| Name and Description | Causes | Symptoms | Treatment | Prevention |
|---|---|---|---|---|
| Wooden Tongue ( Actinobacillus ) | Wooden tongue is a well-defined disease of the soft tissues of the mouth region in adult cattle. It is caused by actinobacillosis lignieresii, part of the normal bacterial flora of the upper digestive tract. The bacteria usually invade the skin through a wound or minor trauma caused by sticks or straw or barley awns. | Inability to eat or drink Drooling/ saliva Rapid loss of condition Painful and swollen tongue Ulcers on tongue Animals may occasionally die from starvation and thirst in the acute stages of the disease. As the infection becomes chronic, fibrous tissue is deposited and the tongue becomes shrunken and immobile and eating is difficult. Local lymph nodes may be enlarged and abscesses may form and discharge creamy pus, which may contain granules. Less commonly the jaw, lungs, oesophageal groove, or udder may be affected. Rarely granulomas may occur anywhere on the skin or internal organs. | It is important to begin treatment early, as advanced cases may fail to respond. The most common treatments are iodine therapy or tetracyclines. Advanced cases may require surgical drainage and irrigation with iodine solution for several days. Treated animals should be observed regularly, as relapses can occur. | There are no vaccines available to treat this disease. Control is best achieved by early recognition and prompt treatment or cases, isolation or disposal of infected animals is recommended. |
| White Muscle Disease. White muscle disease is also known as nutritional myopathy of calves. It is normally is seen in young calves and is associated with deficiencies of selenium or vitamin E, or both. | There are two forms of white muscle disease; a congenital form that affects the cardiac muscle, and a delayed form that is associated with either cardiac or skeletal muscle. | Calves affected by the congenital form of white muscle disease usually die within 2-3 days of birth due to cardiac muscle degeneration. On examination post death, the heart will show white, chalky subendochondral plaques that are most noticeable in the left ventricle. The result is damage to cardiac muscle cells and Purkinje fibers. Cattle affected by the delayed form or white muscle disease may exhibit signs ranging from general unthrift and stiffness, to walking with an arched back and spending more time recumbent, depending on the level of selenium in the diet. Often, the delayed form is brought on by vigorous exercise but if chronically affected, cattle can display splayed toes and a relaxation to the shoulder girdle. If a calf is affected severely it may die of starvation due to an inability to nurse properly due to weakness. The skeletal muscle lesions associated with the delayed from of white muscle disease are usually bilaterally symmetrical and can affect one or more muscle groups. The muscle will have white striations and feel dry and chalky due to abnormal calcium deposits. | Cattle affected by white muscle disease have been treated with sodium selenite and vitamin E in sterile emulsion. This can be administered SC or IM, at 1 mg selenium and 50 mg (68 IU) of vitamin E per 18 kg (40 lb) body wt. If necessary, the treatment may be repeated two weeks later, but no more than four doses total should be given. In calves affected with simple vitamin E deficiency, treatment with dietary supplementation using ?-tocopherol or substances rich in vitamin E can be used. Calves have been cured using 600-mg of alpha-tocopherol initially; followed by daily doses of 200-mg. Any polyunsaturated fats should be removed from the diet as these may be causing the vitamin E deficiency. | To prevent white muscle disease within four weeks after birth, cows are given 15 mg of selenium, usually as sodium selenite four weeks before calving. To prevent the delayed type, calves are given 5 mg of selenium at two to four weeks of age and twice more at monthly intervals. A selenium and vitamin E mixture is advocated in some areas. Other procedures for selenium supplementation include administration of intraluminal selenium pellets, use of selenium-fortified salt or mineral mixtures, SC implantation of selenium pellets, or soil application of selenium at 4 g/acre (10 g/hectare) in fertilizer. Adding selenium to feed for breeding animals or their young is useful in areas of known deficiency. The recommended supplemental level is 0.3 ppm selenium, calculated on the basis of total dry-matter intake. It is added as sodium selenite, which contains 45.65 per cent selenium. Because of the minute quantities involved and the toxicity of excess intake, premixing and thorough subsequent mixing is necessary. In some countries, including the USA, addition of selenium to feeds is controlled by law, and appropriate authorities should be consulted; in all areas, caution in the use of selenium is indicated. |
| Trypanosomiasis / Sleeping Disease / Nagana. Mainly occurring in Africa, Trypanosomosis, or Sleeping Disease, is a infection affecting both animals and humans. The disease mainly occurs in areas where Tsetse flies inhabit. Tsetse flies infest 10 million square kilometers and affect 37 countries, mostly in Africa. It is the most economically important livestock disease of Africa, as it can have a devastating impact on rural areas. | 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 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 | 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 developed 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, organization and specialist expertise. | 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 resistance and now various strains of Trypanosomosis to occur. |
| Vibriosis (Campylobacter Infection). Vibriosis is an important infectious venereal disease of cattle. It is a cause of infertility and abortion. | Vibriosis is caused by the bacterium Campylobacter fetus and is spread by infected bulls when they mate susceptible cows and heifers. Once infected, a bull remains an asymptomatic carrier of the condition. Non-venereal transmission of campylobacteriosis is unlikely to occur. When introduced to a herd, the disease spreads rapidly, as cows and heifers in such herds have no immunity. Conception rates can then drop to around 40 per cent. As immunity develops, the disease rate drops, but reinfection often occurs because immunity normally wanes about a year after the initial infection. Conception rates in these chronically infected herds are usually between 65 per cent and 75 per cent, with replacement heifers typically the most severely affected. Infertility normally occurs from an infection in the uterus after the heifer has mated with an infected bull. This infection can prevent the implantation of a fertilized egg, or more commonly results in the loss of the developing embryo in the uterus. When this happens, the animal usually returns to oestrus, but often with prolonged and irregular cycles. By this time, immunity against the disease has normally developed, and re-mating can result in pregnancy. Occasionally the disease results in permanent infertility. | Identifying Vibriosis is difficult because of the absence of clinical signs. The disease is insidious and often remains unrecognized in herds, causing continuing production losses. Abortion Poor conception rates Long calving interval Uterine infection The disease is confirmed by measuring antibodies in the vaginal mucus of infected cows and heifers. Bulls can also be tested for the presence of infection, though it is not always reliable. | Where available, all breeding animals can be vaccinated to eliminate the disease from an infected herd. In many instances vaccinating and treating only the bulls can break the transmission cycle, with the disease gradually dying out in the herd. Natural immunity will eliminate the disease from the herd, however replacement heifers will still remain at risk. | Bulls can be vaccinated annually against the disease. Vaccinations are also available for cows and makes the animal highly resistant to infection. Biosecurity and screening of bulls bought in can help identify the disease. If a bull has to be bought the best policy is the younger the better. If you have to buy in a mature bull, treat it with antibiotics before it is used to mate cows and use it on a small number of cows only so that its fertility can be monitored before it is used for service in the main herd. |
| Ulcerative Mammillitis. Ulcerative mammillitis is a relatively uncommon condition but it can spread rapidly in herds which are affected for the first time and cause significant pain and discomfort. It tends to occur most commonly in early winter and in first lactation heifers. | 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). | Lesions of mamillitis can spread over the entire udder and perineum, as well as this, the mouths of nursing calves might be affected. The clinical signs vary from small irregular fluid-filled blisters to larger areas of ulcers and scabs. | No specific treatment is available. Infected cows should be separated from others. Iodine dips may help disinfect teats to prevent the spread of the disease. An emollient udder cream can speed healing of skin. | Once on a farm ulcerative mammillitis is difficult to eliminate. Precautionary measures should be taken when bringing cattle onto the farm. Good parlour hygiene and controlling biting flies can significantly reduce the impact of this disease. |
| Acetonaemia (Ketosis) | Ketosis is a metabolic disorder that occurs in cattle when energy demands (e.g. high milk production) exceed energy intake and result in a negative energy balance. Ketotic cows often have low blood glucose (blood sugar) concentrations. When large amounts of body fat are utilised as an energy source to support production, fat is sometimes mobilised faster than the liver can properly metabolise it. If this situation occurs, ketone production exceeds ketone utilisation by the cow, and ketosis results. 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. | Reduced milk yield Weight loss Reduced appetite Dull coat Acetone (pear drop) smell of breath/ or milk Fever Some develop nervous signs including excess salivation, licking, agression etc. For every cow with clinical signs there are probably a number of others with sub-clinical signs. | The initial aim of treatment is to restore the lack of glucose in the body. A quick-acting glucose supplement is required immediately. Follow-up treatment is aimed at providing a long term supply of glucose. Glucose replacement Intravenous administration of a dextrose solution by a veterinarian is effective in the short term, but follow-up treatment is essential if relapses are to be avoided. Drenching with propylene glycol or glycerine has longer term effects. It also has the benefit of ease of administration. Treatment should be continued for two to four days. Several commercial compounds contain propylene glycol and glycerine. Hormonal therapy Many of the long-acting corticosteroids have beneficial effects in ketosis. They are administered by the veterinarian as a single injection. Corticosteroids have the ability to break down protein in muscles to produce glucose, which immediately replenishes the depressed blood glucose levels. When using corticosteroids, it is important to supply an adequate amount of glucose either as a high carbohydrate diet and/or propylene glycol drenches to prevent excessive breakdown of muscle protein. | It is important to prevent ketosis from occurring, rather than treating cases as they appear. Prevention depends on adequate feeding and management practices. In times of feed deficiency because of drought or other reasons, the provision of supplementary feed with adequate amounts of carbohydrate is essential. The best feeds tend to be good quality hay, silage, or cereal grain. The body condition of the dairy cow is important at calving. Cows should be on a rising plane of nutrition up to calving with the aim to calve in good condition. After calving, the cow has the potential to reach maximum efficiency in milk production, but feed requirements for high production are often greater than the voluntary intake of pasture can provide. Therefore an energy supplement is required and there is evidence that this will improve production and reproductive performance, and decrease the risk of ketosis. The best supplements are good quality hay, silage, or cereal grains. Supplements should be fed at least until the peak of lactation is reached or longer depending on the quality and quantity of available pasture. Occasionally, very high-producing cows will be susceptible to ketosis every year. In these cases a preventive drenching program of propylene glycol immediately after calving may avert ketosis in individual problem cows. |
| 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. | |||
| 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. | 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. | 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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| Anaplasmosis | Anaplasmosis is a vector-borne, infectious blood disease in cattle caused by the rickesttsial parasites Anaplasma marginale and Anaplasma centrale. It is also known as yellow-bag or yellow-fever. This parasite infects the red blood cells and causes severe anemia. It is most usually spread by ticks. | Anemia Fever Weight loss Breathlessness Jaundice Uncoordinated movements Abortion Death | Tetracycline is often used for clinical anaplasmosis. However it cannot be used in every country. General supportive care is also important for anemic animals. Blood transfusions are of limited benefit. The incubation time for the disease to develop varies from two weeks to over three months, but averages three to four weeks. Adult cattle are more susceptible to infection than calves. The disease is generally mild in calves under a year of age, rarely fatal in cattle up to two years of age, sometimes fatal in animals up to three years of age, and often fatal in older cattle. Once an animal recovers from infection, either naturally or with normal therapy, it will usually remain a carrier of the disease for life. Carriers show no sign of the disease but act as sources of infection for other susceptible cattle. | Typically, cases of anaplasmosis increase in late summer and fall as insect vectors increase. Therefore, control of vectors is key to preventing anaplasmosis. If necessary herd treatment with oxytetracycline injection every 3 to 4 weeks during high risk times may be necessary will prevent clinical disease but animals can become carriers. Chlortetracycline also known as CTC can reduce the risk of anaplasmosis. A consistent intake of the correct amount of mineral is crucial to a anaplasmosis prevention programme. CTC is available in medicated feed, free choice salt-mineral mixes or medicated blocks. In some places, vaccines are available to increase resistance to anaplasmosis. |
| Anthrax Anthrax, a highly infectious and fatal disease of mammals and humans, is caused by a relatively large spore-forming rectangular shaped bacterium called Bacillus anthracis. Anthrax occurs on all the continents, causes acute mortality in ruminants and is a zoonosis. The bacteria produce extremely potent toxins which are responsible for the ill effects, causing a high mortality rate. While most mammals are susceptible, anthrax is typically a disease of ruminants and humans. It does not typically spread from animal to animal nor from person to person. The bacteria produce spores on contact with oxygen. | 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. Treatment Due to the rapidity of the disease treatment is seldom possible, although high doses of penicillin have been effective in the later stages of some outbreaks. | Infection is usually acquired through the ingestion of contaminated soil, fodder or compound feed. Anthrax spores in the soil are very resistant and can cause disease when ingested even years after an outbreak. The spores are brought to the surface by wet weather, or by deep tilling, and when ingested or inhaled by ruminants the disease reappears. Where an outbreak has occurred, carcases must be disposed of properly, the carcase should not be open (exposure to oxygen will allow the bacteria to form spores) and premises should be quarantined until all susceptible animals are vaccinated. Vaccination in endemic areas is very important. Although vaccination will prevent outbreaks veterinary services sometimes fail to vaccinate when the disease has not appeared for several years. But because the spores survive for such lengthy periods, the risk is always present. Anthrax is a disease listed in the World Organisation for Animal Health (OIE) Terrestrial Animal Health Code, 2011, (Article 1.2.3) and must be reported to the OIE (Chapter 1.1.2 Notification of Diseases and Epidemiological Information). |
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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 grasp 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. | 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. | 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. | 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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| Botulism | Botulism is caused by Clostridium botulinum bacteria that produce toxins under certain environmental conditions. C. botulinum bacteria are commonly found in the environment and will grow to high levels in decaying organic matter including animal and bird carcases. It is believed that contamination of broiler litter with the carcases of chickens that have died, from various causes during production, can render the litter dangerous for ruminants. Even small fragments of carcases transferred onto pasture by scavenger animals, such as foxes, dogs or crows may pose a risk to grazing ruminants. Scavengers may gain access to this material during storage or following spreading on land. While the Animal By-Products (Enforcement) Regulations (NI) 2011 permits the spreading on land of poultry litter, the spreading of litter contaminated by carcases is an offence. It is important to note that that manure from egg laying hens has not been associated with outbreaks of botulism in cattle. A possible reason for this is that husbandry arrangements for layers reduce the likelihood of contamination of litter with carcases. | Cattle and sheep of all ages are susceptible to botulism, which is characterised by a progressive muscle weakness (paralysis). Affected animals may be weak, stagger about, or go down. Cattle characteristically display flaccid paralysis and occasionally protrusion of the tongue. Signs in sheep and goats are similar to cattle but protrusion of the tongue may not be as obvious. In most cases the disease is fatal although some animals may recover. In many cases of botulism euthanasia is justified on welfare grounds. Cattle are extremely sensitive to the effects of the toxin meaning that ingestion of very small amounts of toxin can result in clinical disease. The progression and severity of the disease depends on the amount of ingested toxin. When a large amount of toxin has been ingested, the animal may be found dead without having shown any signs of disease. Conversely if only a small amount of toxin is ingested the progression of the disease may take a more chronic course and clinical signs may be less severe. Diagnosis of botulism is based primarily on clinical signs and a history of known exposure to risk factors such as contaminated broiler litter or carcase material. Laboratory confirmation is frequently difficult and relies on detection of the toxin in samples harvested from suspect cases and elimination of other possible causes of disease. | Vaccination is available. However, in some countries no vaccines are available under a general licence, although special treatment certificates can be obtained. | Careful disposal of all animal or bird carcases and poultry litter is essential to minimise the risk of botulism to livestock. Poultry carcases should be promptly removed and disposed of by incineration, or rendering as required by EU Regulations No. 1069/2009 and 142/2011. Following removal of the broiler crop, all poultry house doors should be kept closed until the litter is removed. The litter should not be removed from the house until it can be loaded directly onto spreading equipment, covered vehicles or immediately stacked and covered. At no time should it be accessible to dogs, foxes, crows or other scavengers that may carry carcases onto adjacent pasture or into livestock housing. Washings from poultry houses and yards should be collected in tanks rather than be allowed to flow onto adjacent land. Poultry litter should not be spread on agricultural land that is to be grazed, or from which silage or hay is to be harvested, in the same year. Spreading litter on a windy day may also pose a risk of contaminating adjacent fields. Any animal or bird carcases, or portions of carcasses, visible on pasture or in livestock houses, should be promptly removed. Even small fragments of such material may be dangerous to livestock and should be disposed of by incineration or rendering, as required by current legislation. |
| Brucellosis | Brucellosis is an infectious disease that occurs from contact with animals carrying Brucella bacteria. Brucella can infect cattle, goats, camels, dogs, and pigs. The bacteria can spread to humans if you come in contact with infected meat or the placenta of infected animals, or if you eat or drink unpasteurised milk or cheese. Brucella is highly contagious, spreading very easily between cattle as the calf, the membranes and the uterine fluids all contain large quantities of bacteria. | Abortion; Stillborn Weak calf born Retention of fetal membranes; Signs of infection in the membranes; Swollen testicles in bulls Infection of the testicles is also seen in bulls. Diagnosis can be done by laboratory testing of blood or milk samples or by laboratory culture of brucella abortus from the placenta, vaginal discharge or the milk of infected cows. | No treatment is available, which makes detection and prevention essential. | Brucellosis is a notifiable disease. Because of this most countries have strict regulations in place to control brucellosis, however it is still a threat. Testing herds regularly and culling has been an effective way of eradicating the disease in individual herds before. Quarantines are placed on infected herds and good sanitation and biosecurity will protect uninfected herds. In endemic areas vaccination is available. In some areas wild populations of buffalo, bison or cattle can carry the disease and infect domestic animals if they come into contact. Vaccination is not a guarantee but can increase resistance to infection. |
| Calf Pneumonia | Calf pneumonia is a major problem in dairy and beef herds. It is a multifactorial disease, and the most common post-mortem diagnosis in calves between one to five months of age. Infectious agents involved include Mannheimia haemolytica, Haemophilus somnus, Infectious Bovine Rhinotracheitis (IBR), bovine Respiratory Syncytial Virus (RSV) and Parainfluenza III Virus (PI3), along with many other bacteria and mycoplasma species and viruses. Environmental factors include low environmental temperatures and high humidity and poor ventilation and also direct draughts onto calves themselves. The relationship between season and outbreaks may also be related to management practices including calving pattern and mixing of different ages of calves. There are two types of the disease, acute and chronic. | Dull and depressed High temperature Raised breathing due to lung damage Nasal discharge Coughing Reduced food intake Chronic pneumonia is more gradual in onset with no distinct ill phase and the cow may appear to still eat well but may have a slight nasal discharge, sometimes with an increased respiratory rate and cough. Both forms of the respiratory disease cause production losses as there is a reduction in liveweight gain and there may be deaths in the acute syndrome. | Antibiotics, anti-inflammatories or anthelmintics can be prescribed for treatment. | It can be difficult to control pneumonia when calves are placed in communal pens. Improved husbandry, ventilation and good nursing care can all reduce risks of pneumonia, as well as ensuring that young animals receive appropriate amounts of colostrum within the first 24 hours of birth. Colostrum: : All calves must have one gallon of colostrum within four to six hours of birth to receive adequate immunity. Calves that are not given enough antibodies at birth are at increased risk for pneumonia and scours throughout the entire growing period. The most important step in any calf health-management programme is a successful colostrum-management programme. Ventilation: Often if ammonia can be smelled it is a sign of poor ventilation. Nutrition: Feeding calves inadequately will reduce calf growth and their immune system response. Vaccination: Vaccines are available to reduce risk of infection, however they must be used alongside an effective management programme. |
| Calf Scour | Calf scour is the most important disease problem in dairy calves and causes more financial loss to the calf producer than any other syndrome. Rotavirus is most common cause of diarrhoea, with over 30% lab diagnoses being rotavirus. The virus is present on nearly every farm so virtually all calves are at risk, though the risk is highest on farms where other agents, particularly E. coli, coronavirus and cryptosporidia, are present. These agents often combine with rotavirus to cause more severe diarrhoea than either would on their own. Controlling rotavirus can thus significantly reduce your losses due to calf scour even if you have other problems on farm. | The level of antibodies in colostrum depends on what the cow has been exposed to (and how long ago the exposure was). Vaccinating pregnant cattle between one and three months before calving will significantly increase the amount of antibodies in colostrum. This means that the colostrum produced by vaccinated cows can have antibody levels high enough to protect the calf from rotavirus for seven days if two litres of colostrum are given within 12 hours of birth. However the best value for vaccination is obtained when colostrum from vaccinated cattle is fed to calves for at least two weeks after birth (and preferably longer), so that the calf continues to have high levels of protective antibodies in the gut during the critical period. | Good hygiene reduces the spread of disease between calves. Ensure that bedding is clean and dry, don’t mix different ages of calves, remove sick calves to a sick pen as soon as possible (and don’t return them to their old group) and above all use an all-in, all-out policy with disinfection between groups. Colostrum is the key to immunity in the young calf. Colostrum contains both antibodies which protect against specific diseases, such as rotavirus, and non-specific protective systems such as lactoferrins which prevent bacterial growth. Ensuring that the calf receives sufficient colostrum (at least two litres within six hours of birth) is vital in the control of calf diarrhoea. It is best if the calf gets its colostrum by sucking its mother as this ensures that it absorbs the maximum amount of antibodies. Bucket or bottle feeding colostrum results in fewer antibodies being absorbed; stomach tubing is even less efficient, so should only be used as a last resort for calves too weak to suck. A second feed of colostrum in the first 24 hours is also important in maximising the value of the first feed, so if possible leave calves with their mothers for at least 24 hours. The protection from the first dose of colostrum lasts for only three to four days, whereas rotavirus and other infections can occur at any time in the first few weeks, so in order to prevent scour, continued colostrum feeding (at least 2.5 litres every day for two to three weeks) is important. This is because although the antibodies in the colostrum will no longer be absorbed they remain in the gut and can thus prevent gut infections such as rotavirus. If you do feed colostrum for three weeks you will need to store it. There are lots of different ways of doing this with freezing being the simplest. If you do store colostrum make sure that you separate day 1 and 2 colostrum from day 3 and 4 as earlier colostrum has many more antibodies. If early colostrum is in short supply it should be preferentially fed to the younger calves. |
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| Bovine Babesiosis (Redwater, Tick Fever) | Bovine Babesiosis (BB) is a tick-borne disease of cattle. The principal strains are babesia bovis and babesia bigemina, with Rhipicephalus ticks being the major vector. Babesia divergens is also found, with the major vector being Ixodes ricinus. BB is found in areas where its arthropod vector is distributed, especially tropical and subtropical climates. Babesia bovis and B. bigemina are more widely distributed and of major importance in Africa, Asia, Australia, and Central and South America. Babesia divergens is economically important in some parts of Europe and possibly northern Africa. Transmission of B bovis takes place when engorging adult female ticks pick up the infection. They pass it on to their progeny via their eggs. Larvae (or seed ticks) then pass it on in turn when feeding on another animal. B bigemina is also passed from one generation of ticks to the next. Engorging adult ticks pick up the infection and nymphal and adult stages (not larval stages) of the next generation pass it on to other cattle. Morbidity and mortality vary greatly and are influenced by prevailing treatments employed in an area, previous exposure to a species/strain of parasite, and vaccination status. In endemic areas, cattle become infected at a young age and develop a long-term immunity. However, outbreaks can occur in these endemic areas if exposure to ticks by young animals is interrupted or immuno-naïve cattle are introduced. The introduction of Babesia infected ticks into previously tick-free areas may also lead to outbreaks of disease. | BB is predominantly observed in adult cattle. Infected animals develop a life-long immunity against re-infection with the same species and some cross-protection is evident in B. bigemina-immune animals against subsequent B. bovis infections. B. bovis Conditions are often more severe than other strains. High fever Parasitaemia (percentage of infected erythrocytes) – maximum parasitaemia is often less than one per cent. Neurologic signs such as incoordination, teeth grinding and mania. Some cattle may be found on the ground with the involuntary movements of the legs. When the nervous symptoms of cerebral babesiosis develop, the outcome is almost always fatal. Dark coloured urine Anorexia B. bigemina Fever Anorexia Animals likely to separate from herd, be weak, depressed and reluctant to move Haemoglobinuria and anaemiaDark coloured urine Central nervous system (CNS) signs are uncommon Lesions In b. bigemina parasitaemia often exceeds 10 per cent and may be as high as 30 per cent. Clinical symptoms for Babesia divergens are similar to B. bigemina infections. The survivors may be weak and in reduced condition, although they usually recover fully. Subacute infections, with less apparent clinical signs, are also seen. Treatment Mild cases may recover without treatment. Sick animals can be treated with an antiparasitic drug. Treatment is most likely to be successful if the disease is diagnosed early; it may fail if the animal has been weakened by anemia. Imidocarb has been reported to protect animals from disease but immunity can develop. There are also concerns with regard to residues in milk and meat. In some cases blood transfusions and other supportive therapy should be considered. | Differential Diagnosis Babesiosis resembles other conditions that cause fever, and hemolytic anemia. The differential diagnosis includes anaplasmosis, trypanosomiasis, theileriosis, bacillary hemoglobinuria, leptospirosis, eperythrozoonosis, rapeseed poisoning and chronic copper poisoning. Rabies and other encephalitides may also be considerations in cattle with central nervous system signs. | Effective control of tick fevers has been achieved by a combination of measures directed at both the disease and the tick vector. Tick control by acaracide dipping is widely used in endemic areas. Dipping may be done as frequently as every 4-6 weeks in heavily infested areas. The occurrence of resistance of ticks, chemical residues in cattle and environmental concerns over the continued use of insecticides has led to use of integrated strategies for tick control. Babesiosis vaccines are readily available and are highly effective. Anti-tick vaccines are also available in some countries and can be used as part of an integrated program for the control of ticks. Babesiosis can be eradicated by eliminating the host tick(s). In the US, this was accomplished by treating all cattle every two to three weeks with acaricides. In countries where eradication is not feasible, tick control can reduce the incidence of disease. |
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