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Acorn calves (chondrodystrophy)

Chloe Hawthorne, Sydney University Veterinary Intern and Rachel Kent, Sydney University Veterinary Intern

Posted Flock & Herd August 2007


RLPB Young was contacted on 20/08/2006 to investigate two cases of Acorn calf syndrome. The herd consisted of 32 cows of mixed age and breed, some with 3-5 month old calves at foot and one Angus bull.

Six or seven of these cows had produced normal calves in the past few weeks. One Belted Galloway cow had produced a live affected Acorn calf, whilst one Angus cow had produced an affected calf which died two days after birth.

The paddock contained a sparse mix of grass pastures (Fescue, Cocksfoot, Phalaris, Sub-clover, Patersons Curse). The herd had been receiving supplemental oaten hay since March/April. Various lick blocks were provided throughout the year. The property had received 175mm of rain so far this year (average annual 650mm).

The live calf was a week old male Belted Galloway. It was stunted, with short, thick limbs. It was able to suckle and walk, the calf moved its forelimbs in a paddling motion and it had hyperextended pasterns.

The dead calf was a two-day-old Angus heifer. This calf had very stunted limbs with enlarged joints, and a mildly short maxilla (undershot jaw).

Post-mortem findings

Samples of myocardium, bone and cartilage were submitted to a diagnostic laboratory for analysis. The histopathology report indicates that within the long bone growth plates, the zones of chondrocyte proliferation and hypertrophy within the physis show that the chondrocyte columns are shorter and less regular than normal. In summary the growth plate shows mild disorganisation.

Image of affected calf prior to post-mortem
Affected calf prior to post-mortem. Note shortened limbs and enlarged joints.
Image of cross-section of humerus
Cross-section of humerus. Note shortness of shaft relative to joint size.


Over July/August, there have been several reports of acorn calves in the Young district. Similar outbreaks have occurred previously in the Hume, Gundagai, Cooma and Young districts, as well as areas of Victoria in 2003/2004 and 1991. Between 1-50% of calves born may be affected. Outbreaks coincide with very dry seasonal conditions, most commonly in the autumn preceding a spring calving.

Affected calves demonstrate varying degrees of limb deformity, such as shortening and rotation. Other abnormalities include shortening of upper and/or lower jaw, domed skull and spinal distortion. The dams of affected calves are normal.

Calf deformities result from an impact on foetal development between day 45 and 245 of gestation. The type and severity of deformity depends on the stage of pregnancy at which development was affected.

There are numerous potential causes of this syndrome, including infectious (viral) diseases, plant toxins, chemicals and dietary deficiencies. The most current hypothesis is that the deformity is the result of a deficiency of the trace element, manganese.

Further studies need to be completed to come up with a definitive cause. Once this is identified, work can then go into disease prevention and management strategies.


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