Polioencephalomalacia

The thiamine deficiency of PEM is suspected to be caused by proliferation of bacteria in the rumen that produce thiaminase, which in turn breaks down thiamine.

Ruminal acidosis may create favourable conditions allowing proliferation of thiaminase-producing bacteria. 

High sulphur intake is suspected to cause high concentrations of hydrogen sulphide (H2S) to be formed in the rumen, which is absorbed into the body. Feeds such as lucerne, canola (rape), and high protein pastures are rich in sulphur, as are some water supplies. Accelerated intake of sulphur can occur from high water consumption in hot weather, increased appetite after fasting, or sudden onset of cold weather to which the animal cannot adapt. 

PEM is usually sporadic but can occur as an outbreak. Animals of any age can be affected, but it occurs more in young animals. The conditions of thiamine deficiency or sulphur excess described above can potentially occur at any stage of the export process.

Injections of large doses of thiamine (vitamin B1) at this stage may be diagnostic if they cause rapid recovery (within hours). If untreated they will become recumbent with retraction of head, arching of back, rapid eye movement, dog-sitting, convulsions and death. 

Differential diagnoses in cattle include lead poisoning, water deprivation/salt poisoning, Histophilus meningoencephalitis, coccidiosis with nervous involvement, nervous ketosis and vitamin A deficiency. 

At necropsy, flattening of the gyri of the brain and coning of the cerebellum may be suggestive. The whole brain should be submitted to the laboratory in buffered formalin for histology. Water and fodder may be tested in the laboratory for sulphur levels. 

PEM in sheep and goats needs to be differentiated from salt intoxication/water deprivation, lead toxicity, and bacterial and viral brain infections.

If cases continue to occur, feed more roughage, and reduce or replace water and feeds that contain sulphur.