Transition, what are our expectations?

Is it our goal to just get cows through calving without clinical milk fever or ketosis? Or, do we see it as an opportunity to achieve high milk production, good health and optimal fertility. Needless to say there is a vastly different financial outcome between these two alternatives. We see both every year.

Obviously transition management should be aimed at the second of these two goals. There is no other stage in a cow’s yearly cycle than transition to determine our financial success. I now count transition as beginning at the day the cow is dried off until three weeks post-calving. My reason is that I’ve become convinced from experience in a number of herds that much of our failings in the above three categories that determine lactation success – milk production, health and fertility, are perpetrated in the dry phase. This is a major problem in Australian dairy production.

Last month’s article addressed this subject; especially calcium nutrition, which we’ve learnt is far from adequate. Energy and protein intakes to sustain a stable live-weight go without saying, but we fail our dry cow in these two as well.

Two defining issues: blood calcium (but also general mineral nutrition) and energy/protein intakes in both dry cows and springing cows. Traditionally, dry cows ingest around 25% of their calcium requirement when on ryegrass pasture, silage or hay. Blood samples we’ve taken from dry cows verify this. Our dry cow is most frequently in subclinical milk fever (subclinical hypocalcaemia) and not even milking! Likewise, blood tests would expose negative energy balance (subclinical ketosis) in many dry cows. Our dry cow is already in deep trouble and still maybe five or six weeks off calving.

Low blood calcium is highly likely to produce impaired immune function, delayed reproduction and bring on other metabolic disorders such as ketosis. We are trialling several methods to lift dry cow calcium intakes this January/February. The herds in which we are having very good success with, apart from adequate calcium intakes (and other minerals too), have the same forage ration as dry cows as they do as springer cows. The only difference is the addition of 3 or 4 kgs of a good Lead Feed grain mix to increase energy and protein intake, and a correct DCAD to mobilise calcium/magnesium reserves from skeletal frame. As we shift our dry cow into the springer cow group, DCAD, or Dietary Cation-Anion Difference, becomes a major management issue; and it can be managed very effectively without feed testing every feed in the ration.

DCAD and cow health and performance are closely intertwined. However, there may be some lack of understanding of this, leading to failure to achieve the best possible results from post-calving feeding. DCAD equation is (sodium + potassium) – (chlorine + sulphur). Sodium and potassium are positively charged ions. Conversely, chlorine and sulphur are negative charged ions. Our goal is a negative DCAD for springing cows for 21 days.

The negative DCAD ration will cause mild blood acidosis and instigate calcium reabsorption from bones to neutralise blood acidity. This then reduces dramatically the massive demand for calcium both, just prior to calving (colostrum contains 9 times the cows whole calcium pool), and post-calving, avoiding both clinical, and if calcium reserves are adequate, subclinical milk fever and their devastating impacts on lactation/fertility performance and profit.

Managing DCAD to ensure it is correct, and it must be correct to be effective, can be done by checking urine pH of a random group of springer cows at least weekly. We want a urine pH of around 6 for Holsteins and 5.8 for Jerseys. Simply adjust the Lead Feed grain up or down to correct this pH reading. We typically run a 3 kg Lead Feed grain mix at -3200meq.

The reward is dramatically reduced milk fever (clinical or subclinical), dystocia (long/difficult calvings), ketosis and retained placenta. Assuming adequate energy/protein post-calving, we have just set up our cow for high milk production potential, good health and high fertility.

A subject virtually unheard of is lactating DCAD; like negative protein balance, they don’t appear on the discussion agenda, yet have significant impacts on all performance parameters. Lactating DCAD should be positive. This is not difficult in our potassium charged pastures, silages and pasture hays. In fact it is commonly way too high inducing both calcium and magnesium deficiencies manifesting, at worst, mid-lactation milk fever and hypomag (flightiness in cows). Lactating cows need a positive DCAD around +200/250. Needless to say, any metabolic disruption from excessive DCAD will impinge on all the production goals.

The other insidious evil so prevalent in our fresh cows is ketosis. The clinical ketosis cow has a very limited future, but the subclinical ketosis cow will be quietly draining your bank account from low productivity in all its forms: Impaired immunity manifesting in mastitis, metritis and other infections; demolishing our fertility goals and as she progresses into mid-lactation and still empty, her feed conversion efficiency plummets – a costly passenger. In many of our clients herds, as fertility has improved providing an abundance of replacement heifers, carry-over cows no long exist. Seasons like this spring/summer we’ve reduced herd size to match feed reserves, and in so doing, rid our herds of any underperforming cows. There is a synergetic benefit of a rising herd genetics as progeny outperform their dams in first lactation. A recent USA speaker at the AARN Nutrition Conference last September, while addressing the subject of amino acid nutrition (fractions/types of protein), stressed: “the highest producing herds in the USA have the highest milk solids tests and the highest fertility”. His stress was necessary, as common belief is the opposite of this, but possibly created by the above issues.

John Lyne is a dairy production specialist with Dairytech Nutrition

johnlyne@dairytechnutrition.com.au