Peri-Weaning Diarrhoea

Peri-Weaning Diarrhoea

Peri-weaning (or post-weaning) diarrhoea is becoming a significant and increasing disease of calves on many farms

What is peri-weaning diarrhoea?

Peri-weaning diarrhoea is an apparently new syndrome in calves around the time of weaning (usually, but not always, after weaning). The cause of the disease is unknown, infectious agents, managemental, environmental and nutritional factors have all been implicated.

The diarrhoea is usually first seen fairly soon after group housing, particularly if the animals were previously kept in outdoor hutches. However, in some outbreaks diarrhoea can begin up to two weeks before weaning.

Clinical Signs

• Profuse watery grey diarrhoea.
• Most calves affected, but death usually rare
• The calves tend to be bright and continue eating
• Dehydration tends to be moderate
• Pot-bellied appearance common in ‘recovered’ calves
• Reduced growth rate, and uneven batches of calves has significant economic effect.
• Significant faecal staining of the coat and appearance of ‘ill thrift’.

Diagnosis

• On the clinical signs described above
• Usually a diagnosis of ‘exclusion’, i.e. other diseases ruled out by investigation

Treatment

• Treatment, except for electrolytes to treat dehydration, is often ineffective, with the duration of the disease seeming to depend on the age at which it developed (younger animals tend to have more persistent diarrhoea)..
• Many antibiotics have been tried but none are routinely effective. Ask your vet for further advice on

Prevention

The cause is unknown so no specific prevention programme has been developed. However several management and nutritional factors have been implicated, and preventing these has reduced the incidence of peri-weaning diarrhoea on many farms: Management: Avoid abrupt weaning and ensure calves get colostrum for at least the first week after birth. Nutritional: Avoid the use of calf pellets that rapidly ferment in the rumen, use slower fermenting coarse mixes. Also avoid products containing heat treated soya.

Unknown

6:38 PM

اقرأ المزيد

Nitrate Poisoning

Nitrate Poisoning

Nitrate poisoning is a rare but important cause of poisoning in cattle. It can occur as the result of eating crops such as Brassicas, green cereals or sweet clover that contain high levels of nitrate. However, the most common source is inorganic nitrate fertiliser, either directly (straight from an open bag), via grazing an over-fertilised field, or via water run-off from heavily fertilised fields. Spring is the most common season for nitrate poisoning.

Nitrate poisoning occurs because the nitrate is broken down to nitrite in the rumen. In normal circumstances this nitrite is further broken down to ammonia in the rumen and is then used by the rumen microbes to make protein. However, when large amounts of nitrate are eaten over a short period of time, the nitrite accumulates in the rumen and is absorbed. Once in the bloodstream it reacts with iron in the red blood cells so that they can no longer bind oxygen.

Clinical Signs

The signs are usually seen within a few hours of eating the nitrate. The higher the dose the faster the signs develop.

• Abdominal pain
• Scour
• Weakness
• Muscle tremors
• Drooling of saliva
• Blue discolouration of the mouth
• Mouth breathing
• Collapse
• Coma
• Death

Diagnosis

The clinical signs are vague, particularly early on. Early veterinary involvement is therefore important. If your cattle have had access to nitrate and start showing signs of illness, get them checked as soon as possible.

Nitrate poisoning can be identified using a blood test for either nitrate or methaemoglobin (the product formed when nitrite reacts with the red blood cells). In severe cases and at PM the methaemoglobin is visible as high levels in the blood result in the blood becoming chocolate in colour

Treatment

Remove the source of nitrate. Veterinary treatment with methylene blue can be very effective at reversing the changes in the blood, particularly in the early stages.

Prevention

Prevent access to nitrate sources. In particular, prevent cattle getting into fertiliser stores. Ensiling high nitrate pastures will usually reduce the nitrate levels to safe levels (as will allowing the pasture to set seed). Feeding a high grain diet alongside high nitrate forage has a protective effect because carbohydrates enhance the conversion process from nitrate to microbial protein

The animal can become conditioned to eat larger amounts of feed with a high nitrate content if the increase is gradual. Healthy animals are less likely to be adversely affected than animals in poor health. Adequate amounts of available carbohydrates (grain) allow the animal to consume more nitrate.

Unknown

6:33 PM

اقرأ المزيد

New Forest Eye

New Forest Eye

Whilst no epidemiological data exists, it is suspected that New Forest eye is the most common eye condition seen in cattle in the UK. The disease has a world-wide distribution and is usually seen in epidemics when a chronically or subclinically infected animal enters a herd. The clinical symptoms vary depending on the animal's susceptibility and the level of other contributing factors, but the main symptoms are runny eyes, red and inflamed conjunctiva and corneal ulcers in the later stages of infection.
The causative agent is a bacterium Moraxella bovis. As the condition is seen commonly during the summer months, it is suspected that ultraviolet light, dust and flies act as predisposing factors. The condition can be seen in housed animals, and it is suggested that these predisposing factors are not needed for an epidemic to occur (Bedford, 1992).
Young animals are more susceptible than older animals and exhibit severer clinical symptoms. Most clinical cases are seen in animals under two years of age (Webber and Selby, 1981).
Keratoconjunctivitis can also be caused by Listeria monocytogenes of silage origin, resulting in silage eye

Unknown

6:18 PM

اقرأ المزيد

Neosporosis in cattle

Neosporosis

One of the most recently identified causes of abortion is neosporosis, however recent studies suggest that neosporosis causes over 10% of all abortions in UK cattle

What is Neosporosis

Neosporosis is caused by infection with the protozoa Neospora caninum. Neospora has been found world-wide and in many species other than cattle. Currently abortion due to Neospora has been shown in cattle, sheep and dogs. The dog and other canids (such as foxes) are the definitive host. That is they are the animals in which the parasite becomes sexually mature and reproduces.

Clinical Signs

• Abortion, between 3 and 9 months of pregnancy (particularly 5 to7 months)
• Still birth or premature calf
• Occasionally, calves will have brain disease at birth
• No other signs seen in the mother
• Repeat abortions possible in the same cow

Diagnosis

• Clinical signs of little help
• Characteristic heart and brain damage in aborted calf
• Identification of parasite in the calf tissue
• Antibodies in the mother's blood

However, as a large number of healthy calves can be infected with Neospora it is important to eliminate other causes of abortion, particularly BVD or leptospirosis before a diagnosis of neosporosis is made

Treatment

• No treatment of any proven benefit

Prevention

Dogs are potentially a source of disease. So prevention must include:

1. Keeping cattle food and water away from dogs and foxes
2. High hygiene standards at calving. Dispose of placental membranes and aborted or dead calves before dogs can get them

However, transmission from mother to calf (known as vertical transmission) is far more important. Over 90% of calves born to mothers with antibodies to Neospora will have been infected in utero. The importance of transmission between cattle is less clear. Nevertheless, vertical transmission alone can maintain infection in a herd. To eliminate Neospora you need to:

1. Identify infected cattle and cull them: All cattle with antibodies to Neospora are sources of infection to their calves, have a significantly increased risk of abortion, and, on average, produce less milk than antibody negative cows.
2. Select only seronegative cattle for breeding. Heifers with antibodies should be sold for meat not bred

These strategies look expensive to achieve, however the cost of neosporosis far outweighs the cost of eliminating it from the herd

Unknown

6:03 PM

اقرأ المزيد

Necrotic enteritis in cattle

Necrotic enteritis

Records from NADIS vets show that the first cases of necrotic enteritis this year were recorded in April. This uncommon but serious disease is usually only seen in late spring/early summer

What is necrotic enteritis?

Necrotic enteritis is a disease of unknown cause, seen in spring-born suckled calves at grass. These calves are usually between 6 and 16 weeks of age.

Clinical Signs

• Diarrhoea often with blood and mucous
• Inappetance, lethargy,
• Loss of condition, dehydration
• Ulcers may be present on lips, gums or tongue
• Death in over 95% of cases
• Other calves in group may show a mild diarrhoea, but rapidly recover

Diagnosis

• On the clinical signs described above
• Other diseases such as salmonellosis, coccidiosis and BVD need to be ruled out
• A post-mortem on fresh material is essential to confirm necrotic enteritis

Treatment

• None. The mortality rate is so high that euthanasia after eliminating other possible diseases is usually the best option.

Prevention

The cause of necrotic enteritis is not yet known. This means that there are, as yet, no effective preventative regimes. There may be some link to specific pastures, so if you have an outbreak, using a different pasture the following spring might reduce the risk of disease

Unknown

5:32 PM

اقرأ المزيد

Molybdenum Toxicity

Molybdenum Toxicity

There has been much recent discussion in the farming press about ‘molybdenum toxicity’ and its role in cattle fertility. Despite the discussion, it is unclear how much of a role molybdenum toxicity actually plays in poor fertility.

There are two types of molybdenum toxicity. The first, which is well recognised, occurs on high molybdenum pastures (often referred to as ‘teart’ pastures) containing around 20 – 100 mg of molybdenum per kg. Within a few days of being placed on such pastures, cattle start scouring and develop stary, harsh coats. This can be effectively prevented by high doses of copper, because it has been demonstrated that such levels of molybdenum affect the absorption and metabolism of copper.

The second type of molybdenum toxicity, which is the type discussed recently in the press, is more controversial. This is the suggestion that at much lower levels of molybdenum (figures??, problems of toxicity can occur even in animals which are being fed more copper than their calculated dietary requirements and have an apparently normal copper status. It is suggested that in adult cattle affected by this version of molybdenum toxicity, the most common problem reported by the farmer is poor fertility. Like teart pasture toxicity, it is suggested that this “low level “ molybdenum toxicity also responds to further copper supplementation.

Does low level molybdenum toxicity exist?

The answer has to be that we don’t know. Even at low levels molybdenum will alter copper metabolism, but it is unclear whether or not it can cause problems in animals which show a normal copper status. The proponents of molybdenum toxicity suggest that molybdenum causes poor fertility as a result of binding to copper (as a compound called thiomolybdate) in the body and preventing its action, without affecting our current tests for copper status. Opponents suggest that thiomolybdates are not necessarily harmful and that molybdenum doesn’t cause problems in animals with normal copper status.

The main problem linked with this “low level” molybdenum toxicity is poor fertility. Fertility in the UK dairy herd is decreasing and many farms have got poor fertility for many different reasons. The most common reason for poor fertility is output exceeding input, that is cows losing more energy in their milk than they can eat. Cows in negative energy balance have reduced fertility, and, while the mechanism for this is far from simple, generally the worse the imbalance the worse the fertility. Any investigation of poor fertility should focus on overall feeding and management first before looking at micronutrients such as copper and molybdenum. So if someone suggests to you, without such an investigation, that molybdenum toxicity is likely to be your main problem, such a suggestion should be taken with a pinch of salt (do not take any Molybdenum).

Can we diagnose toxicity?

Diagnosis of copper deficiency isn’t simple. Cattle can have normal blood copper in the early stages. Thus when investigating deficiency it’s important to sample several cows (at least six), and, ideally, measure liver coppers (which is a better test of status). The proponents of molybdenum toxicity suggest that, because the molybdenum binds but does not remove the copper, blood and liver measurement are not of much value in detecting molybdenum toxicity. They suggest that we need to look at the activity of a copper-containing enzyme, caeruloplasmin. This test seems to show that a high percentage of cattle in the UK have molybdenum toxicity. However, it isn’t a validated test and it is possible that factors other than molybdenum may alter the test’s result.

From a farmer’s point of view, if you are going to use this test ensure that you use it as part of an investigation of fertility and not on its own. Get veterinary advice first.

Can we treat toxicity?

If molybdenum toxicity exists then increasing the intake of copper can prevent it by binding the molybdenum in the gut and thus preventing it getting into the body. However, copper is a poison, so if you are going to feed more copper you should only do so once you have calculated exactly how much copper you are feeding your cows. Too much copper will cause copper toxicity. This used to be a problem almost entirely confined to sheep and young calves, but it’s now being diagnosed in adult cattle. In most cases, the main problem leading to toxicity was that farmers with fertility problems did not know how much copper they were feeding. This meant that they did not appreciate that when the copper in the diet was increased to try and improve fertility, it resulted in toxic levels of copper being fed. Extra copper should not be fed unless there is a proven need for it.

Unknown

5:30 PM

اقرأ المزيد

Mastitis in dairy cattle

Mastitis

Introduction
Mastitis is one of the three most significant health problems of the UK dairy herds, together with lameness and fertility problems (Kossaibati and Esselmont, 1997). The effect of mastitis on milk quality has recently gained added importance with the introduction of an EU-wide upper legal limit for somatic cell counts in milk destined for liquid market at 400 000 cells/ml. Public interest in the welfare of production animals and the recognition of mastitis as a major source of pain for affected cows give added focus to mastitis concerns (Fitzpatrick et al., 1998).
Organic dairy farmers have identified mastitis as a major concern in the UK, mainly due to non-use of antibiotic dry cow therapy and the need to maintain low somatic cell counts in the milk (Roderick and Hovi, 1999). Animal welfare aspects of controlling and treating mastitis are also important on organic farms, where the maintenance of high welfare standards is important.

Mastitis – causative factors
Our understanding of mastitis has developed in several stages over the past 100 years. An association between mastitis and pathogenic micro-organisms was established in 1887 (Munch-Petersen, 1938). Most major pathogens were identified by the 1940s. When antimicrobial therapy became available for production animals in 1945 it proved effective in the control of some, but not all, mastitis pathogens (Edwards et al, 1946; Downham et al, 1946) . This prompted further research into potential husbandry related causes of mastitis. In the 1960s, the multifactorial aetiology of bovine mastitis was commonly recognized (Neave, 1959; Fell, 1964).
Today, mastitis is considered to be a multifactorial disease, closely related to the production system and environment that the cows are kept in. Mastitis risk factors or disease determinants can be classified into three groups: host, pathogen and environmental determinants (see Control and Prevention).

Mastitis and somatic cell counts (SCC)
Somatic cell counts (SCC) have long been used as a way of measuring milk quality. Most dairy companies base their milk pricing policy, among other things, on SCC values of the milk. The SCC levels in the national dairy herd in the UK have declined steadily since the 1970s and are now well below 200 000 cells/ml, both in bulk tank milk and in average individual cow milk in milk-recorded herds. The maximum legal limit for saleable milk is 400 000 cells/ml.
The somatic cells consist mainly of immune cells that enter the milk compartment of the udder. Only a minority of these cells are dead cells from the udder tissue. There are always small quantities of immune cells in the cow’s milk, and their function is to protect the udder against infection by bacteria. The older the animal gets, the more somatic cells it tends to have in its milk. Similarly, the SCC levels are higher immediately after calving and towards the end of each lactation.
When bacteria do enter the udder, the number of immune cells increases rapidly, as the immune system attempts to overcome the infection. Once the infection has been cleared, the SCC levels gradually drop to normal. This can sometimes take weeks, however. In cases of chronic infection, where the bacteria persist in the udder, the SCC levels can remain high throughout the lactation.
High SCC levels in the milk cause deterioration of the milk quality. It has been shown that levels above 500 000 cells/ml decrease cheese yield and affect yoghurt making. The shelf life of milk is also affected, but at a higher level of SCC.
Consistently high SCC levels in a herd are usually a sign of high levels of subclinical mastitis. Most cases of subclinical mastitis are caused by contagious mastitis bacteria (S. aureus or Str. agalactiae), even though Str. uberis is increasingly considered to cause chronic mastitis as well.

Masititis in the UK
In the UK, no national survey data on clinical mastitis has been produced since 1986 (Wilesmith et al., 1986). Annual incidence in England and Wales was reported at 54.6 cases per 100 cows in 1980 and 41.2 in 1982. A recent survey of DAISY (Dairy Information System) recorded herds in England and Wales reported the following parameters for clinical mastitis: 39.9 cases per 100 cows; 25.9% of cows affected and a recurrence rate of 18.3% (Kossaibati et al., 1998). Another survey of English and Welsh dairy herds participating in an udder health programme found an average clinical incidence rate of 34 cases per 100 cows (Berry, 1998). Whilst these surveys offer no data on the prevalence of different mastitis pathogens, sporadic evidence from small field surveys and summaries of VI-centre isolations of mastitis pathogens suggest that E. coli has become the most important mastitis pathogen in the UK, with Str. uberis as the second most important pathogen (Bradley and Green, 1998; Jones, 1998). This anecdotal evidence also suggests that staphylococcal mastitis has significantly declined in significance in the past 30 years. It is, however, suggested that there are great regional variations in the prevalence of different mastitis pathogens, and that S. aureus still remains an important mastitis pathogen in the north of England and Scotland (Logue et al., 1997).
During the past 30 years, there have been even more significant changes in the levels of somatic cell counts of the milk produced in the UK. Bulk tank somatic cell counts have dropped from an estimated 750,000 cells/ml in 1968 to a present estimate of 180,000 in 1996 (Booth, 1997). Individual cow milk cell counts (CMSCC) in the milk recorded herds have similarly declined from an average of 573,000 cells/ml in 1971 (Booth, 1997), to 168,000 in 1996 (NMR, 1997). A similar decline in both bulk tank and individual cow somatic cell counts has been observed in other European countries during the same period.
Whilst mastitis control programmes have had a major impact on the improvement of udder health in the British national dairy herd, it has been suggested that introduction of milk quota systems within the EU, quality payments based on bulk milk somatic cell counts and, most recently, legislation setting maximum somatic cell count levels for saleable milk within the EU have been the major encouraging and motivating factors in bringing about the changes described above. It has also been pointed out that the incidence of clinical mastitis has not declined at the same rate as the somatic cell counts in the past 15-20 years, but has rather remained at an endemic level in the national herd (Booth, 1997).

Mastitis in organic dairy herds
Mastitis incidence and patterns were surveyed in 16 organic and 7 conventionally managed dairy herds in the south of England and Wales in 1997-1998 (Hovi and Roderick, 1999). Clinical mastitis incidence in survey herds is presented in the table below. Whilst overall mastitis incidence was significantly lower (P<0.001) in O herds than in C herds, the incidence rates during the dry period were significantly higher in O herds than in C herds (P<0.001). There was a wide variation in incidence rates amongst both O and C herds. The lower incidence in O herds was related to a very low incidence in one large herd.

Table 1. Mastitis incidence (cow cases/100 cow years)
	O herds	C herds
Overall	36.4	48.9
Lactation	37.6	54.5
Dry period	28.9	9.2

Average individual cow SCC levels were significantly higher in O herds (135,000 cells/ml) than in C herds (84,000 cells/ml; P<0.001), resulting in high subclinical mastitis levels in O herds (individual cow SCC> 200,000 cells/ml in 34% of all measurements).

Another UK survey of dairy farms converting to organic milk production (Weller et al., 1996) found average levels of 45.8 cases of clinical mastitis/100 cows on 11 farms at the end of the conversion period, with mean annual somatic cell counts of 299,000.
A German study of 268 organic dairy herds identified mastitis as the most important health problem. Whilst incidence rates for mastitis were similar to those on conventional farms, the culling rates for mastitis were higher than on conventional farms (Krutzinna et al., 1996). Vaarst (1995) studied health and disease control on 14 organic dairy herds in Denmark, and found similar levels of mastitis incidence to comparable conventional herds. A Dutch study has identified somatic cell count control as a critical area in mastitis control under organic production standards. In the study, S. aureus mastitis is seen as the main mastitis problem on organic dairy farms, and the difficulty in controlling it is attributed to poor diagnosis and non-use of antibiotic DCT (Baars and Barkema, 1998).

Unknown

10:26 AM

اقرأ المزيد

Mange / Lice in cattle

Mange / Lice

Mange is a collective name for allergic dermatitis caused by ectoparasitic infestation by mites that are obligate parasites and spread from animal to animal by direct contact. Mange usually appears as a skin condition associated with irritation and scratching that leads to inflammation, exudation and crusts and scabs forming on the skin. Untreated mange leads to thickening of the skin and loss of condition of the animal. The disease is often seen in animals in generally poor condition and during the winter season. The condition sometimes causes welfare problems in dairy herds as the treatment of lactating animals is not carried out due to long withdrawal periods required in connection with the efficacious treatments.
The mange mites prevalent in the UK can be divided into burrowing and non-burrowing mites. The only burrowing mite of importance in the UK, Sarcoptes scabiei, has a life cycle of about three weeks from egg to adult, after which the adult female will lay eggs for up to 60 days. The most common sites for sarcoptic mange on cattle are inner thigh, underside of neck and brisket and around the root of the tail. Small areas of infestation do not cause major irritation to the animal, but a generalised condition can be extremely distressing.
The non-burrowing mites, Chorioptes and Psoroptes, have a similar life-cycle to the burrowing mites, with a slightly shorter adult phase of 40 days. The predilection site for Chorioptic mites is at the base of the tail, in the perineum and at the back of the udder in the winter. Long-haired, highland cattle are considered to be particularly susceptible to infection. Psoroptic mites are initially found on the withers, with the condition rapidly worsening to exudative dermatitis, associated with severe irritation.
The prevalence of mange in cattle in the UK is considered to be at a low level. A summary of surveys reported by Bates (1998) suggests that the prevalence in dairy herds ranges from 1-10% and in beef herds from 1-50%. Whilst dairy cattle are generally less susceptible than beef animals, all cattle are less susceptible to mange than sheep, as grooming is more efficient in cattle and acquired infections are usually eliminated by the animal.

Mange in Cattle

Mange is the term used to describe infection by mites, microscopic relatives of spiders. They inhabit and damage the skin of domestic animals and man. Problems are most frequently seen in the autumn and winter but can occur all year round. There are three main species of mite that affect cattle in the UK, the surface mite (Chorioptes bovis), the burrowing mite (Sarcoptes scabiei) and the sheep scab mite (Psoroptes ovis) The surface mite is the most commonly seen in the UK

Chorioptes bovis – the surface mite

The effect of mites

The surface mite is usually found on the neck, legs, and tail head. It produces limited hair loss, which only increases slowly in size. However, the lesions are obviously itchy which results in hide damage elsewhere as the cattle try to rub the affected areas.

The sheep scab mite is found on the flanks and around the tail head and anus. Although this mite feeds on the surface of the skin, its mouthparts pierce the skin, producing blisters, which are very irritant.

The burrowing mite prefers the neck and the loin area next to the tail (leading to the description of ‘neck and tail’ mange). As they burrow into and out of the skin they produce a much more intense irritant reaction so that the skin damage rapidly develops with much larger areas being affected and the skin becoming very thickened and crusty. Infection of the damaged areas often develops and affected animals have much reduced production

Life cycle

The surface mite and the sheep scab mite both spend their entire life cycle on the surface of the skin. Females lay around 90 eggs which once hatched take around ten days to develop into mature adults.

The burrowing mites lifecycle is more complex. The female mite tunnels into the skin, and lays around 50 eggs. These hatch in four or five days, each releasing a larva. Some of these tunnel to the surface to become adult others develop in the tunnels; this process takes around two weeks. More tunnels are often formed during the mating process.

For all three species, infection is spread mainly by direct contact between cattle. However, the burrowing mite can survive for some time off the host, so, for this species, bedding and objects that come into contact with infected animals may become contaminated and help spread the infection. For the sheep scab mite, although mites found on cattle are very similar to those found on sheep, it is very unlikely that natural spread from cow to sheep (and vice-versa) occurs.

Diagnosis

Areas of thickened skin in obviously itchy animals are very suggestive of mites, particularly if there is no evidence of lice. To confirm a diagnosis get your vet to take a skin scraping for examination under a microscope.

Treatment

A range of products is available to treat mange in cattle. The choice is between pour-on products and injections. The first are easier and quicker to use and are often cheaper. However, in severely infected animals (as is often seen in burrowing mite problems), the skin reaction can mean that contact between the product and the mite is limited. In such cases, scabs may have to be removed before treatment. If very severe then injectable products are probably a better bet. For very severe surface mite problems, an injection should be followed up by a pour-on treatment when the skin has recovered, as in this species (unlike the burrowing mite) injections only control but do not eliminate. Sheep scab mite can be effectively controlled with injections

The timing and frequency of treatments depend very much on individual circumstances. In most clinical cases, two treatments will give adequate control of cattle mites for the housing period. Whichever product you use, dose accurately, ensuring that you do not under-dose as under-dosing is the best way of ensuring the development of mites that are resistant to treatment.

Treat all cattle on the property at the same time if possible, choosing a time when they are not stressed or in poor condition. If groups have to be treated separately, such groups should be kept apart to ensure there is no contact between treated and untreated groups.

Unknown

10:12 AM

اقرأ المزيد

Bovine fasciolosis

Liver Fluke

Bovine fasciolosis is an important disease of cattle, especially in the wetter western half of the British Isles. Calves and yearlings are most commonly affected, but any age of animal may be susceptible to the effects of infection. Climatic and hydrological factors play an important part in the epidemiology of the disease, and restrict the geographical distribution as well as affecting the severity of the disease encountered.
Eggs from the adult fluke are passed into the intestine to be voided in the faeces. One fluke can pass between 5000 and 20,000 eggs per day. When conditions are moist and warm, the fluke eggs hatch into small infective larvae (miracidia). Propelled by cilia, these larvae actively seek a snail host of the genus Lymnaea. The mud snail Lymnaea truncatulata is the host snail in the United Kingdom. In the digestive tract of the snail, they develop into young sporocysts which then follow one of two courses. The first is for the sporocysts to develop into rediae which enter the liver of the snail and produce daughter rediae; the second is to produce second generation sporocysts which cannot produce rediae. From the rediae, daughter rediae or second generation sporocysts, cercaria are produced. From one miracidium, six hundred or more cercariae are produced, emerging from the snails after about 5 to 10 weeks, depending on the weather. The cercariae swim to attach themselves to herbage where they lose their tails and secrete a tough cyst wall to become metacercariae. At 12-14 ° C, up to 100% of metacercariae can survive for six months, though only 5% survive for 10 months. For prolonged survival, the relative humidity needs to be above 70%.
Once ingested by cattle, the young fluke burrow through the gut wall and pass to the liver. They are voracious feeders and migrate through the liver parenchyma to reach the bile duct, where they mature. Egg laying takes place some 10-12 weeks after the initial infection.
Most development of the larval stages takes place during the spring and summer months and ceases during the winter. The 'summer' infection of snails results from the hatching of overwintering eggs or eggs passed in the spring. The metacercariae then appear on pasture from August to October. A smaller 'winter' infection of snails is due to the infection of snails in the autumn; larval development in the snails ceases during the winter months and commences again in spring resulting in pasture contamination with metacercariae in May and June.
Acute fasciolosis is uncommon in cattle. The clinical signs of chronic fasciolosis are variable and depend upon the number of metacercariae ingested. Weight loss is common. Anaemia, oedema and cachexia develop gradually. Diarrhoea and constipation have also been described (Torgerson, 1999).

Unknown

10:10 AM

اقرأ المزيد

Listeriosis in cattle

Listeriosis

Listeriosis is an infectious disease caused by a bacterium, Listeria monocytogenes. This is a zoonotic disease that can be spread from animals to humans and has been implicated as a potential human health risk, associated with consumption of contaminated milk or meat (Doyle, 1994; Vishinsky, 1993; Pearson and Marth, 1990).
In cattle, the most common manifestations of listeriosis are meningoencephalitis, abortion, mastitis and septicaemia. Very little current information on the prevalence of Listeria infections in British cattle is available. Earlier surveys from the 1970s and 1980s suggest that abortion is the most common form of disease in cattle, with encephalitis and mastitis occurring more sporadically (Gitter, 1985; Anon, 1983; Gitter, 1979; Sharp, 1989; Vishinsky, 1993). Skin infection with L. monocytogenes, cutaneous listeriosis, has also been reported in the UK (Allcock, 1992). In recent years, an increasing number of cases of uveitis, iritis and keratoconjunctivitis caused by L. monocytogenes of silage origin have been reported (Watson, 1994; Morgan, 1977; Mee and Rea, 1989; Bardsley, 1989; Pohjanvirta and Hedlund, 1984; Joncour, 1998).
Many animals excrete L. monocytogenes in their faeces as a normal part of the intestinal flora. Oral infection via contaminated silage is the most common route of infection, but nasal or venereal infections can also occur. This type of infection is seen most often in 1-2-year old animals as result of cutting of molar teeth. There are a number of predisposing factors that cause disease by the agent. Nutritional deficiency, particularly malnutrition, poor quality silage (high pH), heavy silage feeding, cold and wet periods, stress caused by long transport, potential feed contamination by vermin and the entry of clinically normal carrier animals into a clean herd have been recognised as risk factors for listeriosis (Sanaa et al., 1993; Fenlon et al., 1996).
The bacteria persist up to two years in slurry, manure and straw and appear to persist better in cold than warm conditions (Kearney et al., 1993).
Abortion caused by L. monocytogenes tends to occur in late gestation (6-8 months), during the winter months, is sporadic by nature and recurs year after year (Gitter, 1979; Anon, 1980).
Certain serotypes of L. monocytogenes are particularly associated with listerial encephalitis. Many reported cases are associated with fermented silage and are sporadic. Listerial encephalitis symptoms can be confused with those of BSE (Jeffrey et al., 1990).
Chronic mastitis caused by L. monocytogenes has also been reported in dairy cows and is of particular concern for farms that process unpasteurised milk for consumption (Vishinsky et al., 1993; Sharp, 1989).

Unknown

10:05 AM

اقرأ المزيد

lice infestation in cattle

Lice in Cattle

The NADIS data show that last winter there was an increase in the number of cases of lice seen by NADIS vets. Lice populations are highest in winter and lowest in summer. There are two main reasons for this. Firstly, housing significantly increases the rate of transfer of lice between cattle. Secondly, low light levels and cooler skin temperatures are associated with increased louse activity. The denser winter coat and cooler weather thus favours lice survival.

The effect of lice

Lice cause irritation of the skin. This leads to biting, scratching and rubbing by affected cattle. These cows may also damage fences, trees and buildings while rubbing

The effect of lice on the production and growth rate of cattle has been the subject of much research but is still is a matter for continued debate. Their effect on the skin of cattle is probably best understood. Lice are probably the primary cause of “light spot and fleck”, a blemish visible on the hide of cattle which down grades the value of leather and is estimated to cost the leather industry £20 million per year.

Other effects such as weight loss, poor milk production and anaemia are less proven, even when there are large numbers of lice involved. This is probably because large numbers of lice are usually seen in animals that are under stress or under-fed or that have other current disease, which can all result in poor productivity without lice involvement

Types of lice.

There are four common species of lice in the UK, which can be divided into two different categories:

1. Sucking lice
   There are 3 species commonly found in the UK. These have relatively small narrow heads designed piercing the skin and sucking blood. In large numbers they can cause anaemia. They are usually found around the head and neck of cattle
2. Biting lice
   Biting lice have larger rounder heads. They feed on skin debris, blood and scabs. Despite being apparently less invasive than sucking lice, it is biting lice that produce the most severe irritation. There is one species of biting louse found throughout the world. It is a reddish-brown louse about 2 mm long with a brown head. It is mostly found on the neck, shoulders, back and rump.

Bovicola bovis: The biting louse

The life cycles of all species are similar. The female lays a few hundred eggs over the period of one month. These eggs are glued to the hair shafts, and hatch within a few days as nymphs (which resemble small soft adults). These develop, grow and moult three times before they become adult, with each stage lasting approximately one week. The entire life cycle takes between three and six weeks.

Diagnosis

On clinical signs and finding one of the three stages of the life cycle. Eggs are usually the easiest stage to spot, being found on hairs adjacent to bald, rubbed areas. Careful examination of nearby skin , with a magnifying glass, will usually detect nymphs and adults.

Treatment

Lice are spread only by direct contact between cattle. Adults, nymphs and eggs cannot survive more than a few days if removed from cattle. If properly applied treatment can eradicate lice from a farm.

Most insecticides are effective against adult lice and nymphs. However most are not very active against louse eggs. This means that after treatment, eggs can still hatch and continue the infestation, unless there is some residual action. Ask your vet for advice as to which product has the best persistence.

It can be important to know whether you have sucking or biting lice, because the different method of feeding means that they have different susceptibilities to treatments. This is particularly important if you are going to use an avermectin injection (such as ivermectin) as these are much more effective against sucking than biting lice. If you want to use such a product ensure you have the lice on your cattle identified.

The timing and frequency of treatments depend very much on individual circumstances. In many cases treatment in late autumn or early winter will give adequate control of cattle lice for the whole housing period. Whichever product you use, dose accurately, ensuring that you do not under-dose as under-dosing is the best way of ensuring the development of lice that are resistant to treatment.

Treat all cattle on the property at the same time if possible, choosing a time when they are not stressed or in poor condition. If groups have to be treated separately, such groups should be kept apart to ensure there is no contact between treated and untreated groups.

Is lice treatment necessary?

For cattle that have light to moderate numbers of lice, treatment cannot be justified in terms of improving growth rate, body condition or productivity. Treatment can improve hide quality, but as yet this is not of economic importance in the UK. However some quality assurance programmes in other countries (e.g. Australia) have made hide quality of economic importance and it is possible that this will come in the UK. Treatment may also become necessary on welfare grounds because of the easily appreciated discomfort that even moderate lice infestations cause.

Unknown

10:01 AM

اقرأ المزيد

Leptospirosis

Leptospirosis

Leptospirosis is a zoonotic disease, caused by bacteria of genus Leptospira. The disease that affects cattle (and man) in the UK is caused by two serogroups of the serovar Leptospira hardjo.
Cattle, sheep and goats can get infected, but the disease does not normally manifest itself in sheep that remain carriers. In cattle, after the first phase of the infection, the bacteria localise in the uterus and sex glands and in the kidneys. The early symptoms of infection are often so transient that in breeding cattle abortion and lowered fertility are usually the first symptoms to be noticed.
Milk drop
In cattle, the first symptom is often a drop in milk yield in all infected animals. This can be accompanied by transient fever, mastitis-like changes in the milk and sudden loss of all milk with flaccid udder (flabby bag).
Abortion
The abortion usually occurs 6-12 weeks after the initial infection. If the infection occurs in the late gestation, an infected calf may be born. Diagnosis of leptospiral abortion is difficult and based on maternal and foetal serology, as no obvious lesions are associated with the infection.
In herds contracting the infection for the first time, up to 30% of the animals may abort (Ellis, 1994). In endemically infected herds, a 5% abortion rate is suggested (Anon, 1986).
Infertility
The main manifestation of the effect of the infection on fertility is low pregnancy rates and high culling rates for fertility. The manifestation of these symptoms varies in a herd depending of the status of the infection. In a chronic inactive state, very few signs of poor fertility are seen, but during the initial infection of the herd, or when the herd infection becomes active acute infection, the symptoms are more apparent. What changes the health status of a herd from chronic inactive to acute active is not well understood, apart from in cases where a susceptible animal is introduced to an infected herd and is infected.
Whilst a natural immunity is established in a herd after the initial infection phase, all new animals that enter the herd are susceptible and suffer from an acute infection with the associated symptoms. So do animals that were not present in the infected herd during the initial infection but join later (e.g. dry cows). Consequently the abortions and infertility problems can go on for quite a while, causing major losses. In endemically infected herds, the drop in 1^st service conception rates has been reported to be 16-32% (Dhaliwal et al., 1996).
Prevalence of infection in the UK
Reports on the prevalence of Leptospira infection in the UK vary (Pritchard et al., 1989; Anon, 1986; Pritchard et al., 1987; Ellis et al., 1982). Based on various surveys, it has been estimated that some 70-80% of beef herds and 20-55% of dairy herds are infected with leptospirosis (Bennett, 1999). There is no reliable information on the occurrence of clinical episodes in endemically infected herds.
Leptospirosis is a notifiable disease in man, and farmers/farmworkers, abattoir workers and vets have been found to be the main risk groups in the UK. The disease in man is usually acquired from contact with the urine, placental material or aborted foetus of an infected animal or with contaminated water. Clinical signs of the disease are flu-like, with headaches and fever, occasionally progressing into meningitis.

Unknown

12:01 PM

اقرأ المزيد

Lead Poisoning

Lead Poisoning

Lead poisoning is still the commonest poisoning of cattle reported by NADIS vets, although evidence from NADIS and the veterinary laboratories suggest that it is becoming less common (or, at least, reported less frequently). The peak time of the year for lead poisoning is turnout. Of UK farm livestock, cattle appear to be the most vulnerable to lead poisoning, with calves being the most likely victims. However, lead poisoning can occur in all domestic animals including horses, poultry and dogs. Pigs appear to be the least susceptible farmed species.

The main source of lead in most cases is rubbish. Discarded sump oil, dumped lead batteries, unwanted putty and old paint tins are amongst the commonest sources. In many cases cattle will actively eat these products as they are attracted to the oil or to the taste. Calves often ingest lead while they are playing with discarded rubbish. Drinking water from lead pipes is often suggested as a possible source of lead poisoning, but cattle do not appear to be susceptible to poisoning by this route.

As the total number of cases of lead poisoning have decreased from over 100 in 1994 to less than 50 in 2001, it has become apparent that there is a significant number of lead poisonings in grazing animals where high concentrations of lead in the soil have been implicated. These outbreaks have mostly been seen in areas where lead has been mined. Feed contamination is also a potential problem, indeed contaminated rice bran from Burma was the primary source of the last major outbreak of lead poisoning in the UK in 1989.

Clinical Signs

The signs of lead poisoning depend very much on the species involved. The description here refers only to cattle Lead poisoning can be divided into three forms: Acute, where the signs develop rapidly, chronic where the signs develop over a long period, and subacute, which has a time-scale between the first two. The type of disease seen is primarily dependent on the amount of lead eaten, the more thatfs eaten the faster the signs develop. (The source of the lead can also affect the signs, but this effect is more complex). Because of their susceptibility to lead poisoning, cattle very rarely develop chronic poisoning

Acute disease .

• Sudden death
• Muscle tremors
• Frothing at the mouth
• Colic (stomach pain)
• Head pressing
• Apparent blindness
• Fits
• Aggressive behaviour (particularly adults)
• Death after 12 to 24 hours of the above signs

Subacute disease

• Dull
• Loss of appetite
• Apparent blindness
• Colic

Constipation followed by diarrhoea

Not all cases will show all the signs. In some cases the only presenting will be blindness or other nervous signs. It is thus important to get any animal showing strange blindness or other nervous signs checked by your vet, as they could be lead poisoning.

Diagnosis

On clinical signs noted above you can be suspicious of lead poisoning, particularly if a source of lead can be identified. However the signs of many other nervous diseases, including listeriosis, grass staggers and vitamin A deficiency are all similar to lead poisoning, so a veterinary examination can be very valuable. This is especially important for adult cattle as BSE cases can show many of the same vague nervous signs. Also, even if the signs are suggestive of lead poisoning, further testing is necessary to confirm lead poisoning, as there may be food safety implications:

1. Blood lead . will be elevated in ill animals and in many apparently normal animals (unless there is a single small point source of lead). Blood lead measurement can thus show the extent of the problem. However blood lead concentrations decline more rapidly than tissue lead concentrations once the source of lead is removed, so they cannot be used to assess food safety of milk or meat.
2. Tissue lead: Measurement of liver and kidney lead is the gold standard test. This can be done by biopsy, but is best done post-mortem. This is the only way to assess food safety in beef animals

Treatment

Treatment of acute cases is not worthwhile. The disease has usually progressed too far to be treated once signs are seen. Treatment has to begin early if an animal is to be saved. Treatment is complicated, costly and long. It is also NOT effective at eliminating lead faster from affected animals, so cannot be used to make cattle fit for human consumption more quickly.

Prevention

In the vast majority of cases lead poisoning can be avoided by good waste management on the farm. Prevention is easier, cheaper and more effective than treatment by a vet. The most important areas for prevention are:

1. Place used motor oil in sealed containers.
2. Keep rubbish out of pastures and other sites that are used by animals.
3. Prevent access by cattle to areas where rubbish is dumped.. A single site is far safer than several sites.
4. Dispose of used vehicle batteries carefully. Do not leave them around the farm
5. Remove all lead paint. If this is not feasible, ensure livestock canft get access to painted areas.
6. Service farm machinery away from animals.
7. Check all areas carefully before introducing animals to them as most poisonings occur following a change of location. Lead poisoning cases usually increase after turnout in spring when the animals find all the junk discarded over winter
8. Work with your neighbours to prevent lead poisoning. If soil contamination rather than rubbish is the cause of your problem, prevention is more difficult and has to be farm-specific. Get advice from your vet and local veterinary laboratory.

Unknown

11:59 AM

اقرأ المزيد

Navel ill

Joint ill (Navel ill) of Calves

The NADIS data show that the number of cases of joint ill in calves this spring is much higher than normal for the time of year:

Joint ill, Navel ill - All Calves

What is joint ill?

Navel or joint ill is a disease of young calves, usually less than one week of age. It occurs as a result of infection entering via the umbilical cord at, or soon after, birth. This infection can result in a range of signs depending on where the bacteria spread to.

Clinical Signs

Navel ill

• If infection stays mostly confined to the navel, the primary sign is a swollen, painful navel that does not dry up
• An abscess may develop from which pus (often like a thick custard) may burst
• The calf may have a high temperature and reduced appetite

Joint ill

If infection spreads from the navel, or navel ill is not treated, further signs will develop as bacteria spread via the bloodstream and settle in other parts of the body.

• The commonest sites for bacteria to settle are the joints. This leads to swollen stiff painful (often hot) joints
• Temperature will be raised while the bacteria spread but by the time the disease is noted it may be normal
• Loss of appetite and depression
• Usually only a few calves in a batch are infected though outbreaks can occur where hygiene is very poor

Other sites where bacteria can settle include the eyes, around the heart and the brain. Death is common in the latter cases. In some calves infection spreads from the navel to the liver causing a liver abscess. In this case problems may not be noted until the calves are older (1 .3 months)

Diagnosis

The diagnosis of joint or navel ill is usually based on the clinical signs. If a swollen navel is the main sign, ensure that it is not a hernia before treating All calves that die suddenly should be have a PM examination

Treatment

• Early prompt treatment is important as early treatment is much more effective
• Separate the infected animals and isolate them. TLC is an essential part of treatment.
• Antibiotics and painkillers are effective in most mild cases. Antibiotic treatment should continue until after the signs have disappeared (which can take over a week even in mild cases)
• Severe cases may not recover even with prolonged antibiotic treatment
• For large navel abscesses, veterinary intervention to drain and remove the infected tissue is often necessary

Prevention

Prevention is the key to this disease. Ensuring that the cow calves in a clean environment will significantly reduce the risk of joint ill (and many other diseases such as toxic mastitis and metritis). Proper planning and preparation can prevent the build-up of disease that occurs in too many calving areas.

Applying a disinfectant (such as iodine) to the navel can reduce the risk of bacteria entering via the navel, but it is no substitute for good hygiene. No amount of disinfectant can overcome being born in a dirty wet yard. Because of the anatomy, bulls navels tend to dry slower than heifers and they are thus at more risk of navel ill. Applying disinfectant two or three times to bulls can reduce the risk.

It is also important to ensure that if cattle are born in a nice clean environment that they aren't moved to other pens or contaminated pastures until the navel has dried completely.

Finally, like all diseases of young calves getting sufficient colostrum is essential. Ensure that all calves get a good suck in the first 6 hours of birth. If this doesn't happen ensure that they get at least 2 litres of colostrum as soon as possible. Colostrum works best if calves take it from a bucket, but if stomach tubing is the only option it's a lot better than no colostrum.

Unknown

11:57 AM

اقرأ المزيد

chronic enteritis of ruminants

Johne's Disease

Johne's disease is a chronic enteritis of ruminants caused by the aerobic bacterium Mycobacterium johnei (syn. M. paratuberculosis). The disease is widely distributed and causes substantial economic losses through death and loss of productivity during the prolonged preclinical stage. The disease has remained a problem for so long because of the absence of a simple, accurate diagnostic test.
M. johnei is spread via faeces and milk. It is excreted by infected animals before clinical signs appear, although bacteria numbers increase once clinical signs have developed. It is believed that most infections occur during the first day of life of a calf and originate from the dam. After ingestion with faeces or milk, M. johnei invades the lymphatic tissue in the mucosa of the small intestine, where it multiplies over the next 2-3 months and spreads to the draining mesenteric lymph nodes. The outcome of the infection depends on both the ability of the host to mount a cell-mediated immune response and the dose of the initial infection.
The course of the infection depends on the host's response: the initial infection is overcome; the infection persists for many months or years; or the intestinal lesions slowly progress until they interfere with normal function. There is loss of plasma proteins into the lumen and malabsorption of amino acids. Faecal pellets are often soft rather than diarrhoeic, and anaemia occurs in some animals. Appetite usually persists, until the disease reaches advanced stages and animals become emaciated and weak.
Johne’s disease has been associated with reduced milk production and increased culling of infected cows in dairy herds (Wilson et al., 1993; Ott et al., 1999).
Recently, Johne's disease has been implicated in Crohne's disease in humans, as it has been shown that there is a high risk for the presence of residual M. johnei bacteria in milk even after pasteurisation (Millar et al., 1996).
The prevalence of subclinical Johne’s disease in UK cattle was estimated in an abattoir survey in the south-west of England in 1996. A total of 2.6-3.5% of the animals were infected, depending on the diagnostic test used (Cetinkaya et al., 1996). In a questionnaire survey of southern English and Welsh farmers, 17.4% of the farms reported having had the disease at some point, but only 0.9% of the farms had had recognised clinical cases in the past 4-year period (Cetinkaya et al., 1998).

Unknown

11:53 AM

اقرأ المزيد

Duck Septicaemia

Introduction

An acute or chronic septicaemic disease caused by Riemerella anatipestifer, syn Pasteurella, or Moraxella a. It affects ducks of any age, sometimes turkeys, and may also be isolated from chickens, game birds and wild waterfowl. Mortality is 2-75% in young ducks. Transmission is mainly direct, bird-to-bird, via toenail scratches, especially of the duckling foot, or through respiratory epithelium during respiratory disease. It can also be by faecal contamination of feed, water or the environment where survival of the infectious agent may be prolonged. Adverse environmental conditions and pre-existing disease are predisposing factors.

Signs

• Weakness.
• Neck tucked in.
• Head/neck tremor.
• Ataxia.
• Disinclined to walk.
• Incoordination.
• Dyspnoea.
• Ocular and/or nasal discharge.
• Hyperexcitability

Post-mortem lesions

• Perihepatitis without much smell or liver damage.
• Pericarditis.
• Airsacculitis.
• Enlarged liver and spleen.
• Occasionally fibrinous meningitis.
• Salpingitis
• Purulent synovitis.
• Chronic arthritis, sometimes with erosions of the joint cartilage.

Diagnosis

Lesions, isolation and identification of organism - blood or chocolate agar in candle jar or 5% CO₂. Differentiate from duck viral enteritis, duck viral hepatitis, fowl cholera, colibacillosis, coccidiosis, chlamydiosis.

Treatment

Sulphonamides and potentiated sulphonamides are the products most commonly recommended for drinking water application. Subcutaneous injections of penicillin + dihydrostreptomycin, or streptomycin + dihydrostreptomycin are also highly effective.

Prevention

Good husbandry and hygiene, rigid depopulation and disinfection, adequate protection, 'hardening off', correct house relative humidity, sulphonamides in feed. Inactivated and attenuated vaccines available in some countries. Autogenous bacterins sometimes used.

Figure 40. Erosions of the cartilage of the hock joint in a duck with chronic Riemerella anatipestifer infection

Unknown

6:21 PM

اقرأ المزيد

Amyloidosis

Introduction

A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%, depending on secondary infections. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. The infection spreads rapidly by contact, fomites or aerosol. Some birds/viral strains can be carriers for up to 1 year. The virus, which may survive 4 weeks in premises, is sensitive to solvents, heat (56°C for 15 mins), alkalis, disinfectants (Formal 1% for 3 mins). Poor ventilation and high density are predisposing factors.

Signs

• Sudden death.
• Muscular shivering.
• Otherwise as for standard IB.

Post-mortem lesions

• Oedema of pectoral muscles and subcutaneously on abdomen, lesions progress to necrosis and scarring of deep pectorals in convalescence.
• In layers the ovules may be intensely congested.
• Other lesions of 'classical' IB may be encountered.

Diagnosis

3-5 passages in CE allantoic cavity, HA-, typical lesions, FA, ciliostatic in tracheal organ culture, cell culture (Vero, CK) only after adaptation Serology: HI, Elisa (both group specific), SN (type specific), DID (poor sensitivity, short duration, group specific).

Treatment

Sodium salicylate 1gm/litre (acute phase) where permitted - antibiotics to control secondary colibacillosis (q.v.).

Prevention

Live vaccines of appropriate sero-type and attenuation, possible reactions depending on virulence and particle size.

Unknown

9:26 PM

اقرأ المزيد

Colisepticemia

Introduction

Coli-septicaemia is the commonest infectious disease of farmed poultry. It is most commonly seen following upper respiratory disease (such as Infectious Bronchitis) or Mycoplasmosis. It is frequently associated with immunosuppressive diseases such as Infectious Bursal Disease Virus (Gumboro Disease) in chickens or Haemorrhagic Enteritis in turkeys, or in young birds that are immunologically immature. It is caused by the bacterium Escherichia coli and is seen worldwide in chickens, turkeys, etc.

Morbidity varies, mortality is 5-20%. The infectious agent is moderately resistant in the environment, but is susceptible to disinfectants and to temperatures of 80°C.

Infection is by the oral or inhalation routes, and via shell membranes/yolk/navel, water, fomites, with an incubation period of 3-5 days.

Poor navel healing, mucosal damage due to viral infections and immunosuppression are predisposing factors.

Signs

• Respiratory signs, coughing, sneezing.
• Snick.
• Dejection.
• Reduced appetite.
• Poor growth.
• Omphalitis.

Post-mortem lesions

• Airsacculitis.
• Pericarditis.
• Perihepatitis.
• Swollen liver and spleen.
• Peritonitis.
• Salpingitis.
• Omphalitis.
• Synovitis.
• Arthritis.
• Enteritis.
• Granulomata in liver and spleen.
• Cellulitis over the abdomen or in the leg.
• Lesions vary from acute to chronic in the various forms of the disease.

Diagnosis

Isolation, sero-typing, pathology. Aerobic culture yields colonies of 2-5mm on both blood and McConkey agar after 18 hours - most strains are rapidly lactose-fermenting producing brick-red colonies on McConkey agar.

Differentiate from acute and chronic infections with Salmonella spp, other enterobacteria such as Proteus, as well as Pseudomonas, Staphylococcus spp. etc.

Treatment

Amoxycillin, tetracyclines, neomycin (intestinal activity only), gentamycin or ceftiofur (where hatchery borne), potentiated sulphonamide, flouroquinolones.

Prevention

Good hygiene in handling of hatching eggs, hatchery hygiene, good sanitation of house, feed and water. Well-nourished embryo and optimal incubation to maximise day-old viability.

Control of predisposing factors and infections (usually by vaccination). Immunity is not well documented though both autogenous and commercial vaccines have been used.

Figure 17. Severe perihepatitis in colibacillosis in a broiler parent chicken. The liver is almost entirely covered by a substantial layer of fibrin and pus.

Unknown

9:23 PM

اقرأ المزيد

Infectious Bovine Rhinotracheitis {IBR}

Infectious Bovine Rhinotracheitis (IBR)

Infectious bovine rhinotracheitis (IBR) is a viral disease caused by bovine herpesvirus 1 (BHV-1) that can also cause a mild venereal infection in adult cattle or a brain infection in calves. IBR is a highly contagious disease of the upper respiratory tract and can lead to serious primary or secondary pneumonia. The clinical signs of the disease are nasal discharge, fever and conjunctivitis. Acute disease in dairy cattle is usually accompanied by a severe and prolonged drop in milk production. Adult cows may also suffer from abortion and reduced fertility. Animals suffering from IBR are highly susceptible to secondary bacterial infections.
The exposure of cattle to BVH-1 has been known to be widespread in the UK since the 1960s (Dawson and Darbyshire, 1964), but the disease was generally considered unimportant as clinical signs were mild or rare. In the late 1970s, a more virulent form of the disease was reported (Wiseman et al., 1978), and it is believed that a more virulent strain of the virus entered the country (Edwards et al., 1990). In 1992, 34% of farms in the UK had one or more calves with antibodies against BHV-1 (Hogg, 1992). In 1996, some 70% of 360 tested dairy herds were positive for BHV-1 antibody in the bulk milk (Bennet et al., 2000).
Based on collated and unpublished data, it is suggested that the incidence of IBR outbreaks in beef and dairy herds in the UK has declined steadily between 1980 and 1995, in spite of low level of estimated vaccine use (Bennet et al., 2000).
Herds with IBR suffer mainly from low-grade problems associated with calf pneumonia, decreased fertility and occasional abortions. More serious problems are seen on farms that have not been exposed to IBR before. Outbreaks with milk-drop and fever in most cows and subsequent abortions and increase in calf pneumonia are seen.

Unknown

8:49 PM

اقرأ المزيد

Hypomagnesaemia in cattle

Hypomagnesaemia (Grass Staggers)

The NADIS data shows that in previous years the number of cases of hypomagnesaemia (grass staggers, grass tetany) increases each spring after turn out reaching a peak incidence in May, with another peak in October.

Hypomagnesaemia - All Cattle
Average 1997 - 2002

What is Hypomagnesaemia?

Hypomagnesaemia occurs when the intake of magnesium is exceeded by its output. The clinical signs can occur very quickly because the cow does not store magnesium, and is thus reliant on its daily dietary intake. Hypomagnesaemia is most commonly a disease of lactating cows at grass, because grass can be very low in magnesium and the output in milk is high. When the losses in the milk exceed the dietary intake, clinical hypomagnesaemia occurs. Like most nutritional diseases, the animals showing clinical signs are just the tip of the iceberg, for every cow with obvious disease many more will be affected sub clinically.

The increase in disease in spring occurs because rapidly growing grasses, particularly ryegrasses, are very low in magnesium. This low concentration of magnesium can be further reduced by the application of fertiliser, partly because of the increase in growth rate, but also because application of potassium directly inhibits uptake of magnesium by the grass. Slower growing forages, particularly clovers and other broad-leaved plants contain much higher levels of magnesium.

The significant increase in late autumn, may be partly due to the increase in forage growth that occurs at this time, particularly after a dry summer, and also to the feeding silage produced from spring grass that was low in magnesium.

Clinical Signs

The signs of hypomagnesaemia are vary variable ranging from mild apprehension and tremor to sudden death. Hypomagnesaemia is probably the major cause of sudden death in lactating cows at grass The signs of hypomagesaemia are probably best visualised by detailing the changes in an untreated animal with mild hypomagnesaemia.

1. The animal appears apprehensive with the head held high and a mild tremor.
2. The gait stiffens, and the animal begins to stagger and frequently falls over
3. The animal becomes recumbent (lies on its side unable to get up), with marked convulsions Other signs, which may be seen at any of these stages, include watery diarrhoea, skin that is cold to the touch and a low body temperature
4. Death

Often there are signs of struggling evident on the ground around the cow

For every cow obviously affected with hypomagnesaemia, there are many more with marginal magnesium levels. Some of these animals mild show very subtle behavioural changes but the most common effect is a small reduction in milk yield.

Diagnosis

Clinical signs

Blood magnesium Individual cows
For most animals treatment will have to begin before a diagnosis is confirmed as there are no rapid cow-side tests available, but individual measurements can be useful retrospectively in animals where treatment has been unsuccessful
Herd
As hypomagnesaemia is primarily a herd disease, in most cases it is important to assess the extent and severity of the hypomagnesaemia in the rest of the herd, This is best done by testing six cows at the same stage of lactation as those clinically affected. Care must be taken when handling such animals as stress could initiate clinical hypomagnesaemia.

Aqueous humour magnesium concentration.
Samples can be taken by a veterinarian in animals suspected to have died of hypomagnesaemia, however results must be interpreted with caution

Treatment

1. All animals that are suspected of having hypomagnesaemia should be immediately treated with 400ml of 25% magnesium sulphate given subcutaneously. A 25% solution of magnesium should never be given intravenously as it can cause a heart attack. No further action is necessary for mild cases that respond to treatment, but if mild cases do not respond to treatment or if the animal is recumbent a veterinarian should be called.
2. Veterinary treatment usually involves further infusion of magnesium, often intravenously diluted a calcium solution. For severely affected animals a sedative may be given. As both of these treatments are unlicensed they should only be given by a veterinarian.

Following treatment it is important to prevent stimulation for 10-15 minutes to prevent further convulsions. For recumbent animals they should be put on their breastbone and left to get up.

Oral administration of magnesium bullets is recommended to prevent relapses as is moving affected groups to fields with slower-growing pastures.

Prognosis

Animals treated at an early stage have a very good prognosis. For recumbent animals, the prognosis is very poor if they do not rise within two hours of treatment and casualty slaughter should be considered.

Prevention

Feeding magnesium in the concentrates to the cows. Giving magnesium bullets at turn out to cover the period when the animals are most at risk. For some farms, several bullets per cow are needed to prevent hypomagnesaemia. Buffer feed silage with magnesium added Supplement the water supply (this is only effective if the cows have no access to natural water supplies, and may depress water intake) Avoid potassium fertilisers if possible. Adjust grazing sward to a clover/grass mixture

Unknown

8:44 PM

اقرأ المزيد

Parasitic Gastroenteritis

Gut Worms (Parasitic Gastroenteritis or PGE)

Warm moist summers and autumns are ideal for gut parasites as they can reach higher peak numbers and stay near those numbers for longer. In cattle the primary effect of gut worms is poor growth (or weight loss) with diarrhoea, death is rarer in cattle than sheep. Controlling worms is thus important in cattle, particularly in youngstock, and should form an integral part of your herd health plan. It is also important to be aware of the rising problem of resistance in worms, particularly those found in sheep, and to use all wormers carefully to minimise the risk of resistant worms being found on your farm.

Clinical Signs

• Diarrhoea – often green and profuse
• Weight loss
• High proportion of animals affected

There are two main seasons for gut worm problem in cattle, July to November and February to May. In the summer/autumn the problems are caused by worms picked up from the pasture; in the winter, most, but not all, cases are caused by larvae which have hibernated in the calf’s stomach reviving and resuming their development

Diagnosis

• Worm egg count – collect ten faecal samples as fresh as possible and send them to your vet or lab. They will bulk them together and give you a WEC. Several samples are important, as not all animals will have high WEC’s.
• Other blood tests may be useful such as pepsinogen or minerals to rule out additional problems.
• PM – these can be extremely helpful in confirming a diagnosis.

Treatment & Prevention

Prevention is far more cost effective than treatment; planning worm control can thus save significant amounts of money. For most farms wormers will still be an essential part of economic stock production, so strategic wormer use needs to be built into the worm control plan. Each individual farm should have its own individual worm plan, based on farm management, previous worm history and type of stock. Nevertheless there are several factors to bear in mind when developing the plan:

1. Use pasture effectively so that cattle avoid grazing contaminated pasture during the peak season. This can be as simple as moving cattle onto fresh ungrazed pasture (such as silage aftermath) just before the summer rise in larval numbers.
2. Reduce routine worming by monitoring, particularly WEC and growth. This will save you money and reduce the risk of resistance developing on your farm.
3. Worm at housing in stock susceptible to hibernating larvae
4. Don’t forget lungworm control; this is an increasing problem on many farms. Control measures such as pasture management are less effective for lungworm than gut worms, so use vaccination to control lungworms.

Unknown

10:57 AM

اقرأ المزيد

foot foul

Foul in the foot

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.

Unknown

10:51 AM

اقرأ المزيد