D.C.Dalton: Published papers

(In alphabetical order)

BASS, J.J.; KIRTON, A.H.; DALTON, D.C. (1977)
Body composition of cull ewes from New Zealand hill country.
N.Z. Journal of Agricultural Research 20: 7-11.

BIGHAM, M L; ELLIOTT, K H; DALTON, D C (1977)
Wool production of sheep breeds on hill country.
Proceedings of the NZ Society of Animal Production, 37:218-219.

BIGHAM, M L; SUMNER, R H W; DALTON, D C (1977)
Seasonal wool production of Romney and Merino x Romney wethers.
NZ Journal of Experimental Agriculture, 5:257-260.

BIGHAM, M L; SUMNER, R H W; DALTON, D C (1978)
Wool production of different breeds of mixed-age ewes on hill country.
NZ Journal of Agricultural Research, 21:119-126.

BINNIE, D B; DALTON, D C (1980)
Using Sheeplan to buy a ram.
NZ Journal of Agriculture, 141(1):25-27.

BLOCKEY, M A deB; DALTON, D C (1968a)
Procedures in the AI of sheep.
NZ Journal of Agriculture, 117(6):70-71.

BLOCKEY, M A deB; DALTON, D C (1968b)
Artificial Insemination of sheep.
NZ Journal of Agriculture, 117(5):94-95.

BLOCKEY, M A deB; DALTON, D C (1969)
Genetic Aspects of AI in sheep.
NZ Journal of Agriculture, 118(1):77.

BOAZ, T.G.; DALTON, D.C. (1967)
Progeny testing for meat for sheep in Great Britain.
EAAP Association for Animal Production. Commission on sheep and goat production.
Oslo August 14-15. 1967.

DALTON, D.C. (1962)
Characters of economic importance in Welsh Mountain sheep.
Animal Production, 4 (2): 269-278.

DALTON, D.C. (1963)
Effect of dilution of the diet with an indigestible filler on feed intake in the mouse.
Nature, 197, (No 4870):March 2 1963, 909-910.

DALTON, D.C. (1965)
Dilution of the diet and feed intake in the mouse.
Nature, 205 (No 4973), 807.

DALTON, D.C. (1967)
Selection for growth in mice on two diets.
Animal Production, 9(4): 425-434.

DALTON, D C (1969)
Sheep breeding developments in New Zealand.
NZ Journal of Agriculture, 118(5):13-15.

DALTON, D C (1970)
Merino-Romney crossbreeding.
NZ Journal of Agriculture, 120(1):46-49.

DALTON, D.C.(1970)
The application of genetic principles in future farming.
Proceedings of the Hawke’s Bay Conference. 66-81.

DALTON, D.C. (1970)
Cattle breeding. I Genetics.
New Zealand Journal of Agriculture, 121(6); 22-37.

DALTON, D C (1971a)
Theory of group sheep breeding schemes.
NZ Meat Producer, 15(a):41.

DALTON, D C (1971b)
Sheep breed performance in New Zealand. Part I.
NZ Agricultural Science, 5(5):2-5.

DALTON, D C (1971c)
Sheep breed performance in New Zealand. Part II.
NZ Agricultural Science, 5(6):3-6.

DALTON, D.C. (1971)
Selection of Friesian bulls for growth.
N.Z. Agricultural Science, 6 (2); 6-8.

DALTON, D.C. (1972)
Performance testing and beef AB.
Proceedings Veterinary Services Council Course, October 27, 1972. 25-32.

DALTON, D.C. (1974)
New Zealand: cooperative livestock breeding schemes.
Span, 17 (2): 66-68.

DALTON, D C (1975a)
Sheeplan - what's it all about?
Meat and Wool, September.

DALTON, D C (1975b)
Sheeplan - Modified flock recording scheme for 1976.
NZ Journal of Agriculture, 131(1):7-8.

DALTON, D.C. (1976)
Animal breeding – first principles for farmers.
Aster Books. Editorial Services Ltd, Wellington NZ, 48pp.

DALTON, D.C. (1975?)
Approaches developed in New Zealand in the application of the objectives of genetic improvement of beef cattle and the methods and organisation used for this purpose.
Workshop on genetic improvement of beef cattle for Southern Australia. Hamilton, Australia

DALTON, D C (1976a)
Sheeplan and the Carpetmaster's future.
Proceedings of the Carpetmaster Conference, Ruakura Agricultural Research Centre, July 1976.

DALTON, D C (1976b)
Sheeplan - National flock recording scheme.
Meat and Wool, April.

DALTON, D.C. (1976)
An analysis of Angus central bull performance tests in New Zealand.
Proceedings of the NZ Society of Animal Production, 36: 210-5.

DALTON, D C (1978)
A sheep recording scheme in New Zealand.
Span, 21(3):119.

DALTON, D.C. (1979)
Beef cattle improvement Seminar. Performance and progeny testing.
Animal Breeding Research Organisation, Edinburgh, July 19, 1979.

DALTON, D C (1980a)
Lamb deaths - look the other way.
NZ Journal of Agriculture, 141(1):13-16.

DALTON, D C (1980b)
Sources of perinatal mortality.
Proceedings of the Lincoln College Farmers' Conference 109-123.

DALTON, D.C. (1980c)
The New Zealand Charolais.
Paper to the World Charolais Convention, Christchurch, New Zealand, March19-22, 1980.

DALTON, D.C. (1980d)
An introduction to practical animal breeding.
Granada Publishing. 162pp.

DALTON, D.C. (1980-81e)
Applying genetics to sheep breeding.
Wool, 7 (2): 23-28.

DALTON, D C (1981a)
How best to select commercial flock replacements.
Proceedings of the Gore Sheepfarmers' Conference, 79-86.

DALTON, D C (1981b)
Hogget lambing: how to make it worthwhile.
NZ Journal of Agriculture, 143(2):3-4.

DALTON, D C (1981c)
Big profits from hogget fleece weighing: here's how.
NZ Journal of Agriculture, 143(3):5-7.

DALTON, D.C. (1982)
Agricultural glossary.
NZ Ministry of Agriculture and Fisheries. 80pp.

DALTON, D.C. (1970)
Scientists get their teeth into teeth.
N.Z. Journal of Agriculture, 114 (2) 2-4.

DALTON, D.C. (1974)
New Zealand: Cooperative livestock breeding schemes.
Span, 17(2); 66-68.

DALTON, D C (1982a)
Performance recording.
Sheep Production. Vol 1. Breeding and Production. Ed. G A Wickham & M F McDonald, NZ Institute of Agricultural Science, 199-210.

DALTON, D C (1982b)
Scientists get their teeth into teeth.
NZ Journal of Agriculture, 144(2):2-3.

DALTON, D C (1983)
Well, lets get into it.
NZ Journal of Agriculture, 147(1):14.

DALTON, D.C. (1984)
Improving the Limousin for New Zealand.
Paper to the 6th World Limousin Conference, Rotorua, New Zealand, November 3, 1984.

DALTON, D.C. (1985)
Crossbreeding in sheep and beef – principles and methods.
Lincoln College Canterbury Animal Industries Workshop. 105-113.

DALTON, D.C. (1986)
Early lamb at not extra cost.
N.Z. Farmer, June 12, 1986. 17-18.

DALTON, D.C. (1986)
Interest in Angora rabbits as fibre producer.
N.Z. Farmer, 107 (17); 56-57.

DALTON, D.C. (1986)
Cattle yards – a small layout.
N.Z. Farmer, 107 (12): 23-24.

DALTON, D.C. (1988).
Promotion and marketing of Devon cattle.
Proceedings of the 1988 Bicentenary World Devon Conference, Sydney, Australia. March 23-26, 1988.

DALTON, D.C. (2000)
Devon cattle farmers – do you have a future?
World Devon Cattle Breeders’ Conference, Hamilton, New Zealand, 13 February, 2000.

DALTON, D.C.(1991)
New Zealand sheep breeds and their wool.
Ed. David Bateman. 32pp.

DALTON, D C; ACKERLEY, L R (1974)
Performance of sheep on New Zealand hill country. I. Growth and wool production of wethers of five breeds.
NZ Journal of Agricultural Research, 17:279-282.

DALTON, D C; ARMSTRONG, D (1981)
Looking after rams.
NZ Journal of Agriculture, 143(5):2-3.

DALTON, D.C.; BAKER, R.L. (1979)
Beef cattle improvement Seminar. Selection experiments with beef cattle and sheep.
Animal Breeding Research Organisation, Edinburgh, July 19, 1979.

DALTON, D C; BALL, S (1976)
Performance of Romney and crossbred sheep on east coast hill country.
NZ Journal of Experimental Agriculture, 4:35-40.

DALTON, D.C.:BYWATER, T.L. (1963).
The effect of selection for litter size and litter weight in mice maintained on two diets.
Animal Production, 5 (3): 317-326.

DALTON, D C; CALLOW, C F (1975)
Sheeplan progress report.
Sheepfarming Annual, 187-191.

DALTON, D C; CALLOW, C F (1976)
Why sheeplan is necessary.
Proceedings of the Ruakura Farmers' Conference, 13-17.

DALTON, D C; CLARKE, J N (1977)
Some sheep breeding topics: Progeny testing, Crossbreeding and Sheeplan.
Proceedings of the Coopworth Sheep Society of NZ, 34.

DALTON, D.C.; DAVIS, W.P. (1967).
A note on feeding trials with mice.
Journal of the institute of animal technicians, 18 (3): 131-133.

DALTON, D.C.; EVERITT, G.C. (1972).
Meat production from Friesian and Angus bulls.
Proceedings of the NZ Society of Animal Production, 32:11-18.

DALTON, D.C.; GIBSON, A.E. (1974?)
Breeding high-performance Angus cattle – a Lands and Survey Project.
Proceedings of the Massey Sheep and Beef Conference. 7-19.

DALTON, D.C.: HALL, D.R.H. (1978).
Exotic x Friesian beef cow performance. Final report of first trial.
NZ Journal of Agriculture, 136 (1). 8-11.

DALTON, D C; HIGHT, G K (1972)
Breeding better livestock for hill country.
Proceedings of the Ruakura Farmers' Conference, 62-74.

DALTON, D C; KILGOUR, R (1977)
Droving hill-country sheep.
NZ Journal of Agriculture, 135(1):13-14.

DALTON, D C; KIRTON, A H (1973)
Sheep meat from hill country.
Meat and Wool, November 1973.

DALTON, D.C.; MORRIS, C.A. (1978)
A review of central performance testing of beef bulls and of recent research in New Zealand.
Livestock Production Science, 5: 147-157.

DALTON, D C; RAE, A L (1978)
The New Zealand Romney sheep: a review of productive performance.
Animal Breeding Abstracts, 46:657-680.

DALTON, D.C.; STIRLING, J. (1977)
Bad feet in bulls.
N.Z.Journal of Agriculture, 134(2); 13-15.

DALTON, D C; SUMNER, R M W (1972)
Merino-Romney crossbreeding - the MR report.
NZ Journal of Agriculture, 124(6):51-53.

DALTON, D.C. (1980)
Applying genetics to sheep breeding.
Wool, 7 (2): 23-28.

DALTON, D.C.; LANG, D.R. (1994)
Landcorp group breeding- a challege to be grasped.
In Lab Coats to Gumboots. NZ Society of Animal Production. 1-11.

DALTON,D,C; RUMBLE, C. (1985)
50 years of artificial insemination and herd improvement in New Zealand.
Pub. Livestock Improvement, Hamilton, NZ. 65pp.

DALTON, D C; BIGHAM, M L; ELLIOTT, K H (1977)
Black spots in sheep.
NZ Journal of Agriculture, 134(5):26-27.

DALTON, D C; BIGHAM, M L; SUMNER, R M W (1976)
A comparison between the Romney and Merino x Romney on hill country.
NZ Journal of Experimental Agriculture, 4:27-33.

DALTON, D C; BIGHAM, M L; SUMNER, R M W (1980)
Applying genetics to sheep breeding in the 1980's.
Wool, 7(2):23.

DALTON, D C; BIGHAM, M L; WIGGINS, L K (1973)
Specialist carpet wool sheep.
Proceedings of the Ruakura Farmers' Conference, 21-33.

DALTON, D C; CALLOW, C F; ULJEE, A E (1984)
Recording systems and their use for coloured sheep.
Proceedings of the Second World Conference of Coloured Sheep, Ed H T Blair, 203-211.

DALTON, D.C.; GILBERD, D.J.; ALISON, A.W. (1980).
The Red Devon in New Zealand.
World Devon Convention, United Kingdom, May 19, 1980.

DALTON, D C; JOHNSON, D L; CALLOW, C F (1982)
Sheeplan's breeding values: what are they?
NZ Journal of Agriculture, 144(2):25-26.

DALTON, D.C; JURY, K.E.; HALL, D.R.H. (1975).
Growth rate and oestrous behaviour of Friesian, Hereford x Friesian, Simmental x Friesian and Angus heifers.
Proceedings of the NZ Society of Animal Production, 35: 129-136.

DALTON, D C; KNIGHT, T W; JOHNSON, D L (1980)
Lamb survival in sheep breeds on New Zealand Hill Country.
NZ Journal of Agricultural Research, 23:167-173.

DALTON, D.C.: PEARSON, M.E.: SHEARD, M. (1967)
The behaviour of dairy bulls kept in groups.
Animal Production, 9 (1):1-5.

DALTON, D.C; RAE, A.L; CLARKE, J.N. (1970).
A review of genetic parameters, performance and progeny testing and genetic aspects of artificial insemination of beef cattle in New Zealand.
NZ Beef Production, Processing and Marketing. NZ Institute of Agricultural Science, Wellington 1970. 141-153.

DALTON, D C; CLARKE, J N; RATTRAY, P V; JOYCE, J P; KELLY, R W (1978)
Romneys, Coopworths and Perendales: A breed comparison.
Proceedings of the Ruakura Farmers' Conference, FPP 13.

DOBBIE, J B; DALTON, D C (1972)
Missing sheep - a multi-million dollar loss.
NZ Journal of Agriculture, 124(2):19-20.

ELLIOTT, K H; BIGHAM, M L; SUMNER, R M W; DALTON, D C (1978)
Wool production of yearling ewes of different breeds on hill country.
NZ Journal of Agricultural Research, 21:179-186.

ELLIS, M.; DALTON, D.C. (1995)
NZ Dairying. Let’s get the basics right.
The Dairyman – NZ Rural Press publication. 64pp.

ELLIS, M.; DALTON, D.C. (1996)
NZ Dairying. Increase production – lower costs.
The Dairyman – NZ Rural Press publication. 64pp.

ELLIS, M.; DALTON, D.C. (1997)
NZ Dairying. The best practices.
The Dairyman – NZ Rural Press publication. 48pp.

EVERITT, G.C.; JURY, K.E.; DALTON, D.C.; WARD, J.D.B. (1978a)
Beef production from the dairy herd. I. Calving records from Friesian cows mated to Friesian and beef breed bulls.
N.Z. Journal of Agricultural Research, 21: 197-208.

EVERITT, G.C.; JURY, K.E.; DALTON, D.C.; WARD, J.D.B. (1978b)
Beef production from the dairy herd. II.Growth rates of straight-bred and beef-cross Friesian steers and heifers up to 4 months of age in several environments.
N.Z. Journal of Agricultural Research, 21: 209-14.

EVERITT, G.C.; JURY, K.E.; DALTON, D.C.; HALL, D.R.H. (1980)
Beef production from the dairy herd. III. Growth and reproduction of straight-bred and beef-cross Friesian heifers.
N.Z. Journal of Agricultural Research, 23: 1-10.

EVERITT, G.C.; JURY, K.E.; DALTON, D.C.:LANGRIDGE, M. (1980).
Beef production from the dairy herd. IV. Growth and carcass composition of straight-bred and beef-cross Friesian steers in several environments.
N.Z. Journal of Agricultural Research, 23: 11-20.

JURY, K.E.; EVERITT, G.C.; DALTON, D.C. (1980).
V. Growth of steers and heifers in different environments to 600 days of age.
N.Z. Journal of Agricultural Research, 23; 21-25.

GIBSON, A.E. : DALTON, D.C. (1973)
Beef breeding programme: Lands and Survey Department, Rotorua.
Massey Sheepfarming Annual: 9-19.

HIGHT, G K; DALTON, D C (1974a)
Existing sheep breeds in New Zealand and the way to exploit their potential.
Proceedings of the Lincoln College Farmers' Conference, 42-53.

HIGHT, G K; DALTON, D C (1974b)
The role of integrated breeding groups in the sheep and cattle industries.
Sheepfarming Annual, 128-135.

HIGHT, G K; DALTON, D C; LANG, D R (1970)
Large scale integrated sheep and beef cattle.
Proceedings of the Ruakura Farmers' Conference Week, 38-54.

HUGHES, I.R.; PETERS, G.P.; DALTON, D.C. (1978).
Wool and leather production from 150month wethers of different breeds on hill country.
N.Z. Journal of Agricultural Research, 21: 383-388.

KILGOUR, R.; DALTON, D.C. (1984)
Livestock behaviour – a practical guide.
Methuen, New Zealand. 320 pp.

KIRTON, A H; DALTON, D C; ACKERLEY, L R (1974)
Performance of sheep on New Zealand hill country II. Growth and composition of wethers of five breeds at three ages.
NZ Journal of Agricultural Research, 17:283-293.

KIRTON, A H; DALTON, D C; ACKERLEY, L R; WOODS, E G (1982)
Performance of sheep on New Zealand hill country III. Growth and composition of wethers born in three further years and slaughtered at three ages.
NZ Journal of Agricultural Research, 25:1-13.

KIRTON, A.H.; DALTON, D.C.; WINN, G.; DUGANZICH,D.M. (1985).
Body composition of cull Romney, Dorset x Romney, and Cheviot ewes from New Zealand hill country.
N.Z. Journal of Agricultural Research, 28: 241-247.

KNIGHT, T W; DALTON, D C; HIGHT, G K (1979)
Identification of barren ewes by vasectomised rams.
NZ Journal of Experimental Agriculture, 7:125-130.

KNIGHT, T W; DALTON, D C; HIGHT, G K (1980)
Changes in the median lambing dates and lambing pattern with variation in time of joining and breed of teasers.
NZ Journal of Agricultural Research, 23:281-285.

LANG, D.R.; DALTON, D.C.; HIGHT, G.K. (1970).
Artificial breeding in beef cattle.
Proceedings Ruakura Farmers’ Conference, 1970. 68-77.

LANG, D.R.; FERGUSON, A.B.; DALTON, D.C. (1980)
Ova transfers and frozen embryos.
Proceedings of the world conference on sheep and beef cattle. October 1980.

PASSMAN, A; DALTON, D C (1982)
Influence of Romney, Coopworth and Perendale breeds on lambskin leather quality.
NZ Journal of Experimental Agriculture, 10:7-13.

SORRENSON, W.J.; DALTON, D.C.; HALL, D.R.H.; SCOTT, M.E. (1981)
Profitability of different breeds of sheep on New Zealand hill country.
Research paper 8/81, October 1981. NZ Ministry of Agriculture and Fisheries, Research Section, Economics Division, Wellington NZ.

STEPHENSON, S K; DALTON, D C; KIRTON, A H (1980)
The relationships of growth, body shape and body composition to the initiation of oestrus activity in different sheep breeds.
Proceedings of the NZ Society of Animal Production, 40:258-267.

WHATELEY, J; KILGOUR, R; DALTON, D C (1974)
Behaviour of hill country sheep breeds during farming routines.
Proceedings of the NZ Society of Animal Production, 34:28-36.

D.C.Dalton: Published books

Clayton, D. (1988) with contributions from Dalton, D, C. & Jones, V.
Low cost dairying – the basics
N.Z. Gallagher Group of Companies.
ISBN: 0473006243 (pbk.)

Dalton, D. C. (1976)
Animal breeding : first principles for farmers.
Aster Books

Dalton, D. C. (1980)
An introduction to practical animal breeding.
Granada
ISBN: 0246111941 (hbk.) 0246113510 (pbk.)
Editio2nd ed. ISBN: 000383025X

Dalton, D.C. (1985)
An introduction to practical animal breeding.
2nd Edition
Collins
ISBN: 000383025X

Dalton, D. C. (1991)
New Zealand sheep and their wool.
David Bateman
ISBN:1869530659
Revised 2006. ISBN 13:978-1-86953-663-3

Dalton, D. C. Rumble, C. (1985)
50 years of artificial insemination and herd improvement in New Zealand.
N.Z. : Auckland Livestock Improvement Association,
ISBN: 0473002949

Dalton, D. C. (1986)
Angora rabbits.
MAF Promotions, Ministry of Agriculture & Fisheries
ISBN: 0477030572

Dalton, D.C. (2007)
Internal parasites of sheep and their control – now and in the future.
Reward Publishing
ISBN: 978-0-473-12133-3

Dalton, D.C.: Orr, M.B. (2004)
Sheep farming guide – for small and not-so-small flocks.
Hazard Press
ISBN: 1-877270-72-5

Kilgour. R; Dalton, D.C. (1984)
Livestock behaviour: a practical guide.
Methuen
ISBN: 0456031901

Cattle farm husbandry - some common diseases

Cattle, farming, husbandry, diseases, cause, signs, treatment, prevention

By Dr Clive Dalton

Internal parasites Cause

• There are many species of “worms” that live inside the animal’s gastrointestinal tract (stomach and intestines) of cattle and cause serious economic loss. The main ones are “round” worms but there are also others that inhabit the liver (liver flukes) and the lungs (lungworm).
• Their general life cycle is for the mature parasites to live and mate inside the animal, and then pass eggs out on to the pasture. Here they hatch into larvae and move up the grass leaves in a moisture film and are ingested by animals again.
• Most species of worm are host specific, i.e. cattle worm species will not infect sheep or goats and vice versa. This is not the case with sheep and goats that share worm species.
• Spring and autumn are the times when worm larvae “rise” rapidly on pastures.
  

Signs
There is a range of signs and cattle may show some or all of them.

• General unthrift and looking tucked up and lethargic. They are said to look “wormy”.
• Poor performance – nil liveweight gain and big weight loss.
• Diarrhoea (scouring) instead of well-formed dung.
• Mucous from the gut lining seen in the faeces.
• Pot belly and low body condition (skinny).
• Anaemia leading to death.
• A “pokey jaw” – skin pouch hanging down from lower jaw (liver fluke).
• Wheezing with persistent dry cough, especially after activity (lungworm).
  

Treatment and prevention

• It’s now very important to consult your veterinarian for a correct diagnosis of any worm problem and an appropriate drenching programme to avoid drench resistance developing or getting worse.
• The three drench families have ugly names! They are the white drenches (benzimidazoles or BZs), clear drenches (levamisoles), and third generation drenches (macrocyclic lactones, MLs or mectins). Then there are combination drenches made up from the three families. But beware as all clear drenches are not clear and all white ones are not white!
• Then there is the choice of an oral drench, pouron that is absorbed through the skin (both cattle and human so take precautions), injectable and long-acting capsule or bolus. There are also endectocides that kill internal and external parasites at the same time.
• This potential confusion is why you must take veterinary advice to get the right product. In May 2005 there were 45 products on the market from 10 companies with 18 different concentrations and dose rates from 0.5mg/kg to 15mg/kg live weight. Withholding periods varied from 0-49 days for meat and 0-35 days for milk. Safety margins varied from 3 to 30x the correct dose rate.
• The continual use of long-acting drenches is now accepted as one of the worst options and will create drench resistant worms very quickly.
• Faecal egg counts (FECs) are used widely in sheep to indicate parasite load so talk to your vet about their use in cattle where they have been used as widely.
• Always check that drench guns are delivering the correct dose.
• Drench to the heaviest animal in the mob so all animals receive an adequate dose of chemical. If there is a wide variation in size, draft them into two groups of similar size and drench accordingly.
• If resistance has not yet developed – and you know this for sure, use combination drenches to further delay its onset.
• Don’t bother to starve animals for a period before drenching. This has been shown to cause other problems.
• If possible, rotationally graze pastures with different species of stock that are not affected by the worms from the other species. This will help break the cycle.
• Allow as long an interval as possible between grazings to allow sun and frost to dehydrate and kill larvae. But remember that certain larvae can live in the ground for periods in excess of 12 months.
• Graze the re-growth of hay or silage paddocks, or new pasture or forage crops to reduce exposure of vulnerable stock to parasites.
• Drain swampy areas that may harbour snails that are the intermediate hosts for liver fluke.
• Often it’s not worms that are the primary problem but stress caused by hunger and lactation. This will affect the animal’s immune system so keep stock in good body condition and well fed.
• Double check the withholding periods of any products used as these vary with brand and manufacturer.
  

Drench resistance

• Drench resistance is an increasing problem on cattle farms but thankfully nothing near what it is on sheep farms. Resistance is where a drench correctly used fails to remove a worm burden from a host. Too many farmers are not aware of the drench resistance status of their farms. They need to find out quickly.
• Currently the complete picture of worm resistance in cattle in New Zealand is not fully known. But we do know it’s getting worse with 80% of cattle farms resistant to endectocides and 60% resistant to white drench.
• Terminology is important and potentially confusing. We now talk about “resilience” and “resistance” animals and the difference is important. A resilient animal has a high worm burden but it does not affect performance. The problem is that they continue to contaminate pasture.
• Resistance has two meanings – you can have resistant animals with genetic resistance to worms (sometimes called host resistance), and resistant worms that are not killed by drenches.
• Genetic resistance to drench in worms occurs when some of the worms on the pasture and in the animal have developed survived a particular chemical family used in the drench. The result is that they have a “reproductive advantage” and drenching with that particular drench will no longer be effective.
  
• Veterinarians or farm advisers will advise on how to test for drench effectiveness where appropriate by doing faecal egg counts (FECs) before and after drenching.
• If drenching was not effective in reducing FECs to zero, and the drenching technique was not faulty, then you can conclude that drench resistance is probably the problem.
• Resistance is usually defined when there is less than 95% decrease in FEC after drenching.
• Once internal parasites have become resistant to the three main drench chemical families now being used, there are currently no others to use.
• Note that changing the brand or method of delivery (e.g. from oral drench to pouron) may not mean a change in the drench chemical family. So check the label to see what the active ingredient is.
• The latest advice is to leave about 5-10% of the heaviest healthy animals in a group undrenched. They are obviously not affected by the parasites and will be a reservoir of worms that have not yet developed a resistance. When their non-resistant worms breed with resistant worms, the offspring will be less resistant and hence killed by the drench. This concept is called “refugia”.

Natural or organic methods or worm control

• Where chemicals are not allowed, organic farmers have to resort to other methods including grazing “safe” clean pasture.
• Garlic and cider vinegar are recommended to help suppress the egg-laying of worms, and may even remove a few worms, but they cannot be relied on as a consistent means of worm control.
  

Quarantine drenching

• There is a risk that cattle arriving on or returning to your farm could introduce worms that are resistant to some drench families.
  
• To prevent this, all cattle coming onto the farm should be given a “quarantine drench” – usually a combination double or triple drench. Check with your veterinarian for the latest recommendations.
• The cattle should then be held in a “quarantine paddock”, i.e. a separate holding area for 7-10 days (with adequate feed and water) before being released on to the farm.
• The quarantine paddock can be grazed by sheep or horses as well as newly-introduced and newly-drenched cattle.
  

External parasites Cause

• These parasites live on the skin (also called ectoparasites). The main ones are lice but there are also mange mites and ticks.

Signs

• Lice are very host-specific and spend virtually all their life on the animal.
• Heavy infestations occur mainly in winter in young in unthrifty cattle that are poorly fed.
  
• Signs of lice are rubbing, licking the coat and loss of hair often on the brisket and neck. Eggs may be seen attached to the hair shafts.
• If you handle stock you’ll feel them on your skin and not appreciate their bites.
• With mange mites you will see hair loss, itchiness, pimples or red or scaly areas of the skin.
• Ticks are found in the warmer northern parts of New Zealand and are most easily seen when they are engorged with blood before dropping off into the pasture.
  

Treatment and prevention

• Check with your veterinarian for the correct treatment. The most convenient form of treatment is a pouron.
• Veterinarians are now very aware that external parasites are developing a resistance to chemicals like internal parasites so care is needed in deciding on a programme.

Calf scours Cause

Calf with scours and swollen joints

• Calf scours are caused either by faulty nutrition or by disease organisms (bacteria, viruses and protozoa).
• Nutritional scours are most often due to problems with milk powders or excess liquid intake by gorging calves.
  
• The disease organisms involved are.
• Irritants can also cause scouring.
  

Signs

• Any calf that stops eating and stands looking “sad” should be suspected of oncoming scours. (A healthy calf should look “cheeky”).
• Scouring calves become dull and listless with droopy ears and will not feed.
• Fever is also an early sign of approaching scours.
• Diarrhoea – faeces are soft, watery and even blood stained.
• The calf will be soiled with faeces around and below the anus down to the back legs.
  
• Eventually, loss of nutrients and fluid into the intestine, and persistent severe diarrhoea causes dehydration and the calf may die after a few days.

Treatment and prevention

• Correct diagnosis of the cause of the scour is vital – so consult your veterinarian.
• Do this without delay as sick calves are poor patients.
• Treat affected calves immediately with electrolytes to prevent further dehydration and cut out milk if they will still drink it.
• Keep sick calves warm and on a dry bed and away from draughts.
• Antibiotics are the key to treating bacterial infections but they do NOT cure virus infections.
• Cows can be vaccinated against scours caused by E coli and salmonella to boost the immunity that calves get via colostrum.
• Ensure that all calves have been fed colostrum – a minimum of 2 litres before 6 hours.
• Good hygiene in the calf rearing shed is very important.
• With virus infections (e.g. rotavirus), the shed should be cleaned out and disinfected but this is not always effective. Continual spraying of the bedding tends to make it damp and it has to be replaced more often. This dampness is bad for calf health, especially in cold weather.
• It may also be wise to vaccinate the cows against rotavirus for next season. Consult your veterinarian.
• To prevent coccidiosis, make sure the calf meal used contains a coccicidiostat. But again be aware of the possibility of resistance building up to these chemicals over time too. So only use them if you are sure coccidiosis is a risk factor on the farm.
• When put out to grass, try to find a clean pasture that has not been grazed by calves the previous season. This is hard if not impossible to find on most farms.
  

Emergency electrolyte

• Proprietary electrolytes are best but if you have a sick calf and have nothing else to give it, then don’t delay treatment and try the following as a last resort:
• A quarter of a teaspoon of common salt.
• One tablespoon of baking soda.
• Four tablespoons of glucose or dextrose.
• Make up approximately 2 litres and feed the calf twice-a-day so it will get 4-6 litres of the mix/day. Continue the treatment for 2 days.
  

Mastitis Cause

• Mastitis is a bacterial infection of the udder and many different bacteria are involved. In New Zealand Streptococcus and Staphylococcus groups are the main ones.

Signs

• The udder will have hard swollen quarters, there will usually be clots or blood in the milk which may smell foul.
• The cow will be in pain so she will kick when you touch her udder and teats.
• An individual udder quarter may be red and hot, or in advanced stages darkened and cold (gangrenous or dead).
• Mastitis can occur at any time but it’s most common during lactation, soon after calving or at drying off.
• It sometimes develops before calving and even in heifers that have not milked.
  
• It is most common in older cows but it can occur at any age.
• In severe cases the cow may be dull, off her food, have an elevated temperature, be dehydrated and unwilling to move. In acute cases she may die.
  
• Some badly infected quarters are destroyed by the black mastitis infection and may slough off over a period of about 6 weeks.
• From a Somatic Cell Count (SCC) of a milk sample, a veterinarian can assess the degree of infection in the udder. A high SCC may indicate a sub clinical (hidden) infection that can then develop into a clinical one.
  

Treatment and prevention

• Seek veterinary help to find the cause of the infection so the correct antibiotic can be used. The vet may need to test the milk for this.
• Before inserting a tube of antibiotic up a teat canal, remove as much milk as possible and make sure the animal is well restrained to avoid being kicked.
• Read the label on the antibiotic tube and follow the instructions fully. The print is miniscule so keep the leaflet in the package if you get one or double check with the vet.
• Take special care to use the full treatment and note the approved “withholding period” for the milk or meat during which it may not be sent to market.
• After handling an infected teat, avoid touching other teats and wash, disinfect and dry your hands carefully. The drying part of this routine is most important and use disposable towels.
• Keep a record of your actions, dates, quarters infected and drugs used. Your veterinarian will find this useful in later consultancies.
• It is illegal not to treat a cow with mastitis and it is certainly illegal to put a rubber ring on her teat to remove it in bad cases of the disease.
  

Clostridial diseases Cause

• These are caused by a range of Clostridium bacteria that cause diseases such as pulpy kidney, enterotoxaemia, gas gangrene, black leg, black disease, tetanus, and malignant odema.
• These bacteria live in the animal’s gut and it’s when conditions change that they multiply rapidly and produce toxins that damage the animal and kill it.
  

Signs

• Animals are found dead and blow up in a very short time.

Treatment and prevention

• Discuss a vaccination programme with your veterinarian.
• There is now a 5-in-1 and a 10-in-1 vaccine to cover these diseases. Your vet will advise which is the most suitable one and its correct use.
  

Metabolic diseases

• These diseases listed in Table 24 occur in late pregnancy and early lactation when cows are under great “metabolic stress” hence the name.
• The foetus is growing fast in late pregnancy and after birth, cows have to produce a lot of milk.
• If feeding is interrupted or its quality changes, e.g. by bad weather or by yarding, cows can easily be tipped into metabolic imbalance.
  
• In all these diseases the cow will probably be down on the ground and unwilling to get up.
• Remember she may also be down because of paralysis from calving – and the stress of being down may trigger metabolic diseases.
  

Grass staggers (hypomagnesaemia) Cause

• Low magnesium status is common in dairy and beef cows in late winter and spring when magnesium concentrations in pasture are low and potassium concentrations are high.
• Feed shortage, cold weather and stress may make things worse.
  

Signs

Cow down with staggers

• Very fat beef breeding cows that hit a feed shortage are at risk, as are thin cows in the first few weeks of lactation.
• Early signs can be subtle, with slight changes in behaviour that can easily be overlooked or misinterpreted.
• Cows with clinical disease stagger, walk with stiff limbs, and are nervous and even aggressive which may progress to fits and death after 1-2 hours.
  
• Lying on the ground and paddling with head back are very characteristic signs.
  

Treatment and prevention

• If you are fairly sure the cow has hypomagnesaemia, give it an urgent injection of magnesium – now available in sachets with needle attached.
• Injections are best given subcutaneously.
• Magnesium sulphate should not be given quickly intravenously as you can kill the cow.
  
• It’s a good idea to treat the cow for milk fever at the same time, as there may be concurrent hypocalcaemia.
• Magnesium reserves in the cow need to be built up over winter, so get your veterinarian to check blood or liver concentrations in the autumn if there is a history of the disease.
• Magnesium oxide powder or calcined magnesite can then be fed on hay, silage or dusted on pasture. Wear a face mask when dusting pasture to prevent breathing it in.
• Dusted pasture may not be very palatable and if the powder is applied too liberally the stock may go hungry to avoid it. This can precipitate ketosis.
• Provide shelter for calving cows in bad weather.
• Don’t let beef cows get too fat and keep them active. Keep them on bare pasture so they have to work hard and walk for their feed.
  

Milk fever (hypocalcaemia) Cause

• Milk fever is caused by low calcium concentrations in the blood as a result of increased demand for calcium during lactation.
• Calcium deficiency occurs most often in high-producing older cows (5 to 9 years old) within 72 hours of calving. But it can occur several weeks before or after calving and may affect more than 5% of cows in the herd.
  
• Sometimes cases occur after a change of feed especially on to green cereal crops.
• The stress of transport can also trigger it in non-lactating cows (transport tetany).
• Cows affected by facial eczema the previous season and have liver damage are prone to milk fever at calving.
  

Signs

• Early signs include restlessness, muscle tremors, reduced appetite with a preference for roughage, a drop in milk production and staggering.
• Dullness, low body temperature, no urination or defaecation, reluctance to move or “drunken” behaviour, walking in circles aimlessly with vigorous licking, great anxiety and trembling.
• A mild form of the disease in dairy cows is a drop in milk production and infertility problems. This has recently been called the “sad cow syndrome”.
• The disease may be brought on within 24 hours of a sudden stress such as mustering and yarding, transport, forced exercise, very bad weather or insufficient feed.
  

Treatment and Prevention

• Recumbent cows should be propped up with hay bales to to get them off their sides to prevent bloat.
• Treat them urgently with an injection of calcium such as calcium borogluconate. Check with your vet to make sure you have the correct product as many of these metabolic treatments are in similar packs.
• Inject it subcutaneously.
• Feed a high plane of nutrition in late pregnancy and early lactation, and high calcium or phosphorus in the diet in late pregnancy.
• Feeding acid or anionic salts in the weeks before calving can help prevent the disease, as can vitamin D by injection a week before calving.
  

Ketosis (Acetonaemia) Cause

• Ketosis occurs when cows are subjected to heavy demands on their glucose and glycogen reserves.
  
• It most often occurs from 10 days to 6 weeks after calving in early lactation when energy output exceeds energy input.
  
• In poorly-fed herds, 10% of cows or more may develop clinical ketosis each year. The disease is most common in cows that are over 4 years of age.
  

Signs

• Signs include loss of appetite, loss of body condition, ruminal atony (rumination stops) and either unusual dullness or unusual excitability and aimless wandering.
  
• Cows may stagger, grind their teeth, show compulsive licking, head pressing, circling, staggering and may seem blind. Coma and death can follow in 2 to 7 days.
• Only about 50% of people can smell the ketones on the cow’s breath and urine – it’s a human genetic problem. Ketones smell like nail varnish remover.
• Blood ketones rise before signs develop, so blood tests can be used by a veterinarian to predict problems.
  

Treatment and prevention

• Provide energy supplements (check with your vet) some with electrolytes that can be given by mouth.
  
• Intravenous glucose and glucocorticoid injections can be given by a veterinarian, and they can be helpful if given very early in the course of the disease.
• Avoid excessive fatness and checks in nutrition during late pregnancy and early lactation.
  
• Checks can be caused by interruption of feeding by yarding or inadequate shelter in bad weather.
• Provide a rising plane of nutrition during late pregnancy and early lactation.
  

Downer cows
In the interests of precision veterinarians talk about “a down cow” which can be raised with assistance, and “a downer cow” which cannot. To a farmer both these types of cows are called downer cows. Then timing comes into the definition where a good rule is that if a cow doesn’t make an attempt to get up after 5 minutes, then veterinary advice is recommended. If a cow cannot rise after 4 hours, then she is in serious trouble.

Cause

• A cow may be down because of metabolic disease, or nerve damage and paralysis from a difficult calving – or both.
• Sometimes uterus infections (metritis) can contribute.
• The stress of being down can then trigger metabolic diseases.
• Veterinarians can now do a blood test that will predict the cow’s chances of recovery.
  

Treatment

• First try to determine why the cow is down.
• Get a veterinary diagnosis as early as possible regarding the cow’s prospects.
• She must be provided with protection from wind and rain. Light thermal blankets are now available for such cows.
• Treat the cow with calcium or magnesium as an insurance, and if she’s had a difficult calving – consult your veterinarian.
• If paralysis is the diagnosis then the cow will need careful nursing.
• If she’s been down for a while, her body weight crushes her muscles and she may not be able to get back on her feet unaided, especially if she is heavily pregnant or very thin or weak after calving.
• Hip clamps should not be used to get the cow up if there is a possibility of pelvic damage as a result of calving. So a veterinary diagnosis of the cow’s prospects is essential before using hip clamps.
• If hip clamps are used, they should be used with padding and not so tightly applied that they cause damage to the hips, skin or pelvis.
• The hip clamps must be removed if the cow makes no weight bearing after 5 minutes.
• Slings under the abdomen can be used for longer periods of time attempt to help the cow recover. You may need to use the hip clamps to lift the cow to get the sling under her.
• Make sure the cow in a sling can breathe freely and not suffer any unnecessary discomfort.
• A cow must not be suspended in a sling for more than one hour at a time.
• The longer the cow is down, the lower are her chances of recovery.
• See the Dairy Cow code of welfare for advice on using lifting equipment for downer cows.
  

Abortions Cause

• There are many causes of abortions, and often the cause is difficult to diagnose from lab tests.
• Causes include bacterial diseases such as leptospirosis and BVD, then fungi in silage and bad hay, eating macrocarpa leaves or a tiny parasite called neospora.
• Abortions can occur at any time during pregnancy but very early aborted foetuses are usually never noticed.
  

Signs

• You may see an aborted foetus in the paddock with a small afterbirth.
• The mother will rarely show any interest in it so it’s usually difficult to find her.
• The aborted cow may appear unwell and have blood on her vulva or tail.
  

Treatment and prevention

• If possible, collect the aborted foetus and contact your vet for a lab test to investigate the cause. The overall diagnostic success rate is around 40% but can reach 60% from good samples. You should expect more than 50% diagnostic success.
• This is important if there are multiple cases to prevent or minimise an outbreak, as early treatment of sick cows can save their lives.
• If there is only a single abortion, spread the cows out to reduce the risk of any infection spreading from it, and pick up and bury any aborted foetuses and membranes.
• Vaccinate your stock against leptospirosis.
• Never feed mouldy silage, balage or hay to pregnant cattle.
• Provide good shelter and good feed to minimise stress that can precipitate more abortions.
• Prevent dogs from eating afterbirths or aborted calves, and keep pastures clear of dog faeces. This is the neospora link where the dog is an intermediary host. It has also been shown to be spread in muscle so don’t feed dogs raw beef either.
• Trim and remove macrocarpa branches around paddocks. Cows are most likely to eat them if they are hungry or bored – and if the branches have been cut off and are wilted.
  

Prolapse Cause

• Prolapse happens when the vagina and sometimes the uterus is everted (i.e. pushed inside-out to protrude from the vulva) and the prolapse can swell to a large size. It can be a terrifying sight!
• Prolapse in cows often occurs after a difficult birth (dystocia) after a lot of straining. Hypocalcaemia may be involved in some cases too.
• The mass of tissue becomes congested with blood and it is easily damaged and infected. Unless it is cleaned and replaced quickly the cow usually dies.
  

Treatment and prevention

• Call a veterinarian urgently as the prolapse will have to be cleaned and put back inside the cow. The prolapse is large and replacement is a job for an expert.
• The veterinarian may require assistance so have help available if possible.
• The cow will need careful nursing in case the prolapse comes out again.
• Consider the cow as a future cull as this problem is often repeated.
  

Bloat Cause

• Bloat is caused by a build-up of gas or stable foam in the rumen. Carbon dioxide and methane are products of rumen fermentation and normally escape by belching.
• The chemicals in clover are regularly blamed as the main culprit but allowing hungry stock to graze lush pasture is the main threat.
• Chicory is also blamed as causing bloat but again management is more likely to blame.
• Bloat can also be caused by a gullet blocked by a potato, kiwi fruit or piece of turnip where the beast chokes.
  

Signs

Beast with bloat - still able to walk. Next stage is to go down and die!

• Bloat is most common in spring when grass and clovers are growing rapidly, as these feeds contain natural foaming agents that generate stable foam in the rumen.
  
• The bloated rumen sticks out from the abdomen on the left flank area behind the rib-cage in front of the hip where there is normally a depression.
  
• Only individual animals in the herd may be affected and they may be regular bloaters for some frustrating reason.
• The cow will stop eating and become restless; she may bellow or moan, try to defaecate or urinate repeatedly and regurgitate boluses of herbage.
  
• Her breathing will become rapid and more laboured, maybe with the mouth open and tongue protruding. She may groan and grind her teeth because of the pain and discomfort.
• If she gets worse she’ll become staggery, mucous membranes in the mouth, nose and eyes will become pale blue. She’ll go down, develop convulsions and die of asphyxiation (suffocation) and heart failure.
• Sometimes a cow may die in 30 minutes.
  

Treatment and prevention

• If seen early, take the cow off pasture and give her proprietary anti-bloat or anti-foaming agents by mouth. These break down the foam in the rumen.
  
• In an emergency, 100 ml of vegetable oil, or 250 ml cream, or 1 Litre of milk may help.
  
• A little gentle exercise may help break down the foam and make the animal start to belch.
• When the bloat is severe and the cow distressed, call the veterinarian right away. The vet may need to make an incision into the cow’s rumen from the outside to release the pressure caused by the gas and foam.
• If the cow is very distressed and gasping with head extended and tongue protruding, and a veterinarian is not available, you may have to resort to an emergency rumen puncture with a knife. This is not for the faint-hearted and should only be a last resort.
  
• The stabbing spot is not always easy to find on a bloated cow. Locate the hip bone on the LEFT SIDE of the cow. When you stand beside the cow its head should be on your left. This is also called the “near side” of the cow as opposed to the “far” side. It’s the side you mount a horse!
• Press hard on the cow to locate the hip bone and then measure one hand width in front of it pointing down towards the cow’s front feet.
• Stab the cow here to make a short incision. Be warned - the gas may explode outwards and you may need to scoop the excess stable foam out by hand.
  
• Use a knife with a good hand grip and fore guard as when the knife hits the skin, it may stop and your hand may keep going down the blade. Don’t smoke as methane burns with a nice blue flame and removes eyebrows and hair!
• You can also stab the cow with a “trochar and canula” where the dagger is inside a plastic tube. When you pull the dagger out you leave the tube in. Check with your vet clinic on its availability and correct use.
  
• Oils like liquid paraffin or antifoaming agents like pluronics should be added to the rumen contents, after the operation to prevent the rumen contents spilling into the body cavity. The site should then be cleansed and sutured like a standard operation site. Call the veterinarian the same day to sew the cow up again and do not leave it to heal naturally as it won’t.
• To prevent bloat, avoid offering cows lush clover-dominant pasture when they are hungry, as they may gorge themselves. Offer them hay first.
• Anti-foaming agents can be sprayed on to risky pasture before it is grazed but this is never a very practical option.
• Milking cows can be drenched twice daily at milking with proprietary anti-bloat substances that contain pluronics, detergents or alcohols.
• Some antibloat treatments can be given in the drinking water, but this may be insufficient in wet weather when the cows may not drink as much.
• A combination of drinking water medication plus once-daily drenching may be a practical approach. It’s not an option for most beef stock.
• Cows can be dosed with long-acting (controlled-release) antibloat capsules, and these have the advantage of lasting for 100 days or more and are ideal for beef cows that cause problems.
• Anti-bloat blocks and licks are also available.
  

Grain overload Cause

• Occurs when hungry cattle suddenly over-eat carbohydrate-rich food such as root crops, grain, bread or potatoes.
  
• The rumen pH drops dramatically because of excess lactic acid production by rumen microorganisms. The result is acidosis and dehydration that can be fatal.
  

Signs

• Signs are loss of appetite, and swelling of the rumen seen as abdominal swelling, dullness, diarrhoea, dehydration, staggering, recumbency and death within a few days.
  
• Sometimes affected animals seem to recover then go down again a few weeks later with fungal infections in the rumen.
  

Treatment and prevention

• Give the animal sodium bicarbonate by mouth to help neutralise the acid in the rumen and call the veterinarian if the animal is distressed.
• To prevent the problem, introduce carbohydrate-rich food into the diet very gradually over a period of at least a week or two, as it takes time for the digestive system of herbage-eating animals to adapt to significant amounts of any new food.
• When starting to feed grain or concentrates, offer it at about 50 gm/head/day for each of the first 10 days. Then increase it gradually over 1-3 weeks until all animals are eating their full ration.
  
• Oats are probably less likely to cause problems than wheat or barley which require a longer conditioning period.
  
• Stock should not be hungry before any new feed is offered; otherwise they are more likely to gorge. Feeding hay first can help prevent this.
• Concentrate feed can be sprinkled on hay or silage, or spread out in long lines on the ground, allowing ample room for all animals to feed and acquire a liking for the new food. The shy animals should then have plenty of space to eat.
  
• Try to make sure all animals get about the same amount. Grain should always be fed with roughage such as pasture, stubble, hay or straw, and not as the sole diet.
  

Foot problems Cause

• Foot problems are mainly bruising, abscesses or footrot and result from physical damage to the foot or bacterial infections of the damaged areas.
• There are bacterial infections of areas where the underside of the foot has been injured, or wet muddy conditions where mud or grit has been trapped between the toes leading to an infection.
  

Signs

• Cows become lame and are clearly in great pain and may even refuse to walk, or they walk trying to avoid putting weight on their sore foot.
• Cows will go off their feed and milk production will drop.
  

Treatment and prevention

• Don’t let the cow suffer hoping that she will recover on her own – she rarely does.
• Seek veterinary help to diagnose the problem and which claw on which foot is affected. This is sometimes not easy.
• The foot may need to be trimmed to aid diagnosis and hasten effective treatment and cure. This can be a dangerous job if you don’t know how to do it, and don’t have good facilities to restrain a beast.
• Intramuscular antibiotic injections will probably be needed to treat the infection and the foot may have to be protected during treatment.
• On dairy farms races need to be well maintained (surface, width and camber).
• Stock need to moved at their own pace and not be hurried by impatient staff on bikes or biting dogs.
• Lame cows can be separated off into a separate mob for regular treatment where they are not expected to walk far.
• It is very difficult to cure infections that have spread into a joint in the foot.
  

Facial eczema (FE) Cause

• FE is caused by toxins produced by rapidly-growing spores of a fungus called Pythomyces chartarum. It grows on the dead litter in mid to late summer and autumn pastures (January to April) when grass minimum temperatures are above 12°C for two-three nights and humidity is high.
• The toxin damages the liver and bile ducts so it cannot rid the body of wastes and a breakdown product of chlorophyll builds up in the body causing sensitivity to sunlight (photosensitisation), especially on non-pigmented areas.
  

Signs

A heifer at the saleyards showing clincal sunburn from FE.
She's stressed and without doubt will have liver damge.
She shouldn't be at the sale and should be out of the sun.

• FE occurs mainly in the North Island of New Zealand but can occur in the parts of the South Island, e.g. Canterbury under irrigation and the West Coast.
• First signs are usually reddening and swelling or thickening of skin exposed to the sun, i.e. the skin around the eyes, ears, nose, on the udder, vulva and under white hair along the back. Any areas of white skin on the body are first to show up with eczema.
• Signs will occur about 3 weeks after a large ingestion of spores, e.g. 100,000 spores/g of pasture.
• But a series of small spore rises or around 20,000/g of pasture can be dangerous too as their combined effect sensitises the animal.
• The skin eventually sloughs off and the raw skin below can become infected.
• Affected cattle are restless, shake and rub their head and ears. Their eyelids don’t swell and close like sheep.
• They can be quite frantic to lick the bits where skin has sloughed off, especially in the rain. It seems the wetting increases the itching.
• They are also desperate to find some shade and get out of the direct sun.
  
• Cattle with severe liver damage appear jaundiced, seen in a yellowish tinge to the whites of their eyes. Milk production drops markedly.
• Some liver repair happens but future performance is most likely to be affected – e.g. at the next calving.
  

Treatment and prevention

• Provide some shade for affected stock. If there is no natural shade, allow them access to a barn and provide feed or let them graze at night.
• Remove them from the “hot” pasture to allow the skin and liver to recover.
  
• Provide good high-energy feed – not high protein pasture which puts strain on their damaged livers.
• Give affected stock an oral dose of zinc oxide. Check with your vet as too much can be toxic.
• Jaundiced stock should be offered a diet of hay and water for a few days before gradually introducing high-quality nutritious feed to help the liver recover.
• Apply opaque protective cream to damaged skin to hasten healing and screen the skin from sunlight.
• Put a cover on a badly scarred cow if no shade is available.
• A veterinarian may give antibiotic injections if severe skin infections occur, and also vitamin B12 injections to boost appetite. It has very little benefit.
  
• Jaundiced cattle will not be accepted by meat companies or if slaughtered their carcasses will be condemned.
• Check the area spore counts regularly through your vet clinic, local newspapers or websites.
• Pastures can be toxic once spore counts reach over 40,000 but damage can occur with low spore intake over a long period.
• Obtain the equipment (microscope and slide) to monitor spores on the pasture in your own paddocks or join with neighbours to share the information. Note there is great variation between paddocks, and areas within paddocks, so take plenty of samples.
• You can use the same equipment to measure spores in faeces which is easier to do and more meaningful as you know the animal has ingested these spores.
• By the time 5% of a herd have obvious clinical signs; up to 50% or more of the group will be liver-damaged.
• Regular drenching with zinc oxide or putting zinc sulphate in the water supply is effective if started well before spore counts rise. Never drench with zinc sulphate as it will damage the rumen. (Check with your vet clinic for dose rates).
• Cattle can be given a slow-release zinc bolus that stays in the rumen but it must be the correct size for the weight of the animal to avoid toxicity. (Check with your vet clinic).
• Zinc can be toxic so make sure you do not overdose and that only licensed products are used.
• Pastures can be sprayed with fungicides to make “safe areas” on the farm safe for periods of high spore counts. (Check with your vet clinic).
• Any animals that have been badly affected should be culled after they have recovered.
• Make sure you boost copper levels in all stock that have been on long-term zinc treatment as zinc strips copper reserves from the animal’s system.
  

Ryegrass staggers Cause

• Ryegrass staggers is a brain disease caused by the ingestion of a neurotoxin produced by a fungus in perennial ryegrass.
  
• The fungus is an “endophyte” meaning it grows within the living plant in the leaf sheath, at the base of the pasture and in the seed heads.
  

Signs

• It is common in summer and autumn throughout the North Island and as far south as North Otago.
• Affected cattle become anxious when approached and in mild cases there is slight trembling of the head and of the skin of the neck, shoulder and flank.
• More severe cases show head-nodding and jerky movements, swaying while standing and staggering during movement.
• In the most severe cases animals have a stiff-legged gait, short prancing steps, and may collapse with rigid spasms that last for up to several minutes.
• Affected cattle lose weight as they don't graze as much, and may not be able to drink enough water.
• They can become caught up in obstacles like electric fences and fall into holes and over bluffs. They can drown in creeks, dams, drains and swamps.
  

Treatment and prevention

• The disease is not fatal, but there is a real risk of injury or death as a result of accidents.
• Move stock from high-risk ryegrass pastures to safe pastures until they recover which may take several weeks. You may have to use trial and error to find out which pastures on the farm are less prone to the problem than others.
• It might be possible to put calves or dry cows into yards for a while and feed them hay or silage and plenty of clean water.
• Handle affected cattle quietly and disturb them as little as possible.
• Replace affected pastures with “endophyte-free” grasses. Check with your seed company about the best cultivars to use and any disadvantages they may have such as being prone to insect attack. .
  

Paspalum staggers Cause

• Paspalum staggers is caused by a toxin produced by the fungus Claviceps paspali, in the northern areas of New Zealand (particularly Northland, Auckland and Taranaki) during summer and autumn when stock have been grazing Paspalum grass.
  
• nThe disease resembles ryegrass staggers and the toxin is produced by an ergot-like fungus in the seed head on Paspalum (Paspalum dilatatum).
  

Signs

• Animals behave in a similar way to ryegrass staggers.

Treatment and prevention

• There is no effective treatment.
• Remove stock from pastures with a high Paspalum content and they will recover within 2 to 10 days.
• Handle stock with care as described for ryegrass staggers.
  

Trace element (mineral) deficiencies General

• There is a long list of minerals and trace elements that are involved in cattle health and it’s easy to get confused over what is needed and even panic.
• They are needed in only tiny amounts but are essential for good health.
• Healthy animals that are performing well are not likely to be deficient, but in some parts of New Zealand, soils and pastures are deficient in specific minerals and trace elements.
• Veterinarians and farm advisors can arrange the tests to determine the mineral status of soils, pastures and animals. This can be done by soil tests, then herbage tests and then blood tests from the stock that have eaten the pasture.
  

Selenium (Se)

• About 30% of New Zealand farmland is deficient in selenium.
  
• Se deficiency can cause ill-thrift, especially in young growing calves.
  

Signs

• These are congenital and delayed white muscle disease in calves, poor growth, and it has been associated with infertility (early embryonic loss) and retained membranes in cows.

Treatment and prevention

• Consult your veterinarian about a treatment programme.
• Serum tests, whole blood tests and liver tests can all be used to indicate the current selenium status of cattle.
• It’s convenient to test liver samples collected from stock sent to the meat works.
• The initial check should be made in winter because selenium deficiency is known to depress milk production, and may cause problems like retained placentas at calving.
  
• Tests should also be carried out on growing cattle in marginal or deficient areas.
  
• Selenium can be given as a drench, or administered as an injection (sometimes with clostridial vaccines) and this may be effective for 3 months.
  
• It can be administered as a long-acting ruminal capsule releasing selenium for up to 12 months (for cattle over 8 weeks old). Selenium prills can be top-dressed on to pasture.
  
• In areas of mild deficiency, a salt lick containing selenium may help, but the only way to ensure every animal gets an adequate dose in areas of significant selenium deficiency is through drenches, injections, intraruminal capsules or topdressing.
• Take care not to overdose with selenium as even 2-3 times the recommended dose can be toxic.
• Selenium should not be given by mouth if it has already been top-dressed on to the paddocks.
  

Copper

• Copper deficiency is more common in peaty soils and leached sandy soils.

Signs

• Deficiencies result in poor growth rates, changes in coat colour from black to brown and infertility. (Remember that ill-thrift and infertility may be due to other causes).
• Some other minerals in the diet, such as molybdenum, sulphur, iron and zinc, can inhibit the absorption of copper.
• Copper availability is often lowest during winter and spring because this is when molybdenum and iron concentrations are highest. Iron intake is often increased by soil eaten when pastures are muddy which then lowers copper.
• Copper requirements are highest during late pregnancy and early lactation, and growing stock also have a relatively high requirement for copper.
• Cattle grazing kale (Choumoellier) for more than 12 weeks may require copper supplements.
  

Treatment and prevention

• Consult your veterinarian about a treatment programme.
• Serum and liver samples can be tested for copper status. Liver samples are better than blood. Your vet can arrange for liver samples to be collected at the meat works from animals sent for slaughter.
• Copper salts can be added regularly to food or water supply as a supplement, or can be injected into the muscle. Check with your vet for the best system.
• Long-acting copper oxide bullets or capsules can be given by mouth, or copper salts can be top-dressed on to pasture.
  
• However, top-dressing may not raise the copper concentration high enough in forage when molybdenum concentrations are high.
  

Cobalt (vitamin B12)

• Cattle are not as susceptible as sheep but cobalt deficiencies can occur.
  
• Cobalt is needed for the micro-organisms in the rumen to synthesise Vitamin B12.
• The deficiency seems to increase as farming becomes more intensive.
  

Signs

• Cattle will be unthrifty, lose weight and show anaemia.
• Dairy cows will show depressed milk production.
  

Treatment and control

• Cobalt deficiency is most common on farms in the central plateau of the North Island, Southland and Coastal Otago.
• Your vet can take blood samples or liver biopsies to check levels.
• Arrange through your vet to take liver samples from cattle sent to the meat works.
• The best long-term prevention is the addition of cobalt sulphate to fertiliser.
• Injections of B12 can be given but they need to be repeated.
• There are also oral Cobalt drenches available.
  

Iodine

• Iodine deficiency can occur occasionally in calves in some areas.
  
• It’s often implicated in reduced oestrous activity in dairy cows.
  

Signs

• It can be induced by feeding brassicas and clovers, which contain goitrogens that block the uptake of iodine by the thyroid gland.
• One of the main signs of iodine deficiency is goitre, a swelling of the thyroid glands in the neck just below the throat of calves.
  

Treatment and prevention

• Consult your veterinarian before deciding on a treatment programme.
• Cows can be dosed with potassium iodide before calving.
• A long-acting iodine injection is also available.
  
• In lower-risk areas, providing iodised salt licks may be sufficient.
• A few ml of iodine is often put in water troughs for dairy cows – check with your vet.
  

Salmonellosis Cause

• Salmonellosis is caused by various Salmonella bacteria species and can occur in batches of calves or dairy cows.
• Stress predisposes stock to infection so overcrowding, transport and lack of feed can all trigger outbreaks.
  

Signs

• Pregnant cows that get salmonellosis are likely to abort.
  
• Signs include dullness, dehydration and often severe blood-stained diarrhoea. In cows there will first be a sudden drop in milk production.
  

Treatment and prevention

• Isolation and veterinary treatment are the first actions to help contain the outbreak and prevent deaths.
  
• Vaccines are available to prevent infections but it takes at least 10 days for immunity to develop.
• Salmonellosis can cause disease in humans so exercise good hygiene when working with affected cattle.
  

Pneumonia Cause

• Pneumonia is caused by various micro-organisms in the lungs.
• In individual animals, clumsy drenching hence squirting liquid into the lungs instead of correctly down the gullet can cause pneumonia and it’s usually fatal.
  

Signs

• Sudden breathing difficulties and death, sometimes with coughing.
  
• In more chronic forms of the disease, especially in calves, there may be few obvious signs apart from reduced thrift.
  

Treatment and prevention

• Consult a veterinarian to prescribe antibiotics.
• Handling stock in dusty yards in hot weather can bring it on.
  

Leptospirosis Cause

• Lepto is caused by bacteria and three main species are common in New Zealand, one being carried by pigs and another by rats.
  
• The disease can affect humans.
• The bacteria are carried in the kidneys and excreted and spread through urine.
• The clinical disease is seen in adult cattle and calves.
  

Signs

• Infected cows show no clinical signs of the disease other than abortions in late pregnancy. If they abort earlier you will never see the foetus.
• Infected calves will show red urine – called red water disease.
• Infected humans are very sick with flu-like symptoms and bouts of extreme tiredness which keep reoccurring.
  

Treatment and prevention

• Discuss a vaccination programme with your veterinarian. It needs to be put in your OSH farm safety programme and listed as a hazard to human health.
• Calves need to be vaccinated twice and adults have an annual booster vaccination.
• Avoid contact with cattle urine and exercise personal hygiene when working with cattle. Cover all cuts and abrasions.
• Kill all rats on the property and keep pigs away from cattle.
  

Johne’s disease Cause

• Johne’s disease (pronounced “yonees”) is a chronic bacterial disease that is widespread in NZ cattle herds.

Signs

• Loss of milk production, severe diarrhoea, very rapid wasting and death.
  
• It develops slowly and infected cattle may spread the disease through the herd before the disease is diagnosed.
• Very watery dark-coloured scour.
• Lack of feed and very bad weather seem to bring on the disease.
• It most commonly occurs in cattle from 3 to 5 years old, and it is more common in the North Island than in the South Island.
• Diagnosis is confirmed by blood and faecal tests arranged through a veterinarian.
  

Treatment and prevention

• There is no effective treatment but losses can be reduced by management methods and vaccination.
  
• Cull affected cattle from the herd as soon as possible.
• Try to avoid stress caused by too little feed and cold weather in winter.
• Newborn calves( after being fed colostrum) should be fed separately from adult cattle for the next 6-12 months as this is the period when they are most likely to become infected. This is very hard to do on most farms.
• Discuss a vaccination programme with your veterinarian.
  

Woody tongue Cause

• A bacterial infection of the tongue.

Signs

• The animal will not eat with any enthusiasm.
• It may be slobbering from the mouth.
• There are firm lumpy abscesses, usually on the tongue but sometimes elsewhere in the mouth area.
  

Treatment and prevention

• Early antibiotic treatment prescribed by a veterinarian is usually effective.
  
• Check your drenching technique to prevent damage to the mouth.
  

Ringworm Cause

• The cause is a fungus that lives under the skin surface.
• It can spread to humans.
  

Signs

• Ringworm mainly affects calves and yearlings, and they are more susceptible if they are in poor condition or kept in crowded unhygienic conditions.
• The lesions most often occur on the head and neck, and are usually round and spreading, with central hair loss and scaliness or thick crusty plaques, and they may be itchy.
• There are other conditions where bare patches and round scabby areas appear on a beast’s skin that are not ringworm so check with your veterinarian.
  

Treatment and prevention

• Use ointments and lotions (often containing iodine).
  
• In severe cases, oral fungicides or iodine medication may be prescribed by a veterinarian.
  
• Humans should exercise personal hygiene when handling affected stock.
  

Poisons Cause

• Cattle may be accidentally poisoned from plants, algae, and chemicals.

Signs

• The most common signs of poisoning include diarrhoea, regurgitation of rumen contents, unusual excitement, or dullness, body tremors, pain (teeth-grinding, reluctance to move, arched back) and convulsions.

Treatment and prevention

• If poisoning is suspected, a veterinarian should be consulted without delay.
• Garden prunings should not be thrown into the paddock. Many plants are poisonous to cattle and are often more palatable when wilted.
• Even lawn clippings can cause severe indigestion if cattle gorge on them.
• Rubbish dumps should be fenced off and native scrub checked for poisonous plants before allowing cattle access to it.

Some poisonous garden plants, shrubs and weeds

Rhododendron

• Blue lupin (a fungal toxin in lupins can cause lupinosis)
• Bracken (Pteridium esculentum)
• Devilwood (Ageratina adenophora & A. riparia)
• Foxglove (Digitalis purpurea)
• Goat’s rue (Galega officinalis)
• Hemlock (Conium maculatum)
• Jerusalem cherry (Solanum diflorum & S. pseudocapsicum)
• Laburnum
• Macrocarpa (Cupressus macrocarpa)
• Ngaio (myoporium laetum)
• Oak (acorns) (Quercus sp.)
• Oleander
• Orange cestrum (Cestrum aurantiacum)
• Ragwort (Senecio jacobaea)
• Rhododendron
• Rhubarb
• St John’s wort (Hypericum perforatum)
• Tutu (Coriaria arborea)
• Yew (Taxus baccata)
  

Poisons in pasture

• Some of the most serious diseases of cattle are caused by fungal toxins in pasture (see ryegrass staggers, facial eczema).
• Phalaris grasses can cause signs of brain disease (phalaris staggers).
• Some rapidly-growing pastures and crops, especially after nitrogen application contain toxic quantities of nitrate.
• Kikuyu grass found in Northland after 2-3 days of warm wet weather in late summer can be toxic and can cause disease in cattle.
  
• The signs are loss of appetite, depression, abdominal pain, constipation, salivation, thirst, dehydration, ataxia (staggering), tetany (rigours), recumbancy and death.
  

Algae

• Algal bloom in stagnant water (blue-green algae) can cause kidney damage, with incoordination and death.

Chemical poisons

• Cattle can be overdosed with zinc, copper or selenium.
• Superphosphate poisoning can occur when cattle are put on to top-dressed pasture before the fertiliser has been washed into the soil, especially when pasture is short.
• Basic slag – a byproduct from iron smelting has caused poisoning when applied and not washed into the soil.

Keep stock off pasture after spreading fertiliser until is has rained - if you can!

• 1080 poisoning has occurred in cattle when poisoned bait was accidentally dropped on to their pasture or when they gained access to land used for a poison drop.
• Overdosing with organophosphate insecticides or anthelmintics can cause toxicity.
• Calves can be poisoned from making feeders out of old chemical containers (e.g. bloat drums) and from licking old doors and sheds painted with old lead paint.
  

Nitrate poisoning Cause

• The disease is caused by high concentrations of nitrate in the diet.
• Nitrate itself is relatively non-toxic but rumen micro-organisms convert it to nitrite which is toxic.
  
• During dry periods, nitrates accumulate in and near the roots of plants and are taken up rapidly when growth occurs following rain or irrigation. Dull weather with few bright sunny days makes conditions worse.
• Poisoning can occur in brassicas such as rape, turnip tops (especially second growth) and also other crops like certain ryegrasses and immature green oats.
  
• You expect it in new pastures but it can even occur on old pastures which have been dressed with nitrogen fertiliser.
• t can occur where there are a lot of rapidly-growing weeds like red-root (Amaranthus sp.)
  

Signs

• Affected animals are often found trembling, weak, staggery, and characteristically their mucous membranes and blood are a brownish colour.
  
• They die very quickly so prompt veterinary attention is necessary.
  

Prevention

• Always be suspicious of grazing lush green crops or lush pasture, especially after a period of dull weather.
• Get a sample of feed checked through your vet clinic.
• Only graze at-risk high-nitrate feed for very short intervals (15-20 minutes) before moving stock on to other pasture, or feeding hay or silage from low-nitrogen crops.
• Or do the opposite – feed safe pasture or hay before grazing the high-nitrate crop.
• Review and reduce the amount of nitrogen fertiliser used if the problem is common on the farm.
  

Tuberculosis (Tb) Background

• Bovine Tb is not a common disease in New Zealand but is important as we have to reduce its incidence to very low levels to comply with overseas market requirements.
• However, bovine Tb also affects humans as well as farmed deer, pigs and birds (avian Tb). Sheep and goats are relatively resistant to Tb.
  
• The disease is harder to eliminate in New Zealand because it is also carried by possums, ferrets, stoats, weasels, feral pigs; even feral cats and rabbits are at times under suspicion as vectors.
• So whereas Tb in cattle and deer can be controlled by testing and culling, there is no way it can be eliminated once it gets into wildlife or feral animals.
  

Cause

• Tb in cattle is an infectious disease caused by the bacterium Mycobacterium bovis.
  
• It is a slowly progressive chronic debilitating disease but it can take a more rapid course.
  

Signs

• With regular testing of herds for Tb, early reactors to the Tb test would be culled out so you would not see any signs of the disease.
• Tb causes small abscesses (called tubercules) in the lungs or intestines and in lymph nodes that drain them, or in the throat.
  
• These are found by meat inspectors at licensed slaughter premises and by licensed home-kill butchers.
• Watch for sick possums with large cheesy round lumps in their armpits and groins. They are highly likely to have Tb so report them to MAF and do not handle them.
  

Treatment and Prevention

• Animals with Tb are not treated.
• Control is through the National Tb Control Scheme run by the Animal Health Board with money levied from farmers for testing or slaughter.
• It is compulsory for all cattle and deer farms on farms to be tested, so if you have cattle you must inform your nearest AgriQuality office (in the yellow pages) if they have not found you!
• There is also a compulsory ear tagging scheme for all cattle and deer, and strict regulations relating to the movement of stock.
• Any animal that reacts to a Tb test has to be slaughtered and your herd will be put under “movement control” until the infection has been sourced and cleaned up. This will greatly restrict your farming business and that of your neighbours.
• Make sure all stock are tagged correctly to comply with the regulations (see below).
  
• Cattle over one month old must be identified with a bar-coded primary tag and a secondary ear tag unless they are going direct to slaughter, in which case they only need a primary tag, or a “direct to slaughter” tag. Animals are exempt from ear tags if they have been moved from grazing and kept under your day-to-day management and not mixed with animals from other herds.
• Make sure all stock moved to and from your farm have the correct documentation – an “Animal Status Declaration (ASD)” form. Get copies from the NZFSA website (www.nzfsa.govt.nz) stock and station agents or meat companies.
• If you graze stock off the farm, check the Tb status of the farm they are going to by contacting AssureQuality.
  
• This is described using the letter C, e.g. C6 means a farm that has had clear Tb tests for six years.
• Wage a constant war against possums, ferrets, stoats and weasels, as well as feral cats and pigs. Get advice from DOC, your Regional or District Council or AgriQuality how to do this.
• For general information about Tb and the Tb control scheme, cattle farmers should phone 0800 4TB INFO (0800 482 4636).
  

Enzootic bovine leucosis (EBL)
This disease and BVD are not economically important in New Zealand but due to pressure from overseas markets, we have to prove that we are working on eradicating them. So you need to be aware of their names if nothing else.

Cause

• EBL is a slow spreading virus disease that affects the immune system by attacking white blood cells, and a small proportion of affected cows develop fatal blood cancer.
• It can be spread by any action that exposes healthy animals to blood or milk from infected cattle.
  

Signs

• Abortions.
• Leukaemia and solid tumours.
  

Treatment and prevention

• There is no treatment.
• Practice good hygiene when vaccinating, drenching and dehorning to avoid bleeding.
• Prevention is by blood and milk tests, and a dairy industry control scheme based on herd testing and culling of infected cows is planned to eradicate it by 2005.
  

Bovine viral diarrhoea (BVD) /Mucosal disease (MD) Cause

• BVD – a complex disease caused by one virus leading to two syndromes.
• BVD - Infection happens after birth. Animals recover.
• MD - foetus is infected by the dam in mid pregnancy.
• MD – animal is re-infected after birth from the dam.

Signs

• BVD - Shallow ulcers in the mouth. Mild infections.
• MD – fever, depressed, no appetite, profuse diarrhoea, high mortality
  

Prevention

• Live vaccines are available that need to be used with care so consult a veterinarian.

Cancer eye Signs

• Growths appear on the eye lids or eyeball.
• They are seen most often in breeds with white heads.
• The condition seems to be on the increase with greater sun radiation.
  

Treatment and prevention

• There is no cure and little you can do about prevention.
• Make sure the animal is seen by a veterinarian as soon as you see the problem.
• Do not leave the animal until it has finished milking or has weaned a calf before consulting your vet.
  
• Too many cattle are left until their growths are enormous on the assumption that they are not suffering. It is an offence not to treat cattle with cancer eye.
  

Disclaimer This material is provided in good faith for information purposes only, and the author does not accept any liability to any person for actions taken as a result of the information or advice (or the use of such information or advice) provided in these pages.

Cattle farm husbandry – body condition scoring

Cattle, farming, husbandry, body condition scoring, easy method to learn & use, implication of scoring errors, replacing body condition

By Dr Clive Dalton

What is Body Condition Scoring ( Condition Scoring)?

• Condition Scoring (CS) is when you assess a beast’s status by the amount of condition it is carrying. “Condition” means fat under the skin that you can see and feel, but fat reserves in and around internal organs such as kidneys that you cannot see are also part of the story.
  
• Condition scoring also includes muscle mass, because when the cow has used up all its fat reserves it will break down muscle tissue to provide energy to survive.
• From an animal’s condition you judge its state of current health and well-being and its ability to keep on producing.
• Weighing an animal tells you its overall body mass but not necessarily its condition. So you can have a heavy big-framed cow that is a walking skeleton, that weighs the same as a light-weight cow rolling in fat.
• So both weight and CS are needed to give the total picture. Scales will alert you to changes very quickly, whereas changes in condition score may be more difficult to pick up quickly, especially if you see your stock every day.
• Visiting friends never tell you what your stock are really like and never tell you when they are getting really skinny. If asked, it’s safest to score all animals at CS 4.5. This is the “non-confrontational” condition score that won’t upset anyone and you’ll be asked back.
• There are a few different methods to CS cows but they all use the same scale. This goes from 1 to 10, but a CS1 cow would be so thin it would be near death, and a CS 10 cow would be so fat it would be at death’s door through obesity or ready to explode! So a scale from 1 to 8 is enough.
• The same scale applies to both beef and dairy cattle, but you don’t see any dairy cows above CS 6.
• Don’t try to get more accurate than assessing half scores as the whole business is not an exact science. Indeed, if you can score accurately and honestly to single scores, that would be good enough for most management decisions.
  

What happens if you get it wrong?
If you unknowingly ‘underscore’ cows by being too generous with your scores – there are a number of consequences, some very serious. The following is what can happen, either singly or in combination:

• Cows are milked too long at the end of lactation when they should be dried off. This risks milk quality penalties from high Somatic Cell Counts.
• You won’t feed animals enough when their nutritional needs are critical. This is the with dairy cows coming up to calving when your error will only feed them maintenance, and they need much more. Cows should calve at the recommended CS 5 and heifers at CS 5.5.
• So immediately after calving, and during the weeks up and including peak lactation when there is maximum nutritional drain on the cow, her performance will be below expectations. The cow will not regain this lost production during the rest of the lactation resulting in large financial loss.
• It takes 180kg of Dry Matter to replace 1 Condition Score, on top of maintenance, and this can take at least 3 weeks to happen with good quality feed.
• This works out at feeding a thin cow when dry the same as if she was in full milk, so farmers regularly run out of time, and they run out of good quality pasture and supplements to achieve the result.
• Increasing CS from 3-4 increases production by an extra 17.5kg MS, from 3.5-4.5 will increase MS by 15kg MS, and increasing from 4-5 will produce an extra 12kg MS.
• Inevitably low CS cows cause more work for staff at calving as thin cows are more prone to problems.
• Low CS cows will have more metabolic diseases in late pregnancy, at calving and in early lactation. Production losses will occur and even deaths.
• Higher calf mortality and retained foetal membranes (RFM) are likely.
• Low CS cows are slow to return to heat, after calving and will be late calving next season with consequent loss of income.
• Research has shown that at CS 4 18% cows will be non-cyclers, whereas cows at CS5 only 9.7% will not have cycled.
• Maintaining an annual calving pattern will need resorting to inductions (abortions) to fix this, which means veterinary costs, has animal welfare implications and includes the loss of genetic potential from the calves which either die or must be culled.
• Thin cows calving late will need hormone treatment devices to start them off cycling, and this requires vet and drug charges.
• Thin cows which calve late, will most likely need more than one insemination to get pregnant and this will increase costs and waste good semen.
• You will need the added cost of obtaining a bull to mate these late cows when the AI period is over.
• Your farm budget will now have extra (unplanned) costs which bank managers don’t like.
• Cows under CS 3 are officially ‘emaciated’ and risk a prosecution under the Animal Welfare Act 1999. As a ‘boner’ cow killed for meat, their meat yield is too low for an economic return to the meat processor.
• Working with skinny cows is depressing for staff and can kill motivation. They will be looking for other jobs and changing staff can cost the farm business thousands of dollars.
  

An easy method to learn
The following method was developed by M. Ellis and C. Dalton at the Waikato Polytechnic around 1998. There was an urgent need to find a quick, easy and repeatable method to teach new farming recruits as the current system was too vague. Learning how to CS had been far too big a mystery up till then, and we found that most farmers and veterinarians were consistently half a score too generous, and there were many others who were even a whole score wrong.

The problem was that none of us had actually been taught how to condition score; we were supposed to have learned it from photos of dairy cows’ rear ends. And none of us when challenged dared admit we couldn’t do it. So we always fudged and dived for the safety of “around 4.5”. If you felt threatened then you’d say 4.4 and if you felt confident you’d say 4.6. It was all a big con job and in too many situations nothing has changed today.

There are only two steps to learning how to do condition score using the Waikato Polytech method:

Step 1.
Learn where 7 points are on a cow in a set order from 1 to 7. Think of them as bus stops on a journey and you have to decide where to get off. (See Figure below).

Diagram to show the points to locate and feel in the cow

Step 2.
At each stop decide if you are at the right one, and if not, whether you should go back or forwards. As CS 5 is the middle of the range, and you won’t see many dairy cows above this, it’s a great place to start and then most often go up for beef and down for dairy cows.

Scoring going down from CS 5
Stop 1 – the hip bone.
Press the palm of your hand on the hip bone and feel if it’s rounded or flat.

• A rounded hip that fills your cupped palm is CS 5 or above.

Rounded hip well covered must be CS5 or above Viewed looking to the rear of the cow

• A flat hip is below CS 5 so go down to the next stop.

Very flat top on the hip bone of a thin Holstein Friesian cow.
This cow must be below CS5.

Use the palm of your hand to feel how flat it is

Stop 2. The backbone
Press your outstretched fingers along the backbone and “jiggle” them to feel any gaps between the vertebrae.

• If there are no hollows – that’s CS 4.5
• If you feel definite hollows and bumps for the vertebrae – that’s below CS 4.5. Go down to the next stop.

Ph0to of "bumpy" backbone. This cow must be below CS 4.5

On a hairy cow 'Jiggle' you fingers along the backbone to feel for hollows

Stop 3 –The pin bone “dimples”
The pin bone has a flat top and a bone that goes down from it in the shape of a capital letter “T”. With your finger and thumb, pinch the dimples at either side of the stem of the T. This bone is sometimes called the “tap” as it’s shaped like the top of a water tap.

• If there are no dimples – that’s CS 4.
• If there are dimples – that’s below CS 4. Go down to the next stop.
  

Pin bones showing the hollows (dimples) either side of the ridge in the centre of the pin bone.
This cow has no muscle or fat there so she cannot be above CS 4.

On a hairy cow use your finger and thumb to 'pinch' the dimples

Stop 4 – The rear-end view from the side
Here check the cow's rear end where the last bit of the pin bone sticks out. Look to see if she is concave (hollow), straight, or convex (protrudes). Make sure you view a straight leg that she has weight on, and not one that she has moved forward.

• Straight down or convex – that’s CS 3.5.
• Hollow (convex) – that’s below CS 3.5. Go down to the next stop.
  

Photo shows the hollow (concave) rear end of the cow behind the pin bones. She is missing a mass of muscle due to underfeeding. A cow in good condition will be vertical or convex in this area. She cannot be above CS 3.5

On a hairy cow, use your hand to feel for the protruding pin bone

Stop 5 – The shoulder
Here check the shape of the shoulder ridge with your thumb one side and fingers the other.

• Make sure the cow has its head up.
• If you feel a definite ridge – that’s below CS 3. Go down to the next stop.
  

This photo shows a very prominant shoulder ridge on this very skinny cow.
She cannot be above CS 3.

This photo shows where your hand is placed on the high point of the shoulder, near the shoulder blades. Here you can see the thumb being pressed in to feel any protruding bones at the side (see below).

Stop 6 – The side of the shoulder
Here feel the small bones that stick out from the sides of the shoulder vertebrae. So with thumb on one side and fingers opposite, squeeze to see what you can feel.

• No prominent bones is CS 2.5.
• Prominent bones and where your fingers go right below the processes, is below CS 2. Go to the next stop.
• Look back at the photo above and you can see that if you pressed at the sides of that shoulder ridge, she's so thin that your fingers would go right in.
  

Stop 7 – The pelvic ridge (the ski jump)
This is the sharp ridge on the pelvis that stretches from the backbone to the hip bone. Run your fingers along the cow’s back and over this bone like a ski jump to see if the journey is smooth, or the bone sticks up and blocks the way.

• If there is no sharp ridge sticking up – that’s CS 1.5
• If the ridge is very prominent and almost sticking through the skin – that’s CS 1.
  

Note very protruding pelvic ridge ( the ski jump).
When you run your hand along this cow's back it won't ski over the ridge.
They'll hit it head on and stop.

Picture shows the action of your hand as you slide it towards the back
of the cow over the 'ski jump'. Long hair on a skinny cow can hide how sharp the bone is.

KEY POINT: As far as animal welfare is concerned, veterinarians now accept that CS 3 or below as “emaciated” as the beast will have severely depleted fat reserves and will also have lost considerable muscle mass. It will require immediate action to improve its condition and health as you could easily risk prosecution.

Scoring going up from CS 5
In terms of animals at risk, any beast above CS 5 will have no problems. Indeed. above CS 6 the concern will be with obesity and the effects it may have on health such as at calving, and animals being too fat for the meat works. Forget about half scores between scores above CS 5.

• CS 6 - Rounded across the loin and you cannot feel the ends of the short ribs.
• CS 7 – Flat across the loin and you have to press really hard on the backbone to feel it.
• CS 8- Big ugly folds of fat hanging around the tail head.
  

Forget about scoring above this and call them all obese.

An obese pet cow - she must be at least CS 10 and very happy cow!

Scoring in the paddock from a distance
You’ll be doing most condition scoring in the paddock a distance from the animal, but you’ll find the close-up “hands-on” knowledge above will give you the confidence to score accurately from a distance, now that you know what to look for.

The impact of getting condition score wrong
Getting condition scoring wrong can have serious implications for the stock and your income. If you’re a bit skeptical about the importance of cow condition, consider these issues below that will compound if you underscore animals and don’t realise you are doing it:

The farmer who has put these cows for sale as "boners" probably
doesn't realise they are CS 2.5 and are "emaciated".

• You won’t feed the animals enough – they’ll probably get only maintenance when they need feed to replace lost condition on top of their production needs.
• Their performance will be below your expectations, and you may not notice until you have to spend money to fix things.
• Cows will be more prone to metabolic diseases in late pregnancy and at calving.
• Cows will be slow to return to heat after calving and will be late calving next season.
• So if you want to maintain an annual calving you will have to resort to inductions (abortions) to fix this and accept the cost and welfare implications.
• You’ll have to spend money on intra-vaginal hormone treatment devices to start them off cycling.
• Cows will need more than one insemination to get pregnant which will cost more and waste good semen.
• Your farm budget will now have some surprises, and you’ll have to explain them to your bank manager - and bank managers don’t like surprises.
• You’ll be the farmer in the district with the skinny cows and everybody will be talking about them behind your back. They won’t tell you of course. They’ll phone MAF or the SPCA first.
• If you have staff they will probably (or they should) leave to go and work with some decent well-fed stock.
  

Feeding to replace condition
The general rule is that it takes 180 kg of DM to replace 1 CS, above what the animal needs to be fed for maintenance. It’s extremely important to realise this is extra to maintenance. This 180kg is a very general value, and can vary from say 150kg DM for a small cow, to 250kg for a large cow.

And remember the impact of the time limit there may be to put this condition back. Many farmers have great intentions to build their stock up in condition before calving, when the accepted rule is that cows calve at CS 5 and heifers at CS 5.5. But in practice they regularly run out of time and run out of feed so never make their targets. They permanently have skinny stock so think this is normal and everyone else’s cows are too fat and their stocking rate is too low!

Beef farmers who buy boner dairy cows (that are nearly always skinny) to put weight on them for the export trade comment make an interesting comment. They have noticed that these poor beasts need a month’s total rest before they start to put on any weight at all because they are physically exhausted from the stress of being in a big herd and constantly disturbed for grazing and milking. It’s maybe why cows seem to need a much longer period to build up condition than the nutrition tables say!