Bloat In Cattle

Bloat In Cattle

There was an increase in the number of reports of bloat from NADIS vets this spring. Bloat is most commonly seen in spring and autumn, when grass growth is at its peak. It is one of the most common causes of death in adult cattle at grassp>

What is bloat?

Bloat is simply the build up of gas in the rumen. This gas is produced as part of the normal process of digestion, and is normally lost by belching (eructation). Bloat occurs when this loss of gas is prevented. There are two sorts of bloat. The least common type is gassy bloat, which occurs when the gullet is obstructed (often by foreign objects such as potatoes) or when the animal can’t burp (such as with milk fever or tetanus). The second type of bloat is frothy bloat, which happens as the result of a stable foam developing on top of the rumen liquid, which blocks the release of the gas. This is by far the most common form of bloat, and unlike gassy bloat, it is highly seasonal with peaks in the spring and autumn. This is because the foam is formed by breakdown products from rapidly growing forages (particularly legumes such as clover and alfalfa). These increase the viscosity (stickiness) of the rumen fluid and prevent the small bubbles of gas formed by rumen fermentation from coming together to form free gas that can be belched off

Clinical Signs

• Distended left abdomen is the most obvious sign
• Usually associated with pain, discomfort, and bellowing.
• Death can occur within 15 minutes after the development of bloat
• Gaseous bloat is usually seen in one or two animals. Frothy bloat can affect up to 25% of cases
• In some cases sudden death may be the first sign seen by the stockman, although in such cases it is likely that there will be other cattle with bloat that are still alive

Diagnosis

• On the clinical signs described above
• History of access to lush pasture
• Passing a stomach tube will distinguish between gassy and frothy bloat. If it’s gassy bloat a stomach tube passed into the rumen will allow the gas build-up to escape through the tube. No such gas is seen in frothy bloat.

Treatment

• Passing a stomach tube is the best treatment for gassy bloat. Once the gas has been released, the cause of the obstruction should be looked for.
• In a few cases a trochar and cannula punched through the side into the rumen will relieve gassy bloat when a stomach tube has not worked. But such cases are rare, and as the trochar provides a tremendous opportunity for introduction of infection, it should only be used as a last resort.
• For frothy bloat, antifoaming agents that disperse the foam should be given by stomach tube. Old-fashioned remedies such as linseed oil and turpentine are effective but newer treatments such as dimethicone or polaxolene are easier to give as the effective dose is much smaller.
• If an outbreak of frothy bloat occurs all cattle on that pasture should be removed immediately and put onto a high fibre diet (hay or straw), and any cows showing bloating signs treated with an anti-foaming agent. The pasture should not be grazed for at least ten days.

Prevention

It is much more effective to prevent bloat than treat affected animals. Management and planning can significantly reduce the number of cases. To prevent frothy bloat: 1)

1. If possible avoid using high-risk pastures at high-risk times. Pastures with a history of bloat problems or with a high clover content should not be used for cows soon after turnout.
2. Stagger turnout with buffer feeding as this will allow the rumen to adapt to the new diet. In particular try and keep up fibre intakes at risk periods.
3. If you have to use high-risk pastures, introduce the cattle to them slowly. In some cases restricting access to as little as ten minutes per day at the start may be necessary to prevent bloat.
4. Avoid starting to graze high-risk pastures when they are wet.
5. Administer anti-foaming agents daily if bloat is a severe problem. If this is the case and you can strip graze then spraying antifoaming oils (emulsified with water) onto the grass can significantly reduce labour costs.
6. Remove high-risk animals. Some animals have recurrent bloat despite prevention and treatment.

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Blackleg {Clostridial myositis}

Blackleg (Clostridial myositis)

Cases of blackleg often increase when animals are turned out or moved to new pastures, so farmers need to be aware of the signs so that action can be taken to prevent further disease

What is Blackleg?

Blackleg is a highly fatal disease of muscle caused by the bacterium Clostridium chauvoei. Infection begins when bacterial spores are eaten (usually as result of eating soil, but occasionally from contaminated feed). These spores enter the bloodstream and travel to organs and tissues throughout the body (particularly muscles). They remain dormant until a trigger (usually an injury) stimulates them. The trigger reduces blood flow and thus the supply of oxygen to the tissues. In the absence of oxygen the bacteria multiply and produce a local infection. As they grow, the bacteria produce poisons that destroy the surrounding tissues. This damage shows as the characteristic black muscle with gas. The poisons do not stay in the muscle but enter the bloodstream, resulting in animal that very rapidly goes downhill and dies. The disease is most commonly seen in calves between six months and two years of age, but occasional cases are seen in adults and it can occur in younger animals (particularly if they have not had sufficient colostrum). Disease is definitely more common in animals that are growing well

Clinical Signs

• Lameness may be seen before death if you’re lucky
• In a few cases the first sign seen is tongue and throat swelling with the tongue protruding
• However, the most common sign is sudden death in an otherwise apparently normal animal
• The carcass often looks like a much less fresh carcass, with bloating and gas under the skin
• Bloody discharge from the nose, mouth and other body openings are also seen

Diagnosis

• A post mortem is essential to diagnose blackleg. Many other diseases cause sudden death and need to be ruled out. The most important of these is anthrax, which must be ruled out before a PM is done
• The changes in the muscle are characteristic, but the extent of the damage can vary considerably. Some cases have black oozing muscle throughout the hindquarters, others have much smaller areas of damage which may not involve the limbs at all.
• It is worth getting further lab tests done to confirm it is Cl. chauvoei as other clostridial bacteria can cause similar muscle damage Don’t do a PM on farm. Opening the carcass can liberate bacteria which will form spores to contaminate the ground and subsequently infect other cattle.

Treatment

• In very early cases very high doses of penicillin may prevent death, but the extent of muscle damage means that in most cases this will not be economic

Prevention

As the bacteria are present in the soil, preventing access to soil by not grazing freshly sown pastures with youngstock can reduce the risk, but vaccination is really the only effective means of controlling blackleg. The main choice is between vaccination against Cl. chauvoei alone or with vaccines that are effective against other clostridial disease. Ask your vet for advice

With clostridial vaccines, like all vaccines, care should be taken to follow the manufacturers' instructions. The best protection is a two-dose course followed by annual revaccination. Other regimes can be effective but check with your vet before using these. Vaccination takes 10-14 days to become effective, so it’s best to vaccinate before a problem occurs or a risk period is encountered.

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Blackleg

Blackleg

Clostridia are group of anaerobic, spore-forming organisms found in the soil/environment, which produce rapidly fatal disease by secretion of potent toxins. Conditions such as botulism, blackleg, bacillary haemoglobinuria, malignant oedema and tetanus are all caused by clostridia.
Botulism
Botulism is a lethal food poisoning in cattle caused by eating material that contains Clostridium botulinum toxins. The incubation period before clinical signs appear varies from a few hours to two weeks, making it difficult to identify the causative material eaten by affected animals. The most common manifestation of the disease in cattle is a subacute disease with restlessness, incoordination and difficulty to swallow developing into recumbency, paralysis and death within 1-7 days.
The bacteria and the disease occurrence are world-wide. In the UK, cases are likely to occur either due to ingestion of contaminated silage or contact with animal carcasses or skeletons of dead animals containing the toxin. The use of poultry litter as fertiliser on cattle pastures has been identified as a risk factor, due to the poultry mixed with the litter.
Bacillary haemoglobulinuria
Bacillary haemoglobulinuria is a rapidly fatal disease caused by C. oedematiens type D. The disease is associated with liver damage primarily caused by liver fluke. The condition is fairly rare in the UK. Young stock or dry cows inspected less regularly are often found dead. In lactating cows, a sudded drop in milk yield associated with high fever is seen. Other clinical signs include ruminal stasis with or without apparent abdominal pain, rapid breathing, dark red urine, jaundice and death within a short time of the onset of clinical signs.
Spores of C. oedematiens type D can be found both in the soil and in the livers of normal cattle on farms where the disease occurs.
Blackleg
Blackleg infection is caused by Clostridium chauvoei and is almost allways associated with wound infection in cattle. Most cases occur in young stock between 10 months and two years of age. Feet or legs and the tongue are often the predilection site. Within 48 hours there is a high fever and if limb muscles are involved the animal becomes stiff and unwilling to move. Skin discolouration, subcutaneous oedema and gas production may be present and perineal oedema is sometimes seen. Infections of the head may produce marked oedema and even bleeding from the nose. Death usually follows a period of anorexia, profound depression and prostration.
The spores of C. chauvoei survive well in the soil.
Malignant oedema
Malignant oedema is caused by the infection of wounds with bacilli of the genus Clostridium (C. oedematiens type A; C. chauvoei; C. perfringens; C. sordellii; C. septicum). The condition is fairly rare and sporadic, but outbreaks involving several animals may occur after an event that has caused bruising or wounds (e.g. penning for a short period). Clinical signs appear rapidly after infection and at the site of infection a swelling will develop which will 'pit' on pressure. Gas may be detected, as the skin becomes darkened and tenser. A high fever is present and toxaemia develops. The animal dies within 1 - 2 days.
Tetanus
Tetanus is caused by the toxin tetanospasmin released from the spore-forming bacillus Clostridium tetani. The disease in cattle occurs most often after surgical intervention or difficult calving after spores gain entry to a wound. Germination of spores occurs only if the microenvironment is anaerobic. After germination of the spores within the wound the C. tetani bacilli proliferate and produce toxin.
The incubation period can be very variable from 3 days to several months but most cases occur usually after about 10 days. At first the animal appears slightly stiff, becomes unwilling to move and develops a fine muscle tremor. The temperature rise is variable (39 - 42°C). The general stiffness of the limbs, head, neck and tail increases after 12 - 24 hours. The animal shows hyperaestesia and repeated spasms. Mastication becomes difficult due to tetany of the masseter muscle (lockjaw), food is chewed with difficulty, the animal drools saliva and bloat often occurs. There is retention of the urine and constipation. The animal becomes recumbent, with the legs rigidly extended, opistotonos and the jaws become rigid. The animal usually dies due to respiratory failure 3 - 4 days after the onset of clinical signs. Milder cases, which develop more slowly, can recover over a period of weeks or even months.

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Babesiosis{Redwater fever}

Babesiosis (Redwater fever)

This parasitic disease is usually first reported in May/June when its tick host first becomes active.

What is Babesiosis?

Babesiosis is an infection of the red blood cells by a single cell parasite of the genus Babesia. In the UK, babesiosis is usually caused by Babesia divergens. The disease is spread between cattle by ticks (Ixodes ricinus in the UK). The babesia is injected into the bloodstream by the tick and then invades the red blood cells and begins dividing, eventually rupturing the cell. Clinical signs begin around 2 weeks after infection.



Babesiois is rare except in known tick areas. However in these areas even though disease is often relatively mild there is a significant imact on productivity and fertility in affected cattle.



Clinical Signs

Increased temperature

Diarrhoea which ceases after around 36 hours and then becomes constipation

Red urine (due to haemoglobin produced by the rupture of the red blood cells) which becomes darker with time

Increased pulse rate

Abortion of pregnant cows

Death is rare in babesiosis in the UK.

Diagnosis

On the clinical signs described above

Recent movement to pastures known to harbour ticks

Blood smears can show up the parasite

Treatment

Mild cases may recover without treatment.

More severe cases need treatment. This is often best combined with a preventative treatment for the as yet unaffected cattle. This choice is best made on an individual farm basis in consultation with your vet.

Prevention

Identification of risk areas

Prophylactic treatment of cattle about to be moved to a risk area

Tick control

Vaccine not yet available in UK

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Acetonaemia

Acetonaemia


The NADIS data show that the number of cases of acetonaemia (or ketosis) increase significantly during the winter, and the number of cases continue to increase until turnout. So it is particularly important to look out for acetonaemia until at least a month after turn-out.



Like most metabolic diseases it is important to remember that for every cow that shows clinical signs, there will be several more which are affected sub-clinically.

What is acetonaemia?

Acetonaemia occurs when the cow's energy intake does not match its requirement and the cow is unable to compensate and mobilises its body reserves too quickly. In the beef cow, this is most likely to occur in late pregnancy when the cow's appetite is at its lowest and the energy requirement of the growing calf near its peak. In the dairy cow, the mismatch between input and output usually occurs in the first few weeks of lactation, because the cow is not able to eat enough to match the energy lost in the milk.

Clinical Signs

Reduced milk yield: Initially a moderate decline, eventually a sudden drop

Body condition and weight loss

Reduction in appetite (initially non-forage feeds)

Dull, stary coat

Firm, 'waxy' dung

Acetone (pear drop) smell of breath or milk - not always detectable

Temperature, pulse rate and respiratory rate usually normal

A few develop nervous signs including excess salivation, licking, incoordination, aggression.

Acetonaemia is more common in the dairy cow, probably because the energy difference of the lactating cow is more difficult to overcome than that of the pregnant cow, which means that most dairy cows in the UK are in negative energy balance during the first few weeks of lactation. Acetonaemia occurs when the cow is not able to cope with this energy deficit, either because it is too great or if it continues for too long.



If it occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from an energy deficit that is significantly reducing their productivity. A clinical case of acetonaemia is the tip of the iceberg, and therefore it is advisable to discuss blood testing other cows in the same lactation group, for the subclinical form of the disease.



Prevention

Each treated cow is the tip of the iceberg, so prevention is very important. The aim of any prevention regime is to maximise dry matter intake during the critical period. This can be achieved by:



Avoiding over-fat and over-thin cows: Aim to calve cows at condition score (CS) 3.0. Fat cows have lower appetites and mobilise more fat and so are more prone to ketosis Dry-off cows at CS 3.0. Cows should not gain or lose weight during the dry period. Thin cows should be fed to gain condition during late lactation. Fat cows should be fed to lose condition during late lactation.

Preventing disease around calving. Cows with calving difficulties, retained membranes, endometritis, milk fever, toxic mastitis, and hypomagnesaemia all have an increased risk of acetonaemia, so preventing these diseases reduces the risk of acetonaemia.

Feeding correctly Introduce the milking ration to the dry cows from two weeks before calving. This allows the rumen time to adapt to the milking diet Maximise palatability. Good quality forage and feeding as a total mixed ration both increase intake and thus reduce the energy deficit Maximise feeding time. Increasing the feeder space, particularly for self-fed silage, can increase intake and thus reduce energy deficit Keep the diet consistent. Avoid sudden changes to the diet even if only batch changes of concentrate.

Reduce stress Keep freshly-calved cows separate from the milking herd for at least two weeks after calving. Acetonaemia is a significant cause of economic loss, but these losses can be reduced by good management and attention to detail.

Early treatment leads to early recovery, so treat as soon as possible Veterinary advice should be sought to ensure that displaced abomasum is ruled out as a cause of the acetonaemia.



If acidosis occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from sub-clinical acidosis that is significantly reducing their productivity. A clinical case is the tip of the iceberg, and therefore solutions have to be for the whole herd not the individual animal.



Many diseases have been linked to acidosis. For some, such as liver abscesses, the evidence is very strong. For others, such as sole ulcer and white-line disease, the link is not so strong.

Diagnosis

Difficult as signs are non-specific

Ketosis (acetonaemia) must be ruled out

Reduced milk fat is strongly indicative of excess starch feeding

Most diagnoses are based on eliminating other causes of reduced appetite and yield



Treatment

Most treatment is supportive to allow the rumen to return to normal

Ruminal stimulants are of little value

Feeding of buffers such as sodium bicarbonate can help in the short term, particularly in animals in the same group.

Prevention.

Every treated cow is the tip of the iceberg, so prevention is vital. The aim of any prevention regime is to give the cow time to adapt to change and not to expect the rumen to be able to adapt to whatever is thrown at it.



There are two types of sub-acute acidosis. The first occurs in freshly calved cows (up to 20 days after calving). This occurs because of a failure to adapt the rumen to the lactation diet before calving. In this case, dry cow management is the key to prevention. In particular, feeding a transition diet and minimising calving stress are important.



The second type of acidosis affects cows from peak to mid-lactation. At this time rumen adaptation to the diet should have occurred, so acidosis in these cows occurs as a result of feeding diets that are low in fibre and high in starch (or which allow for feed selection).



In all herds with an acidosis problem there needs to be a full assessment of the feeding, with attention paid to what the cows are being fed and to what they are eating. Each individual situation will be different and require a different range of solutions. Nevertheless there are several factors which are likely to be of importance in most situations:



Forage to concentrate ratio. Except in very high yielding cows a ratio of 60:40 will significantly reduce the risk of acidosis

Feeding total mixed rations with forage and concentrates mixed can significantly reduce acidosis, provided selection of the concentrate portion doesn’t occur

Feeding space: If there is insufficient space average meal size will increase, increasing the risk of acidosis (even with a TMR). (This can also occur if feeding time is restricted or if feeding times are irregular).

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Abortion

Abortion


Cows can suffer abnormalities during pregnancy leading to mummification of the foetus or resulting from maternal or foetal abnormality. All cases where the pregnancy terminates early and the foetus is expulsed are called abortions.



As there are multiple causes of abortion and the detection of abortions in a herd can vary significantly depending on the husbandry system and calving pattern, the incidence of abortion at herd level also varies markedly. It has been suggested that an abortion rate of 5% or more in a herd should be considered an indication of an abortion problem (Deas, 1981).



The causes of abortion have been classified by Boyd and Gray (1992) as follows:



Infectious:

Non-specific

Specific

Miscellaneous:

Drug-induced (prostaglandins)

Insemination/intra-uterine infusion

Hypothyroidism

Trauma/stress (transport, noise, veterinary treatment etc.)

High fever and endotoxins (toxic plants, nitrate/nitrite, fungal toxins, other disease)

Nutritional (malnutrition, vitamin A/selenium/vitamin E deficiency, goitre)

Twin pregnancy

Genetic (malformation)

Both non-specific and specific infectious causes of abortion can lead to "abortion storms" in a herd, whereas the miscellaneous causes often result in sporadic, individual cases.



The most important infectious abortion agents are:

Salmonellosis (particularly Salmonella dublin)

Listeriosis

Leptospirosis

Neospora caninum abortion

Bovine Viral Diarrhoea (BVD)

Infectious Bovine Rhinotracheitis (IBR)

Campylobacteriosis (see below)

Fungal/mycotic abortion (see below)

Epizootic/chlamydial abortion (see below)

Trichomoniasis (see below)

Brucellosis (see below)

Campylobacter jejuni is seldom reported as a primary cause of abortion in cattle in the UK. This may be due to the limitations of current diagnostic procedures. It has been suggested that the pathogen may be a significant cause of infertility in suckler herds.



Fungal abortions are associated with contaminated feed and are either sporadic or occur in small outbreaks, typically between the fifth and seventh months of pregnancy.



Epizootic abortion in cattle, caused by Chlamydia spp., has been reported in the UK in recent years and is seen as an emerging cause of contagious abortion in cattle.



Abortions caused by trichomoniasis and brucellosis are extremely rare in the UK, as both diseases have been subject to statutory disease control measures. Brucellosis is a notifiable disease and its control is still carried our as a statutory measure under the Brucellosis Order.

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Pseudocowpox ,false cowpox, milker’s nodule

This is the most common infectious cause of teat disease in cattle. Because immunity is short-lived, cows can get infected fairly soon (often less than 6 months) after recovering from the disease. This means that many herds have a chronic grumbling problem with pseudocowpox with up to 100% of the herd affected (although only 5% are affected at any one time).

Pseudocowpox, caused by a parapox virus, should not be confused with true cowpox, which is a rare disease of little current importance

What are the signs of Pseudocowpox?

Initially infection causes a small area of swelling and reddening on the teat. This is painful and makes the cow difficult to milk. Over the next two days, the affected area elevates into an orange papule, which then scabs over. Tissue developing under the scab pushes it up further. Once the lesion has scabbed over, it becomes much less painful and milking is no longer so difficult

Seven to ten days after first signs the scabs start dropping off. This often leaves a horse-shoe or ring shaped area, which is very characteristic of pseudocowpox. Affected areas may grow together leading to scabs covering the entire length of the teat. Damaged teats are usually healed around a month after first signs.

Most pseudocowpox is found on the teat. However up to 10% of affected cows may have lesions on the udder skin.

Pseudocowpox can spread from cattle to man by contact. Skin infection in man is known as milker’s nodules, and is a painful localised infection.

Diagnosis

• Clinical signs – if you have seen it before pseudocowpox is relatively to diagnose. However other disease, particularly herpes mammilitis can occur at the same time, so if you are unsure get your vet to check.
• If signs alone are not sufficient, the virus can be isolated from the teat skin

Treatment

Removal of the scabs followed by the application of an astringent disinfectant has been suggested for severely affected individual cases. Locally applied teat ointments appear to have little effect. Emollient teat sprays and dips can have a beneficial effect by reducing the numbers of bacteria and viruses on the teat skin and by aiding the healing of damaged skin.

Prevention

1. Prevent infected cows getting in your herd – Quarantine cows for at least 14 days before they enter the milking herd
2. For pseudocowpox, effective teat dipping with an iodophor teat dip is probably the most effective means of control
3. Improving parlour hygiene by using disinfectable gloves, disposable towels and teat cup disinfection may reduce disease spread

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Traumatic Reticulitis

Though far less common than it used to be 30 years ago, NADIS data shows that Traumatic Reticulitis has increased in recent years and is a significant cause of ill-thrift and culling on many farms What is traumatic reticulitis Traumatic reticulitis is primarily a disease of adult cattle. It occurs when pieces of wire, or other sharp metal objects, which have been eaten by the cow along with its food penetrate the reticulum wall (as a result of the contractions during the cudding process). Infection spreads along the wire to the surrounding abdomen, producing an abscess and adhesions. In some cases the wire will penetrate into the chest of the animal causing abscess in the chest, and in severe cases infection of the outside of the heart (pericarditis). In the UK the most common cause of traumatic reticulitis is tyre wire, coming from old tyres used on silage clamps.

Clinical Signs

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

Diagnosis

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

Treatment

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

Prevention

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

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8:42 PM

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Land Application for Livestock and Poultry Manure

Livestock and poultry manures contain nutrient elements that can support crop production and enhance the chemical and physical properties of soil. Manure can be an asset to livestock and poultry operations when its nutrients are used for fertiliser.

This publication provides information on (1) the nutrient content of manures available for land application, (2) how to determine manure application rates and whether supplemental fertiliser will be needed for maximum crop production and (3) how to use management techniques to maximise the fertilization potential of farm manures.

Factors Affecting Fertiliser Value of Manure and Recommendations for Application

The type and amount of nutrients in livestock and poultry manures and the nutrients’ eventual availability to plants may vary considerably. Some factors affecting nutrient value of applied manure are type of ration fed, method of collection and storage, amount of feed, bedding and/or water added, time and method of application, soil characteristics, the crop to which the manure is applied, and climate.

Increasing levels of various elements (copper, arsenic, etc.) and inorganic salts (sodium, calcium, potassium, magnesium, etc.) in feed will increase their concentrations in manure. There is concern about the potential toxic effects to plants of high concentrations of heavy metals and salts in soil as a result of high application rates of manure to the land. Perform regular soil tests and manure analyses to monitor the balance of nutrients in the soil on your farm, especially on land receiving heavy manure applications. From an environmental standpoint, limit the rate of manure application to the needs of the crop grown on the land.

Bedding and water dilute the nutrient concentration of manure and reduce its value. On the other hand, feed spilled and incorporated into the manure increases the nutrient concentration. Excessive feed spillage and/or inadequate agitation may cause sludge build–up in liquid systems, making removal of the manure more difficult.

The type of housing and/or waste handling system you use greatly affects the nitrogen (N) concentration of manures (Table 1). Major nitrogen losses occur when manure is dried by sun and air movement or leached by rain, as is the case in open lot systems. In contrast, manure loses comparatively little nitrogen in a completely covered facility using a manure pack or liquid pit storage system. Loss of nitrogen is greatest in long-term treatment or storage systems such as oxidation ditches or lagoons.

Table 1. Approximate nitrogen losses from manure as affected by handling and storing methods
Handling, Storing Methods	Nitrogen Loss*
Solid Systems:
Manure Pack	35%
Poultry Litter	35%
Liquid Systems:
Anaerobic Pit	25%
Oxidation Ditch	60%
Lagoon	80%
* Based on composition of manure applied to the land vs. composition of freshly excreted manure.

Phosphorus (P) and potassium (K) losses are minimal (five to 15 per cent) for all but open lot and lagoon manure handling systems. In an open lot, you can lose from 40 to 50 per cent of the manure‘s phosphorus and potassium to run–off and leaching. However, most of the phosphorus and potassium can be retained for fertiliser use by run–off control systems (setting basins, detention ponds). In lagoon systems, from 50 to 80 per cent of the phosphorus in manure can settle in the sludge layer and thus be unavailable if only the liquid portion is applied to the land.

It is possible to realise maximum nutrient benefit from manure if you incorporate it into the soil immediately after land application (Table 2). Incorporation minimises nitrogen loss into the air and/or in run–off and also allows soil microorganisms to start decomposing the organic matter in the manure, thus making nutrients available to the plant sooner. In addition, incorporation of manures into the soil minimises odour.

Table 2. Approximate nitrogen losses from manure to the air as affected by application method
Application	Type of Nitrogen Manure	Method Loss
Broadcast without cultivation	Solid Liquid	20% 25%
Broadcast with cultivation1	Solid Liquid	5% 5%
Knifing	Liquid	5%
Irrigation	Liquid	5%
* per cent of total nitrogen in manure applied which was lost within 4 days after application. 1 Cultivation immediately after application

Generally, phosphorus and potassium losses are negligible and are not affected by the method of application; however, incorporating manure minimises phosphorus and potassium losses due to surface run–off. Apply manure as uniformly as possible to prevent local concentrations of ammonium–nitrogen or other inorganic salts that can reduce seed germination and crop yields.

By applying manure just before the planting date of crops, you maximise plant nutrient availability, especially in high rainfall areas and on porous soils having rapid percolation. However, do not plant immediately after heavy manure application. Salt accumulation near the soil surface and/or a temporary excess of ammonia resulting from the break–down of organic nitrogen lower germination and reduce seedling growth. As an alternative, late fall applications may be desirable because of labour availability, field conditions, etc. Even though fall applications may result in five to 10 per cent total nitrogen loss, the extra time allows soil microorganisms to more fully decompose the manure and release its nutrients for use during the following cropping season. This is especially advantageous for solid manure that contains much organic matter.

For sandy or coarse-textured soils, manures can best be applied frequently and at low rates throughout the growing season to provide environmental protection and maximum plant growth. Soils with more than 10 per cent slope should not have manure applied or if applied, use injection of liquid manure into sod.

Not all manure nutrients are readily available to a crop in the year of application. To be used by plants, nutrients in manure must be released from the organic matter in a water-soluble form. Manure nitrogen is in ammonium (inorganic) and organic forms. Potentially, plants could use all of the ammonium–nitrogen in the year of application. Nitrogen in the organic form, however, must be ‘released’ before plants can use it. In other words, the organic nitrogen must be converted to ammonium (NH4)⁺ or nitrate (NO₃)^- before it can be used by plants. Approximately 75 per cent of the total nitrogen will be available to crops during the year of application with the remainder carried over and available the next cropping season.

However, the rate of availability of nitrogen is largely influenced by soil, climate, etc. In contrast, nearly all the phosphorus and potassium in manures are available for plant use during the year of application.

Table 3 shows the pounds of nutrients excreted annually by various livestock per 1,000 pounds liveweight. The nutrient content of manure from your farm might differ considerably from the values presented here. These figures can, however, serve as a guideline for planning purposes. Nutrient analysis of the manure is highly desirable.

Table 3. Annual pounds of nutrients in manure as excreted per 1,000 pounds liveweight
	Dairy Cow	Beef Feeder	Swine Feeder	Laying Hen	Broiler
Nitrogen, N	150	124	164	263	423
Phosphate, P2O5*	60	91	124	232	216
Potash, K2O	118	106	132	136	158
Elemental P and K conversion can be made as follows: to convert P2O5 to elemental P, multiply by 0.44; and to convert K2O to elemental K, multiply by 0.83.

 

Determine How Much Manure Can Be Applied

You can only determine the exact amount of nutrients available for land application from your operation by laboratory analysis. But you can use Tables 1, 2 and 3 to calculate the approximate nutrient value of your manure from Table 3, then subtract storage and handling losses (Table 1) and application losses (Table 2) to get the nutrients available at time of application. With these figures you can estimate the amount of manure to apply to a given crop area and whether your crop will require additional commercial fertiliser.

If you know the quantity of nutrients available from your operation per year, you can determine how much land is needed for manure disposal. Table 4 gives nutrient needs for various crops. Apply to the land at such a rate that the amount of available nutrients does not greatly exceed the amount removed by the growing crop.

Table 4. Approximate N, P2O5 and K2O utilization by various crops
Crop	Yield/Acre	Nutrient Uptake, lb/A*
		N	P2O5	K2O
Corn (grain)	150 bu 180 bu 32 tons	170 225 480	80 100 80	215 240 245
Corn silage
Wheat	40 bu 70 bu 100 bu	80 140 200	27 47 68	81 142 203
Bermudagrass (Hybrid)	6 tons 8 tons	258 368	60 96	288 400
Clover/grass	6 tons	270	90	360
Sorghum/Sudan Hybrid	8 tons	360	122	466
Grain Sorghum	6,000 lb	225	63	180
Barley	100 bu	150	55	150
* Figures given are total amounts taken up by the crop in both the harvested and the above-ground unharvested portions. These numbers are estimates for indicated yield levels taken from research studies, and should only be used as general guidelines.

Example

A swine producer has a 1,000–head finishing operation (averaging 125 pounds weight per animal) in an enclosed confinement building. Liquid manure is collected in a lagoon. If the manure is spread by irrigation annually on land producing 150 bushels of corn per acre, how many acres are required for maximum fertiliser utilisation?

Step 1

Determine the nutrient needs of the crop. From Table 4, for 150 bushels of corn: N = 225 pounds/acre, P₂O₅ = 80 pounds/acre, K₂O = 215 pounds/acre.

Step 2

Determine the nutrient value of manure from Table 3. Pounds nutrient/year/animal unit in manure as excreted: N = 164, P₂O₅ = 124, K₂O = 132. Reduce nitrogen value 80 per cent for storage losses (Table 1) and 30 per cent for application loss (Table 2). This means only 23 pounds of N/1,000 pound animal unit are available for crop utilisation. At 125 pounds/head, the number of 1,000–pound animal units = 1,000 head × 125 lbs/head divided by 1,000 lbs/animal unit = 125 animal units.

To determine total pounds of each nutrient available, multiply unit values by number of animal units:

N = 23 × 125 = 2,875 pounds
P₂O₅ = 62 × 125 = 7,750 pounds*
K₂O = 66 × 125 = 8,250 pounds*

* Assumes 50 per cent recovery with little or no agitation of the lagoon.

Step 3

Determine number of acres required for maximum nutrient utilisation. Divide total pounds of each nutrient (from Step 2) by pounds of that nutrient required per acre (from Step 1).

Acres Required for N = 2,875 ÷ 225 = 12.8
Acres Required for P₂O₅ = 7,750 ÷ 80 = 96.8
Acres Required for K₂O = 8,250 ÷ 215 = 38.4

Thus P₂O₅ is the acreage-determining nutrient if nutrients are fully used. Manure should be applied over 96.8 acres to assure maximum utilisation of the manure (in actual practice, phosphorus and potassium are often over–applied to allow more nitrogen application). Make up the remaining nitrogen and K₂O required for production with commercial fertiliser.

Step 4

Determine supplemental fertiliser needed (total needs - supplied). Since manure will be applied over 96.8 acres, the following total amounts of N, P₂O₅, and K₂O will be required:

N = 96.8 × 225 (from Table 4) = 21,780 pounds
P₂O₅ = 96.8 × 80 (from Table 4) = 7,744 pounds
K₂O = 96.8 × 215 (from Table 4) = 20,812 pounds

Supplemental nutrient requirements may be determined by subtracting nutrients available in manure (from Step 2) from total nutrients required as follows:

Supplemental N required = 21,780 – 2,875 = 18,905
Supplemental P₂O₅ required = 7,744 – 7,744 = 0
Supplemental K₂O required = 20,812 – 8,250 = 12,562

Solids in Liquid Manure

Flushing gutters with recycled water from lagoons can be a major obstacle when solids content is higher than pumping equipment can handle. A major handicap can occur when dairy free–stall bedding, for example, gets in the flush gutters and ultimately into lagoons. Table 5 shows typical solids content of some liquid waste handling systems.

Table 5. Typical solids content of some liquid waste handling systems
	VS/TS* (%)	Solid Content (%)
Manure Pit
Swine	80	4-8
Cattle	82-85	10-15
Poultry Layers	69.8	25
Holding Pond
Pit Overflow		1-3
Feedlot Run–off		Less than 1
Dairy Barn Wash Water		Less than 1
Lagoon
Single or First Stage Swine		1/2-1
Cattle (no bedding)		1-2
Second Stage		Less than 1/2
Volatile Solids/Total Solids. Volatile solids will dissipate and volatilize into the air over time. Values do not include any bedding.

The chart in Figure 1 shows the relationship of the liquid manure solids content to viscosity or consistency and type pump required.

Figure 1. Solids content and pump type required

Management Factors

Some additional management techniques that will help ensure safe and effective application of manure to crop–land follow:

• Incorporate manure into the soil immediately. Otherwise, apply manure to surface at reasonable distances from streams, ponds, open ditches, neighbouring residences and public buildings to minimise run–off and odour problems.
  
• Minimise odour problems by using common sense, especially during the summer. Spread early in the day when the air is warming up and rising rather than later when the air is cool and settling, and do not spread on days when the wind is blowing toward populated areas or when the air is still. Good management helps avoid neighbour complaints. Analysis from liquid manure varies considerably depending on the amount of dilution. Laboratory analysis is recommended for all animal waste and soil samples are recommended as well. Table 6 shows average nutrients in liquid manure.
  
• Apply manure to relatively level land — if slope exceeds 10 per cent, knife liquid manure into sod.
  
• Agitate or mix liquid manure thoroughly in pits to facilitate removal of settled solids and thus ensure uniform application of the nutrients.
  
• Consider irrigating with dilute manures (lagoon or run–off liquids) during dry weather to apply needed water and nutrients to growing crops.
  
• Wash the plants with clean water to avoid leaf burn when irrigating manure on growing crop.
  
• Avoid spreading liquid manure on water-saturated or frozen soils where run–off is apt to occur.
  
• Apply sufficient water sometime during the year to avoid accumulation of salts in the root zone of soils in arid regions.
  
• Use good safety measures when moving manure from tanks or pits. Because of oxygen deficiency or toxic gas accumulation, avoid entering storage structures when agitating the liquid manure.

The chemical and physical properties of soil, such as water infiltration rate, water–holding capacity, texture and total exchange (nutrient–holding) capacity also affect how much manure can be safely applied to land. Fine–textured soils have low water infiltration rates; therefore, the rate at which liquid manure, especially lagoon effluent, can be applied without run–off may be restricted to the intake rate of the soil.

Coarse–textured soils, on the other hand, are quite permeable and can accept higher rates of liquid manure applications without run–off. But because most coarse soils have a very low exchange (nutrient–holding) capacity, you may have to apply smaller amounts of manure during the growing season to minimise the chance of soluble nutrients entering ground water. Organic matter in the manure is decomposed more rapidly in coarse–textured than fine–textured soil and during warm, moist conditions rather than cold, dry conditions. However, fine-textured soils will retain the nutrients longer in the upper profile, where plants can get them.

Table 6. Nutrients in liquid manure: approximate fertiliser value of manure – liquid handling systems
Animal	Waste Handling	Dry Matter	Available N	Total N	P2O5	K2O
		%	lbs/1,000 gal of waste
Dairy cattle	Liquid pit Lagoon*	8 1	12 2.4	24 4	18 4	29 5
Swine	Liquid pit Lagoon*	4 1	20 3.2	36 4	27 2	34 4
Beef	Liquid pit Lagoon*	11 1	24 2	40 4	27 9	34 5
Poultry	Liquid pit	13	64	80	36	96
* Lagoon – Including lot run–off water Note: There will be little odour if manure is immediately incorporated.

Unknown

11:01 PM

اقرأ المزيد

Plan To Improve Calving Weight

“The breeding programme; which bull was used to breed a cow or group of cows, determines the genetic potential of the newborn calf or group of calves,” says Barry Yaremcio, beef/forage specialist with Alberta Agriculture and Rural Development. “Birth weight, frame size and growth rate are all genetically controlled and cannot be changed. On the other hand, management on farm or on the ranch impacts the animals’ growth potential. You can affect the size and weight of the calf come weaning time and, therefore, your profitability. If poor decisions are made, the genetic potential of the calves will be negatively affected.

“Management changes must be evaluated, not just made on a whim. The change or changes should move the operation towards long term goals and make economic sense. Be it a change in bull genetics, or changes in the feeding and grazing programmes, the short and long term benefits need to be greater than the added costs or potential down side.”

There are several things producers can do to improve calf weaning weights without wholesale changes:

Watch body condition score of the cows prior to calving - colostrum quantity and quality are impacted by body condition of the cow. If a cow is thin, less colostrum is produced, reducing the passive immunity provided to the calf. This can lead to a greater risk of disease or infection in these calves.

A cow in good condition is able to mobilize fat reserves. A pound of fat provides enough energy to produce seven pounds of milk. This is very important for the first 12 weeks of lactation when feed intake is limited.

Castrate or ring bull calves at birth – the practice of leaving bull calves intact until weaning to improve growth rates has been disproven. Bull calves do not reach puberty until 9- to 10-months-of-age. At puberty, bull calves start producing hormones to increase growth rates. Unfortunately, most calves are castrated before this time.

As bull calves grow, the stress associated with castration increases. An 8- or 9-month-old calf may experience reduced average daily gain of 0.3 to 1.3 pounds per day throughout the 30-day period after castration, adding up to a total ‘lost’ gain of 39 pounds.

Move cow calf pairs to a clean open area – keeping newborn calves in a tight pen with many other animals presents ideal conditions for diseases to spread. If possible, move cow-calf pairs to clean pens away from cows that have not calved, or to pastures. Minimizing calf contact with other animals, and standing water puddles contaminated with urine and manure, reduces disease pressure.

Use a fortified trace mineral salt with selenium – in most parts of Alberta, copper, manganese, zinc and selenium are deficient. Cobalt and iodine are virtually absent from all forges and grains. The use of a cobalt (red) or cobalt/iodized (blue) salt does not provide any of the four trace minerals mentioned above.

Changing from a blue salt on pasture to a fortified trace mineral salt with selenium resulted in an additional 20 pounds of weaning weight. There can also be improvements in cow fertility when the trace mineral salt with selenium is fed year round.

Develop a water system where cows do not walk into the water supply – water quality impacts average daily gain. Work done in the Barrhead/Westlock area in the early 1990s, found an improvement in calf growth rate if stock drank from a nose pump or from a storage tank. Over the grazing season, there was a 20 pound improvement in calf weight gain.

Creep feed calves – cow milk production peaks about eight weeks after calving. After this, milk yield declines. Creep feed should be provided when nutrients from the fresh grass and milk do not provide what the calf requires. Grazing management, weather, moisture and pasture fertility all impact when the creep feed should be provided.

Calves that consume creep feed prior to weaning have less difficulty adjusting to a ration that includes grain after weaning.

Manage forage resources – let the grass grow in the spring before turning the cows out to graze. There should be a minimum of three to four leaves of new growth to allow the plant to start replenishing food reserves in the root zone. For continuous grazing systems, every day the cows are turned out too soon in the spring, will result in a reduction of fall grazing of two to three days if a continuous grazing system is used.

Forage quality drops rapidly after the seed head has emerged from the boot. The use of rotational grazing to allow plants to recover after grazing events and to keep grass vegetative, maintains quality and increases potential yield. When a seed head is fertilized, the plant allocates nutrients to fill the head rather than initiating vegetative growth; overall yield potential is reduced.

Minimize weaning stress – vaccinating calves four to six weeks prior to weaning provides a higher level of immunity compared to calves vaccinated at weaning. Having a stronger immune system helps combat disease and the associated reduction in animal performance.

“Prior to weaning, move the calves and cows into the pens or corrals where the weaned calves will stay after weaning,” says Mr Yaremcio. “Let the cows teach the calves where the feed bunks, feeders, water bowl and loafing areas are. When the cows are moved out of the pen, the calves know where everything is. Less stress results in less illness and reduced performance.”

Once weaned, place the cows in an adjacent pen to the weaned calves. Allowing the two groups to see each other and touch noses also reduces stress.

“Even if you are selling the calves at weaning, inform the buyers that the calves have been vaccinated,” says Mr Yaremcio. “This information may entice the buyers to add a few cents a pound to the settlement price.”

Unknown

12:43 PM

اقرأ المزيد

Economics Of Dairy Beef Production Systems

Summary

• Projected increases in dairy cow numbers will increase the number of calves becoming available for beef production.
• There has also been an increase in interest in bull finishing systems due to the greater growth potential of bulls relative to steers.
• A number of alternative dairy calf-to-beef systems were compared in terms of financial performance.
• In terms of profitability, systems were ranked as follows from most to least profitable; 22 month bull finishing, 24 month steer finishing, 19 month bull finishing, eight month veal finishing, under 16 month bull finishing and 12 month bull finishing.
• All systems were highly sensitive to calf, concentrate and beef price and thus, the careful preparation of production system budgets is recommended.

Introduction

With the impending abolition of milk quotas in 2015, it is projected that dairy cow numbers in Ireland will increase substantially. This will result in a greater number of dairy male calves becoming available for beef production. Although the majority of beef cattle from the dairy herd are currently finished as steers, there is increasing interest in bull finishing systems given the inherent greater live weight gain performance of bulls relative to steers. However, these systems have typically involved greater levels of concentrate feeding than steer systems. The objective of this paper is to examine the economics of a range of options for finishing male calves from the dairy herd. These systems are based on the systems currently under evaluation in the Johnstown Castle dairy calf-to-beef project. Six options were evaluated representing calf-to-beef systems finishing male calves as; veal at 8 months of age, bull beef at 12, 16, 19 and 22 months of age and steer beef at 24 months of age.

Veal finishing systems

Veal finishing systems using Friesian and Jersey crossbred calves were evaluated. In this system calves were finished on ad libitum concentrate diets with straw offered as a source of roughage following a 12 week rearing phase. Live weight gain was lower for the Jersey crossbred calves resulting in a 20 kg differential in slaughter weight and a 14 kg differential in carcass weight in favour of the Friesian calves (Table 1). Approximately 750 kg of concentrates were fed per head. For the financial analysis of the other systems evaluated, cost and price assumptions were based on those prevailing for the Johnstown Castle dairy calf-to-beef project in 2011. Jersey crossbred calves were purchased at €30/head with Friesian calves costing €140/head. Fixed asset requirements were assumed to consist of a calf house and a weanling finishing unit. Both of these were assumed to be in the seventh year of a 20-year life span with interest charged at seven per cent per annum. A similar approach was taken for the remaining production systems evaluated in this paper with finishing housing costs reflecting age and weight at finish. Both Friesian and Jersey crossbred calves returned a positive net margin (Table 1). Systems based on Jersey crossbred calves were somewhat more profitable largely owing to lower calf purchase price and lower concentrate feed requirements. Sensitivity analysis indicated that both systems are very sensitive to calf price and veal price in particular.

Twelve month bull finishing system

The 12 month bull finishing system and the remaining beef systems evaluated in this paper, had a similar rearing phase to the veal production system. Following the rearing phase calves were built up onto ad libitum concentrate with straw offered as a source of roughage. Similar to the veal production system, live weight gain was greater for the Friesian compared to the Jersey crossbred calves such that slaughter weight was 64 kg greater and carcass weight was 40 kg greater for the Friesian bulls. Correspondingly, concentrate consumption was greater for the Friesians. Neither system returned a positive net margin (Table 2). However, gross margin was positive for both systems indicating that a contribution can be made to the fixed costs of the farm. In addition to calf price and beef price, the 12 month bull system is also sensitive to concentrate price.

Under 16 month bull finishing systems

For the under 16 month bull finishing system, calves were turned out to pasture in May at approximately three months of age for a six month grazing season. Two treatments were compared; supplementing at pasture with 2 kg of concentrate (PC) or offering no supplementation during the grazing season (PO). Following housing in early November, all cattle were adapted onto an ad libitum concentrate diet with straw offered as a source of roughage. Cattle remained on ad libitum concentrates for ~200 days before slaughter at under 16 months of age. Friesian bulls were ~50 kg heavier at slaughter than Jersey crossbred bulls and cattle supplemented during the grazing season (PC) were ~45 kg heavier than cattle offered pasture only (PO) (Table 3). Total concentrate supplementation ranged from 2.3 t for Friesians supplemented during the grazing season to 1.5 t for Jersey crossbreds offered pasture only during the grazing season. Financial results indicated that for systems finishing bulls at under 16 months of age, Jersey crossbreds were more profitable than Friesians and pasture only was more profitable than supplementation during the grazing season. All systems returned a positive gross margin ranging from €70/head for the Friesian system where calves are supplemented in the first grazing season to €194/head for Jersey crossbred systems where calves are not supplemented in the first grazing season. However, when full fixed costs are allocated to these systems, only the latter system (Je PO) returned a positive net margin.

Nineteen and twenty month bull finishing systems

These systems operated similar to the under 16 month bull finishing system up until housing in November at the end of the first grazing season. Thus, two treatments were imposed during the first grazing season; calves supplemented with 2 kg concentrate (PC) and calves receiving pasture only (PO). Following housing, bulls were fed ad libitum grass silage plus 1.5 kg of concentrate until turnout to pasture for a second grazing season in early March. The bulls for finishing at 19 months of age were housed in mid May for a 100 day finishing period on ad libitum concentrates with straw offered as a source of roughage. Similarly bulls to be finished at 22 months were housed approximately 3 months later for a similar 100 day finishing period. Bulls finished at 22 months of age were 70 kg and 90 kg heavier for PC and PO groups, respectively, when compared to bulls finished at 19 months of age (Table 4). Total concentrate intake over the lifetime of the animal ranged from 1.4 t for 19 month finishing bulls which were not supplemented during the first grazing season to 1.8 t for 22 month bulls receiving supplementation during the first grazing season. All systems returned positive gross and net margins with net margin ranging from €150/head to €265/head for 19 month bulls not supplemented in the first grazing season and 22 month bulls supplemented in the first grazing season, respectively. Twenty-two month bull systems were more profitable than 19 month bull systems and systems where concentrate supplementation is provided at pasture during the first grazing season were more profitable than systems where no supplementation was provided during the first grazing season. All systems were highly sensitive to beef price in particular and concentrate price. Again, calf price was also important.

Table 1. Economics of veal production systems from Friesian (Fr) and Jersey crossbred (Je) calves (€/head)

Table 2. Economics of 12 month bull production systems from Friesian (Fr) and Jersey crossbred (Je) calves (€/head)

Table 3. Economics of under 16 month bull production systems from Friesian (Fr) and Jersey crossbred (Je) calves receiving concentrate supplementation (PC) or pasture only (PO) during the first grazing season (€/head)

Table 4. Economics of 19 and 22 month bull production systems from calves receiving concentrate supplementation (PC) or pasture only (PO) during the first grazing season (€/head)

Table 5. Economics of 24 month steer production system (€/head)

Twenty four month steer finishing systems

In this system Friesian calves are finished for slaughter as steers at 24 months of age. Calves spend their first season at pasture with no supplementation. Following an indoor winter period during which grass silage is offered ad libitum in addition to ~ 1 kg/day concentrate supplementation, yearlings are turned out for a second season at pasture. Cattle are housed in October/November for a ~150 day finishing period. During the finishing period good quality grass silage was offered in addition to 5-6 kg concentrate daily (Table 5). Target slaughter and carcass weights were 620 kg and 320 kg, respectively. Total concentrate intake was ~1.2 t. Gross and net margins for this system were €355/head and €193/head, respectively. Margins were most sensitive to beef price with concentrate price and calf price assuming similar sensitivity.

Conclusions

All of the systems evaluated in this paper returned positive gross margins indicating that these systems provide a contribution to fixed costs. The 22 month bull finishing system was most profitable with the 24 month steer system next most profitable. The veal production system was also competitive with these systems arising from the much higher price received for veal meat. However, this system is for niche producers with a relatively small market demand. However, for the 12 month and under 16 month systems gross margins were insufficient to cover allocated fixed costs and therefore, these systems returned negative net margins. The exception was the under 16 month Jersey crossbred system where calves were not supplemented during the first grazing season which had a positive net margin. It is apparent that the economics of dairy beef systems are highly sensitive to beef price, concentrate price and calf price and thus, the market outlook is of critical importance when evaluating the profitability of these alternative systems. Thus, it is recommended that detailed enterprise budgets, subject to the prevailing conditions on individual farms and including sensitivity to key parameters, are prepared annually on dairy calf-to-beef enterprises. It should be noted that a constant beef price has been assumed for all scenarios. As the cattle in the Johnstown Castle research project are slaughter, and carcass data becomes available, it will be possible to re-evaluate the economics using the price received for the alternative systems.

Unknown

11:52 AM

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Clinical signs of Foot and Mouth Disease

Signs of Foot and Mouth in Cattle

• Slobbering and smacking lips.
• Shivering
• Tender and sore feet
• Reduced milk yield
• Sores and blisters on feet
• Raised temperature

Pictures of infected cattle

Plate 1 - Tongue of steer with 1-day-old vesicle which ruptured when the tongue was drawn from the mouth.

 Plate 2 - Steer with 2-day-old ruptured vesicle along upper gum and several 1-day-old unruptured vesicles on the tongue.

Plate 3 - Two-day-old ruptured vesicles on the tongue, lower gum and lower lip of a steer. Note sharp edges to ulcerated areas.

 

Plate 4 - A further example of 2-day-old lesions in the mouth of a steer. Again note sharp margins of lesions and red raw appearance of exposed dermis.

 

 Plate 5 - Tongue of steer with 3-day-old lesions. Sero-fibrinous exudation into the lesions has resulted in a loss of earlier red raw appearance and also sharpness of margination. Early granulation evident.

 Plate 6 - Same animal as in plate 5 with 4-day-old lesions. Note progressive loss of lesion margination and extensive fibrin infilling.

 

Plate 7 - Steer’s tongue with a 10-day-old lesion characterised by loss of papillae, indentation at the site of the lesion and fibrous tissue proliferation.

Plate 8 - Foot of a steer with a 2-day-old unruptured vesicle in the inter-digital space.

Plate 9 - A different steer also with a 2-day-old inter-digital vesicle.

Plate 10 - The heel bulbs of a steer’s foot with unruptured 2-day-old vesicles.

 

Plate 11 - The same foot as in Plate 10, 1 day later. The epithelium overlying the vesicle is friable and easily stripped off.

Plate 12 - A 5-day-old lesion on a steer’s foot. Signs of early granulation are evident.

Plate 13 - A 7-day-old lesion on a steer’s foot. Healing is progressing underneath the necrotic epithelium.

 

Plate 14- Another example of a 7-day-old inter-digital foot lesion on a steer.

Plate 15 - An 11-day-old foot lesion on the heel bulb of a steer. Note healing and under-running of horn tissue.

Plate 16- One-day-old vesicles on the teat of a cow. Rupturing has not taken place but several vesicles have coalesced.

Signs of Foot and Mouth in Pigs

• Sudden lameness
• Prefers to lie down
• When made to move squeals loudly and hobbles painfully
• Blisters form on the upper edge of the hoof, where the skin and horn meet, and on the heels and in the cleft
• May extend right round the top of the hoof with the result that the horn becomes separated
• Blisters may develop on the snout or on the tongue

It is important to remember that Swine Vesicular Disease has identical symptoms to foot-and-mouth disease. Therefore anyone who sees blisters in pigs must report the sighting as suspected foot-and-mouth disease until laboratory tests prove otherwise.

Signs of Foot and Mouth in Sheep

Sudden, severe lameness

Lies down frequently and is very unwilling to rise

When made to rise stands in a half-crouching position, with hind legs brought well forward, reluctant to move

Blisters may be found on the hoof where the horn joins the skin which may extend all round the coronet and in the cleft of the foot. When they burst the horn is separated from the tissues underneath, and hair round the hoof may appear damp the dental pad and sometimes the tongue

Detecting the disease in sheep

As a keeper of sheep you are often the first person who could be suspicious that your animals are affected and so we are providing this further information to assist you during your inspections. The disease can be difficult to recognise in sheep as sometimes as little as 5% of animals in infected flocks show any signs. Look for the following signs:

• Sudden death in lambs. In several recent confirmed outbreaks the most obvious sign was apparently healthy lambs dropping dead.
• Abortions
• Lameness (this may only last for a short time)
• Listless and off their food

Inspection of sheep

If you are noticing any of the above signs in your flock then you must inspect individual sheep. Make sure you have plenty of light either daylight or a good torch. For each sheep you must examine both mouth and feet. Do not ask another stock keeper to assist you. If you have any concerns contact your local Animal Health Divisional Office.

Mouth

The typical fluid filled blisters are difficult to see as they usually quickly burst. This will leave erosions or ulcers particularly on the dental pad of the upper jaw where the lower front teeth touch the pad. They may also be seen on the gums, lips and tongue and may be very small.

Feet

Foot lesions are less common but as the disease progresses they may become more obvious. Transient lameness will be a sign but you must look carefully for blisters, particularly between the claws, on the heel bulbs and the coronary band. Turn back the hair over the coronary band to check for horn separation. If the blisters have burst then hair may be damp and bacterial infection may be present, as could foot rot. Affected feet may feel hot and painful.

Unknown

10:50 AM

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Diseases caused by Rickettsia and Mycoplasma spp

Diseases caused by Rickettsia and Mycoplasma spp.


Heartwater (Hydropericardium)

"Black dung" when affecting African cattle and buffalo


"Sheep fever" when seen in sheep

Heartwater is an acute, non contagious disease of cattle, sheep, goats, antelopes and wild ruminants. It is caused by the rickettsial organism Cowdria (Rickettsia) ruminantium.


Transmission:

Heartwater is transmitted by various species of Amblyomma ticks. Transstadial transmission of the organism occur in vector ticks.

Antemortem findings :


Peracute form

1. Incubation 14 – 28 days
2. Fever
3. Diarrhoea
4. Convulsions and death

Acute form

1. Fever up to 41.7°C
2. Rapid breathing
3. Lack of appetite, depression and listlessness

Nervous signs include

1. Twitching of the eyelids
2. Protrusion of the tongue
3. Champing of the jaw
4. Walking in circles
5. Paddling with legs in recumbent animals
6. Opisthotonos and convulsions

Postmortem findings :

1. Hydropericardium
2. Hydrothorax
3. Pulmonary edema and ascites
4. Haemorrhagic gastroenteritis
5. Enlarged liver, spleen and lymph nodes
6. Haemorrhage in the abomasum and intestine
7. Edema and haemorrhage of the brain

Judgement :


Carcass of an animal affected with heartwater is condemned in the acute stage of the disease. In a chronic case, the carcass may be approved if adequately bled and muscles are wholesome in colour and texture. The affected organs are condemned.


Differential diagnosis :



Peracute form of heartwater should be differentiated from anthrax. The acute nervous form of the disease is differentiated from tetanus, rabies, cerebral trypanosomiasis, strychnine poisoning, piroplasmosis, theileriosis, lead and organophosphate poisoning, parasitism, arsenical poisoning and poisoning with certain plants.





Fig. 63 : Heartwater Cowdria ruminantium in bovine brain smear (arrow).



Q fever (Queensland fever, Nine mile fever, American Q fever, Australian Q fever)


Q fever is a disease of cattle, sheep, goats, donkeys, camels, fowl, dogs, cats, pigeons and humans. It is caused by Coxiella burnetii. Q fever is an occupational disease of livestock personnel. farmers and laboratory personnel.

Transmission :

Ticks spread infection to cattle which develop mild disease. The faeces deposited on animal hide by ticks may be the source of infection for humans. Q fever is also transmitted by inhalation or dust contaminated with infected animal secreta or excreta. Healthy animals may serve as a carrier and shed the organism in milk, urine, faeces, placenta and fetal fluids. They harbour the infection and no clinical signs are observed. Contaminated meat and water are further means of infection read.

field cases there are no clinical signs of this disease. In the disease produced by the inoculation of cows via the udder the clinical signs may include:

1. Acute mastitis
2. Loss of appetite and depression
3. Serous nasal and lacrimal discharge
4. Difficult breathing
5. Atony of the rumen
6. Abortion in pregnant cows

No gross lesions are reported in cattle.

Discussions :
Coxiella burnetii is highly resistant and was isolated from farm soil 6 months after the removal of animals. It may persist in the udder up to 3 years. The temperatures of milk pasteurisation (in bulk at 63°C for 30 minutes or the common method at 72°C for 15 seconds) kill this agent in milk. Vaccination will reduce shedding of organisms in milk.

This disease in humans has a sudden onset and is characterized by loss of appetite, weakness and generalized malaise lasting from 1 – 2 weeks. Pneumonia may also be present. Death may be caused by endocarditis in older people. More severe symptoms of Q fever are noticed.

Contagious bovine pleuropneumonia

This is an acute, subacute or chronic highly infectious disease of cattle caused by Mycoplasma mycoides var, mycoides.

Transmission :


Aerosol and droplet infection from the infected animals. The recovered animal called "lungers" act as carriers and shedders, especially under stress.


Antemortem findings :

1. Incubation: acute 10 – 14 days, chronic 3 – 6 months
2. Morbidity: 90 % in susceptible cattle
3. Mortality: 10 – 50 %
4. Fever
5. Depression
6. Lack of appetite and loss of weight
7. Coughing on exercise
8. Shallow rapid respiration, grunting and gurgling
9. Extended neck, lowered head and open mouth
10. Arched back and outward rotated elbow
11. Arthritis in young animals

Postmortem findings :

1. Fibrinous inflammation of the pleura (pleuritis)
2. Straw coloured fluid in the thorax (Fig. 64)
3. Lobar pneumonia with red hepatization, marbled appearance of lung lobules (Fig. 65) due to thickening of interlobular septae and interlobular pulmonary edema
4. Enlarged mediastinal lymph nodes
5. Walled-off sequestra formation in chronic cases
6. Haemorrhage in the heart
7. Arthritis and tenosynovitis

Judgement :

Carcass of an animal affected with contagious bovine pleuropneumonia is condemned if the disease is associated with fever, inadequate bleeding of carcass, serous infiltration of the brisket and emaciation. Recovered animals showing no generalized signs of the disease are approved and the affected organs are condemned.

Differential diagnosis :



Shipping fever (Pasteurellosis). East coast fever, foreign body pneumonia, IBR, tuberculosis, chlamidial infections and lungworms




Fig. 64: Contagious bovine pleuropneumonia. Straw coloured fluid in the thorax and partial lung hepatization.






Fig. 65: Contagious bovine pleuropneumonia. Lobar pneumonia with red hepatization and marbled appearnce of lung lobules

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9:25 PM

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Anthrax

 

 

Anthrax is a peracute disease of ruminants manifested with septicemia, sudden death and tarry blood from the body openings of the cadaver. It is caused by Bacillus anthracis.

TransmissionMan may contract anthrax by inhalation, ingestion and through a wound in the skin. Biting flies have been shown to be transmitters.

Ante-mortem findingsThe peracute and acute forms in cattle and sheep are without clinical signs. Death may follow in the acute form after 1 - 2 hours of illness. The acute form lasts about 48 hours.

In pigs and horses this disease is usually localized and chronic and is often characterized by swelling around the throat and head.

Ante-mortem findings in pigs:
1. Incubation 1 - 2 weeks
2. Edematous swelling of the throat and neck
3. Swallowing and breathing difficulties
4. Death due to choking or toxaemia
5. Septicemia is not observed.

Post-mortem findings1. Dark-tarry blood discharge from body orifices
2. Absence of rigor mortis
3. Haemorrhage of the mucous and serous membranes, lymph nodes and subcutaneous tissue
4. Enlarged spleen
5. Severe haemorrhagic enteritis
6. Degeneration of the liver and kidneys
7. Bloating and rapid decomposition of carcass
8. Localized lesions in the intestine of pigs (dysentery)

JudgmentCondemnation of the carcass and its parts by burning or burial. If disposed by burial, the carcass should be buried at least 6 feet below ground. The site should be surrounded by a foot thick layer of quicklime.

Differential diagnosisPeracute blackquarter and septicaemic form of other diseases. In splenic enlargement as seen in babesiosis, anaplasmosis and leucosis, spleen consistency is firm. In anthrax, the spleen is soft and upon incision the pulp exudes like thick blackish-red blood.

DiscussionIf an animal has died from an unknown cause in an abattoir's pen or in the stockyard, a blood smear from the tip of the ear should be examined to eliminate anthrax as a cause of death. All measures should be taken to prevent further contact with the carcass. The orifices of the nose, vulva and anus should be packed with cotton swabs to eliminate further spillage of discharge. The carcass must not be opened. Due to insufficient oxygen supply in the closed carcass, spores of B. anthracis will not be formed and the organism will be killed. The spilled discharge is firstly removed by drying with sawdust and sand and is then destroyed together with the carcass. The carcass is wrapped in thick plastic sheets and destruction is performed under the supervision of an appropriate government official.

An open carcass facilitates exposure of B. anthracis to air and consequently, spores are formed within a few hours. Anthrax spores are resistant to heat and disinfectants and may survive in a suitable environment for years.

The abattoir's pen or stockyard area suspected of being in contact with an anthrax animal should be disinfected with 10 % NaOH or 5 % formaldehyde and cleaned. This cleaning should also include the cattle trucks or cars used for the transportation of infected animals.

All personnel that were in contact with anthrax or that handled contaminated material, are also subjected to decontamination. The arms and hands should be washed with liquid soap and hot water. After they have been rinsed, they should be immersed for about one minute, in an organic iodine solution or 1 p.p.m. solution of mercuric perchloride or other acceptable agents. This is followed by a potable water rinse. Clothing of the personnel involved should also be cleaned and thoroughly disinfected by boiling.

If the carcass is discovered on the killing floor, all operations must cease. The carcass and its parts including hides, hooves, viscera and blood must be condemned and destroyed. The carcasses which have been dressed by the same abattoir employees prior to or after the affected carcass must also be condemned and destroyed. Those carcasses which had been dressed before the affected carcass may have a second option of being salvaged with sterilization. They must be boiled for a minimum of 3 hours if contamination occurred with blood splashes. If impractical, these carcasses may be used for "canned meat" for which heat treatment is recommended.

Disinfection of equipment used for the dressing of a diseased carcass as well as the infected abattoir area, should be done with 5 % solution of sodium hydroxide (NaOH). This disinfectant is used because of its action on fat and grease removal. Heat in the form of a blowtorch can be used for disinfecting buildings.

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9:18 PM

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