Disease Checklist:

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Mulberry Heart Disease (vitamin E deficiency)
Vitamin E is widespread in feed stuffs including vegetable oils, cereals and green plants but problems arise often from using polyunsaturated fats in diets as sources of energy which destroys the vitamins. Vitamin E is necessary for the optimum function and metabolism of the nervous, muscular, circulatory and immune systems. It helps to maintain the integral structure of muscles in the digestive and reproductive systems and is involved in the synthesis of certain amino acids and vitamin C. It has a close relationship with selenium metabolism. The less selenium in the diet the greater is the requirement for vitamin E.
The recommended requirements are 30 to 100iu/kg in the grower ration and 30 to 60iu/kg in the finisher ration. These levels are probably higher than those necessary for maximum growth, which may be 50% less. When polyunsaturated fatty acids (PUFA) are added to diets 3iu of vitamin E should be added for each g of PUFA.

Symptoms
Piglets
Become sensitive to iron injections if sows deficient.
Sows
N/A
Weaners & Growers

Clinical signs and post mortem lesions of a deficiency vary according to the system affected and include:
Sudden death in rapid growing pigs without any prior clinical signs.
Possibly increased levels of concurrent diseases if selenium levels are low.
Pale pigs.
Post-mortem symptoms are characteristic and include:
Large amounts of fluid around the heart and lungs.
Haemorrhagic and pale areas in heart muscle.
Fluid in the abdomen with pieces of fibrin.
Pale muscle areas (necrosis) particularly in the lumber muscles and hind muscles of the leg which contain excesses amounts of fluid.
If the liver is involved it is enlarged and mottled with areas of haemorrhage interspersed with pale areas.
Vitamin E and selenium related diseases
Gastric ulcers - These are often caused by stress but the incidence increases where vitamin E levels are low.
Hepatosis dietetica - Death of liver cells.
Muscular or nutritional dystrophy. Degeneration of skeletal, smooth or cardiac muscle fibres. Fluid often accumulates around muscles.
Mulberry heart disease (MHD). A disease of the heart muscle resulting in sudden death.
Causes / Contributing factors
Diet i.e. high levels of fat.
Vitamin A deficiency.
Vitamin E and selenium deficiency.
Rapid growth may be a contributing factor.
High stocking densities may predispose.
Grains stored with high moisture content in high temperatures and with fungal growth may have low levels of vitamin E.
Diagnosis
Accurate diagnosis requires histological examinations of the liver, heart or skeletal muscle. Serum samples should be taken from pigs at risk and tested for levels of vitamin E.

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Muscle Tearing
This is a common condition in sows in which the muscle fibres are torn away from their attachment to the bones of the inner surfaces of the elbow and knee joints and the pelvis.
Symptoms
Sows, Weaners & Growers
Painful inflammation of bone and periosteum.
Affected sows often adopt a dog sitting position.
Pigs cannot stand.
Reluctance to move.
Lameness.
Incoordination.
Shivering.
Piglets
Piglet can not stand - legs spread laterally.
Causes / Contributing factors
Torn muscles arise as a sequel to OCD.
Trauma.
Fighting.
Slippery floors.
Weak bones.
Splay leg in piglets.
Diagnosis
This is by clinical signs.

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Mycoplasma Arthritis
Most herds are infected although not all infected herds show clinical signs. Mycoplasma hyosynoviae lives in the upper respiratory tract without causing clinical signs and is spread by droplet infection. It invades the joints and tendon sheaths of susceptible animals and causes lameness and swelling.
Older sows develop a strong immunity which they pass to their offspring in the colostrum.

Infection takes place sometime after this colostral immunity has worn off, usually between 12 and 30 weeks of age but sometimes gilts do not become infected until introduced to a new herd or in early pregnancy.

It is common in purchased gilts which have been reared in isolated grow-outs, but uncommon in mature sows.

Infection with or without disease takes place in the growing pig from approximately 8 to 30 weeks of age.

Symptoms
Sows/Gilts
Clinical signs in the gilt are sudden in onset.
Starting with a reluctance to rise.
Lameness.
Swellings over hock joints visible.
Affected pigs are in pain and only stand for short periods.
The temperature may be normal or slightly elevated.
Shivering.
Piglets
None.
Disease rare.
Protected by maternal antibodies
Weaners & Growers
Reluctance to rise.
Trembling.
Considerable amount of pain particularly when standing.
Only stand for short periods of time.
Temperature normal or slightly elevated.
Lameness swollen joints.
Causes / Contributing factors
The quality of housing - in particular low temperatures and draughts which act as trigger factors.
Mixing and fighting.
Respiratory spread.
High stocking density.
Sudden reduction in energy intake producing stress nutritional changes.
Poor ventilation.
Diagnosis
This is based on clinical signs and the response to therapy. Joint fluid can be aspirated and examined for antibodies and the organism can be isolated.

Serology is not much help because sub-clinical infection is common and so healthy animals often have antibody titres. Rising titres in blood samples taken two weeks apart aid diagnosis.

Post-mortem examination may be necessary to reach a definitive diagnosis.

It must be differentiated from muscle damage, leg weakness, trauma, erysipelas, and Haemophilus parasuis arthritis.

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Mycotoxicosis
Under certain conditions fungi multiply on cereals, corn, cotton seed and other food materials sometimes producing chemicals called mycotoxins. Fungi require adequate moisture, oxygen and carbohydrates to multiply and temperatures from 10?C to 25?C (50?F to 77?F). Multiplication may still take place however outside these ranges and crops that are already diseased are more likely to succumb to fungal infection. The presence of fungi including recognised toxic species however does not necessarily mean that the toxins are present. Each requires precisely the right substrate and environmental conditions to produce toxins. The common fungi causing disease (mycotoxicosis) in the pig include species of Fusarium, Aspergillus and Penicillium, but because of the variable requirements for growth and toxin production, particular species tend to predominate in certain geographical areas. Toxins are not destroyed by heating but modern treatments used in the processing of animal feeds such as temperature and pressure may reduce the actual fungal load.
Fusarium species require high levels of moisture and relative humidity (>88%) for multiplication and toxin production whereas Aspergillus and Penicillium multiply at lower levels.

Aflatoxins and some of the ochratoxins are immuno-suppressive and can enhance effects of generalised disease.

Zearalenone or F2 Toxin (Fusarium Poisoning)
These are related to the type of fungus, the toxin produced and the amounts present. The most important one called F2 toxin or zearalenone is produced by a strain of Fusarium graminearum which is found in maize.
It is an oestrogenic toxin and is produced in high moisture environments in maize growing areas well before harvest.


Symptoms
All Pigs

Rectal and vagina prolapses are common symptoms in the young growing stock.
The most striking clinical feature is the swollen red vulva of immature gilts.
Stillbirths
The other signs are dependent up on the levels present in the feed and the state of pregnancy.
These include:
Returns > 23 days.
Farrowing early.
The following may be used as guidelines to the symptoms that may be observed.
Boars - Semen may be affected with feed levels above 30ppm but not fertility. At higher levels poor libido, oedema of the prepuce and loss of hair may occur.
Gilts (Pre puberty) 1 - 6 months of age - 1 to 5ppm in feed causes swelling and reddening of the vulva and enlargement of the teats and mammary glands. Rectal and vagina prolapses also occur in young growing stock.
Gilts (mature) - 1 to 3ppm will give rise to variable lengths in the oestrus cycle due to retained corpora lutea and infertility.
Sows - Levels of 5 to 10ppm can cause anoestrus, which may also be associated with pseudo pregnancy due to the retention of corpus luteum. F2 toxin will not normally cause abortion however, if sows are exposed during the period of implantation litter size may be reduced. In lactation piglets may develop enlarged vulva.
Effects on pregnancy - Embryo survival to implantation does not appear to be affected at levels less than 30ppm but above this complete loss between implantation and 30 days occurs, followed by pseudo pregnancies. Low levels of 3 to 5ppm do not appear to affect the mid part of pregnancy, but in the latter stages piglet growth in utero is depressed, with weak splay-legged piglets born. Some of these may have enlarged vulvas.
Effects on lactation - 3 to 5ppm has no effect on lactation but the weaning to service interval may be extended.
Causes / Contributing factors
Mouldy feeds:
The purchase of mouldy, damp or badly stored grains.
The mixing of contaminated and uncontaminated grains.
Holding cereals in moist, damp conditions.
Allowing grains to heat.
Prolonged usage of feed bins, feed bridging across the bin and development of moulds.
Placing compounded feeds into bins whilst they are moist and warm.
Poorly maintained bins that allow water to leak in.
The bridging of feed in bins over long periods of time and their sudden descent.
Prolonged use of automatic feeders and retention of mouldy feed.

Diagnosis
Based on the clinical signs and demonstrating the toxin in feed.
Aflatoxins - (Aspergillus Poisoning)
These toxins are common and their effects are dependent upon the dose and age of the pig. Toxins are found in maize, peanuts and soya beans.

Symptoms
Sows

Abortion.
No milk - agalactia.
Liver damage.
Reduced performance.
Immuno suppression.
Piglets, Weaners & Growers
Unlikely to be any symptoms other than poor growth.
Causes / Contributing factors
Wet harvests allow fungi to grow.
Poor storage of feed ingredients.
Diagnosis
Examine feed for evidence of toxin.

Ochratoxin and Citrinin - (Aspergillus & Penicillium Poisoning)
The fungi are found in oats, barley, wheat and maize.


Symptoms
Sows

Liver / kidney damage.
Jaundice.
Reduced performance.
Piglets
Unlikely to be any symptoms.
Weaners & Growers
Reduced growth.
Kidney damage.
Causes / Contributing factors
Poor wet harvests allow the fungi to grow.
Poor storage conditions.
Diagnosis
Clinical and post mortem signs. Toxins identified in feed.
Ergotoxins (Ergot poisoning)
These toxins are produced from the fungus ergot found in wheat, oats and rye grass. They interfere with blood flow.


Symptoms
Sows, Weaners & Growers
Poor growth.
Increased respiration.
Depression.
Reduced blood supply due to blood vessel contractions. Blue skin.
Gangrene at extremities.
Tail, ear necrosis.
Piglets
Unlikely to be any symptoms.
Causes / Contributing factors
Contaminated grains.
Poor storage of grains.
Diagnosis
Examine feed for the presence of small black ergot bodies.

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Navel Bleeding
At birth or within a few hours the piglet becomes extremely pale and in many cases dies.
Symptoms
Sows
Blood may be seen from the vulva.
Piglets
Pale, low viable pigs.
Anaemia.
Blood on the floor of the pen arising from the navel.
Pigs found dead.
Weaners & Growers
N/A
Causes / Contributing factors
The condition arises in one of three ways:
The piglet's blood may be pooled into the placenta during farrowing. If the cord is broken at birth, the piglet will be pale and anaemic. Affected piglets are more likely from old sows and in large litters.
Pigs are sometimes born with a haemorrhage or a haematoma in the cord itself. The cause of this is unknown but in some cases it is related to premature cord cutting and removal of the piglet from behind the sow at farrowing.
Continual bleeding from the navel during the first 3 to 4 hours after birth.
Other factors that predispose:
Navel bleeding is associated with the use of wood shavings as bedding.
Warfarin poisoning can be responsible for haemorrhage.
Mycotoxins from contaminated feed have been implicated
A riboflavin deficiency has been implicated.
In some herds there appears to be an association with the use of prostaglandin to synchronise farrowings.
Do not allow excessive trauma to the cord within 3 hours of birth. This may occur if too many piglets are fastened in the creep area.
Diagnosis
This is by clinical signs.

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Nipah virus disease
This is a totally new disease that first became evident in September 1998 in Malaysia. In March 1999 a previously unknown virus was isolated from an adult male who having had contact with pigs died. The virus was identified as a previously unknown paramyxovirus and the disease was called Nipah Disease from the village in Malaysia where it was first identified.
The virus causes illness and death in both humans and pigs.

Symptoms
Humans
Symptoms may be mild or severe and include:

Fever, headaches, encephalitis.
Drowsiness, confusion leading to coma.
Respiratory failure.
High mortality up to 40% reported.
A few people have shown no symptoms.
The incubation period is from 7 to 21 days.
In 1999 there were over 300 cases and 100 deaths.

All Pigs
Morbidity is usually high but mortality is low.
Rapid laboured breathing.
Very harsh explosive cough.
In sows disease may be more pronounced with severe breathing difficulties.
Convulsions, death.
Pneumonia.
Mucopurulent discharges from the nose.
At post mortem the predominant signs are consolidation of the lungs.
Causes / Contributing factors
Movement of pigs.
Direct pig to pig contact either by mouth, by the respiratory route or aerosol from urinary excretions.
Diagnosis
This is by serological tests, virus isolation and identification. In infected farms sows show high levels of antibodies and in infected areas antibodies have been widespread in dogs but not in rats.
Further Reading
Click on the links below to find out more about this disease, including treatment, management control and prevention information. The top link is the main article on this disease.
Nipah Virus Disease

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Oedema Disease
This is also called gut oedema. It is caused by certain serotypes of E. coli bacteria that produce a powerful toxin. These toxins damage the walls of small blood vessels including those in the brain and cause fluid or oedema to accumulate in the tissues of the stomach and the large bowel. Damage to the blood vessels in the brain results in characteristic nervous signs. Disease is now uncommon and generally only seen 1 to 4 weeks after weaning, the peak being at 14 days.
Symptoms
Piglets & Sows
N/A
Weaners & Growers
Sometimes the only sign is a good pig found dead.
Typically, live affected pigs show:
A staggering gate.
Incoordination.
Puffy eyelids giving a sleepy appearance.
An abnormal high pitched squeak.
Pigs stop eating.
In the later stages become partially paralysed and go off their legs.
Sometimes with nervous symptoms. Muscle twitching, fits.
Diarrhoea is not a feature.
Breathing difficulties become evident.
The damage to the brain is irreversible and most pigs die.
Lameness.
Causes / Contributing factors
Associated with weaning and changes of diet.
Diagnosis
This is made from the typical clinical signs, the sudden appearance of disease after weaning, post-mortem examinations showing oedema (fluid in tissues) of the greater curvature of the stomach wall, coiled colon and eyelids and isolation of the specific haemolytic E. coli serotypes from the anterior small intestine.

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Leg Weakness (Osteochondrosis - OCD)
(270) Trauma is by far the most common cause of lameness in the dry sow from point of weaning to point of farrowing. Environmental trauma to the coronary band area and to the sole or wall of the foot results in penetration of the sensitive tissues, infection and lameness. These foot conditions are called bush foot and foot rot. Trauma however, more commonly arises indirectly from other causes within the environment that create shear forces on the muscles, tendons, bones and bone structures. Such changes associated with cartilaginous structures are referred to as leg weakness or osteochondrosis. The structure of the joint and bone is shown in Fig.7-7.
 

The term Leg weakness" is also used sometimes to describe poor leg conformation or describe a clinical condition associated with lameness and stiffness. It arises due to abnormal changes in the articular cartilage and the growth (epiphyseal) plates. These plates are responsible for the growth of bones both in length and diameter. Whilst the exact mechanisms that cause these changes are not fully understood they arise due to the pressure and shear stresses that are placed upon these rapidly growing tissues. This pressure reduces the oxygen supply, causing abnormal growth and consistency of the cartilage. Damage to the cartilage tends to be progressive and irreversible. The damaged cartilage is replaced by fibrous tissue. This cartilage damage in turn produces shortening and bending of the bones near the joints and at the extremities of the long bones. Weak epiphyseal plates also have a tendency to fracture and cartilage covering the joint surfaces splits and forms fissures. It is important to appreciate that such changes in the cartilage take place in most if not all modern pigs from as early as two months of age. In some cases many of these can only be detected under the microscope. It is interesting to note that such changes can not be detected in the wild boar which takes up to two years to reach maturity. OCD is therefore a fact of life in modern pig production but its severity and its effects depend largely on the environment. OCD results from the many years of selecting animals for rapid growth, large muscle mass, and efficient feed conversion and therefore much greater weight on the growth plates whilst they are still immature, together with the stresses of intensive methods of production. Conversion of cartilage to bone involves the deposition of calcium and phosphorous and while the process of breaking down and reforming bone goes on throughout life, bone growth ceases when the sow is approximately 14 to 16 months of age.

It is not uncommon in breeding enterprises for 20 to 30% of boars and gilts to be culled after completing the performance test, due to leg weakness and leg deformities.

The conformation of the pig is a predisposing factor to OCD, Fig.7- 8 shows some of these traits.

Sows with good leg conformation show angulation of the bones at the hip, knee and hock joints. The bones below the hock slope slightly forwards and the feet are well placed on the ground. Sows that are susceptible to leg weakness are straight legged with little angulation of the bones between the joints and the back tends to be arched. This alignment increases shear stresses on the growth plates.





Clinical signs

Acute disease
This is seen when there is a separation or fracture of the bones at the epiphyseal plate (epiphyseolysis) associated with sudden movement. The animal walks on three legs, the affected leg swinging freely. Crepitus or rubbing of the broken bones together can usually be felt. Sudden fractures can also occur in the knee and elbow joints, which are more common in the young growing pig. Fractures of the vertebrae in the spine occur particularly during lactation and immediately post weaning. In such cases the sow is in acute pain, often in a dog sitting position with the hind legs well forward. Animals housed in farrowing crates with slippery floors tend to slide the back legs forward and there is a risk of the hind muscles pulling away from their attachments to the pelvis (apophyseolysis). In such cases the sow will stand with assistance but it cannot pull the hind leg backwards. When it is placed on to the ground it just slides forward. Such animals should be culled immediately.

Chronic disease
The onset is gradual. The pig shows abnormal leg conformation and gait with or without stiffness and pain. The temperature remains normal and joints will not be swollen unless there are fractures.

Front legs

- These may be straight with the pig walking with a long step on its toes.
- The knees may be bent inwards or flexed which causes the pig to walk with short steps.
- The pasterns may be dropped. This is common in old sows due to shortened bones and slack tendons.
- The feet may be rotated or twisted.
Hind legs
- These are straight with a swinging action from the hips as the pig moves. Avoid selecting such females for breeding.
- The legs are tucked beneath the body.
- The hocks turn inwards and are close together.
- The pig walks with a goose stepping action.
- Likewise in old sows the pasterns may be dropped.
Abnormal gaits arise either from pain in the joints or abnormal movements in the hind legs from the hips which give a swaying motion. The pain is associated with damage to the sensitive membranes around the joints resulting from either splitting or erosion of the cartilage in the joints or movement of the growth plates. Some pigs however may show severe clinical signs yet on post mortem examinations the joints appear normal and vice versa. Joints may become inflamed (arthritis), particularly in the hip, knee and elbow. OCD may be seen within three months of gilts being introduced on to the farm, during their first pregnancy, in lactation or in the first 2 to 3 weeks post weaning.
Diagnosis

OCD is diagnosed on the clinical signs described. There are no serological or other tests and post-mortem examinations may be misleading because many pigs that are found to have joint lesions may not be lame.

Similar diseases

There are two, Mycoplasma hyosynoviae infection and erysipelas. In both of these the disease is usually sudden in onset sometimes with a raised body temperature and there is pain and swelling in the joints. A differentiating feature is the response to treatment. OCD does not respond to antibiotics whereas Mycoplasma hyosynoviae and erysipelas will respond within 24 to 36 hours, the former to lincomycin or tiamulin and the latter to penicillin.

Treatment

There is no specific treatment for OCD, however, at an early stage the sow should be moved from its existing environment to a well-bedded pen where the foot can grip. If not, the lesions progress and ultimately arthritis and permanent lameness develop.
Gilts that are confined in stalls or tethers, or group housed on floors that are wet and slippery should be moved as soon as clinical signs appear.
Management control and prevention
If OCD is causing a problem on your farm check through the list below and identify those points that are important in your system.

Determine the time and place when OCD first becomes evident.
Look carefully at surfaces that cause the foot to slip and result in increased pressure on the growth plates.
If the problem is in gilts look carefully at the conformation of these animals and consider improving the selection procedure.
Animals with a fine bone structure are more prone to leg weakness.
Animals with heavy ham muscles and a disparity between anterior and posterior muscle masses, increases the horizontal pull on the growth plates. Such young gilts do not acclimatise well to stalls or tethers.
If there is a problem in lactating gilts look at the floor surfaces in the farrowing crates. Are these slippery and causing pressure on weakened bones? The use of dry sand in these pens once or twice a week may assist in the prevention of the condition until the floor surfaces can be altered.
The modern hybrid gilt often suckles ten or more pigs and produces a large amount of milk which is high in calcium and phosphorous. The bones are therefore more prone to calcium or phosphorus depletion and if the gilt is mixed at weaning time with older sows, damage and sudden fractures are likely to take place.
The tethering and confinement of gilts during pregnancy can be a major contributing factor. Culling rates in such animals may rise towards 20% if the floor surfaces are very slippery.
The design of slats can contribute to OCD. Some slats slope to the edges from the centre and are so smooth that when the animals stand, the feet slip into the gaps. This causes constant twisting and pressure on the growth plates and a high incidence of OCD may result.
Gilts in the first pregnancy should not be housed on slippery floor surfaces.
High levels of vitamin A (in excess of 20,000 iu/kg) particularly in the younger growing pigs can interfere with the normal growth of the epiphyseal plates. OCD lesions have been seen in piglets as young as 3 to 4 weeks of age where sows have been fed excessive levels of vitamin A.
High lysine levels may also increase the incidence.
High stocking densities, particularly in the growing period and where animals are housed on solid concrete floors or slats, will increase the incidence of OCD in the breeding stock. Such environments cause great stress on the legs and pens tend to be dirty and wet.
Fat sprayed diets can make floor surfaces slippery.
Pigs treated with porcine growth hormone tend to develop severe lesions of OCD at an early age.
New concrete surfaces or slats during the first few weeks of use may develop slippery surfaces after contact with faeces and urine. They should be pressure washed with detergent on two or three occasions.
Variations in nutrition within acceptable limits do not appear to influence OCD but conditions of osteomalacia and osteoporosis (soft and weak bones) occur where there is an imbalance of calcium and phosphorous in the diet or excessive withdrawal of these minerals from the bones. Soft and brittle bones in such deficiencies often fracture across the mid part of the long bones during lactation. Always check the calcium phosphorous ratios of the diet and add additional minerals during lactation, dicalcium bone phosphate could be used.
Pain in the joints from OCD also gives rise to abnormal stresses on the muscles particularly where they are attached to the bone. Tearing of these attachments on the insides of the shoulders and legs and from the muscle masses in the pelvis is common causing severe pain and periostitis.
Smooth concrete surfaces that have been finished with a steel float can predispose to OCD.
The addition of 0.5% sodium bicarbonate/tonne to the ration has been shown to reduce the incidence.

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Lameness
Calcium and phosphorus

Problems that may arise with calcium, phosphorus, vitamin A and D

(625) With modern dietary formulations actual deficiencies arising due to defective diet would be unusual. Problems however occur due to faulty storage, the incorrect application of the feed or interactions that reduce the availability to the pig. The latter can result from intestinal disease, metabolic failures or adverse interactions between nutrition, the pig, management and the environment.

Calcium contributes to wide variety of functions in the body including blood clotting, muscle and nervous activity, hormone production and milk production to name but a few. Its major role however, together with phosphorus is involved in the formation of bone where on a dry matter basis it forms approximately 38% of the structure and phosphorus 20%.

Bone is a very strong and dynamic structure with minerals constantly being removed and replaced. The intestines control the rates of absorption both into the body and skeleton and these are necessary to maintain an equilibrium between demand and excretion. The ratio of calcium to phosphorus in the diet is also an important factor in this equation and this should not rise above 2:1, when it does the absorption of calcium may be impaired, likewise if the ratio drops below 1:1. The ideal is approximately 1.25:1 to 1.50:1. Vitamin D3 is also required in calcium metabolism together with controlling hormones produced by the parathyroid gland.

Osteodystrophy

This is a general term to describe specific diseases that arise whenever there is a failure of bone structure and metabolism due to faulty nutrition. Such diseases include osteoporosis, rickets and osteomalacia, periostitis describing disease of the periosteum and osteomyelitis, disease of the centre or medullary cavity of the bone.

Osteoporosis (OP) and Osteomalacia (OM)

Both these conditions are becoming more common in modern pig producing systems particularly in the first litter gilt where the skeleton is still growing and there are heavy demands on calcium for milk production.

Bones affected with OP are quite normal in their structure but they become thinner particularly in the dense parts and shafts of the long bones. As a result they become more prone to fracture. OP can arise due to a shortage of calcium in the diet and imbalance of calcium and phosphorus, poor or inadequate absorption from the diet, heavy losses during lactation and where there is a lack of exercise. Osteomalacia is the adult form of rickets and is associated with a phosphorus or vitamin D3 deficiency. There is a failure of the mineral to be deposited in the bones, which become soft and they either bend or fracture.

Clinical signs

These are most common in the first litter female and occasionally after the second litter.

The onset may be gradual with the pig having difficulty rising and showing pain or sudden lameness associated with complete fracture of the long bones. Spinal fractures occur in some animals and they often remain in a dog sitting position. Most pigs are affected in late lactation or shortly after weaning associated with the onset of oestrus and the trauma that results from other animals, or the weight of the boar at service.

Diagnosis

This is based on clinical signs, a history in lactating and newly weaned sows and evidence of fractures of the long bones. If the herd has a problem it is necessary to examine the bones of an affected animal by x-ray to differentiate between OP and OM.

Similar diseases

These include:

Leg weakness or osteochondrosis.
Spinal fractures.
Torn muscles at their insertions into the bones.
Mycoplasma hyosynoviae infection
Treatment
In cases of bone fracture the sow is best destroyed on humane grounds.
Management control and prevention
Outbreaks are often more apparent in new gilt herds. Selection of animals for good conformation is essential.
Investigate the growth rates and nutrition and feeding in the gilt.
Increase exercise during pregnancy if possible.
Check the levels of calcium and phosphorus in the diet. They should be 10-12g/kg of calcium and 8-10g/kg of phosphorus.
Only mate gilts from 220 days onwards and if the disease is a persistent problem in a particular genotype change the source.
Check that floor surfaces are not slippery.
The problem is less common in outdoor herds.
Feed a good lactation diet during suckling and consider top dressing the diet daily with 20g of di calcium bone phosphate.
Inject pregnant animals with 50,000iu vitamin D3 three weeks prior to farrowing. Repeat again in the second week after farrowing.
Maximise feed intake to appetite during lactation.
Check the ratio of calcium : phosphorus in bone ash. The normal ratio is approximately 2:1 or less. In problem sows this is often 3:1 or more.
Rickets
This arises in a similar way to OM except it occurs in young growing animals, again as a failure of mineralisation of bone and growth plate cartilage. Phosphorus and vitamin D deficiencies are the common cause but the condition today is rare.

Where it occurs young animals are often housed in dark surroundings and fed starch feed waste with no mineral vitamin supplements. It usually takes 6 to 8 weeks before symptoms become evident, by which time the disease has progressed to become irreversible.

The symptoms are similar to OM but because the growth plate and cartilage does not develop to bone the joints swell with stiffness and pain is evident. Bone fractures are also common. In the few cases treated the response to injections of vitamin D3 has been very poor with pigs being totally uneconomical.

Vitamin A

The classical descriptions of vitamin A deficiency are described in Fig.14-4 but in the authors experience in the field such diseases would be rare. Most if not all rations are well fortified with the vitamin, indeed in many cases to excess and gross intake leading to disease is more likely to be experienced, but not well recognised.

Two problems arise in the field. The first is where high levels of vitamin A up to 15,000 to 18,000 iu/kg are fed. This has been shown to lower the vitamin E status of the pig and therefore make it potentially more susceptible to mulberry heart disease. This depression of vitamin E may also reduce antibody production and thereby increase susceptibility to disease. This scenario has coincided with out breaks of respiratory disease in the field and lowering the vitamin A levels to around 8,000iu/kg and raising the vitamin E by 50-100iu/kg had been undertaken with improvements.

Piglets born from sows fed high levels of vitamin A may produce piglets with a low vitamin E status and this can be a fruitful line of investigation where iron dextran problems persist in sucking pigs.

The second problem arises when excessively high levels of vitamin A - 25,000 to 30,000iu/kg are fed. At these levels the growth plates of the foetus become affected with classical signs of leg weakness and grossly shortened and bent bones in pigs as young as three weeks of age.

Further evidence for the effects of vitamin A on growth plates was also illustrated in a severe outbreak of leg weakness in weaners and growers fed rations containing high lysine 1.5% and high vitamin A levels of 18,000iu/kg. The pigs were housed on very smooth slats the surfaces of which sloped to the edges. This resulted in the claws remaining in the gaps for long periods and by the time the pigs were 16 weeks of age the claws were completely crossed over due to a combination of pressure and weakened growth plates. When levels were reduced to 10,000iu and the lysine levels dropped to 1.1% and the slat surfaces roughened, the problem gradually disappeared.

Leg Weakness or Osteochondrosis

See also chapter 7.
Degenerative changes in the joints and cartilage are generally described under the term leg weakness or osteochondrosis. These changes involve erosion of the articular cartilage and alterations to the normal patterns of growth at the growth plates at the ends of the long bones.

The use of both vitamins and minerals in cases of disease problems to try and prevent the conditions have been singularly disappointing and it is doubtful if specific nutrient factors are involved.

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Osteomalacia
This bone condition is due to inadequate levels of calcium phosphorus and or vitamin D or sows may not be able to absorb sufficient amounts. The density of the bones becomes less and they are prone to fractures particularly mid shaft.
The ratio of calcium to phosphorus in the diet should be 1.0 to 1.6 :1. A calcium and phosphorus ration of less that 1:1 will result in a calcium deficiency.

Symptoms
Sows
Seen in the first litter gilt.
Dog sitting position.
Stiffness
Sudden acute lameness during lactation or immediately post weaning.
Fractures.
Pigs show pain / discomfort.
Piglets
N/A
Weaners & Growers
Stiffness.
Lameness.
High incidence of fractures of he main bones at slaughter.
Causes / Contributing factors
Inadequate diet.
Heavy milk production.
Low feed intake in lactation.
Breed of animal.
Shortage of vitamin D3.
Low calcium in the diet.
Diagnosis
This is by the clinical signs. Similar diseases include:

Leg weakness or osteochondrosis.
Spinal fractures.
Torn muscles at their insertions into the bones.
Mycoplasma hyosynoviae infection

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Osteoporosis
This conditions is becoming more common in modern pig producing systems particularly in the first litter gilt where the skeleton is still growing and there are heavy demands on calcium for milk production which result in demineralisation of bone..
Bones affected with OP are quite normal in their structure but they become thinner particularly in the dense parts and shafts of the long bones. As a result they become more prone to fracture. OP can arise due to a shortage of calcium in the diet and imbalance of calcium and phosphorus, poor or inadequate absorption from the diet, with heavy losses during lactation and where there is a lack of exercise.

Symptoms
Sows
Pigs show pain / discomfort.
Sudden lameness
Fracture of long bones.
Piglets, Weaners & Growers
Rare
Causes
Loss of calcium and phosphorous during lactation.
Faulty nutrition.
Age of sow.
Diagnosis
This is based on clinical signs, a history in lactating and newly weaned sows and evidence of fractures of the long bones. If the herd has a problem it is necessary to examine the bones of an affected animal by x-ray to differentiate between OP and OM. Calcium and phosphorus levels may be normal.
Similar diseases include:

Leg weakness or osteochondrosis.
Spinal fractures.
Torn muscles at their insertions into the bones.
Mycoplasma hyosynoviae infection.

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Navel Bleeding / Pale Pig Syndrome
(375) At birth or within a few hours the piglet becomes extremely pale and in many cases dies. The condition arises in one of three ways:
Anoxia or shortage of oxygen inside the womb during farrowing causes the piglet to pool its blood into the placenta. If it is born and the cord separated at this point, then it will be born very pale and anaemic. This picture is seen when piglets are delivered by hysterectomy and they are removed from the womb at a critical time before the piglet has time to recall its blood from the placenta. Affected piglets are more likely from old sows and in large litters.
Pigs are sometimes born with a haemorrhage or a haematoma in the cord itself. The cause of this is unknown but in some cases it is related to premature removal of the piglet from behind the sow at farrowing. The blood vessels in the cord bleed.
Continual bleeding from the navel during the first 3 to 4 hours after birth.
Clinical signs
Fresh blood on the floor of the pen arising from the end of the navel is diagnostic.

Treatment

Early recognition of a bleeding navel is essential. The cord should be clamped approximately 13mm from the skin using an umbilical clip. (See chapter 15). Those used for babies are ideal. Nylon or plastic ties used to bind together electrical wires are also good
As an alternate and in an acute emergency the navel can be tied in a knot.
A ligature can be applied around the umbilicus but it shrinks and the bleeding often continues. The cord should be bent back on itself and re-tied in the shape of a "U".
Management control and prevention
Navel bleeding is associated with the use of wood shavings as bedding. The reasons for this are unknown but wood preservatives or other substances may be responsible. Change the shavings to an alternate source or use straw for bedding.
Warfarin poisoning can be responsible for haemorrhage.
Vitamin C was thought to be involved and improvements by feeding sows with 1g/day have been reported. Experiences however with this vitamin have been disappointing.
Do not move pigs away from the sow immediately at farrowing. Allow the piglet to break the cord naturally. There is a particular part of the cord where separation takes place naturally without any haemorrhage. The navel cord is always slightly longer than the birth canal so that when the newborn piglet starts to rise and walk the cord is stretched, breaks and recoils to block the blood vessels. It should not be cut.
Supplementing the diet with vitamin K can sometimes help.
Mycotoxins from contaminated feed have been implicated.
A riboflavin deficiency has been implicated.
In some herds there appears to be an association with the use of prostaglandin to synchronise farrowings.
Do not allow excessive trauma to the cord within 3 hours of birth. This may occur if too many piglets are fastened in the creep area.

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Pasteurellosis (Pasteurella multocidia)
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Non-toxin-producing strains of Pasteurella multocidia bacteria are commonly involved in respiratory disease in pigs. They can cause pneumonia in their own right but are usually secondary opportunist invaders associated with primary EP or PRRS infections. The condition usually affects pigs between 10 and 18 weeks of age and rarely sows and sucking pigs unless as secondary bacteria following the introduction of a new pathogen..
Symptoms
Sows & Piglets
Rare
Weaners & Growers

Acute disease is characterised by:
Severe sudden pneumonia affecting all the lung tissue.
High temperatures.
Discharges from the nose.
High mortality.
Pigs show rapid breathing.
Blue discoloured skin particularly on the extremities of the ears (caused by toxins or heart sac infections).
Sub acute disease is characterised by:
Pneumonia which is less severe but often complicated by heart sac inflammation and pleurisy.
Coughing.
Discharges from the nose.
Emaciation. Poor body condition / wasting.
Increased mortality.
Causes / Contributing factors
Concurrent disease such as PRRS, Flu and EP predispose.
Diagnosis
This is carried out by post-mortem examination and isolation of the organism from the lungs.

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Penis Bleeding
This is a relatively common condition, the boar at mating passes fresh blood into the vagina.
Symptoms
Boar
Blood around vulva post service.
Blood in semen.
Blood around the prepuce and skin.
No generalised illness.
Sudden onset.
Haemorrhage only occurs at mating.
Sows, Piglets, Weaners & Growers
N/A
Causes / contributing factors
Damaged penis.
Ulceration of the urethra.
Haemorrhage from accessory glands.
Haemorrhage from the preputial sac.
Trauma to the penis from sows or boars in outdoor mating.
Diagnosis
This is made from the clinical symptoms.
Treatment
Rest the boar for 3 weeks
Treat with a broad spectrum antibiotic for 5 days
If it reoccurs cull the boar

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Peritonitis
Peritonitis is inflammation of the peritoneum, the shiny membrane that covers all the internal surfaces in the abdomen. The onset may be sudden or gradual. A common time is 7-10 days after mating caused by the boar at mating damaging the vagina. It may arise due to a bacterial septicaemia.
Symptoms
Sows
Abdominal pain.
Appetite normal or depressed.
The sow is reluctant to move.
Loses weight.
Has a tucked up appearance.
A discharge from the vulva may be apparent at mating.
The temperature may be normal or elevated.
Weaners & /Growers
Coughing (App)
Loss of condition and growth.
Pale.
Piglets
Swollen abdomen.
Wasting.
Death.
Causes / Contributing factors
Ruptured gastric ulcer.
Perforated bowel.
Penetration of the abdomen via mating.
External trauma to the abdomen and ruptured bowel or liver.
Conditions such as actinobacillus pleuropneumonia, gl?ssers disease, migrating ascarid worms and miscellaneous generalised infections may also result in peritonitis.
Diagnosis
This is based on the clinical signs and history. A post-mortem examination may be required to confirm it.