Overview of Metabolic Disorders in Dairy Cattle

Overview of Metabolic Disorders in Dairy Cattle By Michel Wattiaux University of Wisconsin-Madison Department of Dairy Science Overview Metabolic Disorders, 1 GENERAL CONCEPTS Overview Metabolic Disorders, 2 General Concepts • • • • Nutritional and management problems vs. infectious diseases (noncontagious vs. contagious) Clinical vs. Sub-clinic vs. Acute Prevention vs. treatment Cost of diseases • Veterinary and drug expenses • LOSS of production (unrealized income!) • Early culling / death • One animal vs. the herd • Prevalence Overview Metabolic Disorders, 3 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) 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 Overview Metabolic Disorders, 4 • • Quiz: Is My Cow Sick? Temperature (38.3-39.4°F) Problem SubNormal Normal High Appetite Reduced Normal Udder Full Slack Milk Fever Metritis Pneumonia Ketosis Mastitis Displaced Abomasum Retained placenta Rumen acidosis Diarrhea Instructions: Please fill in the Table by writing the number “1” for temperature, appetite and udder condition that prevails for each of the disorders listed. (“slack” = “not full”) Overview Metabolic Disorders, 5 Metabolic Disorders Calf Health 1- Immune-resistance (Colostrum) Diarrhea and Pneumonia Cow Health Introduction 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 œdema 3- Retained Placenta Overview Metabolic Disorders, 6 CALVES Overview Metabolic Disorders, 7 New Born Resistance to — and Challenge from — Disease Agents Disease Resistance Colostrum feeding Calf’s own immune system Disease Challenge Good sanitation of calving area Proper housing, feeding and management 0 2 4 6 8 Age of the calf (weeks) 10 0 2 4 6 8 Age of the calf (weeks) 10 Overview Metabolic Disorders, 8 Common Bacterial Infections Overview Metabolic Disorders, 9 Calf Management and Likelihood of Illnesses Adequate management: Healthy calves, low mortality High resistance Poor management: Sick calves, high mortality High disease challenge Low disease challenge Low resistance 0 2 4 6 8 Age of the calf (weeks) 10 0 2 4 6 8 Age of the calf (weeks) 10 Overview Metabolic Disorders, 10 Colostrum and Transition Milk Milking number Component 1 Colostrum 2 3 4 5 11 Whole milk Transition milk 17.9 5.4 8.4 4.2 3.9 0.95 --14.1 3.9 5.1 2.4 4.4 0.87 113 13.9 3.7 4.2 0.2 4.6 0.82 --- Total solid, % Fat, % Protein, % Antibody, % Lactose, % Minerals, % Vitamin A, ug/dl 23.9 6.7 14.0 6.0 2.7 1.11 295 13.6 3.5 4.1 0.1 4.7 0.81 74 12.5 3.3 3.2 0.09 4.9 0.74 34 Antibodies are derived from the dam’s blood stream and are based on the disease history to which the cow has been exposed Overview Metabolic Disorders, 11 Antibodies or Immunoglobulins (Ig): “Warriors” Against Disease Agents Type % of all Ig Function IgG 80 - 85% Destroys microbes that have entered the blood stream (systemic infections) IgA 8 - 10% Protects membranes that line many organs (intestine, lung, etc.) against infections by preventing bacterial attachment, and thus preventing antigens from entering the blood. IgM 5 - 10% Same as IgG, but has a low Antiboby turnover Macrophage Engulfing agglutinated bacteria Bacterium Overview Metabolic Disorders, 12 Antibody Absorption 50 Absorption of Antibody trough the intestinal wall, % 40 30 20 range 10 0 0 6 12 18 24 Average Hours after birth Overview Metabolic Disorders, 13 Timing and Amount of Colostrum Feeding Serum IgG (mg/ml) First feeding immediately after birth First feeding 12 hours after birth 15 10 5 0 Colostrum fed (kg/feeding) 2 kg 1 kg 0.5 kg 0 12 Feeding 24 36 0 12 24 36 Hours Feeding Overview Metabolic Disorders, 14 Colostrum Quality: Antibody, g/100 g fresh colostrum Breed Brown Swiss Jerseys Average Min. Max. Average 6.6 2.8 11.5 9.0 Holsteins 4.8 2.0 12.0 5.6 Ayshire Guernsey 8.6 8.1 6.3 Parity (calving number) First Average 5.9 Second Third 8.2 Fourth 7.5 6.3 Overview Metabolic Disorders, 15 From a variety of sources: Quigley, 1994; Pritchett, 1991 and others Colostrum Quality A high quality colostrum: • • • • • • Is thick, creamy and does not contain blood (high specific gravity) Is from a cow that has lived in the herd for a long time Is from a cow that has been vaccinated during the dry period Is from a cow that had a dry period of about 60 days Is from a cow for which the colostrum did not leak before calving Is from a cow free of infections (mastitis, Johne’s disease, etc.) Overview Metabolic Disorders, 16 COWS Overview Metabolic Disorders, 17 Critical Days Deliver a healthy calf -3 wk -8 wk No milk fever No retained placenta 0 6-8 wk 10 wk High peak production Fast increase in intake Limited loss of BCS No mastitis No ketosis 44 wk of lactation High fertility No fatty liver No displaced abom. No metritis Overview Metabolic Disorders, 18 Managing Cow During Critical Days Dry period Dried-off Far-off Calving “Close up” - - 1 2 Early lactation Energy balance -0 + Bred ++ 9 10 11 Successful insemination Production & reproduction are set for the next 200-280 days, respectively. Wk -8 -4 -3 -2 -1 0 3 4 5 6 7 8 Calving stress Depressed Immune system Acute calcium demand High forage diet High Conc. Diet Lowest Req. Highest Req. Fat mobilization Lowest rumen Severe capacity & 50% Slow rise in DMI drop (rumen capacity) loss in absorption in DMI capacity (papillae) Overview Metabolic Disorders, 19 Energy Balance, Body Condition and Fertility Energy (Mcal NEl/day) 44 40 36 32 28 24 20 16 12 8 4 0 4 0 -4 -8 -12 60 Required Ingested 28 24 20 16 12 8 4 0 DMI (kg/d) Balance (Mcal NEl/d) Unavoidable under-feeding Increasing risk of over-feeding Risk of becoming too thin Period of service(s) -8 4 0 4 8 60 12 90 16 120 20 140 24 168 28 Risk of becoming too fat Cow’s fertility 50 (% conception rate) 40 30 20 5 4 3 2 1 BCS Weeks Days 32 36 40 44 -60 -30 Calving 30 196 224 252 Metabolic Disorders, 20 Overview 280 308 In Summary • To maintain a cow’s health during the critical days and help her regain a high fertility as soon as possible after calving, we must: • Manage her properly so to minimize stress: • maximize comfort (easy access to resting and feeding areas) • Avoid heat stress • Avoid “psychological” stress (fear) • Feed her properly so that … • Drop in intake before calving is minimized • A healthy rumen environment is maintained (avoid acidosis) • Rapid increase dry matter intake after calving … Adipose tissue mobilization is limited. Overview Metabolic Disorders, 21 Disorders Related to Energy Metabolism 1 - Fatty Liver Overview Metabolic Disorders, 22 Lower Intake at Calving Means Increased Fat Mobilization (Blood NEFA) Dry Matter Intake Kg/day 25 NonEsterified 1000 Fatty Acids 800 um/l 20 15 600 400 200 -2 -1 0 1 2 3 Weeks relative to calving 30 -35% intake depression 10 5 300% Increased fat mobilization Grummer, 1993 Overview Metabolic Disorders, 23 Intake at Calving is Associated with Intake and Milk Production in Early Lactation Dry matter intake 21day after calving (% of body weight) 6 5 4 3 40 30 r = .54 Milk yield, kg/d Control Force Fed (trough rumen cannula) 50 2 1 0.0 0.5 1.0 1.5 20 0 5 10 Milk fat,% Control 3.88 Force fed 4.22 15 20 25 30 2.0 2.5 Dry matter intake the day prior to calving (% of body weight) Grummer, 1993 Day relative to calving Overview Metabolic Disorders, 24 Estimated Energy Balance Around Calving Balance NEl, Mcal/day (NEl intake - NEl expanded) 5 0 -5 Drop in DMI Colostrum & milk synthesis -10 -15 -21 -14 -7 0 7 14 Days Relative to Calving 21 Grummer, 1995 Overview Metabolic Disorders, 25 Excess Fat Mobilization Means “Liver Problem” Adipose tissue Triglycerides ++ Low blood glucose Low insulin NEFA Liver FFA Energy Triglyceride Ketones TG-r-LP Storage Fatty liver Ketones Key: NEFA = Non-Esterified Fatty Acids FFA = Free fatty acids TG-r-LP = Triglyceride-rich-lipoproteins or Very Low Density Lipoprotein (VLDL) TG-r-LP Energy FFA Glycerol Milk fat (Triglycerides) Overview Metabolic Disorders, 26 “NEFA” and Incidence of Metabolic Disorders Plasma non-esterified fatty acids (NEFA) the week prior to calving, µM, for cows that developed a disorder (positive) and those who did not (negative) Type of metabolic disorder Ketosis Displaced abomasum Retained placenta Negative 452 450 449 Positive 574 619 585 VandeHaar et al., 1995 Overview Metabolic Disorders, 27 Why Do Cows Develop Fatty Liver in Late Pregnancy? • Fetal needs receive top priority in late pregnancy: • Glucose is the primary source of energy for fetal growth • Amino acids requirement for fetal growth is high • Dietary crude protein required for maintenance ± 400 g/d • Dietary crude protein required for fetal growth ± 800 g/d • • • Low efficiency of metabolizable energy (ME) utilization for pregnancy (14%) Dry matter intake (DMI) declines the week before calving (± 30%) The cow must rely on volatilve fatty acids (VFA) and long chain fatty acid (FA) from tissue mobilization as primary fuel for non-pregnant body function Overview Metabolic Disorders, 28 (Byers, 1999) • • Fatty Liver Prevention (Treatment) No treatment is truly effective Prevention of excess fatty tissue mobilization should be a priority. Many prevention measures come down to avoid intake depression around calving: • Body condition score (BCS) management • Avoid BCS > 4.25 to avoid slow rise in intake in early lactation. • Do not make cow lose BCS during the dry period. • Promote high dry matter intake • Use good forage quality • Avoid rapid diet changes and unpalatable feeds • Provide glucose precursors (glucogenic rather than ketogenic precursors, especially if ketosis is a problem) • Close up dry ration should contain 6-10 lbs of grain • 6 - 10 oz (200 - 300 ml) propylene glycol (as a daily drench or mixed with concentrates) • 8 - 12 oz (225- 350 ml) calcium propionate Overview Metabolic Disorders, 29 Glucogenic vs. Ketogenic Nutrients Sugars Propionate, Lactate Glycerol Certain amino acids GI tract Liver Liver Liver, adipose tissue Amino acids Peptides Acetate, Butyrate Fatty acids (long chain) Glycerol Certain amino acids GLUCOGENIC Blood Amino acids Amino Acids KETOGENIC -Hydroxy-butyrate Aceto-acetate (Acetone) Milk fat (short chain) Glucose Udder Milk lactose Milk protein All organs Cellular respiration (release of energy) Overview Metabolic Disorders, 30 Disorders Related to Energy Metabolism 2- Ketosis Overview Metabolic Disorders, 31 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 Intake during Dry period: ~0 g/d Lactation: ~0 g/d Body reserve: 0 g Glucose lost in feces: ~0 g/d Glucose secretion in milk (as lactose): 2.3 kg/d (for 45 kg/d of milk) Overview Metabolic Disorders, 32 Ketosis Occurrence: • Occurs 2 to 4 weeks after calving (peak incidence is about 3 week) • Affect most high producing cows (sub-clinically) in early lactation Symptoms: • “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 Detection: • Two changes in the blood related to liver functions • Drop in blood glucose (<50 mg/100 ml) • Rise in -hydroxy butyrate (>14.4 mg/dl) • Presence of ketones in urine (“Ketostick”): • -hydroxy butyrate; Acetone; Aceto-acetic acid. Overview Metabolic Disorders, 33 Ketosis - Prevention • • • • Avoid excessive fatness at calving (proper BCS) Smooth dietary transition between dry cow ration and early lactation ration • Gradual change in forage types • Gradual change in amount of concentrates 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.) Propylene glycol drench • 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). Overview Metabolic Disorders, 34 Disorders Related to Energy Metabolism 3- Rumen Acidosis Overview Metabolic Disorders, 35 Acidity In The Digestive System Feed (Forestomachs) Glandular stomach HCl Saliva Small intestine Large intestine Pancreas 1.0 - 2.0 6.0 - 7.0 Liver Feces pH 6.0 - 8.0 7 2 Overview Metabolic Disorders, 36 Rumen Anatomy and Physiology Ideal pH? Re = Reticulum DR = Dorsal Rumen VR = Ventral Rumen Om = Omasum Ab = Abomasum DR Om Ab Re VR Du Du = Duodenum Overview Metabolic Disorders, 37 Forage to Concentrate Ratio And Rumen pH Volatile fatty acids (VFA) produced in the rumen Total VFA production (moles/day) 60 % 50 40 Propionic Acid 30 Acetic Acid 20 Butyric Acid Rumen pH 6.5 6.0 Milk production and composition 5.5 5.0 Milk production (kg/day) Fat in the milk (%) Concentrates Forages 20 80 40 60 60 40 80 % ration dry matter 20 % ration dry matter Overview Metabolic Disorders, 38 Rumen Acidosis 1-Buffering capacity Level of effective fiber Saliva Diet suppl. 2-Rate of acid production Level of concentrate Total acids Type of acids VFA pKa 9 8 Bicarbonate 7 6 5 Ac. Ac. 4.76 Pr. Ac. 4.87 Bu. Ac. 4.82 Lactate 3.86 pH Scale 3-Rate of acid absorption: (rumen papillae, rumen pH) Overview Metabolic Disorders, 39 “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 pH of rumen content Rumen Acidosis 5.5 Sub Acute Rumen Acidosis 5.0 4.5 - Poor appetite - Little cellulose digestion - Poor microbial growth. - Deep physiological changes - May cause death Acute Rumen Acidosis 0 6 12 18 24 Hours Overview Metabolic Disorders, 40 Risk Factor • • Highest risk: • Last week before calving (if poorly managed transition diet) • The first few month after calving (high concentrate diet) Risk factors: • High concentrate diet (>55% diet DM) • High level of dry matter intake (i.e., high producing cows) • Lush Pasture (less salivation) Dorsal rumen papillae • Method of feeding (TMR vs. separate ingredient) • Poor transition between dry cow diet and high producing cow diet (rumen papillae atrophy) Reticular papillae Overview Metabolic Disorders, 41 Acute Ruminal Lactic Acidosis Fermentable CHO Growth Rate (all Bacteria) pH < 5.0 S. Bovis Lactobacilli VFA pH S. Bovis M. Elsednii Growth Rate (many Bacteria) Rumen Acidosis pH Stasis in Fermentation Nocek, jds 80:1005 Lactic Acid Metabolic Acidosis Overview Metabolic Disorders, 42 D- and L-Lactic Absorbed Rumen Acidosis (Prevention) - Effective Fiber • • • • • Avoid ration with more than 50% Concentrates Limit high starch concentrates (corn or wheat grain) Maintain Sufficient “Effective Fiber” • Ration NDF > 28% • Ration Effective NDF > 21% Changes in diets should always be gradual (over 7-10 days) Total Mixed Rations (TMR) Overview Metabolic Disorders, 43 4 - LAMINITIS Locomotion Score Overview Metabolic Disorders, 44 Locomotion Score Score = 1 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 Overview Metabolic Disorders, 45 Score = 3 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 Overview Metabolic Disorders, 46 5- Displaced Abomasum Overview Metabolic Disorders, 47 Cross Section Abdominal Cavity D A B C A B C D Abomasum = A Rumen = B C = Omasum D = Liver Overview Metabolic Disorders, 48 Detection: Displaced Abomasum (DA) • • Sharp and sudden drop in feed intake “Ping Test” 80% of DAs occur within the first month of lactation. 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., overconditioned cows, overcrowding, etc.,) Cause: • • Prevention: • • • • • 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) Overview Metabolic Disorders, 49 6- Milk Fat Depression Overview Metabolic Disorders, 50 Milk Fat Depression and Forage to Concentrate Ratio Volatile fatty acids (VFA) produced in the rumen Total VFA production (moles/day) 60 % 50 40 Propionic Acid 30 Acetic Acid 20 Butyric Acid Rumen pH 6.5 6.0 Milk production and composition What is the origin of milk fat? Concentrates Forages 20 80 40 60 60 40 5.5 5.0 Milk production (kg/day) Fat in the milk (%) 80 % ration dry matter 20 % ration dry matter Overview Metabolic Disorders, 51 Theories Regarding Milk Fat Depression • • • Acetate deficiency • Low acetate: propionate ratio is not due to lower acetate, but rather an higher amount of propionate. Vitamin B12 deficiency • Ruminal synthesis of vit. B12 is low under high grain diet. Vit B12 is required for propionate metabolism in the liver and elongation of fatty acid chains with acetic acid or -hydroxy-butyrate (BHBA) in milk fat synthesis. Insulin and suppression of fat mobilization • Hormonal messages, with high amount of propionate and possibly glucose absorption in the lower intestine elicitng an insulin response which ten to inhibit fat mobilization and the availability of ketones for fatty acids synthesis in the udder. • Inhibition of the de novo synthesis of short and medium chain of fatty acids in the mammary gland by trans fatty acids (TFA). • TFA are produced during ruminal hydrogenation of polyunsaturated fat supplements (vegetable oils) Overview Metabolic Disorders, 52 Origin of Long Chain Fatty Acids (LCFA) and Short Chain Fatty Acids in Milk Fat Diet Blood/ Lymph Carbohydrates Acetate -hydroxy-butyrate Lipid Long chain fatty acids (LCFA ≥ C16) Udder secretory cells De Novo synthesis Inhibition “Direct” Incorporation of LCFA Milk fat Saturated, short chain fatty acids: C4, C6, C8, C10, C12, C14, C16 Saturated or unsaturated long chain fatty acids: C16, C18, C18:1, C18:2, C18:3 Theories Overview Metabolic Disorders, 53 Role of Trans Fatty Acids (TFA) in Milk Fat Depression • Milk fat depression results from change in rumen hydrogenation (saturation) of fats rather than change in rumen VFA patterns. • TFA are produced from incomplete saturation of polyunsaturated fatty acids (PUFA). • TFA in milk fat is high on high grain-fat depressing-diets. • Vegetable or marine PUFA depress milk fat% even in diets with normal amounts of forage. • Addition of buffer decreases production of TFA in rumen, decreases TFA in milk fat and alleviate milk fat depression • Lower rumen pH (insufficient effective fiber) favors the production of TFA with fat-depressing effects. Fat depression does not occur if rumen pH remains > 6.0 Overview Metabolic Disorders, 54 Dietary Induced Milk Fat Depression Milk fat, % Effective fiber Reduced forage particle size High grain diet 3.0 4.0 Buffer (rumen pH 3.5 above 6.0. Ac:pro Milk Fat ratio per se is not important) restoration High levels of unsaturated Fatty acids Milk fat depression 2.5 Erdman, Tri-State Dairy Conference 1996. Overview Metabolic Disorders, 55 Disorders Related to Mineral Metabolism 1 - Hypocalcemia (Milk Fever) Overview Metabolic Disorders, 56 Hypocalcemia and milk fever Introduction: • • • • • • 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. 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 % of cases 3% 6% 75 % 12 % 4% Timing relative to calving Before calving At calving 1 - 24 h. after calving 25 - 48 h. after calving More than 48 h. after calving Overview Metabolic Disorders, 57 Timing: Calcium balance in dairy cow Fecal loss: 8 g/d Urine loss: 0.5-2 g/d Fetal need: 4.5 g/d Ca intake Dry period: 50 g/d Lactation: 100 g/d Blood Ca: 10 mg/ 100 ml Ca Pool: 3 g Body reserve: Total 6000 g Mobilizable 15-20 g/d Calcium secretion: colostrum: 20 kg x 0.015 = 0.3 kg = 300 g Ca (?) milk: 0 - 50 g/d (milk contains 0.95% Ca) Overview Metabolic Disorders, 58 Hypocalcemia - Symptoms Blood Ca (mg/100 ml) Signs Normal Blood Ca Sub-clinical hypocalcemia Clinical hypocalcemia (Milk Fever) 9 - 11 8-9 7 6 4 Lethargy (dullness and listless behavior) unsteady gait Unable to stand Coma and death Cow has cold ears and a dry muzzle Cow does not eat, and the digestive tract is inactive Overview Metabolic Disorders, 59 Clinical hypocalcemia (milk fever) Inability of the cow to respond to the extra calcium drainage from the blood into the milk at calving. Sudden high demand of Ca Increased diet Ca and P delays the responses (“too little too late”) Drop in blood ca (<5 mg/100 ml) MILK FEVER Parathyroid hormone Vitamin D Synthesis Ca absorption from intestinal tract urinary losses bone mobilization Maintain blood Ca constant (10 mg/100 ml) Overview Metabolic Disorders, 60 Calculating DCAD Milk fever and other metabolic problems: Impact of “hypocalcemic cascade” = Increase Ca demand hypocalcemia (subclinical / clinical) smooth muscle function rumen and GIT mobility left displaced abomasum feed intake mobilization adipose tissue ketosis Milk yield energy balance uterine mobility retained placenta Metritis uterine involution Reproduction performance Overview Metabolic Disorders, 61 Milk fever (MF) - prevention Diet very low in Ca: Lowering dietary Ca to 15 g/c/d for the last 10 days before calving will reduce incidence of milk fever Avoid feeding excess calcium during the dry period: Limit the usage of legumes (alfalfa, clover) in favor of low Ca forages: Corn silage vs. 1/2 corn silage 1/2 alfalfa? Grass hay, oat silage, cornstalks Avoid feeding excess phosphorus during the dry period: Normal Ca, but excess P increase risk of milk fever Ca:P ratio of 2 - 2.5 to 1 is usually the most desirable ratio, but what counts is feeding the correct amounts.... Feeding more P to correct excess Ca adds to the problem! Balance diet for a DCAD of -10 to -15 meq/100 g dietary DM: Overview Metabolic Disorders, 62 Dietary Cation Anion Difference: DCAD Facts about DCAD: • • • • • DCAD = (K + Na) - (Cl + S) expressed as meq / 100 g dietary DM • [(%Na/0.023) + (%K/0.039)] - [(%Cl/0.0355) + (%S/0.016)] DCAD that are positive (0 to 300) indicate an “alkaline” (cationic) ration which tend to alkalinize body fluids (pH>6.4?) DCAD that are negative (-100 to 0) indicates an “acidic” (anionic) ration which tends to acidify body fluids (pH<6.4?) Most of our “typical” diets have feeds high in Na and K leading to DCAD > 0 Recent research showed that DCAD < 0 during the last 3 to 4 weeks before calving have beneficial effects: • Ca status --> “ Hypocalcemic Cascade” • Peri partum health --> • Post partum productive and reproductive performances --> Overview Metabolic Disorders, 63 Calculating DCAD of a ration Diet 1 Ca, % P, % Na, % K, % Cl, % S, % Diet 2 JDS 67: 2939 0.63 0.69 Two year study 0.25 0.24 10 cows/treatment/year 0.53 0.16 1.22 1.22 0.42 0.57 0.15 0.56 DCAD (Meq/100 g Diet DM): [(%Na/0.023) + (%K/0.039)] - [(%Cl/0.0355) + (%S/0.016)] [(0.53/0.023) + (1.22/0.039)] - [(0.42/0.0355) + (0.15/0.016)] [(23.0) + (31.3)] - [(11.8) + (9.4)] [(54.3)] - [(21.2)] DCAD +33.1 -12.8 Milk Fever 47.4% 0% Overview Metabolic Disorders, 64 Disorders Related to Mineral Metabolism 2 - Udder Œdema Overview Metabolic Disorders, 65 Udder edema Symptoms: • • • • Incidence range from 8 to 96% of cows in different herds. Excessive accumulation of fluid in the udder. The source of the fluid is seepage from blood into “interstitial cells” with inability of lymph system to remove “excess” fluid Gravity causes most of the accumulation to occur at the bottom of the udder between the skin and secretory cells. Does not interfere with milk production directly, but may cause: • interference with milk let-down • Difficulty of milking • Long term damage to udder attachment. Overview Metabolic Disorders, 66 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. Prevention: • • Avoid excess salt during the dry period (0.25% of diet DM, 1 ounce/d or 28 g/d). New evidence and possible causes indicate that: • Vit. A, vit. E (1000IU/d) and B-carotene may help alleviate the problem because of their anti-oxidant effects • Avoiding excess iron (Fe) may also be helpful. Overview Metabolic Disorders, 67 Udder edema - Possible cause Increased metabolic activity Increased formation of free-radicals (O2-) Interference with cell membrane structure Interference with steroid hormone synthesis imbalance in fluid balance Udder edema Back to prevention Overview Metabolic Disorders, 68 Disorders Related to Mineral Metabolism 3 - Retained Placenta Overview Metabolic Disorders, 69 Retained Placenta Overview Definition: • • Retention of placental membrane for more than 12 hours after calving Often time this condition is due to bacterial infections, but it might also have a nutritional component Cause: • • Lack of very good sanitation at calving (reduce infections) Deficiency of selenium and vitamin E may be implicated in increased incidences of retained placenta Prevention: • • Daily supplementation: 100,000 IU of vit A; 20,000 IU vit D, and 400 IU vit E., with 3 mg/d of selenium Injections of Se and Vit E: • Twice: 30 and 15 days prior to calving • Once: 15 - 21 days prior to calving Overview Metabolic Disorders, 70