Chapter 5

The Effect of Nitrogen Fertiliser Use on Dairy Cow Health and Production

 

Richard J. Eckard

ILFR, The University of Melbourne &

Agriculture Victoria, Ellinbank

 

 

In this chapter, find information on:

 

·        The effects of high nitrogen levels in pasture on animal health and milk production

·        Ways of managing potential nitrogen-related health problems in dairy cows

 

With the increasing use of nitrogen fertiliser on dairy pasture in Victoria, farmers have been noting an increase in nutritional disorders in their cows. It is stressed that these disorders are usually associated with the following:

¨      volunteer weeds (i.e. capeweed);

¨      volunteer regrowth of brassicas (i.e. turnips), and

¨      sometimes stressed annual ryegrass, short-rotation ryegrass, oats or kikuyu fertilised with nitrogen.

It is important to note that perennial ryegrass and/or cocksfoot and white clover pastures are NOT known to accumulate excessive nitrate.

 

The other important point is that these adverse symptoms are almost exclusively associated with combinations of:

¨      starved or hungry cows;

¨      dry cows or heifers;

¨      cows with no energy supplement (i.e no grain in the diet), and/or

¨      cows unadapted to the forage on offer (i.e for some reason the diet changed suddenly, like moving from a paddock with no capeweed, to one with lots).

 

Grazing management

 

The timing of grazing, relative to nitrogen fertiliser application, may adversely affect cows. Figure 1 shows the pattern of nitrogen uptake, as nitrate-nitrogen or crude protein in the plant, after grazing and subsequent application of nitrogen fertiliser. The following observations, from Figure 5.1, are important:

¨      depending on condition, it usually takes around 4 to 5 days for the applied nitrogen fertiliser to dissolve into the root zone and to be taken up by the plant;

¨      nitrate levels in the plant peak around 7 to 14 days post nitrogen application;

¨      protein levels in the plant peak slightly later, usually around 16 to 18 days;

¨      usually nitrate levels in the pasture drop off to acceptable levels by 18 to 21 days post nitrogen application.

¨      note that the data in Figure 5.1 is for annual ryegrass, a nitrate accumulating species, and not perennial ryegrass, which has much lower nitrate levels (see Table 5.1).

 

Figure 5.1.  The pattern of nitrate and crude protein accumulation in annual ryegrass following nitrogen fertiliser application post grazing. Dotted line represents Nitrate-N and solid line crude protein, with horizontal lines indicating potential toxicity limits.

There are two main health problems that may be associated with nitrogen fertiliser management, namely nitrate toxicity and ammonia induced bloat.

 

Nitrate Toxicity

 

Nitrate toxicity is not common in dairy pasture systems in south eastern Australia and almost always associated with a volunteer forage crop or capeweed. Death from nitrate toxicity usually occurs when unadapted, hungry and/or dry cows (no grain), are subjected to a sudden change of diet. A good example of this is moving dry cows or heifers from a pure perennial ryegrass/white clover pasture, to a pasture in which a volunteer forage crop or cape weed has invaded. This does not have to be associated with nitrogen fertiliser applied to the weeded paddock, as these crops can accumulate high levels of nitrate in response to stress (i.e. frost) or time of the year (i.e a warming soil in spring releases nitrogen).

 

Whilst nitrate is a normal plant product, when it enters the rumen it is converted into nitrite.  At low levels nitrite is converted into ammonia in the rumen, however at high rumen nitrite levels, or if nitrite production is rapid, then the nitrite diffuses into the blood and competes with oxygen for uptake by haemoglobin. This results in a decrease in the oxygen carrying capacity of the blood and thus the cow suffers from anaemia.

 

Symptoms in the live animal include marked anaemia (pink mucous membranes), bright-red (changing to brown) blood, profuse salivation and purging and muscular spasms leading to paralysis.  Treatment usually involves an intravenous injection of methylene blue solution repeated every 4 to 5 hours as required. However, this should be administered in consultation with a veterinarian.

 

It is important to note that there are pastures and forages that are known to accumulate potentially toxic levels of nitrate, and others that are not. From the list in Table 5.1 it is important to note that nitrate toxicity is not know to occur on a perennial ryegrass/white clover pasture, but may occur in annual ryegrass and short-rotation ryegrass (ie. Concord), given the right conditions.

 

Table 5.1. Some of the forages and weeds grown in Victorian dairy pasture systems, categorised according to their potential to accumulate toxic levels of nitrate, given the right conditions

 

Forages which are KNOWN to accumulate potentially toxic levels of nitrate

Forages which are NOT KNOWN to accumulate potentially toxic levels of nitrate

¨      Annual ryegrass (i.e. Tama)

¨      Short Rotation ryegrass (i.e Concord)

¨      Oats, Rye, Wheat and Barley

¨      Maize

¨      Millet

¨      Kikuyu

¨      Cape Weed

¨      Brassica tops (i.e turnips, pasja)

 

¨      Perennial ryegrass

¨      White clover

¨      Red Clover

¨      Cocksfoot

¨      Timothy

¨      Brome grass

 

In discussing potentially toxic limits it would be important to stress that these are applicable to unadapted or hungry stock. Ruminants can tolerate excessive nitrate in their diet if adapted first.

¨      plant nitrate levels above 0.65 % NO3-N in pasture are potentially dangerous;

¨      plant nitrate levels above 0.90 % NO3-N are potentially fatal, and

¨      plant nitrate levels above 1.2% NO3-N will cause death in most unadapted stock.

 

Refer to Figure 5.1 for the context of these levels for annual ryegrass.

 

There are certain conditions that will lead to accumulation of nitrate in plants

¨      Soil Nitrate: The most obvious factor affecting nitrate levels in plants would be an excess of available soil nitrate. This may result from fertiliser application, but may just as easily result from clover and natural soil mineralisation at the autumn break or in spring.

¨      Plant stress: Any stress on plants causes them to accumulate higher nitrate levels than normal. Common examples are water stress, herbicide application and frost.

¨      Weather: Plants subjected to a combination of low soil moisture, continuous cloud cover (low irradiance) and high temperature for a period of 4 to 5 days will accumulate nitrate.

¨      Plant age: Newly sown pastures and crops, as well as young regrowth tends to be higher in nitrate. A practical application of this would be to avoid young capeweed or regrowth, but plan to grazed it off when fully grown out. Also, do not apply nitrogen fertiliser to Brassica crops within 6 weeks of the expected grazing.

 

Ammonia Induced Bloat, Clinical and Sub-clinical Ammonia Toxicity

 

This is also referred to as ‘free gas bloat’, ‘sad-cow syndrome’ or 'belly-ache'. Please note that, at this stage there is no formal name known for these disorders, with the name used in the title merely the best available description of the problem.

 

Historically, most disorders associated with nitrogen are blamed on Nitrate toxicity. However, a number of dairy farmers in Victoria are now reporting cows with 'belly-ache' or 'sad-cow syndrome', with symptoms NOT usually associated with nitrate toxicity.  As these disorders are distinctly different in cause and effect, it important to identify the specific cause, as preventative management may be very different.

 

Again it must be emphasised that these disorders are more commonly associated with annual or short-rotation ryegrass, fed with high rates of nitrogen in spring or autumn, and that unadapted, hungry and/or dry cows (no grain) are most susceptible.

 

Ammonia-induced bloat occurs with animals not used to high levels of dietry nitrogen.  Where cows are adapted to a high level of dietary nitrogen, the ammonia released in the rumen is quickly assimilated into microbial protein, particularly if an energy supplement is given. However, if unadapted cows are subjected to a sudden increase in protein intake, excess ammonia builds up rapidly in the rumen and, together with other gasses, may result in a free-gas (non-frothy) bloat.

 

Clinical Ammonia Toxicity is not common, but has been noted in extreme cases. Excessive rumen ammonia is absorbed through the rumen wall into the blood stream resulting in nervous symptoms, paralysis and death. Blood-ammonia levels are part of a natural apatite repression mechanism regulating protein intake in cows. When hungry animals are released into a pasture, the animals engorge themselves on the new forage.  If the pasture contains high levels of nitrogen, the empty rumen may be filled with herbage high in nitrogen. By the time the intake-control mechanism signals the animal to stop eating, the rumen is already full of excess ammonia.

 

Sub-Clinical Ammonia Toxicity is of more concern to dairy farmers because of the production losses associated with sub-clinical ammonia toxicity. Typically, animals on high nitrogen pastures are under an energy stress, due to:

·        an inverse relationship between plant nitrogen and available carbohydrate (i.e high nitrogen, low sugar), and

·        rumen microbes require extra energy to metabolise the surplus rumen nitrogen.

·        excess blood ammonia must be excreted as urea in the urine. The energy used to convert ammonia in the blood to blood-urea has been estimated to cost the equivalent of 2 to 3 litres of milk per day.

 

Lactating dairy cows require around 16 - 18 % crude protein (2.6 - 2.9 % nitrogen) in their normal diet. Most ryegrass and clover pastures have nitrogen levels above 20% crude protein. Again it must be emphasised that ruminants can adapt to diets high in nitrogen, and that potential toxic limits apply to unadapted or hungry stock.

·        Crude protein levels above 22 to 25 % would be loading cows with an energy stress;

·        Crude protein levels above 30% may cause ammonia-induced disorders in unadapted stock, dry stock (no grain) or hungry stock.

 

Common early warning signs of ammonia-induced bloat and sub-clinical ammonia toxicity are:

·        'belly-ache' or 'sad-cows'. Cows refusing lush pasture, usually due to a build up of ammonia, carbon dioxide and methane distending the rumen;

·        an ammonia smell in the dairy from cows belching rumen gas higher in ammonia, and

·        urine scalding in the pasture, as cows excrete the excess ammonia as urea in urine. Within a urine patch the nitrogen rate is equivalent to between 800 and 1600 kg nitrogen fertiliser/ha (1.7 – 3.5 tonnes urea/ha).

 

Treatment

·        Cows with an ammonia-induced bloat usually seek out lower quality roughage as a 'scratch factor' to get the rumen moving again. A low quality bale of hay in the corner of the paddock may be used as a useful indicator, if you suspect a problem.

·        In extreme case of ammonia induced bloat a stomach tube will relieve the pressure, as will making the cows run (jogging the rumen sometimes results in belching).

·        Other options in extreme cases include an oral drench of vinegar to counteract the ammonia, or the use of a heavy gauge needle to release rumen gas. However, these should preferably be left to a veterinarian as the rumen may require re-inoculation after a vinegar drench, and a needle may rip the rumen wall if the rumen moves during the procedure.

 

Conclusions

 

·        Most cases in Victoria are related to dry cows or heifers being subjected to a rapid change in diet, most times without the farmers conscious knowledge. A good example is moving cows from as pure ryegrass pasture, to one with a large amount of young capeweed or volunteer Brassica – this should be avoided;

 

·        Do not graze pastures seven to 14 days after nitrogen fertilisation, as nitrate levels are highest. However, nitrate levels in perennial ryegrass pastures seldom reach toxic levels, regardless of time of year, or period of regrowth;

 

·        Do not graze pastures 14 to 18 days after nitrogen fertilisation, if protein problems are suspected;

 

·        Do not apply more than 50 kg Nitrogen per hectare in a single application, particularly after the autumn break and in spring;

 

·        Never give starved, unadapted or dry cows, unrestricted access to highly nitrogen-fertilised pastures, and

 

·        Cows that are suffering as a result of excess nitrogen in their diet tend to select for lower quality roughage. A bale of low quality ‘bedding’ hay in the corner of the paddock can be used as an indicator of nitrogen stress.

 

For more information, or a more detailed article, please contact the author.

Data from a completed project funded by DPI and the Dairy Research & Development Corporation

Return to Home Page

Last modified:29 January, 2002                         Please Note: Disclaimer             Authorised and maintained by:Richard Eckard
Copyright © 1997-1999, The University of Melbourne.