DairyRec1- Transition Diets

prevents clinical and subclinical hypocalcemia and ketosis

• hypocalcemia
• ketosis
• DA
• mastitis
• RP/metritis
• hoof problems/ lameness

• DA b/c of decreased intake
• mastitis d/t depressed immune function
• metritis d/t depressed immune function

• Se deficiency; hypocalcemia
• (high incidence of RP? --> what is their clinical milk fever rate?--> now extrapolate that to include subclinical b/c clinical is just the tip of the iceberg)

• Clinical: down cow, cold ears, dilated pupils, etc
• Subclinical: blood Ca <8-8.5mg/dL

• Clinical: lethargic, off-feed, dehydrated, ADR
• Subclinical: BHBA > 1200mM/L

ketone bodies are derived from fat oxidation (burning up fatty acids--> ketone bodies are what's left)

BHBA/ketones and NEFAs; BHBA

• feeding a lot of fat in the diet (this isn't usually the cause because we don't feed dry cows a lot of fat)
• mobilization of body fat d/t higher BCS and decreased intake

go to the dry group and get blood to rest NEFAs so you can determine if this is a pre-partum problems (you don't want to test BHBA because if they have DAs, you already know it will be elevated; NEFAs normally spike at calving)

• Pre-partum: NEFAs
• Post-partum: BHBA
• both are indicators of negative energy balance/ fat mobilization/ ketosis

Higher milk production

• the cows will be alkalotic--> higher risk for hypocalcemia
• this is usually associated with high K+

• Low Ca and High Ca
• Low Ca diets basically do not exist in the U.S. because our forages are very high in Ca
• High Ca diet is more likely to be related to hypocalcemia in the US

• high Ph increased milk fever risk
• Ph inhibits the enzyme that activates Vit D--> Ph excess--> less active Vit D--> less Ca absorption--> hypocalcemia

• Mg deficiency is a factor for hypoCa
• Mg stimulates the enzyme that activates Vit D--> Mg deficiency--> less active Vit D--> less Ca absorption--> hypocalcemia

• Vit D excess or deficiency is related to hypocalcemia
• Vit D is linked to Ca absorption from the gut

• K, Na, Cl, S must be looked at TOGETHER as a unit
• the biggest offender is K; high K causes hypoCa; forages are high in K+
• Na and Cl don't change very much ever, they are completely dependent on salt content of feed
• S can change a lot depending on fertilization of the soil
• high K is relative to the other DCAD ions; for instance, if you also have high S, the cow can handle higher K

10% of heifers (good herd can get it as low as 4%)

50% of cows in the US have subclinical milk fever

feed DCAD diet—> induce metabolic acidosis—> blood pH drops—> the cow needs to buffer this with Ph from bone—> CaPh is released from bone (the Ca comes along for the ride)—> the excess Ca is removed by the kidney (remember: the cow isn’t producing milk yet)—> cow calves, the bone is already releasing Ca, so once the demand for Ca occurs at freshening, the Ca goes to the mammary instead of being peed out

• gut absorption
• bone deposition/ mobilization
• kidney excretion

feed a marginally Ca deficient diet, the gut will up-regulate and be very efficient at extracting Ca—> feed low Ca diet during dry period so gut gets more efficient at absorbing it, then increase Ca in diet after calving and the gut will absorb a lot of the Ca for milk production [this works in theory but in the US its hard to get a Ca deficient diet]

• once a cow calves, the increase in calcium absorption must occur within 30 hours after she starts producing milk; the gut cannot respond that fast, so blood calcium levels drop transiently after calving
• [this is the rationale behind feeding a marginally deficient Ca diet, so the gut becomes more efficient at absorbing Ca before calving]

• maximize ability to absorb Ca by the gut
• increase Ca resorption from bone
• reduce urinary loss of Ca
• [all require PTH and production of active vit D]

• Very easy to achieve: adequate Mg and Vit D with supplementation
• Usually easy to achieve: low Ph (avoid cheap feeds, which are high in Ph)
• Difficult to achieve: low Ca and Low K (high amounts of these in US forages)

• straw- low Ca, low K [the problem with straw is expense]
• grasses- low Ca

• usually Mg Oxide because is less expensive
• SHOULD USE Mg sulfate because it helps lower blood pH, which can help compensate for high K (remember:we want metabolic acidosis to mobilize Ca in bone)

• -20mEq/100g
• since you can't really reduce Na, you need to reduce K or feed more Cl (not in salt form...don't want to increase NA too)

pre-fresh group; you don't want to feed DCAD more than 2-3 weeks because you can cause osteoporosis if they are mobilizing Ca in bone for that long

• if it's done incorrectly, you will fix the hypocalcemia and cause major ketosis problems
• the biggest reason this causes ketosis is you’re dropping blood pH too much—> with blood pH too low, the cow will stop eating to try and increase blood pH—> low intake—> ketosis

• monitor urine pH (should be ~6.5)
• start DCAD at ~-10mEq/100g, check urine in 2-3 days, titrate DCAD as needed
• continue monitoring urine pH because %K in forages is EXTREMELY variable, between batches and even between spots in one batch

• you often get a bimodal distribution: a group with low urine pH and a group with high urine pH
• this means that some cows aren't eating the diet because it's not palatable

• feed cow starch--> starch is converted to proprionate in the rumen--> proprionate is absorbed into the blood and travels to the liver--> in the liver, proprionate is converted to glucose (almost none of the blood glucose is from the feed; it is all made by the cow)
• ketosis is glucose deficiency, so either the cow is lacking substrates proprionate and AAs (type 1) or the cows liver is not functioning to synthesize glucose (type 2)

• Type 1 (classical ketosis): 2-4 weeks post-partum, cow is not getting enough substrate to make glucose (feed more starch and protein); responds well to therapy
• Type 2 (peri-partum ketosis): pre-partum or 2-3 days fresh; caused by fatty liver; does not respond well to therapy

• [SUBSTRATE PROBLEM] 
• the cow is lacking in proprionate or amino acids--> no substrate for the liver to synthesize glucose--> glucose deficiency--> mobilize and oxidize fat--> increase ketone bodies
• Evaluate the starch and protein in the diet and ensure intake is adequate: 25% starch and 17-19% protein are the goals (adequate proprionate and amino acids)

dry cows are not lactating and have low energy requirements--> positive energy balance, gaining weight--> she gets close to calving and intake drops--> body goes into starvation mode at neutral energy balance and starts mobilizing fat--> NEFAs increase--> high circulating NEFAs go to the liver (b/c they can't go to milk when she isn't making any)--> fat accumulates in liver--> she calves and starts lactating and glucose requirement goes up dramatically--> fatty liver has lost synthetic ability and con't make glucose--> clinical ketosis

they do NOT NEED TO GO INTO NEGATIVE ENERGY BALANCE to get fatty liver and type 2 ketosis

• don't overfeed energy to your dry cows and let them get fat (keep them at neutral energy balance)
• minimize the pre-partum drop in intake as much as possible

• don't overfeed dry cows and give her more energy than she needs--> energy intake drop is much less pre-partum--> she does not enter starvation mode and start mobilizing fat
• FEED LOTS OF FIBER to fill her up so she eats less during the dry period

• 25-27# DMI
• start with 45% NDF (remember: NDF limits intake)--> measure pen intake--> titrate NDF until intake is ~25-27# DMI
• feed straw ideally- high NDF, low Ca and K
• second option is mature grasses- but these have high K so be careful not to cause HypoCa
• feed to NEL requirement (not above or below)

• rumen-protective choline: helps mobilize fat in the liver; expensive so you should have a pre-fresh group if you're going to feed this
• rumensin: stimulates proprionate production and helps stabilize intake; helps with both types of ketosis
• Niacin: NOT PROVEN, don't waste money on this; B vitamin

• Dry Cows--> Lactating Cows
• Dry Cows--> Pre-fresh Cows--> Lactating Cows
• Dry Cows--> Fresh Cows--> Lactating Cows
• Dry Cows--> Pre-fresh Cows--> Fresh Cows--> Lactating Cows

• to feed DCAD because of milk fever problems
• can have a pre-fresh group for management reasons without feeding a specific pre-fresh diet

• Pre-fresh group to feed DCAD
• Or if you're just going to feed low Ca diet, Dry group will work well too

• Type 1: you need a fresh group to ensure fresh cows are getting enough feed
• Type 2: you need to address you dry cow diet

• Add a fresh group
• feed fresh cows higher protein (still 25% starch)--> higher peak milk

more grain

• feed HIGHEST quality forages (50-60%)
• adequate, but not excess, starch (25%)
• high crude protein (17-19%)
• limit fat (<5%) (high fat in early lactation will decrease intake--> type 1 ketosis)
• ADEQUATE BUNK SPACE