Cattle Diseases Guide:

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

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

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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
Depression
Colic (abdominal pain)
Paleness and jaundice (yellowing)
Reduced appetite and milk yield.
Dark red urine (haemoglobinuria)
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:

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
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
Ensuring you know what the copper intake of your cows. Pay particular attention to the copper content of your mineral and your forage
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.
Do not supplement with copper unless you have clear evidence of copper deficiency (or molybdenum toxicity)

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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
Diarrhoea – profuse watery and green, occasionally bloody
Colic and pain
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:

Regularly moving feed and water troughs
Preventing faecal contamination of feed and water troughs, by raising or covering
Increasing the bedding to reduce contamination
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.

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
Diarrhoea – profuse watery and green, occasionally bloody
Colic and pain
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:

Regularly moving feed and water troughs
Preventing faecal contamination of feed and water troughs, by raising or covering
Increasing the bedding to reduce contamination
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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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:
Ensuring cows calve with a condition score between 2 and 3
Correct formulation of the ration
Maximising dry matter intake
Minimising metabolic disease
Maximising the care of the cow at and just after calving

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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.

[mikey]

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:
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
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:
Ensure cattle are not too fat at calving (i.e. >3.5 BCS)
Feed high quality feeds, with good quality forage


Feeding a total mixed ration as opposed to concentrates


Ensure plenty of space at feeding sites


Minimise changes between late dry and early lactation ration


Prevent and promptly treat, diseases such as milk fever, metritis, toxic mastitis and retained afterbirth which reduce feed

intake
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.