In most high rainfall sub-tropical climates of the world, many livestock producers are intensifying their pasture systems in response to research input and increased financial constraints. With the intensification of grazing systems, adequate fertilization of the pastures is required to produce the dry matter yields required to maintain high levels of herbage and animal production. In recent years there have been many reports of stock mortality, bloat, reduced animal growth rates and apparent lack of acceptability of intensive pastures. A number of these adverse affects may be due to the presence of high nitrogen levels in the herbage. Research at the Cedara Agricultural Development Institute, South Africa, has suggested that nitrogen (N) fertilizer applications above 50 kg N/ha/application, at certain times of the year, may result in plant N levels of 4.0 to 5.4% (25 to 34% crude protein) and plant nitrate levels as high as 0.9 to 1.0% nitrate nitrogen (NO3-N) in the herbage. These high levels of N in the herbage are not only in excess of plant requirement, but are in excess of animal requirement. Furthermore, the high levels of N in the herbage are potentially toxic to ruminants.
Ammonia-induced bloat (as opposed to frothy-bloat) results from ruminants eating herbage containing high levels of rumen-degradable nitrogen. In the rumen, the ingested nitrogen is rapidly converted to ammonia, which is then converted into microbial protein and other forms of nitrogen. The ingestion of excessive quantities of such nitrogen may result in a build-up of ammonia gas in the rumen, as rumen micro-organism's, that convert ammonia to microbial protein, may be limited. In most grasses, the carbohydrate and nitrogen fractions are inversely related. Furthermore, the energy required to metabolize the excess nitrogen increases as the nitrogen content of the herbage increases. Under conditions of high nitrogen, without sufficient energy for microbial assimilation, a build-up of ammonia occurs in the rumen. This excess ammonia may lead to alkalosis and rumen stasis (paralysis of the rumen wall), thus preventing eructation (release of stomach gas via the mouth). Without the release of this ruminal (ammonia) gas, the animal bloats. Samples of ruminal contents, from animals suffering from an ammonia bloat, will show a strong alkaline reaction (pH 7.5 plus).
High blood-ammonia levels form a negative feedback to control intake. When the levels of blood ammonia reach a critical cut-off point, a "message is sent to the animal to stop eating". Where ruminants are not under an intake stress, this intake-control mechanism maintains the control of nitrogen intake by controlling intake of herbage with a high nitrogen content.
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 content. By the time the intake-control mechanism signals the animal to stop eating, the rumen is already full of herbage with a high N content, the total effect of which is potentially toxic to the animal.
TWO COMMON SCENARIO'S FOR AMMONIA BLOAT
When ruminants are grazed on a lush ryegrass pasture they tend to select less lush and more fibrous herbage. Possible causes of ammonia bloat on ryegrass are therefore, (a) that the ruminants preferentially graze the wilted ryegrass for its higher fibre content and, in eating it, ingest a more concentrated form of nitrogen due to the wilting, and (b) that the wilted or stressed ryegrass may contain small quantities of prussic acid, which may contribute to rumen stasis, thus aggravating the ammonia bloat. As ryegrass has not yet been proven to contain prussic acid, further research is still required. However, animals on ryegrass have been noted to exhibit the symptoms of mild prussic acid toxicity. Furthermore, many of these pastures may contain clover which, when stressed, may accumulate prussic acid.
Management of Ammonia Bloat
In most cases, good management will control instances of ammonia bloat. The following management practices should be borne in mind:
Treatment of Ammonia Bloat
If not administered early, treatment is unlikely to be effective. On positive identification of ammonia bloat, immediate treatment would be an oral drench of vinegar or 5% acetic acid (1l for sheep and 4l for cattle), diluted with an equal amount of water, to acidify the rumen (reduce alkalosis). Bloated animals should be made to walk till eructation occurs and allowed low quality hay or rangeland, to stimulate rumen function. Unaffected animals, from the same camp, should be allowed access to low-quality hay or rangeland, or be moved to a pasture of lower quality. If the high-N pasture is dry, irrigation should be applied immediately. A high energy, low protein concentrate or complete feed may be fed.
Only in severe cases, where mortality is likely, should a trochar-cannula be used. A large injection needle (3", 12-gauge) on a syringe without plunger may also work since the gas is a non-frothy ammonia. The needle should be stabbed through the rumen wall; stabbing the same spot each time it blocks, thus allowing the ammonia to escape. However, needles, being shorter than a trochar-cannula may severely tear the rumen wall when the rumen muscles contract, resulting in severe peritonitis.
Ammonia toxicity (also known as urea poisoning) in ruminants is usually caused by the ingestion of pure urea i.e. urea fertilizer. Ammonia toxicity has, however, been recorded on intensive pastures. This condition is usually related to, and associated with, ammonia-bloat. It occurs when the affected animal has managed to eructate the ammonia gas, thus not succumbing to ammonia bloat. The excessive rumen ammonia is absorbed through the rumen wall into the blood stream, leading to paralysis of the muscles and brain. This condition is usually fatal. Animals tend to show extreme nervous symptoms. Blood samples show an alkaline pH under such conditions.
Preventative management and treatment of animals suffering from ammonia toxicity is the same as for ammonia bloat.
Nitrate toxicity in ruminants on intensive pastures has appeared to cause occasional stock losses in European countries. Researchers in the Netherlands, where nitrate toxicity is more common, regard nitrate toxicity as extremely rare in tropical or subtropical climates. Stock losses, attributed to nitrate toxicity, normally affect a large proportion of the herd and may therefore cause concern. In most high rainfall, sub-tropical climates only two pasture species namely, kikuyu and Italian ryegrass, are known to accumulate potentially toxic levels of nitrate given the predisposing conditions.
Evidence from experiments at the Cedara Agricultural Development Institute, South Africa, suggests that nitrate toxicity is unlikely to be the causative agent in most cases of suspected nitrate toxicity. Confirmed cases of nitrate toxicity are uncommon, as the true diagnostic symptoms are often masked by the time a post-mortem investigation is conducted. For example, nitrate toxicity causes anaemia, brown blood, and high non-protein nitrogen (NPN) levels in the blood and rumen digesta. All the above symptoms will be present in an animal that died of redwater or ammonia toxicity while grazing an intensive pasture. Many cases of suspected nitrate toxicity have turned out to be redwater, anaemia associated with mineral deficiencies, or ammonia toxicity/bloat.
The toxic level of nitrate in the plant was originally reported to be in the order of 0.22 % NO3-N. Recent literature reports suggest these levels may be as high as 0.6 to 1.0 % NO3-N. Evidence from studies at the Cedara Agricultural Development Institute, South Africa, has shown that sheep can graze ryegrass, with a nitrate content more than 1.1 % NO3-N, with no apparent ill effect. This indicates the ability of ruminants, under correct management, to adapt to high nitrate or ammonia levels in pasture. However, these animals, although not succumbing to the high nitrogen levels, may be under a sub-clinical nitrogen toxicity stress.
Further evidence from nitrogen fertilization studies, conducted in Natal, South Africa, show a correlation between plant protein levels and nitrate content. Previous studies have shown that pasture protein levels above 22 to 25% are in excess of plant requirements, and are potentially toxic to the ruminant. As mentioned earlier, high protein levels may cause a non-frothy bloat, or at least, an appetite repression. From the relationship between nitrate and protein in the plant it appears that, under normal conditions, appetite repression due to high protein levels would occur before toxic quantities of nitrate could be ingested. Thus, the only way to induce nitrate toxicity in ruminants would be to starve the animals before grazing them on a potentially nitrate-toxic pasture. Even under such conditions the animals are still more likely to suffer from ammonia bloat/toxicity, with the situation being aggravated by sub-clinical nitrate toxicity.
Causes of Nitrate Toxicity
Some important factors leading to a build-up of nitrate in the plant include continuous cloudy conditions for 4 to 5 days, high temperatures, low moisture, frost, high applications of nitrogen fertilizer (over 60 - 100 kg N/ha in one application), and the season of the year (first grazing in May, and during the spring growth period). These conditions, in isolation, may not lead to a significant rise in plant nitrate levels. If, however, several of these factors coincide and are sustained for a period of 4 to 5 days, then an appreciable rise in plant nitrate levels is likely.
Management of Nitrate Toxicity
Nitrate toxicity is a disorder that should never occur, because it is easy to control by applying correct management principles. A common cause of both nitrate toxicity and ammonia toxicity on high quality pastures is the moving of unadapted animals (i.e. from rangeland) onto such a pasture. A rule of thumb is never to allow hungry or unadapted animals to have unrestricted access to high quality pasture, especially not during peak pasture growth periods (spring), or within 21 days of heavy nitrogen fertilizer applications.
Treatment of Nitrate Toxicity
Nitrate toxicity is difficult to diagnose as affected animals are usually found dead. 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. Animals may be given an intravenous injection of a 4% methylene blue solution (sheep 8 to 12 cm3; cattle 50 cm3). The treatment may be repeated every 4 to 5 hours as required.
POOR PERFORMANCE ON INTENSIVE PASTURES
Poor animal performance (ADG) is often noted on highly nitrogen-fertilized pastures. Typically, animals on such pastures are under an energy stress (carbohydrate and nitrogen being inversely related in grasses) as the rumen microbes require energy to metabolize the extra nitrogen. The energy used to convert ammonia in the blood to blood-urea has been calculated to cost the equivalent of 2 to 3 litres of milk. Blood urea levels over 19 mg/kg have been shown to reduce fertility in cattle. These animals may be suffering from a sub-clinical nitrate and/or ammonia toxicity stress or reduced intake due to appetite repression, due to the high nitrogen content of the pasture. These factors, in combination, could result in poor performance.
When ruminants are moved from a low-nitrogen to a high-nitrogen pasture, with a full rumen, there is a high probability that they will reject the new pasture. This is usually related to the appetite repression mechanism (ammonia-based), controlling their intake of the high nitrogen pasture. As the rumen microbes adjust to the higher nitrogen, less of the ammonia enters the blood, and the pasture becomes more acceptable as the appetite repression effect is reduced.
In such cases, one could provide a low quality hay, or include some adjacent rangeland or roadway to provide access to low quality roughage. Within a few days the animals will adjust to the new pasture and begin to graze normally.
The following two management practices, if followed, should prevent the listed disorders from occurring:
Dr M D MacFarlane, Veterinarian, Howick, South Africa for advice on veterinary aspects and contribution of suggestions.
SOURCES OF INFORMATION
Eckard R J, 1984. Factors affecting nitrate accumulation in herbage. M.Sc. Seminar no.1. Dept of Grassland Science and Animal Science, University of Natal, Pietermaritzburg.
Eckard R J, 1986. The nitrogen nutrition of Italian ryegrass (Lolium multiflorum). M.Sc. Thesis, University of Natal.
Eckard R J, 1990. The relationship between the nitrogen and nitrate content and nitrate toxicity potential of Lolium multiflorum. J.Grassl.Soc.South.Afr 7(3):174-178.
Mönnig H O & Veldmann F J, 1976. Handbook on stock diseases. Tafelberg, Cape Town.
Go To Home Page
Last modified:16 August, 2004
Please Note: Disclaimer
and maintained by:Richard Eckard
Copyright © 1997-1999, The University of Melbourne.