An update on leucaena toxicity: Is inoculation with Synergistes jonesii necessary?

Concern about mimosine toxicity and its management has contributed to the restricted adoption of leucaena as a forage for ruminants. The toxicity is a function of the antimitotic effects of mimosine, which is rapidly converted to isomers of hydroxypyridone (DHP), also toxic compounds, by plant and microbial enzymes. Work by R.J. Jones and colleagues (1960-1994) identified a rumen bacterium (Synergistes jonesii) capable of degrading DHP, and rumen fluid containing this bacterium was subsequently made available in Australia as a commercial inoculum for cattle producers.Research by University of Queensland and CSIRO over 15 years, commencing in 2003, found evidence for another pathway of toxin management in Indonesia, where hundreds of Balinese farmers had fed uninoculated Bali bulls (Bos javanicus) up to 100% leucaena without experiencing toxicity symptoms, apart from an initial 1-2 week period while their cattle became adapted to the new diet. Tests showed that the Indonesian cattle were not degrading all DHP, as it appeared in high concentrations in urine samples, predominantly as 2,3-DHP and almost all (>97%) in a conjugated form. The conjugating compounds (glucuronic acid and sulfate compounds), produced in the liver, appeared to be the major pathway for neutralizing the toxicity of DHP. Other work revealed that S. jonesii was a ubiquitous organism in the rumen fluid of animals in all countries but always as a minor population, just detectable using new PCR-based assays, and sometimes not detected in all animals studied.Since the Indonesian cattle fed leucaena suffered symptoms of mimosine toxicity for only a short time before quickly recovering, we hypothesize that conjugation of DHP by the liver was the major detoxification pathway for these animals. This detoxification pathway is also operative in Australia and other countries but further studies are needed to determine its significance