Cattle Diseases Guide:

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Abortion
Cows can suffer abnormalities during pregnancy leading to mummification of the foetus or resulting from maternal or foetal abnormality. All cases where the pregnancy terminates early and the foetus is expulsed are called abortions.

As there are multiple causes of abortion and the detection of abortions in a herd can vary significantly depending on the husbandry system and calving pattern, the incidence of abortion at herd level also varies markedly. It has been suggested that an abortion rate of 5% or more in a herd should be considered an indication of an abortion problem (Deas, 1981).

The causes of abortion have been classified by Boyd and Gray (1992) as follows:

Infectious:
Non-specific
Specific
Miscellaneous:
Drug-induced (prostaglandins)
Insemination/intra-uterine infusion
Hypothyroidism
Trauma/stress (transport, noise, veterinary treatment etc.)
High fever and endotoxins (toxic plants, nitrate/nitrite, fungal toxins, other disease)
Nutritional (malnutrition, vitamin A/selenium/vitamin E deficiency, goitre)
Twin pregnancy
Genetic (malformation)
Both non-specific and specific infectious causes of abortion can lead to "abortion storms" in a herd, whereas the miscellaneous causes often result in sporadic, individual cases.

The most important infectious abortion agents are:
Salmonellosis (particularly Salmonella dublin)
Listeriosis
Leptospirosis
Neospora caninum abortion
Bovine Viral Diarrhoea (BVD)
Infectious Bovine Rhinotracheitis (IBR)
Campylobacteriosis (see below)
Fungal/mycotic abortion (see below)
Epizootic/chlamydial abortion (see below)
Trichomoniasis (see below)
Brucellosis (see below)
Campylobacter jejuni is seldom reported as a primary cause of abortion in cattle in the UK. This may be due to the limitations of current diagnostic procedures. It has been suggested that the pathogen may be a significant cause of infertility in suckler herds.

Fungal abortions are associated with contaminated feed and are either sporadic or occur in small outbreaks, typically between the fifth and seventh months of pregnancy.

Epizootic abortion in cattle, caused by Chlamydia spp., has been reported in the UK in recent years and is seen as an emerging cause of contagious abortion in cattle.

Abortions caused by trichomoniasis and brucellosis are extremely rare in the UK, as both diseases have been subject to statutory disease control measures. Brucellosis is a notifiable disease and its control is still carried our as a statutory measure under the Brucellosis Order.

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Acetonaemia
 The NADIS data show that the number of cases of acetonaemia (or ketosis) increase significantly during the winter, and the number of cases continue to increase until turnout. So it is particularly important to look out for acetonaemia until at least a month after turn-out.

Like most metabolic diseases it is important to remember that for every cow that shows clinical signs, there will be several more which are affected sub-clinically.
What is acetonaemia?
Acetonaemia occurs when the cow's energy intake does not match its requirement and the cow is unable to compensate and mobilises its body reserves too quickly. In the beef cow, this is most likely to occur in late pregnancy when the cow's appetite is at its lowest and the energy requirement of the growing calf near its peak. In the dairy cow, the mismatch between input and output usually occurs in the first few weeks of lactation, because the cow is not able to eat enough to match the energy lost in the milk.
Clinical Signs
Reduced milk yield: Initially a moderate decline, eventually a sudden drop
Body condition and weight loss
Reduction in appetite (initially non-forage feeds)
Dull, stary coat
Firm, 'waxy' dung
Acetone (pear drop) smell of breath or milk - not always detectable
Temperature, pulse rate and respiratory rate usually normal
A few develop nervous signs including excess salivation, licking, incoordination, aggression.
Acetonaemia is more common in the dairy cow, probably because the energy difference of the lactating cow is more difficult to overcome than that of the pregnant cow, which means that most dairy cows in the UK are in negative energy balance during the first few weeks of lactation. Acetonaemia occurs when the cow is not able to cope with this energy deficit, either because it is too great or if it continues for too long.

If it occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from an energy deficit that is significantly reducing their productivity. A clinical case of acetonaemia is the tip of the iceberg, and therefore it is advisable to discuss blood testing other cows in the same lactation group, for the subclinical form of the disease.

Prevention
Each treated cow is the tip of the iceberg, so prevention is very important. The aim of any prevention regime is to maximise dry matter intake during the critical period. This can be achieved by:

Avoiding over-fat and over-thin cows: Aim to calve cows at condition score (CS) 3.0. Fat cows have lower appetites and mobilise more fat and so are more prone to ketosis Dry-off cows at CS 3.0. Cows should not gain or lose weight during the dry period. Thin cows should be fed to gain condition during late lactation. Fat cows should be fed to lose condition during late lactation.
Preventing disease around calving. Cows with calving difficulties, retained membranes, endometritis, milk fever, toxic mastitis, and hypomagnesaemia all have an increased risk of acetonaemia, so preventing these diseases reduces the risk of acetonaemia.
Feeding correctly Introduce the milking ration to the dry cows from two weeks before calving. This allows the rumen time to adapt to the milking diet Maximise palatability. Good quality forage and feeding as a total mixed ration both increase intake and thus reduce the energy deficit Maximise feeding time. Increasing the feeder space, particularly for self-fed silage, can increase intake and thus reduce energy deficit Keep the diet consistent. Avoid sudden changes to the diet even if only batch changes of concentrate.
Reduce stress Keep freshly-calved cows separate from the milking herd for at least two weeks after calving. Acetonaemia is a significant cause of economic loss, but these losses can be reduced by good management and attention to detail.
Early treatment leads to early recovery, so treat as soon as possible Veterinary advice should be sought to ensure that displaced abomasum is ruled out as a cause of the acetonaemia.

If acidosis occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from sub-clinical acidosis that is significantly reducing their productivity. A clinical case is the tip of the iceberg, and therefore solutions have to be for the whole herd not the individual animal.

Many diseases have been linked to acidosis. For some, such as liver abscesses, the evidence is very strong. For others, such as sole ulcer and white-line disease, the link is not so strong.
Diagnosis
Difficult as signs are non-specific
Ketosis (acetonaemia) must be ruled out
Reduced milk fat is strongly indicative of excess starch feeding
Most diagnoses are based on eliminating other causes of reduced appetite and yield

Treatment
Most treatment is supportive to allow the rumen to return to normal
Ruminal stimulants are of little value
Feeding of buffers such as sodium bicarbonate can help in the short term, particularly in animals in the same group.
Prevention.
Every treated cow is the tip of the iceberg, so prevention is vital. The aim of any prevention regime is to give the cow time to adapt to change and not to expect the rumen to be able to adapt to whatever is thrown at it.

There are two types of sub-acute acidosis. The first occurs in freshly calved cows (up to 20 days after calving). This occurs because of a failure to adapt the rumen to the lactation diet before calving. In this case, dry cow management is the key to prevention. In particular, feeding a transition diet and minimising calving stress are important.

The second type of acidosis affects cows from peak to mid-lactation. At this time rumen adaptation to the diet should have occurred, so acidosis in these cows occurs as a result of feeding diets that are low in fibre and high in starch (or which allow for feed selection).

In all herds with an acidosis problem there needs to be a full assessment of the feeding, with attention paid to what the cows are being fed and to what they are eating. Each individual situation will be different and require a different range of solutions. Nevertheless there are several factors which are likely to be of importance in most situations:

Forage to concentrate ratio. Except in very high yielding cows a ratio of 60:40 will significantly reduce the risk of acidosis
Feeding total mixed rations with forage and concentrates mixed can significantly reduce acidosis, provided selection of the concentrate portion doesn’t occur
Feeding space: If there is insufficient space average meal size will increase, increasing the risk of acidosis (even with a TMR). (This can also occur if feeding time is restricted or if feeding times are irregular).

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Acorn Poisoning
 
The NADIS data show that acorns are one of the commonest causes of plant poisoning especially late summer in years when acorns are abundant. As the autumn continues with stronger winds and gales the problems are can increase.


Clinical Signs
Sudden death can occur (although poisoning generally occurs over a period days)
Constipation initially, followed by black watery diarrhoea.
Depression and loss of appetite
Straining to pass faeces and urinate is very common
Weakening, collapse and death (usually within seven days of the onset of signs)
The animals have a normal temperature in most cases
Acorns can cause birth defects if eaten in sufficient quantities by pregnant cattle Acorns contain gallotannin. In the rumen, gallotannin is broken down to gallic acid and tannic acid. Tannic acid causes ulcerations in the mouth, the oesophagus, and the rest of the intestines. It also damages the kidneys, and it is kidney failure which causes most of the death associated with acorn poisoning. Acorn poisoning will generally affect only a few animals in the herd, as acorn poisoning only occurs if animals eat large amounts of acorns (which will only occur in cattle which develop a taste for them). As tannins concentrate in milk fast-growing calves on heavy-milking dams will often be the first animals to show signs.
Diagnosis
On the clinical signs described above
Finding large amounts of acorns and/or oak leaves at post mortem (although in advanced cases this may not be the case)
In live animals, blood and urine tests can identify those with kidney failure
Treatment
There is no specific antidote for acorn poisoning.
If the cattle are removed from the acorn pasture in the early stages, most cattle will recover in two to three days
Good supportive therapy is the only treatment available: a) Fluid therapy: Oral and intravenous fluids will help keep the kidney functioning b) Broad-spectrum antibiotics to prevent secondary infection c) A single dose of a laxative mineral oil may help in the early stages
Cattle that survive are often economically worthless, so euthanasia may be the best option in more severe cases
Prevention
Feeding 1kg/head/day of calcium hydroxide (hydrated lime) can significantly reduce the risk of poisoning


However, anticipation of outbreaks, fencing off oak trees and removal from pasture are still the best option

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Anthrax
In the UK, all cases of unexplainable sudden death have to be reported to the Divisional Veterinary Office, so that a decision can be made whether the animal is to be tested for anthrax as sudden unexplained death is the most common presentation of anthrax in cattle.

However, although the number of cases of sudden death has increased there have been no cases of anthrax in cattle for over three years. However, it is important that owners and stock people are aware of anthrax, as contact with animals or animal products is, despite the recent American outbreak, still the most important cause of human anthrax.

Clinical Signs
Sudden death (often within 2 or 3 hours of being apparently normal) is by far the most common sign
Very occasionally some animals may show trembling, a high temperature, difficulty breathing, collapse and convulsions before death. This usually occurs over a period of 24 hours
After death blood may not clot, resulting in a small amount of bloody discharge from the nose, mouth and other openings
Diagnosis
On the clinical signs described above
Rod-shaped bacteria surrounded by a capsule are visible in blood smears made from surface blood vessels
Post-mortem examinations should not be undertaken on suspected anthrax cases (including any cow that has died suddenly for no apparent reason) until a blood smear has proved negative)
If a carcass is opened accidentally, the spleen is usually swollen and there is bloodstained fluid in all body cavities Suspected anthrax cases are covered by the Anthrax Order 1991 (which replaced the Order of 1938). Any suspicion of the disease must be notified to the DEFRA Divisional Veterinary Manager (DVM), who if they see fit will instigate a veterinary enquiry to determine whether anthrax is present on the farm. Usually the DVM will arrange a visit (often by the ownerfs own vet) to take a blood sample to look for bacteria with capsules. The animal or carcass must not be moved before this has been done, fines will be levied if movement does occur. If the tests prove negative, the veterinarian will send in a certificate stating this and nothing further will happen. If anthrax is still suspected then orders banning movement and requiring disinfection will be instigated.
Treatment
Due to the rapidity of the disease treatment is seldom possible
High doses of penicillin have been effective in the later stages of some outbreaks
Prevention
Infection is usually acquired through the ingestion of contaminated soil, fodder or compound feed. Sterilisation of meat and bone meal used in animal feed (and more recently its complete removal from cattle feed) has been the main factor responsible for the rarity of anthrax in the UK over the last few years.

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Babesiosis (Redwater fever)
This parasitic disease is usually first reported in May/June when its tick host first becomes active.
What is Babesiosis?
Babesiosis is an infection of the red blood cells by a single cell parasite of the genus Babesia. In the UK, babesiosis is usually caused by Babesia divergens. The disease is spread between cattle by ticks (Ixodes ricinus in the UK). The babesia is injected into the bloodstream by the tick and then invades the red blood cells and begins dividing, eventually rupturing the cell. Clinical signs begin around 2 weeks after infection.

Babesiois is rare except in known tick areas. However in these areas even though disease is often relatively mild there is a significant imact on productivity and fertility in affected cattle.

Clinical Signs
Increased temperature
Diarrhoea which ceases after around 36 hours and then becomes constipation
Red urine (due to haemoglobin produced by the rupture of the red blood cells) which becomes darker with time
Increased pulse rate
Abortion of pregnant cows
Death is rare in babesiosis in the UK.
Diagnosis
On the clinical signs described above
Recent movement to pastures known to harbour ticks
Blood smears can show up the parasite
Treatment
Mild cases may recover without treatment.
More severe cases need treatment. This is often best combined with a preventative treatment for the as yet unaffected cattle. This choice is best made on an individual farm basis in consultation with your vet.
Prevention
Identification of risk areas
Prophylactic treatment of cattle about to be moved to a risk area
Tick control
Vaccine not yet available in UK

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Blackleg
Clostridia are group of anaerobic, spore-forming organisms found in the soil/environment, which produce rapidly fatal disease by secretion of potent toxins. Conditions such as botulism, blackleg, bacillary haemoglobinuria, malignant oedema and tetanus are all caused by clostridia.

Botulism

Botulism is a lethal food poisoning in cattle caused by eating material that contains Clostridium botulinum toxins. The incubation period before clinical signs appear varies from a few hours to two weeks, making it difficult to identify the causative material eaten by affected animals. The most common manifestation of the disease in cattle is a subacute disease with restlessness, incoordination and difficulty to swallow developing into recumbency, paralysis and death within 1-7 days.

The bacteria and the disease occurrence are world-wide. In the UK, cases are likely to occur either due to ingestion of contaminated silage or contact with animal carcasses or skeletons of dead animals containing the toxin. The use of poultry litter as fertiliser on cattle pastures has been identified as a risk factor, due to the poultry mixed with the litter.

Bacillary haemoglobulinuria

Bacillary haemoglobulinuria is a rapidly fatal disease caused by C. oedematiens type D. The disease is associated with liver damage primarily caused by liver fluke. The condition is fairly rare in the UK. Young stock or dry cows inspected less regularly are often found dead. In lactating cows, a sudded drop in milk yield associated with high fever is seen. Other clinical signs include ruminal stasis with or without apparent abdominal pain, rapid breathing, dark red urine, jaundice and death within a short time of the onset of clinical signs.

Spores of C. oedematiens type D can be found both in the soil and in the livers of normal cattle on farms where the disease occurs.

Blackleg

Blackleg infection is caused by Clostridium chauvoei and is almost allways associated with wound infection in cattle. Most cases occur in young stock between 10 months and two years of age. Feet or legs and the tongue are often the predilection site. Within 48 hours there is a high fever and if limb muscles are involved the animal becomes stiff and unwilling to move. Skin discolouration, subcutaneous oedema and gas production may be present and perineal oedema is sometimes seen. Infections of the head may produce marked oedema and even bleeding from the nose. Death usually follows a period of anorexia, profound depression and prostration.

The spores of C. chauvoei survive well in the soil.

Malignant oedema

Malignant oedema is caused by the infection of wounds with bacilli of the genus Clostridium (C. oedematiens type A; C. chauvoei; C. perfringens; C. sordellii; C. septicum). The condition is fairly rare and sporadic, but outbreaks involving several animals may occur after an event that has caused bruising or wounds (e.g. penning for a short period). Clinical signs appear rapidly after infection and at the site of infection a swelling will develop which will 'pit' on pressure. Gas may be detected, as the skin becomes darkened and tenser. A high fever is present and toxaemia develops. The animal dies within 1 - 2 days.

Tetanus

Tetanus is caused by the toxin tetanospasmin released from the spore-forming bacillus Clostridium tetani. The disease in cattle occurs most often after surgical intervention or difficult calving after spores gain entry to a wound. Germination of spores occurs only if the microenvironment is anaerobic. After germination of the spores within the wound the C. tetani bacilli proliferate and produce toxin.

The incubation period can be very variable from 3 days to several months but most cases occur usually after about 10 days. At first the animal appears slightly stiff, becomes unwilling to move and develops a fine muscle tremor. The temperature rise is variable (39 - 42°C). The general stiffness of the limbs, head, neck and tail increases after 12 - 24 hours. The animal shows hyperaestesia and repeated spasms. Mastication becomes difficult due to tetany of the masseter muscle (lockjaw), food is chewed with difficulty, the animal drools saliva and bloat often occurs. There is retention of the urine and constipation. The animal becomes recumbent, with the legs rigidly extended, opistotonos and the jaws become rigid. The animal usually dies due to respiratory failure 3 - 4 days after the onset of clinical signs. Milder cases, which develop more slowly, can recover over a period of weeks or even months.

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Blackleg (Clostridial myositis)
Cases of blackleg often increase when animals are turned out or moved to new pastures, so farmers need to be aware of the signs so that action can be taken to prevent further disease

What is Blackleg?
Blackleg is a highly fatal disease of muscle caused by the bacterium Clostridium chauvoei. Infection begins when bacterial spores are eaten (usually as result of eating soil, but occasionally from contaminated feed). These spores enter the bloodstream and travel to organs and tissues throughout the body (particularly muscles). They remain dormant until a trigger (usually an injury) stimulates them. The trigger reduces blood flow and thus the supply of oxygen to the tissues. In the absence of oxygen the bacteria multiply and produce a local infection. As they grow, the bacteria produce poisons that destroy the surrounding tissues. This damage shows as the characteristic black muscle with gas. The poisons do not stay in the muscle but enter the bloodstream, resulting in animal that very rapidly goes downhill and dies. The disease is most commonly seen in calves between six months and two years of age, but occasional cases are seen in adults and it can occur in younger animals (particularly if they have not had sufficient colostrum). Disease is definitely more common in animals that are growing well
Clinical Signs
Lameness may be seen before death if you’re lucky
In a few cases the first sign seen is tongue and throat swelling with the tongue protruding
However, the most common sign is sudden death in an otherwise apparently normal animal
The carcass often looks like a much less fresh carcass, with bloating and gas under the skin
Bloody discharge from the nose, mouth and other body openings are also seen
Diagnosis
A post mortem is essential to diagnose blackleg. Many other diseases cause sudden death and need to be ruled out. The most important of these is anthrax, which must be ruled out before a PM is done
The changes in the muscle are characteristic, but the extent of the damage can vary considerably. Some cases have black oozing muscle throughout the hindquarters, others have much smaller areas of damage which may not involve the limbs at all.
It is worth getting further lab tests done to confirm it is Cl. chauvoei as other clostridial bacteria can cause similar muscle damage Don’t do a PM on farm. Opening the carcass can liberate bacteria which will form spores to contaminate the ground and subsequently infect other cattle.
Treatment
In very early cases very high doses of penicillin may prevent death, but the extent of muscle damage means that in most cases this will not be economic
Prevention
As the bacteria are present in the soil, preventing access to soil by not grazing freshly sown pastures with youngstock can reduce the risk, but vaccination is really the only effective means of controlling blackleg. The main choice is between vaccination against Cl. chauvoei alone or with vaccines that are effective against other clostridial disease. Ask your vet for advice

With clostridial vaccines, like all vaccines, care should be taken to follow the manufacturers' instructions. The best protection is a two-dose course followed by annual revaccination. Other regimes can be effective but check with your vet before using these. Vaccination takes 10-14 days to become effective, so it’s best to vaccinate before a problem occurs or a risk period is encountered.

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Bloat In Cattle
There was an increase in the number of reports of bloat from NADIS vets this spring. Bloat is most commonly seen in spring and autumn, when grass growth is at its peak. It is one of the most common causes of death in adult cattle at grassp>

What is bloat?
Bloat is simply the build up of gas in the rumen. This gas is produced as part of the normal process of digestion, and is normally lost by belching (eructation). Bloat occurs when this loss of gas is prevented. There are two sorts of bloat. The least common type is gassy bloat, which occurs when the gullet is obstructed (often by foreign objects such as potatoes) or when the animal can’t burp (such as with milk fever or tetanus). The second type of bloat is frothy bloat, which happens as the result of a stable foam developing on top of the rumen liquid, which blocks the release of the gas. This is by far the most common form of bloat, and unlike gassy bloat, it is highly seasonal with peaks in the spring and autumn. This is because the foam is formed by breakdown products from rapidly growing forages (particularly legumes such as clover and alfalfa). These increase the viscosity (stickiness) of the rumen fluid and prevent the small bubbles of gas formed by rumen fermentation from coming together to form free gas that can be belched off

Clinical Signs
Distended left abdomen is the most obvious sign
Usually associated with pain, discomfort, and bellowing.
Death can occur within 15 minutes after the development of bloat
Gaseous bloat is usually seen in one or two animals. Frothy bloat can affect up to 25% of cases
In some cases sudden death may be the first sign seen by the stockman, although in such cases it is likely that there will be other cattle with bloat that are still alive
Diagnosis
On the clinical signs described above
History of access to lush pasture
Passing a stomach tube will distinguish between gassy and frothy bloat. If it’s gassy bloat a stomach tube passed into the rumen will allow the gas build-up to escape through the tube. No such gas is seen in frothy bloat.
Treatment
Passing a stomach tube is the best treatment for gassy bloat. Once the gas has been released, the cause of the obstruction should be looked for.
In a few cases a trochar and cannula punched through the side into the rumen will relieve gassy bloat when a stomach tube has not worked. But such cases are rare, and as the trochar provides a tremendous opportunity for introduction of infection, it should only be used as a last resort.
For frothy bloat, antifoaming agents that disperse the foam should be given by stomach tube. Old-fashioned remedies such as linseed oil and turpentine are effective but newer treatments such as dimethicone or polaxolene are easier to give as the effective dose is much smaller.
If an outbreak of frothy bloat occurs all cattle on that pasture should be removed immediately and put onto a high fibre diet (hay or straw), and any cows showing bloating signs treated with an anti-foaming agent. The pasture should not be grazed for at least ten days.
Prevention
It is much more effective to prevent bloat than treat affected animals. Management and planning can significantly reduce the number of cases. To prevent frothy bloat: 1)
If possible avoid using high-risk pastures at high-risk times. Pastures with a history of bloat problems or with a high clover content should not be used for cows soon after turnout.
Stagger turnout with buffer feeding as this will allow the rumen to adapt to the new diet. In particular try and keep up fibre intakes at risk periods.
If you have to use high-risk pastures, introduce the cattle to them slowly. In some cases restricting access to as little as ten minutes per day at the start may be necessary to prevent bloat.
Avoid starting to graze high-risk pastures when they are wet.
Administer anti-foaming agents daily if bloat is a severe problem. If this is the case and you can strip graze then spraying antifoaming oils (emulsified with water) onto the grass can significantly reduce labour costs.
Remove high-risk animals. Some animals have recurrent bloat despite prevention and treatment.

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Bluetongue (BTV)
Bluetongue is an insect-borne, viral disease primarily of sheep, occasionally goats and deer and, very rarely, cattle. The disease is non-contagious and is only transmitted by insect vectors. The disease is caused by a virus belonging to the family Reoviridae.
Species affected
Primarily a disease of sheep but other species such as goats, cattle, buffaloes, camels, antelopes and deer can be infected. Humans are not affected.
Distribution
The virus is present in most countries of Africa, the Middle East, India, China, the United States, and Mexico. Bluetongue virus infection, without associated clinical disease, is present in Southeast Asia, Papua New Guinea, northern South America and northern Australia. A strain of bluetongue virus was first identified in Australia in 1975 from trapped insects but despite its long-term presence, it has not caused any clinical disease.
Key signs
The disease is characterised by fever, widespread haemorrhages of the oral and nasal tissue, excessive salivation, and nasal discharge. In acute cases the lips and tongue become swollen and this swelling may extend below the lower jaw. Lameness, due to swelling of the cuticle above the hoofs and emaciation, due to reduced feed consumption because of painful inflamed mouths, may also be symptoms of this disease. The blue tongue that gives the disease its name occurs only in small number of cases. Convalescence of surviving sheep is slow. The high fever in sheep results in wool breaks, which adds to production losses.
Spread
The virus cannot be transmitted between susceptible animals without the presence of the insect carriers. The incidence and geographical distribution of bluetongue depends on seasonal conditions, the presence of insect vectors, and the availability of the susceptible species of animals. The insect carriers, biting midges, prefer warm, moist conditions and are in their greatest numbers and most active after rains.
Persistence of the virus
Bluetongue virus does not survive outside the insect vectors or susceptible hosts. Animal carcases and products such as meat and wool are not a method of spread. Survival of the virus within a location is dependent on whether the vector can overwinter in that area.
Control strategy
The strategy is to contain the outbreak and minimise trade impact by:
using a combination of quarantine and movement controls to prevent spread
treatments and husbandry procedures to control vectors, reduce transmission and protect susceptible animals
tracing and surveillance to determine the extent of virus and vector distribution
zoning to define infected and disease-free areas.
There is no justification for stamping out but some animals may need to be destroyed for welfare reasons. It is not possible to eradicate the bluetongue vectors.

Note: The Exotic Animal Disease Response Agreement only apply to bluetongue disease in its classical virulent form.

© The State of Queensland (Department of Primary Industries and Fisheries) 1995 - 2007.
Post-Mortem Blue Tongue Pictures
Bluetongue is an insect-borne viral disease to which all species of ruminants are susceptible. The virus is transmitted by a small biting midge of the Culicoides genus rather than from animal to animal. The virus does not affect humans. Bluetongue is a notifiable disease and, where suspected, should be reported to Animal Health.

VLA is involved in the surveillance for the disease and was responsible for the detailed post mortem examinations of the first cases in the UK. The images below illustrate the pathology associated with this disease as shown by the first 3 cattle cases in East Anglia.

 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive superficial erosion of the muzzle with a mucopurulent nasal discharge
 
 
Cow 1 bluetongue case – clinically affected Highland cow. Diffuse reddening of the dental pad with multifocal haemorrhages on the upper lip and dental pad
 


 
Cow 1 bluetongue case – clinically affected Highland cow. Ocular discharge visible at the medial canthus (wrinkling of the cornea reflects post mortem change)


 
 
Cow 1 bluetongue case – clinically affected Highland cow. 'Coronitis’: skin reddening around and above the coronary band intensifying distally with serous crusting at the coronary band
 


 
Cow 1 bluetongue case – clinically affected Highland cow. Multifocal haemorrhages with oedema visible on the cut surface of the submandibular lymph node
 
 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive ecchymotic subepicardial haemorrhages


 


 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive subendocardial haemorrhages in the left ventricle






 
 
Cow 2 bluetongue case – Gloucester cow. Identified as PCR positive. Multiple pinpoint haemorrhages in the skin around the bases of the teats. There were also scattered petechial haemorrhages on the skin of the ventral abdomen. No other lesions distinctive of bluetongue were seen in this cow
 


 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive necrosis at the mucocutaneous junction of the nares.





 
 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive area of haemorrhage (with associated ulceration not clearly visible in this image) on the ventral surface of the tongue. There are multifocal pinpoint haemorrhages covering most of the ventral surface of the tongue
 


 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive haemorrhage involving the bulbar conjunctiva with associated subconjunctival petechiation
 
 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Generalised lymph node enlargement with oedema



 

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Bovine Diarrhoea Virus (BVDV)
(BVDV)
BVDV is one of the commonest causes of infectious abortion. It is also associated with a wide range of diseases from infertility to pneumonia, diarrhoea and poor growth. BVDV is normally the most important viral cause of disease in cattle in the UK (at least outside of an FMD outbreak!)

What is BVDV?
BVDV is a member of the family of pestiviruses. Other diseases associated with other pestiviruses include classical swine fever and border disease in sheep. Pestiviruses infect cloven-hoofed stock only, BVDV has been found in pigs and sheep (indeed many cases of border disease are caused by BVDV not border disease virus)

Clinical Signs
Calf diarrhoea
o Mild diarrhoea of a few days duration.
o This was the initial disease associated with BVDV but is rare as a syndrome in the UK.
o In the US a new type of BVDV has been identified associated with outbreaks of severe diarrhoea with very high death rates.


Mucosal disease
o Sudden onset weight loss and inappetance in cattle between 6 and 24 months of age (usually 12 to 18)
o Drooling and salivating
o Profuse foul smelling diarrhoea
o Usually only one or two animals infected at any one time
o Erosions and reddening on gums, cheek, tongue and muzzle
o Over 90% die within 7 days
o Only occurs in calves persistently infected while in the uterus with BVDV


Unthrifty calves
o Small at birth or fail to grow properly
o May be blindness, incoordination
o Hair loss or abnormal hair
o Other defects such as bulldog face can be present


Calf pneumonia
o BVDV infection suppresses the immune system, so calves with BVDV have a significantly higher risk of developing viral pneumonia
o Pneumonia generally more severe than that caused by infection with other viruses alone


Infertility
o Infection <16 days after service – apparently normal return to oestrus but reduced herd pregnancy rate
o Infection >16 days after service, but in early pregnancy – embryo loss and delayed return to oestrus
o Infection mid to late pregnancy – abortion or stillbirth
o Not all pregnant cattle infected by BVDV will show infertility, some will fight off infection and have normal calves
o Other cattle, particularly if infected before 120 days, will have apparently normal calves but these calves will be
persistently infected spreading the virus and being at high risk of developing mucosal disease. These animals are often referred to as PIs
Diagnosis
BVDV causes such a wide range of disease it is rare to be able to diagnose cause on clinical signs alone (except for IBR infections which can have a characteristic conjunctivitis)
Testing the blood for antibodies and/or virus is the best method of diagnosis.
A paired blood sample for antibodies is useful for pneumonia, diarrhoea and infertility. If the first sample is taken when the animal is ill and the second two to three weeks later, a rise in antibodies suggests that there was active infection
For most cattle with mucosal disease there will be no rise in antibodies. However, because they are persistently infected with BVDV, their blood will be virus positive
Some unthrifty calves will show a rise in antibodies, others will have virus in the blood, but some will have neither. In the latter case a diagnosis of BVDV is made on the presence of other animals excreting virus or having raised antibodies.
Prevention and control
There are two routes for control.

The first and best is to eliminate BVDV from the herd by testing and slaughtering. In most herds BVDV is spread by PIs. Getting rid of these PIs and closing the herd can be significantly economically beneficial. Discuss with your vet the testing options, which can include testing the milk for virus and antibodies as well as the more routine blood testing. The problem with this route is that it may take two or more attempts to eliminate BVDV from the herd and becoming closed is vital because as BVDV is extremely common

The second route is vaccination. This can be used in combination with blood testing. There are two vaccines available in the UK for adult cattle, both of which claim to prevent the effects of BVDV on fertility. Ask your vet for advice as to which vaccine to use and when to use them

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Bovine Spongiform Encephalopathy (BSE)
BSE was first recognised as a separate disease entity in the UK in 1986. The disease agent is believed to be a scrapie-like agent (an infectious protein) that causes destruction of the grey matter in brain, leading to a progressive disease. The main clinical symptoms are hypersensitivity to external stimulus, lack of coordination, wasting and death. The disease has a long incubation period, from 2 to 8 years, and is mostly seen in adult cattle (youngest diagnosed animal 20 months). Stress appears to induce the symptoms in cattle, and many cases are diagnosed around calving and after transport.

It is currently believed that BSE originated from either sheep or cattle infected with a scrapie-like agent. Meat and bone meal made from infected animals was recycled back to susceptible cattle in feed, and infection followed. Changes in the processing of meat and bone meal in the early 1980s is believed to have allowed an increased infectivity build-up in the meal (Bradley, 2000). There is some evidence of maternal transmission of BSE to offspring, but it is suggested that this form of disease spread is not significant (Wilesmith et al., 1997). Other theories about the origin of BSE have been developed, suggesting that factors like organophosphorous dipping rendered some animals more susceptible to infection than others (Purdey, 1994).

The UK has been the main geographical focus of the disease epidemic, which is declining rapidly. Currently, the number of suspected cases per week is 55, whereas in 1993, at the peak of the epidemic, the weekly number of suspected cases was 1000. Almost 180,000 confirmed cases have been identified in the UK since 1986. The majority of these cases (81%) have occurred in dairy herds, whilst only 11% of cases have been reported in suckler herds. There is also a clear geographical distribution within the UK, where the majority of cases have been diagnosed in the south of England and Wales. (Data from a MAFF web site, 28/04/00).

In recent years, some other European countries have experienced an increase in BSE cases, with Switzerland and Ireland leading in the number of identified cases (323 and 424, respectively).

Natural occurrence of BSE in other animal species has been confirmed in several captive ruminant and feline wild animals. A closely similar agent has been found causing spongiform encephalopathy in domestic cats in the UK. The same biological strain type of BSE agents as found in cattle has been identified in three human patients suffering from the new variant CJD in the UK (Bruce et al., 1997).

BSE is a notifiable disease and any suspicion of the disease on the farm should be reported to the nearest State Veterinary Services office immediately. Suspected animals are either put under restriction orders and observed or destroyed immediately. Due to concerns over the link between BSE and new variant CJD, no meat from cattle over 30 months of age enters the human food chain in the UK at the moment. These animals are slaughtered through a specific slaughter scheme and the meat, bones and offal are processed into meat and bone meal and destroyed. Only cattle from the UK beef assurance scheme can be slaughtered for human consumption at over 30 months of age (up to 40 months).

The UKROFS standards (UKROFS) prohibit the purchase of cattle into an organic herd from herds that have had BSE within the past six years. All cohort and offspring of BSE cases on organic units must be removed. The Soil Association further defines that if an animal has been bought since 31 December 1993 from a herd with an unknown BSE histroy, it must be removed.

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Bovine Viral Diarrhoea (BVD)
BVD is a viral disease of cattle caused by a pestivirus (similar to Border Disease virus in sheep and swine fever virus in pigs). It has many different manifestations in a herd, depending on the herd’s immune and reproductive status. Transient diarrhoea, mixed respiratory infection, infertility or abortion and mucosal disease are the most common clinical signs of the disease and can be seen simultaneously in a herd. Due to its varied manifestations and subclinical nature in many herds, the significance of the disease has not been understood until recently, when diagnostic methods improved.

Currently, BVD virus infection is considered to be widespread in the UK cattle herds, causing significant financial losses to affected farms during an outbreak (Pritchard et al., 1989). Paton et al. (1999) report that 95% of 1071 dairy herds in England and Wales were positive for BVD virus antibodies in bulk milk, with 65% of the herds likely to have suffered an outbreak in the recent past and currently having persistently infected animals in the herd.

Apart from causing an outbreak of acute diarrhoea at the time of introduction into a herd, the following short- and long-term effects are caused by a herd infection: infertility, embryonic death, foetal mummification, abortion, congenitally damaged calves and persistently infected (PI) calves that are likely to die of mucosal disease before two years of age. BVD virus has also been identified as an immunosuppressive agent, increasing the risk of infections such as respiratory disease in calves, salmonellosis, interdigital dermatitis and mastitis (Pollreiz al., 1996; Penny et al., 1996; Waage, 2000).

To be able to understand the epidemiology of BVD infection in a herd it is important to know how the virus affects the host at different stages of life:
Adult, non-pregnant cows: acute diarrhoea or no clinical signs;
Adult, pregnant cows, first 3 months of gestation: acute diarrhoea or no clinical signs, foetal loss, abortion, congenital defects in calf or PI calf;
Adult, pregnant cows, mid-gestation: acute diarrhoea or no clinical signs, foetal loss or congenital damage to calf or no effects;
Adult, pregnant cow, last three months of pregnancy: acute diarrhoea or no clinical signs, calf born with antibodies against BVD;
Calves that have not been exposed in uterus: acute diarrhoea or mixed respiratory infections, possibly due to immunosupressive effect of BVD;
PI animals: mixed infections, mucosal disease (usually lethal).
Further information
Further information on Bovine Viral Diarrhoea (BVD) in cattle can be found by following the links below. This information references cattle health and welfare in organic cattle production systems and is part of a compendium on animal

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Bracken Poisoning In Cattle
Many plant poisonings, including bracken poisoning, are common in the autumn. The highest risk period is when grass growth is poor, particularly if this has been combined with bracken control so that rhizomes or new young fronds are available for cattle to eat.

 Bracken contains a variety of toxins. For cattle the two most important are a toxin that depresses the bone marrow, and a cancer–causing toxin. These toxins are still active in hay made from pastures with bracken

Clinical Signs
Acute poisoning
This occurs as a result of eating large quantities of bracken. Disease develops because of depression of the bone marrow, which stops the production of the white cells that fight infection and the platelets that help blood to clot. Signs can up to eight weeks after cattle have stopped eating bracken

Depression and loss of appetite
Bloody diarrhoea accompanied by straining
High temperature
Weakening, collapse and death (usually within five days of the onset of signs)
Secondary infection is very common
Enzootic haematuria This occurs as the result of eating small quantities of bracken over a long period of time. Cancerous changes occur in the bladder leading to:
In mild cases - persistently bloody urine (haematuria)
In severe cases – severe blood loss and difficulty passing urine with visible blood clots
In some animals, cancer occurs in the gut as well as the bladder. The signs depend on the site of the tumour. Get veterinary advice in animals showing unusual gut signs that have had access to bracken
Diagnosis
On the clinical signs described above
History of access to bracken
Blood sample for haematology
In many cases a post mortem will be essential to confirm the diagnosis
Treatment
here is no specific antidote for bracken poisoning.
Broad-spectrum antibiotics to prevent secondary infection can help in acute cases
For animals with haematuria no treatment is effective
Prevention
Limit access to pastures with bracken, particularly if grazing is poor
Never allow cattle access to recently ploughed land where bracken has been. Exposed rhizomes are the most dangerous part of the plant as they are attractive to cattle. Particularly if they have started to reshoot
Bracken control by burning, ploughing, reseeding, and herbicide is the best method of prevention.

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Brucellosis
 Until the cases of brucellosis in Eastern Scotland and Northern England in 2003 mainland UK had been free of for almost ten years. However, the disease is still regularly seen in Ireland and other European countries. Thus imported cattle pose a major risk to Great Britainfs brucellosis status

What is Brucellosis?
Brucellosis is infection with the bacteria Brucella abortus. The most important outcome of infection is abortion, but infection of the testicles (orchitis) is also seen in bulls. Brucella is highly contagious, spreading very easily between cattle as the calf, the membranes and the uterine fluids all contain large quantities of bacteria. Infected cattle will often abort only once due to brucellosis and have apparently normal calvings in subsequent years, but will continue to excrete large amounts of bacteria after calving.

Brucella can infect humans, causing a chronic disease known as undulant fever, which is often very resistant to treatment. Infected cattle will also have bacteria in their milk, so pasteurisation is essential to prevent human infection.

Clinical Signs
Abortion or premature calving
The fetal membranes are virtually always retained.
The membranes also often show signs of infection (placentitis)
In bulls - Swollen testicle (one or both may be involved)
Joint infection has been reported in other countries)
Diagnosis
Brucellosis cannot be diagnosed on signs alone
Diagnosis is by laboratory testing of blood or milk samples and by laboratory culture of Brucella from the fetal membranes, vaginal discharge or the milk of infected cows.
Routine blood and milk testing is used as part of the UKfs strategy to prevent brucellosis
Treatment
No treatment is allowed. All infected cattle and contacts that have been exposed to infection must be slaughtered.
Prevention
Brucellosis is a notifiable disease, which means that its control is regulated by law, and all cases where brucellosis might be suspected must be reported to the local divisional animal health office. Because the signs associated with brucellosis are not specific this means that ALL abortions (or premature calvings) of cattle MUST be reported. The legal definition of an abortion or premature calving is ean abortion or calving which takes place less than 271 days after service, or 265 days after implantation or transfer of an embryo, whether the calf is born dead or alive

Once an abortion is reported the animal health office will then decide whether a visit to take samples is needed, based on the type of farm and cow factors (such as whether she is home-bred). If an investigation is required, it is usually carried out by the farmerfs private veterinary surgeon who will come and take the required samples. There is no cost to the farmer for this unless tests for diseases other than brucellosis are required. Due to Great Britainfs brucellosis status the number of such tests has fallen by 75% since 1995 (despite the NADIS data showing no fall in the number of abortion cases seen by NADIS vets). With the recent cases, it is likely that the number of investigations will go up, and it is essential for the prevention of this disease that all cases of abortion are reported to the animal health office.

It is particularly important to be vigilant with imported cattle. They may have been tested negative before they were imported but in many cattle the test will be negative until the cow calves or aborts. (Indeed this was the case in the recent Scottish outbreak). It is vital that all imported cattle are tested after calving even if that calving is normal.

Current regulations require all cattle that have had contact with infected animals to be slaughtered. This means that if imported cattle, which are subsequently found to have brucellosis, are mixed with the main herd before they calve, the cattle they have been mixed with will have to be slaughtered as well. It is therefore essential to ensure that imported animals are properly quarantined until they have tested negative for brucellosis after calving in the herd for the first time. Work out a proper biosecurity with your vet before you bring the cattle on-farm.

Brucellosis has been effectively controlled by a statutory testing programme to identify infected cattle. This has changed brucellosis from a very common cause of abortion to a very rare disease. However, as the more recent cases show the farming industry needs to be vigilant to prevent it from becoming a major problem once again.

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Bulls and Biosecurity
The purchase of a bull is one of the commonest ways in which disease enters farms. Too many farms think they are closed but buy bulls. A bull is as likely to be infected with an important disease as a cow and, because of the close contact during mating, far more likely to spread it.

So what should you be doing when buying a bull to prevent disease getting on your farm?
Bull Health Declaration
The first thing to do is determine his disease status. The best bulls will have a Bull Health Declaration covering the major diseases: BVD, Leptospirosis, IBR, TB and Johne's. This declaration will show whether the bull’s herd is free of the specific disease in addition to showing that the bull is free of that disease. In addition it will show whether the bull has been vaccinated.


Testing
If such a declaration is not available then you should get the bull tested. This is best done before moving the bull onto the farm. If this is not possible then the testing should be done as part of the quarantine system. Bulls should be tested for BVD, Leptospirosis, IBR, TB and (if older than two) Johne's. The test results need to be interpreted by your vet as the bull’s history (particularly vaccination) can have a major impact on the test results. However, it is important to remember that a negative Johne's result does not mean a bull is free of disease as many infected bulls can test negative. The only way of ensuring that an animal is free of Johne's is to buy it from a herd that has been tested and shown to be free of disease. Never buy a Johne's vaccinated bull as this is likely to have come from a farm with a significant disease problem and vaccination does not prevent infection.


Quarantine
If the bull passes these initial tests it should then go into quarantine on your farm. For BVD, Leptospirosis and IBR, it pays to retest negative animals that you have bought at a sale as they could have been infected at the sale and so be capable of spreading disease for another eight to ten weeks. Also ask your vet about treating the bull with antibiotics to prevent the excretion of Leptospirosis, which can happen even if the bull has no antibodies.


Other Disease Checks
The quarantine period is also useful for checking for digital dermatitis, Salmonella and Campylobacter. The latter is one of the commonest causes of infectious infertility, but only occurs in herds using natural service. Get your vet to test for Campylobacter and if necessary wash the prepuce with antibiotics to clear potential infection. Bulls bought from TB areas should also have an additional TB test while in quarantine, so that the only bulls from such areas which are allowed to enter the herd have had two recent clear TB tests

This testing will significantly reduce the risk of bulls bringing disease onto your farm, preventing such disasters as the 80-cow suckler farm that lost 30 calves in one year due to BVD and the farm on which less than half of the cows got pregnant during the service period as a result of a bull infected with Campylobacter.


Vaccinate
Although the biggest risk is the bull bringing disease onto your farm, don’t forget that infection can spread the other way. So if you have IBR, BVD or Leptospirosis and the bull you are buying tests negative, vaccinate to prevent it getting infected as these diseases can have significant effects on bulls as well as cows.