History
Breed:
Corriedale
Size of Flock:
'Rowan' runs about 200 stud sheep - stud established 45 years ago. 1200 commercial sheep - ewes, lambs, no wethers.
Source of Rams:
The last ram bought was in 1978. A ram was also bought in 1976 but before that, no rams were purchased for about 15 years.
Location:
Walla Walla, about 55 km north-west of Albury.
Type of Farming:
Cereal cropping and sheep grazing.
Other Animals on Farm:
Steers at times for fattening - local purchases, some farm dogs and cats.
1974 Lambing:
85% market - spring lambing.
5.8.75
Two dead lambs were sent in by owner and forwarded to the D.V.R., Glenfield. Odd lambs had been born dead over the years.
Laboratory Findings
Lamb 1 a male, 5 kgs, antiparturient (sic) death, showing generalised subcutaneous oedema, blood stained, up to 1.5 cm thick. Brachygnathia inferior, scoliosis (left deviation of thoracic vertebrae column between T5 & 8). Hydranencephaly and cerebellar hypoplasia, moderate arthrogryposis. Complete extension of limbs was not possible. Fibrin clots were present over organs.
Lamb 2 a male, 3 kg, parturient death, generalised subcutaneous oedema up to 0.5 cm over rump. Excess fluid in body cavities, swollen liver, less than 5% of lung aerated.
The provisional diagnosis was developmental abnormalities and/or intrauterine infection.
Bacteriology revealed no significant organisms.
Histopathology of Lamb 1 revealed changes typical of Hydranencephaly arthrogryposis observed in calves due to Akabane virus.
In Lamb 2, the brain showed mild leuco-encephalomalacia. This could have been due to Toxoplasmosis.
Enquiries revealed that grain was fed to ewes from 6 to 8 weeks before lambing started and feeding stopped after lambing was over. Grain was stored in silos. Cats lived about the sheds.
The dams of Lambs 1 & 2 could not be identified but the owner was asked to endeavour to identify any affected lambs and their dams in 1976. This request was again made in 1978.
27.9.78
A 2 year old ewe had a lamb with abnormal jaw development. The ewe was located after lambing was finished and a blood sample obtained. It proved to be negative to the Akabane Neutralisation Test. Ten sera were tested for Mucosal Disease and all were negative.
16.8.79
A still born lamb with abnormal jaw development born the previous night was sent in by the owner and forwarded to Glenfield. This lamb, 16 kg male, had joints fixed in flexion, muscle atrophy, generalised oedema, excess body fluid, brachygnathia inferior.
The CNS showed Hydranencephaly, cerebellar hypoplasia and hypoplasia of the spinal cord. The findings were typical of Hydranencephaly - arthrogryposis c.f. Lamb 1 of 1975.
Virology revealed negative GEL Diffusion Precipitin Reactions of both CSF and heart blood for mucosal disease, Bluetongue, M3, Akabane and Aino/Peaton viruses.
27.8.79
Two more lambs dead at birth were examined at Albury, both female, full-size large lambs. Both showed joints fixed in flexion, poor muscle development, generalised oedema and excess body fluid of clear colour, brachygnathia inferior.
In the CNS, there was hydranencephaly, cerebral hypoplasia and hypoplasia of the spinal cord (3 mm diameter).
The 2nd lamb had oedematous tissue over the cranium and dark red, port wine coloured fluid in the cranium.
Virology of heart blood. again gave negative GDP reaction to mucosal disease, Bluetongue, M3, Akabane and Aino/Peaton viruses.
Virus isolation was attempted from these 3 lambs, but no virus was isolated.
Immunoglobulin levels were determined but these findings did not indicate that an infectious agent was involved.
An attempt will be made during the 1980 lambing to identify those ewes which give birth to this type of lamb, so that the cause may be further investigated.
Acknowledgement
The writer wishes to thank Mr. J. Plant and colleagues at Glenfield Research Station for assistance and comments in this investigation and the Chief, Division of Animal Health for permission to report it.