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This article was published in 1977
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Microencephaly and Related Abnormalities in Lambs
H.C. Grant-Frost, B.V.Sc., Veterinary Inspector, Coonabarabran
Introduction
Micrencephaly and other developmental abnormalities in lambs in N.S.W. were described by Hartley et al. (1974). This paper describes another outbreak on a Dorset stud at Gilgandra, and mentions briefly a further occurrence of the condition on a property near Coonabarabran.
History of Outbreak
The Gilgandra Dorset stud property consists of 1120 hectares running approximately North-South along the Eastern bank of the Castlereagh River about 3 km north of Gilgandra. About 400 hectares of lucerne, 320 hectares of wheat, 160 hectares of oats plus some small areas of summer crops and sub-clovers are grown. The stud comprised 140 ewes and 3 stud rams which were joined in February 1976 for 8 weeks. On the same property, 1700 Border Leicester Merino cross ewes were running with flock rams from the stud over the whole year.
The second property is situated 55 kilometres east of the first property. 300 Merino and Merino X Border Leicester ewes were joined to Dorset rams in February / March 1976.
Losses were first observed on 28.6.1976 in the stud ewes at Gilgandra and on 15.7.76 on the second property. No abnormal lambs were seen in the crossbred ewes lambing at the same time at Gilgandra.
Pathological Findings
Similar conditions were seen in both flocks. These included:—
(a) Microencephaly in apparently normal lambs. Some of these lambs showed a deformity of the frontal bones of the head. In the brain, the corpus callosum was either absent or reduced. There was a gross dilation of the lateral ventricle and some showed cavitation or gelatinous areas in the cerebral or cerebellar white matter.
(b) Microencephaly associated with brachygnathia inferior.
(c) Hydranencephaly / arthrogryposis with or without brachygnathia with or without cerebellar hypoplasia. In these Lambs there was no corpus callosum and the lateral ventricles were dilated.
Virological examination
Neutralising antibody to Akabane virus was detected in 6 of 11 ewes examined, including 4 ewes which gave birth to affected lambs and 2 ewes which gave birth to dead lambs. Antibody was also detected in the peritoneal fluid of a lamb with microencephaly and hydranencephaly.
Mucosal Disease virus precipitating antibody was detected in 5 of 11 ewes examined including 3 ewes giving birth to affected lambs and 2 ewes giving birth to dead lambs. No Mucosal Disease antibody was detected in any of the lambs examined.
In the indirect fluorescent antibody test for toxoplasmosis (1 Fat one ewe with a titre of 1/64 had evidence of recent infection and other ewes with a titre of 1/6 gave birth to dead lambs. No evidence of toxoplasma infection was seen on histological examination.
Discussion
Dennis (1975) has made a detailed study of lambs with congenital defects in W.A. However, Microencephaly was only seen in one lamb out of a total of 401 lambs studied. Arthrogryposis was commonly seen, with 32 cases, or 8%, in abnormal lambs. Conversely, agnathia, seen in this series only once, was by far the most common abnormality in the West Australian study (70 cases, or 17.5% of abnormalities).
It is considered likely that the abnormal lambs on these two properties did not comprise the complete syndrome, since foetal death and abortions also occurred. Examination of reproductive tracts from ten Dorset ewes from the Gilgandra stud culled for infertility revealed evidence of recent pregnancy in six cases.
It is likely that the condition is due to an insult to the dam at some time between 25 and 50 days gestation. Brachygnathia is likely to result from an insult at about 25-30 days, AG/HE has been produced by inoculation of the pregnant ewe with Mucosal Disease Virus at about 50 days gestation (J.W. Plant, personal communication, 1976).
The pathogenesis of the clinical condition probably involves two stages:—
a) An agent destroying or interfering with germ cells in the early stages of development resulting in abnormal development.
b) An interference with normal development gives rise to other changes including dilation of the lateral ventricles and leads to degeneration of brain tissue and muscle atrophy in association with AG.
The possible causes of the condition include viral agents, ingestion of some teratogenic material or an environmental insult. The condition was only reported from 2 properties in the district; and in one flock, only the younger ewes gave birth to affected lambs, suggesting some immunity had developed in the older animals.
In August/September 1976 calves with AG/HE, and 'dummy' calves were born in this area. It has been shown that there is a direct association between infection with Akabane virus in cattle and the occurrence of AG/HE and HE/ME in calves in the Moss Vale area of N.S.W. (Hartley et al. 1975). Furthermore, the isolation of Akabane Virus from ovine foetuses out of ewes which had been naturally infected during pregnancy has recently been documented (Della-Porta et al.., 1977). The ewes in this instance were part of a flock of 50 ewes at Badgery's Creek, N.S.W. In view of the serology results in the present series indicating exposure of the ewes to Akabane virus infection with this agent is considered the most likely cause of the condition, infection having taken place some time in March/April, 1976.
Summary
The birth of Lambs with congenital abnormalities including Microencephaly and Arthrogryposis on two properties on the Central West Slopes of N.S.W. is described. It is postulated that the cause of the condition is exposure of the dam to Akabane virus at a critical stage of pregnancy, probably between 25 and 50 days gestation.
Acknowledgements
These are made to the staff of the Veterinary Research Station, Glenfield, who carried out examination of material from the two properties. Special thanks are due to S.V.R.O. John Plant who provided much of the material used in this essay. I also acknowledge the help of Mr. R. Marchant, L.S.O. (S. & W.) Dubbo, who collected and sent some of the specimens to the laboratory. Finally, thanks are due to Mr. Max Chandler, 'Bowenleigh' Gilgandra, whose keen co-operation is appreciated.
References
Dennis, S.M. (1975) Aust. Vet. J.51:80
Hartley, W.J., & Haughey, K.G. (1974) Aust. Vet. J. 50:55
Hartley, W.J., Wanner, R.A., Della-Porta, A.J. and Snowdon, W.A. (1975) Aust. Vet. J. 51:103
Della-Porta, A.J., O'Halloran, M.L., Parsonson, I.M., Snowdon, W.A Murray, M.D., Hartley, W.J. and Haughey, K.J (1977) Aust. Vet. J. 53:51
Table 1
| LAMB BIRTH DATE | AGE OF EWES | PATHOLOGICAL CHANGES IN LAMB | BRAIN WEIGHT (gm) | SPINAL CORD WEIGHT (gm) | SEROLOGY ON EWE MUCOSAL DISEASE VIRUS gel DIFFUSION PRECIPITATION TEST | AKABANE VIRUS NEUTRALISATION TEST |
|---|---|---|---|---|---|---|
| 28.6.76 | Born alive, had fed, hydranencephaly (Akabane antibody in peritoneal fluid) | 6.50 | - | |||
| 28.6.76 | ? | Arthrogryposis/hydranencephaly Brachygnathia, Scoliosis | 2.0 | |||
| 29.6.76 | 2 | 2 day old lamb, appeared normal | +ve | -ve | ||
| 1.7.76 | 4 | Born dead, appeared normal | +ve | -ve | ||
| 5.7.76 | 3 | Arthrogryposis/hydranencephaly Brachygnathia | 2 | 1.7 | +ve | +ve |
| 5.7.76 | 2 | Microencephaly, brachygnathia, abnormal frontal bones | 9.0 | 1.7 | +ve | +ve |
| 5.7.76 | 2 | Cavitation of cerebrum | 67.7 | 14.7 | +ve | +ve |
| 6.7.76 | 3 | Microencephaly | 18.0 | 6.8 | -ve | +ve |
| 6.7.76 | ? | Microencephaly | 11.8 | 8.1 | ||
| 6.7.76 | 2 | Dystocia | -ve | -ve | ||
| 21.7.76 | ? | Microencephaly, brachygnathia | ||||
| 3.8.76 | ? | Arthrogryposis/microencephaly/ hydranencephaly/scoliosis |