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This article was published in 2005
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A history of the 'Acorn Calf' syndrome

Alex Stephens, District Veterinarian, Cooma RLPB

The term 'Acorn calves' came from the US (specifically California), where it has been used to describe congenitally malformed calves showing varying degrees of chondrodystrophy and with a resemblance to inherited dwarfism calves. In unscientific terms these calves are often described as having a typical bull dog appearance with varying degrees of limb deformities.

This description of the condition by John Maars in 2001 gives a good generalised summary of the condition. "'Acorn calves' are congenitally malformed calves born to cows that have ingested large numbers of acorns under very poor forage conditions during the second trimester of pregnancy (3-7 months of pregnancy). The cause appears to be a combination of poor nutrition and exposure to acorns. The calves have very short legs, abnormal hooves, and misshapen heads. These calves look like dwarves in most instances. Occasionally, more than 10% of the calves in a herd will be acorn calves." Interestingly, the term may be a misnomer, as when the condition could not be reproduced experimentally, by feeding acorns to pregnant cows, severe nutritional deficiency during the 3rd to 6th months of pregnancy was suggested to be an aetiological factor (Hart et al. 1947).

It has also been suggested (Ribble et al. 1987) that 'acorn calves' and CJLD syndrome (congenital joint laxity and dwarfism in beef calves) are part of the same disorder. CJLD has been seen frequently in Canada and there are many papers coedited by Ribble on the topic. In one paper he reports it as a "congenital joint laxity and dwarfism-a feed associated congenital anomaly of beef calves". He describes it as a 'distinctive and recurring congenital anomaly in beef calves associated with feeding clover or grass silage without supplementation to pregnant cows over the winter'. Although the etiologic (sic) can not be determined, the disease can definitely be induced experimentally by restricting nutritional intake of the dam, supplementary feeding during pregnancy eliminates the problem.

Thus both problems have been induced in controlled feeding experiments causing a nutritional deficiency between 3 and 6 months of gestation.

One of the problems associated with recording and reporting this condition is the wide range of abnormalities seen in affected calves. The syndrome is characterised by dwarfism and marked congenital deformities of the limbs. Generally there is marked chondrodystrophy leading to proportionally widened joints and twisting and shortening of the limbs. Both arthrogryposis and joint laxity may or may not be seen. Deformities of the spinal column can be seen, kyphosis, lordosis and scoliosis have been reported (Glastonbury). Often there is a domed head and an abnormal shortening of the maxilla resulting in an overshot jaw. Occasionally almost the entire range of deformities can be seen on the same property.

Other causes of congenital deformities such as inherited syndromes, teratogenic plants and treatments, and infectious causes have been analysed through the use of laboratory testing and questionnaires.((Cave and Jubb)(Glastonbury)). Investigation by Cave and Jubb found no mutagenic plants were reported on any of the affected properties and all serological results for Akabane virus, Aino virus, Pestivirus and bluetongue were negative. Immunoglobulin levels in calves were <200U /L. It should be noted that these style of deformities can be caused by anything that temporarily reduces foetal movement in utero (comment Ross McKenzie).

In Australia the condition seems to occur in poor range country and similarly is thought to be due to a maternal deficiency during the middle trimester of pregnancy. 'Acorn calves' were first reported in the literature in Australia by Barry and Murphy in 1964, occurring in the Albury region and the upper Murray. In 1991 another outbreak was recorded in properties from the Wagga, Gundagai, Murray and Young RLPBs (Glastonbury). It was reported that 179 affected calves from 977 cows on over 20 properties were seen. Again in 1994 the condition was reported in Western Australia in cattle run or relatively poor non-irrigated pastures with partially improved pastures during a period of drought. No congenital deformities were reported on an adjoining property, where the cows were on an improved and fertilised pasture and their diet was supplemented with hay at a more generous rate. (Peet and Creeper).

In Southern Australia during a period of reasonably severe drought and dry summers in 2003, 2004 and possibly 2005 the 'acorn calf' syndrome has been seen through the South of NSW and in the Upper Murray of Victoria. The exact numbers and figures of this outbreak are being collated by Sarah Robson but it seems to be the largest outbreak to date. At least 620+ calves from 64+ properties were born over the spring calving in 2003-2004 with the acorn calf syndrome in the Hume, Gundagai and Cooma boards of NSW and the upper Murray of Victoria.

A generalised summary of reported observations from this outbreak are as follows. The condition has been seen in the spring calving cattle only. Dams of any age give birth to calves with the reported deformity but heifers may have a higher incidence. It was seen more often in cattle in poorer condition and those running in rough hilly country. The nutrition in the affected cattle had often not been carefully monitored but generally they were often reported to have had a "tough time". Immunoglobulin assays on those tested have been negative (<12lug /m1).

The New Zealanders in their report of the condition have taken it a possibly questionable step further. Valero et al. reporting it in 1990 as "Chondrodystrophy in calves associated with manganese deficiency". The congenital chondrodystrophy reported was very similar to the conditions that we have seen. A low level of manganese was found in the liver of the affected calf, and a link was thus drawn between cause and condition.

There is ample evidence to indicate that Manganese deficiency produces a number of striking effects in the experimental animal (Merton and Utter). Skeletal lesions related to manganese (Mn) deficiency have long been described in poultry, swine, Guinea pigs and cattle (Valero et al.).

The Mn requirement for growing and finishing cattle is approximately 20mg Mn/kg diet. Skeletal abnormalities were noted in calves where the pregnant cows were fed diets containing 15.8mg Mn/kg, but were not present when diets were supplemented to contain 25mg Mn/kg (Rojas et al. 1965). The concentration of manganese in forages varies greatly depending on plant species, stress on the plants, soil ph, and soil drainage (Minson 1990). Dietary manganese is poorly absorbed by cattle, with only 1-4% of the dietary content (irrespective of the magnitude) taken up and transferred by the erythrocytes (Hurley and Keen, 1987). In addition, absorption is inhibited by many factors, including presence of high levels of cobalt and iron, and high levels of calcium and phosphorus.

In summary at least 620+ calves from 64+ properties were born over the spring calving in 2003-2004 with the acorn calf syndrome in the Hume, Gundagai and Cooma boards of NSW and the upper Murray of Victoria. General evidence suggests that the condition has been brought on by nutritional stress from the 3rd to the 6th month of gestation. The specific underlying etiologic of the condition still eludes us with the most popular theory being that it is linked to a Mn deficiency. Vitamin A deficiency is also a distinct possibility. With the financial impact of this latest outbreak fresh in our minds it is an issue that needs to receive attention and research dollars so that recommendations can be made to avoid the recurrence of such widespread outbreaks of this condition in the future.

References

  1. Australian Soil Fertility manual CSIRO 2000 Editor J.S. Glendinning p65
  2. Barry MR and Murphy WJB (1964) Acorn calves in the Albury district of New South Wales Aust. Vet. J. vol. 40, p195
  3. Blood and Radostits 9th edition "Acorn Calves", "Congenital joint laxity and dwarfism in beef calves" pp 1810-1811, manganese deficiency pp1513-1514
  4. Cave JG and Jubb T (unpublished 2004) Calf deformities in the Upper Murray of Victoria
  5. Godwin J, Philbey A, Glastonbury J, Searson J, Links I (1992) Bovine Congenital Chondrodystrophy Annual Conference Proceedings, Australian Society for Veterinary Pathology, Adelaide, May 1992 p22
  6. Hart G, Guilbert H, Wagnon KA and Goss H (1947) "Acorn Calves" A non hereditary congenital deformity due to maternal nutritional deficiency calif Agric Exp st Bull, No 699, p1
  7. Hurley LS, Keen CL, Manganese Trace elements in human and animal nutrition. 1987 5th Ed Mertz W (editor) academic press, USA
  8. Nutrient requirements of Beef cattle, p65
  9. Maas J Oak toxicity, California Cattleman January 2001
  10. Merton F Utter, Phd (1976) The Biochemistry of Manganese symposium on Trace Elements Medical clinics of north America, Vol 60, No.4, july 1976 p713-
  11. Peet RL and Creeper J (1994) Congenital joint laxity and dwarfism in calves Aust. Vet. J. 71:2
  12. Philbey AW, Godwin J, Glastonbury JRW and Morton AG, An epidemic of congenital dyschondroplasia in calves 2001, unpublished
  13. Ribble CS, Janzen ED and Proulx JG (1989) Congenital joint laxity and dwarfism: A feed-associated congenital anomaly of beef calves in Canada. Canadian Veterinary Journal 30:331
  14. Rojas MA, Dyer IA, Cassatt WA (1965) Manganese deficiency in the bovine, Journal of Animal Science 24: 664-667
  15. Valero G, Alley MR, Bradcoe LM, Manktelow BE, Merrall M and Lawer GS (1990) Chondrodystrophy in calves associated with manganese deficiency, New Zealand Veterinary Journal 1990 38:161-7

 

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