Polioencephalomalacia (PEM) is a pathological diagnosis that describes necrosis within the grey matter of the cortex of the brain. It is a common domestic ruminant neurological disease caused by a disruption of glucose metabolism within the cerebral cortex due to thiamine deficiency. This report describes a mortality event characterised by sudden death in a cohort of feedlot lambs attributed to PEM in which a presumptive diagnosis was made on observation of gross brain lesions at necropsy. Diagnosis was confirmed by histopathology.
Approximately 500 prime wether lambs, 12 months old, were inducted into a feedlot with the aim of finishing the group on a barley/lucerne mix plus a vitamin/mineral premix. The animals had received a primary course of 5-in-1 clostridial vaccination and been recently drenched. Six animals were found dead with no premonitory signs over a one-week period. No clinical signs were observed in the surviving group members. Two dead lambs were presented for necropsy examination.
Both lambs were well grown with a body condition score (BCS) of 4. There was formed rectal faeces and grain/herbage in the rumen. The brains were removed and sectioned longitudinally revealing multifocal, irregular, soft, pale areas in the cerebral cortex (Figure 1). Histopathology revealed multifocal cerebral laminar necrosis with sub-meningeal oedema and haemorrhage, confirming the diagnosis of PEM.
No further cases were seen.
Thiamine is required for carbohydrate metabolism. PEM develops after disruption of cellular respiration in the cerebral cortex when thiamine is limiting. In ruminants this is usually secondary to a proliferation of thiaminase-producing ruminal microorganisms. High sulphur rations have also been associated with thiamine-responsive PEM.
Sheep with PEM may be found dead or present with progressive neurological signs, including anorexia, separation from the mob, stargazing, central blindness, head-pressing, ataxia, hypermetria, recumbency and convulsions. Mildly affected animals can recover spontaneously.
The adult ruminant thiamine (vitamin B1) requirement is met by thiamine-producing ruminal microorganisms. Thiaminase degrades thiamine, rendering it unavailable to the animal. Feedlot ruminants are particularly susceptible to PEM due to the tendency of highly fermentable, grain-based, low-roughage rations to favour the predominance of thiaminase-producing microorganisms. High sulphur rations might also be contributory.
Potential sources of excessive sulphur available to feedlot animals include contaminated water, brassica products (e.g., canola meal) and lucerne. By-products of sugar beet and corn processing can also be high in sulphur.
Treatment with injectable thiamine can be successful early in the course of disease. Prevention requires a review of the feedlot induction strategy and ration. Consider the addition of roughage to the diet. Identify and remove sources of excessive sulphur. Commercially available feed mixes with added thiamine are available but the efficacy of oral thiamine supplements in PEM prevention in ruminants has not been established.