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This article was published in 2005
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ACORN CALVES OUTBREAK INVESTIGATION IN SOUTHEAST NSW AND NORTH EAST VICTORIA IN 2003 AND 2004
Luzia Rast, District Veterinarian, Gundagai RLPB
Background
In 2003 and 2004 outbreaks of acorn calves were reported in the Gundagai, Cooma and Hume RLPB districts and in northern Victoria. No prevalence survey was conducted, however collation of data from these districts estimated that there were 50 to 70 affected properties. On affected properties 1-50% of calves were affected. Prevalence in some individual mobs reached >75%. Cases occurred mostly in spring (July to October) born calves. Seven affected calves born in autumn (March to June) were reported in the Gundagai RLPB.
A case-control study was attempted early in 2005 in the Gundagai RLPB. The aim was to collect data from affected and non-affected farms through a questionnaire to establish if certain risk factors could be identified that were apparently associated with the condition. As a first step, questionnaires were mailed to 80 randomly selected properties (20 per Board division) with no known reports of acorn calves. A 30% response rate was achieved and of the responses 50% reported to have had acorn calves in 2003 and/or 2004. The plan was to apply the same questionnaire to the 18 known affected farms in the Gundagai RLPB district. Because of the unexpected high number of case reports in what we thought were unaffected farms and the poor quality of data obtained through the questionnaires the study was not continued. However this preliminary result indicates a much higher prevalence than assumed.
There have been previous recordings of similar outbreaks of calf deformities termed 'acorn calves' in Australia in 1991 in the southwest slopes of NSW (Philbey et al. unpublished) and in 1957, 1958 and 1960 (Barry & Murphy, 1964). Similar syndromes have been reported overseas in New Zealand (Valero et al. 1990), in Canada (Ribbe et al. 1989), the United Kingdom (Davies, 2000; Gunn et al. 2000) and in the USA (Hart et al. 1947). The syndromes have been termed acorn calves, chondrodystrophy, congenital dyschondroplasia.
Hart et al. work put forward the hypothesis that dams of affected calves ingested acorns (quercus species) producing calves with typical chondropathy. It is from that work that the condition got to be known as 'acorn' calves. However the condition could not be reproduced by feeding acorns to pregnant cows. Another study produced acorn calves with pregnant cows fed on a low energy, low protein (<9%) and at least 20% acorns in diet (Personal communication VIN, 2004). Other work hypothesised infectious, toxic or mineral/vitamin deficiencies as cause but to date the etiology of remains uncertain.
Syndrome description
The affected calves during 2003 and 2004 showed shortened front limbs leading to an outward bowed appearance of the front legs (like bulldogs- hence some people refer to the condition also as 'Bulldog' calves).
Other traits of the condition were domed foreheads, shortened maxilla and spinal deviations. In affected herds the owners generally noted an increase in dystocia and stillborn calves. Because of the varied signs and severity of deformities a precise case definition was difficult if not impossible to establish. In my opinion some uncertainty remains that the various reports of acorn calves outbreaks in Australia and overseas were all the same condition.
Investigations/Methods
On farm investigations: Investigation initially occurred at random on some farms that reported cases. Necropsies were performed on 20-25 cases and samples submitted to regional veterinary laboratories during the 2003/2004 outbreaks.
Case- control study Gundagai RLPB: a questionnaire based around some hypothesizes risk factors was developed. Risk factors considered were soil type and ph, chemical treatments of pasture and stock , supplementary feed, plants accessible by stock, water source, climate, location and topography of farm/paddocks where dams of affected calves were kept during pregnancy. There were 18 confirmed affected farms in the Gundagai RLPB district. The aim was to complete a questionnaire for all affected farms and apply the same questionnaire to at least 2 to 3 times the number of control or unaffected farms. Twenty farms for which we had no reports of occurrence of acorn calves from each of the four Board divisions (80 farms total) were selected randomly from the Gundagai RLPB ratepayer database. A four page questionnaire and covering letter including photographs of affected calves was mailed to the 80 selected farms. 24 (30%) questionnaires were returned.
Results
On farm investigations: Post-mortem and histopathology revealed shortening of the long bones (mainly humerus but also radius) and growth plates with prematurely closed regions. If calves survived birth and got up this led to malposition of limbs and irregular wearing and severe erosion of joints.
Serology was negative for Akabane, Pestivirus, Bluetongue, Simbu group virus suggesting Immunoglobulin levels were low.
Manganese levels were measured in tissues of a limited number of affected calves in Victoria in 2004 and showed low levels.
In the 1991 outbreak samples from a similar number of cases were submitted to regional veterinary laboratories. No aetiology could be established from these investigations either (Philbey et al. 2001 unpublished).
Case control-study Gundagai RLPB: 24 from 80 questionnaires mailed out were returned.
Number of affected calves on 24 surveyed farms.
| Number of affected calves 2003 (%) | Number of affected calves 2004 (%) | Number of normal calves 2003 | Number of normal calves 2004 | ||||
|---|---|---|---|---|---|---|---|
| Spring | Autumn | Spring | Autumn | Spring | Autumn | Spring | Autumn |
| 21 (1.06) | 1 (0.19) | 86 (3.81) | 6 (1.21) | 1988 | 529 | 2255 | 494 |
Reported calving rates ranged from 36.21 — 100% m 2003 and 48.19 — 100% in 2004.
Soil types reported were sandy loam (4 cases; 4 non-cases), granite (1 case; 4 non-cases), and basalt (2 cases and 2 non cases).
90% of unaffected farms and 73% of affected farms provided supplementary feed to cattle at some time during pregnancy.
Stagnant water (dams or troughs) was the only water source on 10% of unaffected farms and on 37% of affected farms.
73% of unaffected and 82% of affected herds gave clostridial vaccine to cattle during pregnancy.
90% of affected farms and 55% of unaffected farms treated cattle with anthelminitcs during pregnancy (macrolytic lactones, triclabendazole).
60% of affected and 45% of unaffected farms ran their cattle on hilly country during pregnancy.
Several affected farms reported cases only in mobs that were kept on hilly country during pregnancy.
All farms had below average rainfall in 2003 and 2004.
Discussion and conclusion
Due to the poor response rate, the high percentage of reported cases in the assumed non-affected farms (see results) and the poor quality of data obtained through the questionnaires the study was not continued to date. Data obtained allows a limited descriptive analysis only.
The questionnaire design in hindsight was unclear to many respondents. For example the question 'how many normal calves did you have in spring 2004?' was answered in percentage by some and in numbers by others or not at all.
Half of the farmers who responded to the questionnaire sent out to farms from which we had no previous reports of acorn calves did report having cases in 2003 and/or 2004. This indicates that the condition was underreported and the true prevalence likely to me much higher than thought. Potential reasons for underreporting are speculative. Reasons may have been reluctance to report because of fear of potential regulatory measurers or unwillingness to report a presumed genetic disorder for fear of implicating owners as 'bad' cattle breeders.
While efforts were made to describe the condition accurately and provide photos with the questionnaire it may be that reported cases were more than one disease syndrome.
The major challenge with investigation of the acorn calves syndrome was the retrospective nature. There is still uncertainty about when exactly during the gestation period the insult leading to acorn calves occurred. Histopathology suggests that growth plates close prematurely and partially and it can therefore be assumed that the cause occurs in the first or second trimester of pregnancy. This means that by the time affected calves are born we are looking for risk factor that occurred at least 3 to 8 months earlier.
A prevalence survey would be needed to estimate the prevalence and its economic impact more precisely. Due to the varied severity of cases or potential different syndromes occurring at the same time and due to the retrospective nature face-to-face interviews for data collection are likely to provide more accurate data than if questionnaires were mailed out. Any further data collection using questionnaires will need very careful wording of the questions to make them less ambiguous. The questionnaire should also first be tested on some volunteers.
All previous reported outbreaks as well as the most recent one during 2003 and 2004 occurred during or following drought condition. Association of this syndrome with drought makes it likely that the cause is a factor related to nutrition. However these nutritional causes could include deficiencies or toxins due to either supplementary feeds (i.e. mycotoxins) or cattle ingesting unusual plants because of being hungry or plants that only grow during dry times. Available data does however not allow making any conclusions.
Negative serology and low inununoglobulin levels suggest that an infectious cause is unlikely unless the infectious challenge occurred very early during pregnancy. Above described results show higher rates of anthelmintic use and clostridial vaccination in affected herds during pregnancy, however not enough data is available to show any causal association.
The aetiology of acorn calves continues to be unresolved. The size of the most recent outbreak warrants further investigations. Appropriate resources will need to be allocated in any future efforts to identify the cause of this condition. This recent outbreak of acorn calves is a nice example of where regional coordination and approach to investigations may provide a more efficient use of resources and more powerful results.
Acknowledgment
Justin McKay designed the questionnaire and completed an initial literature search. Jeff Cave, DNRE Victoria, John Glastonbury, CSU Wagga, Joan Lloyd, MLA Sydney, Tony Morton, Wagga RLPB, Alex Stephen, Cooma RLPB, Steve Whittaker, Hume RLPB and Peter Windsor, University of Sydney all provided very useful data, advice and discussion. Peter Windsor provided histopathology as did the regional veterinary laboratories in Orange and Menangle.
References
- Barry M.R. & Murphy W.J.B., 1964, Acorn calves in the Albury district of New South Wales, Australian Veterinary Journal 40: 195-198
- Cave J.G. & Jubb T., 2003, Calf deformities in the upper Murray of Victoria, unpublished
- Philbey A.W., Godwin J., Glastonbury J.R.W. & Morton A.G. (2001) An epidemic of congenital dyschondroplasia in calves, unpublished
- Ribble C.S., Janzen ED. & Proulx J.G. (1989), Congenital joint laxity and dwarfism: a feed-associated congenital abnormality of beef calves in Canada, Canadian Veterinary Journal 30: 331-338
- Valero G., Alley M.R., Badcoe L.M., Manktelow B.W., Merrell M. & Lawes G.S. (1990), Chondrodystrophy in calves associated with manganese deficiency, New Zealand Veterinary Journal 38: 161-167
- Staley G.P., Lugt J.J., van der Axsel G. & Loock A.H. (1994) Congenital skeletal malformation in Holstein calves associated with putative manganese deficiency, Journal of the South African Veterinary Association 65:2 73-78
- www.vin.com accessed October 2004