Showing posts with label sheep diseases. Show all posts
Showing posts with label sheep diseases. Show all posts

April 2, 2011

Facial eczema – NZ disease scourge for 100 years

By Dr Clive Dalton


Clinical cases of Facial Eczema showing typical lesions on ears
and around they eyes, and sometimes along the back.


Problem for 100 years
For over a century now, Facial eczema (FE) has caused massive animal suffering and economic loss to New Zealand flocks and herds, and every year it still takes its toll. It’s a fungal disease of the autumn, thriving in a combination of soils still warm from summer, dead pasture litter, and moisture from autumn rains and heavy dews.

Looking down a microscope, it’s hard to imagine how the tiny hand grenade shaped fungal spores can produce a toxin that can permanently damage an animal’s liver, leading to photosensitivity, great suffering and often death. When cases get really bad the animal has to be euthanased. Stock sent for meat processing end up being condemned, as their flesh is jaundiced and has an unacceptable 'off' smell.

The Fusarium fungus (Pythomyces chartarum) which produces the spores, is common in many other countries such as Australia, South America and South Africa, but for some unknown reason does not produce the ‘sporidesmin’ toxin. The toxin is most dangerous from young rapidly-growing spores like the ones in the picture below.

Spores of the fungus Pithomyces chartarum

Finding the cause

Facial eczema has been known in New Zealand since the importation of modern grasses in the 1870s, and it was certainly reported by J.A Gilruth in the Department of Agriculture's Annual Report in 1897.

Finding the cause and working out prevention measures took 40 years of solid research, (including many setbacks) by scientists at the New Zealand government’s, Ministry of Agriculture and Fisheries, Ruakura Animal Research station, working in close cooperation with local farmers desperate to find a solution, many of whom regularly lost more than half of their sheep flocks in bad years. It took them years to get over one bad FE year.

Farmer demands
In fact, it was farmer action led by a Waikato farmer, Mr F.C. (Togo) Johnstone in 1939, strongly supported by Waikato Federated Farmers, that got Ruakura under P S Smallfield to take a serious look at the problem. A long hard road of research was started and got a major boost in 1943 when Dr C.P. McMeekan was recruited from Massey College (later University) to develop the Ruakura Animal Research Station.

McMeekan recruited a team (many from overseas), to find the cause and then provide a prevention to the scourge causing massive economic losses on farms in the warmer northern parts of the North Island of New Zealand.

Today, with the climate warming and more dry summers, the disease is being found in many other areas of New Zealand.

When I arrived at the Whatawhata Hill Country Research Station in 1968, researchers had done most of the hard work. The fungus and its toxin had been identified, and treating animals with zinc salts was the accepted prevention.

Gladys Reid


Gladys Reid OBE

A famous part of the zinc research story was Mrs Gladys Reid who farmed at Te Aroha in the Waikato. There was always an argument, which continues to this day even after her death at age 92, as to who was first to ‘discover’ zinc to prevent FE. As a former dental nurse she knew about the qualities of zinc, and tried throwing zinc sulphate into water troughs with clear benefits to preventing the disease.

To her dying day, she declared that she told the scientists at Ruakura about the value of zinc, and that they needed to follow it up. She must have spent 30 years goading them on to do more, and they certainly didn’t like it, and to this day they claim to have discovered zinc before Gladys.

Things certainly got heated from time to time and much of it was played out in the local newspaper - the Waikato Times under farming editor Peter Bourke. I got involved in the cross fire at one stage when Scientific Liaison Officer at Ruakura and in the end, I and Dr Rex Munday were the only two scientists at Ruakura who Gladys would talk to, and who were in contact with her. We always listened to her, difficult though it was at times as she was so deep into biochemistry and certainly well ahead of my knowledge of the subject. Rex could certainly follow her theories and ideas. Scientists from all around the world kept in touch with her and used to visit her.

There was the famous letter from overseas addressed to ‘The zinc lady, Te Aroha, New Zealand’ that got to her with no problems!

Before she died, I managed to get most of her original papers and correspondence into the archives at the Hamilton City Council’s public library, where they are publically available. In my opinion, from reading all her original letters, she clearly was the first to see zinc as a practical preventative for FE.

But I don’t expect my former colleagues to ever agree with me, and even years after it was all over ( I thought !), I was reprimanded by the President of the Waikato branch of the NZ Institute of Agricultural Science, for some words I had written for a display in the Hamilton City Museum of Art and History on the history of FE research. My scolding was because I had ‘given overdue emphasis to the role of Mrs Reid in the story of FE research’. Certain scientists never gave up their pique.

What made things worse for them was that Gladys was awarded an OBE for ‘Services to Agriculture’, an honour she always felt was a ‘sop’ to compensate her for the years of insults and rebuffs she’d had from Ruakura scientists as well as MAF's Director General of Agriculture.

One of the wonderful switchboard staff at Ruakura - Ruth Utting, told me that she was told by certain scientists and the Director that if 'that woman phoned', she was to tell her the person she wanted was not available. Ruth told me that Gladys got wise to this, and once got her daughter to phone the Director who then handed the phone to Gladys!

Google ‘Gladys Reid’ for her obituary.

Easy for dairy farmers
Daily drenching dairy cattle with zinc oxide was easy for farmers, as for most of the year cows had to be dosed for bloat and were well used to being handled – almost opening their mouths when approached with a drench gun. And when technology advanced, zinc sulphate could be applied via drinking water systems which circulated around the farm.

Messy chore
However, for sheep farmers where prevention involved weekly drenching with zinc oxide, it was just not practical, which was good because it got them determined to find an alternative solution.

I well remember seeing the mess in many woolsheds, as old washing machines were being used to mix the powder and water. You would think the shed and the sheep yards had been whitewashed – which was in stark contrast the shepherds’ blue language over their weekly mustering and drenching chore. The stress on sheep, dogs and staff was too much.

Why did some sheep survive?
Some smart farmers noticed that there were individual sheep that survived whatever the season (based on the survival of the fittest), so Ruakura researchers picked this up and started a flock selected for high and low FE resistance along with a randomly selected control group, and it continued for many years.

This was possible as the toxin (sporidesmin) had been isolated from the fungus (Pythomyces chartarum) grown in the lab at Ruakura, so sheep could be dosed with it to measure their liver reaction. As this was a very nasty toxin, handling and dosing animals with it had to be done by veterinarians, or under their supervision.

FE resistance heritable
These selection flocks soon showed that FE resistance was heritable and quite strongly too with heritability around 45%. This was similar to wool production, so it allowed farmers to start selecting for it along with their other important production traits. And they did – with great enthusiasm and success, working closely with Ruakura staff.

Colin Southey
A major driving force in this was the late Colin Southey who was a Farm Adviser at MAF Pukekohe, along with former Farm Advisor Andy Dalton. In their Raglan coastal hill country area in the early 1970s, FE was killing off over 40% of flock replacements causing enormous economic loss to hill country farmers. Many farms were losing 1000 sheep every year, and the losses in their replacement hoggets were particularly devastating.

It was Colin who drove the FE testing from the Ruakura labs into woolsheds and sheep yards for vets to administer the toxin and measure the response in blood tests using the enzyme GGT (gammglutylthiamase) which had been developed for measuring liver damage in human alcoholics.

Colin was a great driving force to get groups of breeders working together to select for FE resistance, and share the genetic gain made between their own flocks before passing it on to commercial ram buyers.

Two-tooth rams tested
Farmers put up the best of their top two-tooth rams for testing, and only kept those that survived the increasing levels of toxin as the years went on. In theory, if the flock had been achieving overall genetic gain over time, the two-tooths were the best genetics so were the obvious age group to test.

It’s a pity that the test was so expensive, around $300/ram, as it prevented stud breeders testing females, and hence speeding up overall genetic gain in their flock to pass on to commercial buyers. Selection on the female side had to come through survival of the fittest.

Dose rates
Dose rates were based on weight, so when farmers started, this was 0.1-0.2mg of sporidesmin/kg of body weight. Today most Waikato sheep breeders have sheep that will now take 0.6 mg/kg. In today’s flocks even in severe years, they never see a clinical case of FE so the programme has been a massive success.

Disappointing uptake
But the disappointing feature to me was that after 40 years of hard work and investment, none of the Romney, Coopworth or Perendale breeders who put large amounts of time and money into their flocks, got rich selling their FE-resistant rams to committed commercial sheep farmers.

The main reason was farmer complacency – as FE was never severe every year. Farmers seemed to believe that like lightning, it never strikes twice in the same place. So after a bad year, panic many drive farmers to buy FE resistant rams, but it may not based on the 'lightning logic'. But if they did buy the progeny of tested rams from stud breeders as they didn’t see the impact for some years which may not be bad seasons, they concluded that nothing had worked.

Genetic change takes time
Commercial sheep farmers didn’t seem to understand that genetic change took time, especially as new genes were only entering the flock on the ram side. So it took many sheep generations (average 3 years) to see any dramatic change, and it needed a few bad FE seasons to show this.

Buying rams locally
The other frustration was that even after massive losses, too many sheep farmers were loathe to buy rams from their local area. There seemed to be something wired into farmers that made them assume that you had to travel well out of the district to get ‘good rams’!

These 'good rams' were inevitably massive animals, covered in wool and usually very fat, as they’d come from very good farming areas. Some had even been on ‘hard feed’ and regularly drenched before buyer inspection time. Inevitably, these rams came from areas where FE did not occur!

Buying replacement ewes
After a devastating season, farmers never bought replacement sheep in their own area – they always went well away south to sales, which was the very worst thing genetically that they could do, as this diluted any genetic gain made by resistant rams that they had been using.

Stock agents
Stock agents who still have a big effect on farmers' decisions
on where they buy their rams.


Stock agents had a major part to play in this misguided practice, and I battled with many of them over the years about their role in improving hill country sheep flocks in the Whatawhata Research Station (Raglan) area, where lambing percentages were the lowest in the country.

Agents always reckoned that rams from Raglan breeders were ‘too blardy small’, assuming size was a major indicator of genetic merit for sheep to survive and perform on hard hill country. They could never understand that most of a ram’s size was caused by the environment (feeding) and not genetics.

The visual look of a ram always took pride of place in ram selection by agents in those days and any records were a mystery that only held up the 'ram picking' job and delayed the time spent by the drinks cabinet in the front room of the house!

I always suspected there were Company deals going on to move surplus big fat rams from, the classical ram breeding areas (we called them ram alley) in theWairarapa and Manawatu up to the Waikato, as a sort of clearing house for their surplus.

Agents would take off with a car load of buyers at crack of dawn, pick the rams for the client, empty a whiskey bottle or two, and be home after the last pub closed on the way. It was great business as the rams didn’t live long, and the agents got regular business each season and the ram buyers had their ‘ram picking trip’ to look forward to as an annual feature!

I once met a very tired farm manager at 6pm, who had just been dropped off at a friends house where he’d left his car at 4am to be picked up by his agent. He was proud to tell me he’d been ‘to pick the rams’. I asked him where he had been, and he wasn’t sure – other than it was somewhere in the Manawatu and it had taken over 5 hours to get there. I then asked about selecting the rams and he said the agent had done this for his boss, and he just looked on to give them a final approval. I asked if the Sheeplan performance records had been used to pick the rams but he didn’t know what I was talking about. He had not seen any paper sheets around.

Dalton’s 13-pub rule for genetic gain
Once in a farmers’ meeting discussing this issue, I formulated a ‘natural law’ which said that if any sheep farmer wanted to be sure of getting genetic gain through his or her Stock agent, then they had to go past at least 13 pubs in the agent’s car, listening to all the agent’s wisdom and war stories, before genetic progress could be guaranteed from anything they bought! I sometimes still meet many farmers who can remember this – but nothing else I said!

Things have changed
But things have changed, and especially in the last five years, with this year seeing a total clearance of breeders’ rams selected for FE resistance. This is mainly due to increasing dry seasons (climate change or not) and the appearance of FE in new areas of the North Island.

What’s good for stud breeders selecting for resistance, is that seeing FE every year and enough losses to show on the bank balance, has made commercial farmers concentrate on finding a solution – which is through genetics and not their veterinarians. This has never been helped by veterinarians as they are not strong on genetics – and in any case genetics do not sell the farmer anything off their shelves.

Zinc boluses
Zinc oxide boluses for lambs showing the zinc inside
the wax protective cover


Veterinarians do sell zinc boluses for both sheep and cattle. When Ruakura scientists recognised the difficulty of regularly drenching sheep with zinc oxide, they developed these to stay in the rumen and be effective for a month. This delivers a slow rate of zinc as the exposed end of the bolus dissolves.

The bolus is used by farmers who see it, and the costs and work involved in inserting it, as a basic protection. The problem is that it does not provide enough zinc when spores rise rapidly and dangers of toxicity are high. The sheep in the picture at the top of this post were all given a bolus which clearly was not enough zinc to protect them from the 'natural challenge' they got on the farm.

Ramguard
All the past years of research at The Ruakura Agricultural Research Centre has been built into a programme called ‘Ramguard Facial Eczema Tolerance Testing Service’. Here sheep breeders can get information on how to test for FE tolerance and how to build this information into an overall breeding programme. Google ‘Ramguard’ for details.

Tolerance and resistance
I have been involved in many academic arguments about which is the correct term to use. I don’t really think it’s important – I use resistance.

Breeders need thanks
The sheep industry should be grateful to these Waikato breeders of FE-resistant sheep who never gave up, and were prepared to invest in on-farm R & D to deal to a major animal scourge. They have also proved conclusively that to farm sustainably in today’s world, genetics will have a better long-term outcome than chemotherapy.

Further reading
John D.J. Scott (1989). Ruakura - 50 Years of Research and Recreation.
Facial Eczema. Page 29. Chapter by John Scott and Archie Campbell
ISBN 0-477-08021-9.

January 2, 2009

Sheep Farm Husbandry - Common diseases: Causes; Signs; Treatment; Prevention

Health, diseases, signs, treatment, prevention, when to seek advice, poisons, poisonous plants

By Dr Clive Dalton & Dr Marjorie Orr

Note
This is not a veterinary text book and the listed diseases are very selective. They are in the order which you’ll be most likely to meet them (if they occur) on most farms. This information will help you have a meaningful discussion with your veterinarian who must be called if you have any doubts about the health and welfare of any animals.

Feet problems (lameness)
Cause
  • Footrot is the main problem and is caused by a bacterium. It’s more often seen in older sheep.
  • Foot scald (interdigital dermatitis) is also caused by bacteria and can affect ewes and even young lambs.
  • Foot abscesses are also bacterial infections and are often seen in rams.
  • All these bacteria live in the soil and infect the sheep when their skin or hooves are soft after prolonged wet periods or on lush pasture.
Signs
  • Sheep have varying degrees of lameness from a slight limp to grazing on their knees. Bad cases are very reluctant to move and are clearly in pain.
  • In foot scald the area between the toes is red or blanched and looks sore.
  • In footrot the horn separates from the foot wall, which is spongy and smells very sour and rotten.
Treatment and prevention

  • For scald, moving sheep to drier pastures often cures them.
  • Putting them through a footbath of 10% zinc sulphate or 5% formalin usually works well.
  • For footrot, more drastic action is often needed, first to trim the overgrown hoof and expose the area to the air and then footbathing.
  • A footbath in the form of a pen that they can be held in is better than a race, as some sheep learn to run through holding up sore feet or running along the nib wall on the side.
  • Over zealous foot paring that leads to bleeding should be avoided.
  • Treating sheep and then turning them out on to the muddy paddock they came from won’t do much good. After treatment, try to let them stand on a clean hard area for some time.
  • Abscesses need veterinary treatment and antibiotics, and may be slow to recover.
  • Cull persistent sufferers of all foot problems as there is strong farmer evidence that foot problems are inherited and can be eliminated by selection.

Internal parasites
Cause

  • These are generally understood to be roundworms found in the fore stomachs of the sheep and also in the small and large intestine.
  • The most important roundworms in sheep are Haemonchus, Ostertagia, Trichostrongylus and Nematodirus.
  • There are also lungworms (Dictocaulis), liver flukes (Fasciola) and tape worms (Monezia).
Signs
  • General unthrift and lethargic.
  • Loss of appetite and massive weight loss.
  • Diarrhoea (scouring).
  • Mucus in the faeces.
  • Anaemia.
  • White sections of tape worms in the faeces.
  • Bottle jaw (fluke)
Treatment and prevention
  • Because of the increasing risk of worms becoming resistant to the chemicals in drenches, consult your veterinarian to ensure the problem really is worms and that you have a farm plan to deal with them to avoid or delay drench resistance.
  • Read the details in Dalton (2006) – see references.

External parasites
Cause
  • As the name suggests, external parasites or “ectoparasites” live on the outside skin of animals.
  • The main ones are body lice but there are also foot lice and face sucking lice as well as keds, itch mites and ticks.
  • Body lice are the main issues and tend to remain in preferred body sites feeding on surface debris. They don’t suck blood like ticks.
  • They move up and down the wool staples and this is how they get from sheep to sheep.
  • In ideal conditions they complete a life cycle in about 34 days.
  • Lice also cause a defect in sheep pelts called “cockle”.
Signs
  • Sheep rub themselves on any convenient objects like fences leaving wool behind.
  • They may bite themselves where the parasites are active.
  • The sheep’s fleece looks rough with some fibres pulled out.
  • Lice and keds are very host-specific and spend virtually all their life on the animal.
  • Keds are not very important but can cause problems in fine-woolled sheep where their faeces stain the wool.
  • Heavy lice infestations occur mainly in winter in young and/or in unthrifty sheep that are poorly fed.
  • To look for lice, turn the sheep towards the sun and part the wool to expose about 10cm of skin. The lice will move away from the light. Do this two or three times on the sheep as lice live in colonies.
Treatment and prevention
  • Up to the 1980s it was compulsory to dip sheep once a year to control lice. This law now does not apply.
  • “Dipping” is still the main prevention method and it includes plunge dipping, spray dipping and using pourons.
  • Check with your veterinarian for the correct treatment for all external parasites as they too are now building up resistance to the chemicals in treatments.
  • The most convenient form of treatment for small flocks and even for some large flocks is now pouron product.
  • Injectable formulations are very effective against itch mites.
  • Sheep that are kept in good condition generally don’t suffer major problems from external parasites.
  • Treat sheep soon after shearing when the wool is short.
  • Do not treat sheep with any approved product for at least 6 weeks before shearing unless the directions differ.

Flystrike Cause
  • Flystrike is where blowflies lay their eggs on sheep and the resultant maggots eat the sheep’s skin and flesh, often leading to a very painful death.
  • There are three species in New Zealand.
  • Dirty damp woolly areas on the sheep attract the flies and warm humid conditions favour the eggs to hatch. This takes about 12 hours.
  • The Australian green blowfly will strike clean areas of the sheep and is active over a longer period.
Signs
  • Affected sheep are distressed and will stop and bite the area where the maggots are active. They may run around or stamp their feet.
  • The struck areas on the sheep may look dark and wet.
  • Struck sheep will hide away in scrub searching for relief as struck areas will attract more flies, both blowflies and others.
Treatment and prevention
  • Suffering sheep must be caught and the affected area treated to kill the live maggots. Methylated spirit is a good product for this.
  • Shear the woolly area if the wool is long to expose the skin to the air. Maggots don’t like fresh air.
  • Put some insecticide on the affected area to prevent further strikes. Many shepherds carry a bottle of dip with them for this job.
  • Crutch and dag dirty sheep and if many are getting struck, it may pay to shear and dip them all.
  • Good worm control will prevent scouring and hence attracting flies.
  • Watch all lambs after docking to make sure none of them have their tail wounds attacked by blowflies. Also watch any sheep with shearing cuts.
  • Don’t leave anything dead around the farm to attract blowflies – or use this fact in fly traps baited with rotten meat.
  • Pouron or spray-on treatments are available. Consult your veterinarian for advice on which products to use and the time it remains effective. Pay special attention to meat withholding times for the products.
  • Remember not to dip for at least 6 weeks before shearing.

Pregnancy (metabolic) diseases
Here the concern is over what are called “metabolic diseases” as they are caused by a ewe’s metabolism going wrong close to birth and soon afterwards. The three main metabolic diseases are shown in the Table below:

Names of metabolic diseases in sheep


Grass staggers
Note this is different to Ryegrass staggers (see later)

Cause
  • Low magnesium in the bloodstream which has to be built up for storage in the liver.
  • It can occur both before and after lambing.
  • Rapid changes in the diet from hay to lush pasture can cause it.
Signs
  • Ewes are simply found dead. Perhaps there will be scruff marks where she has been staggering and froth on the mouth.
  • Very early signs can be subtle and not noticed in a big mob.
  • This may progress to increased nervousness and slight shaking when disturbed.
  • These can lead to quite dramatic signs like walking with stiff legs, staggering and falling over when mustered.
  • When the sheep goes down she will paddle with her legs and hold her head back.
Treatment and prevention
  • Treat any ewe showing early signs with magnesium. Check with your vet for the correct product and the way to give it.
  • Check with your vet whether to give a calcium injection at the same time as milk fever could be involved.
  • Dust paddocks with calcined magnesite before grazing if you expect major problems. Wear a mask when applying the dust.
  • Check the soil tests to see if potassium levels are excessively high as this can be a predisposing factor.

Milk fever Cause
  • An imbalance of calcium.
  • It occurs mainly in older ewes which produce a lot of milk.
  • It can happen both before and after lambing.
  • Often happens within 24 hours of a sudden stress, e.g. yarding, transport, mustering, bad weather or feed shortage.
Signs
  • Affected ewes may just be found dead with no obvious signs.
  • Restlessness, trembling, staggering, depression and lying down.
  • Ewes go down on their chests (rather than on their sides) with their hind legs extended behind them, and head down and extended forwards or turned into their flank.
  • May be a discharge from the nose, bloated, and they usually abort dead lambs.
Treatment and prevention
  • At the first sign of problems give the sheep a calcium injection. Check with your vet for the correct product and the way to give it.
  • It may be wise to give her a magnesium injection too as the two conditions are often seen together.

Sleepy sickness, pregnancy toxaemia
Cause
  • This is the most common metabolic disease in sheep and occurs in the six weeks before lambing, especially with ewes carrying multiple lambs (hence the name of twin-lamb disease).
  • It is regularly triggered by underfeeding which can happen in snow storms, especially after a period of good feeding. Cold weather and lack of shelter add to the problem.
  • Any condition that increases the stress on ewes, e.g. footrot, foot abscess and internal parasites may trigger it.
  • Lack of exercise such as when ewes are yarded or held under cover, may also cause it.
Signs
  • Slow onset of the disease as opposed to the other two metabolic diseases.
  • You will notice slowness to move, lethargy, not eating, staggering or aimless wandering, twitching of the face and ears, blindness causing the sheep to lie down usually with her head up.
  • Coma and death can occur from 2-7 days.
  • 50% of people should be able to smell the ketones (nail varnish smell) in the sheep’s breath. Blood tests will confirm this.
  • Dead ewes will have a fatty liver.
Treatment and prevention
  • As soon as you suspect the disease, treat the sheep with energy supplements – (some with electrolytes) given by mouth. Check with your vet for the correct products and the way to give it.
  • Good feeding is the key to prevention and avoiding variation in the feeding level in the last weeks of pregnancy. Feed high energy concentrates as the sheep’s appetite for bulky feeds will be reduced.
  • Make sure ewes have gentle exercise before lambing.
  • For valuable ewes, performing a caesarian section will save her life and her lambs.

Bearings (vaginal prolapse)

Bearings can be a frightening sight and the ewe risks infections if she lies on muddy ground.
Cause
  • Bearings can be caused by high pressure in the abdomen from a womb full of lambs, a rumen full of frothy herbage, a lot of fat in the abdomen and a full bladder. It’s possible to have a combination of these factors.
  • Bearing problems vary greatly between farms and between seasons.
Signs
  • A mass of pink flesh hanging from the vulva of usually a heavily-pregnant ewe.
  • Dry ewes can also have bearings.
  • The “bearing” may be the inverted (inside out) vagina.
  • If it’s big it may contain the bladder, the cervix and the uterus (womb).
Treatment and prevention
  • If it is a massive bearing, call the vet urgently and leave the sheep undisturbed.
  • If the bearing has been out a long time and is dry, then the chances of success are poor and euthanasia may be the best option. Saving the lambs by caesarian may be possible immediately after the ewe is dead.
  • If the bearing is recent and small, i.e. only a prolapsed vagina, then gently clean and disinfect the prolapse and push it back in. It’s important to empty the bladder before doing this. It helps to point the ewe down hill or get someone to hold her up by the back legs during the task.
  • The bearing will then have to be retained to prevent it coming out again. Veterinary treatment involves placing sutures around the vagina and vulva.
  • The best farm treatment is to use a commercial plastic retainer held in the vagina by tapes to the sheep’s wool.
  • Old methods using safety pins, clips, wool or twine tied across the vagina have variable results and should be used only in the last resort. For any problems seek veterinary help.
  • Make sure all these devices are removed before the ewe lambs and before shearing.
  • Keep at risk ewes off hilly pasture as lambing approaches and make them take gentle exercise.
  • Keep a steady feed supply, avoiding putting ewes into long lush pasture.
  • Mark all bearing ewes for culling at the first opportunity.
  • Note: There is also “rectal prolapse” which is where the rectum is pushed out and can happen in male sheep too. Often these go back in again on their own, but it’s best to cull the sheep to avoid future problems.

Mastitis Cause
  • This is an infection of the udder caused by various bacteria.
  • It usually happens in the first weeks of lactation and at weaning.
  • There are two main types – simple mastitis and gangrenous mastitis.
  • Cold stress and lambing on bare muddy paddocks are often part of the cause.
Signs Simple mastitis
  • With simple mastitis there is little obvious sickness.
  • The udder is hot, swollen and painful, usually just on one side.
  • The milk is watery, clotted and discoloured.
  • The ewe may look lame due to the extra pain in her udder when she walks.
  • She will not let the lamb suck so the teat and udder are very extended.
  • After a few days the affected side shrinks and becomes hard.
Gangrenous mastitis
  • This is often rapidly fatal.
  • Affected ewes are very dull and show little interest in their lambs or eating.
  • In the early stages the udder is hot, swollen and painful but soon becomes cold and turns blue-black in colour.
  • Only blood-stained watery fluid can be expressed from the teats.
  • If the ewe survives, the damaged tissue may slough off leaving an unsightly cavity which heals over leaving a large scar.
Treatment and prevention
  • Treatment often fails as the sheep is seen too late.
  • For simple mastitis, treatment with antibiotics over three days will work if the ewe is seen early. (Check with vet for correct antibiotic treatment into the udder and into the muscle).
  • Empty the udder before putting antibiotic into the teat.
  • For gangrenous mastitis, amputation of the teat by a veterinarian allowd the tissue to drain and may save the ewe’s life.
  • In both cases of mastitis, udder function will be severely affected for next lactation and the ewe should be culled.
  • Little is known about prevention other than lambing on clean paddocks and culling all ewes that have been affected.
  • Put ewes that have just weaned lambs on to short feed to reduce milk supply but do not restrict water.

Clostridial diseases Cause
  • These are caused by a range of bacteria that are widespread in animals and their environment. Being anaerobic they reproduce in the absence of oxygen in the tissue and produce powerful toxins.
  • When oxygen is present they form spores that can live in the soil for many years.
  • These are mainly diseases of lambs as older sheep have developed an immunity to them, assisted by yearly vaccinations.
  • They include pulpy kidney, tetanus and the gangrene diseases (malignant oedema, blackleg and black disease) which are almost always fatal.
Signs
  • These vary with the disease but generally death is very rapid.
  • Pulpy kidney is a good example where often the biggest lambs in the flock are found dead with little signs of a struggle. They may scour and show convulsions and die within 4-5 hours of the onset.
  • With blackleg and malignant oedema (blood poisoning) they are found with blood-stained froth at the nose. They may be sick for 12 hours to a couple of days.
  • Often the dead animal may blow up quickly and the skin goes blue/black very quickly.
  • With tetanus (lockjaw), lambs gradually become stiff and may show muscular spasms. It is common in lambs within three weeks of docking but it can occur in older animals too.
Treatment and prevention
  • Treatment of these conditions is not effective.
  • A vaccination programme with a 5-in-1 or a 10-in-1 vaccine is the best prevention as ewes pass immunity on to their lambs. The programme is to vaccinate hoggets twice then do ewes about a month before lambing.
  • If lambs need further protection (check with your vet) then they are done at 2-3 months of age when their maternal immunity has passed.
  • If ewes are not vaccinated, then lambs should be done at docking (4-6 weeks old).
  • Or lambs can be vaccinated from 10-12 weeks old with a sensitising dose followed by a booster 6 weeks later.

Trace element & mineral deficiencies Cause
  • These diseases are caused by lack of a range of minerals or trace elements which are deficient in some New Zealand soils and can be induced by fertilisers and feeding.
  • Some are called “trace elements” as they are needed in very small amounts (traces).
  • The main ones for sheep are cobalt, selenium, copper, magnesium and iodine.
Cobalt
  • Ill thrift in lambs with loss of appetite, poor growth, wasting away, watery eyes, scabby ears and death.
  • Deficiency is also associated with brain and liver diseases in older sheep.
Selenium
  • A third of New Zealand soils are deficient in selenium.
  • Ill thrift in young lambs leading to white muscle disease.
  • Infertility in ewes.
Copper
  • Not common and seen on peat soils and leached sandy loams.
  • Weak hind legs, fragile bones, poor growth, infertility, low fleece weight and wool loss.
Magnesium
  • Seen on pastures where high nitrogen and potassium fertilisers have been used over time, especially after spring applications.
  • Pregnancy and lactation increase the demand for magnesium.
  • Ewes show agitation before convulsions and death, especially after the disturbance of yarding or in bad weather like snow storms.
Iodine
  • Some alluvial soils are deficient in iodine, and deficiencies can be induced by feeding brassicas and clovers which contain chemicals (goitrogens) that reduce thryroid hormones.
  • Goitre is the main sign of the disease seen in swollen thryroid glands in the neck.
  • Poor survival in newborn lambs, and reduced wool production in ewes.
Treatment and prevention
  • Both treatment and prevention depend on supplementing animals with the required trace elements well before they need them so body reserves (except for Iodine and magnesium) can be built up.
  • Review your fertiliser programme to see what trace elements can be added in the mix.
  • Body reserves can be checked by blood tests and liver biopsies through your veterinarian.
  • Don’t overdose. Don’t dose with selenium if it has been applied in the fertiliser.
Scabby mouth Cause
  • Also called orf, contagious pustular dermatitis, and is a virus disease seen in lambs.
  • The scratches caused by eating thistles and gorse seem to predispose lambs to the infection.
  • It is classed as a zoonoses as it can be picked up by humans, especially meat workers handling affected lambs.
Signs
  • Crusty sores mainly around the lips of lambs up to 6 months old.
  • Scabs can also form on the muzzle, ears, lower legs and around the teats of ewes caused by lambs sucking.
  • Ewes not letting their lambs suck and lambs not thriving because they are not eating.
Treatment and prevention
  • Treatment is not worthwhile. Sores generally heal naturally.
  • Antiseptic creams can help secondary infections for small numbers of sheep.
  • If the disease occurs regularly on farms, a vaccination programme should be used every year.
  • Lambs are vaccinated by scratching the bare skin in the loin area soon after birth or at docking.
  • Always wash your hands after handling lambs, especially at docking time.

Johnes disease Cause
  • This disease (pronounced as Yoh-neez) is caused by a bacterium that lives in the soil and can persist for years. It’s of growing concern in New Zealand.
  • Affected stock pass out the bacteria in faeces to infect other sheep.
  • It’s a wasting disease that develops slowly and is seen most often in sheep from 2-4 years of age.
Signs
  • Many affected animals don’t show signs, especially in younger age groups.
  • In the early stages sudden loss of condition in older sheep.
  • Severe scouring.
  • Lab tests are needed to confirm the disease.
Treatment and prevention
  • There is no treatment for affected stock.
  • All infected stock should be destroyed to prevent spread of the disease.
  • Avoid introducing it to the farm with purchased stock.
  • Don’t have any suspect animals on the farm over lambing.
  • A live vaccination is available – check with your vet for details.

Facial eczema (FE) Cause
  • FE is caused by a toxin produced by the rapidly growing spores of a fungus in the dead litter of pastures, especially when conditions are warm and moist in autumn.
  • It is most common in the North Island of New Zealand.
  • 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

Stressed sheep showing swollen closed eye, bleeding from rubbing to stop the itch. Should not be out in the sun and should not have been at the saleyard!
  • Reddening and swelling of the skin around the eyes, ears, lips, nose and vulva exposed to the sun.
  • Sheep rub these itchy areas and make them bleed.
  • Affected stock are restless and continually seek shade.
  • The skin reddens, swells and then sloughs off leaving raw skin that can become infected.
  • Severely affected sheep will be jaundiced seen in a yellowish tinge in the whites of their eyes.
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.
  • A veterinarian may give antibiotic injections if severe skin infections occur, and also vitamin B12 injections to boost appetite.
  • Jaundiced sheep 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 flock 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).
  • Sheep 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. If there is no chance of recovery then they should be euthanased.
  • 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 (RGS) Cause
  • This is a brain disease caused by a toxin from a fungus that grows in perennial ryegrass.
  • It’s not common in the southern half of the South Island of New Zealand.
  • The fungus is an “endophyte” i.e. it grows inside the plant where the highest concentrations are in the leaf sheath at the base of the pasture and in the seed heads.
  • The toxin damages parts of the brain that coordinate movement.
Signs
  • When disturbed, affected sheep appear nervous and in mild cases they show slight trembling of the head and of the skin on the neck, shoulder and flank.
  • More severe cases show head nodding and jerky movements, swaying while standing and staggering when walking.
  • In the worst cases sheep have a stiff-legged gait, take short prancing steps and may collapse with rigid spasms that last for several minutes.
  • The disease is not fatal but sheep often die as a result of accidents – falling into holes, drains and creeks. They may not be able to drink.
Treatment and prevention
  • There is no cure for severely affected stock.
  • Remove affected animals from the hazardous pasture if you have other pasture available.
  • If not then hold them in yards and feed supplements (hay/silage/meal) with plenty of water.
  • Try to avoid stressing them through excess handling.
  • The best long-term solution is to replace ryegrass pastures with endophyte-free cultivars or safe endophytes.

Poisons Cause
  • These include poisonous plants, fungal toxins in pasture, algae and chemicals.
  • Many cases of poisoning are accidental.
Signs
  • One or more of the plants can cause diarrhoea, regurgitating rumen contents, unusual excitement, 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 sheep and are often more palatable when wilted.
  • Rubbish dumps should be fenced off and native scrub checked for poisonous plants before allowing sheep access to it.
Some poisonous plants, shrubs & weeds

  • 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)
Chemical poisons
  • Sheep can be overdosed with zinc, copper or selenium.
  • Fertilisers should be allowed to wash in before grazed by stock.
  • 1080 poisoning can occur when poisoned bait is accidentally dropped on to pasture or when stock gain access to land used for a poison drop.
  • Overdosing with organophosphate insecticides or anthelmintics can cause toxicity.
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.

December 20, 2008

The Dosin 'O the Hoggs - Part 1

Border Shepherding - Prevention of Braxy


By Clive Dalton

In our “Daft Laddies” book, on this blog Don Clegg and I report the story about “Braxy Mutton” in which our great friend, the late Willie Robson gives details of the performance when he shepherded ootbye at Willow Bog, to prepare a concoction of pig dung and fresh milk to dose the hoggs to prevent them dying of “Braxy”, a disease we now know is caused by the Clostridial group of bacteria.

In the late 1800s and early 1900s, the cause of the disease was a mystery, so anything was worth a try to kill whatever was in the sheep’s innards that caused such rapid death. Imagine the despair of a shepherd going out in a morning to find his best hoggets dead and blown up, because the nature of Clostridial diseases like Braxy is that it’s most commonly found in the better bigger hoggets that are doing well and it kills rapidly with large amounts of gas produced in the intestines. The runts in the flock never seem to be affected in the same way.

Goodness knows who ever came up with the idea of a pig-dung brew as a preventative – but anything would be worth a try.

So here’s it’s story which was both recited and sung at many a Shepherd’s supper in Northumberland and is still a well-loved party piece.

There seems to be no record of an author, so I’d be interested in any information about such this perceptive knowledgeable person who clearly understood the problem, the way to make the brew as well as local scepticism.
(Spiered – sought opinion)

Some magnificent Blackface ewe lambs/hoggs from Sundaysight at Bellingham mart in 2003. It was sheep like these that lived with the threat of Braxy before modern vaccines.
(Photo copyright of Helen Brown)

Acknowledgement: To Helen Brown for permission to use her material. She can be contacted at Burnbank Cottage, Tarset, Hexham, Northumberland, NE 48 1LY. Phone 240-427