drench or paste Propylene glycol is a glucose precursor which is effective in reducing blood NEFA and the severity of fatty liver at calving and blood ketones after calving (~300 g/cow/day for 20 days starting 10 days before calving). Can add niacin to drench

5- Displaced Abomasum

Cross Section Abdominal Cavity Abomasum = A C = Omasum Rumen = B L = Liver

Displaced Abomasum (DA) Sharp and sudden drop in feed intake “Ping Test” 80% of DAs occur within the first month of lactation.

Displaced Abomasum (DA) Exact cause is unknown, but incidence has been associated with: High concentrate diet during the transition period and/or early lactation (high ruminal gas formation and passage into the abomasum) (Difficult) calving leaving “open space” into the abdominal cavity Stress conditions that limit dry matter intake and gut fill in early lactation (e.g., over-conditioned cows, overcrowding, etc.,)

Displaced Abomasum (DA) Avoid over-conditioned cows (body condition score >4.0) Begin concentrate feeding (0.5-0.75% of body weight) during the last three weeks before calving (“close-up” ration) Feed long and / or coarsely chopped good quality forage during the dry period and early lactation. Keep a minimum of 50% forage in the diet Minimize stress due to other peri-parturient diseases (milk fever, ketosis)

Prevention Management is implicated in too many cases of DA’s!

Disorders Related to Energy Metabolism 6- Rumen Acidosis

Acidity In The Digestive System Feed (Forestomachs) Glandular stomach Small intestine Large intestine HCl This slide shows the general pattern of acidity within the digestive tract. Generally, the saliva of ruminants is higher in sodium bicarbonate and phosphate buffer than the saliva of non-ruminants. Thus, the pH of ruminant saliva is higher than the pH of non-ruminant saliva. In ruminants, there is a need to maintain a pH above 6.0 in the reticulo-rumen to maximize the fermentation of feed and the growth of desirable bacteria. Also, the microbes that populate the rumen have enzymes that degrade feed components including starches. Thus, the low activity or absence of -amylase in the saliva of ruminants is explained by the fact that ruminal microbes carry out that function. From an evolutionary viewpoint, the synthesis of -amylase in the saliva became obsolete. In all animal species, the hydrochloric content of gastric secretion reduces its pH to values as low as 1.5 - 2.5. Pepsin is a gastric enzyme that breaks down specific peptide bonds in a strong acidic environment only. The pancreatic secretion in the small intestine are rich in bicarbonate buffer, which helps to raise the pH progressively. The optimal pH of pancreatic enzymes is generally in the range of 5.0 - 6.0. One of the main challenges in feeding high producing ruminants is to avoid the excess of readily fermentable starch that might overwhelm the natural buffering capacity provided by the saliva. A drop in rumen pH (rumen acidosis) lowers intake and production in the short term, and it causes foot and leg problems in the long term. It might also be associated with reproductive problems. Excess starch reaching the cecum of dairy cows can also cause undesirable fermentation with possible risk of diarrhea. Saliva Pancreas Liver Feces pH 1.0 - 2.0 6.0 - 8.0 6.0 - 7.0 7 2

“Average” pH vs. Length of Time Under 6.0 Length of time under pH 6.0 and cow-to-cow variations must be taken into account in the diagnosis of rumen acidosis - Good appetite - Good cellulose digestion - Good microbial growth. 6.0 Rumen Acidosis - Poor appetite - Little cellulose digestion - Poor microbial growth. 5.5 pH of rumen content Sub Acute Rumen Acidosis 5.0 Acute Rumen Acidosis - Deep physiological changes - 4.5 6 12 18 24 Hours

Rumen Acidosis (Prevention) - Effective Fiber Avoid ration with more than 50% Concentrates Limit high starch concentrates (corn) Maintain Sufficient “Effective Fiber” Ration NDF > 32% Ration Effective NDF > 22% Gradual Changes in diets Total Mixed Rations (TMR)

7 – LAMINITIS Locomotion Score

Locomotion Score Score = 1 Score = 2 Walk rapidly and confidently, making long strides with a level back Score = 2 Walk more slowly, making shorter strides with an arched back Difficult to detect any weight transfer from affected limb

Score = 3 Score = 4 Often thin, walk slowly making deliberate short steps with an arched back and frequent stops Weight transfer will cause sinking of the dew claws on the contra-lateral limb Stand with an arched back and frequently rest lame foot Encounter some difficulty turning Score = 4 Usually very thin, move very slowly making frequent stops to rest affected limb, which is only partially weight-bearing Grinding of teeth and/or drooling of saliva are signs of acute pain Stand and walk with an arched back Extreme difficulty turning

8- Milk Fat Depression

Milk Fat Depression and Forage to Concentrate Ratio Propionic Acid Milk production (kg/day) Total VFA production (moles/day) Volatile fatty acids (VFA) produced in the rumen 50 Concentrates 20 % ration dry matter 80 % ration dry matter Forages 80 60 40 20 60 % 30 Acetic Acid Butyric Acid Rumen pH 5.5 5.0 6.0 6.5 Milk production and composition Fat in the milk (%)

Udder edema Cause: Exact cause is unknown, but incidence of udder edema has been associated with management and feeding practices during the dry period: Excess salt (>0.5 lb/d, 230 g/d or 2.5% diet DM) aggravates the problem Excess energy, sodium and potassium in pre-partum diet; First calf-heifers (primiparous cows) in excess BCS at calving show an increased incidence of udder edema.

So How Do We Feed 1. Forages should be of very high quality to encourage intake of roughage NDF 32% ADF 22% 2. Maintain at least 45% of ration DM in forages Corn Silage Alfalfa Hay Other Silages Other Hays

So How Do We Feed 3. Supply Adequate Energy (NFC <40%) Carbohydrates – grain (starch & sugar <30%) Corn Sorghum Other Grains Lipids (EE 3.5-5.5%) tallow by-pass fat (Megalac, Energy Booster) Pay attention to specific LCFA

So How Do We Feed 4. Feed high quality protein sources Ration DM Protein% 14.5- 18.5% Soybean meal Cottonseed meal Blood meal Fish Meal

So How Do We Feed 5. Allow rumen synthesis of proteins by feeding a balance of forage, energy and protein precursors. Watch manure for indicators of acidosis Watch manure for tightness or looseness

So How Do We Feed 6. Balance remaining fraction or ration for minerals, vitamins, etc Calcium ~1% Phosphorus~.35% Potassium 0.0-1.1% + DCAD Balance Magnesium .35-40% Vitamin A – 240 (KIU/day)