Dealing with Milk Fever Challenges

Irish dairy farms operate with a compact calving pattern and maximising milk from grass, a compact calving season of 6-8 weeks with more cows creates a very stressful time on dairy farms. This coincides with a period when farmers are exposed to one of the most costly disease on the dairy farm, milk fever.  Milk fever is known as the ‘’GATEWAY DISEASE’’ leading to other metabolic disorders such as retained placenta. Milk fever is a major challenge and cost, not only in terms of cow health but also in lost productivity. Milk fever can be clinical and sub-clinical and recent research has shown that sub-clinical milk fever has a major unseen cost and is responsible for 80% of the annual cost of milk fever. Reducing the risk of clinical and sub-clinical milk fever is a key management priority for farmers.

MILK FEVER PREVELANCE

Many studies have been carried out to quantify the incidence and cost of clinical milk fever (blood Ca of <5.5mg/dl).

DeGrais and Lean (2009) average incidence in 10 European countries was 6.2%.

Mulligan and Doherty 2008; Goff 2008; incidence reported 5-7%

Reinhardt in 2011 put the scale in focus, 50% of second lactation and older cows were in the sub-clinical range and 25% of first lactation heifers were also in the sub-clinical range (blood Ca 5.5-8.0mg/dl).

As these studies indicate more cows are in the sub-clinical range than clinical showing that 80% of the annual cost is coming from sub-clinical.

MILK FEVER AND MINERALS

Metabolic problems are mainly caused by nutrition. With milk fever it is an issue of balancing and maximising calcium availability at calving. In the transition period of the dry cow and freshly calved cow factors affecting the ability of the cow to regulate calcium availability are,

1. Calcium, colostrum, has a high demand for calcium. This calcium is taken from the blood and can be 8-10 times greater than in the blood supply causing a rapid drop in the calcium pool. High levels of oestrogen around calving inhibit the mobilisation of calcium.

2. Magnesium, low magnesium intake reduces the ability of the gut to absorb calcium. The role of magnesium cannot be understated, magnesium is critical for the release of PTH and the synthesis of1-25dihydroxy-VitD3. She cannot mobilise magnesium and is dependent on her supply. The potassium reading for the forage/total diet will determine the requirement. The requirement can range from 0.4% – 0.6% magnesium per kg DM in the total diet with Irish potassium readings.

3. Potassium and sodium, cause metabolic alkalosis. Hormones normally work to mobilize calcium from the cow’s bones to increase the efficiency of dietary calcium absorption at calving, but these are inhibited when diets are high in potassium and sodium. These alkalize the blood raising its pH. High potassium will also decrease the availability of dietary magnesium by binding it up in the rumen. The potential issue with metabolic alkalosis can be assessed by having a mineral analysis of the forage so that the DCAD (Dietary Cation Anion Difference) can be calculated. It’s calculated as follows (K+Na)-(Cl+S).

4. Phosphorous, high phosphorous has been shown to increase the risk of milk fever by inhibiting the enzyme converting 25-hydroxy-VitD3 to 1-25-dihydoxy-Vit D3. This inhibition compromises the cow’s ability in the transport of Ca in the intestine which impacts on the balancing of the calcium pool of the cow. A forage or total diet with a phosphorous reading > 0.4%/kg dm is high.

OTHER RISK FACTORS

  1. Age of the cow. Older cows are less able to mobilize calcium.
  2. Breed, Jerseys and their crosses are more likely to have clinical milk fever as they have less receptor sites for vitamin D3.
  3. BCS, body condition score, the ideal score at calving is 3.25. This is assessed externally but one needs to bear in mind the visceral fat around the organs this will also be mobilised on calving. Excess body fat mobilised will coat calcium and magnesium forming soaps and reducing their availability.

5. Toxemia, some cases of milk fever are complicated by a toxemia from infection in the udder, reproductive tract, or digestive system.

THE ROLE OF CALCIUM

Calcium plays a critical role in key areas in the transition period from

1. muscle and nerve function

2. physical barriers of the innate immune response

3. phagocytic response

Muscle function

Calcium is required to optimise muscle function along with magnesium to ensure labour will not be long with expulsion of the calf. Long labour will result with a stressed calf with high cortisol levels, this impacts on the absorption of colostrum and the immune system. One of the early indications of milk fever is a staggered walk. Huber et al (1981) found that rumen contractions ceased well before the onset signs of clinical milk fever. This can result in reduced dry matter intake, research showing 37 kg DM over ten days resulting in a higher risk of displaced abomasum.

Innate Immunity – Physical Barriers X

Increased risk of mastitis

With milk fever the resulting low calcium on muscle function includes the muscle at the end of the teat opening the teat to more infection and mastitis. Curtis (1983) reported that cows with milk fever were eight times more likely to suffer from a case of mastitis.

Tight junction permeability

Ma et al (2000) demonstrated the role of extracellular calcium levels play in the permeability of the intestinal tight junction, a key physical barrier to infection.

 Innate Immunity – Phagocytic Response X

Parturition places a lot of stress on dairy cows increasing cortisol (stress hormone) and is linked with a large impact on immune suppression giving rise to increased susceptibility to disease. The intracellular reserve of Ca is responsible for signalling within the cell and initiation of the immune response to bacterial challenges. Martinez et al (2012) found that sub-clinical milk fever resulted in a higher risk of metritis occurring. The study found that the risk of metritis decreased by 22% for every 1mg/dl increase in blood calcium level recorded over the first three days after calving.

METABLIC DISORDERS

Retained Placenta and Metritis

Retained placentas, also known as retained fetal membrane (RFM) delay uterine involution and increase the incidence of metritis. Metritis is a uterine infection.

In a healthy cow, the immune system attacks specific cells to release the placenta after calving. Hormonal changes and the outpouring of antibodies in colostrum naturally compromise the cow’s immune system at calving. By enhancing the immune system through nutrition, the incidence of retained placenta and metritis will be reduced. Selenium and vitamin E are important here, establish the selenium status of the herd including the in-calf heifers with a blood profile and supplement 1,800 ius of vitamin E. If a diet is high in iron this creates oxidative stress increasing the demand for antioxidants selenium and vitamin E.

As cortisol increases naturally at parturition this can be raised further with over stocking poor head space and not enough cubicles, this increases the demand for energy by 1-2 kg of glucose or the equivalent energy required for 14 litres of milk.

Maintain body muscle tone with protein supplementation, required in the transition period is 1-1.2 kg of metabolizable protein or PDIE. This can be achieved with a crude protein = 13.5%-14% with adequate energy.

ECONOMIC LOSSES OF METABOLIC DISORDERS

Milk fever is a very costly disease as can be seen in the table below in a survey carried out by Nutribio across Ireland with 152 farmers surveyed totalling 16,141 cows. Using the Irish Veterinary cost per incident of metabolic disorder the average cost for a 106 cow herd was €4,767.00. There will always be incidents of metabolic disorders, but they can be reduced and their economic impact to the farmer.

Source:                                      C Guard, Cornell – 1998  

Milk Fever

 

Retained Placenta

 

Ketosis

 

LDA

Deaths% 4 1.5 0.5 2
Culls% 5 6 5 8
Delayed conception days 13 15 10 12
Discarded milk-kg 0 145 0 135
Lost Milk – Kgs 286 550 500 880
 

 

Source: 

Nutribio Data Base

 

Milk Fever

 

Retained Placenta

 

Ketosis

 

LDA

No. of Cows-16,141
% Metabolic disorders 3.8 4.7 1 1
Average No. of Cows/herd-106 4 5 1 1
Average Cost Vet. Ireland-€ 423.00 448.00 320.00 515.00
€ per herd 1,692 2,240 320 515
Total Cost – € 4,767.00
Per Cow – € 44.97

 

SUMMARY

Metabolic problems are nutritional. Playing a central role in milk fever clinical and sub-clinical is calcium metabolism and putting a management strategy in place is key in minimising milk fever and its associated metabolic disorders.

Management strategy,

  1. Analyse the grass silage for its mineral status, potassium, sodium, chloride, sulphur, magnesium, phosphorous and calcium. A dry cow mineral based on Irish silage analysis and background readings needs to supply a minimum of 30 grams of magnesium per cow per day for the dry period.
  2. If the forage has a high DCAD reading (+)150mEq/kg dm then the use of anion salts can play an effective role in calcium metabolism. This would be fed 3 weeks pre calving.
  3. Administration of a calcium bolus can also be of benefit at calving, particularly to older cows.
  4. Critical to managing the calcium status is ensuring the freshly calved cows diet has 0.8% to 9% calcium per kg dm in the total diet.
  5. As calcium is required for muscle tone critical here in addition to calcium is the protein% in the total diet to ensure muscle density is maintained. The diet needs to supply 1.0-1.2 kg of metabolizable protein.
  6. Reduce stress, one cubicle per cow and adequate head space. Increase in stress impacts on the immunity system and therefore increases the demand for energy ensure this is being met.
  7. Body condition score (BCS) at calving critical, ideal a BCS = 3.20. Excess reduces calcium and magnesium availability and reduces dry matter intake.
  8. Feed adequate long fibre to the transition cow.
  9. Retained placenta is failure of to get rid of the placenta by 24 hours. Maintaining the immune system and body muscle stores is critical. Selenium status and vitamin E supplementation critical. A blood profile can establish the selenium status.