A local producer runs a mixed beef herd on 2 holdings in the Alstonville area.
The stocking rates are high, even by North Coast standards with 39 cattle and 13 sheep on a 17 ha property and 98 cattle and 2 horses on another 49 ha property.
Despite the high stocking rates, the cattle are kept in good order, with good growth rates, due to hand feeding. Pasture on the holdings can be quite short, particularly in the winter months.
The smaller of the two holdings is in dress circle Macadamia red soil country with a backdrop of rainforest in the gully.
On the afternoon of Saturday 29th July, 2000, a 4 month old bull calf presented with ataxia. It was examined by a local practitioner and treated with Ixodes antiserum.
Later that night another bull calf became ataxic.
The calves were staggering, swaying and generally unbalanced in the hindquarters and stiff and proppy in the fore.
By the following morning the first calf was recumbent, unable to rise, had hyperaesthesia to both touch and sound which increased to tetanic fits during the day, muscle tremors and a regular nystagmus.
The second calf also became progressively worse during the course of the day until it was unable to rise and developed similar signs to the first. It was treated that morning with Ixodes antiserum and the group of 16 calves treated with Thiamine.
A further 4 calves developed ataxia during the course of the day.
When I was referred the case on the Monday morning, 31st July, a total of 8 of the 16 calves were affected to varying degrees.
The most recently affected 2 calves had a mild wobbly unbalanced hind gait.
The others varied from knuckling in the hind, with a weaving gait, slow muscle tremor and a head wobble (3 calves) through to marked tetany, hyperaethesia particularly to sound, opisthotonus, unable to blink, fine muscle tremor and nystagmus in the worst 3 calves.
A plant poisoning was suspected.
The owner informed me that she had noticed that the fence was down bordering the rainforest, and this was close to where the first 2 affected calves were found.
Inspection of the rainforest found native wandering jew, birds nest fern and hoya vine all recently eaten.
A quick phone call to Ross McKenzie confirmed that the signs were typical of Hoya australis toxicity. With careful nursing a good prognosis was given.
Attention was given to shade, particularly over the eyes, as the worst affected calves could not blink. Hydration with subcutaneous and intraperitoneal fluids was important to prevent dehydration.
The other important consideration was preventing injury or drowning from misadventure. During the tetanic stage, particularly in recovery, the calves were given to throwing themselves about violently. One calf down in the yard developed blight, one near the dam ended up in it and another down amongst rocks had a prolonged downer syndrome in recovery.
The duration of the clinical signs was varied and generally prolonged. Convalescence was up to 2 weeks and the calves lost significant condition during that time.
Subsequent visits on the Tuesday and Wednesday found the last 2 calves affected to be the worst.
I suspect that the thick waxy nature of the leaf, and hence slow breakdown in the rumen may have been responsible for both the long period from ingestion to onset of clinical signs seen in some calves, and the generally prolonged duration of signs.
One calf that appeared to be recovering and was able to drink relapsed several hours after being given water.
Hoya australis is an attractive perennial native vine, found in rainforests, rocky peaks and dry scrub in coastal and subcoastal Queensland and Northern NSW.
The plant has been grown for may years as a garden plant. The plant is sought after by cattle as a source of green feed, during dry times.
For those cattle that die, postmortem and histopathology signs are minimal.
The toxin has not yet been identified.
With general nursing, prognosis is usually good.