Diseases

Polioencephalomalacia

Other Names

Cerebrocortical Necrosis, PEM, Star Gazing

Species

All.

Description

Polioencephalomalacia (PEM) refers to the nervous disease caused by degeneration (malacia) of the brain associated with thiamine (vitamin B1) deficiency or sulphur excess.

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

High sulphur intake is suspected to cause high concentrations of H2S to be formed in the rumen which is absorbed into the body. Feeds such as lucerne and 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 or increased appetite after fasting or sudden onset of cold weather to which the animal cannot adapt.

PEM is usually sporadic but can occur as outbreaks. 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.

Clinical Signs and Diagnosis

Ear twitching, incoordination and hypersensitivity to any stimulus are earliest detectable signs. Cases are often dull, apparently blind and they may head press against fixed objects or stand with the head pulled back (stargazing). Sometimes they are found convulsing, comatose or dead.

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 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.

Treatment

Injectable thiamine (vitamin B1) is highly effective at rapidly reversing signs if given early and in massive doses. Intravenous products are available and should be administered slowly. Dexamethasone may be useful to decrease oedema and inflammation of the brain. Sulphur induced PEM has a poorer response to thiamine treatment. In-contact animals may be supplemented with oral thiamine added to the feed.

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

Prevention

Adequate dietary fibre and gradual dietary changes are necessary to prevent acidosis or indigestion leading to thiamine deficiency. Avoid rations and water high in sulphur.

Syndromes