5 Lactation Curve Lactation curve Gradually increases following calving Peaks at days in milk (DIM)Stage 1 is where most metabolic diseases occur.
6 CuresThere 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”
7 Critical Days 90-100 days Deliver a healthy calf No milk fever No retained placenta-8 wk44 wk oflactationIncrease DMINo fatty liverNo displaced abom.No ketosisLimited loss of BCSNo mastitisHigh peakproduction6-8 wk-3 wkdays10 wkHighfertilityNo metritisNot 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 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 days after calving.The usual problems usually interfereing with these objectives include:….
8 Managing Cow During Critical Days Early lactationDry period-8Dried-offWkFar-off-4Calving“Close up”-1-2-32315647810911Energy balance- - -- --++ +SuccessfulinseminationBredFat mobilizationHigh forage dietHigh Conc. DietHighest Req.Lowest Req.Calving stressDepressed Immune systemAcute calcium demandProduction &reproare set for thenext 200- daysSlow rise in DMI(rumen capacity)Lowest rumencapacity & 50% loss in absorption by papillaeSeveredropin DMI
9 DMI is the Key Dry matter intake (DMI) General shape of curve is same as for milkPeak is later in lactation than milk curve
10 About Metabolic Disorders Metabolic disorders occur primarily in early lactationperiod of great stress and drastic changes in nutritional requirementEnergy metabolism(ketosis, fatty liver, rumen acidosis)Minerals and vitamin metabolism (milk fever, metritis, udder edema, retained placenta)
11 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
12 DMI Dry matter intake Factors used to estimate DMI: body weight milk productionfat testdays in milk
13 Overview of Metabolic Disorders in Dairy Cattle
15 Disorders Related to Mineral Metabolism 1 - Hypocalcemia (Milk Fever)
16 Hypocalcemia and milk fever Most cows suffer from (sub-clinical) hypocalcemia in early lacationClinical 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.
17 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 repeatMore than about 5-8 % incidence in a herd is cause for concernIf you find milk fever in dry cows, there is a problem with your mineral balance of Ca:P
18 Prevention Calcium levels during Close-up period Check forage levels?DCAD level – negative 20 (neg )Urine pH 5.5 to 6.0 during the close up timeUse palatable sources to lower DCADSoy-clor, Bio-clor, MolassesAnionic Salts - less palatable
19 Disorders Related to Mineral Metabolism 2 - Retained Placenta
20 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 componentDeficiency of selenium and vitamin E and imbalance of Calcium may be implicated in increased incidences of retained placenta
21 Prevention Provide 2400 – 2500 IU Vitamin E during close up Provide selenium in combination with vitamin EMonitor forage Calcium levelsThis can sneak up on you!
22 Disorders Related to Energy Metabolism 3 - Ketosis
23 Glucose secretion in milk (as lactose): Ketosis or AcetonemiaInsufficient glucose is the source of ketosis or acetonemia:Blood concentration of glucose drops from 50 mg/100 ml to< mg/100 ml Signals cow to digest body fat!Body reserve: 0 gGlucose lost infeces: ~0 g/dIntake duringDry period: ~0 g/dLactation: ~0 g/dGlucose secretion in milk (as lactose):2.kg/d(for 35 kg/d of milk)
24 KetosisOccurs 2 to 4 weeks after calving (peak incidence is about 3 week)Affect most high producing cows (sub-clinically) in early lactationDetection: Urine - Ketostik
25 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 dullnessSymptoms:
26 Ketosis - PreventionAvoid excessive fatness at calving (proper BCS) < 4.25Smooth dietary transition between dry cow ration and early lactation rationClose-up ration should contain same feeds with anions and NiacinNo BicarbGradual change in forage typesGradual change in amount of concentrates
27 Disorders Related to Energy Metabolism 4 - Fatty Liver
28 Lower Intake at Calving Means Increased Fat Mobilization (Blood NEFA) 510152025Dry Matter IntakeKg/dayWeeks relative to calving-1-21232004006008001000Non-EsterifiedFatty Acidsum/l300% Increasedfatmobilization30 -35% intakedepressionGrummer, 1993
29 Excess Fat Mobilization Means “Liver Problem” TriglyceridesAdipose tissueNEFAFFALiverEnergyTriglycerideLow blood glucoseLow insulin++TG-r-LPStorageFatty liverKetonesUptake 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.FFAMilk fat(Triglycerides)GlycerolEnergyTG-r-LPKetonesKey:NEFA = Non-Esterified Fatty AcidsFFA = Free fatty acidsTG-r-LP = Triglyceride-rich-lipoproteins orVery Low Density Lipoprotein (VLDL)
30 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.)
31 Band Aid = Metabolic Switch Propylene glycol drench or pastePropylene 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
34 Displaced Abomasum (DA) Sharp and sudden drop in feed intake“Ping Test”80% of DAs occur within the first month of lactation.
35 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 cavityStress conditions that limit dry matter intake and gut fill in early lactation (e.g., over-conditioned cows, overcrowding, etc.,)
36 Displaced Abomasum (DA) Avoid over-conditioned cows (body condition score >4.0)Begin concentrate feeding ( % 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 dietMinimize stress due to other peri-parturient diseases (milk fever, ketosis)
37 PreventionManagement is implicated in too many cases of DA’s!
38 Disorders Related to Energy Metabolism 6- Rumen Acidosis
39 Acidity In The Digestive System Feed(Forestomachs)Glandular stomachSmall intestineLarge intestineHClThis 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 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 ofOne 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.SalivaPancreasLiverFecespH72
40 “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.6.0Rumen Acidosis- Poor appetite- Little cellulose digestion- Poor microbial growth.5.5pH of rumen contentSub Acute Rumen Acidosis5.0Acute Rumen Acidosis- Deep physiological changes-4.56121824Hours
41 Rumen Acidosis (Prevention) - Effective Fiber Avoid ration with more than 50% ConcentratesLimit high starch concentrates (corn)Maintain Sufficient “Effective Fiber”Ration NDF > 32%Ration Effective NDF > 22%Gradual Changes in diets Total Mixed Rations (TMR)
43 Locomotion Score Score = 1 Score = 2 Walk rapidly and confidently, making long strides with a level backScore = 2Walk more slowly, making shorter strides with an arched backDifficult to detect any weight transfer from affected limb
44 Score = 3 Score = 4 Often thin, walk slowly making deliberate short steps with an arched back and frequent stopsWeight transfer will cause sinking of the dew claws on the contra-lateral limbStand with an arched back and frequently rest lame footEncounter some difficulty turningScore = 4Usually very thin, move very slowly making frequent stops to rest affected limb, which is only partially weight-bearingGrinding of teeth and/or drooling of saliva are signs of acute painStand and walk with an arched backExtreme difficulty turning
46 Milk Fat Depression and Forage to Concentrate Ratio Propionic AcidMilk production(kg/day)Total VFAproduction(moles/day)Volatile fatty acids(VFA) producedin the rumen50Concentrates20 % ration dry matter80 % ration dry matterForages8060402060 %30Acetic AcidButyric AcidRumen pH5.55.06.06.5Milk productionand compositionFat in themilk (%)
47 Udder edemaCause: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 problemExcess 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.
48 So How Do We Feed1. Forages should be of very high quality to encourage intake of roughageNDF 32% ADF 22%2. Maintain at least 45% of ration DM in foragesCorn SilageAlfalfa HayOther SilagesOther Hays
49 So How Do We Feed 3. Supply Adequate Energy (NFC <40%) Carbohydrates – grain(starch & sugar <30%)CornSorghumOther GrainsLipids (EE %)tallowby-pass fat (Megalac, Energy Booster)Pay attention to specific LCFA
50 So How Do We Feed 4. Feed high quality protein sources Ration DM Protein% %Soybean mealCottonseed mealBlood mealFish Meal
51 So How Do We Feed5. Allow rumen synthesis of proteins by feeding a balance of forage, energy and protein precursors.Watch manure for indicators of acidosisWatch manure for tightness or looseness
52 So How Do We Feed6. Balance remaining fraction or ration for minerals, vitamins, etcCalcium ~1%Phosphorus~.35%Potassium % + DCAD BalanceMagnesium %Vitamin A – 240 (KIU/day)