Feeding the Dairy Cow Have to Understand the Lactation Curve.

Feeding the Dairy Cow

Have to Understand the Lactation Curve

Your Handout

Lactation Curve

Lactation curveGradually 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”

10 wk

Highfertility

No metritis

Critical Days

0

-8 wk

44 wk oflactation

-3 wk

Deliver a healthy calf No milk fever

No retained placenta

Increase DMI

No fatty liver

No displaced abom.

No ketosis

Limited loss of BCS

No mastitis

High peakproduction

6-8 wk

2 31 5 64 7 8 109 11

Energy balance- - - - - - 0 + + +

Managing Cow During Critical Days

-8

Dried-off

Wk

Far-off

-4

Calving stressDepressed Immune system

Acute calcium demand

Calving“Close up”

0-1-2-3

Successfulinsemination

Bred

Fat mobilization

High forage diet High Conc. DietHighest Req.Lowest Req.

Slow rise in DMI(rumen capacity)

Lowest rumencapacity & 50% loss in absorption by papillae

Severedropin DMI

Early lactationDry period

Production &

reproare set for

thenext 200-

days

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

2- Udder edema1- Hypocalcemia (Milk Fever)

2- Ketosis (Acetonemia)1- Fatty Liver Syndrome

3- Retained Placenta

5- Displaced Abomasum

3- Rumen Acidosis

6- Milk Fat Depression

Energy-Related Disorders

Minerals & Vitamins-Related Disorders

4- Laminitis (Locomotion Score)

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

Ketosis or Acetonemia

Glucose lost infeces: ~0 g/d

Body reserve: 0 g

Glucose secretion in milk (as lactose): 2.kg/d

(for 35 kg/d of milk)

Intake during Dry period: ~0 g/d Lactation: ~0 g/d

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!

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)

Grummer, 1993

5

10

15

20

25

Dry Matter IntakeKg/day

Weeks relative to calving

0-1-2 1 2 3

200

400

600

800

1000

Non-EsterifiedFatty Acids um/l

30 -35%intakedepression

300%Increased fatmobilization

Triglycerides

Adipose tissue

NEFA FFA

Liver

Key:NEFA = Non-Esterified Fatty Acids FFA = Free fatty acidsTG-r-LP = Triglyceride-rich-lipoproteins or Very Low Density Lipoprotein (VLDL)

Excess Fat Mobilization Means “Liver Problem”

Energy

Ketones

Triglyceride

TG-r-LP Storage

Fatty liver

FFA

Milk fat (Triglycerides)

GlycerolEnergy

TG-r-LPKetones

Low blood glucoseLow insulin

++

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

A

BC

L

B

C

L

A

Abomasum = A

Rumen = B

C = Omasum

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

pH1.0 - 2.06.0 - 8.0 6.0 - 7.0

7

2

Feed

Feces

(Forestomachs)Glandularstomach

LiverPancreas

Small intestineLarge intestine

HCl

Saliva

“Average” pH vs. Length of Time Under 6.0

pH o

f ru

men

con

tent

Hours

5.5

6.0

5.0

4.5

24181260

Sub Acute Rumen Acidosis

- Poor appetite- Little cellulose digestion- Poor microbial growth.

- Good appetite- Good cellulose digestion- Good microbial growth.

Rumen Acidosis

Length of time under pH 6.0 and cow-to-cow variations must be taken into account in the diagnosis of rumen acidosis

Acute Rumen Acidosis - Deep physiological changes-

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

Walk rapidly and confidently, making long strides with a level back

Walk more slowly, making shorter strides with an arched back

Difficult to detect any weight transfer from affected limb

Score = 1

Score = 2

Often thin,walk slowly making deliberate short steps with an arched back and frequent stops

Usually 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 pain

Score = 3

Score = 4

Weight transfer will cause sinking of the dew claws on the contra-lateral limb Encounter some

difficulty turningStand with an arched back and frequently rest lame foot

Extreme difficulty turning

Stand and walk with an arched back

8- Milk Fat Depression

Volatile fatty acids(VFA) produced

in the rumen

Milk productionand composition

Propionic Acid

Milk production(kg/day)

Total VFAproduction(moles/day)

Milk Fat Depression and Forage to Concentrate Ratio

Rumen pH 5.55.0

6.06.5

Acetic Acid

Butyric Acid

Fat in themilk (%)

50

Concentrates20 % ration dry matter80 % ration dry matter

Forages 80 60 4020 40 60

60 %

20

30

40

Udder edema 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.

Cause:

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)