NADIS disease bulletins are written specifically for farmers, to increase awareness of prevalent conditions and promote disease prevention and control, in order to benefit animal health and welfare.

Farmers are advised to discuss their individual farm circumstances with their veterinary surgeon.

Polioencephalomalacia (CCN; cerebrocortical necrosis)

Several ewes were seen during the last week of July with clinical signs of isolation from the flock, high head carriage, a high stepping gait (due to blindness), aimless wandering and in some cases bouts of head pressing; progressing over a period of 12 - 24 hours to sternal recumbency and depression, with periodic bouts of hyperexcitation and backwards flexion of the neck. Upward and inward rotation of the eyes was observed in some cases. Untreated ewes progressed to a state of lateral recumbency, with periodic convulsions leading to death within a few days. These clinical signs are characteristic of polioencephalomalacia (CCN).

CCN IN A WEANED HALFBRED LAMB

Other diseases which can present with similar clinical signs include -

- focal symmetrical encephalomalacia (enterotoxaemia) in young lambs born to dams which were not vaccinated against clostridial diseases

- abscessation of the cervical spinal cord associated with dosing gun injury

- pregnancy toxaemia

- acute coenurosis or cysticercosis (tapeworm infections)

- listeriosis

Most of these diseases can be differentiated on the basis of veterinary clinical examination.

CCN can be diagnosed by postmortem examination. Affected areas of the cortex of the brain autofluoresce when cut sections are viewed under ultraviolet light. The postmortem diagnosis is confirmed by histopathology.

STERNAL RECUMBENCY AND BACKWARDS FLEXION OF THE NECK DUE TO CCN

The clinical signs of CCN are caused by damage to the superficial tissue of the brain. This brain damage is due to altered glucose metabolism, which usually results from an induced deficiency of vitamin B₁ (thiamine). Thiamine is normally synthesized in the rumen, but overgrowth of thiaminase-producing bacteria in the rumen, which can occur following a change of diet, destroys the vitamin B₁.

Most cases of CCN occur about 2 weeks after movement to lush pasture or other dietary change such as overnight yarding before anthelmintic drenching. The disease occurs in both ewes and weaned lambs, but is uncommon in lambs less than 12 weeks-old. The unusually high incidence of the disease in ewes in the south-east of Scotland was probably a consequence of two days of persistent heavy rain and low temperatures at the end of June. Many ewes would not have fed while seeking shelter during this period, and would have been hungry after the rain stopped. Alterations to the ruminal pH and microflora associated with this extreme change in feeding behavior would have enabled overgrowth of thiaminase producing bacteria and destruction of vitamin B₁ produced by other bacteria in the rumen.

The treatment response to intravenous injections of 10 mg/kg vitamin B₁ (5 ml of the 100 mg/ml product for a 50 kg sheep) and soluble corticosteroids (1 mg/kg dexamethasone) is good, provided that affected animals are identified promptly. Further twice daily intramuscular injections of vitamin B₁ for three days are usually required. Unfortunately vitamin B₁ on its own is not currently available from the manufacturer, so injections of multi-vitamins which include vitamin B₁ are required. The dose rate for these products must be adjusted to ensure administration of sufficient vitamin B₁.