This producer milks dairy buffalo in the Murray Mallee area and reported several, 2-3 month old calves suddenly unwell in early November. No management changes or diet changes had occurred, no obvious toxins were present and thorough investigations by consulting veterinarians failed initially to find causes. Unfortunately over the following 2 weeks a total of 21 buffalo calves died, most with initial lethargy, dropping dead, or being found dead in the morning. Multiple autopsies and exhaustive testing was undertaken to establish a set of consistent findings which pointed to a possibility of ionophore or “Monensin” toxicity. Feeding of grain to young buffalos stopped immediately pending feed sample tests, which confirmed excess Monensin in a batch of feed. Several more calves died following this but no more deaths or illness has been reported a week afterwards. Only one affected calf survived. Buffalo are known to be highly sensitive to Monensin and stringent controls of further feeds has been put in place.
This case demonstrates the benefit of persistence, care, good communications between producers and consulting veterinarians, thorough clinical observations and autopsy techniques, and Government support in the investigation of complex cases. To quote from an international pathologist speaker recently:
This producer breeds and milks Buffalo in a commercial operation. He has 75 milking adults and rears female progeny, with a total of 230 buffalo on the property. AI is used in some cows. This is the only milking buffalo herd in SA at present.
Commencing 12th November calves in the 4-8 month old age group started dying. Some were found dead overnight, others recumbent and moribund, others able to stand and walk, then later died. Deaths seemed to involve mostly younger calves, but some older animals died over a period of 10 days. Initially good sample collection was difficult as post-mortem changes gave poor results, but some fresh cases and blood samples assisted with a final diagnosis. A careful check of paddocks found no obvious poison weeds or sources of other toxins, there have been no introductions into the herd for 4 years, and feed had not been changed with the exception of a new batch of hay and grain mixed ration over the weekend of 10th November. All other stock were also eating these rations without apparent ill effect (note: milking herd were on a different grain mixed ration batch though). As the syndrome progressed some young animals would go to the feeder and on return would “drop dead” in front of the owner- a very distressing situation. All calves are normally vaccinated appropriately with “7 in 1” vaccine - covering a range of Clostridial and other diseases - however were not vaccinated this year. Botulism and anthrax were ruled out on the basis of clinical signs and history. There is no history of internal parasitism, mastitis or any infectious disease on the property, and no obvious sources of plant or other toxins.
Recumbent and sick calves had consistent signs of semi-consciousness, average capillary refill time, elevated heart rate, reduced rumen sounds and normal temperature (bar one severely affected calf with an elevated temperature). On autopsy the pathology noted was unremarkable with some reddening of the abomasum in some cases, rounded liver borders in others, occasional pale musculature, and in two final cases some excessive pericardial, thoracic and abdominal fluid. At this point a strong suspicion of Monensin poisoning was made and the producer instructed to stop feeding any more prepared grain ration.
After this two more calves died, but no more after that. A sample of the ration fed to calves (but not adults) was collected and analysed. It was found to contain more than 10 times the recommended levels of Monensin due to accidental mixing in the feed mill.
Comprehensive testing was undertaken to determine a diagnosis including repeated histopathology of specimens, some cultures, D-lactate and ocular fluid electrolyte and nitrate levels, trace element (copper, cobalt and selenium), whole blood metabolites and haematology, faecal egg counts, epsilon toxin testing (to rule out enterotoxaemia), and pestivirus testing. All tests were negative with the exception of consistently marked increased levels of Creatinine kinase and AST in some but not all live animals. A pathologist's comment was “This is a second animal with a significant increase of AST and CK. Consider a Vitamin E/ selenium toxicity, plant toxins such as Cassia spp - typically this plant is in Qld, blackleg, other bacterial myositis, snake bite, muscle trauma.”
Pathologists noted the lack of reference ranges for this species, but assumed similar to cattle. Histopathology noted hepatic changes in some animals, and muscle damage in others, with myocarditis noted in some samples. Monensin poisoning was mentioned as a possible diagnosis in one report, but samples were inconsistent in all animals.
A very high level of laboratory testing and veterinary input occurred in this case to achieve a diagnosis, and to rule out some other possibilities. Some of these test results may be helpful for “base line” data in this species in the future. An overview of all the results shows that death occurred by primary damage to the heart and other muscles caused by Monensin in toxic levels. This would account for clinical signs observed, as well as the shuffling gait and lack of energy affected animals were observed with before death.
A literature review indicates that Monensin and ionophore toxicity is well known in buffalo1, and the feed manufacturers were aware of this, but an operational error caused a large overdose into the calf feed.
This case highlights the benefit of thorough clinical examinations (and recording of findings), repeated autopsies when a highly unusual syndrome appears, good quality sample collection and the benefits of Government involvement to assist with test costs. Very few veterinarians in southern Australia have experience in dealing with buffalo, especially milking varieties and this investigation has added skills and confidence to local vets, and added to the body of knowledge about this hardy species. Ionophores are regularly used in ruminant nutrition, often as a means of reducing the risk of acidosis, but in the case of this species, the use may be reassessed.