The disease is fairly acute, with swelling in the affected part, under the jaw and in the regional lymph nodes. The clinical symptoms are excess salivation, difficult mastication and inappetance.

The condition is seen either as an outbreak in several animals simultaneously or as an individual case in a single animal, often in association with a diet change

Worms

Parasitic gastroenteritis is associated with large numbers of nematodes in the abomasum and intestines. The nematodes in the abomasum are generally considered to be the primary pathogens, with those in the intestines playing a lesser but synergistic role. In the United Kingdom, the predominant worms in the abomasum belong to the genus Ostertagia, with Ostertagia ostertagi the most abundant. In the small intestine, Cooperia oncophora and Nematodirus helvetianus are commonest. There are two common forms of ostertagiasis, type I and type II.

Type I Ostertagia infection

This disease is most common in late summer and autumn and causes profuse watery diarrhoea in calves at grass. The faeces are usually green because of the grass diet. Developing larvae within the gastric glands of the abomasum cause the lumen of these glands to distend and stretch the cellular lining. As a result, the mature functional parietal and peptic cells are superseded by undifferential cells. As the infection progresses adjacent non-parasitized glands also become affected and their parietal cells replaced by non-functional undifferentiated cells. The pH of the abomasum increases and leakage of macromolecules and protein occurs across the damaged mucosa, resulting in hypoproteinaemia and increased concentrations of pepsinogen in the plasma. There is a rapid loss of weight, largely due to changes in grazing behaviour. In chronic cases, submandibular oedema may result.

The direct cause is the ingestion of large numbers of O. ostertagi infected larvae over a relatively short period of time. The number of infected larvae on pasture is lowest in May and June, but rises to a peak in late August and September. This pattern arises from a sequence of events which starts with calves turned out in April or May onto pasture grazed by cattle (and especially calves) during the preceding year. These calves ingest some of the infective larvae which have overwintered. It takes three weeks for these larvae to develop into adults and start laying eggs. The rate of hatching of these eggs depends on climatic conditions, reaching a peak in midsummer. The hatched larvae migrate or are washed out of faecal pats onto surrounding herbage to await ingestion by the eventual host. Wet summers produce an early peak, but numbers decrease more rapidly due to rapid depletion of numbers in faecal pats and dilution due to the more abundant grass growth. Conversely, dry summers delay the build-up, as the release of the larvae from the faecal pats is delayed until the autumn rains.

In dairy herds typical cases of type I Ostertagia infection occur in spring-born calves turned out in midsummer onto pastures grazed and contaminated in the spring and early summer by autumn-born calves. In a recent survey, it was found that 65% of farmers used the same pasture each year for calves. The disease is not usually a problem in spring-calving beef herds, as the calves are too young to consume much grass in the early part of the season. As a result, the peak of infective larvae does not develop until September or October, when most calves are weaned and housed. However, autumn-born beef calves may suffer from type I Ostertagia infection in the absence of preventative measures. In areas where climatic conditions allow autumn-born calves to be turned out in March or early April, type I Ostertagia infection may occur 4 to 6 weeks after going to grass.

Type II Ostertagia infection

Infective larvae ingested from September onwards undergo a change in their normal parasitic development, resulting in a period of delayed development at the early fourth larval stage while within the abomasal wall. The change is thought to be brought about by either cold or desiccation in their preparasitic exposure. In the late autumn, calves may harbour many thousands of such larvae. Type II ostertagiasis results when these inhibited larvae resume their development, usually from February to May, the emerging larvae causing the same lesions as those causing type I disease.

Although adult cattle acquire immunity by the age of 18 months, occasionally bulls grazing calf paddocks or cows suffering from immunosuppression due to other diseases such as fascioliasis, may suffer from type II ostertagiasis.

Nematodiriasis in calves

Nematodirus battus, mainly a parasite of sheep, has recently been found to be transmittable by cattle, both on farms where annual alternation of sheep and cattle has taken place, and even where cattle only are kept. It has caused severe outbreaks of diarrhoea in calves.

What is ulcerative mammillitis?

Ulcerative mammillitis is an infection of the skin of the teats and udder of dairy cattle. It is caused by a herpes virus (known as BHV-2)

Clinical Signs

The clinical signs vary from small irregular fluid-filled blisters to larger areas of ulcers and scabs

Diagnosis

• A veterinary examination can confirm that ulcerative mammillitis is very likely
• Scrapings of blistered skin will contain virus which can be seen with electron microscope

Treatment

• No specific treatment is available. Treatment should be aimed at speeding the healing of the skin and preventing spread to other cattle.
• Separate and milk affected cows last
• Disinfect clusters between cows and after milking
• Dip teats with iodine-based dip
• Emollient udder cream can speed healing of skin
• Check regularly to ensure tha skin damage hasn’t resulted in mastitis. (In some cases cannulation may be necessary to milk cow properly

Prevention

Once on a farm ulcerative mammillitis is difficult to eliminate. If you are buying in cattle, try and ensure you don’t buy ulcerative mammillitis as well. Check the teats and udder of all cows before you purchase them. This will significantly reduce, but not eliminate, the risk of buying in ulcerative mammillitis.

Once you have ulcerative mammillitis is established on your farm, it will be most commonly seen in first lactation heifers during winter housing. Pay particular attention to this group and separate and treat affected heifers as soon as you see signs of diseases.

Good parlour hygiene and controlling biting flies can significantly reduce the impact of this disease.

The disease mainly occurs in areas where Tsetse flies inhabit. Tsetse flies infest 10 million square kilometres and affect 37 countries, mostly in Africa, where it is known as ‘Nagana’.

It is the most economically important livestock disease of Africa, as it can have a devastating impact on rural areas.

Cause

Trypanosomosis is usually transmitted through blood lymph and other fluids of infected animals. It is caused by Flagellated protozoan parasites that live in the fluids and tissue of its host animal.

Often the disease is transmitted through the bite of an infected tsetse fly which has been feeding on an infected animal.

Symptoms

Symptoms often begin to show four to 24 days after infection. The most important clinical sign is nonregenerative anaemia.

The major clinical signs are:

• intermittent fever
• anaemia
• oedema
• lacrimation
• enlarged lymph nodes
• abortion
• decreased fertility
• loss of appetite, body condition and productivity
• early death in acute forms
• emaciation and eventual death in chronic forms often after digestive and/or nervous signs

Prevention and treatment

At present no vaccine is available.

If detected early, Trypanosomosis can be treated with trypanocidal drugs for therapeutic and prophylactic purposes.

Therapeutic drugs for cattle include diminazene aceturate, homidium chloride and homidium bromide. Prophylactic drugs for cattle include homidium chloride, homidium bromide and isometamidium.

However the effectiveness of these drugs is now questionable following years of use, causing resistence and now variuos strains of Trypanosomosis to occur.

Another area of control that has been studied is to eradicate the tsetse flies which transmit the disease.

The most common of the procedures that have been deveoped are: spraying insecticide on tsetse habitat, destruction of tsetse habitat and alteration of vegetation so that it becomes unsuitable for tsetse flies.

However, these methods are costly and require a high level of management, organisation and specialist expertise.

Clinical Signs

• Traumatic reticulitis is a progressive disease with the signs changing as the infected abscessed area spreads
• Reduction in feed intake
• Reduced milk yield
• Abdominal pain, reluctant to move, often grunts when made to move
• Stands with arched back and tense abdominal wall
• Initially temperature will be raised, but as progresses this can fall to normal
• Rumen movements reduced and weak

Diagnosis

• On clinical signs, but these are often very vague
• Blood tests may show increased white blood cells, a secondary ketosis
• Exploratory rumenotomy can be used to locate wire
• Animals will grunt when withers firmly pressed down
• Pericarditis identified by muffled heart sounds accompanied by splashing
• For many cows in chronic phase the only diagnosis possible is a non-specific indigestion, because the signs of traumatic reticulitis are limited

Treatment

• Surgical treatment (rumenotomy and removal of wire) can be useful in early cases if spread is not too great
• Conservative treatment (antibiotics, anti-inflammatories and a rumen magnet) can also be effective in mild cases.
• Severely affected cases, particularly those with pericarditis, should be humanely slaughtered as soon as possible as treatment will almost certainly be ineffective
• Injections of anti-inflammatories significantly improve cow wellbeing and help to restore the cow to normal production more quickly

Prevention

1. Removing the source of wire is the best method of prevention. Old tyres with wires that show any evidence of wear must be thrown away and not used on silage clamps
2. Magnets can significantly reduce the incidence of clinical disease.

The development of Thrombosis

Most cases of thrombosis occur as a result of an abscess forming in the liver. The infection spreads from the liver to cause a localised infection in the vein that passes near the liver, the vena cava. The localised infection can then result in the development of a solid mass (a thrombus) in the vena cava. The thrombus is made up of made up of clotted blood, dead white blood cells, bacteria and other cells. Once formed, these thrombi can detach from the lining of the vena cava (they are then called emboli) and are carried in the bloodstream through to smaller blood vessels, where they become stuck. The most common site is in the lungs. Emboli in the lungs result in chronic pneumonia and the development of multiple lung abscesses

Clinical Signs

A) Peracute disease

• Sudden death – usually the animal is found dead with a pool of blood in front of it

  B) Acute disease

• Cattle can show respiratory disease for a variable period (from a few days to several months) prior to the development of other signs.
• Affected cattle will cough up blood, with frothy blood often seen around nose and mouth
• Chest pain and difficulty breathing common
• Black, tarry faeces common
• Weakening, collapse and death (usually within seven days of beginning to cough up blood)
• In some animals, heart failure will occur

Diagnosis

• On the clinical signs described above
• Finding liver abscesses and clots in the vena cava at post mortem

Treatment

• No effective treatment
• Casualty slaughter affected animals if they are not severely ill may be the only option

Prevention

1. Prevent liver abscesses. Liver abscesses occur primarily as a result of acidosis.
   To prevent acidosis:
   a)Make sure that all changes in feeding are undertaken as slowly as possible

   b)Maximise forage intake

2. Treat all abscesses, wherever found, adequately to minimise the risk of spread.

1. Trauma at or after calving: Bone fracture or nerve paralysis
2. Metabolic: Milk fever or hypomag
3. Toxic disease: Metritis or mastitis

A cow becomes a downer cow when the initial cause resolves but the cow still doesnft rise. This failure to rise is usually observed within 24 hours of the cow going off her feet, as a result of muscle and nerve damage. This damage occurs because a cow going off its feet results in heavy pressure on its muscles and nerves, this is made worse in many diseases by the cow being unable to shift position to prevent continuous bearing of weight.

Clinical Signs

• Recently calved cow (usually less than 48 hours)
• Unable to rise for no apparent reason
• Lie in sternal recumbency (on the breast bone)
• Alert, will often eat and drink and pass urine and faeces
• Most make no effort to rise, but some move around on forelimbs (creeper cows)

Diagnosis

• On the clinical signs described above
• The downer cow is a diagnosis of exclusion, so a veterinary examination is essential to rule out broken bones, nerve paralysis, unusual milk fevers, metritis etc.
• Blood tests can be very useful in assessing the prognosis, as can the presence of reflexes

Treatment

• Move to a well bedded yard or loose-box if housed
• Good nursing care is the key to success, e.g. providing food and water in easy to reach wide-based containers
• Mechanically raising the cow, followed by hobbling, can help in many cases
• Observe closely for toxic mastitis, as this is very common, even in cows which did not have mastitis originally
• Give calcium, phosphorus and magnesium as necessary
• Local disinfection and treatment are necessary in more severe cases

Prevention

1) In 46% of downer cows the primary problem was a difficult calving. So good management at calving is vital. Good calving management is dependent upon a vast number of factors, but probably the four most important are:

1. Provide a good environment: Clean, dry, low stocking density
2. Ensure the cows are between BCS 2 and 3.5 at calving
3. Observe from a distance, donft interfere too readily
4. Know when to get help and assistance

2) 38 percent of downer cows had milk fever as the primary cause. Preventing milk fever will significantly reduce the number of downer cows.

What is tetanus?

Tetanus is a highly fatal disease caused by toxins produced by the bacterium Clostridium tetani. This bacterium is found in the soil and the guts of animals and humans. The disease starts when the organism gets into wounded or damaged tissue as a result of contamination. In the absence of oxygen the bacteria multiply and produce a local infection. As they grow, the bacteria produce poisons (toxins), which spread along the nerves to the brain and cause the clinical signs of tetanus. We don’t know how the toxins are transported or how they produce their effect on the nervous system. The time between infection and disease can be very short (two or three days) or quite long (four weeks or more), depending on how long it takes for the contaminated area to develop a low level of oxygen (such as by a wound healing over sealing off the tissue from the outside). The disease is seen in all ages of stock. Calving and castration seem to be the most common procedures linked to the development of tetanus

Clinical Signs

• Stiffness and reluctance to move are normally the first signs
• Twitching and tremors of the muscles
• Lockjaw
• Prominent protruding third eyelid
• Unsteady gait with stiff held out tail
• Affected cattle are usually anxious and easily excited by sudden movements or handling.
• Bloat is common because the rumen stops working
• Later signs include collapse, lying on side with legs held stiffly out, spasm and death.

Diagnosis

The clinical signs are characteristic and in many cases the only information available for making a diagnosis Post mortem investigation is very useful for ruling out other causes of similar disease, such as CCN, staggers or lead poisoning Growing the bacterium from the suspected site of infection is a useful finding. However, it is often very difficult to culture Cl. tetani, because the numbers of bacteria are usually small and the site of infection is often hidden

Treatment

• Cattle with early tetanus probably respond to treatment better than most other livestock
• In very early cases very high doses of penicillin may be helpful, particularly if combined with local treatment of the infected site.
• Antitoxin is probably of little value unless given in the very early stages.
• In some cases sedatives and relaxants can aid recovery
• Good nursing is important. Treated animals need dark quiet surroundings with lots of space and plentiful bedding
• It is not worth treating cattle with fully developed tetanus

Prevention

Undertaking surgical procedures (such as castration) properly, in a clean environment, with disinfected instruments and surgical area, will significantly reduce the risk of tetanus. The same rules apply to calving, be as clean as possible and minimise contamination. Antitoxin can be useful as a short-acting (up to 21 days) preventative if used at high risk times, however on such farms vaccination may be better as a three dose course of vaccination can result in protection for over three years.

M. bovis has been found in several wild mammal species. High rates of infection have been found in badgers and the consensus of scientific opinion is that badgers are a significant source of TB in cattle. However, there appears to be a relationship between the type of landscape (e.g. southwest England) and the risk posed by badgers. M. bovis also infects people and was in the past a major cause of death in humans in the United Kingdom.

Animals are probably more likely to be infected by M. bovis when they are poorly nourished or under stress. Growing heifers and younger cows are most at risk. There is evidence that more intensive dairy farms also have a higher risk of infection.

M. bovis is spread in a number of ways by infectious animals – in their breath, milk, discharging lesions, saliva, urine or droppings. In cattle, excretion of M. bovis begins around 87 days after infection occurs. Entry is usually by inhalation (especially if housed) or ingestion (when badgers are the source of infection). Once in a herd, infection probably spreads from cow to cow by inhalation. Spread from cows to calves may occur via the milk or colostrums.

Various body systems can be affected, but signs are usually confined to the respiratory tract. A soft, chronic cough occurs once or twice at a time. In more advanced cases, there is a marked increase in the depth and rate of respiration as well as dyspnoea. Areas of dullness can be heard in the chest on auscultation or percussion. Some cases may squeak, whistle or have a snoring respiration.

Supervision of maiden and in-calf heifers and dry cows at pasture during the summer months is often sporadic due to other commitments and mastitis may be well advanced before clinical signs are noted.

Clinical signs

During the early stages the diligent stockman will notice:

• Gradual enlargement, both in length and diameter, of the teat(s) of the 0affected gland(s) for up to one week before the heifer/cow becomes sick.
• Large numbers of flies cluster around the affected teat orifice causing considerable irritation with frequent kicking.
• Obvious swelling of the affected quarter.
• Generalised signs of illness including isolation from the group, stiffness and reluctance to walk, lack of grazing giving a gaunt appearance.
• Joint distension of the fetlock and hock joints.
• Rapid loss of body condition.
• Abortion. May occur up to two weeks after the initial episode of mastitis but is not common. More usually the calf has a normal skeletal size at full term but is weak and poorly fleshed as a consequence of growth retardation within the womb. Such calves are prone to a variety of infections unless they ingest sufficient good quality colostrum which is unlikely unless the calf is given colostrum from a healthy cow.

Treatment

Veterinary treatment is essential for these sick cattle. Despite antibiotic therapy and regular stripping of affected quarter(s) the affected glands will not be functional and eventually become hard and indurated. Occasionally, pus may drain through the skin from a superficial abscess in the affected gland. The hopeless treatment response in summer mastitis emphasises the need for effective preventive measures.

Cause

It is probable that the causal bacteria gain entry to the mammary gland after damage to the teat sphincter. While there is circumstantial evidence only to link the sheep headfly Hydrotaea irritans with disease, all recent experimental attempts to transmit disease by this route have failed. It is generally accepted that primary invasion of the mammary gland, with either the anaerobic organism Peptococcus indolicus or Streptococcus dysgalactiae, is followed by Arcanobacterium pyogenes infection. All of the bacteria are present on healthy cattle.

Prevention

1. Dry cow therapy remains the most affective means of preventing summer mastitis both in cows at drying-off, and in susceptible pregnant heifers during the summer months. As a general rule, the longer duration dry cow antibiotic preparations should be used but only after consultation with your veterinary surgeon. In herds with a severe summer mastitis challenge re-tubing cows, or more commonly at-risk heifers, at three week intervals has proven successful but is considered cost-prohibitive in beef cattle. Care must be exercised when infusing intramammary antibiotic preparations in heifers whereby the nozzle of the tube is held at the teat orifice, but not forced into the teat canal lest damage occurs. The teats must be swabbed with surgical spirit before tubing and a teat dip used afterwards. Cattle should not be tubed in wet weather or in unhygienic conditions because of increased risks from introducing infection into the udder. If in any doubt, consult your veterinary surgeon regarding this important aspect of dry cow management.
2. Mechanical barriers such as Stockholm tar or micropore tape have proven successful in the prevention of summer mastitis during high risk periods in dairy herds, but require weekly handling for their application/supervision and are therefore considered unsuitable for beef cows.
3. Fly repellents, whether in the form of pour-on or impregnated ear tag, provide useful protection against nuisance flies but cannot be relied upon in isolation to prevent summer mastitis. Such preparations also assist in preventing New Forest disease (Pink eye). Many dry dairy cows are walked through the milking parlour at regular intervals allowing application of teat dips and attention to teat sores and lesions which attract nuisance flies.

Other factors may predispose hypomagnesaemic tetany. Scouring reduces magnesium absorption. Chewing fibrous material, such as floor bedding, increases salivation and thus causes greater losses of endogenous magnesium. Hypomagnesaemic tetany in calves often coexists with other diseases, especially enzootic muscular dystrophy.

The disease is most common in housed, inadequately fed animals. Calves aged 2-4 months or over are most at risk when fed solely on a diet of whole milk, as with veal calves. However, the disease also occurs in calves running at pasture with their dams. Calves receiving the greatest quantity of milk and growing most rapidly are more likely to be affected, as they have a greater need for magnesium.

Tetany does not occur until serum magnesium levels fall below 0.8 mg/dl (0.33 mmol/l), and is most severe at levels below 0.6 mg/dl (0.25 mmol/l), although calves may have levels even lower than this and show few clinical signs. It is probable that hypocalcaemia precipitates tetany, in animals rendered tetany-prone by low serum magnesium levels.