Second cross Dorper lambs were purchased as store weaners in February 2011. Since that time they had been grazing lucerne or oat crops withad lib. access to a grain supplement of wheat, oats or chickpeas.
Monitoring for internal parasites and drenching had been routine. An effective 6 in 1 vaccination program was in place.
On the 19th June 2011, 6 lambs were found dead in the paddock and a visit was scheduled for the following morning when 4 more animals had to be picked up while mustering to the yards.
There were 1600 lambs in the affected mob and less than 10 showed any clinical signs. Typically affected lambs were depressed with their ears down and slow to move away. Some had a mild signs of lameness although no signs consistent with ovine interdigital dermatitis or footrot were seen. One lamb appeared blind. Moving through the yard, between 5 and 10% of faeces seen on the ground were loose and light in colour with grain in the faeces.
Three lambs were autopsied. The first had died while being trucked from the paddock. Large quantities of wheat were found in the rumen and through into the small intestine. A small number of Haemonchus contortus worms were found in the abomasum but were not consistent with acute haemonchosis. A clinical diagnosis of grain overload was made.
The second lamb had very little grain in the rumen. The liver was pale and enlarged. Because of the neurological signs seen in the mob, the brain was removed for histopathology. When removed the brain seemed to be enlarged with flattened gyri. Blood was also collected from this lamb.
The third lamb once again had large quantities of grain in the rumen. Blood was collected.
D Lactate levels in the blood of third lamb were elevated but not the second. The D Lactate level is a strong indicator of acidosis. Histopathological changes in the brain of the second lamb were consistent with polioencephalomalacia. A FEC on the mob averaged 200 epg with a high of 1120 epg.
Grain overload was clearly involved in these deaths. Large quantities of grain in the gastrointestinal tract, along with the D Lactate levels support this diagnosis. The question is then what to do? The lambs were within a month of sale and had been on grain for 4 months. Removing the grain feeders would slow the growth of the mob and increase the risk of further losses due to grain overload when the feeders were re introduced.
One possible cause of the grain overload was an increase in the proportion of wheat in the mix. Also, there was the possibility that the smaller wheat grains settled through the oats and chickpeas and concentrated in the bottom of the feeder. The flow of grain out of the feeders was slowed for a week and more oats were added to the mix.
The diagnosis of polioencephalomalacia (PEM) in the second lamb autopsied explained the signs of blindness not usually expected in a case of grain overload. Thiamine levels in the grazing oats and lucerne pastures should be adequate so the likely mechanism was due to thiaminase activity by bacteria such as Bacillus thiaminolyticus in the rumen.
The farmer reported no further cases. A paddock move, slowing of the grain flow from the feeder or time appeared to solve the problem.