CASE NOTES


Polioencephalomalacia in a Merino Flock

Steve Eastwood, District Veterinarian, New England Livestock Health and Pest Authority, Armidale

Posted Flock & Herd August 2009

INTRODUCTION

In May 2008 an outbreak of polioencephalomalacia (PEM) occurred in a merino flock in the Walcha district.

HISTORY AND CLINICAL SIGNS

In March 2008, 30 mixed aged, merino ewes died. The 500 head flock had been split into 9 paddocks and rotated with deaths occurring in 5 of the mobs. Pastures consisted of either perennial fescue or Microlaena (native species). Affected ewes suffered ataxia, recumbency and death within 3-5 days.

Ewes were unresponsive to intramuscular thiamine injections despite histopathology results from the investigating private vet demonstrating subtle brain lesions suggestive of polioencephalomalacia (PEM). Deaths ceased in April 2008. In May 2008 deaths resumed. Initial presentation of affected ewes included marked opisthotonous, apparent blindness, ataxia, tremors and dilated pupils.

PATHOLOGY FINDINGS

There were no gross abnormalities detected on post mortem. Initial histopathology was inconclusive. However, requests for further sections to be taken identified marked multifocal PEM.

TREATMENT

Treatment consisted of thiamine IV 10mg/kg and subsequently IM bid for 3 days. Response to thiamine was seen with full recovery at the end of treatment however recovery was not as good as the author would have expected in 'thiaminase responsive' cases resulting from plant toxicities.

Despite response to thiamine ewes continued to be affected and a prevention strategy was sought instead. It was postulated that the PEM was due to an overgrowth of thiaminase-producing bacteria in the gut. All ewes were drenched with virginiamycin (Eskalin) @ 2mg/kg. Cases of PEM-affected ewes ceased a few days after drenching.

DISCUSSION

PEM lesions are caused by:
1. A change in thiamine status resulting from either a. Ingestion of thiaminase containing plants e.g. nardoo b. Increased intraruminal thiaminase production resulting in a decrease in thiamine availability
2. Sulphur toxicity - e.g. brassica toxicity (rape blindness), high sulphur water source
3. Lead toxicity
4. Water-sodium toxicity In this incident it was established that there had been no exposure to unusual thiaminase or sulphur containing plants, lead or salt.

It was hypothesised that there was an overgrowth of thiaminase-producing bacteria in the rumen. The cause of this overgrowth is not understood but may be as a result of normal pasture grazing. There is anecdotal evidence that PEM in the northern tablelands occurs sporadically with no cause identified. However it does not usually involve such large numbers of stock.

Thiamine treatment although moderately effective did not provide any control of the disease. Virginiamycin was used as a preventative because it was registered for oral use in sheep and would be effective in killing lactate producing bacteria. The targeting of these bacteria was designed to upset the ruminal flora and re-establish bacteria which did not produce thiaminase.

 


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