One of my favourite books is Modern Dairy Farming that originally belonged to my great, great grandfather and was printed in 1911. It highlights milk fever as the most formidable of all conditions that attack dairy stock.
It also suggests methods of prevention which include a pound of Epsom salts given once a week, two weeks before calving, and keeping a cow with a tendency to the disease in lower condition prior to calving.
Treatment involved atmospheric air being injected into the udder -- I have visions of a farmer using some form of bicycle pump! Thankfully, things have moved on over the past century and milk fever as a metabolic disorder is now understood. With many dry cows now coming into their final month of pregnancy, it may be timely to prepare ourselves for the management of milk fever but, more importantly, its prevention.
Milk fever occurs when blood calcium (Ca) concentration becomes too low to support the functions of the nerve cells and the contractions of muscle tissue. Adequate status of calcium in the blood is in the range of 2-3mmol/l. This is maintained by contributions from the intestines (dietary calcium absorbed) and bones (where 99pc body calcium is stored) against the losses of calcium in urine, faeces and milk. These losses significantly increase after calving. For example, a 500kg cow can put 30g calcium into 25kg of milk every day.
Most cows manage the transition into lactation by mobilising sufficient skeletal calcium to meet the increase in demand, as a newly calved cow cannot absorb enough dietary calcium to compensate for high milk production.
However, cows with an inappropriate diet, hormonal imbalance or poor condition may lose more calcium than they can replace. Subclinical hypocalcaemia increases the risk of mastitis, ketosis, retained placenta and uterine prolapses. All these conditions are seen at calcium blood concentrations of 1.4-2mmol/l.
Clinical signs of milk fever are usually observed 48 hours after calving, with cows exhibiting hypersensitivity, excitability, muscular twitching, weakness and rumen stagnation. These signs are associated with blood concentration of less than 1mmol/l. A cow with milk fever should be propped up, kept warm and injected subcutaneously or intravenously with 8-14g of calcium as calcium borogluconate. Call a vet if you are unsure of this procedure or if the cow fails to improve within a few hours.
To prevent milk fever, cows, before calving, should receive a diet that will induce the metabolism into a calcium-deficient state. This will activate the parathyroid hormone, or vitamin D system, that acts on the bones to stimulate the release of calcium into the blood and accelerates conversion of the vitamin D precursor to an active form to stimulate absorption of calcium from the diet. So, ideally, feed a low calcium intake 10-14 days before calving of 15-20g/cow/day. Maize silage can be useful if you have it as it contains less than 2.5gCa/ kgDM. In comparison, grass silage contains around 4.5g Ca/kgDM and the odd supplement like citrus pulp that contains around 18g Ca/kgDM is very high.
However, after calving, increase the intake of calcium to restore skeletal reserves.
Effective regulation of calcium also relies on an adequate magnesium (Mg) status as it stimulates the mobilisation of calcium from the bone. It's also important in preventing grass tetany, so cows should be supplemented with magnesium of 10-15g/cow/day from 3-4 weeks before calving to 12-14 weeks after calving. Supplementing with magnesium sulphate or magnesium chloride before calving is more likely to prevent milk fever than using magnesium oxide as they have a higher biological availability.
So, obviously, even 100 years ago they were onto something with the Epsom salts that is magnesium sulphate, although they can have a laxative effect.
However, it can be difficult to supply cows with enough magnesium when using magnesium sulphate or magnesium chloride, so using magnesium oxide may be more appropriate.
High potassium (K) impairs the absorption of dietary magnesium and can be high in spring pastures, so avoid spreading high amounts of potassium fertiliser early on or be careful on paddocks with heavy, high soil potassium readings. Aim is to keep pasture potassium below 3.5g/kgDM. Calcium status can also be affected by the cow's dietary cation-anion difference (DCAD).
Very high cation intake (potassium and sodium) can raise blood pH and impair the mobilisation of calcium from the bone. While large amounts of anion salts can improve DCAD, they are poorly palatable and tend to reduce intake.
Dr Mary Kinston is a farm consultant based in Kerry. Email: email@example.com