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This article was published in 1985
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A Cerebellar Defect of Calves
A.G. Morton, B.V.Sc., Veterinary Inspector, GUNDAGAI
Four ex twenty calves born between early March and late May, 1984 were seen by the owner to have nervous signs at or within a few days of birth. One died of misadventure, one was destroyed and two survived. Another calf found dead may well have been a victim of the same condition.
I was asked to investigate the problem in late May, 1984. Two calves had survived, the first a 6-8 week old red baldy steer ex an aged broken mouth Angus cow, the second a black baldy heifer ex a broken mouth Angus cow. Signs included inability to rise, ataxia, goose stepping, wide stance, walking with a general unsteadiness, wavering of the head and body and mild opisthotonus.
Post-mortem of one calf yielded no significant gross lesions. Initial histopathology suggested oedema of the CNS and the comment 'possibly some spheroid formation in granule cell layer of the cerebellum and dorsal horn of spinal cord. Also isolated vacuole formation in some Purkinje cells. These findings are non-specific. Aetiology? Lead poisoning or an insecticide could be involved.' These histological slides were later examined by Bill Hartley in New Zealand and he felt that there were no significant lesions.
The pattern of calving was one of normal calves followed by a mixture of abnormal and normal calves and then normal calves. This suggested a short term exposure to an effector, e.g. a virus or chemical at some critical stage of gestation.
A new Poll Hereford bull had been used at joining, however, with all the cows being home bred Angus and Angus cross Herefords with the exception of three Murray Greys and four Angus cross Herefords purchased several years earlier as heifers, a genetic basis seemed unlikely.
Neighbouring properties experienced no problems.
Thorough checks of paddocks revealed nothing unusual. The main diagnostic contenders were -
A. A hereditary cerebellar defect ex sire;
B. Mucosal Disease or some other effector.
One of the surviving calves died from misadventure (drowning), during August 1984, gross pathology and histopathology were negative.
In September, 1984 the herd was bled for Mucosal Disease serology and virus isolation. The results provided no evidence for mucosal disease virus involvement in the condition. The surviving calf continued to show similar symptoms to those first observed. The owner had attempted to correlate cows with their calves with little success. The calves were ear tagged to facilitate future investigations.
In January, 1985 the condition suddenly appeared in two sibling calves some eight months old! The cows and calves had been in the new (hill) paddock for 3 or 4 weeks. They were allowed access on 31/12/84 to the long paddock where the original affected calves were seen. The cows had also been in the new (hill) paddock during late gestation. Two calves (784, 795) were found sick 1/1/85. The first (784) was described by the owner as 'very uncoordinated, just like the previous cases.' The following day (2/1/85) I observed that the beast had a high stepping gait of the front limbs, the back was held stiff and the hind limbs exhibited a slightly widened stance. The second (795) when found by the owner was described by him as 'down, very stiff and uncoordinated, almost convulsing (rigid) when down. If helped up it usually fell down, sometimes it would remain standing for short periods.' To the astonishment of all the following day (2/1/85) 795 was almost normal, the only symptom observed being mild ataxia of the forelimbs. The owner later commented that symptoms appeared worst during the afternoon and on hot days. The only surviving calf (252) from the original group affected as perinates appeared almost normal.
On 9/1/85 myself and D. Kennedy, Veterinary Officer (Epidemiology) visited the property while the owner was on holidays. Calves 784 and 795 were much the same as they were on 2/1/85 while a further case 793 a black and white steer was seen. It was more severely affected than 784 and 795. We felt some toxic substance must have been present to precipitate the outbreak in both perinate calves and their siblings some seven months later. A thorough search of the paddocks was made for possible plant or chemical toxins, none were found.
Further checks were made of the hill and long paddocks by the District Agronomist on 22/1/85. One of the Regional Veterinary Laboratory officers (R. Whittington) also observed the calves, his overall assessment was 'hypermetria, unusual posture, wide base stance and gait, ataxia with normal strength and delayed onset of voluntary movements are characteristic of cerebellar disfunction.' The four calves had similar clinical signs that varied only in degree. The clinical signs improved with rest and worsened with exercise.
On 30/1/85 P. Harper, Veterinary Research Officer, Glenfield visited the property to examine and videotape, affected cattle. The cattle had remained in the long and hill paddocks with no new cases since 9/1/85. A check of these paddocks again found nothing suspicious. Attempts to obtain CSF samples from affected animals were unsuccessful.
The 1985 calving commenced with one of the cows believed to be the dam of previously affected calves having two small dead calves. No post-mortem was performed. A further 10 normal calves were born over the next two weeks and then a calf suffering the same symptoms as previous cases was born 10/3/85. Its dam, cow 26 was believed to be the mother of a previous case. The calf was videotaped and post-mortemed at Regional Veterinary Laboratory, Wagga on 13/3/85. Grossly the post-mortem was unremarkable. Serum amino acid concentrations were within the normal range, CSF was collected regrettably it was contaminated with blood. The histopathology on nervous tissues revealed :
| Left sciatic nerve, 2 brachial nerves | There was mild segmental swelling or vaculation of the myelin sheaths around axons |
| Gasserian ganglion | Not remarkable |
| Brain | Astrocyte cytoplasmic swelling in cerebral white matter tracts and cerebral peduncles. Dilated Virchow Robin spaces. |
| Cerebellum | In one area granular cells were seen tracking down a blood vessel into the molecular layer |
| Spinal cord | Not remarkable |
| Diagnosis | Cerebral oedema |
Jim Rothwell (Veterinary Research Officer) commented, 'I'm not sure if the myelin changes in the peripheral nerves are a lesion or not, but I have noted them for interest. I think the cerebral oedema is real.'
This is a most puzzling case with cases of an apparently identical syndrome appearing in perinates and 7-8 month old calves. Histopathology has been unrewarding and a genetic basis for the syndrome seems unlikely with the breed history of the sire and dams. Hopefully, further investigations will shed some light on this unusual condition.