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This article was published in 1975
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Viral-Induced Congenital Development Abnormalities of the Central Nervous System of Calves
W.J. Hartley, M.V.Sc., F.R.C.Path., Dept. Veterinary Medicine, University of Sydney
Congenital anomalies of the nervous system may be caused by a number of factors: namely, chromosomal abnormalities, hyperthermia, nutritional deficiencies or excesses and infections.
Although a wide range of viruses may invade the bovine foetus and/or foetal membranes and cause inflammatory or degenerative lesions therein, to date only a few are known to cause distinct developmental abnormalities of the central nervous system. Bovine virus diarrhoea/mucosal disease (BVD/MD) infection can produce cerebellar lesions and the blue tongue virus is thought to produce hydranencephaly. There is also strong evidence to implicate the Akabane virus with the syndrome of arthrogryposis and hydranencephaly (AG.HE) seen in New South Wales and in Japan.
BVD/MD Infection
Field and experimental evidence indicates that susceptible pregnant cattle between 3 and 6 months of pregnancy when exposed to the BVD/MD infection may produce full term calves with neurologic signs (Ward 1969, Kahrs et al. 1970 a,b; Scott et al. 1973, Brown et al. 1973). Clinical signs ranged from slight inco-ordination to inability to stand and some were blind. Gross lesions ranged from virtual absence of the cerebellum to a cerebellum smaller than normal. Histologically the lesions, which were confined to the cerebellum, ranged from a mild to advanced focal or diffuse atrophy of the folia. Folial changes varied from areas of complete destruction of all cortical layers to areas where there was focal absence of granule or Purkinje cells. White matter adjacent to folial lesions often showed focal or extensive cavitation.
A diagnosis of foetal BVD/MD infection can only be made by the identification of the cerebellar lesions together with demonstration of serum neutralising antibodies to the virus in the serums of unsuckled, affected calves.
In New South Wales I have seen several calves with either complete absence of the cerebellum or a cerebellum reduced in size with similar microscopic lesions to those reported above. It is not known whether any of these represent BVD/MD infection.
Blue Tongue Infection
Field and experimental evidence indicates that the blue tongue virus, either as wild or vaccination strains, can produce abnormalities of the ovine foetal central nervous system when ewes are exposed to this virus in early pregnancy. It is thought on serological evidence that a similar entity occurs naturally in calves in the U.S.A. (Mc Kercher et al. 1970, Richards et al. 1971). Affected calves were born inco-ordinate, blind and dull and on autopsy showed evidence of advanced hydranencephaly.
Although blue tongue does not occur in Australia, this entity is of interest because the lesions of hydranencephaly are similar to those in the entity now to be described.
AG/HE syndrome in N.S.W.
An apparently specific entity characterised by AG and HR has been seen sporadically and in severe epizootics in southern N.S.W. for many years (Blood 1956, Hartley and Wanner 1974). Less spectacular outbreaks of an entity characterised mainly by hydranencephaly and microencephaly (HE/ME) has also been seen in central and northern N.S.W. (Young 1969, Wanner and Husband 1974 Pritchard, pers comm.).
In the spring of 1974 a severe epizootic occurred in southern N.S.W. characterised by HE with some cases of ME and a few of AG. This outbreak was preceded the previous autumn, in the same general area, by the birth of incoordinate or paralysed calves (Sheppherd, Borner, Timmins, Gee and Jessep, pers comm,). In retrospect it would appear probable that the syndromes of paralysis, arthrogryposis, hydranencephaly and microencephaly represent different manifestations of the same disease process, the difference in lesions depending on the gestational age of the foetus at the time of the insult.
Incoordinate calves showed evidence of a mild to moderate non suppurative polio encephalomyelitis and/or a mild to moderate active secondary demyelination of cord and peripheral motor nerves (De Sarampers comm.). Other lesions observed were similar to those already described (Whittem 1957, Young 1969, Hartley and Wanner 1974). Cases of arthrogryposis showed massive loss of motor neurones in the cord in association with massive loss of myelinated fibres in the ventral and lateral tracts of the cord and in peripheral nerves. Most cases of hydranencephaly were characterised by a virtual complete replacement of each cerebral hemisphere by a fluid-filled cavity with preservation of most of the adjacent brainstem. Occasional brains had parts of the cerebro-cortical grey matter remaining. Most microencephalic brains also showed advanced hydranencephaly and in two of these brains there was virtually no anterior or mid brain stem. Several brains with HB and/or ME had abnormally small cerebellums.
Epizootics of AG/HE similar to those seen in N.S.W. have also been reported from Israel (Makusfeld and Mayer 1971) and from Japan (cited by Kurogi et al. 1975). These Japanese workers have also reported a direct association between this entity and the presence of antibodies to Akabane virus in the serums of unsuckled affected calves. Serums collected in N.S.W. from the 1964 outbreak of AG/HE and the 1974 outbreak of HE/ME/AG have also shown an apparent direct association between the presence of lesions and antibodies to the Akabane virus in both calves and dams, (Hartley 1975a,b). No virus was demonstrated in HE/ME/AG tissues examined by CSIRO in 1974 (Snowden pers comm.).
Akabane virus was first isolated from mosquitoes in Japan and later from Culicoides brevitarsis in Queensland (Doherty et al. 1972). In view of the distribution pattern of C. brevitarsis in Australia (Murray 1975) it seems likely that it may be responsible for the periodic transmission of Akabane virus to non immune pregnant cattle in years when it extends beyond the limits of its normal range.
The presence of arthrogryposis in a new born calf should not be taken as positive evidence of involvement by the entity described above. Sporadic cases regularly occur due to a number of other causes, e.g. the inherited arthrogryposis and cleft palate seen in Charolais and cases of spina bifida (Hartley and Warner 1974).
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