Isolation and the early practice of quarantine and disease control have kept New Zealand livestock free of the more serious diseases found in animals in Europe, Asia and the Americas. This is an advantage for New Zealand, and keeps its livestock products in demand worldwide.
An act was passed in 1867 to restrict animal importation. It prohibited the entry of all animals likely to spread disease. Since then, regulations have become more stringent.
Although New Zealand does not have serious infectious diseases such as foot-and-mouth or mad cow disease, there are some that can seriously affect animal health and production. Several may be passed on to humans and are known as zoonotic diseases. New Zealand has specialist veterinary laboratories that diagnose diseases and have developed programmes for controlling tuberculosis (Mycobacterium bovis) and leptospirosis (Leptospira pomona).
The New Zealand farmer is always on the lookout for animal health problems, including contagious illnesses, diseases of reproduction and the nervous system, internal and external parasites, poisoning, and metabolic illnesses caused by nutrient deficiencies. Many of these occur only sporadically and are easy to cure, but two – tuberculosis (TB) and internal parasites of sheep and cattle – may threaten farming in the future. Tuberculosis is difficult to control because it is endemic in wild possums and ferrets, which can reinfect domestic stock. Internal parasites of sheep and cattle can become resistant to the anthelmintics used to control them.
About the 1940s foot-and-mouth disease was spread throughout the world. In 1996, endemic areas included Asia, Africa, and parts of South America. North America, Australia, New Zealand and Japan have been free of the disease for many years. Most European countries are thought to be clear, although there were major outbreaks in the UK in 2001 and 2007.
Perhaps the greatest potential threat to future farming is foot-and-mouth disease (Aphtae epizooticae). It is a highly contagious viral disease that affects cloven-hoofed animals such as sheep, cattle, pigs, goats, llamas and deer, as well as rats and hedgehogs. It can be spread by saliva, mucus, milk or faeces, and carried on wool, hair, hay, footwear, clothing, livestock equipment and vehicle tyres. It can also be spread quickly over long distances by the wind. The virus thrives in damp, cool conditions and can survive for several weeks (although only up to five days on summer pasture) on sheep wool, cattle hair or footwear.
Clinical signs vary between animal species, but there are usually blisters on the nose, mouth and feet. Animals stop eating, become depressed and lame, and salivate a lot. There is continuous vigilance to ensure the disease is kept out of New Zealand – if it was found, almost all exports of meat, dairy products and animal by-products would stop.
There is an old saying that ‘a sheep’s worst enemy is another sheep’ – sheep, like all animals, suffer from a number of contagious diseases. When they were grazed on open country they were generally healthy, but as sheep farming intensified, greater numbers of sheep were confined to smaller paddocks and keeping them healthy became a bigger challenge. The following health problems were present in sheep on open country, but grew worse under intensive farming.
Hydatids (Echinococcus granulosus) was well established in New Zealand in the late 19th century. The disease is caused by a parasite that may occur in dogs as an intestinal tape worm. During the cycle of development it exists as a cyst in the organs of sheep, human beings and other animals. Dogs become infected by eating raw offal from an infected sheep.
In the late 1950s a massive control effort began, including establishing 800 local voluntary committees, education, promotion, peer pressure, dedicated hydatids officers, dog dosing strips and the introduction of the Hydatids Act 1959. In 2002 New Zealand was pronounced provisionally free of hydatids, and the control programme a success.
Lungworm and worms of the gut were major problems, especially in young sheep, in some areas by the early 1880s. In 1881 a stock inspector in North Canterbury reported an outbreak, with the mortality rate of affected flocks being 5 –20%. He recommended turpentine (distilled from the resin of pine trees) as the best remedy. Infected sheep were often dosed with a mixture of turpentine and milk.
Sheep scab was the most serious stock health problem in the early years of large-scale sheep farming in New Zealand. The disease is caused by the mange mite Psoroptes communis ovis, which lives in the skin of sheep. Infected animals lose their wool and condition.
A Scab Ordinance was passed in 1849 to control the introduction of scabby sheep from Australia. Thereafter provincial governments enacted increasingly harsh measures to try to control the problem. Sheep inspectors checked sheep for the disease and courts could order infected flocks to be slaughtered. In the 1850s and 1860s several large stock owners were bankrupted by scab because of the impact of the disease on their sheep, the cost of treatment, or the financial penalties set by the courts.
Dipping was known to be the best treatment for scab, but farmers disagreed on what ingredients made the best dipping solution. The decision was often down to the whim of the person in charge of the job. In 1868 John Robinson, the manager at Whiterock Station, north of Christchurch, dipped the sheep in arsenic. He killed several hundred, and nearly killed the shepherds as well.
Treatment was by dipping the sheep in boiled tobacco water. Sometimes salt, saltpetre, sulfur or arsenic were added. By the end of the 1880s New Zealand was largely free of scab, partly because of the severe penalties imposed by the courts and partly due to the increase of wire fencing, which meant farmers could keep infected sheep away from their flocks.
There were isolated outbreaks of anthrax (Bacillus anthrax) from the 1870s to the early 1900s. The cause was found to be bones, imported from India, which had been crushed and spread on pasture and crops as fertiliser. Between 1903 and 1935 the government put measures in place to prevent the introduction of anthrax, including a ban on importing bone meal.
Anthrax spores have been used as a weapon in biological warfare. In 1942, British bio-weapons trials severely contaminated Gruinard Island in Scotland with anthrax, making it uninhabitable for the next 48 years.
Anthrax is one of the oldest recorded diseases of ruminants (sheep, cattle and goats) and horses, and also affects humans. The spores can survive for decades in the soil and enter an animal by being eaten or breathed in, or through damaged skin. They quickly spread through the body, causing cell destruction and bleeding. In ruminants, death is usually sudden.
Anthrax became known as wool-sorters’ disease after an outbreak in Bradford, England, in the late 19th century, when it was found that humans were ingesting anthrax spores from wool pelts.
Footrot is caused by the anaerobic bacteria Fusobacterium necrophorum, and its transmitting agent, Dichelobacter nodosus. Warm, moist conditions encourage the spread of footrot, which is highly contagious among sheep. As the disease spreads in the hoof it destroys tissue, and the horny part can become almost completely detached. Sheep become lame and are less inclined to graze, resulting in weight loss, scantier wool and poorer lambing performance. They become prone to fly strike (where blowflies lay eggs in the wool and maggots develop), especially where infected hooves have been in contact with the fleece. If not treated, footrot leads to a slow and painful death.
New Zealand’s early sheep flock was founded on Merinos, which are more likely to get footrot than other breeds. Farmers in wetter areas had trouble with the disease from the outset. The problem increased on the big stations after farmers fenced the land and sowed improved pasture, and the intensity of grazing increased.
A variety of treatments were tried. A popular method was to run sheep through a foot bath of bluestone (copper sulfate) and arsenic. However, the cure rate was poor. The problem was only eased temporarily in dry seasons, when the disease went into remission naturally.
The problem of footrot in Merinos encouraged farmers to introduce British sheep breeds that were less susceptible. Footrot remains a major problem in Merino and other fine-woolled breeds when it is wet, although vaccinations are now available. Other methods of control include culling susceptible animals, genetically selecting animals that show resistance to the disease, paring hooves to remove infected tissue, using foot baths containing a disinfecting agent, and dosing with antibiotics.
Foot abscess is an infection of the joints in the foot, generally by Fusobacterium necrophorum and/or Arcanobacter pyogenes. Wet and muddy underfoot conditions predispose the condition. Treatment involves draining the abscess, bandaging and antibiotics.
In the early days of settlement, thousands of sheep newly landed off ships from Australia, or sheep being driven to new grazing areas, died after eating tutu (Coriaria arborea). Some farmers claimed to have lost one-quarter of their flock to tutu poisoning. Tutu has been responsible for most plant poisonings of stock in New Zealand.
Bleeding was the recommended cure for sheep poisoned by tutu. Early runholder Mark Pringle Stoddart wrote: ‘cure is instantaneous if applied in time, and consists simply by boldly cutting across the bars of the palate – the swallowing of blood brings immediate relief.’ 1
This treatment would certainly not be advocated today.
Tutu grows throughout New Zealand on riverbanks and tussock lands, and among scrub. Stock can eat a small amount without any ill effects, but larger quantities can be lethal.
Many other plants can kill sheep, including acorns, yew, St John’s wort, ngaio, oleander, rhododendron, laburnum, delphinium, Iceland poppy, cestrum, foxglove, goat’s rue, ragwort, and blue lupin. Some sheep become sick after grazing on specialist feed crops. They can get nitrate or nitrite poisoning and red gut from grazing lucerne, skin scald from rape, and haemoglobinuria from brassicas (such as swedes and kale).
Sheep can also be poisoned if pasture is contaminated with superphosphate fertiliser. The fluorine in superphosphate is largely the cause.
The most widespread modern health problems in sheep are caused by nematode parasites, which live in the gastrointestinal tract. They cause diarrhoea (also called scours), poor growth and ultimately death, especially in young stock. Some species of worm can cause anaemia and death from blood sucking. Internal parasites can be controlled by an anthelmintic given orally or injected. However, resistance to anthelmintic products has become an increasing problem in sheep as well as goats.
Drench resistance is when parasitic worms in the alimentary canal develop an inherited resistance to specific types of anthelmintic drenches or injections. This occurs when a few worms survive a dose of drench and go on to breed resistant worms, which eventually dominate the population. Drench resistance was common on New Zealand sheep and beef farms in the early 2000s.
Although internal parasites generally have little effect on healthy adult ewes, they contaminate pasture with their eggs, excreted in ewes’ dung. Some of the techniques farmers use to reduce pasture contamination can increase anthelmintic resistance in the parasites, so care must be taken to follow recommended practices and be aware of the resistance status of nematode worms on each farm.
Scours (diarrhoea) can be caused by a number of organisms other than nematode parasites. Gastrointestinal salmonellosis in ewes generally occurs in summer and autumn, and can be controlled by vaccination. A clinically similar disease seen in winter is caused by the bacterium Listeria monocytogenes, which sheep ingest in poor-quality silage or baleage (preserved feed) and hay bales. Enteric yersiniosis is a mild form of diarrhoea that occurs in winter in sheep 9–12 months old.
Johne’s disease in sheep is caused by the bacterium Mycobacterium avium spp. paratuberculosis, which affects the intestine and results in wasting, often without diarrhoea. The intestinal wall slowly thickens and the animal has trouble absorbing nutrition from its food. Infected sheep initially continue to eat and remain bright, but over the months and years lose condition. There is no cure. Lambs usually contract the infection, and shed the bacteria well before signs of sickness show up in two- and three-year-olds.
The disease is endemic, with an estimated 60–70% of New Zealand flocks being affected. Often, less than 1% of the sheep will show clinical signs in any one year. Vaccines can help control the disease.
Pneumonia (an infection of the lungs causing inflammation) and pleurisy (an infection of the layers around the lungs) in lambs are common in late summer and autumn. These diseases have two forms: an acute fibrinous pneumonia, and a chronic non-progressive pneumonia. They are considered to be initiated by para influenza-3 virus (PI3) and adenoviruses with a secondary bacterial infection by Mannheimia (Pasteurella) haemolytica. Infections lasting more than one month are likely to be caused by another bacterium, perhaps Mycoplasma ovipneumoniae or Bordetella parapertussis.
Scrapie is a fatal, degenerative disease affecting the central nervous system of adult sheep and goats. The disease creates sponge-like spaces in the brain in genetically susceptible sheep, who often show signs of nervousness, and in some cases itching – hence the name scrapie.
Badly affected flocks can mean significant production losses, but more importantly the presence of scrapie in New Zealand would prevent the export of sheep products. Despite stringent regulations and quarantine requirements, scrapie appeared in 1952 in a South Island flock with imported stud animals, and there was a second outbreak on another property before the disease was eradicated. Sheep imported for research purposes were diagnosed in 1976 and 1977 while in quarantine on Mana Island. All animals involved in the project were destroyed.
Bacterial infection of the testis and epididymis duct can cause infertility in rams. A significant cause is Brucella ovis, and there is a voluntary, national industry-based programme to record flocks which are free of this bacterium.
There are a number of causes of spontaneous abortion, which can result in high lamb losses. Toxoplasmosis and Campylobacter infections can reduce the lambing rate of some flocks by 25% or more. They can be prevented by vaccines.
Since 1996, in intensively stocked areas of the South Island, Salmonella Brandenburg has caused abortions, and in previously unaffected flocks 50% of the affected ewes have died. A vaccine is available.
Other less common causes of abortion are hairy shaker disease (Pestivirus), Listeria and Fusobacterium organisms. Toxoplasmosis, Campylobacter and hairy shaker disease can also cause lambs to die shortly after birth.
This disease is commonly seen in late summer and autumn, and is caused by sheep ingesting Lolitrem B, a toxin produced by an endophyte fungus in ryegrass. Affected sheep become unsteady on their legs, eat less and lose weight. Ryegrass pastures low in endophytes overcome this problem. Similar to ryegrass staggers, Phalaris staggers can affect animals grazing on new Phalaris tuberosa grass in summer and autumn. This is caused by alkaloids in the plant.
Polio-encephalomalacia can occur in sheep of all ages, but is most common from weaning to 12 months of age and is characterised by impaired vision, blindness, circling, tremors, convulsions and ‘star gazing’. It is thought to be caused by thiamine deficiency and has been associated with a feed change to less roughage. It has also been linked to sulfur intoxication after eating feed rich in sulfur.
Listerosis or circling disease is caused by Listeria monocytogenes, a bacterium which moves up cranial nerves to the brain, where it forms micro-abscesses. Poorly made silage and baleage (preserved feed) and hay bales are often a source of infection, as is the loss of teeth. The disease becomes evident about a month after exposure to the bacteria. Damage to the brain means that treatment is seldom successful.
Clostridial bacteria are found in the soil and intestinal tracts of animals and humans. Outside the body they are transformed into spores that are highly resistant to drying and temperature changes, and can live in the soil for many years. When environmental conditions become favourable, the spore germinates into a vegetative bacterial cell and begins to multiply. This may occur in damaged tissue, such as wounds, or in the intestinal tract, and especially after over-eating grain or lush pasture. When multiplying, the bacteria release powerful toxins into the system of the host animal. Their effects are usually fatal.
Sheep are prone to a number of clostridial diseases, but vaccination can usually prevent them.
Tetanus or lockjaw is a fatal disease of sheep caused by the bacterium Clostridium tetani. Symptoms are muscular stiffness in the neck, difficulty in swallowing, rigidity of abdominal muscles and fever in sheep as well as humans. Deep wounds with devitalised tissue are ideal sites for the proliferation of tetanus bacteria. Most cases occur after lambs have had their tails removed with rubber rings, when Clostridium tetani infests the oxygen-deprived tissue. Prevention is by injecting lambs with tetanus antitoxin at tailing, or by vaccinating ewes so the antibody is available to lambs in their colostrum (first milk).
Enterotoxaemia is caused by type-D Clostridium perfringes. The disease causes convulsions, muscle tremors, then sudden death in well-fed, rapidly growing lambs.
Black leg and malignant oedema are caused by the bacteria Clostridium chauvei and Clostridium septicum, which enter wounds such as those from shearing, castration, docking, fighting and parturition. Both diseases can be prevented by vaccination.
Fly strike (myiasis) was not a problem in the early days of sheep farming in New Zealand. Flies were a nuisance for people and there are plenty of stories of woollen blankets and socks crawling with maggots after being blown by flies. The first reported case of fly strike in sheep is from a South Canterbury farm in 1881. A leading English expert recommended applying coarse whale oil, as the flies would be put off by the strong smell.
Flies are attracted to lay their eggs in dirty, urine- or dung-stained wool, and on wounds. The emerging maggots eat the flesh of the living sheep. If untreated, the sheep will die from secondary complications such as septicaemia or toxaemia. Fly strike can be prevented by crutching to remove dirty wool from the sheep’s tail, and by dipping.
Lambs’ tails are removed, generally at an early age, to reduce faecal contamination of this area and reduce the risk of fly strike. The most common and humane method is to put a rubber ring around the tail, or it can be cauterised or cut off. Ram lambs are usually castrated at the same time.
The sheep louse (Bovicola ovis) spends its entire life cycle on the sheep. Lice numbers can build up to create a heavy infestation in autumn and winter. Infected sheep can be seen rubbing against fences and often leave behind tags of wool. A lice infestation downgrades the quality of wool and the pelt. The best way to control lice is by dipping all the sheep on the farm three to four weeks after shearing, or by using a pour-on dip immediately after shearing.
The sheep ked (Melophagus ovinus) is often called a tick, but is a wingless, bloodsucking fly. Its entire life cycle is spent on a sheep, and if dislodged it can survive only about four days. Blood loss from a heavy infestation of keds can cause anaemia in young lambs and reduced production in older sheep. Reduced capillary flow to the skin lowers the quality and quantity of wool, while ked faeces and pupae give it a dirty appearance. Ked numbers build up in cool weather in full-woolled sheep.
Keds can be controlled using a pour-on dip immediately after shearing or a saturation dip three to four weeks later. This parasite has largely been controlled by the annual dipping for lice that was compulsory until the 1980s, and is unlikely to be a problem in the future.
Facial eczema is a serious disease characterised by photosensitisation (sunburn). It is caused by the fungus Pithomyces chartarum, which develops on pasture and produces a toxin (sporidesmin) that damages a sheep’s liver. Spore numbers increase in warm, humid weather in late summer and autumn in the North Island, and occasionally in the top third of the South Island. Spores in pasture and sheep can be counted to assess the risk of disease.
A pasture fungus (Fusarium sp.) capable of producing an oestrogenic compound, zearalenone, is found throughout the country and can cause infertility in ewes.
These include scabby mouth, a virus generally spread after thistle prickles or other trauma has irritated skin and lips, and periodontal disease, which results in loose teeth, especially incisors.
One of the earliest serious threats faced by New Zealand farmers was bovine pleuro-pneumonia in cattle, which appeared in the South Island in 1864. The gravity of the disease was recognised, and it was eradicated by slaughtering the affected animals.
Bovine tuberculosis (TB) is a dangerous illness, and controlling it is important for the farming industry as well as the health of farmers. TB is a chronic, infectious bacterial disease caused by Mycobacterium bovis, which can take years to develop and results in weakness, coughing and weight loss.
In 1961 a compulsory control programme was set up for herds supplying town milk, and by 1970 all cattle were being tested. Voluntary testing of beef herds began in 1968, and by 1977 it was compulsory for all beef cattle to be tested. The Animal Health Board has responsibility for TB control.
A herd is classified infected if TB has been confirmed by testing or post-mortem. A herd is classified as ‘suspended’ if TB is suspected and further confirmation is being sought, if it has received stock from an infected herd or one with unknown status, or if testing obligations have not been met. For an infected herd to be reclassified as clear, the whole herd must have two consecutive clear tests, with a minimum of six months between tests and no further evidence of disease. A herd’s classification will determine what tests are carried out and whether controls are put on its movement.
Eradicating TB in cattle is complicated because the disease can be transmitted by ferrets and wild possums, which are abundant. In the late 1960s TB was diagnosed in brushtail possums (Trichosurus vulpecula), and since 1972 major effort has gone into controlling them. Infected possums tend to occur in clusters, depending on an area’s vegetation type and topography. Estimates of infection therefore vary, and usually range from 2–5%, although one five-year study in an area of the North Island indicated that 11% were infected. Cattle contract the disease when they come across a dying possum and sniff or lick it.
Although the disease has not been eradicated from cattle, regular testing means it is well under control. Cattle cannot be moved from one district to another without a permit. The control programme aims to have less than 0.2% of herds infected by 2013.
Bovine brucellosis causes abortions in cattle. In 1989, after 23 years of control measures, it was declared eradicated.
Leptospirosis or lepto (Leptospira pomona) causes abortions, red water (haemoglobinuria or red urine) and death in calves. The bacteria is excreted in the urine and can infect humans if it comes into contact with scratches or cuts, or through soft tissues. There is always a risk of people becoming infected at slaughtering plants. Vaccinating cattle can help control the diseases in both cattle and humans.
Mad cow disease (bovine spongiform encephalopathy) is a chronic degenerative disorder affecting the central nervous system of cattle. It was first diagnosed in the UK in 1986, and has not been found in New Zealand. It is probably caused by a prion (self-replicating protein) spread through contaminated feed. In 1996 researchers linked the disease with the human variant, Creutzfeldt-Jakob disease.
Enzootic bovine leucosis (EBL) is a virus that causes enlarged lymph nodes and can infect almost any organ. A voluntary eradication scheme funded and operated by the dairy industry since 1996 has almost completely controlled the disease.
Mannosidosis is where an inherited, defective enzyme fails to break down complex sugar molecules, resulting in the harmful accumulation of these products. It particularly affects calves of Angus and Murray Grey breeds, and may be evident at birth or develop later. Calves show unsteadiness and lack of co-ordination (ataxia), have a high-stepping gait in the forelegs, or may not be able to stand to suckle. By using blood tests to detect and cull heterozygote animals (those with one normal and one mutant gene), the disease has been reduced to a negligible level.
One of the most common diseases of cattle is bovine viral diarrhoea, caused by a Pestivirus. Although diarrhoea can be a transient occurance in previously unexposed cattle, it can cause abortions, congenital defects, the birth of weak calves and of calves that fail to thrive, as well as mucosal disease and diarrhoea in adult cattle.
Mucosal disease is a severe affliction that produces mouth ulcers, eruptive lesions on the hooves, and fever in 6–24-month-old animals, as well as diarrhoea and dysentery. Current research is looking at the feasibility of a disease control programme.
In cattle this disease is caused by the bacterium Mycobacterium avium spp. paratuberculosis, which is closely related to bovine tuberculosis. Johne’s disease affects the intestines, leading to diarrhoea, wasting or loss of body condition, and ultimately death. It is present at a low level in many dairy herds. Some infected animals show little or no signs of disease, but pass it on to others.
The disease is difficult to control because there is no accurate test. In 2008, vaccinations were done only where bovine TB was not present in wildlife, because of problems in developing a test that could distinguish between Johne's vaccination and TB. The only other method of control is to restrict contact between infected and uninfected animals.
This disease causes occasional dysentery and lost milk production in dairy cows. Salmonella Brandenburg can also cause abortions.
Colostrum is the first milk produced after giving birth. This special milk is yellow-orange, low in fat, and high in carbohydrates, protein, and antibodies. It is extremely easy to digest and provides perfect nutrition for a newborn, as well as living cells which provide defence against many harmful agents. The concentration of immune factors is much higher in colostrum than in mature milk.
Calves are particularly susceptible to diarrhoea in their first month of life, especially if deprived of colostrum (the first milk produced by the mother). Colostrum is highly nutritious and contains antibodies to help fight infections.
Common infectious causes of diarrhoea in calves are rota virus, Salmonella, Escherichia coli infections and cryptosporidiosis. Some species of Coccidia can affect calves from about four weeks of age. Calves 6–12 months old can develop diarrhoea from yersiniosis (Yersinia pseudotuberculosis or Y. enterocolitica).
Ticks and lice are external parasites of cattle. The tick (Haemaphysalis longicornis) can infest cattle, sheep, goats, dogs, horses, deer, and other mammals including humans, and many species of bird. Adult ticks can cause deaths of cattle, sheep and deer from blood loss. They can be controlled using showers, sprays and pour-on treatments.
The female cattle tick is a dark-brown, eight-legged insect which inserts her mouthpiece through the skin of an animal or human to drink its blood. The tick will balloon from just 2 millimetres wide and 3 millimetres long to over 10 times that size.
Gastrointestinal worms are parasites that live in a cow’s abomasum (fourth stomach) and intestines. Large numbers of them can reduce appetite, skeleton growth and the metabolism of protein and minerals – especially in young animals.
Worms lay their eggs inside the cow, and the eggs are passed out in dung onto the pasture. If the pasture is moist, larvae hatch and are eaten by grazing animals. An infected calf may develop diarrhoea and fail to grow and develop. Beef calves can be treated with an anthelmintic drench at weaning. Dairy calves are treated in spring or early summer, including for lungworm, which causes coughing.
Gastrointestinal worms are difficult to control if they become resistant to drenches. Farmers can avoid the problems associated with resistance if they understand how the various drenches work, and use strategies to minimise their animals’ intake of larvae.
Several organisms can cause abortions in cattle, the most common being Neosporum caninum, a protozoan parasite. Less frequent causes are bovine viral disease and fungi such as Mortierella wolfii, Aspergillus and bacteria such as Salmonella Brandenburg and Leptospirosis. Eating the leaves of macrocarpa (Cupressus macrocarpa) and radiata pine (Pinus radiata) trees can also cause abortions.
Campylobacter fetus (subspecies venerealis) causes early foetal loss, but is rare in New Zealand cattle, probably due to the widespread use of artificial insemination. Trichomonasis is also rare, but has been diagnosed more recently in beef cattle.
Mastitis (inflammation of the mammary glands and reduction in milk) is caused by a bacterial infection. The problem is very widespread and costly to the dairy industry. The main strain of infective bacteria has changed with time – in the 1940s it was Streptococcus agalactiae, by the mid-1960s it was Staphylococcus aureus, and since the mid-1990s Streptococcus uberis and coagulase-negative staphylococci have been the most common bacteria. Mastitis is treated with antibiotics, and can be prevented by hygienic milking, dipping or spraying teats with a mild disinfectant, and injecting long-acting antibiotics into the mammary gland at the end of lactation.
A number of diseases produce nervousness in cattle: listeriosis, haemophilosis, tetanus, malignant catarrhal fever, polioencephalomalacia, ryegrass staggers, lead poisoning, brain abscess, neoplasia and metabolic diseases.
In cows, facial eczema appears as sunburn, especially on lightly pigmented areas such as the udder and teats. This is caused by liver damage after eating the toxin sporidesmin, produced by the fungus Pithomyces chartarum, which grows on pasture in late summer and autumn in the North Island and occasionally the top third of the South Island. Spores in pasture and faeces can be counted to assess the risk of disease.
Fescue toxicosis, fescue foot, fat necrosis and heat stress have all been associated with cattle grazing tall fescue grass infected by the fungal endophyte Neotyphodium coenophialum.
Other fungus-related diseases are Paspalum staggers and Claviceps (ergot) toxicosis.
Lameness in dairy cattle affects milk production, fertility and animal welfare. Lameness, including bruising or abscesses on the sole of the hoof, may be caused by poor-quality raceways, an impatient stockperson bringing in cattle for milking, long walking distances to and from the shed, continuously wet underfoot conditions, and nutritional factors.
Young calves can get lead poisoning if they lick lead paint or batteries. A number of plants are poisonous to cattle, including yew leaves, and acorns. On North Island hill country in particular, cows can be poisoned after eating bracken fern and tutu plants.
Bloat in dairy cows is a major concern to farmers. A cow’s abdomen becomes distended when gases accumulate in the rumen (first compartment of the stomach) after eating clover-rich pasture, and if untreated the cow collapses and may die. Treatment is by oral drench to stabilise the foam, inserting a tube down the cow’s throat to release the gas, or as in earlier days, stabbing the cow in the rumen to release the gas.
Cattle suffer nitrate poisoning when there are high nitrate levels in pasture and brassica crops, especially after dry weather or where a lot of nitrogen fertiliser has been applied in winter or spring. Poisoning occurs because nitrate accumulates at a faster than normal rate in the rumen. Nitrate gets converted to nitrite in the rumen, and is then absorbed into red blood cells, discolouring them and blocking the transport of oxygen. In extreme cases the animal dies from lack of oxygen.
When red blood cells are destroyed they release haemoglobin, which is filtered by the kidneys and released into the urine, turning it red. In grazing animals, this can be caused by a chemical (S-methyl cysteine sulphoxide) in brassica crops.
Early wild deer in New Zealand were generally healthy, as they were well fed and had plenty of space. However, as their numbers increased they began to get diseases associated with malnutrition and stress. Bovine tuberculosis and parasitic infection were widespread in wild herds and became problems from the 1970s when deer were caught for farming. Even so, the death rate of deer on farms is low compared with sheep and cattle. The group at greatest risk are young deer from birth to weaning, and those 10–12 months old at the end of spring. A three-year study of deer deaths on South Canterbury farms, compiled in 2000, showed that 34% of hinds’ and 47% of stags’ deaths were a result of disease.
Some 10–20% of deaths of farmed deer may be due to accidents, so farm facilities and management need to be of a high standard. Many accidents occur in poorly designed deer yards, and a quiet but firm approach when handling deer can avoid harm to animals and handlers.
The government’s Code of Welfare (Deer) describes the minimum standards for handling facilities, feeding and nutrition, and health treatment and care to ensure deer are kept healthy and free of stress.
Malignant catarrhal fever is less common than it used to be, but is a severe disease that cannot be treated and usually causes death. In deer it is associated with a herpes-type virus and probably comes from a form that affects sheep. Stags are more susceptible than hinds, and winter is the worst time for infection. Prevention is the best approach, and this is done by separating sheep from deer, feeding deer well and minimising their stress.
Bovine tuberculosis (TB) probably poses the biggest threat to the deer-farming economy, and also risks the health of farmers and slaughterers. New Zealand has a scheme aimed at controlling and eventually eradicating the disease. The Animal Health Board is responsible for controlling TB and accredits farms after tests are clear. Eradicating TB in farmed deer is complicated because it can be transmitted back to them by cattle, possums and ferrets.
Johne’s disease was first identified in farmed deer in the late 1990s. It is caused by the bacterium Mycobacterium paratuberculosis, which can be passed to deer by cattle and sheep. It is related to TB and their symptoms are similar, which complicates diagnosis of both. Johne’s disease affects the intestines, leading to failure to thrive and in many cases death (up to 20% of infected animals die quickly). In cattle and sheep it does not affect young animals, but in deer it does, especially at the end of winter and other times of stress. In a herd of deer, some infected animals show little or no signs of the disease, but can pass it on to others.
Deer Industry New Zealand and the New Zealand Deer Farmers’ Association (NZDFA) support research and practical activities towards controlling the disease. The NZDFA Johne’s Research Group has written a manual on how to manage the disease and minimise its effects on farms.
A mysterious disease of deer and elk in Canada and the central US appears to be spreading. It riddles the brain of infected animals, which lose condition and die. There is no evidence yet of humans contracting the disease.
Young deer are generally more susceptible to leptospirosis than adults, and some can die. The bacteria can infect humans, and there is always a risk of infection for those working at slaughtering plants. Animals with the disease are treated with antibiotics.
Clostridial diseases (blackleg, pulpy kidney) in deer have similar symptoms to those in sheep and can be prevented by vaccination. Yersiniosis strikes sporadically, and cryptosporidiosis is a recent disease of newly weaned deer.
Lungworm and internal parasites are major problems in young deer, causing failure to thrive and death. Problems are worse when nutrition is inadequate and animals have been poorly managed. These parasites can be treated with regular doses of anthelmintics, given to young deer orally or as a pour-on drench. Drenching can start before weaning in January and should continue every three to six months until natural immunity occurs around 11–12 months of age.
Internal parasites in deer are becoming resistant to drenches. Research is being done to modify drenching programmes and find alternative methods of control.
External parasites of deer include ticks and lice. Nymph (larval) ticks can be a major problem on newborn fawns, causing some deaths. Tick infestations of velvet antler during growth in the spring can be a problem in some years. Shower and spray treatments are available, but these are licensed for cattle and sheep and not usually for deer. An insecticide worn as an ear tag, effective for up to eight weeks, has recently been developed for hinds during the fawning season where there is high risk of infection.
To be healthy, animals need a balanced diet. Livestock need at least 13 mineral elements, or nutrients.
An animal health problem caused by lack of a nutrient is called a metabolic disease because it affects the animal’s ability to convert food into energy and growth. This is distinct from viral or bacterial diseases, which are spread from animal to animal or by other agencies.
The trace element content in pasture is measured in parts per million (ppm). There should be at least 10 ppm of copper, but only 0.25 of iodine, 0.10 of cobalt, and a mere 0.03 ppm of selenium is enough for animals to grow well.
Grazing animals rely on pasture for their nutrition; however, animals and plants have different mineral needs. Pasture plants do not need cobalt, selenium or iodine to grow, but if the soil is low in these then the plants cannot provide enough for animals. Between 1930 and 1960, when agriculture in New Zealand expanded and intensified, trace-element deficiencies of cobalt, selenium, copper and iodine were identified in livestock. Nationally, 13% of pastures are deficient in cobalt and 30% need selenium supplementation for stock growth.
Detecting trace element deficiencies in animals can be difficult because poor growth and reproduction are signs associated with many diseases and nutritional problems. However, the amount of trace elements in the blood or liver is related to growth, and can be tested. A low content means the animal will have poor growth, while a high content means the animal should have a near-maximum growth rate. This is the ‘reference range’ for expected animal production and is particularly useful for managing lambs and calves, which are sensitive to trace element deficiencies.
Applying fertilisers with added trace elements (cobalt, selenium or copper) to pasture is one way of overcoming trace element deficiencies, and is how cobalt deficiency (called bush sickness) is remedied. The trace elements are absorbed by pasture plants, which increase their trace element content over the next three to five weeks. This drops over the 18 weeks after that, so the fertilisers should be applied annually. If animals take in more trace elements than they need, the excess is stored in their liver and other tissues and released when intake is low.
Cud-chewing animals can be treated by giving them a long-acting bolus, or large pill, which remains in their reticulorumen (first and second stomachs). Another method is to inject a small quantity of an element under the skin, which is slowly released into the bloodstream for six months to a year. Oral doses with liquid supplements (drenching) lasts only two to four weeks.
Sometimes the best way to supply minerals to young stock is to treat the pregnant mother. Vitamin B12, selenium, copper and iodine are readily transferred across the placenta and also, with the exception of copper, secreted into the milk. Treating the mother before mid-pregnancy will prevent deficiencies in the young from birth to weaning.
Cobalt deficiency was the cause of bush sickness, particularly on the pumice soils of the North Island, and was widespread among livestock in the early 1930s. It was known as Morton Mains disease in Southland, and Glenhope ailment in Nelson. The condition still occurs, particularly in lambs, and results in appetite loss, poor growth, wasting, failure to thrive and eventual death. Ruminants need cobalt for the production of vitamin B12 by micro organisms in the gut. This vitamin is then absorbed and stored in the animal’s liver. Vitamin B12 is needed for energy and protein metabolism – so cobalt deficiency is really a vitamin B12 deficiency. Lambs seem to need more cobalt than cattle and deer.
Since many New Zealand soils are deficient in selenium, so are the plants that grow in them. Selenium is one of the antioxidants that enhance immune responses and protect against toxic metabolites. A deficiency causes white muscle disease (muscular dystrophy), poor growth in lambs, calves and fawns, low fertility in ewes, and poor milk production in cattle.
Selenium deficiency can be corrected by using fertilisers containing selenium at the rate of 1 kilogram per hectare. A pour-on animal treatment is also available.
Copper levels in pasture are lowest in winter and animals are often tested at this time.
Animals will be deficient if their feed is low in copper, or suffer induced deficiency when copper intake is high but there is high molybdenum content in the feed – the molybdenum interferes with the absorption, use and storage of copper. Cattle and deer are more sensitive than sheep to induced copper deficiency because their requirements are about twice that of sheep.
Copper assists in the formation of the myelin sheath around nerves, and in bone development. Some copper enzymes have antioxidant properties. Copper deficiency causes a nerve disorder (enzootic ataxia), weak bones (osteoporosis) and poor growth in lambs and calves. Fewer lambs and calves are born, and adult cattle can lose weight and suffer bad diarrhoea (peat scours). Livestock can suffer copper deficiency in spring on peat soils when the molybdenum concentrations in pasture are at their highest.
In the 1920s and 1930s people in much of New Zealand had mild to moderate iodine deficiency. In some areas up to 30% of schoolchildren had goitre. The introduction of iodised salt in 1939 helped to eradicate this by the 1950s. In the 1960s, milk-equipment cleaners contained iodine, which was absorbed by the milk. These are no longer used, and salt intake has also diminished. Recent studies show that adults may be becoming mildly deficient in iodine again.
Iodine deficiency causes an enlarged thyroid gland (goitre) in the neck of newborn animals, particularly lambs. Goitrous thyroid glands grow larger to compensate for insufficient iodine in the blood. Humans show the same effects of iodine deficiency.
Most iodine deficiencies occur when brassica crops are fed to pregnant ewes during the second half of their pregnancy. These crops are low in iodine and contain chemicals which interfere with the use of iodine by the thyroid gland. Deficiency results in lower lambing and a higher death rate of newborn lambs. Adding iodine to the diet corrects the problem.
A shortage of calcium in ewes, but more commonly in breeding cows, and especially older, high-producing cows, causes milk fever or parturient paresis (hypocalcaemia). It can be triggered by stress or a sudden change of feed. Animals with milk fever become restless, suffer lost appetite, muscle tremors and staggers, and usually die if left untreated. Most pastures in New Zealand provide animals with enough calcium, but the sharp increase in demand for this mineral by cows at the start of lactation in early spring can lead to deficiency. Cows with milk fever should be injected under the skin with calcium borogluconate and kept warm.
In March 2007 the Hopkirk Research Institute was opened at Massey University to accommodate up to 400 scientists working on animal diseases. Bovine TB, Johne’s disease, and the development of parasite-resistant drenches were highlighted as priorities for the AgResearch and Massey University Veterinary School staff who will work there.
Grass staggers or grass tetany (hypomagnesaemia) is caused by a shortage of magnesium in the diet and an impaired ability to absorb magnesium by lactating sheep and cows. Animals with grass staggers have body tremors, walk with a stiff-legged gait, and are liable to collapse on their side kicking their legs in a paddling motion. Affected cows are injected under the skin with magnesium chloride. To limit grass staggers in a herd their diet should be supplemented with magnesium three to four weeks before calving, and up to 12 weeks afterwards, by dusting pasture or hay with magnesium oxide, or adding magnesium to drinking water. The absorption of magnesium and calcium is affected by too much potassium in the diet, so farmers avoid using large amounts of potassic fertilisers in spring.
Sleepy sickness or twin lamb disease (acetonaemia or ketosis) is the most common metabolic disease of sheep in New Zealand. It occurs in the weeks before lambing, and ewes carrying two or more lambs are particularly at risk. Signs include lethargy, staggering and not eating. The main cause is underfeeding in late pregnancy. The best prevention is to scan pregnant ewes and give those carrying multiples more feed near lambing.
Davidson, R. M. ‘Control and eradication of animal diseases in New Zealand.’ New Zealand Veterinary Journal 50, no. 3 (2002): supplement, 6–12.
Parton, K., and others. Veterinary clinical toxicology. 3rd ed. Palmerston North: VetLearn, Massey University, 2006.
Pomroy, W. E. ‘Anthelmintic resistance in New Zealand: a perspective on recent findings and options for the future.’ New Zealand Veterinary Journal 54 (2006): 265–270.
West, David Michael, and others. The sheep: health, disease & production: written for veterinarians and farmers. 2nd ed. Palmerston North: Veterinary Continuing Education, Massey University, 2002.