FMD

Foot-and-Mouth

Foot-and-mouth disease (FMD) is a severe, highly contagious viral disease of cattle and swine. It also affects sheep, goats, deer, and other cloven-hooved ruminants. FMD is not recognized as a zoonotic disease

This country has been free of FMD since 1929, when the last of nine U.S. outbreaks was eradicated.

The disease is characterized by fever and blisterlike lesions followed by erosions on the tongue and lips, in the mouth, on the teats, and between the hooves. Most affected animals recover, but the disease leaves them debilitated. It causes severe losses in the production of meat and milk.

Since it spreads widely and rapidly and because it has grave economic as well as clinical consequences, FMD is one of the animal diseases that livestock owners dread most.

What Causes It

FMD is caused by a virus. Signs of illness can appear after an incubation period of 1 to 8 days, but often develop within 3 days.

The virus survives in lymph nodes and bone marrow at neutral pH, but is destroyed in muscle when pH is less than 6.0, i.e., after rigor mortis. The virus can persist in contaminated fodder and the environment for up to 1 month, depending on the temperature and pH conditions.

There are seven known types and more than 60 subtypes of the FMD virus. Immunity to one type does not protect an animal against other types.

How It Spreads

FMD viruses can be spread by animals, people, or materials that bring the virus into physical contact with susceptible animals. An outbreak can occur when:

• Animals carrying the virus are introduced into susceptible herds.
  
  
• Contaminated facilities are used to hold susceptible animals.
  
  
• Contaminated vehicles are used to move susceptible animals.
  
  
• Raw or improperly cooked garbage containing infected meat or animal products is fed to susceptible animals.
  
  
• People wearing contaminated clothes or footwear, or using contaminated equipment, pass the virus to susceptible animals.
  
  
• Susceptible animals are exposed to materials such as hay, feedstuffs, hides, or biologics contaminated with the virus.
  
  
• Susceptible animals drink common source contaminated water.
  
  
• A susceptible animal is inseminated by semen from an infected animal.

Signs

Vesicles (blisters) followed by erosions in the mouth or on the feet and the resulting excessive salivation or lameness are the best known signs of the disease. Often blisters may not be observed because they easily rupture, leading to erosions.

These signs may appear in affected animals during an FMD outbreak:

• Marked rise in body temperature for 2 to 3 days.
  
  
• Vesicles that rupture and discharge clear or cloudy fluid, leaving raw, eroded areas surrounded by ragged fragments of loose tissue.
  
  
• Production of sticky, foamy, stringy saliva.
  
  
• Reduced consumption of feed due to painful tongue and mouth lesions.
  
  
• Lameness with reluctance to move.
  
  
• Abortions.
  
  
• Low milk production (dairy cows).
  
  
• Myocarditis (inflammation of the muscular walls of the heart) and death, especially in newborn animals.

Animals do not normally regain lost weight for many months. Recovered cows seldom produce milk at their former rates, and conception rates may be low.

Confusion With Other Diseases

FMD can be confused with several similar but less harmful diseases, such as vesicular stomatitis, bluetongue, bovine viral diarrhea, foot rot in cattle, and swine vesicular disease. Whenever mouth or feet blisters or other typical signs are observed and reported, laboratory tests must be completed to determine whether the disease causing them is FMD or not.

Where FMD Occurs

While the disease is widespread around the world, North America, Central America, Australia, New Zealand, Japan, Chile, and many countries in Europe are considered free of FMD. Various types of FMD virus have been identified in Africa, South America, Asia, and some parts of Europe.

Prevention and Control

FMD is one of the most difficult animal infections to control. Because the disease occurs in many parts of the world, there is always a chance of its accidental introduction into the United States.

Animals and animal byproducts from areas known to be affected are prohibited entry into this country. Livestock animals in this country are highly susceptible to FMD viruses. If an outbreak occurred in the United States, this disease could spread rapidly to all sections of the country by routine livestock movements unless it was detected early and eradicated immediately.

If FMD were to spread unchecked, the economic impact could reach billions of dollars in the first year. Deer and other susceptible wildlife populations could become infected and potentially serve as a source for reinfection of livestock.

Vaccines for FMD are available, but must be matched to the specific type and subtype of virus causing the outbreak. Vaccination can help contain the disease if it is used strategically to create barriers between FMD-infected zones and disease-free areas.

What You Can Do

You can support U.S. efforts against FMD by:

• Watching for excessive salivation, lameness, and other signs of FMD in your herd; and
  
  
• Immediately reporting any unusual or suspicious signs of disease to your veterinarian, to State or Federal animal disease control officials, or to your county agricultural agent.
  
  
• When traveling outside the United States, ensuring that you do not bring back prohibited animal products or other at-risk materials (see APHIS Factsheet on Protecting America from FMD).

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Foot Rot in Cattle

Foot Rot in Cattle

Foot rot is a term loosely used to describe lameness associated with the bovine foot. However, true foot rot is characterized by acute inflammation of the skin and adjacent soft tissues of the interdigital cleft or space. It is accompanied by diffuse swelling, varying degrees of lameness and in most cases, by a foul-smelling necrotic lesion of the interdigital skin. Foot rot is the term commonly used in the United States for this lameness disorder, but internationally the disease is better known as foul, foul-in-the-foot, interdigital phlegmon, interdigital necrobacillosis, or infectious pododermatitis. It is a frequent problem of beef and dairy cattle, especially in poorly drained, muddy pens or lots and pastures. Normally, occurrence is sporadic, affecting only 1 or 2 animals at a time, but it may affect larger numbers of cattle in outbreak situations or problem herds.

Causes and Contributing Factors

For many years Fusobacterium necrophorum or Bacteroides melaninogenicus were considered the primary causes of foot rot with F necrophorum most commonly isolated. Recently with improved technology and taxonomic changes there is evidence that the companion organism Porphyromonas levii (formerly considered in the Bacteroides genus) may play an important role with F necrophorum in foot rot infections.

Healthy epithelium (skin) is resistant to bacterial organisms, whereas diseased or injured epithelial tissues are susceptible to infection. High rainfall with wet feces and mud can soften the interdigital skin, making it susceptible to injury. Infectious agents gain entry through the skin as a consequence of injury caused by sharp pieces of stone, metal, wood, stubble, thorns, and frozen manure. Other factors that may encourage damage to the interdigital skin may include irritation and erosion of the interdigital skin caused by interdigital dermatitis, believed to be in part a consequence of the constant exposure of feet to mud and manure.

Clinical Signs and Diagnosis

The earliest and most obvious clinical sign of foot rot is lameness, which increases in severity as the disease progresses. Once the infectious organisms become established, they cause inflammation and necrosis of tissue, resulting in slight to severe swelling and pain. The swelling is usually more evident in the interdigital space and around the coronet (or skin horn junction). The swelling is usually sufficient to cause separation of the digits. A break or fissure in the interdigital space develops which may extend from the front of the foot to the bulbs of the heel. These lesions are sometimes difficult to see unless the foot is elevated and properly restrained for examination. The interdigital lesion is often necrotic along its edges and has a characteristic fetid or foul odor, hence the name foul-in-the-foot.

The signs of foot rot in cattle include lameness with holding or raising a foot, reluctance to move, impaired locomotion, loss of appetite, weight loss, low-grade fever and reduction in milk yield for lactating cows. Hind feet are affected most often and cattle tend to stand and walk on their toes. If left untreated, lameness becomes increasingly severe with infection extending to the distal and proximal interphalangeal joints and other deeper structures of the foot.

Diagnosis of foot rot is made by observation of the animal and physical examination of the foot for the characteristic gross lesions. Cattle producers often diagnose any lameness associated with foot swelling as foot rot, but a more careful examination may reveal other causes of the swelling and lameness.

Treatment

The affected foot should be cleaned and inspected for characteristic clinical signs and to rule out other causes for the swelling and lameness such as foreign bodies, infectious arthritis, or wounds caused by trauma. Historically, an antiseptic and bandage were applied after cleaning and trimming the foot, but topical treatment and bandaging are considered less important than systemic therapy. Prompt diagnosis and initiation of antimicrobial therapy are essential to achieve a satisfactory response. The treatment of choice is parenteral antibiotics administered for three to five days. In commercial beef cattle that are difficult to handle, feed additives such as chlortetracycline and oxytetracycline have been used for control and treatment of large numbers of cattle with the disease. Although this is convenient, there are no feed-grade antimicrobials labeled for control or treatment of foot rot. According to the Animal Medicinal Drug Use Clarification (AMDUCA) extralabel use of feed additives is prohibited in the United States. Readers are advised to seek advice from a veterinarian for specific recommendations. In some severe cases where the infection has extended into deeper tissues of the foot, surgical correction including amputation of the affected claw may be indicated. Recovered cattle can usually function well with one claw.

Prevention

Preventive measures include removing sources of injury and keeping feet dry and clean. Mudholes should be filled and stagnant pools drained or fenced off. Lots should be well drained and manure removed frequently to reduce the amount of muddy filth. In areas where cattle walk frequently, such as in lanes or gateways, grading or filling in low areas to provide a well-drained pathway for walking may help to prevent foot rot cases. Pouring a concrete pad around feed bunks and water troughs will help keep feet dry. In dairy cows, beef cows and bulls, regular foot care including claw trimming as needed helps prevent foot diseases and injuries. Animals may also be walked through a foot bath containing copper sulfate, zinc sulfate or formalin (where permitted). Footbaths are more commonly utilized in dairies and may be impractical for most beef herds.

Historically organic iodide (EDDI) was added to salt mixtures to reduce the incidence of foot rot. Although organic iodide can be effective, the current US Food and Drug Compliance policy guide states that all therapeutic and prevention claims for EDDI are considered as unapproved new animal drugs, thus restricting their use.

Foot rot can be a cause of economic losses in beef and dairy herds. Early treatment, control and prevention under the direction of a veterinarian will help to keep losses to a minimum.

Footnotes

^1. This document is VM26, one of a series of the Veterinary Medicine-Large Animal Clinical Sciences Department, Florida Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida. Original publication date July, 1975. Revised February, 2007. Visit the EDIS Web Site at http://edis.ifas.ufl.edu.

^2. M.B. Irsik , D.V.M. MAB, Beef Cattle Extension Veterinarian, College of Veterinary Medicine, Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL, 32610-0136.

J.K. Shearer DVM, MS, Dairy Extension Veterinarian, College of Veterinary Medicine, Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL, 32610-0136.

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acute pneumonia of adult cattle

Fog Fever

NADIS data show that fog fever is a disease of the autumn. This is because it is almost always associated with cattle who have moved from a dry summer pasture to a lush autumn one

What is Fog Fever?

Fog fever is an acute pneumonia of adult cattle which occurs within 4 to 10 days of moving from an over grazed pasture to a fresh one. A wide range of forages have been associated with fog fever, including, rape, kale, turnip tops, alfalfa and many grasses. This is a disease caused by a toxin, 3-methylindole. This is a toxin produced as a result of breakdown in the rumen of D,L,tryptophan, present in high levels in lush forage. Once absorbed from the rumen the toxin damages the cells lining the lungs resulting in pneumonia.

Clinical Signs

• Severe difficulty breathing, often noisy and accompanied by open-mouthed breathing and frothing
• Anxiety, often separate themselves from the rest of the herd
• Collapse and death
• Coughing infrequent, temperature usually not very high

Diagnosis

• On the clinical signs described above
• Only occurs in animals over 1 year in age
• Time after change in pasture very characteristic (4 to 10 days)

Treatment

• There is no specific treatment for fog fever. Indeed mild cases will commonly recover without treatment. Seek veterinary advice for moderately or severely affected cows
• Removal from pasture is controversial, it may not actually prevent further cases, while moving very sick cows can make the disease worse and should be done with extreme care. Furthermore, leaving cows on pasture will often not result in new clinical cases. Seek veterinary advice

Prevention

1. Limit total grazing time in the first 10 days when cattle are moved to a new pasture. The cattle should graze the pasture for 1 or 2 hours the first day increasing gradually by 10 days.
2. Feeding monensin or chlortetracycline for the first 10 days has been shown to be effective, if grazing management is not possible.

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Fatty Liver in cattle

Fatty Liver Syndrome

What is Fatty Liver?

Fatty liver syndrome is the accumulation of fat within the cow's liver. The dairy cow does not normally store fat in the liver, so fatty liver does not occur when a cow increases its body condition and puts fat on its back. Fatty liver occurs as a result of the cow breaking down too much fat for the liver to process properly, the broken down fat products are then converted back to fat in the liver to prevent them becoming toxic. Thus the liver becomes fat when the cow is losing condition, the more loss in condition the more fat in the liver.

Fatty liver syndrome (> 20% fat) reduces liver function, depresses appetite and milk yield, increases the risk of diseases such as RFM, metritis and mastitis, reduces fertility, and when severe (when it is usually called fat cow syndrome) can lead to death. Once it is deposited in the liver, the concentration of fat in the liver does not fall until the cow gets into positive energy balance, which can be over ten weeks after calving, particularly if the fatty liver is severe. Fat cows (>BCS 3.5) are much more prone to fatty liver.

Causes of Fatty Liver

Fatty liver, ketosis and displaced abomasum are closely interconnected. Cows which have one of these conditions are much more likely to get another. The most important cause of fatty liver is negative energy balance.

Clinical Signs

• High incidence of diseases such as milk fever, ketosis, mastitis after calving
• Reduced fertility
• Rapid weight loss after calving particularly in cows that were fat at calving
• Reduced milk yield (often on a herd basis).

Diagnosis

• Clinical signs
• Blood samples: increased NEFA (free fatty acids), increased ketones (such as beta-hydroxy butyrate), increased liver enzymes Liver biopsy: this the best diagnostic test.

Treatment

• Use the same treatment as for ketosis: Glucose, propylene glycol, corticosteroids.
• However treatment is often ineffective.
• Prevention is far more important.

Prevention and control

Fatty liver occurs because of too much fat breakdown after calving. This occurs primarily in cows that are too fat at calving. Therefore ensuring that cows calve at a body condition score between 2.5 to 3.0 will significantly reduce the risk of fatty liver. Cows should be dried off at a body condition score of 2.5 to 3.0 and maintain their body condition during the dry period. Any alteration of body condition score is best done during mid to late lactation.

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Diarrhoea caused by E.coli

E.coli Diarrhoea

According to NADIS data most common cause of diarrhoea in calves continues to be E.coli .

What is E.coli?

E.coli is a bacterium that is present in the guts of normal animals. Most types of E.coli do not cause disease, however three types of E.coli are associated with diarrhoea in calves.

One type (known as ETEC) attach to and damage the small intestine and produce a special type of toxin (known as an enterotoxin), the second (EPEC) attaches to and damages the small intestine but do not produce enterotoxins, and the third (EHEC) attaches to and damages the large intestine

Clinical Signs

ETEC:
Young calves (usually <3 days old)
Calves become depressed, don’t drink, dehydrate and die rapidly Diarrhoea is very watery

EPEC:

Older calves (usually <21days)
Usually not so rapid or as severe as ETEC
Diarrhoea yellow and watery

EHEC

Older calves (around 14 days)
Often bloody diarrhoea

Diagnosis

ETEC

• Age of calf
• Severity and nature of diarrhoea
• Laboratory tests can identify the protein used by bacteria to attach to the gut

EPEC/EHEC

• Difficult to diagnose as signs are very similar to diarrhoea caused by other organisms, and non-disease causing E.coli are present in most faecal samples
• Examination of material from post-mortems can confirm E.coli –related disease

Treatment

• Replacing lost fluids is the most important part of treatment. This can range from oral electrolytes for moderately affected calves to intravenous fluids for severely affected calves.
• Commercial electrolytes are more expensive than the home-made version but in moderate to severe cases they are much more effective
• Antibiotics can help in some cases, but they should be used with caution and if possible sensitivity testing should be undertaken.

Prevention

1. Keep the environment as clean as possible, this refers to the calving yards as well as the calf pens.
2. Single penning of young calves will significantly reduce the spread of diarrhoea
3. Sick calves will pass a vast number of disease-causing bacteria. Disinfection is vital
4. If possible use an all-in-all-out system. This allows pens to be disinfected between batches and prevents disease being passed on to every new calf that enters the building.
5. Ensure good colostrum intake. In herds with problems, feeding bulked colostrum for at least 7 days can significantly reduce the number of cases of scour
6. For ETEC diarrhoea only, vaccination is available. This is given to the mother in late pregnancy. The colostrum then contains antibodies that help prevent ETEC infection. For the best effect colostrum feeding should continue for at least a week

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Displaced Abomasum in Cattle

Displaced Abomasum in Cattle

What is a Displaced Abomasum

The abomasum (or true stomach) normally lies on the floor of the abdomen, but can become filled with gas and rise to the top of the abdomen, when it is said to be ‘displaced’. The abomasum is more likely to be displaced to the left (LDA) than the right (RDA). Two main risk factors have been implicated:

1. Calving: The majority of cases occur soon after calving. During pregnancy the uterus displaces the abomasum, so that after calving the abomasum has to move back to its normal position, increasing the risk of displacement
2. Atony of the abomasum: If the abomasum stops contracting and turning over its contents, accumulation of gas will occur and the abomasum will tend to move up the abdomen

Clinical Signs

• Inappetance, milk yield drop, reduced rumination are the most common signs
• Can be scanty diarrhoea, mild colic and distended abdomen
• Normally, very like acetonaemia, with ketones in blood, milk, breath and urine. It often responds to treatment but relapses.

Diagnosis

• On the clinical signs above, but cannot be distinguished from ketosis on these alone.
• On examination with a stethoscope the presence of a pinging noise, that sounds like a tap dripping into a steel bucket, is indicative of a gas-filled organ, which is almost certain to be a displaced abomasum.
• A blood sample can be useful in identifying the severity of the ketosis and other metabolic changes

Treatment

• Veterinary advice and assessment is essential.
• Treatment can be conservative or surgical
• Conservative treatment: This involves casting and rolling the cow and manipulating the abomasum so that it returns to its normal position. This can be effective, if done early but about 50% relapse. Rolling can be used in conjunction with toggling, where a toggle is passed through the skin into the abdomen and twisted fixing the abomasum in the correct position. This significantly reduces the relapse rate.
• Surgery: Many surgical techniques have been used some involving opening both flanks.

Prevention

Of the two major risk factors, only atony of the abomasum is preventable. Thus prevention should be aimed at ensuring dry matter intake is maintained in early lactation:

1. Ensure cattle are not too fat at calving (i.e. >3.5 BCS)
2. Feed high quality feeds, with good quality forage
   
   
3. Feeding a total mixed ration as opposed to concentrates
   
   
4. Ensure plenty of space at feeding sites
   
   
5. Minimise changes between late dry and early lactation ration
   
   
6. Prevent and promptly treat, diseases such as milk fever, metritis, toxic mastitis and retained afterbirth which reduce feed
   
   intake
7. Maximise cow comfort, minimise stress

It is likely that a farm with DA problem (>3% of calving cows) is feeding the late dry and/or early lactation cows wrongly. If you get the nutrition right to prevent DA’s, you will also increase your milk production as cows with DA’s are just the tip of an iceberg.

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Digital Dermititis

Digital Dermititis

Lameness is a common problem in all classes of cattle and can greatly affect the welfare and productivity of the animals. Esslemont and Kossaibati (1996) reported 24% lameness in a DAISY survey of 90 herds in 1992-1993, while a more recent survey (Kossaibati and Esslemont, 1999) on 50 farms during 1995-1996 found 38% lameness. There are a large number of factors contributing to lameness in cattle. These can be broken down into external, farm, animal and foot factors.
External Factors
One of the most important external factors is the time of year, the number of cases being greater in winter than in summer (Rowlands et al., 1983). Wet weather conditions are also conducive to maintaining high bacterial levels. Lameness in grazing cattle tends to increase about three weeks after heavy rainfall (Williams et al., 1986).
Farm Factors
Farm factors associated with lameness include herd size: veterinary practitioners saw proportionally fewer cases of foul-in-the-foot but more cases of sole ulcer in larger than in smaller herds (Rowlands et al., 1983). Overcrowding, especially of first calved heifers, leads to reduced lying times and increased lameness.
Stockmanship is important, as farmers who know more about lameness or who have been trained tend to have lower overall prevalence of lameness in their herds than untrained herdsmen (Ward, 1999). Housing is a very important factor. The overall incidence of lesions is lower in strawyards (0.71 cases/100 cows/ month) than in cubicles with yards (0.93 cases/100 cows/ month) (Rowlands et al., 1983). The difference is thought to be due largely to longer lying times in strawyards (Ward, 1999). Cattle at pasture tend to lie down for longer periods than those in cubicles (Ward, 1999). This is thought to be beneficial. Straw yards also reduce the exposure to bacteria causing digital dermatitis (Laven, 1999).
The floor surface is another important factor. A two-year survey of 37 farms showed that only 25% of floor surfaces were satisfactory in the first winter and 34% in the second winter. 55% and 33% were considered smooth or very smooth and 20% and 33% were rough or very rough in the two periods (Faull et al., 1996).
There is no doubt that feed input has an important role to play in lameness associated with lesions of hoof horn and laminitis.
Animal Factors
Huang et al. (1995) found differences between breeds in claw score traits for certain foot conditions. Ayrshires and Jerseys had better scores than other breeds. The Brown Swiss had the worst scores for corkscrew claws, laminitis and sole ulcers. White line score was worst in Guernseys and heel erosion and digital dermatitis were worst in Friesians. There is evidence that Jerseys tend have harder feet and less lameness (Chesterton et al., 1989). It has also been suggested that heavier cows are more prone to clinical lameness (Boettcher et al., 1998). Claw colour has also been implicated in lameness, with cattle with less pigmented feet being more prone to lameness (Chesterton et al., 1989). The heritability of clinical lameness in dairy cows from 24 herds was estimated as 0.10 and 0.22 using linear and threshold model analysis respectively (Boettcher et al., 1998). Enevoldsen et al. (1991) reported that a cow with a sole ulcer in one lactation was more likely to have one in a subsequent lactation.
Age is also important with regard to lameness. An initial peak in lameness occurs in young first calving heifers. There appears to be a marked reduction in horn growth in late-pregnant heifers, making them more prone to bruising and haemorrhages when housed on concrete floors. The reduced growth leads to softer horn formation, causing a weakening and possible separation at the white line and predisposing to mechanical bruising of the underlying sensitive corium. Older cows are mainly affected between five and eight years old (Choquette-Levi et al., 1985). Huang et al. (1995) found that the risk for six different foot disease traits increased with age.
There is evidence that low dominance-ranked cows spend less time lying down than high-ranking animals, leading to higher lameness risks. Many foot lesions are also related to the early post-calving period.
Lameness lesions
Over 90% of lameness involves the foot, with leg injuries being far less common. Lameness lesions can be classified into four main categories: horn, skin, joint and leg problems:
Horn Diseases:
Laminitis
Laminitis is an acute or chronic inflammation of the laminae, which lie immediately below the outer horny wall of the foot. The disease may cause lameness in its own right, often in all four feet, but usually it is a predisposing cause or risk factor for other types of lameness lesions, such as sole ulcer and white line abscesses.
Factors causing laminitis include housing systems and management factors that decrease lying times and increase stress on the feet, such as:

• cubicle design and overall cow comfort;
• competition for cubicle space;
• cubicle bedding material;
• sudden changes in calving, especially at calving.

(Philipot et al., 1994).
Nutritional factors have also been implicated in predisposing laminitis. These factors include:

• diets high in starch and low in fibre, leading to ruminal acidosis;
• possibly, diets high in crude protein content;
• sudden, major changes of diet at calving, especially from low to high concentrate diets;
• Excessive cow condition at calving, where overfat cows have a lower appetite for forage and hence are more prone to ruminal acidosis;
• The way food is offered - large amounts of concentrates at one time can produce acidosis.

Sole ulcer
Sole ulcers are the most common disease of the foot and most typically occur in the outer claw of the hind foot. Events such as laminitis may cause the pedal bone to drop and damage the underlying horn of the sole. As a result, an ulcer appears in the typical position - the centre of the sole towards the heel. The ulcer sometimes appears as a haemorrhage, with a softening and yellowing of the horn, progressing to necrotic tissue and often infection. Lumps of proud flesh - granulation tissue - may protrude from the ulcer area.
Sole ulcers can cause severe losses and reduced fertility, especially when occurring 70-120 days after calving. Many sole ulcers never fully heal and cows may suffer from chronic lameness for the rest of their productive lives. Solar ulcers may also predispose other conditions, such as septic arthritis.
White line abscess
The white line is the site at which the horn of the wall of the hoof joins that of the sole. It is a naturally weak area in the horn and cracks can allow dirt and bacteria to enter, causing abscess formation, pain and lameness. The initial weakness in the white line may be a result of laminitis, abnormal conformation and possibly dietary effects. The abscess most commonly occurs on the outside of the outer claw of the hind foot.
This type of lameness is the most common form of lameness in yarded cattle, especially on slats. Excessive activity on poor underfoot surfaces can lead to a high incidence of the condition. Restrictions of trough space in yarded cattle may also predispose the condition.
Slurry heel
Slurry heel is also known as heel erosion and is very common. Almost all older cattle which are housed show some degree of irregular loss of the bulbar horn. The problem may occur in all four feet, but often it may only affect the hind feet. The lateral digit is most commonly involved. It is thought the bacterium Dichelobacter (Bacteroides) nodosus, an obligate anaerobic bacterium producing keratolytic enzymes that are able to erode the horn, is involved (Toussaint Raven et al., 1985). As a result, the hoof might rotate backwards and the toe may no longer be weight-bearing, the pedal bone rotates and leads to an increased risk of lameness. The predisposing factors include moist conditions, which soften the horn, unhygienic conditions allowing bacterial proliferation, and overgrown feet and chronic laminitis, which produce poor quality horn.
Skin Diseases:
Digital dermatitis
Digital dermatitis is the most common skin disease of the foot, often associated with housing. It is a contagious inflammation of the epidermis. Classically, it occurs between the bulbs of the heels, but more recently it has also affected the interdigital space. There is a severe form that attacks the horn/skin junction at the coronary band.
Digital dermatitis is likely to be caused by an infection. Spirochaetes (a type of bacteria) are most probably involved (Woodward, 1999). They have a predilection for keratinised cells and produce a toxin which is keratolytic (Blowey et al., 1994). It can produce two types of lesion: erosive (strawberry-like) or proliferative (wart-like). The erosive form is most commonly found in the United Kingdom. It is very painful and has a pungent smell. The wart-like lesion occurs when the infection is not treated and is due to a chronic irritation reaction of the skin.
Foul-in-the-foot
Foul-in-the-foot is caused by an infection with Fusobacterium necrophorum, usually following damage to the interdigital skin by a foreign body. The infection results in sudden lameness, often in one limb. Body temperature is raised. There is swelling of the coronary band area, forcing the claws apart, and a split in the interdigital skin often associated with pus and dead tissue. The degenerated skin causes a 'foul' odour. At certain times of the year (wet, muddy and often warm at grazing) there can be herd outbreaks.
'Super foul' is an aggressive form of the disease that has become more common in recent years. It produces severe interdigital necrosis with rapid extension deep into the surrounding structures.
Joint Diseases:
Septic Arthritis
Septic arthritis usually involves the pedal joint between the pedal bone and the second phalangeal bone. It results from the direct extension of infection from a foot lesion (e.g. sole ulcer or white line infection) into the surrounding tissues and eventually involving the structures such as the joint itself. It is associated with swelling of the joints, acute pain, reduced appetite, weight loss and longer periods of recumbency.
Joint-Ill
Joint-ill is a disease of newborn calves and results from any form of septicemia that spreads to the joints of the limbs. The most common causative bacteria involved are E. coli and Streptococcus, which are found in great numbers in damp, dirty bedding. It causes severe lameness, usually in one or two joints.
Leg Injuries:
Hock Damage and Carpal Hygromas
Hock damage, such as hygroma and traumatic arthritis, primarily results from chronic mechanical irritation due to rough floors with little or no bedding, poor cubicle or building design, and poor hygienic conditions. A hygroma is a swelling on the outside face of the hock joint and is produced by changes in the skin and underlying structures. The skin is often hairless, thickened and flaky. The underlying tissues are thickened and swollen, mainly with fibrous tissue. A cavity may develop, containing blood clots and serum, but infection often produces an abscess, which will eventually burst and drain. A fibrous lump will remain.

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7:42 PM

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Cystic Ovaries

Cystic Ovaries

Theis year cystic ovaries have been occurring very commonly, and have been one of the most important causes of cows being presented to the vet for not being seen bulling

What are cystic ovaries

A cystic ovary is an ovary with a large (usually greater than 2cm), persistent (usually for more than 10 days) fluid-filled structure.

Cysts are often divided into two groups (luteal and follicular), based on production of progesterone and appearance. However, there is a vast amount of overlap between the two types and it is probably best to treat them just as cystic ovaries.

A cystic ovary

Clinical Signs

Cows with cystics ovaries usually have abnormal oestrus cycles; persistent oestrus, shortened oestrus intervals or failure to cycle (anoestrus). Anoestrus is by far the most common sign.

Persistent bulling behaviour, or nymphomania, is by far the least common clinical sign associated with cystic ovaries.

Diagnosis

• Best done by ultrasound examination by a veterinarian

Treatment

• Early prompt treatment is important as most cysts will not resolve on their own.
• A wide range of products have been used to treat cystic ovaries. Progesterone, prostaglandins and gonadotrophin-releasing hormones are the most commonly used products

Prevention

We do not fully understand the causes of ovarian cysts, which means that there are no specific prevention regimes. However energy deficiency is a major factor, and reducing the depth and length of the period of negative energy balance after calving, will significantly reduce the incidence of cystic ovaries

This can be achieved by:

1. Ensuring cows calve with a condition score between 2 and 3
2. Correct formulation of the ration
3. Maximising dry matter intake
4. Minimising metabolic disease
5. Maximising the care of the cow at and just after calving

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7:41 PM

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Cryptosporidiosis

Cryptosporidiosis

Cryptosporidiosis in recent years has come to national attention as a potential cause of water-borne disease in humans, due to contamination of the water supply by infected animal faeces. However, as well as being a potential human disease, cryptosporidiosis is also a significant cause of disease in young farm animals.

What is Cryptosporidiosis?

Cryptosporidiosis is caused by infection with the single-celled parasite (not bacterium) Cryptosporidium parvum. This parasite is found in many mammals including lambs, calves, goat kids, piglets and humans. Research so far has shown two basic types, the bovine type which affects most species, and a second human type which causes disease in humans only. Outbreaks of human disease, where large numbers of people are affected, are usually water-borne and usually associated with the bovine type of cryptosporidium. Individual sporadic cases of cryptosporidiosis in humans are mostly (around 60%) associated with the human type of cryptosporidium.

Cryptosporidiosis is usually seen in calves between one and two weeks of age. It is very rare in animals older than a month old, because by this age most animals will have become immune to infection.

Clinical Signs

1. Diarrhoea – profuse watery and green, occasionally bloody
2. Colic and pain
3. Depression, loss of appetite, weight loss

Many infected calves will not develop diarrhoea, the reason for this is not known In many cases cryptosporidia is seen with other diseases, particularly rotavirus. In this case disease is often more severe with more affected calves.

Diagnosis

• On the clinical signs described above
• Examination of diarrhoea for the presence of cryptosporidia. However, care must be taken when interpreting these results and it is best to consult a veterinarian in suspect cases

Treatment

• Many cases will recover without treatment.
• If calves become dehydrated then electrolytes should be given.
• If disease is severe, halfuginone can be used to reduce disease severity and prevent spread to other animals. However this product needs to be used with advice from your vet as it can cause problems if not used correctly, particularly in ill animals vAll calves with diarrhoea should be separated from clinically normal calves, to reduce contamination of environment with oocysts.

Prevention

To achieve effective control of cryptosporidia, good management and hygiene is vital. The major source of cryptosporidia is left-over oocysts from previously infected calves. These oocysts can be killed by freezing and by composting, but they are very resistant to disinfectants. Hot washing of surfaces followed by thorough drying is effective. Most commercial disinfectants are ineffective at recommended safe concentrations, except for some ammonia-based disinfectants.

Prevention of disease is therefore based on:

1. Regularly moving feed and water troughs
2. Preventing faecal contamination of feed and water troughs, by raising or covering
3. Increasing the bedding to reduce contamination
4. Clean and disinfect all buildings with products that kill oocysts vMass medication can be used as a preventative, but it is no substitute for improving management.

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7:40 PM

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Copper Poisoning in Cattle

Copper Poisoning in Cattle

Cattle are commonly supplemented with copper to prevent copper deficiency (often due to molybdenum toxicity). Unlike sheep, which are very prone to copper poisoning, it has been thought that cattle are relatively resistant. In the past most cases of copper poisoning have been associated with cattle inadvertently eating pig food or grazing pastures fertilised with pig manure (pigs are fed high levels of copper to increase growth rates). However, cases of copper toxicity are now being seen in cattle with no connection to pigs or pig by-products.

Copper toxicity in cattle is usually chronic in development (occurring as the result of a build–up over a long period of time), but is usually seen as an acute disease. The signs occur as the result of liver failure when the level of copper stored in the liver gets too high and damages the liver cells it is stored in)

Clinical Signs

1. Depression
2. Colic (abdominal pain)
3. Paleness and jaundice (yellowing)
4. Reduced appetite and milk yield.
5. Dark red urine (haemoglobinuria)
6. Death

Diagnosis

On clinical signs noted above you can be suspicious of copper poisoning. However your veterinary surgeon would carry out further tests to confirm copper poisoning:

1. Blood copper – will be elevated in ill animals, and in many apparently normal animals (unless there is a single small point source of copper. Blood copper measurement will show the extent of the problem
2. Tissue copper: Measurement of liver and kidney copper is confirmatory. This can be done by biopsy, but is best done post-mortem.

Treatment

Identify dietary sources of copper, and if possible remove them. Remove copper from all minerals. Individual treatment with ammonium molybdate and sodium thiosulphate can be effective but may not be economic. Other supportive therapy such as fluid therapy and antibiotics is of limited value

Prevention

It has not yet been clearly established what the cause of the increased rate of copper poisoning in cattle is. However, the risk of copper poisoning can be reduced by

1. Ensuring you know what the copper intake of your cows. Pay particular attention to the copper content of your mineral and your forage
2. Using chelates with care. So-called ‘organic copper’ may be better absorbed than inorganic copper, but this increase the risk of copper toxicity, particularly if the same amount of copper is fed.
3. Do not supplement with copper unless you have clear evidence of copper deficiency (or molybdenum toxicity)

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7:39 PM

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Cold Cow Syndrome

Cold Cow Syndrome

Cold cow syndrome is an unusual disease of unknown cause, which usually occurs in early spring in lactating cows grazing ryegrass pastures. It has been seen in most areas of the UK. The syndrome can affect up to 80% of a group of cows The most likely cause is the intake of very high levels of soluble carbohydrates, but other suggestions include oestrogenic compounds in the plants and mycotoxins. There does not appear to be any link with weather conditions

Clinical Signs

• Cow appears drunk, wobbling and falling over
• Cow cold to the touch, but body temperature normal
• Profuse non-smelling diarrhoea
• Sudden dramatic milk drop ( up to 100% in affected cows)

Diagnosis

• On the clinical signs described above

Treatment

• There is no specific treatment, except that affected herds should be housed for at least 24 hours before they are moved to a new pasture Cows unable to stand will require nursing care

Prevention

1. The problem may occur on the same pasture each year, thus avoiding the use of that pasture in early spring may be helpful
2. Until the cause of the diseases is better understood then further preventative measures are not possible

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7:37 PM

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Coccidiosis in Cattle

Coccidiosis in Cattle

The Nadis data show that the number of cases of coccidiosis is at its lowest in late winter, and then rises during the spring to peak in June and July. This peak is followed by a slight,short-lived fall in late summer, and then another rise to a peak in November.

Coccidiosis - Cattle
Average 1997 - 2001

What is Coccidiosis

Coccidiosis is caused by single-celled parasites (not bacteria) known as coccidia. There are several species in cattle, not all of which cause disease. The species that cause disease are primarily found in the large intestine, and the diarrhoea results from damage to the cells lining it.

Coccidiosis is seen in animals up to two years old, and is particularly common in calves between three weeks and six months of age. Cattle become infected when placed in environments contaminated by older cattle or other infected calves. This can happen either indoors on bedding, or outdoors around drinking or feeding troughs. In order for the coccidial oocysts (the egg stage of the parasite) to become infective they require warmth and moisture. It is probably the lack of moisture in late summer and the low temperatures in late winter that result in the low level of coccidiosis during these times, however coccidiosis can be a significant problem at any time of year.

Clinical Signs

The most common sign is a watery diarrhoea, which because the coccidia damage the large intestine is often accompanied by straining (which can become very severe), mucous and blood. Other signs can include depression, loss of appetite, weight loss, and, much more rarely than with diarrhoea in milk-fed calves, dehydration. Death is rare. Infections that fail to produce diarrhoea can, nevertheless, result in reduced growth and weight gain. This sub-clinical infection is very common, with up to 95% of cases being of this type.

Diagnosis

• On the clinical signs described above
• Examination of diarrhoea for the presence of large numbers of oocysts. However, care must be taken when interpreting these results and it is best to consult a veterinarian in suspect cases

Treatment

• Most cases will recover without treatment. Discuss the necessity of treatment in particular cases with your veterinary surgeon.
• If calves become dehydrated then electrolytes should be given.
• Once high numbers of oocysts are found, then treatment is unlikely to be of any benefit
• Treatment is better given to in-contact animals that have not yet started showing signs, or to combat secondary infection. A large number of products are available for treatment, but only two are licensed. Specific recommendations should be obtained from your veterinarian.
• All calves with diarrhoea should be separated from clinically normal calves, to reduce contamination of environment with oocysts.
• If possible, during an outbreak stressful procedures, such as dehorning, castration and weaning should be avoided

Prevention

To achieve effective control of coccidia, good management and hygiene is vital. This should include:

1. Reducing stocking density
2. Regularly moving feed and water troughs
3. Preventing faecal contamination of feed and water troughs, by raising or covering
4. Increasing the bedding to reduce contamination
5. Clean and disinfect all buildings with products that kill oocysts
6. Mass medication can be used as a preventative, but it is no substitute for improving management.

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7:35 PM

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Campylobacter infection (Vibriosis)

Campylobacter infection (Vibriosis)

The NADIS data show that abortion and infertility remain significant problems on farm. One of the most important causes of infertility and abortion in UK cattle is infection by Campylobacter fetus. This organism can cause sporadic abortion, abortion storms, metritis, delayed return to heat, and very low pregnancy rates.

How do cows get infected?

Sporadic abortion, that is the one-off case, is probably associated with the bacteria getting in via the guts. However the vast majority of problems associated with Campylobacter are linked to venereal infection. In most cases the source of infection is an infected mature bull bought onto the farm, which then spreads the bacteria as it mates. The most high-risk animal is a hire bull. Younger bulls and breeding females are less common sources of infection but any animal that has been previously mated is a potential source.

In bulls, infection is not associated with clinical signs, problems with Campylobacter are exclusive to the female

Clinical signs

• Mild endometritis
  
  
• Failure to conceive .. Return to service at normal time
  
  
• Early embryonic death .. Delayed return to service
  
  
• Late embryonic death .. Abortion (usually 4 to 5 months)

Cows (but not bulls) readily become immune to infection, so quite often Campylobacter is first seen as a problem after the introduction of a bull, which resolves itself over the period of a few months. However, heifers served by the bull for the first time remain susceptible and immunity is often not protective for more than one year. Additionally the bacterium can be found in vaginal mucous for more than a year after infection even after the development of immunity. Such cows are good sources of infection for new uninfected bulls Diagnosis

• Campylobacter can be isolated from aborted fetuses and fetal membranes – the bacterium is found in about 3% of abortion cases in which a diagnosis is made.
  
  
• Most commonly Campylobacter is suspected when there are high return rates or poor pregnancy rates in a herd using natural service. However, proving the role of Campylobacter can be difficult as we have no test which has a sufficiently low rate of false negatives
  
  
• Sheath washing of bulls followed by culture in the laboratory is the best available method of identifying infected bulls. However, although a positive test
  
  is a useful indication of infection, a negative result is not; the test is insensitive and does not pick up all infected bulls
• Identifying infected cows is more difficult. Culture of vaginal mucus is less sensitive than culture of sheath washings so more infected cows will be missed. If you suspect Campylobacter get your vet to collect samples from at least 12 cows served by the suspect bull or bulls as this will significantly increase the chances of finding the bacterium.

Treatment

In cows treatment is not very effective, and, particularly because diagnosis is often made in the late stage of the disease, it is usually best to wait for natural immunity to eliminate the disease. Routine treatment of bulls bought onto a farm can reduce (but NOT eliminate) the risk of them spreading disease.

Control

In infected herds stop using natural service until at least two years after initial infection began. If oestrus detection is a problem then synchronisation with fixed time AI should be used. Vaccination is extremely effective n the control of Campylobacter, however no authorised vaccines are available in the UK. For severe problems your vet can get an autogenous vaccine made up which can be used on your herd only.

Prevention

As there are no authorised vaccines available in the UK, prevention is based on maximising biosecurity. In an uninfected herd maintaining a closed herd will prevent disease, but if this is not possible then a buying policy of purchasing virgin heifers and bulls only will not significantly increase the risk. 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.

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7:32 PM

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Calf Pneumonia

Calf Pneumonia

Respiratory diseases in young animals
Enzootic pneumonia in young calves is a multifactorial disease that occurs mainly in two different systems: in housed dairy calves reared for replacement or in housed calves reared for beef in a herd other than the herd of origin. Dairy calves are likely to suffer from the disease at any age, with it manifesting itself as a chronic, coughing pneumonia, or as a more acute, enzootic calf pneumonia. Older dairy calves are also vulnerable after housing in the autumn. Suckler calves are more likely to suffer from respiratory disease between two and five months of age, following weaning or transport from one herd to another. Outdoor reared beef suckler calves can also be severely affected by pneumonia (Peters, 1986; Scott, 1997).
In older calves, mainly in weaned suckler calves aged six months to two years, respiratory disease is likely to occur after transport or other environmental stress and is often called shipping or transit fever. This condition is discussed elsewhere in this compendium (see: Pasteurellosis). Similarly, a respiratory disease caused by lung parasites, husk, occurs in older calves and is discussed elsewhere. A viral respiratory disease caused by the infectious bovine rhinotracheitis virus is also more significant in older animals and discussed under its own heading.
Respiratory diseases in young animals were ranked very low in importance in a survey of British organic beef and dairy farmers (Roderick and Hovi, 1999). Late weaning, a whole milk diet, the requirement for good housing standards and a closed herd policy reduce the risk factors for respiratory disease in calves in organic dairy herds (UKROFS, 2000). The Soil Association standards further prevent the sale of calves via the cattle markets when calves are sold for fattening (Soil Association Certification Ltd., 2000). This should reduce the stress of moving from one farm to another and the risk of acquiring new infections.
Enzootic pneumonia in calves
Enzootic pneumonia in young calves may be a chronic disease with very few clinical signs apart from a dry cough and slightly increased respiratory rate. The acute form of the disease usually manifests itself in an outbreak involving several calves going down with the disease within a 48-hour period. Fever, dullness, inappetance and coughing, often combined with nasal discharge, are the most common symptoms.
There is very little data available on the prevalence of enzootic pneumonia in UK cattle herds, as recording of calf diseases is seldom carried out. Respiratory diseases are, however, considered the second most important cause of death and ill drift in calves. The condition is farm related, with some farms suffering serious losses due to calf pneumonia, while on others the disease is either very mild or non-existent. Sporadic outbreaks can, however, be experienced by farms that normally see very little respiratory disease in calves.
Causes of enzootic pneumonia
Enzootic pneumonia in calves is a multifactorial disease. Infectious agents, environment, management and the immune status of the calves are all-important factors in determining the outcome of an infection.
A multitude of infectious agents, including viruses, bacteria and Mycoplasma, are involved in different combinations on different farms (Dyson and Linklater, 1976; Bryson et al., 1987; Caldow et al., 1988; Uttenthal et al., 1996). It is often suggested that the viral and mycoplasmal agents are the primary infections and the bacterial agents cause a secondary infection in an animal whose defences have been weakened by the first infection. The most common viral agents isolated from enzootic pneumonia cases are respiratory syncytial virus (RSV), parainfluenza III virus (PI3), infectious bovine rhinotracheitis virus (IBR) and bovine viral diarrhoea virus (BVD), some of which are discussed separately as herd problems elsewhere in the compendium.
Mycoplasmal agents are usually considered to be the most common agents causing the chronic form of enzootic pneumonia, even though Mycoplasma bovis has been identified as the causative agent in many acute outbreaks as well.
The most commonly isolated bacterial organisms are Pasterurella and Hemophilus subspecies.
The main environmental factor predisposing calves to respiratory disease is poor ventilation in calf housing (Anderson et al., 1978; Lamprecht, 1982; Pritchard, 1982). Cold, humid conditions, sudden changes in air temperature, stress due to different causes and change in the environment have also been associated with outbreaks of pneumonia in young calves. (Phillippo et al.,, 1987; Webster et al., 1985; Roe, 1982; Scott, 1995).
Inadequate intake of colostrum or poor quality colostrum will affect the calves' defence against respiratory agents and make them more susceptible to infection (Virtala et al., 1999). Weaning of calves before five weeks of age has been associated with increased respiratory disease. Rearing systems where calves of different origin are mixed together at a young age suffer from high levels of respiratory diseases (Miller et al., 1987). Large , shared air spaces, calves from different age groups and poor sanitation between calf batches often make these systems even more vulnerable (Ostergaard et al., 1986; Losinger and Heinrichs, 1996). Calves that have suffered from diarrhoea are also more likely to suffer from respiratory disease. The stress associated with management procedures such as disbudding and castration may also be associated with a high respiratory disease incidence.

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7:31 PM

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Calf Diphtheria

Calf Diphtheria {Necrobacillosis}

What is calf diphtheria?

There are two forms of calf diphtheria. The most common is an acute oral (mouth) infection, usually seen in calves less than 3 months old. The second form is usually seen in older calves and affects the larynx (or voice-box), Both forms are caused by the bacteria Fusobacterium necrophorum, which also causes foul-in-the foot and liver abscesses in older cattle.

Clinical Signs

Oral form

• Initial presenting sign may just be a swollen cheek
• Calf may be otherwise bright and active with no temperature
• Examination of the inside of the mouth shows a foul-smelling ulceration and swelling of the cheek
• Temperature may be normal at the start

If untreated more signs develop:

• High temperature
• Coughing
• Loss of appetite and depression
• Difficulty breathing, chewing and swallowing
• Swollen pharyngeal region
• Deep ulcers on the tongue, palate, and inside of cheeks
• Pneumonia

Usually only a few calves in a batch are infected though outbreaks can occur where hygiene is poor

Laryngeal form:

• Coughing : Moist and painful
• High temperature
• Loss of appetite and depression
• Difficult breathing, chewing and swallowing
• Pneumonia

Diagnosis

• The diagnosis of calf diphtheria is usually based on the clinical signs.
• For one-off cases rule out other problems such as BVD and foreign bodies by getting your vet to do a thorough oral
• examination
• Bacteriology can be also useful.
• A post-mortem can confirm the ulcerative nature of the disease, particularly in calves with the laryngeal form

Treatment

• Early prompt treatment is important as early treatment is much more effective
• Separate the infected animals and isolate them
• Antibiotics and pain killers are effective in most cases
• The laryngeal form is much more resistant to treatment. Get veterinary advice

Prevention

Fusobacterium necrophorum is a normal inhabitant of cattle intestines and the environment. Under unhygienic conditions, infection may be spread on feeding troughs and dirty milk buckets. Some of the contributory factors for occurrence of this disease include abrasions in the oral mucosa (such as those from erupting molar teeth), poor nutrition and the presence of other diseases present in young calves.

If animals are closely confined, the spread of this infectious disease can be prevented by thoroughly cleaning and disinfecting of all calf feeders. Young calves must be examined daily to identify early stages of the disease.

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7:29 PM

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Bulls and Biosecurity

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?

1. 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.
   
   

2. 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.
   
   

3. 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.
   
   

4. 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.
   
   

5. 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.

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7:26 PM

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Brucellosis

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's 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's 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 an 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's 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's 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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7:24 PM

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Bracken Poisoning of Cattle

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

1. Limit access to pastures with bracken, particularly if grazing is poor
2. 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
3. Bracken control by burning, ploughing, reseeding, and herbicide is the best method of prevention.

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7:23 PM

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Bovine Viral Diarrhoea {BVD}

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).

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Bovine Spongiform Encephalopathy (BSE)

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 Diarrhoea Virus (BVDV)

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

1. 
   
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.
2. 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
   
   
3. 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
   
   
4. 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
   
   
5. 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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Bluetongue (BTV)

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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