NZ Lifestyle Block

FE mysterious­ly affects NZ, but nowhere else

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In the late 1930s, facial eczema was decimating sheep flocks in the greater Waikato, with farmers regularly losing 1000 sheep each year, especially hoggets. The dry coastal hill country from Port Waikato down to Raglan was especially hard hit.

Things got so bad that Federated Farmers demanded that research be started to find the cause and a cure. The government responded and Dr CP Mcmeekan moved from Massey College to start a new Animal Research Station at Ruakura.

The answer would take 30 long years to find. The breakthrou­gh came when the groundsman at Claudeland­s in Hamilton noticed black dust on his boots when mowing the grass. That dust turned out to be the fungal spores of Pithomyces chartarum which was shown to produce the toxin sporidesmi­n.

Few could believe that a fungus could be the cause, when so much time and money was spent investigat­ing all sorts of other daft suggestion­s and quack cures which MAF was committed to testing.

This fungus is present in other countries, but the spores are not toxic anywhere else. Why they would be so damaging in NZ conditions has never been explained. It was a pity that so much energy was wasted by Ruakura scientists arguing with Te Aroha farmer and former dental nurse, Gladys Reid. She discovered zinc was the best prevention for the liver damage caused by FE back in the late 1940s, thanks to her work in the dental industry and years of research. Gladys would throw zinc salts into farm water troughs, even testing her livestock by dosing some and not others to check her (correct) hypothesis.

While farmers in NZ and the USA followed her lead and raved about her work, the Ruakura team never liked it and a pointless argument over who was first to ‘discover zinc’ went on for 30 years. Before Gladys died in her 90s in 2006, I got her to put a collection of her papers in the Hamilton City Library archive. Gladys always believed that she was awarded her OBE to placate her over the way MAF had treated her. What Ruakura did do was isolate the best zinc dose rates which was very important work as too much zinc can be toxic and damages the rumen.

Zinc oxide was used as a drench, which was easy for dairy farmers as cows almost opened their mouths when they saw the drench gun. But it was a disaster for sheep farmers who had to mix the powder and water in the woolshed (an old washing machine was good) and dose them twice a week. The whole place and the staff would get covered in the stuff.

Zinc could also be put into the water trough, but it had to be zinc sulphate, and there was always the problem of controllin­g the amount individual animals were drinking.

In the late 1970s the team at Ruakura came up with a bolus to solve the problem. This could be administer­ed by mouth and would last in the rumen for about a month before the animal needed another one. Some sheep farmers started noticing that after the decimation of their flocks, there were always some sheep that survived to keep on performing. Two drivers of

the belief that there must be a genetic component were farm advisor (and former All Black captain) Andy Dalton and his colleague, the late Colin Southey.

They believed some stock were geneticall­y more resistant to FE. To test this concept, Ruakura staff started by breeding a line of highly-resistant sheep, a line of low-resistant sheep, and a control line. These lines were formed by drenching sheep with the sporidesmi­n toxin harvested from fungi at Ruakura, then measuring the effect on the liver using a GGT test developed in human medicine to check the state of the livers of alcoholics. Spectacula­r progress was made in both directions of selection, proving FE resistance (or tolerance) had a clear genetic base.

This led Colin Southey to demand that toxin drenching before selecting rams was made available to farmers in his area, and flocks have now been on that programme (called Ramguard) for over 40 years, with spectacula­r results. Commercial farmers buy tested rams and their genes flow through the flock to spread the resistance genes. Some farmers who have specialise­d in testing for the longest period to guarantee their sheep have now developed the recent ‘Fegold’ brand.

Breeding cattle for FE resistance has been sadly neglected, even though research at Ruakura some years ago showed the trait in cattle was also something geneticall­y inherited. Dairy breeding organisati­ons have been slow to recognise that half the calves born are males reared for beef, and drenching them for FE as they grow large is a chore that beef farmers and small block owners want to avoid. FE spores are easy to see down a microscope, looking like tiny brown hand grenades. Early on, staff at Ruakura developed a ‘wash method’: they would cut a sample of grass and dead litter at the pasture base, mix it with water in a jar, shake it, then count the spores from a drop of it on a special calibrated slide. This is still the way it’s done by vet clinics, and kits can be purchased for farmers to use themselves.

It’s the young, rapidly-growing spores that produce the toxin. Old dead spores that look black and solid down the microscope are harmless.

The trouble with spores is that their numbers are not consistent over a whole farm, or even in the same parts of the paddock. Counts are high in sheltered areas and on different types of slope, depending on sunshine. If you are going to count spores, then sample different areas of the farm or you risk errors by relying entirely on a general spore count. When spore counts are down in the low hundreds and conditions are cold, current wisdom is that there’s no problem until there’s a spike of say a million spores/g of grass. This usually occurs when rain arrives after a long dry spell in the warm humid days of late summer and early autumn. But it’s important to realise that danger can start with a series of low counts because an animal’s liver becomes sensitised. It means when a high level of toxicity is reached, it doesn’t take a very big spore count to have a really dangerous effect, and the level of protection the animals have been given will not be enough for effective protection. It quickly becomes a crisis which needs urgent action, but by that stage it may be too late. Getting minerals into the liver is like charging a battery. It takes at least three weeks after the start of zinc treatment for it to be effective, and this is always a problem for a lot of people as you need to start dosing stock on 1 January. In some places now, even this may not be early enough as FE cases are being found before Christmas.

Administer­ing zinc is a chore that many farmers hate, but don’t delay things until you hear about spore counts rising on some other local farms.

On small blocks, to administer a bolus – your best bet – you’ll need some good yards, preferably a head bail, and you’ll need to get an experience­d person to do it so that the bolus stays in the rumen and no danger is done to man and beast. That often means bringing in your vet.

When to end zinc treatment is getting trickier with cattle as long periods of zinc treatment are needed right into May as seasons stay warmer for longer. But prolonged zinc treatment is known to strip copper from the liver, so veterinary advice is needed on this one, to work out how much copper is needed. This is not an issue with sheep. Spraying the whole farm or selected areas is still recommende­d, and can be an easy

option. But again, knowing how effective it has been will mean you need regular spore counting to keep an eye on things, and it may not be totally effective if there is a massive spike of spores, when zinc drenching will also be needed.

Fungal spores end up on and in the soil, so there is advice around about how a fertiliser programme can affect spore numbers and reduce the risks of FE. Scientific opinion varies on this claim, but plenty of farmers who have applied lime and used fertiliser­s high in trace elements can claim not to have had FE in their stock. It is worth studying for future management to avoid all the work and cost of animal treatment. Sheep suffer more than cattle as their eyes and ears swell. They then rub them until they are red-raw, and until they cannot see. You won’t see great layers of skin come off as you do in cattle. Sunshine drives stock mad as it must increase the itching.

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