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4.4 Management of Anti-nutritive Factors - with Special Reference to Leucaena

R.J. Jones


Introduction
Strategies for Managing Anti-nutritive Factors
The Leucaena Story
Natural Distribution of the DHP Degrading Bacteria
Implications of the Leucaena Work
References


Introduction

In addition to the proteins, carbohydrates, fats and other compounds essential to metabolism, plants also contain 'secondary' metabolites. These occur in a variety of chemical structures and vary from genus to genus and from species to species. They appear to be more widespread in tropical forages than in temperate forages, and are more prominent in woody genera than in herbaceous ones (Jones and Lowry 1990).

The role of the numerous secondary plant compounds in plants is not fully understood. However, it is generally accepted that they may enable a plant to deter or limit predation by herbivores (Culvenor 1970, Rosenthal and Janzen 1979). The compounds may be toxic, confer unpalatability or reduce the intake of grazing herbivores. Ruminants, however, may be less affected by such anti-nutritive substances because of the capacity of the rumen microorganisms and the liver to degrade these compounds and so render them less harmful to the animal.

The range of compounds known to have anti-nutritive qualities is large (Hegarty 1982) and is discussed in Section 4.3. It is very likely that some of these, and possibly new compounds, will be encountered in new species of forage trees that are now being considered for release to industry.

Strategies for Managing Anti-nutritive Factors

A number of approaches could be used to reduce the effects of known anti-nutritive factors remembering that more than one factor may be involved in any given plant.

Avoid using the plant

Clearly this strategy can be used if one has a choice either to plant a problem tree legume species or not. In some cases, however, the tree legume may be a component of the natural vegetation of the area and may have some useful attributes, e.g. mulga (Acacia aneura) in western Queensland.

Use supplements to overcome the anti-nutritive factor

High concentrations of condensed tannins can lower feeding value due to reduced availability of nutrients, especially protein, and lower cell wall digestion (Barry and Blaney 1987). The use of supplements of Na, S, Ca and N (urea) improved wool growth and liveweight gains of sheep fed mulga (Acacia aneura) (Gartner and Niven 1978, Elliott and McMeniman 1987) even though proximate analysis of leaf showed that these nutrients should have been adequate for growth. Interference in their availability, due to the presence of oxalates (as calcium oxalate) and tannins (which bind proteins and necessitates the excretion of sulphur as sulphate), has been proposed to explain the responses obtained with mineral supplementation (Gartner and Hurwood 1976).

Reduction in the level of tannins may be achieved in some herbaceous legumes by improving soil nutrient status - particularly that of P and S. Thus the condensed tannins of Lotus spp., sainfoin (Onobrychis sativa) and Desmodium ovalifolium were reduced by fertilisation (Barry and Blaney 1987, Lascano and Salinas 1982). For the tropical tree legumes, there has been little work done on either supplementation or fertilisation as strategies to alleviate any perceived problems from condensed tannins. However, for Calliandra calothyrsus, increasing levels of fertiliser input did not reduce tannin levels in the leaves (B. Palmer and J.B. Lowry, personal communication).

An effective, though as yet uneconomic, way of reducing the adverse effects of condensed tannins is to feed polyethylene glycol (PEG) with molecular weight of 3,350 or above (see Section 4.6).

Reduce access to the problem feed

By reducing the proportion of the problem legume in the diet, adverse effects can be reduced. This may be readily achieved under a cut-and-carry system but may not be so easy under grazing. The use of small fenced legume paddocks adjacent to the main pasture areas is one way of rationing the feed; another is to plant the legume in widely spaced rows or to grow most of the feed above grazing height as for tree leucaena (Wildin 1985).

Irrespective of the feed, it is always wise to introduce animals to it gradually. This will enable animals to 'adapt' to the new feed. Such adaptation may well involve an increase in the rumen of microorganisms capable of detoxification, or partial detoxification, of the anti-nutritive compounds.

In some cases it may be possible to avoid feeding the plant when levels of the anti-nutritive compounds are high. Another strategy would be to use the forage for fattening of animals prior to slaughter and not to use the forage for long-term feeding of growing animals. It would be important, however, to ensure that such cumulative toxins do not accumulate in the meat and so cause problems when the meat is eaten.

With plant oestrogens, limiting access to non-breeding animals will reduce the adverse effects on reproductive performance (e.g. with subterranean clover). However, no comparable problems have been recorded for tree legumes.

Use cultivars low in anti-nutritive compounds

A breeding programme conducted by the CSIRO Division of Tropical Crops and Pastures successfully produced low mimosine lines of leucaena by crossing L. pulverulenta and L. leucocephala. However, it was not possible to combine vigour with low mimosine concentration (Jones and Bray 1983).

For plant breeding strategies to be effective, a clear identification of the anti-nutritive compounds is needed. These should be readily determined by simple tests, should show a range of variation in the genetic material available, and the character should be highly heritable. Care should be taken to assess levels of other anti-nutritive compounds which may vary together with or inversely with the 'target' compound. Thus low mimosine levels could be associated with high tannin levels and low palatability.

Use rumen microbes to detoxify the compounds

Rumen micro-organisms may metabolise toxins in several ways:

· They may convert the toxin to non-toxic metabolites. Thus, under normal circumstances soluble oxalate in grasses is no cause for concern in ruminants, though if cattle on dry feed are suddenly introduced to lush pasture high in oxalates they can die from accumulation of calcium oxalate in the kidneys (Jones et al. 1970). Unique anaerobic bacteria (Oxalobacter formigenes) have been isolated which convert oxalate to CO2 and formate. They depend on oxalate as their sole energy source (Allison 1985).

· They may convert the toxin to compounds with enhanced activity in the animal, a classic example being the conversion of the isoflavones formononetin and daidzein, present in oestrogenic clover, to equol and O-methylequol by dimethylation and reduction (Cox 1985). These are compounds which are more active in reducing fertility in female sheep.

· They may convert the toxin to substances with a completely different toxic property. For example, the mimosine in L. leucocephala has strong anti-mitotic and depilatory properties but is not goitrogenic, whereas its ruminal metabolite 3,4 DHP is a potent goitrogen (Hegarty et al. 1979). This will be considered in more detail later.

· They may not metabolise the toxin at all, although subsequently some change may occur in the body tissues. For example, fluoroacetic acid, present in some Acacia species and Gastrolobium species, is not metabolised by rumen microorganisms, but is converted to fluorocitrate in the body tissues. This then blocks the carboxylic acid cycle causing citrate accumulation and subsequent toxicity and death (Everist 1974).

In the future, with an increasing understanding of the structure of anti-nutritive compounds and their likely degradation pathways, it may be possible to modify bacteria genetically to contain specific enzymes that detoxify problem compounds. The approach certainly holds promise. However, much basic work will be required to achieve this objective, but the successful use of naturally occurring DHP degrading bacteria to solve the leucaena toxicity problem in Australia (see later) offers hope and encouragement for this area of work.

Thus far, the management of anti-nutritive compounds has been treated in a general fashion. For the remainder of this section discussion will focus on the use of leucaena in northern Australia and summarise progress towards successful management of the toxic amino acid mimosine.

The Leucaena Story

When research started on leucaena in the 1960s, two problems seemed worthy of special effort - slow establishment and the toxicity of leucaena to ruminants. The special advantages of leucaena over other legumes being evaluated at the time gave priority to research on these problems. Advantages were very high animal production potential and persistence in grazed pastures. At Samford, southeast Queensland, a leucaena pasture established in 1959 has produced liveweight gains per hectare double that of Siratro (Macroptilium atropurpureum) based pastures on similar soils (Jones and Jones 1982).

The toxicity

The toxic constituent in leucaena is a non-protein amino acid, mimosine (-[N-(3-hydroxy-4oxopyridyl)](-a -aminopropionic acid) which is an antimitotic and depilatory agent as well as possessing other unusual pharmacological properties (Hegarty et al. 1964). Mimosine occurs in all parts of the leucaena plant, but in particularly high concentrations in the tips of actively growing shoots (8-12%), young leaves (4-6%) and young pods and seeds (4-5%). Although mimosine is the toxic agent in the plant, it is not usually the toxic agent which causes problems in the ruminant. This is because when leucaena leaves are chewed by cattle, part of the mimosine is converted to 3-hydroxy-4(1H)-pyridone (DHP) by enzymes which occur in the plant material. The bolus material reaching the rumen may then have approximately 30% of the mimosine converted to DHP (Lowry et al. 1983). Further conversion occurs in the rumen by bacteria so that, within a short time of entering the rumen, most of the mimosine is converted to 3,4 DHP. When animals are fed dried leucaena material, the enzymatic conversion of mimosine to DHP does not occur when the plant material is chewed since the enzyme in the plant is rendered inactive by the heat treatment. Under these conditions, animals fed leucaena for the first time may initially excrete only mimosine in the urine. However, once the animals have adapted to eating fresh or dried leucaena, they excrete DHP. When first introduced to leucaena pastures, animals can lose hair from the switch of the tail, an effect which is caused by mimosine. However, the toxicity arising from DHP develops more slowly under field conditions and is rarely acute.

The adverse effects of a high leucaena diet include excessive salivation, goitre, depressed serum thyroxine levels (T4 and T3), depressed appetite, poor liveweight gains, ulceration of the oesophagus and rumen, hair loss, lesions on the body, poor breeding performance, the production of weak, goitrous, lightweight calves, and even death. The development of goitre in ruminants in Australia invariably follows sustained leucaena feeding. In cattle, the normal thyroid weight is about 20 g. Following leucaena feeding, thyroid enlargement is often proportional to the time the animals spend on leucaena. In the Ord Irrigation area of northwest Western Australia, thyroids may attain weights of up to 500 g over a 12 month period. Serum thyroxine levels (T4) also decline with prolonged and high leucaena intakes. The decline in serum thyroxine can be rapid if leucaena is the sole diet with levels falling from a normal value of 80 nM to about 5-10 nM in 5-6 weeks (Jones et al. 1978). Jones and Winter (1982) found that liveweight gain of steers over a 300 day period was linearly related to serum thyroxine levels. However, only a few of the animals showed unmistakable signs of leucaena toxicity and these animals had serum thyroxine levels less than 30 nM. Other animals with depressed thyroxine levels showed no outward signs of toxicity and yet their liveweight gain was depressed compared with animals with normal serum thyroxine levels.

Hegarty et al. (1979) showed that DHP is a potent goitrogen although mimosine is non-goitrogenic. It was important to know whether the depressed thyroxine per se was the reason for the poor performance of cattle grazing leucaena. Experiments in which goats were fed leucaena diets supplemented with thyroxine to maintain normal levels, showed that supplemented goats ate their feed more rapidly and were much more alert than unsupplemented goats.

However, they had similar voluntary feed intake and liveweight change except at extremely low serum thyroxine levels. This suggested that the circulating DHP had the major effect on feed intake, and that low serum thyroxine was associated with high levels of circulating DHP. A depression in feed intake was measured when sheep were fed lucerne chaff and infused with DHP into the rumen. In this study, feed intake declined from about 1 kg per day of lucerne chaff to 0.2 kg per day over a 6 day period. Over this period, the thyroxine levels of the animals were not depressed (Bamualim 1984).

Similar clinical signs to those reported in Australia were reported in Papua New Guinea (Holmes et al. 1981). These authors found that some cattle also suffered cataracts, and that heifers had extremely poor breeding performance. Supplementation with zinc sulphate prevented the development of lesions on the bodies of the animals and improved liveweight gain but had no effect on serum thyroxine levels. Possible chelation of zinc and other metals by mimosine and DHP, where concentrations of these elements are marginal in the herbage, could explain some of the variable effects reported in different leucaena feeding experiments.

It seemed clear that in order to alleviate toxicity the amount of leucaena eaten would need to be restricted. In practice, few serious problems were encountered in the subtropics where growth of leucaena was rapid for only about 5-6 months of the year, or where access to leucaena was limited to the autumn/winter period. From pen feeding trials, it was concluded that steers receiving 30% or less leucaena in their diet encountered few clinical problems due to toxicity. Control of grazing to achieve this objective was not difficult in the subtropics. However, in the Ord River Irrigation area, even the use of rotations involving pangola grass-only pastures was not a solution to the problem (Blunt and Jones 1977).

The other approach was to limit mimosine intake by breeding low mimosine varieties of leucaena. This programme, initiated by Dr E.M. Hutton, used crosses of L. leucocephala with L. pulverulenta as the basis of a new cultivar. Unfortunately, the material bred for low mimosine was less productive than the L. leucocephala parent and was not suitable for release as a new cultivar (Bray et al. 1984). It appeared that vigour was inversely proportional to mimosine concentration in the leaves and, under the heavy grazing imposed on the irrigated pastures, the low-mimosine line declined in vigour and many plants died. Survivors had higher mimosine concentrations than the mean value for the original population, and approached the value for cultivar Cunningham.

Towards a solution

By 1979, it was apparent from reports from Hawaii and the Bahamas, and from observations in Timor with tethered cattle, that ruminants were being fed substantial amounts of leucaena without any apparent ill effect. Why was it that animals in some countries appeared to suffer no effect whereas in others severe toxicity occurred? Unfortunately, the evidence from some overseas countries was not well documented although there seemed to be no doubt about the reality of the observations. In 1979, in Hawaii, the performance of goats fed lucerne, leucaena or diets containing 50% leucaena and 50% lucerne were compared. Daily intakes of the leucaena-fed animals varied from 16 to 21 g per day of mimosine and there were no ill effects on the animals. In this experiment, appetite was maintained, serum thyroxine remained normal and thyroids did not enlarge. No lesions developed in the oesophagus and surprisingly, virtually no DHP was excreted in the urine. Some animals excreted a compound which gave a blue (rather than the expected purple) colour in reaction with ferric chloride (Jones and Megarrity 1983). These results contrasted dramatically with those from similar experiments in Australia. What was the explanation? My theory was that the animals in Hawaii possessed rumen microbes which were not present in Australia and which were capable of detoxifying the mimosine and DHP consumed by the animals (Jones 1981). The evidence from in vitro digestion studies indicating that rumen fluid from Australian animals did not degrade DHP whereas the rumen fluid from Hawaiian goats did, supported the theory. However, it was several years before this theory was accepted and practical results achieved.

Proving the theory

It was difficult to convince colleagues and other scientists that the reason for the difference between animals eating leucaena in Australia and Hawaii could be attributed to a rumen microorganism. Further proof was required.

Fortunately, Dr Brian Lowry and his co-workers in West Java, following the work I had done in Hawaii, also found goats capable of degrading DHP in a village in Java. In 1981, the critical experiment was performed at Ciawi in West Java. For the experiment, four Australian goats were flown to Indonesia. They had been fed leucaena for 5 weeks before shipment and, on arrival, were fed dried Australian grown leucaena brought to Indonesia for the purpose. All four goats were fed a salt lick and separated into two pairs which were housed in separate buildings. One pair received an infusion of rumen fluid from an Indonesian goat known not to be excreting DHP when fed on a leucaena diet. The other pair were treated as controls. The results of infusion were rapid and dramatic, with DHP levels in the urine declining to virtually zero after 5 days. There was also a doubling of feed intake and, hence, of the intake of the toxic mimosine. Ten days after infusion, rumen fluid was taken from one of these goats and infused into one of the control goats. The results of this infusion were almost identical to those from the first infused goats (Figure 4.4.1).

Fig. 4.4.1. Effect of infusing Australian goats with rumen fluid from goats adapted to degrade DHP. a) Urinary DHP excretion as a percentage of the DHP equivalent of mimosine ingested. b) Leucaena intake (g dry leaf per day). Maximum offered daily was 400 g. Values prior to infusion are the mean daily output of DHP and the mean daily feed intakes respectively. Arrows indicate date of infusion from a goat able to degrade DHP.

(a) DHP excretion

(b) Feed intake

In vitro degradation of DHP did not occur with rumen fluid from the Australian goats prior to infusion whereas rumen fluid taken from the same animals 10 days after infusion showed rapid and complete degradation of the DHP in vitro within 24 h.

Getting the 'bugs' to Australia

The joint work in Indonesia (Jones and Lowry 1984) clearly showed that it was possible to introduce DHP degrading microorganisms into Australian goats but goats or rumen fluid could not be introduced into Australia for quarantine reasons. However, Hawaii did not have many of the diseases present in Indonesia. Furthermore, a culture of the microorganisms in artificial media would be easier to introduce into Australia This work was done jointly with Mr R. Megarrity.

On the island of Maui, rumen fluid from a donor goat that had been fed almost exclusively on leucaena was used to inoculate culture tubes containing growth medium and the toxins DHP or mimosine. Growth of the microorganisms in the medium occurred and the toxins were degraded. We soon discovered a population of bacteria which was essentially Gram negative rods that were responsible for the degradation. These were shown to be extremely sensitive to oxygen and so strict anaerobic conditions were essential for any work with these bacteria. On the 1st November, 1981, ten tubes each containing 9 ml of culture were introduced to the QDPI Veterinary Laboratory in Townsville, at Oonoonba where they were shown to be effective under strict quarantine conditions. Subsequently, a steer at the CSIRO field station at Lansdown near Townsville was infused with the bacteria. The animal was fed on leucaena before infusion and showed the classic signs of leucaena toxicity. Following infusion, the animal ceased excreting mimosine and DHP and its feed intake increased. For the first time, we were able to record liveweight gain of an animal eating solely leucaena over a period of several months. In a leucaena pasture, he continued to grow and achieved the remarkable liveweight gain of 275 kg in 12 months (Jones and Megarrity 1983).

Transmission of the bacteria naturally from this one animal to four other animals introduced into the same paddock occurred within a 5 week period. Activity of the bacteria was monitored by taking rumen samples and incubating these in vitro with a medium containing DHP or mimosine. This monitoring showed that the animals retained the ability to degrade DHP and mimosine while grazing leucaena pastures though their ability to do this was reduced when the animals were removed from leucaena. Nevertheless, after 9 months off leucaena, rumen fluid from these cattle still retained the ability to degrade mimosine and DHP in vitro.

Subsequent experiments at the Kimberley Research Station (KRS), in the Ord Irrigation area have shown that the bacteria can be transferred to other animals. At KRS, heifers infused with the bacteria did not exhibit the toxicity whereas control animals showed marked clinical signs of leucaena toxicity (Pratchett et al. 1991). At the QDPI Brian Pastures Research Station at Gayndah, steers grazing leucaena grass pastures gained 39% more weight over the 4 month period following infusion compared with controls which were not infused (Quirk et al. 1988). Again the infused animals ceased excreting DHP in their urine and retained normal serum thyroxine levels. In both field experiments, however, animals in the control treatments also ceased excreting DHP in their urine after about 4 months and their serum thyroxine levels began to improve. It was clear that some cross-contamination had occurred although the method was not apparent since the animals were grazed in separate paddocks and were weighed on consecutive days with a period of 4-6 weeks elapsing between the passage of the control animals through the yards.

Subsequent work (R.J. Jones, unpublished data) has shown that it is possible to obtain in vitro degradation of DHP and mimosine by using water extracts from dried dung samples collected in the paddocks grazed by infused cattle. It seems likely, therefore, that the bacteria were picked up from the yards which had been contaminated by dung from the treated animals. This cross-contamination effectively terminated the experimental comparison but at least it showed that the spread of the bacteria under field conditions could be rapid and so only a small proportion of the herd need be infused with the DHP degrading bacteria.

Several attempts to isolate the bacteria from water in drinking troughs situated in leucaena paddocks grazed by cattle have been unsuccessful (R.J. Jones, unpublished data). Presumably the oxygen in the water rapidly kills the bacteria in food particles which may enter the water when cattle drink.

It was a surprise to measure such a large improvement in performance at Brian Pastures since at this station there has been very little evidence of overt leucaena toxicity compared with the situation at the Ord. As noted above, however, the presence of circulating DHP can have quite a substantial negative effect on feed intake. Removal of this circulating DHP following infusion has undoubtedly led to an increased intake and corresponding improved liveweight gain.

The greatest expression of leucaena toxicity had always been observed at Kununurra in the Ord Valley of Western Australia where, under irrigation, leucaena grows rapidly and has a high mimosine concentration in its shoots and young leaves. In an experiment on well established flood irrigated leucaena in rows 4 m apart with pangola grass, six weaner steers per hectare were fattened in a 12 month period with no supplement of any kind. The results of this experiment are given in Table 4.4.1.

Practical use of the bacteria

In our experiments, cattle were infused with bacterial cultures grown in the laboratory or with rumen fluid taken from fistulated animals. In the initial experiments, we dosed cattle with approximately 300 ml of culture or rumen fluid diluted with buffer medium. Subsequently we have used a rumen injector gun to place 10 ml of culture or rumen fluid directly into the rumen from the left side of the animal. The gun is attached to a tank containing the medium or strained rumen fluid under anaerobic conditions. Valves on the tank allow us to pressurise the tank with CO2, and to connect the gun to the tank by butyl rubber tubing. The tank containing 2 litres can then be used to infuse 200 head of cattle. Many herds in Queensland and northwest Australia have now been infused by CSIRO or the QDPI. In every case, the infusions have been successful. Furthermore, I have taken cultures of the bacteria to Ethiopia, where, at ILCA in Addis Ababa, goats and sheep were successfully infused. Similar success was achieved in China with cattle. The infused cattle ate more feed and gained 45% more weight than controls over a 38 day period (Wang et al. 1987).

Table 4.4.1. Summary of a grazing experiment undertaken at Kununurra Research Station using L. leucocephala cv. Cunningham undersown with pangola grass.

Parameter

Value

Stocking rate

6 weaner steers/ha

Gain (head/year)

237 kg (162 to 399)

Gain (ha/year)

1,442 kg

Killing out percent

54%

Carcass weight

215 kg

Age

20 months

It should be noted that prior to the use of the bacteria, steer gains were only 135 kg/steer/year at 6.2 steers/ha or 830 kg/ha/year (Blunt 1976).

Natural Distribution of the DHP Degrading Bacteria

Over the last decade we received, at the Davies Laboratory, samples of urine (1:1 vol/vol urine:conc. HCl) from ruminants fed on leucaena diets in various tropical countries. These were analysed for mimosine and its degradation products 2,3 and 3,4 DHP to assess the presence or absence of DHP degrading bacteria in the countries of origin. In addition, urine tests were made in new countries and reported to us. This enabled us to map the distribution of the DHP degrading bacteria. Distribution proved to be somewhat discontinuous as shown in Table 4.4.2.

An unusual result was obtained from Brazil where approximately 50% of samples analysed on two occasions revealed no degradation of DHP whereas the other 50% were free of DHP. Further work in Brazil showed that DHP degrading bacteria were present (Paul Rayman, personal communication).

Table 4.4.2. Distribution of DHP degrading bacteria.

Countries without the DHP degrading bacteria

Countries with the DHP degrading bacteria

Australia

Indonesia

Papua New Guinea*

Vanuatu

Fiji

Thailand

Japan

Malaysia

China

India

USA**

Seychelles

Africa:


Ethiopia

Mexico

Nigeria


Zaire


Kenya


Zimbabwe


Tanzania


S. Africa


* Later samples, from the site at Lae, showed that DHP degrading bacteria were present. They were probably introduced via Javanese Zebu cattle from Indonesia (Raurela and Jones 1985).

** Dr Milton Allison (personal communication)

However, the situation in other South American countries needs to be clarified. Cattle in Paraguay appear not to have DHP degrading bacteria (Dr A. Glatzle, personal communication) whereas in Venezuela they do (Dominguez-Bello and Stewart 1990).

Isolation of the bacteria

The initial population of bacteria introduced into Australia was mixed. From this mixed culture we have now isolated pure colonies of bacteria with the ability to degrade the two isomers of DHP - 3,4 and 2,3 DHP. The bacteria are small Gram negative rods measuring approximately 1 pm x 0.5 pm. They are extremely anaerobic when actively growing, can be stored at 20°C and will tolerate temperatures up to 50°C. Between 50° and 55°C, the bacteria are killed. Detailed work in the USA on the substrates they ferment, on their cell wall composition and rRNA sequences have clearly shown that the bacteria are not closely related to any other rumen bacterium. As a result this unique bacterium has been assigned to a new genus and species - Synergistes jonesii (Allison et al. 1992). In the laboratory they can be maintained in culture for prolonged periods (one year) without any addition of nutrients and once sub-cultured into new medium they grow and actively degrade the toxins. There is some specialisation within the bacteria in that some are capable of degrading mimosine whereas others may only degrade 3,4 DHP or 2,3 DHP. For practical purposes, I have combined two of the isolates in my cultures in order to degrade mimosine to as yet unidentified end products.

It is now known that in the degradation, mimosine is converted to 3,4 DHP then to 2,3 DHP and finally the pyridine ring is broken (Jones 1985 and unpublished data). Ring cleavage appears to be possible only at the 2,3 DHP stage.

Implications of the Leucaena Work

This work has shown firstly that secondary plant compounds such as mimosine and its degradation products can reduce the voluntary feed intake of ruminants. It would be interesting to know how widespread is the phenomenon and whether its effects can be overcome. Secondly, we have shown that rumen bacteria are not ubiquitous. We may well ask are there other rumen bacteria available overseas which would benefit the animal industries of Australia? In particular, there may be other plant toxins, such as indospicine in Indigofera and oestrogenic compounds found in clovers, which may be overcome by the use of suitable introduced rumen bacteria. It may also be possible to improve the utilisation of low quality forages by using better adapted rumen microbes or rumen microbes that may have been manipulated in some way to improve their ability to degrade plant fibre.

Other work, based at the University of New England at Armidale, seeks to develop bacteria to detoxify fluoroacetate. This toxin is responsible for stock poisonings following ingestion of the native leguminous trees Acacia georginae, Gastrolobium spp. and Oxylobium spp.

It has also been shown that goats grazing Acacia shrublands have populations of bacteria which can metabolise tannic acid. Transfer of rumen fluid from these goats to sheep fed Acacia aneura resulted in an increase in the digestibility of the protein (Matthew et al. 1991) (see Section 4.6).

Improved dry matter digestibility of the tannin-containing tropical shrub legume Calliandra calothyrsus in Dacron bags in the rumen of sheep also occurred when rumen fluid from goats grazing shrubs was infused into their rumens (Palmer and Minson 1993).

These examples clearly indicate a potential to reduce the effects of anti-nutritive factors in forage plants and so improve feeding value to ruminants by the use of introduced rumen microorganisms. The successes thus far have followed the use of naturally occurring organisms. In the future, the scope for improvement may well be extended by the use of genetically modified microorganisms.

References

Allison, M.J. (1985) Anaerobic oxalate-degrading bacteria of the gastrointestinal tract. In: Plant Toxicology - Proceedings of the Australia-USA Poisonous Plants Symposium, Brisbane, Australia, May 14-18, 1984, pp. 120-126.

Allison, M.J. Mayberry, W.R., McSweeney, C.S. and Stahl, D.A. (1992) Synergistes jonesii, gen. nov., sp. nov.: a rumen bacterium that degrades toxic pyridinediols. Systematic and Applied Microbiology 15, 522-529.

Bamualim, A. (1984) The nutritive value of Leucaena leucocephala as a feed for ruminants. PhD thesis, James Cook University of North Queensland, 167 pp.

Barry, T.N. and Blaney, B.J. (1987) Secondary compounds of forages. In: Hacker, J.B. and Ternouth, J.H. (eds), Nutrition of Herbivores. Academic Press, Australia, pp. 91-119.

Blunt, C.G. (1976) Preliminary cattle grazing trials on irrigated Leucaena leucocephala and pangola grass in the Ord Valley N.W. Australia. Proceedings of the Australian Society of Animal Production 11, 10.

Blunt, C.G. and Jones, R.J. (1977) Steer liveweight gains in relation to the proportion of time on Leucaena leucocephala pastures. Tropical Grasslands 11, 159-164.

Bray, R.A., Hutton, E.M. and Beattie, W.M. (1984) Breeding leucaena for low-mimosine: field evaluation of selections. Tropical Grasslands, 18, 194-198.

Cox, R.I. (1985) Immuno physiological control of phyto-oestrogen toxicity. In: Plant Toxicology - Proceedings of the Australia-USA Poisonous Plants Symposium, Brisbane, Australia, May 14-18, 1984, pp. 98-108.

Culvenor, C.C.J. (1970) Toxic plants - a re-evaluation. Search 1, 103-110.

Dominguez-Bello, M.G. and Stewart, C.S (1990) Degradation of mimosine, 2,3-dihydroxy pyridine and 3 hydroxy-4(1H) - pyridone by bacteria from the rumen of sheep in Venezuela. FEMS Microbial Ecology 73, 283-289.

Elliott, R. and McMeniman, N.P. (1987) Supplementation of ruminant diets with forage. In: Hacker, J.B. and Ternouth, J.H. (eds), The Nutrition of Herbivores. Academic Press, Australia, pp. 409-428.

Everist, S.L. (1974). Poisonous Plants of Australia. Angus and Robertson, Sydney, 684 pp.

Gartner, R.J.W. and Hurwood, I.S. (1976) The tannin and oxalic acid content of Acacia aneura (mulga) and their possible effects on sulphur and calcium availability. Australian Veterinary Journal 52, 194-196.

Gartner, R.J.W. and Niven, D.R. (1978) Studies on the supplementary feeding of sheep consuming mulga (Acacia aneura). 4. Effect of sulphur on intake and digestibility and growth and sulphur content of wool. Australian Journal of Experimental Agriculture and Animal Husbandry 18, 768-772.

Hegarty, M.P. (1982) Deleterious factors in forages affecting animal production. In: Hacker, J.B. (ed.), Nutritional Limits to Animal Production from Pastures. Commonwealth Agricultural Bureaux, Farnham Royal, UK, pp. 133-150.

Hegarty, M.P., Schinckel, P.G. and Court, R.D. (1964) Reaction of sheep to the consumption of Leucaena glauca and to its toxic principle mimosine. Australian Journal of Agricultural Research 15, 153-167.

Hegarty, M.P., Lee, C.P., Christie, G.S., Court, R.D. and Haydock, K.P. (1979) The goitrogen 3-hydroxy-4(1H)-pyridone, a ruminal metabolite from Leucaena leucocephala: Effects in mice and rats. Australian Journal of Biological Science 32, 27-40.

Holmes, J.H.G., Humphrey, J.D., Walton, E.A. and O'Shea, J.D. (1981) Cataracts, goitre and infertility in cattle grazed on an exclusive diet of Leucaena leucocephala. Australian Veterinary Journal 57, 257-261.

Jones, R.J. (1981) Does ruminal metabolism of mimosine explain the absence of Leucaena toxicity in Hawaii? Australian Veterinary Journal 57, 55-56.

Jones, R.J. (1985) Leucaena toxicity and the ruminal degradation of mimosine. In: Plant Toxicology - Proceedings of the Australia-USA Poisonous Plants Symposium, Brisbane, Australia, May 14-18, 1984, pp. 111-119.

Jones, R.J. and Bray, R.A. (1983) Agronomic Research in the Development of Leucaena as a Pasture Legume in Australia. In: Leucaena Research in the Asian-Pacific Region. Proceedings of a workshop, Singapore, November 1982, pp. 41-48.

Jones, R.J. and Jones, R.M. (1982) Observations on the persistence and potential for beef production of pastures based on Trifolium semipilosum and Leucaena leucocephala in subtropical coastal Queensland. Tropical Grasslands 16, 24-29.

Jones, R.J. and Lowry, J.B. (1984) Australian goats detoxify the goitrogen 3-hydroxy-4(1H) pyridone (DHP) after rumen infusion from an Indonesian goat. Experientia 40, 1435-1436.

Jones, R.J. and Lowry, J.B. (1990) Overcoming problems of fodder quality in agroforestry systems. In: Avery, M.E., Cannell, M.G.R. and Ong, C.K. (eds), Applications of Biological Research in Asian Agroforestry. Winrock International, Morrilton, Arkansas, USA, pp. 259-275.

Jones, R.J. and Megarrity, R.G. (1983) Comparative toxicity responses of goats fed on Leucaena leucocephala in Australia and Hawaii. Australian Journal of Agricultural Research 34, 781-790.

Jones, R.J. and Winter, W.H. (1982) Serum thyroxine levels and liveweight gain of steers grazing Leucaena pastures. Leucaena Research Reports 3, 2-3.

Jones, R.J., Seawright, A.A. and Little, D.A. (1970) Oxalate poisoning in animals grazing the tropical grass Setaria sphacelata. Journal of the Australian Institute of Agricultural Science 36, 41-43.

Jones, R.J., Blunt, C.G. and Nurnberg (1978) Toxicity of Leucaena leucocephala. The effect of iodine and mineral supplements on penned steers fed a sole diet of Leucaena. Australian Veterinary Journal 54, 387-392.

Lascano, C. and Salinas, J.G. (1982) Effecto de la fertilidad del suelo en la calidad de Desmodium ovalifolium 350. CIAT, Cali, Colombia. Boletin Informativo de Pastos Tropicales 7, 4-5. (In Spanish.)

Lowry, J.B., Maryanto, N. and Tangendjaja, B. (1983) Autolysis of mimosine to 3-hydroxy-4(1H) pyridone in green tissues of Leucaena leucocephala. Journal of the Science of Food and Agriculture 34, 529-533.

Matthew, J., Brooker, J.D., Clark, K., Lum, D.K. and Miller, S.M. (1991) Isolation of a ruminal bacterium capable of growth on tannic acid. Australian Society for Microbiology. Annual Scientific Meeting, Gold Coast, Australia Poster No. 59.

Palmer, B. and Minson, D.J. (1993) The in-sacco digestibility of the tropical shrub legume Calliandra calothyrsus as affected by diet of the fistulated animal, temperature of drying and source of rumen inoculation. Animal Feed Science and Technology. (In press.)

Pratchett, D., Jones, R.J. and Syrch, F.X. (1991) Use of DHP-degrading rumen bacteria to overcome toxicity in cattle grazing irrigated leucaena pastures. Tropical Grasslands 25, 268-274.

Quirk, M.F., Bushell, J.J., Jones, R.J., Megarrity, R.G. and Butler, K.L. (1988) Live-weight gains on leucaena and native grass pastures after dosing cattle with rumen bacteria capable of degrading DHP, a ruminal metabolite from leucaena. Journal of Agricultural Science (Cambridge) 111, 165-170.

Raurela, M. and Jones, R.J. (1985) Degradation of DHP in cattle in Papua New Guinea. Leucaena Research Reports 6, 68-69.

Rosenthal, G.A. and Janzen, D.H. (1979) Herbivores: their Interaction with Secondary Plant Metabolites. Academic Press, New York 718 pp.

Wang, J., Yang, J.H. and Jones, R.J. (1987) Chinese cattle detoxify the leucaena toxin after Australian rumen fluid infusion. In: Proceedings 4th Annual Conference of Chinese Grassland Association, Nanning, Guangxi, November 12-17, 1987.

Wildin, J.H. (1985) Tree Leucaena - Permanent High Quality Pastures. Queensland Department of Primary Industries, Rockhampton, 8 pp.


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