CASE NOTES
Feedlot lactic acidosis despite complete ration, buffer and roughage provided
Courtney Simkin, District Veterinarian, Hay
Posted Flock & Herd October 2019
Introduction
Lactic acidosis (grain overload or grain poisoning) can occur easily in feedlot situations; especially during the transition to a high grain ration. It is vital to get the stock accustomed to the grain ration over a period of at least 2 weeks. Even though a ration may tick all the boxes on paper it is important to observe it being consumed correctly. In this case, the sheep were given access to ad-lib roughage but it had been packed into the hay dispenser too tightly and could not be eaten by the sheep.
History
Late November 2017, a producer near Rankin Springs NSW was preparing his lambs by feed-lotting before sale. The lambs, 4 months old, July/Aug 2017 drop, were grazed on a failed pea stubble crop and fed barley and barley hay. The lambs were shorn, vaccinated (5in1) and had been moved into the feedlot. On 12.12.2017 the producer reported a large 'tail'-in the mob and continued deaths (total now 25 since November).
The lambs were in two holding paddocks next to the shearing shed. They hadad lib loose lick (salt and lime) in dishes next to water-troughs. There was ad lib. barley hay in bale holders and a concentrate mix of barley, peas and buffer pellets (brand not recorded but did contain added Ca, Mg and buffer - ionophore), added at the recommended rate. The lambs were divided into two weight classes and if lambs lost condition they were moved in with the low weight lambs. There was good shade from multiple gum trees with some grass (well eaten down) and lots of young toxic weeds (estimate covering 10% of the area in low weight yards). The toxic weeds were heliotrope (Heliotropium europaeum), paddymelon (immature Citrullus lanatus or Cucumis myriocarpus), marshmallow (Malva parviflora) and caltrop (Tribulus terrestris). However, on inspection there appeared to be minimal consumption of the potentially toxic weeds.
On inspecting the lambs in the feedlot, an estimated 5% of the lambs were lying down (scattered across the shaded area, as the ambient temperature was over 37°C with strong northerly winds) but the whole mob appeared dull. Lamb one was found under gum tree (sunny side), sternal recumbency, head turned to flank, ears drooping. This was described by the producer as a typical appearance of the lambs prior to death.
Clinical Signs
Lamb One: The merino lamb was 20-25kg, BCS 2/5, dull, had to be lifted to stand and carried to the shed for examination. She had a rectal temperature of 40.7°C, an increased respiratory rate, but the heart rate was slow and strong. She had her eyes closed and bilateral inflammation of lids (slightly swollen and pink) and clear discharge from medial canthus. The mucous membranes were pink, moist and CRT <2 sec. There was no menace response, the pupils were dilated (may be due to lighting of shed) and the pupillary light response was normal. All four limbs had normal proprioception although, had slightly widened stance. The faeces green odorous, soft and semi-formed.
Producer elected not to sacrifice the lamb for necropsy. Instead, blood samples were taken.
Additional fresh faeces were collected for testing from low weight lamb mob.
Laboratory Results
The blood picture suggested subclinical dehydration, with moderate to marked azotaemia, consistent with lactic acidosis (or less likely from consuming some of the toxic plants that were available). With the benefit of hindsight a D-lactate determination would have been worthwhile.
WEC was low with low coccidia.
Post-mortem Results
The following morning a lamb (lamb two) was found dead and brought into the office for post-mortem examination.
Lamb two: The lamb was 20-25kg, BCS 2/5, with poor fat coverage. The rumen was filled with barley and peas, with little to no roughage and rumen had a pH of 4. The rumen epithelium was easily removed exposing red, inflamed/degenerated tissue. The liver was grey and necrotic. There was little ingesta beyond the rumen.
Figure 1 - whole carcass at PM with rumen open - lamb two
Figure 2 - close up of exposed ruminal lining showing red inflammation/decomposition - lamb two.
Outcome and follow-up
Based on the post-mortem indicating lactic acidosis, the producer planned to buy lucerne hay to try to encourage the lambs to eat some roughage. However, when assessing his current arrangement see why the lambs had rejected the hay he found it was tightly packed in the holders. After he spread some out the lambs 'swarmed on it'.
Discussion
The toxic plants in the feedlot were all non-palatable plants and did not have evidence of being eaten. Paddymelons are described as very bitter, with symptoms including diarrhoea, dyspnoea, pulmonary oedema, hepatic myocardial necrosis and sudden death. Marshmallow weeds induce staggers and nitrate toxicity. Heliotrope causes hepatic damage leading to secondary photosensitivity and also predisposes stock to copper toxicity. Caltrop causes hepatic, kidney and other organ damages. Based on the lack of evidence of consumption of the plants and the symptoms displayed by the lambs, toxic plant consumption was excluded as the cause of morbidity and mortality.
The necropsy of lamb two, including the rumen pH of 4.0 confirmed lactic acidosis. Post-mortem testing of the rumen for acidosis needs to be analysed with care as post-mortem changes can decrease the ruminal pH over time. Depending on the time since death, a pH of 4-5 is indicative of lactic acidosis; although ruminal wall histology and D-lactate levels can also be tested.
Despite the producer introducing the lambs to grain over a few weeks, with lime/salt and buffered pellets available, there was still lactic acidosis. Unfortunately, the only roughage, the barley hay, was packed tight in the holders making the ration fibre-deficient and the lambs developed lactic acidosis.
References
- Tom Westermann, EMAI (Pathology Resident), personal communication
- Duddy G, Shands C, Bell A, Hegarty R and Casburn G (2016) Primefact 523 - Feedlotting lambs, 2nd Edition
- Radostits OM, Gay CC, Hinchcliff KW and Constable PD (2007). Veterinary Medicine, 10th ed, pp314-325
- West DM, Bruère AN and Ridler AL (2002). The Sheep, 2nd ed, pp214-215