Sub-clinical Milk Fever & Ketosis (The silent thieves of profit)

Worse than a second mortgage – we can see the damage this one does on monthly bank statements. Sub-clinical metabolic disease (MF & Keto) work silently against milk production, immunity, mastitis, metritis, displaced abomasum and worse, our equal profit driver with milk production; fertility!

Awareness of their existence is often hazy, let alone their prevalence in the herd. Sub-clinical milk fever and ketosis are often described as “iceberg” diseases: what is visible is only the tip of the iceberg with a far greater portion under the surface, and far more costly.

Sub-clinical milk fever usually occurs with 24 to 48 hours after calving (and often lingering for some time after as random blood testing in a client’s herd has well verified), however, in light of the average cow’s calcium intake in late lactation, and especially during the dry and springer phases, it is highly likely it exists even prior to calving. Bear in mind, the first test bucket of colostrum contains nine times the cow’s whole calcium pool. She has already shifted a very significant volume of calcium from her reserves into colostrum synthesis. And that’s assuming she had a good calcium reserve to start with, which we are now questioning based on general calcium nutrition and recent research on this subject.

Research has quantified the cumulative effects of sub-clinical milk fever: 3.2 times increased risk of metritis. 2.4 times increased risk of fever post-calving. Almost without saying, induces sub-clinical ketosis if not already present. Longer average days open. If you are aware or suspicious this is an issue in your herd; you are not alone. Estimates are 54% of mature cows and 25% of heifers succumbing to sub-clinical milk fever. These are big numbers in anyone’s herd to be underperforming.

Where do we go from here? Firstly, I think calcium nutrition through the whole annual cycle of a cow’s life is number one. We are currently doing our own research/trials in this based on dramatic improvement, particularly in fertility, we’ve witnessed when calcium has not been a limiting or debilitating issue. At present, this is a work in progress, but showing very favourable response.

Detection of sub-clinical milk fever can only be through blood tests for blood calcium concentration. If you have the vet coming for other reasons, I strongly urge you to hold back a random half dozen very fresh cows for blood samples to be taken from. This will give some idea of the prevalence of the problem. Calcium drench is the remedy.

Obviously a good quality Lead Feed grain mix for springers is next; however, this MUST be verified by checking urine pH of springer cows at least weekly, but preferably twice weekly to ensure DCAD is right (Holstein 5.8 to 6.5 pH & Jerseys 5.6 to 6.2 pH). If every other task related to milk production were less diligent, this one could go a long way to compensate. Healthy, uninhibited cows produce milk, get in calf and make profit.

The greatest danger in not checking urine pH comes from varying potassium levels in the springer ration’s forage. Silage or hay from different paddocks on farm, and more so, bought-in forage, can have dramatically differing potassium contents. Potassium is a very strong positive charged ion and has power to decimate the best designed transition program. We have seen herds with ‘seamless’ transition plummet to cows going down with clinical milk fever, some even before calving, and some never rose again. A DCAD either too high or too low will have the same devastating effect in milk fever; entirely due to variations in potassium content of forages. It is not practical to test all forages to be used for springers: urine pH checking alerts immediately to a problem. Urine pH strips are cheaply available at www.animart.com. We also have them in stock – call Tina on 0400 991 814.

The other twin, sub-clinical ketosis, as rarely are they not ‘co-joined’: equally as devastating to overall profit and equally as prevalent. Again research shows sub-clinical ketosis affects 40% to 60% of fresh cows at a cumulative impact average of $300/case. This one regularly starts in dry cows due to insufficient energy intake to sustain the dam’s maintenance energy requirement and her unborn calf. Inadequate energy can also be induced by a low protein dry cow diet. Worse, often the quality of the dry cow ration is inadequate in both energy and protein.

The onset of ketosis is usually five to nine days post-calving. However, we have certainly verified its sub-clinical existence in dry cows through blood tests. Post-calving, sub-clinical ketosis is easier to both detect and treat. Milk Keto Test strips to check milk of fresh cows will soon identify its presence. The treatment is very simple – 250 mls of propylene glycol drench. I suggest you check treated cows again three or four days later to ensure the cow has passed from sub-clinical ketosis. If not, drench again with propylene glycol. Milk Keto Test Strips are available from either www.animart.com or call Tina in our office and she will post some to you.

Sub-clinical ketosis is usually in this early stage of lactation and relatively easy to remedy. The later stage, around five to six weeks after calving, is a more severe scenario and usually is clinical in nature – downer cow. This cow needs both propylene glycol to ‘kick-start’ the liver to process excess fat accumulation, but also dextrose to give her an energy boost.

John Lyne is a dairy production specialist with Dairytech Nutrition

www.dairytechnutrition.com.au