Pinoyagribusiness

Abortion and embryo / foetal loss
Abortion means the premature expulsion of dead or non-viable foetuses. Embryo loss occurs when there is death of embryos followed by absorption, or expulsion. Healthy embryos grow into foetuses.
There is often alarm when an abortion is seen but it should be remembered that there can be loss of embryos at any time during early pregnancy, which often go unseen.

Embryo loss or abortion can be considered in three main groups:

During the period from fertilisation to implantation
During the period of implantation at around 14 days post-service to 35 days.
During the period of maturation, which results in premature farrowings. It can be seen therefore that losses can take place at any stage from approximately 14 days after mating, when implantation has taken place, through to 110 days of pregnancy.
Records help to identify reproductive problems. These should include information on:

- Age (or parity) profile of the herd.
- Failure to come on heat.
- Culling rates.
- Bleeding and discharges from the vulva.
- Repeats, sows not in pig.
- Lameness.
- Litter sizes.
- Mastitis, lack of milk, swollen udders.
- Deaths and their likely causes.
- Poor conformation.
- Prolapse of the vagina or rectum.
- Savaging.
Symptoms
Piglets, Weaners & Growers
N/A
Sows
The delivery of a premature litter with or without mummified pigs.
Mucus, blood, pus discharges from the vulva.
Sow may be ill or normal.
Symptoms of a specific disease.
Sows not in pig.
Usually less than 2% of sows affected, however acute PRRS may cause rates to rise to 20% or more.
Causes / Contributing factors
Infectious Causes (common ones). Consider the following:
Aujeszky's disease.
Influenza virus.
PRRS (Blue ear disease).
Leptospira.
Specific bacteria, E. coli, klebsiella, streptococci, pseudomonas.
Parasite burdens.
Cystitis, nephritis.
Non Infectious Causes
Seasonal infertility.
Decreasing daylight length, poor lighting.
Low temperatures.
Chilling, draughts.
Poor nutrition.
Mouldy feeds.
Contaminated water.
Stress.
No boar contact.
Vaccine reaction.
Lameness.
Poor hygiene.
Diagnosis
Fresh, aborted foetuses should be submitted to a competent diagnostic laboratory where examinations can be carried out for evidence of viral and bacterial infections, together with histological examinations and toxic studies. In many cases the end results of post-mortem and serological tests do not identify any particular infectious organism, which may seem disappointing. However, it is useful in telling us what is not present.
A Checklist for Abortions
Abortion Level. Is this more than 1.5% of sows served? Take action.
Are sows ill? Probably disease.
Are sows otherwise normal? Probably non infectious, Maternal failures.
Is the problem seasonal? Autumn abortion syndrome.
Do they occur in a particular part of the farm? Environmental.
Are the aborted pigs fresh or alive? Suggests the environment.
Are mummified pigs present? Suggests infection.
Is the dry sow accommodation uncomfortable? Suggests the environment.
Are sow pens wet, draughty, poorly lit? Suggests the environment.
Does the ventilation system chill the sows? Suggests the environment.
Are there factors that place the sows in a negative energy state? e.g.: High chill factors, draughts, low feed intake, a change in bedding or availability.
Are sows short of food - Check feed intakes by volume and weight.
Is the food mouldy? Check for mouldy feed.
Do the sows experience 14 hours of good light at eye level?
Are the lights dirty, covered in fly dirt?
Can you read a newspaper in the darkest corner?
Do your sows have boar contact in pregnancy?
Are any other diseases evident in the sows? e.g.: lameness , cystitis, kidney infections.
Are the abortions associated with stress?
Increase feed intake from days 3 to 21 after mating according to body condition and environmental temperatures.
Increase the mating programme by 10-15% over the anticipated period of infertility.
Because boar semen can be affected, particularly by environmental temperatures, follow each natural mating 24 hours later by purchased AI.
Further Reading

Abscesses
Pockets of pus that contain large numbers of bacteria which usually enter the body through damage to the skin. Near the skin surface they may become painful.
Symptoms
All Pigs
Possibly emaciation and death.
Small to large swellings.
Pigs show pain / discomfort.
Evidence of fluid - pus or blood in the swellings.
Red skin may be ulcerated.
Often damage evident to the skin.
Lameness from spinal abscesses.
Causes / Contributing factors
Fighting.
Secondary infection arising from other conditions such as PRRS, pneumonia or tail biting.
Small widespread abscesses in the skin (pustular dermatitis) may be seen following general illness, septicaemia and or greasy pig disease.
Damage to the skin by sharp objects in the environment.
Trauma to feet, knees, tail.
Teeth removal.
Poor injections.
Chronic abscesses may from around joints following fractures.
Diagnosis
Feel and press the swelling to ascertain if the contents are fluid or solid. Sample the contents by inserting an 18mm 16 gauge needle attached to a 10ml syringe at the lowest soft point of the swelling.
Haemorrhage into the tissues is the only condition likely to be confused with an abscess. In such cases either pure blood or a very thin blood stained liquid will be withdrawn. Such pockets of blood are called haematomas.

Actinobacillosis
This is caused by the bacteria, Actinobacillus suis and Actinobacillus equuli. The first of these is present in most herds and lives in the tonsils of older pigs, particularly sows. It usually only effects piglets.
Symptoms
Sows
Rarely applicable.
Piglets
Sudden death.
Discoloration of skin (blue).
High fever.
Coughing.
Pneumonia.
Skin lesions (not to be confused with Erysipelas).
Arthritis.
Lameness.
Septicaemia.
Weaners & Growers
Rarely seen.
Symptoms as for piglets
Causes / Contributing factors
It can be precipitated by PRRS.
Teeth clipping .
De-tailing.
Scrubbed knees.
It may enter the piglet via the respiratory system or via cuts and abrasions.
It occasionally multiplies in the blood stream and settles out in various parts of the body, particularly the lungs and the joints. Here it produces multiple small abscesses.
Diagnosis
Post-mortem and laboratory examinations to demonstrate characteristic lesions and the presence of the organism. It has to be differentiated from meningitis, acute E. coli infection, erysipelas, clostridial diseases and piglets that have been laid on.

Actinobacillus Pleuropneumonia (App)
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Nuflor
DRAXXIN®
EXCEDE®
EXCENEL® RTU
Porcilis APP
Porcilis Cobactan 2.5%
Tiamutin
The bacterium Actinobacillus pleuropneumoniae (App) consists of at least twelve different serotypes, some of which produce no disease but others cause severe disease. Serotypes vary in different countries. Types 1, 5, 9, 11 and 12 are usually highly virulent and strains 3 and 6 are mild. App is carried in the tonsils and upper respiratory tract. It is transmitted short distances by droplet infection and only survives outside the pig for a few days.
The organism may affect the pig from weaning through to slaughter but usually the age is from 8 to 16 weeks. The incubation period is very short, as little as 12 hours. Toxins produce severe damage to the lungs.

App is uncommon in sows unless they are naive or disease is triggered by PRRS or flu.

Symptoms
All Pigs
Unusual in adult and very young pigs unless a naive herd.
Sudden death/mortality may be low or high - only sign a bloody discharge from the nose.
Sudden death/mortality - no symptoms and more than 1 % of such deaths. Post mortems required.
A short cough perhaps 1 to 3 coughs at a time - different from the prolonged coughing of EP.
Severe heavy breathing difficulties.
Blueing of the ears.
Badly affected pigs are:
- Severely depressed.
- Off feed.
- Body temperatures are high.
Pleurisy.
Haemorrhage from the nose.
Lameness - occassionally.
Pale pigs.
Pneumonia.
Poor pigs - wasting and hairy.
Causes / Contributing factors
Contaminated or carrier incoming pigs.
Can be spread mechanically by equipment and visitors.
Water deprivation.
Low temperature and low humidity predisposes.
Stress / movement.
Nutritional changes.
Continual production.
High stocking densities.
Diagnosis
This is based on herd history, clinical signs, post-mortem examinations including slaughter house checks and culture of the organism in the laboratory. The lesions in the lung are very characteristic. Serology can be used to identify different serotypes but the interpretation can be difficult because of cross reactions between serotypes.

App must be differentiated from enzootic pneumonia, PRRS, flu, and Salmonella choleraesuis pneumonia.

Agalactia
This is a failure of milk let down, shortage of milk or no milk in an otherwise healthy animal.
Symptoms
Lactating Sows only
Inappetence may or not be present.
May have slight fever but usually no temperature.
Udder tissue is poorly developed and disappearing.
Oedema of the udder.
No milk.
Piglets starving due to no milk.
Piglets, Weaners & Growers
N/A
Causes / Contributing factors
Old age.
Excess body condition.
Water shortage.
Poor crate design.
Sequel to oedema or mastitis.
Diagnosis
This is based upon the appearance of the litter, piglets showing starvation, and the udder which lacks milk and is "drying up", or the udder may be hard with oedema or fluid.
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.
Agalactia - No Milk
Mastitis - Inflammation of the Mammary Glands

Anaemia
Anaemia is caused by the lack of sufficient, or diseased red cells in the blood. This is mainly a disease of the piglet because it is born with limited supplies of iron, a vital component in blood cells. If the piglet does not have access to iron in the first 2 - 3 weeks it's red cell capacity to absorb oxygen (anaemia) is impaired. Anaemic animals will be susceptible to infertility.
Symptoms
All pigs (mainly seen in piglets)
Pale skin.
Rapid breathing.
Jaundiced sometimes(Skin slight yellow appearance).
Mucous membranes of the eyes are pale.
Scour, sloppy diarrhoea.
Signs of haemorrhage.
Symptoms of specific disease.
Weakness.
May be increased stillbirths.
Causes / Contributing factors
Eperythrozoonosis (Epe)
Gastric ulcers
Haematoma
Internal bleeding
Loss of blood visible
Porcine enteropathy (PE)
Prolapse of the rectum
Torsion of the stomach and intestines
Faulty nutrition.
Lack of iron or copper.
Warfarin poisoning.
Diagnosis
This is based on the clinical signs and examination of blood samples by red cell counts, levels of haemoglobin and visual appearance of the red cells under the microscope.

Anthrax
This is an uncommon disease of pigs in most parts of the world. Care however should always be taken in handling diseased pigs or carcasses because anthrax is communicable to people. Effective vaccines are available in some countries for both pigs and people.
Symptoms
All Pigs
Acute illness.
Bloody faeces.
Haemorrhage from the nose.
Fever.
Respiratory distress.
Sudden death.
Swollen discoloured neck.
Blue skin.
Unusual in piglets
Causes / Contributing factors
Contaminated feed or water.
Diagnosis
Anthrax should be suspected if a sow is found dead and post-mortem examination shows copious blood tinged tissue fluid and large red lymph nodes under the skin of the neck and in the abdomen. The post-mortem examination should be discontinued immediately and veterinary help sought.

Arthritis, joint infections
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Porcilis Cobactan 2.5%
SS Pac®
Tiamutin
Arthritis is inflammation of one or more joints and is common in all sucking, growing pigs and sows. The causes are mainly bacteria. The bacteria include Actinobacillus suis, Haemophilus parasuis, E. coli, staphylococci and streptococci and Mycoplasma hyosynoviae. The commonest in sucking pigs is Streptococcus suis type 1 which causes chronic lesions sporadically in individual pigs but Streptococcus suis type 14, which is less common, also causes severe sudden outbreaks of very painful arthritis. Mycoplasma arthritis is rare in piglets. Erysipelas is uncommon due to the presence of maternal antibody but as this disappears from between 6 - 10 weeks of age disease may develop.
Symptoms
Sows
Lameness.
Stiffness.
Piglets
Sudden death.
Shivering.
Lameness.
Pigs show pain / discomfort.
Reluctance to rise.
Hairy appearance.
Swollen hock and elbow joints.
Stiffness or lameness
Weaners & Growers
Lameness, swollen joints.
Reluctance to stand.
May be signs of specific disease.
Diamond lesions on skin - raised skin patches.
Causes / Contributing factors
Trauma.
Knee necrosis *.
Faulty iron injections.
Poor floor surfaces.
Faulty teeth clipping, tail docking, worn equipment *.
Navel infection *.
Poor sow immunity.
Brucellosis (in countries where this exists).
Gl?ssers disease (Haemophilus parasuis). *
Erysipelas.*
Mycoplasma arthritis (Mycoplasma hyosynoviae infection). *
Leg weakness, Osteochondrosis (OCD) .*
Streptococcal infection .*
Trauma. *
(* common)
Diagnosis
In many cases the only clinical sign is lameness. If a problem exists it is necessary to identify the organisms or diseases

Atresia Ani - No Anus or No Rectum
The piglet is born with a blind end to its rectum, 5-10mm in length with no anus. It is not worth attempting surgical repair. Death invariably ensues. The incidence in mature herds is usually less than 0.5% but it can be much higher in newly established gilt herds. The condition is heritable but of low penetrance. Records may indicate that a certain boar is involved. The abdomens of affected piglets becomes enlarged. Some piglets may survive to weaning. Affected piglets should be destroyed.

Atrophic Rhinitis (AR)
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Aurofac / Aureomycin
Econor
Porcilis ART
Rhinitis is inflammation of the tissues inside the nose and in its mild form it is very common. During the process of infection the delicate turbinate bones in the nose become damaged and may shrink or become distorted (atrophy). This condition rarely causes clinical disease in the mature animal but if the breeding female has been infected early in life it could still show distortions of the face in adulthood.
There are two forms of the disease: mild and non-progressive where the infection or irritation occurs over a period of 2 to 3 weeks. However, the inflammation does not progress and the turbinate bones repair and return to normality.

The serious disease is progressive atrophic rhinitis (PAR) where toxin producing strains of the bacterium Pasteurella multocidia, present in the herd cause a continual and progressive inflammation and atrophy of the tissues and nose distortion. Progressive atrophic rhinitis is a serious condition both in sucking and growing pigs.

All herds will show some degree of non-progressive atrophic rhinitis.

Symptoms
Sows
None clinically. They may carry the pasteurella organism.
Possible distortion of the face.
Piglets, Weaners & Growers
Early signs can be seen in sucking pigs; sneezing, snuffling and a nasal discharge.
Sneezing often blood stained. Haemorrhage.
Runny eyes, tear staining. Conjunctivitis.
Twisting, shortening and wrinkling of the nose and or upper jaw.
Reduced daily gain and variable growth.
Poor body condition.
Reduced feed efficiency.
Difficulty eating.
Inappetence.
Increase in respiratory diseases.
Pneumonia.
Causes / Contributing factors
More common in young herds particularly those containing large numbers of gilts.
Large permanently populated farrowing houses.
Multi suckling increases the spread of infection.
Poor ventilation, low humidity.
Dusty atmospheres predispose.
Toxic gases predispose.
The presence of diseases such as EP, PRRS, Hps and Aujeszky's disease.
Milder rhinitis, in the absence of toxigenic pasteurella (non progressive disease) in which the turbinate bones heal and regenerate, may be caused by the following.
Air containing high bacterial counts.
Aujeszky's disease (pseudorabies).
Bordetella bronchiseptica infection.
Chronic respiratory disease.
Dust.
Gl?ssers disease.
High levels of ammonia.
Porcine cytomegalovirus infection (inclusion body rhinitis).
Porcine reproductive and respiratory syndrome (PRRS).
Poor humid conditions.
Diagnosis
This is based on clinical signs. However do not assume if sneezing alone is occurring in young pigs that it will necessarily lead to progressive atrophic rhinitis. Individual piglets may also develop distortion of the nose from trauma or some cause other than PAR. The disease is easily identified by post-mortem examinations of the nose and culture of the organism from nasal swabs.

Aujeszky's disease AD,
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Porcilis Begonia
PRV/Marker Gold-MaxiVac FLU
PRV/Marker Gold®
This is an important disease of pigs caused by a herpes virus. The virus can remain hidden in nerves of the pig in a carrier state for long periods of time and then be reactivated. Once introduced into a herd the virus usually remains there and it can continually affect reproductive performance at varying levels. The virus can survive for up to three weeks outside the pig. Acute outbreaks of disease occur when virulent strains of the virus first infect an unvaccinated susceptible herd. The virus crosses the uterus and placenta and infects the foetuses.
The pig is the main host. Dogs and cattle may become infected, show nervous signs and die.

Symptoms
Sows
Coughing.
Fever
Nervous signs
Reproductive failure.
Abortions.
Mummified piglets.
Stillbirths.
Birth weak litters.
Piglets
Nervous signs.
Incoordination.
Sneezing.
Coughing.
High mortality.
Low / poor viable piglets.
Weaners & Growers
Fever.
Sneezing.
Coughing.
Pneumonia.
Nervous signs including incoordination, fits and meningitis.
Some strains of the virus can cause severe respiratory disease and others severe rhinitis.
Usually low mortality.
All Other Species
Nervous signs.
Death.
Causes / Contributing factors
Movement of carrier pigs.
Virus airborne - at least 3km (2 miles).
Infection from feral (wild) pigs.
The role of mechanical spread by birds is questionable.
Contaminated carcasses may spread infection.
Mechanically on people.
Contaminated vehicles.
Through infected semen via AI or a carrier boar.
From infected slurry.
Within herds it may be spread by nose to nose contact, or by aerosol droplets.
Periods of stress may activate disease.
Continual production systems perpetuate disease.
Additionally:
The presence of other infections such as PRRS and leptospira may increase the severity of disease.
Diagnosis
When a susceptible breeding herd first breaks down with this disease the clinical signs described above strongly suggest aujeszky's disease and are almost diagnostic. Laboratory tests are required to confirm the diagnosis.

Back Muscle Necrosis
Back muscle necrosis is part of the porcine stress syndrome and in affected pigs degenerative changes take place in the back muscles along each side of the spine. It is usually seen in the young growing gilt although occasionally it occurs in the adult female. The disease is relatively uncommon.
Symptoms
Growing Pigs and Gilts/Sows
The symptoms are sudden in onset after exercise.
Severe pain in the lumber muscles with obvious swellings.
Incoordination.
Death (necrosis) of muscle fibres with haemorrhages into the tissues themselves.
Lameness - reluctance to stand.
Adopt a dog sitting position.
The temperature is usually normal but may be elevated.
Discoloration of the skin over the affected area.
Piglets & Weaners
N/A
Causes / Contributing factors
Sudden movement e.g. from confinement to outdoor accommodation.
Presence of the halothane gene.
Diagnosis
Based on the clinical signs. The pig can be made to stand with difficulty but there is no evidence of fractures. Examine the lumber muscles carefully, they will be swollen and painful on pressure. History includes sudden lameness associated with movement and acute pain.

Biotin Deficiency
Biotin is present in most nutrient sources and deficiency is unlikely. The role of biotin in nutrition and the changes that result when it is deficient are not clear. Reports and field studies however have highlighted the following associations:
Symptoms
Piglets
N/A
Sows, Weaners & Growers

Lameness throughout the herd or a group of sows.
Laminitis.
Hooves will be soft over the walls.
Haemorrhage over the solar surfaces of the feet.
Dark transverse cracks in hooves.
Excessive hair loss.
Extended weaning to mating intervals - Anoestrus (sows only).
Poor litter size.
Causes / Contributing factors
Biotin deficiency in the diet.
Possible cause trauma from poor floor surfaces.
Diagnosis
Based on the clinical picture and the fact that the herd or a group of animals will be affected. Chronic lesions of swine vesicular disease could be confused with biotin deficiency.

Blue Eye Disease
This is a viral disease that causes nervous symptoms, reproductive failure and opacity or blueing of the cornea. It is seen mainly in Mexico but has also been reported in other countries. It is not seen in Europe.
Symptoms
All Pigs
Inappetence.
Corneal opacity - conjunctivitis.
Nervous signs - fits and convulsions.
Dog sitting position.
Fever.
Increased returns.
Increased weaning to mating intervals.
Stillbirths
Mummified piglets.
High mortality in piglets
Swollen testicles
Loss of libido
Causes / contributing factors
Carrier pigs.
Nasal spread.
Mechanical spread.
Diagnosis
Clinical symptoms. HI tests. Virus isolation.

Border Disease (BD)
There are two viruses, which are in the same group of pestiviruses as the virus of swine fever (hog cholera) but which primarily infect cattle and sheep respectively. They can get into pig breeding herds and cause reproductive problems.
The disease is not a common cause of infertility in the sow and would be considered low on the list of possibilities from a diagnostic point of view.

Symptoms
Piglets, Weaners & Growers
N/A
Sows

Poor conception rates.
A few abortions.
Foetal death.
Mummification.
Small litters.
Low birth weights.
Causes / Contributing factors
Exposure of pigs to cattle or sheep faeces.
Feeding of un-pasteurised cow's milk.
Contaminated live-attenuated virus vaccines.
Diagnosis
Laboratory tests. Serology and isolation.

Bordetellosis (Bordetella bronchiseptica)
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DRAXXIN®
Bordetella bronchiseptica is a bacterium found in most if not all pig populations. Some strains cause a mild and non progressive rhinitis that heals spontaneously. The disease is clinically and economically of no consequence. However if toxigenic pasteurella are present in the herd then a combination of the two organisms can produce severe progressive rhinitis (PAR).
Bordetella bronchiseptica can also be a secondary opportunist invader in pneumonia.

Symptoms
Piglets & Growers
Coughing.
Sneezing.
Nasal discharge.
Sows & Weaners
N/A
Causes / Contributing factors
High levels of the bacteria may predominate in poor environments.
Recirculation of air in nurseries allows a build up of organisms.
Continual use of housing.
Diagnosis
This is based on cultural and laboratory examinations.

Treatment
None needed unless levels are high
In-feed medicate with trimethoprim sulpha or chlortetracycline
Inject weaners with oxytetracycline lang acting at weaning

Botulism
Bacteria called clostridia produce toxins (poisons). Clostridium botulinum, which produces this disease grows in decaying vegetable matter producing the toxin which is then eaten. However botulism is rare in pigs. It should be considered as a food poisoning. See also clostridial diseases for additional information.
Symptoms
These are seen 4-48 hours or so after the toxin has been eaten.

All Pigs

Muscle paralysis.
Weakness of limbs leading to complete paralysis.
Blindness.
Excessive salivation.
Loss of bladder function.
Breathing difficulties.
Unusual in piglets.
Causes / Contributing factors
Decaying feed.
Contaminated water or feed.
Diagnosis
This is based on the symptoms, evidence of decomposing food and demonstration of the presence of toxin by a laboratory .

Bovine (Porcine) Spongiform Encephalopathy (BSE)
No naturally occurring cases of this have been identified in the pig. It has been produced experimentally by direct inoculation of infected bovine brain tissue into the brain. Feeding infected brain tissue however has not resulted in disease. The feeding of meat and bone meal to pigs is now banned in the UK but during its use no cases have been identified.

Bovine Viral Diarrhoea Virus (BVD)
There are two viruses, which are in the same group of pestiviruses as the virus of swine fever (hog cholera) but which primarily infect cattle and sheep respectively. They can get into pig breeding herds and cause reproductive problems.
The disease is not a common cause of infertility in the sow and would be considered low on the list of possibilities from a diagnostic point of view.

Symptoms
Piglets, Weaners & Growers
N/A
Sows

Poor conception rates.
A few abortions.
Foetal death.
Mummification.
Small litters.
Low birth weights.
Causes / Contributing factors
Exposure of pigs to cattle or sheep faeces.
Feeding of un-pasteurised cow's milk.
Contaminated live-attenuated virus vaccines.
Diagnosis
Laboratory tests. Serology and isolation.

Brucellosis
This disease is caused by the bacterium Brucella suis, which is one of the six different species of brucella. Brucella suis does not exist in the UK, Ireland and in some other EU countries, Canada and most states of the USA but is widespread through most of the rest of the pig rearing world. It is an important disease not least because some strains of it can be transmitted to people where it can cause serious illness. A carrier state persists for long periods of time.
It can be spread by venereal infection and the boar is a major source either by direct contact at mating or via artificial insemination. The organism can survive outside the pig for long periods of time particularly at or near freezing temperatures. The hare in Northern Europe can also be infected where it is considered a natural host. It can be an important source of infection to the pig.

When a female becomes infected, the organism establishes itself in the placenta, causing inflammation and ultimately abortion. B. suis infects the testicles and accessory reproductive glands of the boar, and can be excreted via semen.

Symptoms
Sows
Bacteraemia (bacteria in the blood).
Infertility.
Abnormal oestrus
Abortions at any time.
Vulval discharges with pus or occasionally blood.
Delayed returns.
Lameness
Swollen/ painful testicles (boar only).
Piglets
Paralysis of hind legs.
Weaners & Growers
Swollen testicles.
Lameness
Causes / Contributing factors
Spread by venereal infection.
The boar is a major source either by direct contact at mating or via artificial insemination.
Pigs can also be infected via the conjunctiva, through the nose or by mouth.
The hare in Northern Europe can also be infected and is considered a natural host.
Carrier sows.
Diagnosis
This can be readily carried out by isolation of the organism. Serology is used to detect carrier sows but cross reactions can occur quite extensively due to another organism called Yersinia enterocolitica. If the serum agglutination test (SAT) is used results of 31 international units (iu) or more are considered positive. The complement fixation test (CFT) is often used in conjunction with the SAT for export testing purposes.

Bursitis
Bursitis is a common condition that arises from constant pressure and trauma to the skin overlying any bony prominence. The membrane or periosteum covering the bone reacts by creating more bone, a swelling develops and the skin becomes thicker until there is a prominent soft lump. Bursitis may cause the skin to become broken and secondary infection can develop. Mycoplasma can also infect the fluid in the swelling.
Under normal circumstances, if there is no secondary infection, the condition is not commercially important but if breeding stock is being produced then the system needs to be adjusted or there will be a drop in selection rates.

Symptoms
All Pigs
Swellings develop over the lateral sides of the hocks and elbows and over the points of the hocks.
Occasional lameness may be seen.
Infection may occur.
If skin is broken and secondary infection occurs abscesses develop.
Ulceration of the skin.
Causes / Contributing factors
Poor floor surfaces.
Lack of bedding.
High stocking densities on slats.
Bad slats in confinement.
Diagnosis
Visual examination.

Bush Foot, Foot Rot
Bush foot results from infection of the claw which becomes swollen and painful around the coronary band. It arises through penetration of the sole of the foot, cracks at the sole-hoof junction, or splitting of the hoof itself. It usually occurs in one foot only and is more commonly seen in the hind feet especially the outer claws, which are the larger ones carrying proportionately more weight. Infection sometimes penetrates the soft tissues between the claws and this is referred to as foot rot. Foot rot involves both superficial and deep infection of the soft tissues between the claws often caused by fusiform bacteria. The claw becomes enlarged and inflamed. Invariably, unless foot rot has developed, only one claw is involved.
Symptoms
All Pigs
Lameness.
Painful swollen claw.
Cracks at the sole-hoof junction, or splitting of the hoof itself.
As the infection progresses inside the hoof, the claw becomes enlarged and infection and inflammation of the joint often develops.
In most cases a swelling is visible around the coronary band which may form an abscess and burst to the surface.
Causes / Contributing factors
It arises through penetration of the sole of the foot.
Cracks at the sole-hoof junction, or splitting of the hoof itself predispose.
Poor floor surfaces.
Poor concrete surfaces with sharp aggregate cause damage.
Biotin deficiency predisposes.
Diagnosis
This is based on the clinical signs. Bush foot has to be differentiated from other forms of trauma and infection including erysipelas, gl?ssers disease, leg weakness or osteochondrosis (OCD) and mycoplasma arthritis.

Campylobacter
Campylobacters are small curved rods which are present sometimes in large numbers in the small intestines and large intestines of most mammals including pigs. There are several species in pigs. Whether or not they cause diarrhoea in naturally reared piglets is debatable because it seems likely that the antibodies in sows milk would prevent this. However oral infections to newborn colostrum-deprived piglets may result in mild diarrhoea with mucus and sometimes blood in it. Spiral helicobacter species, related to campylobacters, may be found adhering to the stomach wall of pigs and in and around gastric ulcers. However, many other factors contribute to stomach ulcers in pigs and it seems unlikely that helicobacters are a primary cause.
Symptoms
Piglets
Mild, sometimes creamy, diarrhoea in piglets lasting several days if untreated.
Dehydration.
Sometimes diarrhoea with blood and mucous.
Loss body condition.
Sows, Weaners & Growers
N/A
Causes / Contributing factors
Dirty pens.
Poor hygiene in farrowing pens.
Poor wet floor surfaces.
Continually used houses without cleaning and disinfection.
Secondary infection to other enteric organisms.
Diagnosis
This is difficult because campylobacters are so common in faeces along with other organisms which can cause diarrhoea such as, E.coli, rotaviruses, coccidia and crytosporidia and it is impossible to decide whether their isolation is significant in any particular outbreak.

Clostridial Diseases
Related Products:
Gletvax 6
Clostridia are large gram-positive spore-bearing bacteria that are present in the large intestine of all pigs. There are several species. They multiply rapidly and produce toxins that rapidly kill the host. Such diseases can be a major problem in outdoor breeding pigs (C. novyi). The organisms may enter the body through damage to the skin and underlying tissues and muscles. Bacterial spores also get carried from their normal habitat, the gut, to the liver where they may lie latent and inactive for long periods. The course of the disease is extremely short and often the only sign is a dead pig.
The most common disease in sows is associated with C. novyi which causes sudden death. Whenever total sow mortality rises above 4%, this disease should be considered.

The species, C. perfringens, types A, B or C, can under certain conditions produce a severe diarrhoea with very high mortality in piglets. Type C is by far the most important and if it gets into the small intestine and becomes established before colostrum is taken in, disease can result. Piglets are normally infected under 7 days of age and more typically within the first 24 to 72 hours of life.

The disease caused by C. perfringens type A tends to be milder, less dramatic and more prolonged but it can look similar to that caused by type C.

Clostridial infections are relatively uncommon in growers, finishers and the sow during lactation.

Symptoms
Sows
Sudden death.
Gangrene, characterised by painful and discoloured swellings.
Fluid and gas are often present in the tissues.
Piglets
Rotten smelling watery diarrhoea often blood coloured with mucous.
Diarrhoea 0-5 days of age.
Diarrhoea 6-21 days of age
The lining of the small intestine sloughs off (necrosis) and may be observed in the scour.
Many piglets die.
Bubble of gas in the small intestines.
Weaners & Growers
Sudden death in well grown pigs.
Haemorrhage - faeces.
Diarrhoea.
Painful and discoloured swellings over muscle masses.
Gangrene.
Causes / Contributing factors
High numbers of bacteria in the environment.
Unknown factors.
Trauma to muscles.
Immuno suppressive diseases e.g. PRRS, fungal poisoning.
Damage to the skin allowing bacteria to enter.
Diagnosis
In acute cases diagnosis is by the clinical signs and post-mortem lesions, which are diagnostic. It is necessary to submit preferably a live or very recently dead pig to the laboratory (within 3 to 4 hours) because the causal organisms multiply after death and cause rapid post-mortem changes. If the abdomen of a dead pig is cut open the middle portion of the small intestine is often claret wine coloured. A characteristic feature is the very rapid post-mortem change particularly in the liver, which is full of gas and turns a chocolate colour. Confirmation of the diagnosis must be carried out in a laboratory by a fluorescent antibody test to identify the bacterium.

Anthrax should also be considered as a possibility.

Coccidiosis (Coccidia)
Coccidiosis is caused by small parasites that multiply inside the host cells, mainly in the intestinal tract. There are three types, Eimeria, Isospora and Cryptosporidia.
Disease is common and widespread in sucking piglets but is seen occasionally in growing and finishing pigs and boars when they are moved or housed into continually populated and infected pens.

Coccidiosis should be suspected if there is a diarrhoea problem in sucking pigs from 7-21 days of age that does not respond particularly well to antibiotics.

Symptoms
Sows
None
Sows are carriers
Piglets
Diarrhoea is the main clinical sign in early stages.
In later stages the faeces vary in consistency and colour from yellow to grey green, or bloody according to the severity of the condition.
Dehydration is common.
Wasting.
Weaners & Growers
Poor growth.
Sloppy diarrhoea may be seen.
Faeces / diarrhoea may occasionally be tinged with blood.
Causes / Contributing factors
Dirty pens.
Poor hygiene in farrowing pens.
Poor wet floor surfaces.
Creep feeding on the floor.
Flies.
Dried faeces behind the sow in lactation.
Continually used houses without cleaning and disinfection.
Diagnosis
Faeces samples for laboratory examination should be taken from semi-recovered pigs rather than pigs with scour. Diagnosis is best made by submitting a live pig to the laboratory for histological examination of the intestinal wall. Isospora suis is the most pathogenic of the three types of coccidia.

Colitis
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Tiamutin
"Colitis" means inflammation of the large bowel. It is common in some countries in growing pigs and is characterised by diarrhoea. It is uncommon in home milled cereal based diets.
Affected pigs are usually 6 to 14 weeks of age and in any one group, up to 50% may be affected. It is not seen in adult or sucking pigs. Colitis may be seen in individual sows. A number of organisms have been implicated but Brachyspira pilosicoli, an organism distinct from the one that causes swine dysentery, is thought to be important.

Symptoms
Sows & Piglets
N/A
Weaners & Growers
Usually appear in rapidly growing pigs from 6 to 14 weeks old fed ad lib on high density diets.
The early signs:
Sloppy "cow pat" type faeces, with no blood and little if any mucus.
Pigs appearing otherwise normal but lose bloom and growth.
As the disease and its severity progress:
Watery diarrhoea.
Dehydration.
Loss of condition.
Poor growth.
During the affected period:
Daily gain and food conversion can be severely affected, with feed conversion worsening by up to 0.2.
Mortality is low but morbidity can be high, ranging from 5 to 50%.
Causes / Contributing factors
Dietary factors. Disease is experienced using all types of diets but particularly those that have been pelleted rather than fed as a meal. It is thought that the pelleting process may have an effect on fats in the diet and thereby initiate digestive disturbances in the large bowel.
It is more common with diets high in energy and protein (14.5MJ DE/kg 21% protein).
Certain components in the feed may also be implicated, such as high levels of wheat.
It is common when fat sprayed diets are fed.
Continual production predisposes.
Diagnosis
This is based on clinical signs and the elimination of other causes of diarrhoea, in particular swine dysentery. Faecal examinations in the laboratory are necessary to assist with diagnosis together with post-mortem examinations and laboratory tests on a typical untreated pig. It is possible that porcine enteropathy may be involved.

Congenital Tremor (CT) - Shaking Piglets
This is a sporadic disease seen in newborn pigs. Usually more than one pig is affected in a litter. If the tremors are too great for the piglets to find a teat and suckle then mortality maybe high. Mortality in an affected litter or in a herd outbreak could increase above the norm by 3-10%. The condition decreases as the affected piglets grow.
It would be unusual to find a pig farm that sometime in its history had not experienced one or more litters of trembling piglets. There are 4 possible group causes. The causal virus in group 2, which is by far the commonest cause, is widespread among most if not all pig populations, yet little disease is seen in most herds, presumably because an immunity is established in the sow herd. In new gilt herds however, there can be major outbreaks involving up to 80% of all litters during the first parity. This is an unquantifiable risk in any new gilt herd.

Symptoms
Sows, Weaners & Growers
N/A
Piglets
Muscle tremor, only seen when piglets are walking around and not when they are asleep.
Nervous symptoms i.e. shaking of the body.
Incoordination.
Often dog sitting.
Increased mortality in piglets.
Causes / Contributing factors
The causes of the condition are classified into 4 groups based on brain histology.
Associated with a classical swine fever.
Caused by an unknown virus, possibly circovirus type 2. Most of the problems in the field are found in this group.
Associated with either hereditary disorders seen in the Landrace or Saddleback breeds or with organophosphorus poisoning.
Includes aujeszky's disease and Japanese encephalomyelitis virus.
Diagnosis
This is based on clinical evidence although histological examinations in the laboratory can help to differentiate the groups.

Cryptosporidiosis
Cryptosporidia are parasites similar to coccidia that can also cause diarrhoea but at a slightly older age of 8 to 21 days. They can infect people and are also found in other species such as rats and mice.
Symptoms
Sows & Growers
N/A
Piglets & Weaner
Watery diarrhoea 8 - 21 days of age.
Poor body condition - wasting.
Dehydration.
Inappetence.
Causes / Contributing factors
Rats and mice.
The main water supplies are sometimes infected.
Poor hygiene.
Dirty pens.
Diagnosis
This is made by examining faeces in the laboratory.

Cystic Ovaries
This is a not uncommon condition particularly in old sows. Large cysts develop in the ovaries which often, but not always produce high levels of oestrogen.
Symptoms
Piglets, Weaners & Growers
N/A
Sows

Abnormal heat.
Not accept the boar at mating.
Continually on heat.
Infertility.
Repeat matings.
Pigs show pain / discomfort.
May grind teeth.
Causes / contributing factors
Age.
Mycotoxins.
Breeding.
Hormonal malfunctions.
Mouldy bedding or food.
Badly stored grains.
Poor feed bin hygiene.
Diagnosis
This is usually made on clinical grounds and normally only involves individual animals. Carry out a post mortem examination of the ovaries.

Cystitis and Pyelonephritis
Cystitis is inflammation of the bladder and nephritis is inflammation of the kidney. The bacteria causing cystitis are usually Actinobaculum suis (originally called Corynebacterium suis or Eubacterium suis) or sometimes E. coli. It is impossible to eradicate these organisms. They are present in every herd.
This disease is an important cause of mortality in all ages of dry sows. Occasionally it may be seen in gilts, even maiden gilts, although this is uncommon unless there has been gross and prolonged faecal contamination of the vulva. In badly affected herds sow mortality can exceed 12% per annum.

Sows die rapidly or respond poorly to treatment remaining chronically diseased. Disease can be so acute that death is the only sign. It is more common in the first 21 days post mating because the urine of the sow becomes alkaline and both A.suis and E.coli will survive and multiply in alkaline urine.

Reproductive failure is not associated with this disease specifically unless the sow is ill and as a consequence either dies or aborts. High mortality affects overall sow mortality and therefore pregnancy survival.

Symptoms
Piglets
None
Weaners & Growers
Uncommon
Sows
Appear ill.
Not eating.
Thin sows.
Red rimmed eyes - membranes red.
The area around the vulva is wet and soiled with evidence of blood and pus in the urine.
Death - high mortality
Abortion
Chalky mineral deposits.
Pigs show pain / discomfort.
May grind teeth.
When cystitis occurs alone:
The disease may be prolonged and not fatal.
Appetite and the general condition of the sow can be normal.
Pus in the urine or a slight discharge clinging to the vulva may be seen.
This should be distinguished from inflammation of the womb or vagina.
Causes / Contributing factors
Low water intake.
Infrequent urination.
Faulty drinkers.
Badly drained boar and sow pens increase the risk of infection
The disease is more common in herds that have high numbers of old sows.
Squeezing the prepucial sac at mating increases the bacterial load transmitted to the vagina, (which may also result in increased returns to service).
Sows that are too big for the stalls often adopt a dog sitting position with the vulva becoming heavily contaminated, allowing excessive bacterial multiplication.
Contamination of the vulva with faeces particularly from weaning to 21 days post mating. This occurs in stalls when solid back boards drop down to the ground level.
Stress at farrowing can occasionally activate disease.
Diagnosis
By post-mortem examination. Examinations should be carried out on all sows that have died without obvious cause.
In the live animal, diagnosis is based upon clinical signs and evidence of blood and pus in the urine. Urine can be tested for the presence of blood, protein and the pH (acidity or alkalinity) by using paper strip tests. Urine can be collected in clean receptacles, especially if sows are made to stand up 2-3 hours after feeding when they tend to urinate. Affected animals show evidence of blood and protein in the urine and a pH of 7 or more. (Normal urine is slightly acid, that is, less than the pH7.) Sows showing a pH of 8 or more may die in their next pregnancy.

Dipped Shoulder (Humpy Back, Kinky Back, Kyphosis)
This is a not uncommon condition seen in both gilts and boars up to six months of age. Mild forms can sometimes be seen in individual mature boars indifferent herds. It has been described in pigs as young as 3 - 4 weeks of age where there may be a genetic predisposition.
As the animal approaches maturity its body changes shape and it starts to give the appearance of two different pigs joined together at the middle. The back above and behind the ribs becomes increasingly dipped and the back above the middle and rear abdomen becomes humped. The condition is abnormal and unsightly but, in the absence of other diseases, the pigs remain healthy and normal in every other way.

In some cases it is a developmental condition and probably environmental although what factors in the environment cause it are not known. The affected farms may have a significant proportion of their growing breeding stock with it but closely related breeding stock on other farms all develop normally. In herds where the condition is common there may be a boar conformation involvement. Record and observe progeny from suspect boars. It has also been associated with excessive riding of boars and back damage. Early onset of puberty has been implicated in boars.

In severe cases partial or complete paralysis may be seen. Such animals should be destroyed. Mortality is usually low.

E. coli - Scour (Diarrhoea)
Of all the diseases in the sucking piglet, diarrhoea is the most common and the most important. In some outbreaks it is responsible for high morbidity and mortality. In a well run herd there should be less than 3% of litters at any one time requiring treatment and piglet mortality from diarrhoea should be less than 0.5%. In severe outbreaks mortality can rise to over 7% and in individual untreated litters up to 100%.
E. coli diarrhoea, clostridial diarrhoea, coccidiosis, TGE and PED all cause diarrhoea in the piglet. E. coli is the most important.

At birth the intestinal tract is micro-biologically sterile and it has little immunity to disease producing organisms. Organisms begin to colonise the tract quickly after birth, among them potentially pathogenic strains of E. coli and Clostridium perfringens. Immunity is initially provided by the high levels of antibodies in colostrum (IgG, IgM, IgA). After the colostral antibodies have been absorbed into the blood stream, the immunity is maintained by the antibody (IgA) which is present in milk. IgA is absorbed into the mucous lining of the intestines. It is essential that the newborn piglet drinks sufficient colostrum soon after birth to prevent potentially pathogenic organisms multiplying against the intestinal wall and causing diarrhoea. It is also essential that the piglet continues to drink milk regularly after the colostrum has gone so that its intestines continue to be lined by protective antibodies.

The antibodies acquired passively from the colostrum and milk are finite and can be overwhelmed by large doses of bacteria present in the environment. The higher the number of organisms taken in, the greater the risk of disease. Environmental stress such as chilling also plays a role because it lowers the piglets resistance. There is thus a delicate balance between the antibody level on the one hand and the weight of infection and stress on the other.

Scour in the piglet can occur at any age during sucking but there are often two peak periods, before 5 days and between 7 and 14 days.

Sudden outbreaks of scour involving large numbers of litters with acute diarrhoea and high mortality suggest TGE, epidemic diarrhoea or PRRS. Rotavirus diarrhoea appears in waves in individual litters or groups of litters and normally in the second half of lactation. Coccidiosis is usually involved in diarrhoea from 7 to 14 days of age. At less than 5 days of age the most common cause is E. coli with acute diarrhoea particularly in gilts' litters. Clostridial infections also occur at this age.

At weaning the loss of sow's milk and secretory IgA allows the E. coli to attach to the villi of the small intestines, the toxins produced then cause acute diarrhoea, usually within five days of weaning.

Symptoms (E.coli)
Sows / Growers
Uncommon.
Usually occur with viral infection.
Piglets
In acute disease:

The only sign may be a previously good pig found dead.
Huddle together shivering or lie in a corner.
The skin around the rectum and tail is wet.
Watery to salad cream consistency scour - distinctive smell.
Vomiting.
As the diarrhoea progresses:
Dehydrated.
Sunken eyes.
Leathery skin.
The scour often sticks to the skin of other piglets giving them an orange to white colour.
Prior to death piglets may be found on their sides paddling and frothing at the mouth.
In sub-acute disease:
Signs are similar but the effects on the piglet are less dramatic, more prolonged and mortality tends to be lower.
This type of scour is often seen between 7 to 14 days of age.
Watery to salad cream consistency diarrhoea, often white to yellow in colour.
Weaners
The first signs are often slight loss of condition, dehydration and a watery diarrhoea.
In some cases blood or black tarry faeces may be seen or they may be like paste with a wide range of colour: grey, white, yellow and green. The colour is not significant.
Poor pigs - wasting, hairy.
Sloppy faeces and often dirty wet pens.
Sunken eyes.
Dehydration results in rapid loss of weight.
Pigs may be found dead with sunken eyes and slight blueing of the extremities.
Good pigs may also be just found dead with no external symptoms.
Occasional vomiting.
Causes / Contributing factors
Sows & Piglets
Poor pen floors.
Poor pen hygiene associated with bad drainage.
Poor hygiene procedures, between pens.
Environmental contamination from one pen to another i.e. boots, brushes, shovels clothing etc.
Continual use of pens.
Moisture, warmth, waste food and faeces are ideal for bacterial multiplication.
Draughts.
Routine use of milk replacers, particularly if they are allowed to get stale or contaminated, may increase the incidence.
Scour is more common in large litters. This can be due to:
- Insufficient colostrum.
- Poor teat access.
- Poor crate design.
- Agalactia in the sow.
Weaners & Growers

Pre-weaning

Are the weaning problems mainly in gilt litters? If so consider E. coli vaccination in gilts:

- Creep feeding. Consider the type, frequency and age of introduction.
- Stop creep feeding before weaning and assess the effects.

At weaning consider:

- Stress.
- Stocking density - group sizes.
- House temperatures and temperature fluctuations.
- Poor house hygiene.
- Continually populated houses.
- Water shortage.
- Feed type: Meal or pellets, wet or dry.
- Feeding practices.
- Quality of nutrition.
After weaning consider the effects of:
- Air flow - chilling.
- Temperature fluctuations.
- High ventilation and humidity.
- Creep feed management.
- Assess the response to different creep diets.
- Consider other diseases present.
- Age and weight at weaning.
- Floor surfaces - provide comfort boards.
- Asses rate and evenness of growth.

A diarrhoea problem in growing pigs is likely to be associated with one or more of the following diseases (Most common *):
Classical swine fever (in those countries where it is still endemic).
Coliform infections. *
Colitis (non specific). *
Parasites.
Porcine epidemic diarrhoea (PED). *
Porcine enteropathy including PIA, NE and RI. *
Rotavirus infection.
Salmonellosis. *
Spirochaetal diarrhoea.
Swine dysentery. *
TGE (rare in Europe now but still common in some other countries).
Diagnosis
This is based on the clinical examination, the response to treatment (viral diseases do not respond to treatment) and laboratory examination of the scour.

Submit a rectal swab and faecal sample of a recently dead pig or a live pig to the laboratory for cultural examinations and antibiotic sensitivity tests.

A simple test to differentiate between virus causes and E. coli diarrhoea involves the use of litmus paper to determine whether the scour has an alkaline or an acid consistency. Soak the paper in the scour, E. coli diarrhoea is alkaline (blue colour change) whereas viral infections are acid (red colour change).

It is not possible to eliminate organisms such as rotavirus, E. coli and coccidiosis from the herd and most if not all pigs will be infected with them. Herds can be maintained free of TGE, PED and PRRS. All herds carry clostridia but other factors are required to cause disease.

Eclampsia
This is an uncommon condition caused by low levels of calcium in the blood stream. It may occur at any stage but is most likely within seven days either side of farrowing. Occasionally seen pre farrowing but normally during lactation.
Symptoms
Sows
Sudden in onset.
The sow becomes distressed.
Panting heavily.
Trembles and shakes.
Fits and convulsions.
Reactive to external stimuli, both touch and sound.
Death often results unless there is prompt treatment.
Piglets, Weaners & Growers
N/A
Causes / Contributing factors
Loss of calcium in the colostrum.
Shortage of calcium in the diet.
Failure of uptake of sufficient calcium.
Heavy milking sows.
Diagnosis
This is based on the clinical signs but it can be confused with the porcine stress syndrome (PSS).

Electrocution
Electrocution of sows and litters occurs sometimes in farrowing houses where electricity is used for heating. Farrowing crates are often connected together throughout the house by various pieces of metal and because of this several animals maybe killed - including piglets.
Symptoms
All Pigs
A variable number of animals are suddenly found dead in one house.
The sows' skin will often be burned or inflamed where it contacted the metal.
Blood and froth are commonly seen around the nostrils and mouth.
Bones may be fractured.
Paralysis in surviving pigs.
Causes
Faulty electricity lines and switches. Trip out switches should be provided in the electricity circuits.
A common cause however is damage by sows that escape from farrowing crates.
Diagnosis
Post-mortem examinations are necessary to differentiate electrocution from other causes of sudden death. Veterinary certification is usually required for insurance claims.

Note - If you go into your farrowing house and find large numbers of dead animals STOP and THINK ELECTROCUTION or TOXIC GASES, and DON'T ENTER!

Encephalomyocarditis
The main reservoir host for the EMC virus is the rat although mice may also spread it. It infects and causes disease in a wide range of vertebrate animals but pigs appear to be the most susceptible of farm animal species. The virus is world-wide but differs in pathogenicity and virulence in different countries and regions. In most countries of Europe, particularly those in the EU, it tends to be relatively mild or non-pathogenic and disease in pigs is rarely diagnosed.
In Australia the strains appear to be much more virulent for pigs than those in New Zealand. Virulent strains in Florida, the Caribbean and probably Central America damage the heart and cause death whereas those in the Mid West of the US tend to cause reproductive problems.

Clinical disease in pigs tends to occur when rat numbers increase to plague levels. Pigs can be infected from rats or from rat-contaminated feed or water. It does not seem to spread very readily between pigs.

In affected herds there are usually no clinical signs in weaned and growing pigs.

Symptoms
Sows
In gilts and sows first signs are often :

A few abortions near the end of pregnancy.
Then over a period of about 3 months
The numbers of mummified foetuses and stillbirths increase and pre-weaning mortality rises.
The farrowing rate worsens.
Affected females may show signs of fever and lack of appetite.
Embryo death
In affected herds there are usually no clinical signs in weaned and growing pigs.
Piglets,
Poor viable.
Usually none.
Weaners & Growers
N/A
Causes / Contributing factors
Pigs can be infected from rats or from rat-contaminated feed, water or bedding.
Disease does not seem to spread very readily between pigs.
Incoming breeding stock with pathogenic strain.
Diagnosis
To make a definitive diagnosis the virus has to be isolated and identified or rising antibodies demonstrated in blood samples taken two weeks apart.

EMC could be confused with AD, parvovirus infection and PRRS although there are distinguishing signs between these four. EMCV would be the last on the list of diagnostic priorities in Europe but to a lesser extent in the Mid West USA. Abortion or illness in sows or piglets due to PPV is uncommon and mummified pigs can be examined for the evidence of this infection.

Further Reading

Endometritis
Since 1985 there has been a gradual reduction in farrowing rates in many herds associated with increased repeats in sows. A survey carried out at that time indicated that up to 24% of herds may have had previously unrecognised problems with this disease.
A discharge from the vulva post-service does not automatically mean there has been a pregnancy failure, but it will in most cases indicate infection. Discharges can arise from the rectum, the vulva, the vagina, the cervix and the uterus. Discharges can also arise from infection of the kidneys (pyelonephritis) or the bladder (cystitis) with pus being passed in the urine. It is important to record the time when discharges are first seen, their colour and composition and effects on the sow.

Vulval discharges are common within 3-4 days of farrowing when a thick viscous material may be excreted. If the sow is healthy, the udder is normal and there is no mastitis, ignore it.

A heavy smelling bloody discharge may indicate a retained piglet or afterbirth.

Discharges are important between 14-21 days post-service. The lips of the vulva of each sow should be parted daily and any tackiness or small discharge noted. The sow should be marked and if she repeats a problem may be developing. Discharging sows may be pregnant and always pregnancy test before culling.

Discharges in healthy sows are normal up to 5 days post farrowing at mating and 3 - 5 days post mating - only if slight.

Symptoms
Piglets, Weaners & Growers
N/A
Sows
Vulval discharges are common within 3-4 days of farrowing when a thick viscous material may be excreted. This is normal.
If the sow is healthy, the udder is normal and there is no mastitis, ignore it. It is common practice to inject such sows, but this is not necessary under these circumstances.
A heavy smelling bloody discharge may be from a retained piglet or afterbirth.
Sow may be ill.
Mastitis.
Increases in returns at 18 - 23 days post service with discharge.
Increases in returns >23 days post service with discharge.
Increases in sows not in pig.
Reduced farrowing rates by 10 - 20%.
Increased negative or doubtful pregnancy tests at 30 days post service.
Litter size normal.
Embryo death.
Abortion.
Anoestrus.
The table below gives the times discharges might be seen and their likely significance.

INSERT TABLE


Causes / contributing factors
Infection can be caused in a number of ways:

Vulval discharges arise from opportunist bacteria in the anterior vagina that cause a womb infection or endometritis. These include:
- Actinomyces pyogenes
- Chlamydia
- E. coli *
- A. suis
- Erysipelothrix
- Klebsiella *
- Leptospira bratislava / muenchen
- Pasteurella
- Proteus
- Pseudomonas
- Staphylococci *
- Streptococci * (* Common causes)
Herds with high numbers of old sows.
A short lactation length (14-21 days).
Multiple matings. Cross mating boars.
Handling the prepuce at mating and squeezing the preputial sac.
No supervision at mating.
Matings towards the end of the oestrus period.
Wet, dirty boar pens. Poor drainage. Continual use.
Dirty, wet sow mating pens and continual use without cleaning.
Small stalls where the sow adopts a dog sitting posture with heavy contamination of the vulva.
Housing maiden gilts in stalls.
Heavy vulval contamination, for example in maiden gilts housed on slats where slurry spills over.
Early embryo mortality.
Re-mating discharging sows.
Using old boars on young sows.
Using young boars on older sows.
Diagnosis
Diagnosis is considered in three parts:

Studying records.
Observations on vulvas 14 - 21 days post service.
Bacteriological examinations of swabs from the prepuce and vagina from all boars and 10 problem sows and post mortem examinations on the uteri of affected sows.
Cultures are carried out on the swabs and the predominating bacteria determined. Sensitivity tests identify antibiotics that could be used.
The main organisms associated with endometritis and vulval discharges are opportunist invaders. In some herds no specific organism can be identified, although bacteriological tests may show one or more bacteria predominating either in the prepuce or vagina. A precise diagnosis can be difficult.

Enteroviruses, SMEDI
These are gut-borne viruses, host specific to the pig, that are included in the group called "SMEDI viruses". SMEDI stands for Stillbirth, Mummification, Embryonic Death and Infertility. The term is now also commonly used for parvovirus infection. Although these groups of viruses are distinct from that of parvovirus, they are often all grouped together clinically because the signs are similar. The enteroviruses are subdivided into serotypes of which at least 11 are known. Four of these, serotypes 1, 3, 6 and 8, have been implicated in reproductive problems in pigs. Serotype 1 is the Teschen/Talfan virus which can also cause paralysis in pigs. Usually, each pig herd has an array of different serotypes which circulate in weaned and young growing pigs sub-clinically. The pigs are protected by circulatory antibodies derived from their dam's colostrum. By the time they reach breeding age they are solidly immune.
Reproductive problems only occur when a new serotype, to which the gilts are not immune, enters the herd and multiplies in the breeding females. This probably does not happen very often.

Symptoms
Sows
Embryo mortality.
Mummification.
Stillbirths.
In some cases infertility associated with absorption of embryos also occur. (Repeats).
If reproductive failure results there will be increases in embryo mortality, foetal deaths and mummified and stillborn piglets.
Infection and disease only occur in non-immune sero-negative animals.
Paralysis.
No symptoms in the adult breeding female.
Piglets, Weaners & Growers
None.
Causes / Contributing factors
Introduction of a new strain of virus into the herd.
Poor gilt acclimatisation.
Virus in semen.
Diagnosis
This is carried out by serology and virus isolation.

The symptoms of SMEDI can be mistaken for other causes. These include AD, Leptospirosis, PPV and PRRS

Enzootic Pneumonia (EP)
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Porcilis M Hyo
Enzootic pneumonia is caused by Mycoplasma hyopneumoniae. It is widespread in pig populations and endemic in most herds throughout the world. As an uncomplicated infection in well-housed and well-managed pigs it is relatively unimportant and has only a mild effect on the pig. However if there are other infections present particularly App, Hps, Pasteurella, PRRS or SI, the pneumonia can become more complex with serious effects on the pig.
EP always attacks the lower areas of each lung lobe causing consolidation. The extent of this consolidation in each lobe is scored out of either 5 or 10 depending upon the lobe affected. Thus a severely affected pig with all lobes involved would score 55. This scoring system can be used to assess the severity of disease and its effects on the pig.

If more than 15% of lungs are affected it is highly probable that EP is present in the population. Herds that do not carry M. hyopneumoniae rarely show consolidated lesions in more than 1 % and even then they are very small.

If EP is not present in the growing population then the effects of the other respiratory pathogens are greatly reduced. It is therefore considered a primary pathogen that opens up the lung to other infections.

Clinical signs of enzootic pneumonia only occur in the lactating sow and piglets when the disease has been introduced into a fully susceptible herd for the first time. The breakdown of disease usually takes place over 6 to 8 weeks with sows coming into the farrowing house continuing to be affected.

There is a widely held but erroneous belief that sows and gilts will become carriers and pass this infection to their next litters. They may do so early on and their piglets may cough but by the time they farrow again 4 to 5 months later they will have eliminated the infection and will provide a solid immunity to their piglets via colostrum. If weaning is at 3 to 4 weeks, subsequent litters are not likely to become infected until after weaning.



 
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Symptoms
All pigs
It usually has an incubation period of two to eight weeks before clinical signs are seen but may be longer. Acute disease is normally only seen in new break-downs of disease.

Over the first six to eight weeks after it enters there may be: (This picture however is extremely variable).

Severe acute pneumonia.
Dehydration.
Heavy breathing.
Coughing, prolonged.
Respiratory distress.
Fever.
High mortality across all ages of stock.
Chronic disease is the normal picture when the organism has been present in the herd for some considerable time.
Maternal antibody is passed via colostrum to the piglets. It disappears from seven to twelve weeks of age after which clinical signs start to appear including:
A prolonged non-productive cough, at least seven to eight coughs per episode, is a common sign around this time, with some pigs breathing heavily ("thumps").
30 to 70% of pigs will have lung lesions at slaughter.
Causes / Contributing factors
It is commonly transmitted through the movement of carrier pigs.
Wind-borne infection for up to 3km (2 miles) if the climatic conditions are right. The organism dies quickly outside the pig, particularly when dried.
Incoming pigs.
Increased clinical disease is associated with the following;
Overcrowding and large group sizes.
Less than 3 cu.m.air space per pig and 0.7 sq.m. floor space per pig.
Houses that are too wide for good air flow control.
Variable temperatures and poor insulation.
Variable wind speeds and chilling.
Low temperature, low humidity environments.
High levels of carbon dioxide and ammonia.
High dust and bacteria levels in the air.
Pig movement, stress and mixing.
Housing with a continuous throughput of pigs.
Other concurrent diseases particularly PRRS, App, flu, and aujeszky's disease.
Poor nutrition and dietary changes at susceptible times.
Diagnosis
This is based on the clinical picture and examination of the lungs at post-mortem examination or at slaughter, combined sometimes with histology of the lesions. However, these do not provide a specific diagnosis and in the herds supplying breeding stock or in special cases (e.g. litigation) it may be necessary to confirm the diagnosis by carrying out one or more of the following tests: Serological (ELISA) tests, microscopic examination of stained touch preparations (TPs) of the cut surface of the lungs, fluorescent antibody tests (FATs), polymerase chain reaction (PCRs) tests and finally culture and identification of Mycoplasma hyopneumoniae.
These tests are becoming more widely available and some diagnostic laboratories cannot do them. The PCR is probably the most sensitive. FAT, serology and cultures are used in Denmark, but only FATs are available in many laboratories.

EP must be differentiated from Flu, PRRS, Hps and other mycoplasma infections. Laboratory tests are required to differentiate them. Furthermore, all or some of these may occur as mixed infections together with Mycoplasma hyopneumoniae.

Further Reading

Eperythrozoonosis
This is a disease caused by a bacterium called Eperythrozoonosis suis which attaches to the surface of red blood cells and sometimes destroys them. The pig may then become anaemic and the products left after the destruction of the cells may cause jaundice. Clinical disease is more commonly seen in young growing pigs. However it can also cause reproductive problems in the breeding herd. A sow may carry Epe and yet remain quite healthy, however, it can cross the placenta resulting in weak pale pigs at birth.
Epe is present in most if not all herds but the mechanisms which allow it to become pathogenic and produce disease in some populations and not in others are unknown. The incidence of disease is low.

Symptoms
Sows
Acute disease:

Affected sows are inappetent with fever 40-42?C (105-107?F) when high numbers of organisms are present in the blood. This clinical picture is often seen after farrowing.
Anaemia
Increased respiration.
Anoestrus.
Pale skin
No milk - agalactia.
Chronic disease:
Sows become debilitated and pale with jaundice.
Poor conception, repeat matings and anoestrus.
Delayed returns to oestrus.
Anaemia.
Jaundice.
Bleeding into tissues.
Abortion.
Thin sows.
Stillbirths.
Reduced conception rates.
Pale skin
No milk -agalactia.
Piglets
In severe cases jaundice may result.
Secondary infections tend to occur.
More chronic cases result in slow growth and poor-doing pigs.
Pale and anaemic pigs.
Increased scour (sloppy diarrhoea).
Pneumonia.
Weaners & Growers
The clinical picture varies:

In weaners the acute disease is manifest by primary anaemia.
In growers it leads to slow growth and poor-doing pigs.
The presence of anaemic and possibly slightly yellow-skinned recently weaned pigs.
Pale pigs.
Slow or variable growth.
Ear necrosis.
Enteritis - sloppy diarrhoea.
Fever.
Pneumonia.
Poor pigs, wasting, hairy.
Pot bellied pigs.
Scour.
Causes / Contributing factors
Biting insects.
Internal parasites
Lice or mange mites.
Cannibalism / vice (Abnormal behaviour).
Sows method of spread:
Vaccinating sows with the same needle.
Tagging gilts.
Feeding placenta or farrowing house material.
Fighting.
Vulval and tail biting etc.
Piglets - method of spread:
Tailing, tooth clipping and iron injections.
Weaners & Growers method of spread
Fighting.
Tail biting and other vices.
Diagnosis
In trying to arrive at a diagnosis, the following should be considered.
The clinical picture.
The identification of the organism in blood smears stained with Wright's stain. Fifty microscopic fields should be examined before a negative diagnosis is arrived at. The presence of Epe in a smear need not necessarily imply disease.
Serological tests, including an ELISA, are still unreliable but are being improved.

Evidence of other causes of anaemia (e.g. iron/copper deficiency).

Examination of blood samples for packed cell volume and haemoglobin levels.
Epe must be differentiated from the following:
- Actinobacillus pleuropneumonia.
- Chronic respiratory disease complexes with PRRS and influenza.
- Gl?ssers disease - Haemophilus parasuis.
- Leptospirosis (L. icterohaemorrhagiae).
- Malabsorption and chronic enteritis.
- Pale piglet syndrome - haemorrhages.
- Porcine enteropathy (PE, NE, PHE and PIA).
- Post weaning multisystemic wasting syndrome (PMWS)
- Other causes of anaemia (e.g. Iron / copper deficiency).

Epitheliogenesis Imperfecta, Imperfect skin
The piglet is born devoid of areas of skin. It usually occurs on legs or flanks.
Symptoms
Sows, Weaners & Growers
N/A
Piglets
Born devoid of areas of skin.
Causes / Contributing factors
A developmental abnormality.
Diagnosis
This is based on the clinical signs.

Erysipelas
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Swine erysipelas is caused by a bacterium, Erysipelothrix rhusiopathiae that is found in most if not all pig farms. Up to 50% of animals may carry it in their tonsils. It is always present in either the pig or in the environment because it is excreted via saliva, faeces or urine. It is also found in many other species, including birds and sheep and can survive outside the pig for a few weeks and longer in light soils. Thus it is impossible to eliminate it from a herd. Infected faeces is probably the main source of infection, particularly in growing and finishing pens.
The bacterium alone can cause the disease but concurrent virus infections, such as PRRS or influenza, may trigger off outbreaks.

Disease is relatively uncommon in pigs under 8-12 weeks of age due to protection provided by maternal antibodies from the sow via the colostrum. The most susceptible animals are growing pigs, non vaccinated gilts and up to 4th parity sows.

The organism multiplies in the body, and invades the bloodstream to produce a septicaemia. The rapidity of multiplication and the level of immunity in the pig then determines the clinical symptoms.

Symptoms
Piglets
Rarely in sucking pigs.
Sows
Per-acute or acute disease

The onset is sudden.
Often the only sign being death.
Death - generalised infection.
High temperatures 40?C (108?F) - Fever.
Obviously ill, although others can appear normal.
May cause abortion.
Mummified piglets.
Stillbirths.
Restricted blood supply causes small raised areas called diamonds in the skin. These are clearly defined become red and finally black, due to dead tissue but no abscesses. Most heal in 7 - 10 days.
Often these lumps can be palpated in the early stages before anything can be seen.
Stiffness or reluctance to rise indicating joint infection - arthritis.
Sudden death is not uncommon due to an acute septicaemia or heart failure.
Sub-acute disease
Inappetence.
Infertility.
Characteristic skin lesions and ulceration.
The temperature ranges from 39-40?C (102-104?F) - Fever.
The disease can be so mild as to be undetected.
Some piglets may die in the womb following sub-acute disease and become mummified.
Abortion with ill sows and dead piglets.
Chronic disease
This may or may not follow acute, or sub-acute disease.
The organism either:
- Affects the joints producing lameness or
- The heart valves producing growths.
Boars
Boars infected with erysipelas develop high temperatures and sperm can be affected for the complete development period of 5-6 weeks. Infertility is demonstrated by returns, sows not in pig and poor litter sizes.
Weaners & Growers
Acute infection:

Sudden death.
Acutely ill pigs running high temperatures.
Characteristic skin lesions may also be evident as large 10 to 50mm raised diamond shaped areas over the body that may turn from red to black. They may be easier to feel than to see in the early stages and often resolve over 7 - 10 days.
Commonly the disease is less acute and mild.
Skin lesions may appear but the pigs may not appear to be ill in spite of a high temperature 42?C (107?F).
The organism may settle in the joints causing chronic arthritis and swellings which can be responsible for condemnations at slaughter.
Lameness.
Causes / Contributing factors
Wet dirty pens.
Wet feeding systems, particularly if milk by-products are used, can become major sources for multiplication of the organism
Continually populated houses with no all-in and all-out procedures and disinfection.
Water systems that have become contaminated with the organism.
Virus infections.
Feed back of faeces.
The movement of pigs involving mixing and stress.
Sudden changes in temperature and warm summer weather.
Sudden changes in diet.
Common in straw based systems.
Feeding milk waste products.
Diagnosis
This is determined by the clinical picture and isolation of the organism which is easy to grow in the laboratory. Serology will only indicate exposure to the organism and not necessarily disease. It can only be used to aid diagnosis if rising titres, 14 days apart, are demonstrated and if clinical signs are evident.

Exudative Epidermitis
This is caused by the bacterium Staphylococcus hyicus which lives normally on the skin without causing disease. It is not known why sometimes it flares up and causes a dermatitis which oozes greasy fluid. It produces toxins which are absorbed into the system and damage the liver and kidneys. In the sucking piglet disease is usually confined to individual animals, but it can be a major problem in new gilt herds and weaned pigs. During the days immediately preceding farrowing the bacterium multiples profusely in the sow's vagina so that piglets are infected during the birth process or soon after.
Symptoms
Sows
Uncommon but localised lesions may be seen particularly behind the face and eyes.
Piglets
Severely affected piglets will die.
Localised lesions on the flanks and behind ears. Lesions usually commence with small, dark, localised areas of infection around the face or on the legs.
The skin along the flanks the belly and between the legs changes to a brown colour gradually involving the whole of the body.
The skin becomes wrinkled with flaking of large areas and it has a greasy feel.
In severe cases the skin turns black due to necrosis and the piglets die.
A more localised picture is seen if the sow has passed some immunity to the piglet, with small circumscribed lesions approximately 5-10mm in diameter that do not spread.
Weaners & Growers
Usually commence about 3 days after weaning with localised, brown areas of infection or dermatitis around the face or on the legs, where the skin has been damaged. It may ulcerate.
The skin along the flanks the belly and between the legs changes to a brown colour gradually involving the whole of the body.
The skin becomes wrinkled with flaking of large areas.
It progresses to a dark greasy texture and in severe cases turns black.
Such cases usually die due to the toxins produce by the staphylococci organisms.
In nurseries up to 15% of the population may be involved.
Dehydration is common.
Causes / Contributing factors
The sharp eye teeth cut the skin around the mouth during competition for a teat.
Abrasions on the knees from sucking may also trigger it off.
Abrasions from poor concrete surfaces or metal floors, side panels.
Faulty procedures for iron injections, removing tails and teeth.
Fighting and skin trauma at weaning.
Mange giving rise to skin damage.
Damage to the face by metal feeding troughs can precipitate disease.
Abnormal behaviour - tail biting, ear biting, navel sucking, flank biting.
Badly clipped teeth at birth.
Diagnosis
This is based on the characteristic skin lesions. It is important to culture the organism and carry out an antibiotic sensitivity test. A moist wet area should be identified, the overlying scab removed and a swab rubbed well into the infected area.

Fever
Fever means a high body temperature of 39-40?C (103-109?F). It may occur with little or no other signs or be part of a specific disease.
Symptoms
All Pigs
Vomiting.
Temperature.
Inappetence.
No milk.
Dehydration.
Dullness / Lameness.
Increased respiration.
Reddening of skin. Blue skin.
Metritis.
Mastitis.
Abortion.
Shivering.
Causes / Contributing factors
Mastitis or metritis.
Retention of a dead pig.
Retention of afterbirth.
A bacterial septicaemia (e.g. erysipelas).
Flu or PRRS.
Secondary bacterial infections associated with flu or PRRS.
Cystitis/ pyelonephritis.
Acute stress or eclampsia.
Heat stroke.
Pneumonia.
Diagnosis
Check for any of the above conditions. If you cannot find out what the cause is and there are a number of animals involved, veterinary advice should be sought. Bear in mind that depending where in the world your herd is located, fever may be the first clinical sign in such diseases as classical swine fever (hog cholera), African swine fever and aujeszky's disease (pseudorabies).

Foot-and-Mouth Disease
Quick Disease Guide:

Foot-and-Mouth disease should always be considered if sudden widespread lameness appears with vesicles or blisters on the snout, tongue and tops of the claws. In most countries it is notifiable and if suspected must be reported to the authorities immediately. Salivation is an obvious symptom.

Fractures
Broken bones are not uncommon and usually result from injury and fighting. Spontaneous fractures can occur in bone diseases such as osteochondrosis and osteomalacia, which are associated with calcium phosphorus and vitamins A and D.
Fractures are common in growing pigs due to environmental trauma and where appropriate high stocking densities.

Symptoms
All Pigs
The onset is always sudden and painful.
The pig is unable to rise on its own without difficulty.
Incoordination.
A significant feature is the reluctance to place any weight on the affected leg and lameness.
The pig is very reluctant to move unless on three legs.
The muscles and tissues over the fracture site are often swollen.
Crepitus or the rubbing together of the two broken ends of the bone can often be felt.
Fractures of the spinal vertebra are common particularly in the first litter gilt during lactation and after weaning.
The pig usually adopts a dog sitting position and exhibits severe pain on movement.
In chronic cases joints may be swollen and abscessed.
Causes / Contributing factors
Bone disease such as osteomalacia, osteoporosis or leg weakness (OCD).
Low levels of calcium, phosphorus and vitamin D levels in the diet.
Trauma.
Fighting.
Fractures in piglets are usually caused by trauma from the sow.
Diagnosis
This is based upon a history of injury, clinical signs and palpation. Fractures must be differentiated from acute laminitis, arthritis, muscle tearing, bush foot and mycoplasma arthritis.

Frostbite
This is the end result of the destruction of the skin and surface tissues by low temperatures. The ears, tail and feet are particularly vulnerable areas. Frostbite is not uncommon in outdoor pigs.
Symptoms
All Pigs
The skin initially becomes pale then bright red, swollen and painful.
If exposure to low temperatures continues, the affected tissues die and a line of demarcation develops between damaged and healthy tissues becoming blue.
Secondary skin infections or dermatitis develop.
Causes / Contributing factors
Exposure to low temperatures.
Diagnosis
This is based upon skin lesions and a history of exposure to low temperatures. It can be confused with acute infection by erysipelas, salmonella or pasteurella bacteria or a toxic condition.
Treatment
Cover affected areas with an antiseptic cream
Topical antibiotic cream may be required to control infections
Move affected animal indoors

Gastric Ulcers
Erosion and ulceration of the lining of the stomach is a common condition in sows and growing pigs. (More common in growing pigs than breeding animals). It occurs around the area where the food pipe (oesophagus) enters the stomach. In the early stages of the disease this area becomes roughened and gradually changes as the surface becomes eroded until it is ulcerated. Intermittent bleeding may then take place leading to anaemia or massive haemorrhage may occur resulting in death. The incidence in sows is usually less than 5% in growing pigs at slaughter is up to 60%.
Symptoms
These depend on the severity of the condition.
Piglets

Uncommon.
Often no symptoms.
Wasting.
Sows
In the less acute form:

Pale skin.
Weak.
Breathless.
Dehydration.
Grinding of the teeth due to stomach pain .
Passing of dark faeces containing digested blood.
Not eating.
Vomiting.
A tucked up appearance.
In its most acute form:
Previously healthy animals are found dead and very pale.
Weaners & Growers
Acute form:

Previously healthy animals are found dead.
The most striking sign is the paleness of the carcass due to internal haemorrhage.
Less acute form:
The affected pig is pale.
Weak.
Shows breathlessness.
Grinding of the teeth.
Vomiting.
The passing of dark faeces containing digested blood is often a persistent symptom.
Usually the temperature is normal.
In chronic cases:
The pig has an intermittent appetite and may lose weight.
Causes / Contributing factors
There is usually more than one causal factor. They may include nutritional factors, management deficiencies that lead to stress, and infections.

Nutritional factors

Low protein diets.
Low fibre diets. (The introduction of straw reduces the incidence).
High energy diets.
High levels of wheat in excess of 55%.
Deficiencies of vitamin E or selenium.
Diets containing high levels of iron, copper or calcium.
Diets low in zinc.
Diets with high levels of unsaturated fats.
Diets based on whey and skimmed milk.
Physical aspects of the feed
Size of feed particle - the more finely ground the meal the smaller becomes the particle size and the higher the incidence of ulcers. This is still the case if the feed is then pelleted.
Pelleting feeds in itself increases the incidence. Feed meal.
However, sometimes changing from pellets to meal itself causes problems. A compromise is to feed alternatively.
Cereals with a high moisture content sometimes seem to contribute to ulcers.
Rolling cereals as distinct from grinding them will often produce a dramatic drop in the incidence but the penalties of feed use have to be taken into consideration.
Managemental factors that increase the incidence:
Irregular feeding patterns and shortage of feeder space.
Increased stocking densities and movement of pigs or any other undue stresses including poor stockmanship.
Transportation.
Excessive aggression between sows.
Poor management of sows in stalls and tethers.
Noisy unsympathetic stockmanship in the farrowing rooms.
Periods of starvation.
Poor availability of food or water.
Fluctuating environmental temperatures.
Other diseases.
There is a clear relationship between outbreaks of pneumonia and the incidence of gastric ulceration.
Ulceration may occur following bacterial septicaemias such as those associated with erysipelas and swine fever.
Breed.
More common in certain genotypes.
Diagnosis
This is based on the clinical signs and post mortem lesions. A sample of faeces should be examined for the presence of blood and to eliminate parasites. An examination of stomachs at slaughter should be carried out.
Gastric ulcers must be differentiated from haemorrhage of the bowel, eperythrozoonosis, the red stomach worm Hyostrongylus rubidus and porcine enteropathy.

Getah Viruses
These have been associated with foetal death and abortion in sows in Japan and Korea but little is seen or noted in other countries. It is not of great significance.

Glässers Disease
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Porcilis Glässer
Glässers Disease is caused by the bacterium Haemophilus parasuis (Hps), of which there are at least fifteen different types. It is found throughout the world and organisms are present even in high health herds. If such herds are set up using SPF or MEW techniques and are free from Hps it can be devastating when they first become contaminated, producing an anthrax-like disease with high mortality in sows.
In the majority of herds in which the bacterium is endemic, sows produce a strong maternal immunity which normally persists in their offspring until 8 to 12 weeks of age. As a result, the effects of the infection in weaners are usually nil or minimal. . Disease may however be seen in sucking pigs. Pigs usually become sub-clinically infected when still protected by maternal antibody and then stimulate their own immune response. If however the maternal immunity wears off before they become infected they may develop severe disease. This is usually sometime after weaning. It can also act as a secondary pathogen to other major diseases particularly enzootic pneumonia (EP) (Mycoplasma hyopneumoniae). Outbreaks of disease are sometimes experienced in sucking pigs, particularly in gilt herds.

Hps attacks the smooth surfaces of the joints, coverings of the intestine, lungs, heart and brain causing pneumonia, heart sac infection, peritonitis and pleurisy. It is respiratory spread.

Symptoms
Sows
Disease is rare in sows, unless the dry sow is naive.
Occasionally seen in gilts:
Lameness / stiffness.
Slight swellings over the joints and tendons.
Meningitis rarely.
Piglets
Acute disease:

Rapidly depressed.
Elevated temperature.
Inappetence .
Reluctant to rise.
Characteristic feature a short cough of 2-3 episodes.
Sudden death in good sucking piglets is not uncommon.
Also causes individual cases of arthritis and lameness with fever and inappetence.
Chronic disease:
Pale and poor growing pigs.
Sudden deaths may occur.
Weaners & Growers
Pigs with glässers disease become rapidly depressed or may be just found dead.
Elevated temperature.
Stop eating.
Reluctant to rise.
Fever.
Nervous signs - fits and convulsions including meningitis.
Poor pigs, wasting, hairy often result.
In young growing pigs the following are common:
Fever.
Mild meningitis.
Arthritis.
Lameness.
Pneumonia.
Heart sac infection.
Peritonitis and pleurisy.
A characteristic feature is a short cough of only 2-3 episodes.
Causes
It is respiratory spread. Disease may be precipitated by PRRS, flu or EP.
Poor environments, draughts etc. predispose.
Stress.
Diagnosis
This is made by clinical observations, post-mortem examinations and isolation of the organism in the laboratory. Gl?ssers disease has to be differentiated from Actinobacillus suis infection, App, mulberry heart disease, streptococcal meningitis and arthritis and bacterial septicaemias.

Greasy Pig Disease
This is caused by the bacterium Staphylococcus hyicus which lives normally on the skin without causing disease. It is not known why sometimes it flares up and causes a dermatitis which oozes greasy fluid. It produces toxins which are absorbed into the system and damage the liver and kidneys. In the sucking piglet disease is usually confined to individual animals, but it can be a major problem in new gilt herds and weaned pigs. During the days immediately preceding farrowing the bacterium multiples profusely in the sow's vagina so that piglets are infected during the birth process or soon after.
Symptoms
Sows
Uncommon but localised lesions may be seen particularly behind the face and eyes.
Piglets
Severely affected piglets will die.
Localised lesions on the flanks and behind ears. Lesions usually commence with small, dark, localised areas of infection around the face or on the legs.
The skin along the flanks the belly and between the legs changes to a brown colour gradually involving the whole of the body.
The skin becomes wrinkled with flaking of large areas and it has a greasy feel.
In severe cases the skin turns black due to necrosis and the piglets die.
A more localised picture is seen if the sow has passed some immunity to the piglet, with small circumscribed lesions approximately 5-10mm in diameter that do not spread.
Weaners & Growers
Usually commence about 3 days after weaning with localised, brown areas of infection or dermatitis around the face or on the legs, where the skin has been damaged. It may ulcerate.
The skin along the flanks the belly and between the legs changes to a brown colour gradually involving the whole of the body.
The skin becomes wrinkled with flaking of large areas.
It progresses to a dark greasy texture and in severe cases turns black.
Such cases usually die due to the toxins produce by the staphylococci organisms.
In nurseries up to 15% of the population may be involved.
Dehydration is common.
Causes / Contributing factors
The sharp eye teeth cut the skin around the mouth during competition for a teat.
Abrasions on the knees from sucking may also trigger it off.
Abrasions from poor concrete surfaces or metal floors, side panels.
Faulty procedures for iron injections, removing tails and teeth.
Fighting and skin trauma at weaning.
Mange giving rise to skin damage.
Damage to the face by metal feeding troughs can precipitate disease.
Abnormal behaviour - tail biting, ear biting, navel sucking, flank biting.
Badly clipped teeth at birth.
Diagnosis
This is based on the characteristic skin lesions. It is important to culture the organism and carry out an antibiotic sensitivity test. A moist wet area should be identified, the overlying scab removed and a swab rubbed well into the infected area.

Haematoma
A haematoma is a pocket of blood that forms beneath the skin or in muscle tissue and usually results from ruptured blood vessels following trauma particularly over the shoulders, flanks or the hind quarters. The most common site is the ear.
Symptoms
Sows
Blood from the vulva.
Head on one side.
Large swellings which develop suddenly.
The swellings contain blood or serum due to haemorrhage.
Piglets
Uncommon but as for sow.
Weaners & Growers
Large swellings which develop suddenly.
The swellings contain blood or serum.
Causes / Contributing factors
Fighting.
Mange.
Trauma.
Diagnosis
This is based on the clinical signs. Differentiate from an abscess, test with a needle and syringe

Hepatitis E Virus
This caused some public concern in 1997 when it was isolated from pigs' livers which were suffering from another condition. Antibodies were found to be widespread in the pig population of the Mid-western United States. It was shown later that the pig hepatitis virus was distinct from the human one and there was no cross-species transmission. Hepatitis E has also been identified in pigs in Australia. This virus should not worry pig farmers

Hypoglycaemia
Hypoglycaemia is the term for low blood sugar level. During the first few days of life the newborn piglet is unable to mobilise the low glycogen reserves in the liver to provide adequate levels of glucose in the blood. It is therefore dependent for energy on a regular intake of lactose from the sows milk. If a piglet cannot obtain sufficient lactose to maintain its energy output, it runs out of energy, its body temperature drops and ultimately it goes into a coma and dies.
Hypoglycaemia usually occurs in the first 12-24 hours of birth.

Symptoms
Sows, Weaners & Growers
N/A
Piglets
Piglet with Hypoglycaemia
Laid on belly.
Shivering.
Becoming very cold.
Starvation.
Paddling.
Fits and convulsions.
Frothing at the mouth - salivation.
Comatosed.
Eyes are sunken and the head bent backwards due to dehydration.
High mortality.
Causes / Contributing factors
Low level of sugar in the blood.
No milk - starvation.
Severe chilling.
Wet pens.
Low viable piglets.
Diagnosis
This is based on the clinical signs. Examine the eyes to see that there is no evidence of rapid back and fore lateral movements which would indicate meningitis not hypoglycaemia.
Diseases associated with Hypoglycaemia
The following diseases can give rise to hypoglycaemia in piglets.
Clostridial Diseases
Congenital Tremour
Diahorrea - acute e.coli infections
Low birth rate / poor maturity
Mastitis, no milk, no colostrum
Navel Bleeding
Porcine Reproductive and Respiratory Syndrome (PRRS)
Pseudorabies / Aujesky's disease
Splay leg
Transmissible Gastro Enteritis (TGE)

Hps - (Haemophilus Parasuis)
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EXCEDE®
Glässers Disease is caused by the bacterium Haemophilus parasuis (Hps), of which there are at least fifteen different types. It is found throughout the world and organisms are present even in high health herds. If such herds are set up using SPF or MEW techniques and are free from Hps it can be devastating when they first become contaminated, producing an anthrax-like disease with high mortality in sows.
In the majority of herds in which the bacterium is endemic, sows produce a strong maternal immunity which normally persists in their offspring until 8 to 12 weeks of age. As a result, the effects of the infection in weaners are usually nil or minimal. . Disease may however be seen in sucking pigs. Pigs usually become sub-clinically infected when still protected by maternal antibody and then stimulate their own immune response. If however the maternal immunity wears off before they become infected they may develop severe disease. This is usually sometime after weaning. It can also act as a secondary pathogen to other major diseases particularly enzootic pneumonia (EP) (Mycoplasma hyopneumoniae). Outbreaks of disease are sometimes experienced in sucking pigs, particularly in gilt herds.

Hps attacks the smooth surfaces of the joints, coverings of the intestine, lungs, heart and brain causing pneumonia, heart sac infection, peritonitis and pleurisy. It is respiratory spread.

Symptoms
Sows
Disease is rare in sows, unless the dry sow is naive.
Occasionally seen in gilts:
Lameness / stiffness.
Slight swellings over the joints and tendons.
Meningitis rarely.
Piglets
Acute disease:

Rapidly depressed.
Elevated temperature.
Inappetence .
Reluctant to rise.
Characteristic feature a short cough of 2-3 episodes.
Sudden death in good sucking piglets is not uncommon.
Also causes individual cases of arthritis and lameness with fever and inappetence.
Chronic disease:
Pale and poor growing pigs.
Sudden deaths may occur.
Weaners & Growers
Pigs with gl?ssers disease become rapidly depressed or may be just found dead.
Elevated temperature.
Stop eating.
Reluctant to rise.
Fever.
Nervous signs - fits and convulsions including meningitis.
Poor pigs, wasting, hairy often result.
In young growing pigs the following are common:
Fever.
Mild meningitis.
Arthritis.
Lameness.
Pneumonia.
Heart sac infection.
Peritonitis and pleurisy.
A characteristic feature is a short cough of only 2-3 episodes.
Causes
It is respiratory spread. Disease may be precipitated by PRRS, flu or EP.
Poor environments, draughts etc. predispose.
Stress.
Diagnosis
This is made by clinical observations, post-mortem examinations and isolation of the organism in the laboratory. Glässers disease has to be differentiated from Actinobacillus suis infection, App, mulberry heart disease, streptococcal meningitis and arthritis and bacterial septicaemias.

Heat Stroke
This usually occurs where ventilation has failed or in extremely hot weather.
Symptoms
Piglets
Uncommon, but as for sow.
Sows, Weaners & Growers
Distress.
A very high respiratory rate.
Muscle trembling.
Skin red.
Weakness.
Prostration.
Vomiting.
Diarrhoea may be seen.
Rectal temperature may rise to 43?C (109?F)
Causes / Contributing factors
High temperatures.
Exposure to sunlight.
Combined with high humidity and poor ventilation in indoor housing.
Diagnosis
The history and clinical signs.
Treatment
Give immediate treatment
Immerse the animal in cold water or spray
Dribbel cold water into the rectum using a flutter valve

Ileitis (Lawsonia intracellularis)
Related Products:
Aurofac / Aureomycin
Enterisol® Ileitis
This comprises a group of conditions involving pathological changes in the small intestine associated with the bacterium Lawsonia intracellularis. This exists on most if not all farms. Disease takes four different forms: porcine intestinal adenopathy (PIA) an abnormal proliferation of the cells that line the intestines; necrotic enteritis (NE) where the proliferated cells of the small intestine die and slough off with a gross thickening of the small intestine (hosepipe gut); regional ileitis (RI), inflammation of the terminal part of the small intestine and proliferative haemorrhagic enteropathy (PHE). In the latter there is massive bleeding into the small intestine, hence the common name bloody gut and this is the commonest form in growing pigs. The other three forms are rarer and progress from PIA. PHE is more common in 60-90kg pigs and gilts.
All are uncommon in the mature female but outbreaks of one of the forms, bloody gut or porcine haemorrhagic enteropathy (PHE), are occasionally seen in maiden and pregnant gilts.

The organism is impossible to keep out of farms probably because it also infects other species. Infected faeces are the major vehicle for spread around the farm.

Symptoms
Weaners & Growers

Clinical signs of PIA, NE, RI are different from PHE.

PIA:
The pig appears clinically normal.
Initially eats well.
Chronic watery, sloppy diarrhoea.
Necrosis.
Gradual wasting.
Loss of condition.
In some cases a pot bellied bloated appearance.
Pigs with the chronic form of the PIA recover over a period of four to six weeks, however there can be considerable losses in feed efficiency and daily gain of up to 0.3 and 80g/day respectively. As a consequence there can be marked variations in sizes of pigs.
NI or RI follow from it with similar signs.
PHE is an acute disease:
Bloody scour.
The pig may die suddenly.
Appears very pale and passes black bloody faeces.
Anaemic.
Sows
Gilts with PHE have pale skins.
Appear weak.
Bloody or black tarry diarrhoea.
May suddenly die.
Abortions
Piglets
N/A
Causes / Contributing factors
These are not fully understood.
The use of continually populated pens.
Lack of all-in, all-out production.
Naive animals.
Change of environment.
Changes in feed.
Carry over of infection between batches appears to be a main means of spread.
Associated with continual population of finishing pens.
Diagnosis
This is based on the clinical picture, post-mortem examinations, histology of the gut wall and demonstrating the organism in faeces by an ELISA test. A serological test is also available. Only a few laboratories can do these tests. Tissue cultures have been recently developed.

Inherited Thick Legs, Hyperostosis
This is a very rare condition of newborn piglets which is thought to be inherited. Individual litters are born with boney thickening of the legs, most notably the front legs. The pigs can not walk properly and usually fail to thrive. If such a condition arises check that the boar has not thrown other similar litters and do not mate the sow with the same boar again.

Internal Parasites (Worms etc.)
In the sow the important parasites are the large white worms ascarids (Ascaris suum), red stomach worms (Hyostrongylus rubidus) and whip worms (Trichuris suis). Pigs can also get ring worm, which although needs treatment, is of little economic significance, however it can be passed to humans.

The sow becomes the source of potential infection to piglets. The threadworm (Strongyloides ransomi) is important in the piglet. The life cycles of all are direct from eggs in faeces to adult in the intestine.
Internal parasites are an uncommon problem in the weaned, growing and finisher pig unless they are housed in continuously occupied straw based or bare concrete pens in which case ascarids may become a problem.

Symptoms
Sows
May include the following:

Coughing.
Loss of body condition.
Hairy pigs.
Vomiting.
Blood in faeces but rarely.
Anaemia.
Diarrhoea - sloppy.
Piglets (Thread Worm)
Coughing.
Stiffness.
Pain.
Vomiting.
Bloody diarrhoea.
Some mortality.
Weaners & Growers
Coccidiosis could cause diarrhoea within 7 to 10 days of entry to continually used pens.
Strongyle infections (poor growth and sloppy faeces) within 3 to 4 weeks
Coughing.
Blood in faeces.
Pneumonia / Heavy breathing.
Pale pigs.
Causes / Contributing factors
Management systems that allow regular access to faeces.
Faeces allowed to accumulate for more than 3 - 4 days (allows eggs to become infective).
Moist wet areas encourage survival of eggs.
No all-in, all-out management.
Permanently populated yards or paddocks outdoors.
Failure to monitor faeces for egg output.
Failure to carry out routine treatments when indicated.
Continuously used pens predispose.
Wet dirty floors.
Carrier pigs.
Diagnosis
This is based on symptoms and identification of the parasites. Laboratory examination of faeces for worm eggs.
Photo's of the various worms
Large white worm Eggs
(Ascaris suum)
 Large white worm
(Ascaris suum)
 
 
Threadworm Eggs
(Strongyloides ransomi)
 Threadworm
(Strongyloides ransomi)
 


--------------------------------------------------------------------------------

   
Whipworm Eggs
(Trichinosis)
 Whipworms
(Trichuris suis)
 


--------------------------------------------------------------------------------

   


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Ringworm in Dry Sows

 

Iron toxicity (Vitamin E Deficiency)
Iron toxicity occurs when the sow and her piglets are deficient in vitamin E. Iron dextran injections become toxic and cause severe muscle reactions at the injection site.
Symptoms
Piglets
The piglets become acutely lame, stiff and the affected muscles swell.
The piglets develop heavy breathing and look pale.
Anaemic.
Death occurs within 24 hours.
Sows
None
Weaners & Growers
Rare
Causes / Contributing factors
Vitamin E deficiency in the sow occurs when fats in the diet become rancid or cereals or corn have fermented and spoiled and the vitamin E is destroyed. Piglets are then born deficient
Poor quality iron dextran will predispose.
Diagnosis
A history of acute lameness within 12 hours of iron injection, often with high mortality. Swellings at the sire of injection.

Japanese B Encephalitis Virus (JE)
This virus is spread by mosquitoes and is only important in countries where the insects are prevalent. Most domestic animals are affected. It causes an encephalitis in the human. The pig is an important source of infection.

Symptoms
Sows, Weaners & Growers
No clinical effects.
Piglets
Mummified piglets
Stillborn piglets
Nervous signs in piglets - Fits and convulsions.
Oedema fluid in piglets.
Boars
Infertility in boars.
Swollen testicles.
Causes / Contributing factors
The presence of mosquitoes.
Susceptible pigs (na?ve).
Viral reservoirs in other species.
Diagnosis
Viral isolation. HI and ELISA tests.

Jaw and Snout Deviation
This is a common yet little recognised condition in the sow. When the jaw is at rest, a proportion of sows (often around 5%) and particularly those housed in confinement, show a misalignment of the lower jaw to the left or right of centre. In extreme cases this can give the appearance of rhinitis but it is of no significance.
Symptoms
Piglets
N/A
Sows
Misalignment of the lower jaw when at rest.
The upper jaw and nose become shortened and flattened, in some cases to a grotesque degree.
Weaners & ocassionally in Growers
Occasionally, as in sows.
Causes / Contributing factors
Constant trauma from bar biting or the use of nipple drinkers.
Infection of the bone as a result of faulty teeth clipping.
Prolonged feeding of very finely ground meal in narrow troughs.
Diagnosis
This is based on the clinical symptoms and absence of rhinitis.

Joint Ill in Piglets
The conditions commonly referred to as “joint ill” is more correctly referred to as an arthritis affecting one or more joints, usually in young pigs. It is a condition seen in the young of most species and results from infection gaining entry to the blood stream at or soon after birth, circulating around the body and then settling out in the joints or occasionally in other parts of the body, particularly the brain causing meningitis.
Cause
The cause of joint ill is bacterial infection of the piglet. The majority of cases are caused by opportunist infection from the environment with, for example, E coli, Staphylococci and Streptococci. There are specific infectious agents that can produce epidemics of joint ill (and meningitis) such as Strep Suis type 14.

There are a number of possible routes by which the bacteria can gain access to the blood stream and, hence, spread to the joints:-
Through the navel
Through badly clipped teeth
Through contamination of a docked tail stump
Through wounds or abrasions
Through the tonsil of the piglet (especially strep suis)
Clinical Signs
The first signs usually seen will be a piglet carrying a leg or reluctant to stand. Some may “dog sit”. As the pigs’ ability to compete for a teat is compromised, loss of condition and starvation will occur.

It is often the case that visible and palpable swelling of specific joints occurs later and, when evident, the hock and knee are most commonly affected.

Without treatment the infection will persist and, in severe cases, the abcessation resulting will burst out from the joint.

Cases of arthritis can be seen post weaning, either as a delayed manifestation of earlier infection or resulting from inadequate treatment of an earlier case.
Treatment
Early individual antimicrobial treatment is essential if a recovery is to be made. The medication used should be tailored to the needs of the farm and laboratory testing of the cause(s) may help. In general, penicillin, ampicillin or lincomycin are likely to be effective. Use of pain killers (e.g. ketoprofen) may also be indicated as this condition can be very painful.

Treatment should be continued for at least 3 and preferably 5 days.

Failure to respond and evidence of burst abscesses from joints should lead to euthanasia. In rare cases an early problem with joint ill can contaminate the end of the bone and affect the growth plates with the result that later in life (e.g. at 3 months) spontaneous fractures occur.
Prevention
The key to controlling joint ill is firstly to improve hygiene in the farrowing area and secondly to identify and rectify the route of entry of infection.
Teeth Clipping - Teeth must be clipped singly with clean sharp clippers or ground off. Some producers stop teeth clipping in the face of joint ill problems but it must be remembered that the fighting damage that results can itself lead to joint ill!
Tail Docking - Always use separate instruments from those used to clip teeth. Ideally, use thermocautery. Tail stumps can be dipped or sprayed with iodine immediately after docking.
Navels - Navels should be dipped in iodine at birth.
Use of dry disinfectants in the farrowing pens can help but are not a substitute for a failure to wash and disinfect or to keep the pen clear of sow faeces. Do not allow sows to spend more than 5 days in the farrowing crate before farrowing.
Where tonsillar penetration is suspected, and in particular with Strep suis 14 infection, prevention can be achieved by:-
a) Routine treatment of piglets at birth with long acting penicillin or amoxycillin.
b) Treatment of the sows in the farrowing area with appropriate antibiotics, either by inclusion in the feed or by top dressing onto the feed.

Lameness
Lameness is a common cause for culling sows second only to reproductive failure. Cases can occur at any time during the dry period or in lactation. Increased unplanned culling for lameness increases the non productive sow days so reducing the litters per sow per year. Often problems involve first parity or second parity animals before they have reached the most productive part of their life. Sows culled for severe lameness have to be shot on the farm because they should not be transported.
Lameness is prevalent in growing pigs with levels ranging from 1 to 5%. If more than 2% of pigs are recorded lame per month further investigations are necessary.

Lameness can account for significant losses in growing pigs either because the pigs are unfit to travel on welfare grounds and require to be destroyed, or they are part or totally condemned at slaughter. Early identification of lame animals and their removal to hospital pens for treatment is a vital part of the control and healing process.

Symptoms
Sows
Pig off food.
Sometimes fever.
Reluctance to stand.
Swollen joints / Fractures.
Evidence of other diseases.
Loss of balance.
Arthritis.
Dog sitting position.
Not accept boar at mating.
Pig shows pain / discomfort.
Piglets
As for sows.
Shivering.
Weaners & Growers
Pig may be off food.
Sometimes fever.
Reluctance to stand. Difficulty moving.
Swollen joints / Fractures.
Evidence of other diseases.
Causes / Contributing factors
The common ones *
Arthritis caused by bacteria. *
Back muscle necrosis - a stress related disease.
Bursitis.
Bush foot. *
Cuts or breaks in the skin related to sharp projections.
Damage to nerves.
Erysipelas. *
Fighting.
Foot-and-mouth disease and swine vesicular disease in those countries where they occur.
Fractures. *
Gl?ssers disease.
Haematomas.
High stocking densities.
Laminitis (inflammation of the tissues attaching to the hoof).
Leg weakness or Osteochondrosis. *
Mycoplasma arthritis. *
Myositis (inflammation of muscles).
Nutritional deficiencies.
Osteitis (inflammation of bone).
Osteochondrosis (degeneration of bone growth plate and cartilage).
Osteomalacia (softening of bone, calcium and phosphorus deficiency).
Osteomyelitis (inflammation of bone and bone marrow).
Osteoporosis (weak bones, imbalance of calcium and phosphorus).
Penetrated sole.
Periostitis (inflammation of the membrane around bone).
Poor floor surfaces. *
Porcine stress syndrome associated with the halothane gene.
Separation of the head of the femur.
Separation of the muscle from the pelvis.
Split horn (poor hoof quality).
Tail biting (see vice - abnormal behaviour). *
Torn muscle and/or ligament. *
Trauma. * (Stocking density and mixing are the two major factors that precipitate traumatic disease).
Diagnosis
This is based on the clinical signs.
Further Reading

Laminitis
Inflammation of the soft highly vascular sensitive tissues that connect the bone to the hoof. It is an uncommon but very painful condition causing animals to walk on their knees.
Symptoms
Piglets, Weaners & Growers
N/A
Sows
Animals walking on their knees. Reluctant to stand.
Lameness.
Pain over hooves.
Causes / Contributing factors
The cause is unknown.
Diagnosis
This is based on the clinical signs.

Leg Weakness
"Leg weakness" is an imprecise term used to describe different forms of lameness. For example, it is sometimes used to describe poor leg conformation. More often it is used to describe a clinical condition associated with degeneration of the bone and cartilage, called osteochondrosis (OCD).
Changes in the cartilage that lead to clinical OCD take place in most modern pigs from as early as two months of age. The severity and its effect depend largely on the environment and the speed of growth of the animal. OCD in modern pigs 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.

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.

Leg deformities are common in the rapidly growing pig but are usually of no commercial consequence. Separation of the head of the femur at the growth plate however occurs in rapidly growing pigs on some farms.

Symptoms
Piglets
None.
Sows

In acute cases of OCD:
There is separation of the bones at the growth plate resulting from sudden movement.
The animal walks on three legs, the affected leg swinging freely.
Crepitus, the rubbing of the broken bones together, can usually be felt.
Fractures in the spine can also 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.
Nervous signs.
In chronic cases of OCD, the onset is gradual.
The sow shows abnormal leg conformation and gait with or without stiffness and pain.
The temperature and affected joints remain normal.
The front legs may be straight, the pig walking with a long step on its toes, or the knees may be bent inwards or flexed, the pig walking with short steps. In some old sows, the pasterns may be dropped. The feet may be rotated or twisted.
The hind legs are often straight, the pig walking with a swinging action from the hips. In some cases the legs are tucked beneath the body. The hocks are turned inwards and are close together. The pig walks with a goose stepping action. Again in old sows the pasterns may be dropped.
Weaners & Growers
Acute cases are characterised by the sudden onset of acute lameness, highlighted by poor conformation of legs, bending of bones and dropped pasterns.
The pig refuses to put the foot to the floor.
Fractures in the hip, knee and shoulder joints. Evident at slaughter or post mortem.
Long-term the joint changes may lead to arthritis.
Causes / Contributing factors
Environmental factors that cause the foot to slip on the floor.
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, causing repeated pressure on the growth plates.
Full confinement of pregnant gilts when they are still growing can be a major contributing factor.
Are the gilts mixed with sows at weaning? The modern hybrid gilt often suckles produces large litters and large amounts of milk which depletes her body calcium and phosphorous. The bones become weak and are therefore more prone to injury.
High levels of vitamin A (in excess of 20,000 iu/kg) particularly in the younger growing pigs can interfere with the normal development of the growth plates.
High stocking densities increase the incidence, particularly in the growing period and where animals are housed on solid concrete floors or slats.
Trauma.
Rapid weight gain.
Diagnosis
This is based on the clinical signs. There are no laboratory tests and post-mortem examinations may be misleading because many pigs that were not lame before death may be found to have lesions.
OCD has to be distinguished from Mycoplasma hyosynoviae and erysipelas arthritis.

Leptospirosis
Leptospira are long slender spiral-shaped bacteria, found in most mammalian host species. Over 160 serotypes are known, generally called serovars, with cross infections occurring between some host species. Each serotype has one or more (usually only two or three) reservoir hosts which multiply it up and maintain it. A serotype can remain as a life-long infection in its reservoir host.
The pig is a reservoir host for Leptospira pomona, L. tarassovi, L. bratislava and L. muenchen, the last two being very closely related. It is not a reservoir host for L. icterohaemorrhagiae but it can be infected from rats urine and become ill. It can also become infected by other serotypes from other animals urine, for example L. canicola from dogs and L. hardjo from cattle but the infections are subclinical and do not result in disease. The pig is then an incidental host i.e. does not perpetuate the infection and is only responsible for minimal spread.

L. pomona causes important reproductive problems in female breeding pigs spreading slowly through the herd. It remains in the herd permanently unless steps are taken to eradicate it. It is not in the UK or Ireland and seems to have disappeared from Western Europe but is widespread throughout the rest of the pig rearing world. In America the skunk is an alternative reservoir host.

L. tarassovi causes a similar syndrome (i.e. a collection of signs and lesions) to L. pomona but tends to be milder and to spread more slowly. It is found in Eastern Europe and the Antipodes. It is thought that some wild animals are also reservoir hosts.

The pig is also a reservoir host for certain subtypes of L. bratislava and L. muenchen which are widespread throughout the pigs of the world. They cause a different syndrome to L. pomona and L. tarassovi and affect mainly pregnant gilts and second litter females because they will not previously have encountered it.

Once these organisms are introduced into a herd the pigs become permanent carriers with infection of the kidneys and intermittent excretion of the organism into the urine. L. bratislava/muenchen also permanently inhabit the fallopian tube of sows and the reproductive organs of boars and they are spread in semen.

Disease is uncommon in the sucking pig and would only infect individuals.

Growing pigs are occasionally exposed to Leptospira icterohaemorrhagiae from the urine of rats.

Remember that this disease can be transmitted to people.

Symptoms
Piglets
Uncommon.
Illness.
Inappetence.
Jaundice.
Blood in urine.
Severely infected pigs die.
Sows In acute outbreaks:
Inappetence.
Fever.
Depression may be observed.
Chronic low grade disease is more common with:
Abortions.
Stillbirths.
Increase in poor, non-viable pigs.
If abortions in a herd are more than 1% then investigations for leptospirosis should be considered. A reduction in farrowing rates and numbers of live pigs born per sow is also an associated factor particularly with L. bratislava infection.
Signs associated with acute L. bratislava disease:

Repeat breeders are common particularly in first and to some extent second pregnancy gilts.
This often follows embryo loss and there may be copious vaginal discharges.
Late term abortions.
An increase in premature piglets.
An increase in stillbirths.
Mixed litters of live poor pigs and dead piglets at birth.
An increase in mummified pigs.
An increase in repeat breeding animals.
Often there is a two year cycle of disease.
Reproductive failure occurs in second litter females, rather than gilts following their introduction to older carrier boars.
Disease is less common in older animals.
In long standing carrier herds disease can be difficult to recognise.
Weaners & Growers
Acute jaundice.
Haemorrhage.
Rapid death.
Pale pigs.
Causes / Contributing factors
Introduction of infected gilts and boars.
The presence of PRRS in the herd.
AI
Infection brought into the herd by other animals; rats, mice and dogs can be reservoirs of infection.
Exposure of the herd to indirect sources of contamination, e.g.: contaminated water, poor floor surfaces allow urine to pool. Spread in urine.
Diagnosis
This is difficult but the following will help:

Records. Study the levels of abortions, repeats, stillbirths, week piglets and the age of occurrence in sows and gilts.

Study the clinical picture.

Blood sample suspicious animals and repeat 2-3 weeks later. Look for rising antibody titres e.g. 1st sample result 1:100, 2nd result 1:800. This would confirm active infection and indicate probable involvement.

Blood sample ten females that have a history of infertility.

In chronic disease however, the significance of titre levels are very difficult to assess.

Test the aborted foetuses, urine or kidneys and fallopian tubes of slaughtered gilts.

Eliminate other diseases - Chronic PRRS, endometritis.

Eliminate non infectious causes of infertility - Summer infertility, management failures.

The symptoms of leptospirosis can be mistaken for other causes of infertility.

Listeriosis
This is caused by the bacterium Listeria monocytogenes which may colonise the tonsils and be passed out in faeces. Listeria are wide spread in nature and are often found in cheese and silage. Exposure results in infection but disease is uncommon.

Symptoms
Sows
None.
Piglets, Weaners & Growers
The bacterium may cause a septicaemia and high temperature in piglets.
Nervous signs possibly meningitis.
Weak piglets at birth.
Pneumonia.
Head on one side.
Middle ear infections.
Causes / Contributing factors
Stress causing the bacteria to invade the system.
PRRS or Flu.
Heavy environmental exposure
Diagnosis
Laboratory examinations are necessary.
Treatment
Listeria are usually sensitive to penicillin and ampicillin
In outbreaks it is necessary to identify the sources of infection and reduce the exposure to them.

Lymphosarcoma
This is a tumour affecting all the lymph glands throughout the body but particularly those of the intestines and lungs. The condition is very occasionally seen in the Large White where a hereditary component is thought to be involved.
Reported levels of lymphosarcoma found at slaughter are extremely low (0.002%).

Symptoms
Piglets
N/A
Sows, Weaners & Growers
These are usually seen in young growing pigs.
Pale skin.
Sometimes slightly jaundiced.
Loss of weight.
Pot bellied appearance - abdomen distended.
Enlarged glands may be seen in the neck.
Most pigs die within 4-5 months.
Causes / Contributing factors
Unknown but thought to be associated with a virus and genetic predisposition.
Diagnosis
This is based on clinical tests confirmed by post mortem examinations.
Treatment
None - Destroy affected pigs

M-Hyo (Mycoplasma Hyopneumoniae) Infection
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M+Pac®
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RESPISURE-ONE®
Porcilis M Hyo
Enzootic pneumonia is caused by Mycoplasma hyopneumoniae. It is widespread in pig populations and endemic in most herds throughout the world. As an uncomplicated infection in well-housed and well-managed pigs it is relatively unimportant and has only a mild effect on the pig. However if there are other infections present particularly App, Hps, Pasteurella, PRRS or SI, the pneumonia can become more complex with serious effects on the pig.
EP always attacks the lower areas of each lung lobe causing consolidation. The extent of this consolidation in each lobe is scored out of either 5 or 10 depending upon the lobe affected. Thus a severely affected pig with all lobes involved would score 55. This scoring system can be used to assess the severity of disease and its effects on the pig.

If more than 15% of lungs are affected it is highly probable that EP is present in the population. Herds that do not carry M. hyopneumoniae rarely show consolidated lesions in more than 1 % and even then they are very small.

If EP is not present in the growing population then the effects of the other respiratory pathogens are greatly reduced. It is therefore considered a primary pathogen that opens up the lung to other infections.

Clinical signs of enzootic pneumonia only occur in the lactating sow and piglets when the disease has been introduced into a fully susceptible herd for the first time. The breakdown of disease usually takes place over 6 to 8 weeks with sows coming into the farrowing house continuing to be affected.

There is a widely held but erroneous belief that sows and gilts will become carriers and pass this infection to their next litters. They may do so early on and their piglets may cough but by the time they farrow again 4 to 5 months later they will have eliminated the infection and will provide a solid immunity to their piglets via colostrum. If weaning is at 3 to 4 weeks, subsequent litters are not likely to become infected until after weaning.



 
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Symptoms
All pigs
It usually has an incubation period of two to eight weeks before clinical signs are seen but may be longer. Acute disease is normally only seen in new break-downs of disease.

Over the first six to eight weeks after it enters there may be: (This picture however is extremely variable).

Severe acute pneumonia.
Dehydration.
Heavy breathing.
Coughing, prolonged.
Respiratory distress.
Fever.
High mortality across all ages of stock.
Chronic disease is the normal picture when the organism has been present in the herd for some considerable time.
Maternal antibody is passed via colostrum to the piglets. It disappears from seven to twelve weeks of age after which clinical signs start to appear including:
A prolonged non-productive cough, at least seven to eight coughs per episode, is a common sign around this time, with some pigs breathing heavily ("thumps").
30 to 70% of pigs will have lung lesions at slaughter.
Causes / Contributing factors
It is commonly transmitted through the movement of carrier pigs.
Wind-borne infection for up to 3km (2 miles) if the climatic conditions are right. The organism dies quickly outside the pig, particularly when dried.
Incoming pigs.
Increased clinical disease is associated with the following;
Overcrowding and large group sizes.
Less than 3 cu.m.air space per pig and 0.7 sq.m. floor space per pig.
Houses that are too wide for good air flow control.
Variable temperatures and poor insulation.
Variable wind speeds and chilling.
Low temperature, low humidity environments.
High levels of carbon dioxide and ammonia.
High dust and bacteria levels in the air.
Pig movement, stress and mixing.
Housing with a continuous throughput of pigs.
Other concurrent diseases particularly PRRS, App, flu, and aujeszky's disease.
Poor nutrition and dietary changes at susceptible times.
Diagnosis
This is based on the clinical picture and examination of the lungs at post-mortem examination or at slaughter, combined sometimes with histology of the lesions. However, these do not provide a specific diagnosis and in the herds supplying breeding stock or in special cases (e.g. litigation) it may be necessary to confirm the diagnosis by carrying out one or more of the following tests: Serological (ELISA) tests, microscopic examination of stained touch preparations (TPs) of the cut surface of the lungs, fluorescent antibody tests (FATs), polymerase chain reaction (PCRs) tests and finally culture and identification of Mycoplasma hyopneumoniae.
These tests are becoming more widely available and some diagnostic laboratories cannot do them. The PCR is probably the most sensitive. FAT, serology and cultures are used in Denmark, but only FATs are available in many laboratories.

EP must be differentiated from Flu, PRRS, Hps and other mycoplasma infections. Laboratory tests are required to differentiate them. Furthermore, all or some of these may occur as mixed infections together with Mycoplasma hyopneumoniae.

Mammary Hypoplasia, Undeveloped Udder
This term defines failure of udder development and is relatively uncommon.

It can occasionally be seen in gilts because the hormones that are responsible for the development of the udder have not been produced in sufficient quantity. Such animals should be culled.

Occasionally herd problems are seen where poor nutrition, heavy worm burdens, chronic disease or mycotoxins may be implicated. The most likely mycotoxin to cause it is from ERGOT poisoning in pregnant gilts running in grass paddocks. Shortage of water is a common cause.

Rarely, hypoplasia may be due to a genetic mutation in the affected gilts ancestors.

Mange Mites, Sarcoptes Scabiei
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IVOMEC Injection
IVOMEC Premix
The IVOMEC HM/LE Program


Acute mange: The skin is covered by minute red pimples.
Mange is a parasitic disease of the skin caused by one of two mites either Sarcoptes scabiei or Demodex phylloides. Sarcoptic mange (sometimes called scabies) is by far the most common and important because it is irritant and uncomfortable for the pig, causing it to rub and damage the skin which becomes unsightly. It significantly depresses growth rate and feed efficiency. The life cycle is direct and takes 14-15 days from adult to adult to complete. The mite dies out quickly away from the pig, under most farm conditions, in less than five days. This is an important factor in control. If a herd is free from mange, it is one of the easiest of diseases to keep out because it can only be introduced by carrier pigs. However, once it is introduced it tends to become permanently endemic unless control measures are taken.

 
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Symptoms
Piglets
Skin irritation after 7 days.
Sows

In acute disease:
Ear shaking.
Severe rubbing of the skin against the sides of the pen causing reddening. Approximately three to eight weeks after initial infection the skin may become sensitised to the mite protein. A severe allergy may develop in some pigs with very tiny red pimples covering the whole of the skin.
Intense irritation and rubbing to the point where bleeding may occur.
In chronic disease:
Thick asbestos-like lesions on the ear, along the sides of the neck, the elbows, the front parts of the hocks and along the top of the neck.
Weaners & Growers
Its presence affects food conversion and daily gain, particularly if the weight of infection is heavy.
Tiny red pimples over the skin.
Irritation and rubbing/scratching.
Ear shaking.
Chronic condition - Thick asbestos like scabs, mainly on the ears, often with slight bleeding and constant rubbing.
Poor growth.
Causes / Contributing factors
The mite spreads directly from pig to pig, either by close skin contact or contact with recently contaminated surfaces.
The boar helps to maintain infection in the herd because he is constantly in direct skin contact with breeding females and he remains a chronic carrier.
If pigs are housed in groups there is increased opportunity for spread.
Newly purchased pigs.
Disease is more easily spread where sows are group housed.
Continually housed pens.
Diagnosis
This is confirmed by demonstrating the presence of the mite. Scrapings are taken from suspicious lesions on the skin and particularly inside the ears. A teaspoon is an ideal instrument to scarify material from the interior of the ear. This material can be spread onto a piece of black paper and left for ten minutes. Mange mites which are rounded in shape and only 0.5mm in length may be just visible to the naked eye. However to positively identify the mite the scrapings should be submitted to a laboratory for microscopic examination. An ELISA blood test is also available.

Mastitis
Mastitis in one or more mammary glands is caused by a variety of bacteria or it may be secondary to other diseases. It is a common condition that occurs sporadically in individual sows or sometimes as herd outbreaks. It starts around farrowing and becomes clinically evident up to 12 hours later. It can arise because bacteria have gained entry to one or more mammary glands for the first time, or it may be a flare-up of a long-standing sub-clinical latent infection. The route of entry of the bacteria is probably the teat orifice but it may be from the blood stream or by injection on piglets' teeth. It also commonly occurs at weaning time.
The bacteria that cause mastitis in the sow can be grouped into three broad categories: coliform bacteria, staphylococci and streptococci, and miscellaneous bacteria.

Coliform mastitis - Coliform bacteria are related to E. coli, the commonest being E. coli itself and klebsiella. They produce a severe acute mastitis which results in reduced milk yield, a very ill sow and poor "doing" piglets. Marked discoloration of the skin over the udder and dark blueing of surrounding skin, ears and tail is a feature.

Herd problems can develop because the organisms are present in faeces and may also be in sows' urine. Consequently, they may be everywhere in a piggery. Coliform mastitis may thus be regarded as environmental in origin.

Staphylococcal and streptococcal mastitis - These are usually less acute and less severe than coliform mastitis. They tend to occur sporadically in individual sows in one or more glands and usually do not make the sow ill. The exception is an acute severe staphylococcal infection usually in a single gland which becomes swollen, hard and discoloured and makes the sow toxic.

Unlike coliform bacteria the source of these organisms is not usually the contaminated environment but the skin and possibly orifices of the sow herself. There is some evidence to suggest that as in the dairy cow and sheep some of these bacteria may persist sub-clinically in the udder and then flare up at or after farrowing

Miscellaneous bacteria - These include organisms such as pseudomonas which can produce a serious mastitis and toxaemia and which are often resistant to antibiotic treatment. Fortunately such infections are rare.

Symptoms
Piglets
Hungry.
Thin.
Squealing due to lack of milk.
Sows
Acute disease

Inappetence at farrowing or before if mastitis is already developing.
Obviously ill will not suckle.
Fever.
Mucous membrane of her eyes are brick red.
Affected glands swollen, red colour and painful.
Discoloration of the ears and the whole of the udder, but particularly over the affected glands.
Blue skin.
Chronic disease (Usually seen in dry sows):
Mammary tissue is infiltrated with hard lumps that are usually not painful when palpated.
They may ulcerate to the surface and become a potential source of infection to other sows.
Weaners & Growers
N/A
Causes / Contributing factors
The continual use of farrowing houses.
Poor farrowing pen hygiene, bad drainage, inadequate and poor quality bedding.
The use of saw dust or shavings for bedding that become soaked in water or urine.
A warm temperature for the organisms to multiply.
Worn pitted farrowing house floors.
Wet farrowing house floors.
Contaminated drinking water.
Adverse temperatures, draughts and poor ventilation in the farrowing houses.
A build up of faeces behind the sows.
Klebsiella in the water system.
Diagnosis
The clinical signs are usually sufficient to diagnose mastitis. However if there is a herd problem with a number of sows affected, you should examine all animals clinically at farrowing and again at weaning, to determine the starting point of the mastitis. A sample of the secretions from the infected quarters should be submitted to a laboratory for examination. This is carried out by wiping the teat end with cotton wool soaked in surgical spirit, injecting the sow with 0.5ml of oxytocin and once there is a good flow squirt the milk on to a sterile swab. The swab should be immersed in a transport medium. It is very important that mastitis is diagnosed early and that prompt treatment is given.

Meningitis
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SS Pac®
See also streptococcal infections
Meningitis is uncommon in the sow but it is sometimes secondary to middle ear infection. If an infectious disease enters a herd for the first time sporadic cases in sows may be seen. Meningitis is seen in the sucking pigs and weaners associated with streptococcal infections. See Streptococcal meningitis.

Symptoms
Piglets, Weaners & Growers
Shivering.
Pigs show pain / discomfort.
Hair raised.
Grinding teeth
Lateral movement of eyes (nystagmus).
Fits and convulsions.
On side paddling.
Sows (unusual)
The sow is off feed.
Trembling with an unsteady gate.
The temperature is elevated, often as high as 42?C (108?F).
As the meningitis develops:
The eye moves sideways.
Fits occur and the sow cannot stand.
The head may be on one side.
Causes / Contributing factors
Middle ear infection.
Specific bacteria e.g. streptococci, Haemophilus parasuis.
Aujeszky's disease.
Poisons.
Poor environments in nurseries.
Diagnosis
This is based upon the signs in an individual sow, or if there are a number of cases, a specific infectious disease. It may require a post-mortem examination, including histology of the brain and culture of the causal organism to confirm the diagnosis.

Meningitis must be differentiated from the following:-

- Acute kidney infection.
- Aujeszky's disease (AD) (PR).
- Brain abscess.
- Heat stroke.
- Middle ear infection.
- Poisons.
- Water deprivation (salt poisoning).

Metritis
Metritis is inflammation of the womb caused by bacterial infection. It is fairly common in the immediate post-farrowing period.
After farrowing the womb contracts and squeezes mucus, white fluid and afterbirth out through the vagina. This discharge can continue for up to 4 days and is normal. If the sow is eating well, has a normal temperature and no mastitis ignore it. However abnormal discharges can also indicate the presence of infection requiring treatment.

Symptoms
Piglets
Starvation - no milk.
Lactating Sows only
Temperature.
Sow is off her food and toxic
Signs of mastitis.
Bright red mucous membranes around the eyes.
Discharge from vulva - white or brown colour.
No milk.
Dry Sows
Discharge from the vulva.
Sow normal in health.
Regular, irregular returns.
Not in pig.
Weaners & Growers
N/A
Causes / Contributing factors
Prolonged farrowings.
Manual assistance during farrowing.
In association with mastitis.
Refuses to suckle.
Diagnosis
This is based on the clinical signs.

Middle Ear Infections
This is caused by a variety of bacteria, that gain access to the middle part of the ear which is responsible for balance. Infection probably arises from the tonsils at the back of the throat and travels down the eustachian tube to the middle part of the ear. The common organisms involved include; Haemophilus parasuis, streptococci, and staphylococci.
The condition is sporadic but common particularly in the weaned pig and sow and occurs occasionally in the sucking pig from 7 to 10 days of age. If treatment is prompt there is usually a good response. If treatment is delayed there is the risk that infection will spread from the middle ear into the inner ear and inwards to cause meningitis

Symptoms
All Pigs
The pig stands with its head to one side often shaking.
As the disease progresses there is a gradual loss of co-ordination until ultimately the pig walks around in a circle eventually falling over.
Jerky eye movements may be evident.
Nervous signs i.e. fits, convulsions and meningitis may result.
Unusual in young piglets.
Causes / Contributing factors
Disease may result from:
Mange.
Skin trauma.
Vice - Abnormal behaviour.
Fighting.
Greasy pig disease.
Joint infections.
PRRS infection.
Diagnosis
Based on clinical signs. Bacteriological examinations should be carried out if many pigs are involved.

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.

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.

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.

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.

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.

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

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.

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.

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.

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

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.

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.

Pasteurellosis (Pasteurella multocidia)
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Porcilis Cobactan 2.5%
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.

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

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.

Pneumonia
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Pneumonia is normally uncommon in mature acclimatised animals (unless exposed to a new organism), it occasionally it occurs in gilts but is very common in the growing animal. Mortality in naive animals can be as high as 10 to 15% (no immunity) if prompt treatment is not undertaken.
The onset of swine influenza is usually sudden and affects most pigs. The onset of enzootic pneumonia in a naive herd may be insidious although it may later develop rapidly affecting many sows severely. There is likely to be severe pneumonia and some mortality if the disease is not controlled in herds infected for the first time.

Of all the diseases that affect growing and finishing pigs, chronic respiratory disease is the most economically important. It is extremely common and can be difficult to prevent and control. Growth rates and feed-intake are depressed together with poor feed efficiency and in some herds there is heavy mortality. The control of respiratory disease requires an understanding of the complexities and interaction between the organisms that are present, the pig and the management of the environment.

Pneumonia is affected by:

The presence of respiratory pathogenic organisms.
The virulence of the pathogens present.
The level of the pathogens in the house environment.
The immunity of the pig and the time of exposure to the organisms
The presence of secondary opportunistic bacteria.
The interactions between management, environment, the diseases and the pig.
Symptoms
Weaners & Growers
Coughing.
Rapid breathing.
Dehydration.
Inappetence.
Discharges from the eyes - conjunctivitis.
Poor circulation.
Blue discoloration of the skin.
Loss of condition.
Huddling.
Fever.
Sows
Widespread coughing.
Some sows obviously very ill.
Respiratory rate is elevated, some showing acute respiratory distress.
Piglets
Coughing.
Heavy breathing.
Loss of condition.
Dehydration.
Causes / Contributing factors
If pathogens such as influenza, PRRS virus, Mycoplasma hyopneumoniae or a virulent strain of Actinobacillus pleuropneumoniae enter a susceptible herd for the first time dramatic outbreaks may occur in sows.
Poor environments.
Incorrect ventilation and humidity.
High stocking densities.
Diseases are commonly transmitted through the movement of carrier pigs.
Incoming pigs.
Increased clinical disease is associated with the following;
Overcrowding and large group sizes.
Less than 3 cu.m. air space/pig and 0.7 sq.m. floor space/ pig.
Houses that are too wide for good air flow control.
Variable temperatures and poor insulation.
Variable wind speeds and chilling.
Low temperature, low humidity environments.
High levels of carbon dioxide and ammonia.
High dust and bacteria levels in the air.
Pig movement, stress and mixing.
Housing with a continuous throughput of pigs.
A combination of diseases, particularly PRRS, App, flu, and aujeszky's.
Poor nutrition and dietary changes at susceptible times.
Diagnosis
This is based on the clinical signs and post-mortem examinations. Laboratory tests involving serology and microbiology are often necessary to identify the precise causes. See also the specific respiratory diseases.

Porcine Cytomegalovirus Infection (PCMV)
This is a herpes virus found in the tissues throughout the body including the nose of newborn piglets where it causes inflammation (rhinitis). PCMV is present throughout the world and exists in most if not all pig populations but most infections are sub-clinical and clinical disease is rare. Serology carried out in the UK, for example, indicates that over 90% of herds have been exposed to infection.
The rhinitis produced by this virus is uncommon and occurs mainly in newborn pigs and has no relationship to atrophic rhinitis caused by the toxin-producing bacteria Pasteurella multocidia. In most herds therefore the infection is insignificant and apart from sometimes causing a mild sneeze has no major effect on the health of the pig.

Symptoms
Piglets / Weaners only
Rhinitis in newborn piglets can be severe enough to cause haemorrhage from the nose if sows are naive which would be very rare.
In herds in which PCMV is endemic there are no symptoms other than mild sneezing in sucking and weaned piglets.
Possibly fever.
Growers
N/A
Sows
Clinical signs are rare and only seen if PCMV infects a sow for the first time when she is late in pregnancy.
Foetal deaths.
Mummified foetuses.
Stillbirths.
Weak piglets.
A slight fever.
Inappetence.
Nasal haemorrhage.
Causes / Contributing factors
The virus is shed in discharges from the nose and eyes, urine and farrowing fluids.
It is also transmitted via the boar through semen and crosses the placenta to infect piglets before birth.
Poor environmental conditions.
Fluctuating temperatures may predispose.
Dust.
Continually populated houses.
Diagnosis
This can be confirmed by serological tests, fluorescent antibody tests and demonstration of inclusion bodies in tissue sections.
The disease might be confused with atrophic rhinitis or bordetella infection of the nose, however the effects are very short lived and there is no progressive atrophy or distortion of the nose.

PCMV rhinitis only occurs in newborn piglets and there is a tendency to assume that sneezing in piglets must be associated with atrophic rhinitis. Rhinitis means inflammation of the delicate tissues in the nose and is caused by dust, gases, bacteria or viruses, in fact any irritant. If toxin producing pasteurella are present the inflammation persists with damage and progressive destruction of the tissues (atrophy). This is a serious disease. It can be differentiated from PCMV by swabbing the noses of sneezing piglets and testing for the presence or absence of the pasteurella. It is important to carry this out because if the tests are negative you have no worries (or expensive treatments).

Porcine Dermatitis and Nephropathy Syndrome (PDNS)
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This disease will be regularly updated as our knowledge base increases.
This disease is not new and has been recognised in most pig producing countries as a minor sporadic condition. In recent years bigger more severe outbreaks have occurred particularly in parts of Europe.

PDNS occurs mainly in growers and finishers but rarely in other age groups.

Clinical signs may occur in a herd in a few pigs sporadically and the disease may then go undiagnosed or they may occur in a bigger proportion of pigs and be economically damaging.

Mortality in affected pigs may be around 15%, death occurring within a few days of onset but mortality can rise much higher.

Pigs that recover are often permanently unthrifty.

Symptoms
Weaners & Growers
Appearance of extensive greasy brown, purplish red slightly raised blotches of various sizes and shapes over the chest, abdomen, thighs and forelegs. The majority of pigs that develop extensive skin blotching die.
Over time the blotches become covered with dark infected crusts (dermatitis) and then fade leaving scars.
The pigs are depressed.
May have a fever.
They are usually reluctant to move.
Lose weight
Sometimes breath heavily.
Mortality high.
Loss appetite.
Piglets & Sows
Rare
Causes / Contributing factors
The cause is unknown.
It is not known how the disease spreads between pigs or between herds or what triggers off a clinical outbreak. However sources of incoming pigs must come from herds with no history of disease.
Diagnosis
The clinical signs are strongly suggestive but not diagnostic. Gross and microscopic post mortem examinations are needed to make a firm diagnosis. At gross post mortem examination lymph nodes, particularly those at the rear of the abdomen which are not usually examined, are reddened and enlarged and there is often fluid in the abdomen. The most consistent lesions are in the kidneys which are swollen, pale and mottled with many small haemorrhages showing through the surface. Tests can be done for high urea and creatinine levels in the blood which indicates severe kidney damage. These tests may be negative if the kidneys are less severely affected. Microscopically, the lesions in the blood vessel walls are distinctive. Since the cause is unknown there are no specific diagnostic tests.


Similar diseases
Classical swine fever (CSF), (Hog cholera), or African swine fever (ASF). Other diseases which might be confused with PDNS include erysipelas and Actinobacillus suis. Other kidney conditions may also be confused with PDNS.

Porcine Enteropathy
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This comprises a group of conditions involving pathological changes in the small intestine associated with the bacterium Lawsonia intracellularis. This exists on most if not all farms. Disease takes four different forms: porcine intestinal adenopathy (PIA) an abnormal proliferation of the cells that line the intestines; necrotic enteritis (NE) where the proliferated cells of the small intestine die and slough off with a gross thickening of the small intestine (hosepipe gut); regional ileitis (RI), inflammation of the terminal part of the small intestine and proliferative haemorrhagic enteropathy (PHE). In the latter there is massive bleeding into the small intestine, hence the common name bloody gut and this is the commonest form in growing pigs. The other three forms are rarer and progress from PIA. PHE is more common in 60-90kg pigs and gilts.
All are uncommon in the mature female but outbreaks of one of the forms, bloody gut or porcine haemorrhagic enteropathy (PHE), are occasionally seen in maiden and pregnant gilts.

The organism is impossible to keep out of farms probably because it also infects other species. Infected faeces are the major vehicle for spread around the farm.

Symptoms
Weaners & Growers

Clinical signs of PIA, NE, RI are different from PHE.

PIA:
The pig appears clinically normal.
Initially eats well.
Chronic watery, sloppy diarrhoea.
Necrosis.
Gradual wasting.
Loss of condition.
In some cases a pot bellied bloated appearance.
Pigs with the chronic form of the PIA recover over a period of four to six weeks, however there can be considerable losses in feed efficiency and daily gain of up to 0.3 and 80g/day respectively. As a consequence there can be marked variations in sizes of pigs.
NI or RI follow from it with similar signs.
PHE is an acute disease:
Bloody scour.
The pig may die suddenly.
Appears very pale and passes black bloody faeces.
Anaemic.
Sows
Gilts with PHE have pale skins.
Appear weak.
Bloody or black tarry diarrhoea.
May suddenly die.
Abortions
Piglets
N/A
Causes / Contributing factors
These are not fully understood.
The use of continually populated pens.
Lack of all-in, all-out production.
Naive animals.
Change of environment.
Changes in feed.
Carry over of infection between batches appears to be a main means of spread.
Associated with continual population of finishing pens.
Diagnosis
This is based on the clinical picture, post-mortem examinations, histology of the gut wall and demonstrating the organism in faeces by an ELISA test. A serological test is also available. Only a few laboratories can do these tests. Tissue cultures have been recently developed.

Porcine Epidemic Diarrhoea (PED)
Porcine epidemic diarrhoea is caused by a coronavirus somewhat similar to that which causes TGE. This virus is widespread in Europe. The virus damages the villi in the gut thus reducing the absorptive surface, with loss of fluid and dehydration. After introduction of the virus into a susceptible breeding herd, a strong immunity develops over two to three weeks. The colostral immunity then protects the piglets. The virus usually disappears spontaneously from breeding herds particularly small ones (< 300 sows).
Acute outbreaks of diarrhoea occur when the virus is first introduced into a susceptible population. In such cases up to 100% of sows may be affected, showing a mild to very watery diarrhoea. Two clinical pictures are recognised: PED Type I only affects growing pigs whereas PED Type II affects all ages including sucking pigs and mature sows. The incubation period is approximately 2 days and diarrhoea lasts for 7 to 14 days. In sucking pigs the disease can be mild or severe with mortalities up to 40%.

In large breeding herds, particularly if kept extensively, not all the females may become infected first time round and there may be recrudescence. This only occurs in piglets suckling from sows with no maternal antibodies and is therefore sporadic.

Symptoms
Sows
This can vary from very mild "cow pat" faeces through to a watery diarrhoea.
Loose faeces.
Piglets
Diarrhoea.
Dehydration.
Mortality may be high.
Weaners & Growers
Acute watery diarrhoea with no blood or mucus.
Mortality is usually low but morbidity can be high.
When the virus is first introduced on to the farm there is a rapid spread of diarrhoea across all breeding and growing pigs with almost 100% morbidity (pigs affected) within 5 to 10 days. The incubation period is 2 to 4 days.
Vomiting.
Causes / Contributing factors
The immunological status of the herd i.e. no immunity.
Disease may be perpetuated as susceptible pigs enter the finishing herd.
Disease normally only seen when virus first enters the herd.
Diagnosis
This is based on the history, clinical signs and examination of faeces samples for evidence of porcine epidemic diarrhoea virus by ELISA tests or electron microscopy. Post-mortem examination of dead pigs and laboratory tests on the small intestine may be necessary to confirm the diagnosis.
PED must be differentiated from TGE by laboratory tests.

Porcine Parvovirus Infection (PPV)
Porcine Parvovirus Infection (PPV) is the most common and important cause of infectious infertility. Porcine parvovirus is a fairly tough virus that multiplies normally in the intestine of the pig without causing clinical signs. It is world-wide in its distribution. If you test for it in your pig herd it is almost certain it will be present unless your herd is less than 100 sows when it might have died out. It is therefore an infection you have to live with and manage. Whereas most viruses do not survive outside the host for any great period of time PPV is unusual in that it can persist outside the pig for many months and it is resistant to most disinfectants. This perhaps explains why it is so widespread and so difficult to remove from the pig environment.
Symptoms
Piglets
None normally.
Occasional low viable piglets are seen.
Increase in stillbirths associated with mummified piglets.
Sows
The virus has no effect on the female only on the foetus.
Small litters associated with embryo loss before 35 days.
Not in pig.
Mummified pigs of varying size, (30-160mm).
Increased numbers of stillbirths.
These are associated with the delay in the farrowing mechanism which occurs because of the presence of the mummified piglet.
Abortions associated with PPV infection are uncommon.
There may be an increase in low birth weight piglets but neonatal deaths are not affected.
The acute disease episode often lasts for up to 8 weeks then wanes for 4-6 weeks, followed by smaller bouts of mummified pigs for a further 4-6 weeks.
The virus can take up to 4 months to infect all sows in a susceptible previously uninfected herd.
Sporadic disease is seen in individual females which are infected for the first time. It is usually confined to gilts.
No other signs of ill health in the breeding female or in individual affected animals.
Weaners & Growers
N/A
Immunity
PPV infection results in high antibody levels in the serum which persist for long periods. You should appreciate that such levels do not necessarily mean that there is or has been a reproductive problem or a higher level of protection. For example, a titre of 1:2 will be equally as protective as a titre of 1:80,000. Blood sampling all the sows in a herd on one occasion only indicates the percentage of animals that have been exposed to parvovirus at some previous period which gives you an idea of the overall breeding herd immunity or susceptibility. Once an animal has been exposed to PPV it remains immune for the rest of its life.
Key points to parvovirus infection:

The virus is widespread throughout all pig populations but it may disappear in small herds (<100 sows).
Infection is endemic (present all the time) in most pig units.
Once a pig is exposed there is a lifelong immunity.
Reproductive problems may appear every 3-4 years in a herd if vaccination is not carried out.
Parvovirus infection in a susceptible female can cause death of the embryo with absorption or death of the foetus with mummification.
The major signs are therefore small litter sizes, mummified pigs of different sizes, and increases in pseudo-pregnancies and not-in-pigs.
Abortion due to PPV is uncommon.
Maternal immunity may persist up to 7 months of age but only in a few gilts. (This interferes with vaccine response).
Up to 50% of gilts may be sero-negative at point of mating.
Causes / Contributing factors
In small herds the virus may die out and sows become susceptible.
In large herds, pockets of naive breeding females, particularly gilts, can maintain the disease.
Failure of virus to circulate in the herd.
A naive herd often < 100 sows at risk.
Failure to vaccinate.
Faulty vaccination.
Incorrect storage of vaccine.
Virus may be in semen.
Diagnosis
In the absence of any other signs of illness in the breeding females, PPV disease can be suspected by increases in variable sized mummified pigs and small litter sizes.
The important features are disease and death in the embryo and foetus from approximately 15-70 days of pregnancy. The mummified pigs can be examined by fluorescent antibody test in the laboratory to confirm the infection. Serology will not help because many sows are positive and normal.

Porcine Reproductive & Respiratory Syndrome (PRRS)
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Porcilis PRRS
PROGRESSIS
PRRS is caused by a virus which was first isolated and classified as an arterivirus as recently as 1991. The disease syndrome had been first recognised in the USA in the mid 1980's and was called "mystery swine disease". It has also been called blue ear disease. The name porcine arterivirus has been proposed recently.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.

Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.

A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.

It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.

The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.

PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.



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Symptoms
Acute disease

When the virus first enters the breeding herd disease is seen in dry sows, lactating sows, sucking piglets and growers.

Sows

Clinical signs in dry sows during the first month of infection
Short periods of inappetence spreading over 7-14 days, 10-15% of sows at any one time.
The body temperature may be elevated to 39-40?C (103-105?F).
Abortions, often late term, may occur at a 1-6% level. These are often the first signs to be noted.
Transient discoloration (blueing) of the ears may be seen (2% level. Blue ear disease).
Some sows farrow slightly early. 10-15% over the first 4 weeks.
Increased returns occur 21-35 days post-service.
Prolonged anoestrus and delayed returns to heat post-weaning.
Coughing and respiratory signs.
Clinical signs in farrowing sows in the first month of infection
Inappetence over the farrowing period.
A reluctance to drink.
No milk (agalactia) and mastitis - significant symptoms.
Farrowings are often 2-3 days early.
Discoloration of the skin and pressure sores associated with small vesicles.
Lethargy.
Respiratory signs.
Mummified piglets. 10-15% may die in the last 3-4 weeks of pregnancy.
Stillbirth levels increase up to 30%.
Very weak piglets at birth.
The initial phase of inappetence and fever will often take 3-6 weeks to move through.
Cyanosis or blueing of the ears is a variable finding and less than 5% of sows show it. It is transient and may last for only a few hours.
Coughing occurs in some sows and a few individual cases of clinical pneumonia may occur.
This acute phase lasts in the herd for up to 6 weeks, and is characterised by early farrowings, increases in stillbirths, weak pigs and an increase in the numbers of large mummified pigs that have died in the last three weeks of pregnancy. In some herds, these may reach up to 30% of the total pigs born. Piglet mortality peaks at 70% in weeks 3 or 4 after the onset of symptoms and only returns to pre-infected levels after 8-12 weeks. The reproductive problems may persist for 4-8 months before returning to normal, however in some herds it may actually improve on the pre-PRRS performance.
Longer term effects of PRRS on reproductive efficiency are difficult to assess, particularly in herds of low health status. In some there are increases in repeat matings, vulval discharges and abortions, all of which may be blamed on PRRS.
The effects of PRRS on reproduction efficiency in herds in which the infection has become enzootic have been observed in the field for up to 12 months after disease has apparently settled.
These are as follows:
A 10-15% reduction in farrowing rate (90% of herds return to normality).
Reduced numbers born alive.
Increased stillbirths.
Poor reproduction in gilts.
Early farrowings.
Increased levels of abortion (2-3%).
Inappetence in sows at farrowing.
Piglets
More diarrhoea.
Less viable piglets.
Increase in respiratory infections such as gl?ssers disease.
Signs in boars
Inappetence.
Increased body temperature.
Lethargy.
Loss of libido.
Lowered fertility.
Poor litter sizes.
Lowered sperm output.
Weaners & Growers

When first introduced into an EP and App free growing herd there may be few signs:
A period of slight inappetence.
Mild coughing.
Hairy wasting pigs.
In some herds there are no symptoms.
If EP and/or virulent App are present but not under control in the herd:
An acute extensive consolidating pneumonia.
Formation of multiple abscesses.
Disease becomes evident within 1-3 weeks of weaning.
Pigs lose condition.
Diarrhoea may be seen.
Pale skin.
Mild coughing.
Sneezing.
Discharges from the eyes.
Increased respiratory rates.
Mortality during this period may reach 12-15%.
Once the acute period of disease has passed through PRRS virus normally only becomes of significance in the early growing period:
Severe pneumonia.
Periods of inappetence.
Wasting.
Pigs become infected as maternal antibody disappears and then remain viraemic for 3 to 4 weeks continually excreting virus. Clinical disease is seen in pigs 4 to 12 weeks of age:
Inappetence.
Malabsorption.
Wasting.
Coughing.
Pneumonia.
In this post-weaning period mortality can rise up to 12% or more and persist inspite of antibiotic treatments.
Secondary bacterial infections become evident in pigs at a later stage from 12 to 16 weeks of age:
Abscesses develop in the lungs and may spread throughout the body.
Lameness with abscesses.
Poor stunted growth.
Causes / Contributing factors
The following are common methods of spread and contribute to overall disease levels.
Droplet contamination from older pigs to younger pigs.
Nasal secretions, saliva, faeces and urine
Permanently populated houses maintain the virus at high levels, particularly in the first and second stage nurseries.
Movement of carrier pigs.
Airborne transmission up to 3km (2 miles).
Adult animals excrete virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
Mechanical means via faeces, dust, droplets and contaminated equipment, lorries etc.
Contaminated boots and clothing.
Vehicles especially in cold weather.
Artificial insemination but only if the boar is viraemic. This period is probably only 3-4 days.
The mallard duck and probably other species of bird.
Diagnosis
This is based on the clinical signs, post mortem examinations and the known presence of the virus in the herd or by serological examinations and isolation of the virus in a laboratory.
If the herd has not been exposed to PRRS then blood sampling and testing a minimum of 12 adult animals (preferably those that have been off their food at least three weeks) provides a reliable means of diagnosis.

Porcine Respiratory Corona Virus Infection (PRCV)
PRCV first appeared in pigs in Europe some ten years or more ago. It is related to but distinct from TGE virus, which is another corona virus. It is thought to spread between farms on wind and so it is extremely difficult to keep herds free from it. Infection often takes place in the sucking pig at 2 to 3 weeks of age but is not of importance. It may have an effect on lung tissue when other respiratory pathogens are present in chronic respiratory disease complexes.
Symptoms
Sows
Usually no symptoms.
In the presence of other respiratory agents coughing may be associated.
Piglets
A transient cough but no other signs.
Weaners & Growers
Herds exposed for the first time have few if any signs of disease.
A transient coughing lasting only a few hours.
Causes / Contributing factors
Field observations indicate the virus is spread for long distances on the wind.
PRCV is respiratory spread.
Diagnosis
PRCV does however cross react with the serological test for TGE and it therefore can confuse the diagnosis. A differential test is available but recently this has failed suggesting a new or different virus has appeared. In such infected herds respiratory disease is becoming evident particularly in the presence of PRRS virus.

Porcine Stress Syndrome (PSS)
This term covers a group of conditions associated with a recessive gene. The group includes acute stress and sudden death (malignant hyperthermia), pale soft exudative muscle (PSE), dark firm dry meat, and back muscle necrosis. Heavy muscled pigs are more likely to carry the gene than leaner pigs. The gene is called the halothane gene because of the adverse effect halothane anaesthetic has on pigs carrying it. Each pig is homozygous (i.e. possessing a pair of halothane genes), or heterozygous (i.e. possessing one normal gene and one halothane gene) or two normal genes. Homozygous pigs or their meat may show any of the four conditions.
Homozygous (but not heterozygous) pigs can be identified by their response to the anaesthetic with halothane. Recent developments have produced a gene probe that identifies both the homozygous and heterozygous carriers using only a drop of blood or a single hair. Back muscle necrosis is a more localised form of PSS.

When the homozygous state is present and following a period of muscle activity, there is a change in muscle metabolism from aerobic to anaerobic and biochemical abnormalities develop. The body tissues become acid with a marked rise in temperature 42?C (107?F).

Symptoms
Piglets
Rarely seen.
If so as in sows.
Sows
The onset is sudden with:-

Marked muscle tremors.
Twitching of the face.
Rapid respiration.
The skin becomes red and blotched.
Death usually occurs within 15-20 minutes.
Rigor mortis (stiffening of the muscles after death) within 5 minutes is a striking feature.
Rise in temperature > 41?C (106?F).
Weaners & Growers
The onset is sudden with muscle tremors.
Twitching of the face
Rapid respiration.
The skin becomes red and blotched.
Death usually occurs within 15-20 minutes.
Back muscle necrosis is a more localised form of PSS.
Whilst the gene produces a leaner carcass, growth rates are slower and the levels of sudden death increase.
Causes / Contributing factors
Disease is precipitated by sudden muscle activity.
The carrier pig is genetically susceptible.
Diagnosis
This is based on the sudden onset, symptoms, breed, susceptibility and the known presence or absence of the gene in the pig. In many cases the pig is just found dead and a post-mortem examination is necessary to eliminate other disease. Rigor mortis (stiffening of the muscles after death) within 5 minutes is a striking feature.
This condition has to be differentiated from other causes of sudden death, twisted bowel, internal haemorrhage, mulberry heart disease and pyelonephritis.

Post Weaning Multisystemic Wasting Syndrome (PMWS)
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This disease has during the past year or so become of significance and considerable concern in many countries particularly Canada, the US and Europe. It is manifest as the name implies by wasting in pigs from 6 weeks of age onwards.
The disease is associated in part with a porcine circovirus (PCV), so called because its DNA is in the form of a ring. It is extremely small and hardy. There are two serotypes, Type 1 causes no known disease. Type 2 can be found in the lesions and can be isolated in pure culture. There are several different strains (biotypes and genotypes). Antibodies to circovirus type 2 have been detected in pig sera collected in Belgium in 1985 but the clinical disease was not described until 1991 in Western Canada. It has since become widespread in North America and Europe.

Young experimentally inoculated colostrum deprived pigs given Type 2 alone sometimes, develop typical lesions. However, they are more likely to develop lesions if another virus, such as porcine parvovirus (PPV) or porcine reproductive and respiratory syndrome virus (PRRSV), is inoculated at the same time. Naturally occurring clinical cases in the field seem always to have a dual infection with PCV Type 2 and some other virus but most pigs which are infected with PCV and PRRS do not develop clinical PMWS.

Serum surveys in Europe and North America have shown that infection has spread widely through the pig population but only a small proportion of seropositve herds have a history of clinical disease. It seems that most infections are sub-clinical. It is not known why some infections result in disease. Piglets may become infected before weaning.



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Symptoms
Weaners & Growers
PMWS tends to be a slow and progressive disease with a high fatality rate in affected pigs.
Starting usually at about 6 - 8 weeks of age, weaned pigs lose weight and gradually become emaciated. Their hair becomes rough, their skins become pale and sometimes jaundiced.
Sudden death.
Enlarged peripheral lymph nodes.
May show diarrhoea.
May show respiratory distress caused by interstitial pneumonia.
Incoordination.
Post weaning mortality is likely to rise to 6 - 10% but is sometimes much higher.
Clinical cases may keep occurring in a herd over many months. They usually reach a peak after 6 - 12 months and then gradually decline.
Sows & Piglets
N/A
Causes / Contributing factors
Infected faeces.
Mechanical means via clothing, equipment, trucks etc.
Possibly birds and rodents.
Circovirus has also been detected in semen from apparently healthy boars.
It is not known what other ways the virus spreads between pigs or between herds.
Mixing and stress.
Continual production.
High stocking densities.
Diagnosis
Since most herds have antibodies to PCV, blood testing a herd usually does not help. The clinical signs are not specific and to make a diagnosis it is often necessary to post mortem several pigs. Diagnosis is based upon the presence of PCV type 2 histological lesions in lung, tonsil, spleen, liver and kidney tissues. Immunohistochemistry is used to demonstrate PCV in tissues. Probably many small mild outbreaks go undiagnosed. The gross post mortem lesions are variable. The carcass is emaciated and may be jaundiced. The spleen and many lymph nodes are usually very enlarged and the kidneys may be swollen with white spots visible from the surface. The lungs may be rubbery and mottled. Microscopically these lesions are characteristic and diagnostic particularly if the circovirus is demonstrated in them. If affected pigs are suspended by their back legs the inguinal lymph nodes appear enlarged often the size of large grapes.
Similar diseases
Many conditions, such as starvation, malnutrition, lack of water, gastric ulcers, enzootic pneumonia, coliform enteritis, swine dysentery, PRRS and other diseases, can cause similar signs. These all have to be eliminated if a specific diagnosis of PMWS is to be made. One disease deserves special mention here, porcine dermatitis and nephrosis syndrome (PDNS) because it sometimes occurs at the same time as PMWS or precedes it in a herd or follows it. The relationship between these two diseases is not known but each can occur in herds without the other being present.

Prepucial Ulceration
This is occasionally seen in outdoor boars and may become a problem in groups of boars. It appears to spread slowly.
Symptoms
Boars
The skin around the prepucial opening is red, inflamed and ulcerated and is clearly evident when the boar is still.
Blood may be seen on the skin and around the prepuce.
Causes / Contributing factors
The cause is unknown but it may be initiated by:

Trauma.
Viral or bacterial infections.
Contact dermatitis.

Atrophic Rhinitis (AR) - Progressive Disease (PAR)
(407) Rhinitis implies inflammation of the nose and it can be caused by a variety of bacteria and irritant substances. During the process of infection the delicate structures or turbinate bones in the nose become damaged and atrophy or disappear. Progressive atrophic rhinitis describes a specific disease where the nose tissues permanently atrophy. It is caused by specific toxin producing strains of Pasteurella multocidia (PMt). There are two types A and D.

Bleeding from nose caused by atrophic rhinitis

Typical signs of atrophic rhinitis

Section through nose - grade 3 atrophic rhiniits
 
Spread of disease between herds is almost invariably by the carrier pig, the organism being found in the respiratory tract and the tonsils. Spread within herds is by droplet infection between pigs or by direct pig to pig (nose to nose) contact. It can also be spread indirectly on equipment, clothes etc. When first infected pigs can carry the infection for many months. Infection is usually picked up during the second half of the sucking period or after weaning and clinical disease may be evident from three weeks of age onwards. The toxin is absorbed into the system where it damages other tissues including the liver, kidneys and lung, resulting in reduced daily gain and depressed feed efficiency. Similar organisms may also be found in the cat, dog, rabbit, poultry, goat, sheep, turkey but it is thought that these are host adapted strains and are unlikely to cause serious disease in the pig. The human may carry PMt in the tonsils for a very short period of time, although the evidence for this is limited and there are no reports of transmission by people to pigs. Experience indicates that the main and probably only method of introduction into the herd is by carrier pigs, although occasionally unexplained outbreaks of disease may occur.

Clinical signs

In sucking pigs sneezing, snuffling and a nasal discharge are the first symptoms, but in acute outbreaks where there is little maternal antibody, the rhinitis may be so severe to the extent that there is haemorrhage from the nose. By three to four weeks of age and from weaning onwards, there is evidence of tear staining and malformation of the nose associated with twisting and shortening.

Severely affected pigs may have problems eating. There is considerably reduced daily gain. In severe outbreaks pigs may not grow to market weight.

Diagnosis

This is based on clinical signs. However do not assume if sneezing is occurring in young pigs that automatically it will be progressive atrophic rhinitis. The disease is easily identified by post-mortem examinations of the nose and culture of the organism from nasal swabs. (See chapter 15 Swabbing). The snout is sectioned at slaughter at a level of the second premolar tooth and an assessment of the degree of atrophy of the turbinate bones made. The snouts are graded from 0 to 5, 0 to being a perfect snout. Grade 1 would show a slight loss of symmetry of the nose, grade 2 a slight loss of turbinate tissue and grade 3 a moderate amount. It is only when grades 4 and 5 are present, when there is severe progressive loss of tissue that PAR will be suspected. (Fig.9-21).




The five grades of Rhinitis


Similar diseases

Rhinitis may be caused by the following but the distinction is less evident, less pigs are obviously affected and the turbinate bones will heal and regenerate.

Air containing high bacterial counts.
Aujeszky's disease.
Bordetella bronchiseptica infection.
Chronic respiratory disease.
Dust.
Glässers disease.
High levels of ammonia.
Porcine cytomegalovirus infection (PCMV) (inclusion body rhinitis).
PRRS.
Treatment
The moment PAR is diagnosed all adult stock should be vaccinated twice with a toxin derived vaccine 4 to 6 weeks apart. Vaccination usually gives excellent control.
Sows should then be vaccinated four to six weeks prior to each subsequent farrowing or as per the data sheet.
All weaned pigs should be medicated in-feed until the clinical outbreak has subsided.
At the same time and until a good immunity has developed, antibiotic treatment should be given to the piglets. Consider using the following routines:
- Day three of age. Inject with either long-acting OTC or amoxycillin.
- Day ten. Inject with either long-acting OTC or amoxycillin.
- Inject again at weaning time with OTC or amoxycillin
Other antibiotics could be used depending on the bacterial sensitivity, such as penicillin, trimethoprim sulphas, tylosin and enrofloxacin.
The sows feed could be top-dressed with either OTC or trimethoprim/sulpha (TMS) commencing five to seven days prior to farrowing and throughout the farrowing period, or the lactating ration medicated with trimethoprim/sulpha (500g).
At weaning time the creep feed should be medicated with OTC or CTC at dose levels of 500-800g/tonne or TMS for three weeks post-weaning.
In acute outbreaks PAR is evident clinically in up to 25% of pigs by the time they have reached 16 weeks of age. Four months after vaccination this should have dropped to around 10% and after six months down to less than 1%. Vaccination will usually prevent the establishment of infection up to approximately eight to twelve weeks of age until the pigs move into finishing houses. Here, unless the houses have been depopulated, the pigs will become infected but with few clinical signs. Infection however increases the predisposition to other respiratory diseases and depresses feed intake and performance.
Management control and prevention

Keep disease out by purchasing pigs only from known negative sources.
Monitor snout sections regularly.
If the herd is infected do not breed from home bred gilts.
Vaccinate sows.
Maintain an old herd to produce good colostral immunity.
Avoid continuously populated housing which may allow organisms to build up to a threshold level and initiate a disease outbreak.
Adopt all-in all-out procedures from weaning to slaughter.
Avoid high stocking levels.
Avoid more than ten sows per farrowing room.
Damp humid farrowing houses increase the risk of spread.
Use solid divisions between farrowing crates to reduce droplet infection
Keep weaners to less than 120 per group.
Poor ventilation and high humidity post-weaning predispose.
Do not re-circulate air in flat decks.
Avoid fluctuating temperatures in flat decks.
Eradication
PAR may be eradicated from the herd after a 12 month period of sow vaccination provided all clinical evidence of disease has subsided. Piglets from vaccinated sows are weaned and segregated from disease carrying pigs until the weaning finishing accommodation has been depopulated and cleaned. The segregated pigs are then returned to the buildings. In the meantime the other finishing pigs are gradually sold to slaughter. The vaccinated "clean" pigs are not allowed contact with infected pigs and separate personnel are used between groups. PAR is only spread by close droplet contamination. An alternate and more successful method is to market all growing pigs over a 6 to 8 week period before bringing the segregated pigs back into the system. (See chapter 3 segregated disease control).

Prolapse of the Bladder
This is an uncommon condition and usually only occurs in the sow. The bladder turns inside out and protrudes from the lips of the vulva.
It is usually seen after mating. Such animals should be culled immediately if it can not be replaced.

Symptoms
Piglets, Weaners & Growers
N/A
Sows
The inside of the bladder appears as a large red mass about the size of an orange.
It can be confused with an early prolapse of the uterus but examination will show that is like a small balloon.
Causes / Contributing factors
It arises when there is a large urethral opening at the floor of the vagina and complete loss of muscle tone in the sphincter.
Possibly cystitis
The presence of calculi and continual straining
Unknown factors
Diagnosis
Veterinary advice is suggested if in doubt. It can be confused with vaginal prolapse and vaginal polyps.

Prolapse of the Rectum
This is not uncommon in sows. It is a widespread condition occurring in growing pigs from 8 to 20 weeks of age. The onset is sudden.
Symptoms
Weaners & Growers
The size of the prolapse varies from 10 to 80mm and if small it will often revert into the rectum spontaneously.
In most cases however the prolapse remains out becomes swollen and filled with fluid.
It is also prone to damage with haemorrhage.
Cannibalism often results by other pigs in the pen as shown by blood on the noses of the offending pigs and on the flanks of others.
Blown up abdomen seen in pigs 2 - 4 weeks after prolapse (rectal stricture).
Pale pigs due to haemorrhage.
Constipation.
Sometimes death.
Piglets
Rare.
Sows
At the onset, the red coloured mucosa of the rectum protrudes from the anal sphincter.
May return on its own or remain to the exterior, become swollen and filled with fluid.
It is prone to damage, haemorrhage and cannibalism.
Pale pigs due to haemorrhage.
Blood in faeces.
Causes / Contributing factors
The exact mechanisms are not understood but the following should be considered as contributory factors.
Prolapses which occur after oestrus in the sow may be related to sex hormone levels.
Penetration of the rectum at mating may result in prolapse 24-48 hours later.
Stalls or tethers with an excessive slope of the floor towards the back.
Sow stalls or farrowing crates with the back retaining gate consisting of parallel bars seem to predispose. If the sow can rest with the tail over the back gait, pressure is placed on the anus. This causes a partial relaxation of the sphincter, poor circulation and swelling. The sow strains and prolapses.
Genetic factors do not appear to have a part to play in this condition.
Trauma
Tail docking - docking tails too short can damage the nerve supply to the anal ring leading to a relaxation of the anal sphincter.
The fundamental cause is an increase in abdominal pressure which forces the rectum to the exterior and a swelling of the mucous lining and then straining.
The following may be considered as causal or contributory particularly in growers.
Diarrhoea - excessive straining.
Respiratory disease - excessive coughing increasing abdominal pressure.
Colitis - abnormal fermentation occurs in the large bowel with the production of excessive gas increasing abdominal pressure.
In cold weather the incidence of rectal prolapses increases. This is associated with low house temperatures and the tendency of pigs to huddle together, thus increasing abdominal pressure.
Wet conditions and slippery floors, particularly those with no bedding, increase abdominal pressure.
If stocking densities reach the level whereby pigs cannot lay out on their sides across the pen the incidence may increase. It is often related to specific houses on the farm.
Nutrition:
Ad lib feeding - Feeding pigs to appetite results in continual heavy gut fill and indigestion. There is then a tendency for abnormal fermentation in the large bowel because undigested components of the feed arrive in greater amounts.
High density diets and in particular lysine levels increase growth rates and outbreaks may often subside either by a change to restricted feeding or using a lower energy / lysine diet.
Diets high in starch may predispose to prolapse - Try adding 2-4% grass meal to the diet.
The presence of mycotoxins in feed - If there is a problem make sure that the bins have been well cleaned out. Examine the cereal sources.
Change of diet - By studying the timing of the problem it is sometimes possible to identify rectal prolapses not only with a change of diet but also a change of housing.
Prolapses may occur with constipation e.g. from feeding a low fibre diet, shortage of water.
Diagnosis
This is based on the clinical picture.

Prolapse of the Uterus
This involves the complete eversion of both horns of the womb which turn completely inside out. It usually takes place within 2-4 hours of the completion of farrowing but sometimes up to 24 hours afterwards. Prolonged straining causes a small part of the tube to be propelled outwards by uterine contractions.
Symptoms
Sows
The prolapse occurs over a period of approximately one hour and commences with the appearance of the red congested lining of the womb.
This rapidly increases in size until the large everted mass is presented.
Piglets, Weaners & Growers
N/A
Causes / Contributing factors
Uterine prolapses are uncommon but usually occur in old sows with large litters or where large piglets have been born.
The supporting structures of the uterus become weak or the uterine wall becomes flaccid.
Faulty farrowing mechanisms.
Previous damage to womb.
Diagnosis
This is obvious by the appearance.

Prolapse of the Vagina and Cervix
Prolapse of the vagina and cervix commonly occurs in the last third of pregnancy including the immediate pre-farrowing period.
Symptoms
Sows
In the early stages the protruding tissues appear between the lips of the vulva and return to their normal position when the sow stands.
With advancing pregnancy the prolapse may remain to the exterior and as soon as this occurs the animal should be removed from it's existing environment and loose-housed.
The tissues become swollen with time.
Piglets, Weaners & Growers
N/A
Causes / Contributing factors
It occurs usually in older fatter sows that are heavy in pig.
It is a response to increased abdominal pressure together with a relaxation of the internal structures that support the neck of the womb.
It is more common in older sows.
Sows housed on tethers with slippery floors are more prone.
Stalls or tethers with floors that slopes too steeply to the rear predispose.
High levels of starchy feed intake, produce excess fermentation and gas and an increase in abdominal pressure.
Diagnosis
This is by clinical signs. It may be confused with eversion of the bladder but may be differentiated by handling the tissues.

Pseudorabies PR
Related Products:
Porcilis Begonia
PRV/Marker Gold®
This is an important disease of pigs caused by a herpes virus. The virus can remain hidden in nerves of the pig in a carrier state for long periods of time and then be reactivated. Once introduced into a herd the virus usually remains there and it can continually affect reproductive performance at varying levels. The virus can survive for up to three weeks outside the pig. Acute outbreaks of disease occur when virulent strains of the virus first infect an unvaccinated susceptible herd. The virus crosses the uterus and placenta and infects the foetuses.
The pig is the main host. Dogs and cattle may become infected, show nervous signs and die.

Symptoms
Sows
Coughing.
Fever
Nervous signs
Reproductive failure.
Abortions.
Mummified piglets.
Stillbirths.
Birth weak litters.
Piglets
Nervous signs.
Incoordination.
Sneezing.
Coughing.
High mortality.
Low / poor viable piglets.
Weaners & Growers
Fever.
Sneezing.
Coughing.
Pneumonia.
Nervous signs including incoordination, fits and meningitis.
Some strains of the virus can cause severe respiratory disease and others severe rhinitis.
Usually low mortality.
All Other Species
Nervous signs.
Death.
Causes / Contributing factors
Movement of carrier pigs.
Virus airborne - at least 3km (2 miles).
Infection from feral (wild) pigs.
The role of mechanical spread by birds is questionable.
Contaminated carcasses may spread infection.
Mechanically on people.
Contaminated vehicles.
Through infected semen via AI or a carrier boar.
From infected slurry.
Within herds it may be spread by nose to nose contact, or by aerosol droplets.
Periods of stress may activate disease.
Continual production systems perpetuate disease.
Additionally:
The presence of other infections such as PRRS and leptospira may increase the severity of disease.
Diagnosis
When a susceptible breeding herd first breaks down with this disease the clinical signs described above strongly suggest aujeszky's disease and are almost diagnostic. Laboratory tests are required to confirm the diagnosis.

Rabies
This is caused by a virus and considered a rare disease in pigs. It is invariably fatal in all species including the human - hence its importance. Rabies is absent from the UK but present in may other countries throughout the world.
Symptoms
Piglets
Rare.
As for sows.
Sows, Weaners & Growers
Onset is sudden with:

Nervous twitching of the face muscles.
Fits and convulsions.
Rapid chewing.
Salivation.
The muscles may also go into spasm.
Posterior paralysis may occur.
Death usually takes place within 3 days.
Causes / Contributing factors
Rabies virus is spread by contact with wild life.
Diagnosis
Consult your veterinarian immediately.

Rectal Stricture
This is a condition often considered a sequel to rectal prolapse in growers and finishers. Approximately a fingers length inside the rectum the tissues gradually shrink, scar tissue develops and eventually the tube completely closes. The area where the stricture occurs is supplied by two tiny arteries that originate from the aorta. Some studies suggest that if these arteries are blocked or thrombosed by bacteria a rectal stricture will result. Erysipelas, Haemophilus parasuis, streptococci and salmonella have been implicated.
Symptoms
Weaners & Growers
Affected pigs in the early stage of the disease often show:

A very loose watery diarrhoea that becomes projectile.
A gradual increase in the size of the abdomen.
Constipation.
Loss of condition / poor growth.
Sows & Piglets
N/A
Causes / Contributing factors
Infection and thrombosis of blood vessels.
Sequel to rectal prolapse.
Diagnosis
Based on clinical signs.

Retroviruses
These are thought to occur within the genome of every cell in every pig's body. The virus genomes have become part of the genome sequence of the pig and are passed on through the cells of the ovum and foetus. Thy are of no consequence to the pig or the pig farmer and are only of concern if the pig has been reared as a source of organs or tissues for human patients. The concern is that a retrovirus may pass from the transplanted organ or tissue into human cells and cause disease. The overriding fear is that this virus might then spread to other people causing an epidemic.

Rotavirus Infection
This virus is widespread in pig populations. It is present in most if not all pig herds with virtually a 100% sero-conversion in adult stock. A further epidemiological feature is its persistence outside the pig where it is resistant to environmental changes and many disinfectants. Maternal antibodies persist for 3-6 weeks after which pigs become susceptible to infection but exposure does not necessarily result in disease. It is estimated that only 10-15% of diarrhoeas in pigs are initiated by a primary rotavirus infection. In a mature herd disease appears after piglets are 7 to 10 days of age. It becomes progressively less important with age. However if pathogenic strains of E. coli are present severe disease can occur with heavy mortality.
Symptoms
Sows
Transient diarrhoea.
Piglets
Watery profuse diarrhoea in younger animals.
Villus atrophy is a consistent feature with dehydration, malabsorption and wasting.
Diarrhoea usually persists for 3-4 days.
Pigs look hollow in the abdomen and become dehydrated.
The eyes are sunken.
The skin around the rectum is wet.
Weaners & Growers
In a mature herd:

A watery profuse diarrhoea appears after piglets are 7 to 10 days of age. It becomes progressively less important with age.
However if pathogenic strains of E. coli are present severe disease can occur with heavy mortality.
Villus atrophy is a consistent feature which results in malabsorption.
Dehydration.
Diarrhoea usually lasts 3-4 days.
Pigs look hollow.
Eyes are sunken.
Skin around the rectum is wet.
The role of rotaviruses in the post-weaned pig is probably less important although they are often identified when acute E. coli diarrhoea occurs in the first 7-10 days after weaning.
Causes / Contributing factors
Poor house hygiene.
Permanently populated houses. Adopt all-in, all-out.
Movement of pigs.
Temperature fluctuations.
Contaminated boots and clothing.
Diagnosis
Whenever there is a diarrhoea problem in pigs between 10 and 40 days of age rotavirus infection either as primary agents or secondary must be considered. Electron microscopy and ELISA tests in the laboratory are required for confirmation. Try the litmus test by soaking scour in litmus paper, E. coli infections turn blue, virus infections red.

Ruptured Blood Vessel
This is often seen post farrowing and can be life threatening. The blood may be fresh and bright red indicating fresh haemorrhage or dark brown previous haemorrhage.
Symptoms
Sows
Blood from the vulva or vagina evident.
Blood in faeces.
Blood in urine.
Pale pig.
Rapid breathing.
Dehydration.
Piglets, Weaners & Growers
Rare
Causes / contributing factors
Damaged vulva.
Ruptured blood vessel at farrowing.
Acute cystitis.
Dead piglet in the womb.
Haemorrhage from the umbilical cord.
Diagnosis
Identify the source of the haemorrhage and ligature if possible.

Treatment
If a fresh haemorrhage, apply pressure
See vulval haematoma for treatment
See also cystitis
Give anticoagulents - vitamin K

Ruptures, Hernias
Of many congenital abnormalities, umbilical or inguinal ruptures are most common. They are considered to be developmental defects and have a very low heritability. Umbilical hernias can sometimes be traced back to a particular boar in which case he should be culled. These are most evident from 6 to 12 weeks of age.
Symptoms
Weaners & Growers
Swellings 30 - 200mm in diameter protruding from the umbilicus and abdomen, or below and in front of the testicles or in the groin (inguinal rupture).
If the swellings are large trauma to the skin may cause ulcerations particularly umbilical ruptures.
Sows & Piglets
N/A
Causes / Contributing factors
Environmental factors can increase the incidence of umbilical hernias so if there is a problem (more than 2% of pigs) consider the following:
Are prostaglandins used to synchronise farrowings. If so check that piglets are not being pulled away from the sow at farrowing and the cord stretched excessively.
Is navel bleeding occurring on the farm? Are naval clips being used to prevent bleeding? If so make sure they are not placed close up to the skin otherwise the tissues will be damaged and weakened.
Identify the precise time when the ruptures appear. Do these coincide with a change of housing?
In housing where the pigs pass through a small hole to the dunging area sudden severe abdominal pressure may cause ruptures.
Are stocking densities high and causing increased abdominal pressure?
In cold weather do the pigs huddle thereby increasing abdominal pressure?
Check records to see if any particular boar is implicated.
If the rupture is large and the pig is on a concrete floor or slats it should be moved to a soft bedded area so that the overlying skin does not become sore and ulcerated.
Examine navels at births and two days later to see if there are any abnormalities.
Diagnosis
Visual evidence. Reduction of the bowel contents in the rupture when squeezed back into the abdomen.

Salmonellosis
Salmonella bacteria are widespread in human and animal populations. Some of them can cause disease in pigs.
They multiply mainly in the intestines of young growing pigs but also in some sows. They may be shed in faeces for several weeks or months with no clinical disease. Salmonella in the gut of the pig can contaminate carcasses during the slaughter process and their presence creates potential public health risks from food poisoning.

Of the many serotypes of salmonella that exist, the ones that are most likely to cause clinical disease in pigs are Salmonella choleraesuis, and Salmonella typhimurium and to a lesser extent Salmonella derby. Other "exotic" salmonella serotypes may infect pigs and be shed in the faeces for limited periods but they usually remain sub-clinical. S. choleraesuis and S. derby are host-adapted to the pig and may be carried for long periods by sows, the former sometimes causing clinical disease in sows (fever, depression, septicaemia, pneumonia, meningitis arthritis and diarrhoea) but rarely in people.

Pigs may become long-term sub-clinical carriers of S. choleraesuis and S. derby, the organisms surviving in the mesenteric lymph nodes draining the intestine. Many such carriers do not shed the bacteria in faeces unless they are stressed. Pigs may be intermittent or continuous faecal shedders of other serotypes but the carrier state is usually short, weeks or a few months and is self limiting.

S. typhimurium and S. derby are more likely to cause milder disease, the main sign of which is usually diarrhoea. The serotype most commonly found in pigs, however, is Salmonella typhimurium which sometimes is associated with diarrhoea in young pigs but which is also a major cause of food poisoning in people. Some strains have multiple medicine resistance. If it is diagnosed in your pigs you should take hygienic precautions not to become infected yourself. Many other so called exotic types may also be detected in pigs without causing disease.

Remember that S. typhimurium, which occasionally can be isolated from pigs, are common causes of food poisoning in people.

Salmonellosis can occur at any age but is most common in growing pigs over eight weeks of age. Severe S. choleraesuis infection occurs typically at around 12 to 14 weeks.

Disease is dose dependent, that is, a relatively large number of organisms are required before clinical signs occur.

Symptoms
Weaners & Growers
The acute septicaemia and pneumonia which may occur with S. choleraesuis may result in fever, inappetence, respiratory distress, depression, coughing, red skin and poor doing pigs.
The skin of the extremities (i.e. tail, ears, nose and feet) become blue.
Foul-smelling watery diarrhoea which may be blood stained, is a common feature.
Yellow jaundice may result from liver damage and lameness from arthritis.
Nervous signs resulting from meningitis.
If untreated, mortality may be high.
Infections with S. typhimurium usually are manifest by diarrhoea.
Piglets
Disease would be uncommon in the piglet and due to passive immunity provided via colostrum.
Sows
Clinical signs of Salmonella choleraesuis and occasionally Salmonella typhimurium infection may include any combination of the following:

A high temperature.
Depression.
Loss of appetite.
Congestion of the ears, snout and tail.
Pneumonia.
Coughing.
Nervous signs.
A smelly sometimes bloody diarrhoea.
Death may occur in the acute phase of the disease.
Causes / Contributing factors
Poor hygiene.
Overcrowding.
Stress by moving and mixing.
Permanently populated houses.
Contaminated boots and clothing.
Mechanical means via faeces and the movement of contaminated equipment.
Vermin and flies.
Contamination of feed by birds, rats and mice
Contamination of raw feed ingredients and thus the final product.
Diagnosis
The post-mortem lesions are strongly suggestive of S. choleraesuis, particularly the generalised pneumonia, the appearance of the lining of the small and large intestine, the congested spleen and multiple small haemorrhages. However, to make a specific diagnosis it is necessary to submit to the laboratory either fresh faecal samples from untreated pigs or where available a dead or live untreated pig.
Severe salmonellosis caused by S. choleraesuis can occur alone but it also commonly occurs with classical swine fever (hog cholera) in those countries in which this disease still occurs. In such countries it is important to ensure by serology and laboratory tests that swine fever is not the primary cause (NB. swine fever usually also affects sows and sucking piglets and also causes mummified litters and abortions).

Severe PRRS in herds with endemic EP may give the appearance of salmonellosis, however PRRS also causes abortions, stillbirths and precipitates scouring in piglets.

Savaging of Piglets (Cannibalism)
This is a condition mainly in first litter gilts that may account for up to 3% increase in piglet mortality.
Symptoms
Sows
Offending gilts can often be identified by their nervous apprehension at the onset of farrowing.
They have a "wild eyed" look.
Piglets, Weaners, Growers
N/A

Causes / Contributing factors

It is thought to be related, in part at least, to the major hormone changes that take place around parturition.
The following factors seem to predispose to it:
A harsh or alien environment.
Poor empathy between the gilts and the stockperson.
Nutritional deficiencies.
The effect of being placed in individual confinement for the first time.
It may also be related to temperament.
It seems to be more prevalent in some breeds than others.
Alarming outbreaks have been experienced in new gilt herds where 100 - 150 pregnant animals have been reared together in straw yards. In such large groups no pecking order develops.
Diagnosis
Severe trauma to the skin and limbs. Clinical picture. History.

Scour (E. coli)
Related Products:
Aurofac / Aureomycin
Gletvax 6
NEOCOLIPOR
SCOURMUNE®
Of all the diseases in the sucking piglet, diarrhoea is the most common and the most important. In some outbreaks it is responsible for high morbidity and mortality. In a well run herd there should be less than 3% of litters at any one time requiring treatment and piglet mortality from diarrhoea should be less than 0.5%. In severe outbreaks mortality can rise to over 7% and in individual untreated litters up to 100%.
E. coli diarrhoea, clostridial diarrhoea, coccidiosis, TGE and PED all cause diarrhoea in the piglet. E. coli is the most important.

At birth the intestinal tract is micro-biologically sterile and it has little immunity to disease producing organisms. Organisms begin to colonise the tract quickly after birth, among them potentially pathogenic strains of E. coli and Clostridium perfringens. Immunity is initially provided by the high levels of antibodies in colostrum (IgG, IgM, IgA). After the colostral antibodies have been absorbed into the blood stream, the immunity is maintained by the antibody (IgA) which is present in milk. IgA is absorbed into the mucous lining of the intestines. It is essential that the newborn piglet drinks sufficient colostrum soon after birth to prevent potentially pathogenic organisms multiplying against the intestinal wall and causing diarrhoea. It is also essential that the piglet continues to drink milk regularly after the colostrum has gone so that its intestines continue to be lined by protective antibodies.

The antibodies acquired passively from the colostrum and milk are finite and can be overwhelmed by large doses of bacteria present in the environment. The higher the number of organisms taken in, the greater the risk of disease. Environmental stress such as chilling also plays a role because it lowers the piglets resistance. There is thus a delicate balance between the antibody level on the one hand and the weight of infection and stress on the other.

Scour in the piglet can occur at any age during sucking but there are often two peak periods, before 5 days and between 7 and 14 days.

Sudden outbreaks of scour involving large numbers of litters with acute diarrhoea and high mortality suggest TGE, epidemic diarrhoea or PRRS. Rotavirus diarrhoea appears in waves in individual litters or groups of litters and normally in the second half of lactation. Coccidiosis is usually involved in diarrhoea from 7 to 14 days of age. At less than 5 days of age the most common cause is E. coli with acute diarrhoea particularly in gilts' litters. Clostridial infections also occur at this age.

At weaning the loss of sow's milk and secretory IgA allows the E. coli to attach to the villi of the small intestines, the toxins produced then cause acute diarrhoea, usually within five days of weaning.

Symptoms (E.coli)
Sows / Growers
Uncommon.
Usually occur with viral infection.
Piglets
In acute disease:

The only sign may be a previously good pig found dead.
Huddle together shivering or lie in a corner.
The skin around the rectum and tail is wet.
Watery to salad cream consistency scour - distinctive smell.
Vomiting.
As the diarrhoea progresses:
Dehydrated.
Sunken eyes.
Leathery skin.
The scour often sticks to the skin of other piglets giving them an orange to white colour.
Prior to death piglets may be found on their sides paddling and frothing at the mouth.
In sub-acute disease:
Signs are similar but the effects on the piglet are less dramatic, more prolonged and mortality tends to be lower.
This type of scour is often seen between 7 to 14 days of age.
Watery to salad cream consistency diarrhoea, often white to yellow in colour.
Weaners
The first signs are often slight loss of condition, dehydration and a watery diarrhoea.
In some cases blood or black tarry faeces may be seen or they may be like paste with a wide range of colour: grey, white, yellow and green. The colour is not significant.
Poor pigs - wasting, hairy.
Sloppy faeces and often dirty wet pens.
Sunken eyes.
Dehydration results in rapid loss of weight.
Pigs may be found dead with sunken eyes and slight blueing of the extremities.
Good pigs may also be just found dead with no external symptoms.
Occasional vomiting.
Causes / Contributing factors
Sows & Piglets
Poor pen floors.
Poor pen hygiene associated with bad drainage.
Poor hygiene procedures, between pens.
Environmental contamination from one pen to another i.e. boots, brushes, shovels clothing etc.
Continual use of pens.
Moisture, warmth, waste food and faeces are ideal for bacterial multiplication.
Draughts.
Routine use of milk replacers, particularly if they are allowed to get stale or contaminated, may increase the incidence.
Scour is more common in large litters. This can be due to:
- Insufficient colostrum.
- Poor teat access.
- Poor crate design.
- Agalactia in the sow.
Weaners & Growers

Pre-weaning

Are the weaning problems mainly in gilt litters? If so consider E. coli vaccination in gilts:

- Creep feeding. Consider the type, frequency and age of introduction.
- Stop creep feeding before weaning and assess the effects.

At weaning consider:

- Stress.
- Stocking density - group sizes.
- House temperatures and temperature fluctuations.
- Poor house hygiene.
- Continually populated houses.
- Water shortage.
- Feed type: Meal or pellets, wet or dry.
- Feeding practices.
- Quality of nutrition.
After weaning consider the effects of:
- Air flow - chilling.
- Temperature fluctuations.
- High ventilation and humidity.
- Creep feed management.
- Assess the response to different creep diets.
- Consider other diseases present.
- Age and weight at weaning.
- Floor surfaces - provide comfort boards.
- Asses rate and evenness of growth.

A diarrhoea problem in growing pigs is likely to be associated with one or more of the following diseases (Most common *):
Classical swine fever (in those countries where it is still endemic).
Coliform infections. *
Colitis (non specific). *
Parasites.
Porcine epidemic diarrhoea (PED). *
Porcine enteropathy including PIA, NE and RI. *
Rotavirus infection.
Salmonellosis. *
Spirochaetal diarrhoea.
Swine dysentery. *
TGE (rare in Europe now but still common in some other countries).
Diagnosis
This is based on the clinical examination, the response to treatment (viral diseases do not respond to treatment) and laboratory examination of the scour.

Submit a rectal swab and faecal sample of a recently dead pig or a live pig to the laboratory for cultural examinations and antibiotic sensitivity tests.

A simple test to differentiate between virus causes and E. coli diarrhoea involves the use of litmus paper to determine whether the scour has an alkaline or an acid consistency. Soak the paper in the scour, E. coli diarrhoea is alkaline (blue colour change) whereas viral infections are acid (red colour change).

It is not possible to eliminate organisms such as rotavirus, E. coli and coccidiosis from the herd and most if not all pigs will be infected with them. Herds can be maintained free of TGE, PED and PRRS. All herds carry clostridia but other factors are required to cause disease.

Seasonal Infertility
Abortion means the premature expulsion of dead or non-viable foetuses. Embryo loss occurs when there is death of embryos followed by absorption, or expulsion. Healthy embryos grow into foetuses.
There is often alarm when an abortion is seen but it should be remembered that there can be loss of embryos at any time during early pregnancy, which often go unseen.

Embryo loss or abortion can be considered in three main groups:

During the period from fertilisation to implantation
During the period of implantation at around 14 days post-service to 35 days.
During the period of maturation, which results in premature farrowings. It can be seen therefore that losses can take place at any stage from approximately 14 days after mating, when implantation has taken place, through to 110 days of pregnancy.
Records help to identify reproductive problems. These should include information on:

- Age (or parity) profile of the herd.
- Failure to come on heat.
- Culling rates.
- Bleeding and discharges from the vulva.
- Repeats, sows not in pig.
- Lameness.
- Litter sizes.
- Mastitis, lack of milk, swollen udders.
- Deaths and their likely causes.
- Poor conformation.
- Prolapse of the vagina or rectum.
- Savaging.
Symptoms
Piglets, Weaners & Growers
N/A
Sows
The delivery of a premature litter with or without mummified pigs.
Mucus, blood, pus discharges from the vulva.
Sow may be ill or normal.
Symptoms of a specific disease.
Sows not in pig.
Usually less than 2% of sows affected, however acute PRRS may cause rates to rise to 20% or more.
Causes / Contributing factors
Infectious Causes (common ones). Consider the following:
Aujeszky's disease.
Influenza virus.
PRRS (Blue ear disease).
Leptospira.
Specific bacteria, E. coli, klebsiella, streptococci, pseudomonas.
Parasite burdens.
Cystitis, nephritis.
Non Infectious Causes
Seasonal infertility.
Decreasing daylight length, poor lighting.
Low temperatures.
Chilling, draughts.
Poor nutrition.
Mouldy feeds.
Contaminated water.
Stress.
No boar contact.
Vaccine reaction.
Lameness.
Poor hygiene.
Diagnosis
Fresh, aborted foetuses should be submitted to a competent diagnostic laboratory where examinations can be carried out for evidence of viral and bacterial infections, together with histological examinations and toxic studies. In many cases the end results of post-mortem and serological tests do not identify any particular infectious organism, which may seem disappointing. However, it is useful in telling us what is not present.
A Checklist for Abortions
Abortion Level. Is this more than 1.5% of sows served? Take action.
Are sows ill? Probably disease.
Are sows otherwise normal? Probably non infectious, Maternal failures.
Is the problem seasonal? Autumn abortion syndrome.
Do they occur in a particular part of the farm? Environmental.
Are the aborted pigs fresh or alive? Suggests the environment.
Are mummified pigs present? Suggests infection.
Is the dry sow accommodation uncomfortable? Suggests the environment.
Are sow pens wet, draughty, poorly lit? Suggests the environment.
Does the ventilation system chill the sows? Suggests the environment.
Are there factors that place the sows in a negative energy state? e.g.: High chill factors, draughts, low feed intake, a change in bedding or availability.
Are sows short of food - Check feed intakes by volume and weight.
Is the food mouldy? Check for mouldy feed.
Do the sows experience 14 hours of good light at eye level?
Are the lights dirty, covered in fly dirt?
Can you read a newspaper in the darkest corner?
Do your sows have boar contact in pregnancy?
Are any other diseases evident in the sows? e.g.: lameness , cystitis, kidney infections.
Are the abortions associated with stress?
Increase feed intake from days 3 to 21 after mating according to body condition and environmental temperatures.
Increase the mating programme by 10-15% over the anticipated period of infertility.
Because boar semen can be affected, particularly by environmental temperatures, follow each natural mating 24 hours later by purchased AI.

Shoulder Sores
They arise due to repeated bruising and pressure over the bony prominences on the shoulder blade in breeding females. Ultimately the skin breaks, there is an erosion and a large sore develops. Such sows should not be kept for future breeding
Symptoms
Piglets, Weaners & Growers
N/A
Sows
Highest point of the spine a reddening of the skin appears, which gradually forms into an ulcer.
In severe cases the lesion may extend to 40 - 70mm in diameter with the development of extensive granulation tissue.
Often both sides of the shoulder are affected.
Causes / Contributing factors
They are associated with totally slatted flooring and individual sows that are too thin and have a prominent spine to the shoulder blade.
First noticed in the farrowing crates where the floors are slippery.
The sow has difficulty in rising, thus constantly bruising her shoulder.
Diagnosis
This is based on the clinical signs and ulcerating shoulders.

Spirochaetal Diarrhoea
This is a disease associated with spirochetes distinct from the one that cause swine dysentery. It occurs mainly in growing pigs appearing very similar to non-specific colitis and PIA caused by Lawsonia intracellularis. Spirochetes are common inhabitants of the large intestine and caecum.
Symptoms
Weaners & Growers
A mild to moderate sloppy diarrhoea develops two to six weeks post-weaning that persists for a few days.
Dehydration.
Loss in growth.
Most cases resolve in 7 to 10 days but in some pigs it becomes chronic.
The disease can be difficult to differentiate from other bacterial infections, particularly non-specific colitis.
Piglets & Sows
N/A
Causes / Contributing factors
A sudden change in diet.
Removal of copper from the diet.
Withdrawal of growth promoters.
Poor hygiene i.e. dirty floor surfaces, water contamination.
Diagnosis
This is difficult because specific organisms cannot usually be identified. If there is an on-going problem on the farm, live diseased pigs showing typical signs, should be submitted for post-mortem and bacteriological examinations to eliminate swine dysentery.

Splaylegs
This is a condition where the newborn piglet is unable to hold the front and/or (more commonly) back legs together and up to 2 % of piglets can be affected. The mobility of the piglet is impaired which makes teat access difficult.
Symptoms
Piglets
The piglets are unable to stand with the hind legs deflected laterally.
As a result they often adopt a dog sitting position.
Death usually ensues either due to starvation or crushing because the pig cannot move away from the sow.
Poor / low viable piglets.
Sows, Weaners, Growers
N/A
Causes / Contributing factors
It is more common in the Landrace breed and in males.
Disease is caused by immaturity of the muscle fibres in the hind legs, over the pelvis and occasionally in the front legs.
The condition is exaggerated when piglets stand on very smooth or wet slippery floors.
Diagnosis
This is based upon the clinical signs.

Stillbirths
When pigs are found dead behind the sow they are usually recorded as stillbirths which may be wrong. They may have died after farrowing having breathed but died of chilling and hypoglycaemia.
Symptoms
Piglets
Found dead behind the sow. They may be fresh or 3 - 4 days old.
Causes / Contributing factors
Stillbirths increase with the increasing age of the sow.
Individual sows may be regular offenders and these can be identified by the sow litter card. The farrowing process should then be monitored.
Stillbirths occur more in larger litters.
Stillbirths are more common in pure breeds.
Stillbirths are common in prolonged farrowings.
Lack of exercise during pregnancy may raise stillbirth rates.
Stillbirths are raised where there is a long gestation period.
Farrowing house temperatures above 24?C (75?F) increase the risk of stillbirths.
Uterine inertia results in stillbirths.
High carbon monoxide levels in the air associated with faulty gas heaters can raise stillbirth rates significantly.
Pigs found dead behind the sow can sometimes be related to particular farrowing crates in certain rooms and are due to draughts behind the sow.
An examination of records should clarify whether the problem is one of individual sows or across the herd.
Diseases of the sow which may result in stillbirths:-

Anaemia.
Aujeszky's disease.
Eperythrozoonosis.
Erysipelas.
Leptospirosis.
Mycotoxicosis.
Parvovirus infection.
PRRS.
Toxoplasmosis (poisoning).
Diagnosis
If the piglet dies before farrowing, it will show varying degrees of post mortem or degenerative changes. A pig that dies during the process of farrowing or immediately afterwards will be fresh and normal. The two can be differentiated easily. The chest is opened and the lungs examined to determine whether the pig had breathed. The lungs of the true stillborn pig are a dark plum colour, showing none of the pink areas associated with breathing. Pigs that attempt to breath during the process of farrowing will show evidence of mucous obstructing the wind pipe. A good target level for stillbirths is 3 to 5 % of total pigs born. At this level there is no point in carrying out investigations because it is unlikely that external inputs can alter the situation. However once the level reaches beyond 7% it is worthwhile carrying out an investigation by records and post-mortem examinations.

Streptococcal Infections
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EXCEDE®
EXCENEL® RTU
Streptococci are common organisms in all animals. They are broadly but not entirely species specific. The main species in pigs is Streptococcus suis which is widespread in pig populations and probably occurs wherever pig farming is carried out. It is associated with a variety of conditions including meningitis, septicaemia, polyserisitis, arthritis, endocarditis and pneumonia. It has also been isolated from cases of rhinitis and abortion. The pattern and relative importance of the different syndromes vary in different countries.
S. suis is sub-divided into at least thirty-four serotypes. They vary in their pathogenicity and the clinical signs they cause, both between and within types. Some types appear to be non-pathogenic and have been isolated mainly from healthy pigs, some are mainly associated with lung lesions, and some have been isolated from other animal species as well as pigs. Some types, mainly 2, can occasionally cause meningitis in people as well as pigs. Fortunately human cases are rare.

The syndrome that is important and worrying to the pig farmer is persistent endemic meningitis caused by type 2.

Clinically healthy pigs can carry the organism in their tonsils for many months and a carrier state exists in some sows. Once a serotype has entered a herd no techniques are yet available to remove it and it becomes established as part of the normal flora. S. suis is quickly killed by disinfectants in common use on farms, including phenolic disinfectants and chlorine and iodine based ones. Detergents will also kill the organism in thirty minutes. 'Savlon ' is particularly effective. Outside the pig, in very cold and freezing conditions, it may survive for 15 weeks or more but at normal room temperatures it dies within one to two weeks. It survives long periods in rotting carcasses.

The sow passes on antibody through colostrum to the sucking pig and the disease is therefore uncommon in this group of animals unless it is introduced into the herd for the first time. It is much more common in the immediate post-weaning period often starting 2 to 3 weeks after weaning and continuing through to approximately 16 weeks of age. In flat decks or nurseries almost 100% of pigs become carriers within three weeks.

There are also strains of low pathogenicity which may be activated by PRRS virus infection. PRRS may also raise the incidence of meningitis caused by pathogenic strains when it first enters a herd. Although PRRS alone does not affect the brain, it has been shown experimentally that many more pigs are affected with meningitis when they are infected with both S. suis type 2 and PRRS viruses than when they are infected with S. suis alone. S. suis type 14 which was first isolated from a case of human meningitis is emerging as a new disease in the UK with the appearance of acute severe outbreaks of arthritis in both sucking and weaned pigs.

Species of streptococci other than S. suis may sometimes cause disease in pigs. For example, Streptococcus equisimilis causes sporadic cases of septicaemia and arthritis in sucking pigs, infection of the heart valves in growing pigs and ascending infection of the womb in sows. In the USA Streptococcus porcinus causes throat abscesses and septicaemia and is sometimes isolated from pneumonia. However, cases of streptococcal throat abscesses have become rare in modern systems of pig housing.

Symptoms
Weaners & Growers

Cases of acute type 2 meningitis:
The pig may just be found dead.
In very early stages of meningitis the pig is laid on its belly, hair standing on end and shivering.
Within two to three hours there are lateral jerky movements of the eye (nystagmus).
The animal then lies on its side paddling and frothing at the mouth. Salivation
The organism invades the blood stream and is carried around the body where it may cause arthritis and pneumonia. Pigs squeal with pain and refuse to stand.
Abscesses.
Fits and convulsions.
Head on one side.
Type 1 occurs fairly commonly in most countries and causes:
Sporadic arthritis.
Occasionally meningitis is seen in sucking piglets usually around one to two weeks of age but sometimes up to six weeks. It is a relatively unimportant condition.

Sows & Piglets
Rare
Causes / Contributing factors
S. suis is spread from one pig to another by direct nose to nose contact.
Carrier boars or gilts.
It can also spread within a herd by indirect contact.
In confined space by aerosol infection.
If you have the disease endemic in your herd the incidence increases with :-
High stocking density in flat decks.
Continuous production systems which perpetuate infection.
Concurrent PRRS infections.
Mixing of pigs post-weaning.
Too small cubic capacity air space per pig. Provide at least 0.8 cu.m. per pig at weaning.
Poor ventilation and high humidity.
High dust levels.
Stress.
Damp pens.
High slurry levels under perforated metal floors.
Weighing pigs and associated stress.
Tattooing, ear notching and extra stress at weaning.
Changes in nutritional status at critical times.
Low vitamin E in the diet. Assess the response to adding 50-100iu/kg.
Diagnosis
A history of the presence of recurring meningitis in weaned pigs is highly suggestive and is confirmed by the isolation of the organism from the brain and its specific identification, which not all diagnostic laboratories are capable of.
Because of the existence of strains that are non-pathogenic or only mildly pathogenic, the isolation of S. suis type 2 from the tonsils of a pig is difficult to interpret. Isolation from the brain of a pig showing signs of meningitis is more conclusive.

The disease must be differentiated from aujeszky's disease, gl?ssers disease or salt poisoning (water deprivation) which all produce nervous signs.

Streptococcal Meningitis
Meningitis denotes inflammation of the meninges which are the membranes covering the brain. In the sucking piglet it is usually caused by Streptococcus suis, Haemophilus parasuis, or sometimes bacteria such as E. coli and other streptococci. S. suis has many serotypes. In most countries S. suis type 1 is the main one in sucking piglets, but this may not be true in other countries. For example in Denmark it is type 7. S. suis also causes joint problems particularly types 1 and 14.
S. suis is carried for long periods in the tonsils and may be transmitted to the sucking piglet from the sow or from other piglets. The sow also provides a variable level of immunity in the colostrum. Streptococcal meningitis in sucking piglets is sporadic in individual piglets. Streptococcal meningitis may be worse in sucking pigs when the organism has been introduced into the herd for the first time, or where it is secondary to infection with PRRS.

Symptoms
Piglets & Weaners
Symptoms of meningitis are rapid in onset.
The piglet lying on its belly and shivering.
It is characterised by a continual movement of the eyes from one side to the other (nystagmus).
Paddling.
Convulsions.
In acute cases the piglet may be found dead.
Sows & Growers
Meningitis is uncommon.
Muscle trembling.
Head on one side.
Nystagmus of the eyes.
Incoordination.
Causes / Contributing factors
S. suis is spread from one pig to another by direct nose to nose contact.
Carrier boars or gilts.
It can also spread within a herd by indirect contact.
In confined space by aerosol infection.
Diagnosis
To confirm the diagnosis, the organism must be isolated from the meninges of clinically affected pigs and identified in a laboratory. The disease must be differentiated from joint infections, gl?ssers disease, generalised septicaemia, salt poisoning, aujeszky's disease and hypoglycaemia.

Sunburn
This is a common condition in sows outdoors particularly in non pigmented breeds.
Ultra violet radiation not only damages the skin but also has an effect on the reproductive system and the maintenance of pregnancy.

Symptoms
Piglets
Reddened skin.
Sows
Reddened skin.
Blistering.
Wet dermatitis.
Pigs show pain / discomfort.
Illness.
Reabsorption of embryos.
Irregular returns.
Abortions.
Will not accept boar at mating.
Weaners & Growers
Reddened skin.
Blistering.
Wet dermatitis.
Pigs show pain / discomfort.
Illness.
Causes /Contributing factors
Non pigmented breeding stock.
Lack of shades.
Lack of wallows.
Poor maintenance of wallows.
Brassica tops e.g. turnips, parsnips may predispose.
Diagnosis
This is by the clinical signs.

Swine Dysentery
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Econor
Tiamutin
Swine dysentery (SD), is caused by a spirochaetal bacterium called Brachyspira hyodysenteriae. This organism causes a severe inflammation of the large intestine with a bloody mucous diarrhoea (i.e. dysentery).
Disease is common in pigs from 12 to 75kg but severe cases occur occasionally in sows and their sucking piglets.

SD will survive outside the pig for up to seven weeks in cold moist conditions but it dies out in two days in dry warm environments.

Spread through the herd is slow, building up in numbers as the dose rate of the causal agent builds up in the environment. Pigs that recover develop a low immunity and rarely suffer from the disease again.

The high cost of disease is associated with mortality (low), morbidity (high), depression of growth and feed conversion efficiency, and costs of continual in-feed medication.

The incubation period in field cases is normally 7 to 14 days but can be as long as 60 days. Pigs may develop a sub-clinical carrier state initially and then break down with clinical disease when put under stress or when there is a change of feed.

Symptoms
Sows
Clinical disease in sows is uncommon unless new disease appears in the herd.
Piglets
Severe acute dysentery may occur.
Sloppy light brown faeces with or without mucous or blood.
Loss of condition.
Sows become symptom less carriers.
Weaners & Growers
The first signs are:-

Sloppy diarrhoea, which stains the skin under the anus.
Initially the diarrhoea is light brown and contains jelly-like mucus and becomes watery.
Twitching of the tail.
Hollowing of the flanks with poor growth.
Partial loss of appetite.
Slight reddening of the skin.
As the disease progresses:
Blood may appear in increasing amounts turning the faeces dark and tarry.
The pig rapidly loses condition.
Becomes dehydrated.
A gaunt appearance with sunken eyes.
Sudden death sometimes occurs mainly in heavy finishers.
Causes / Contributing factors
Pigs become infected through the ingestion of infected faeces.
Spread is by carrier pigs that shed the organism in faeces for long periods.
It may enter the farm through the introduction of carrier pigs.
Mechanically in infected faeces via equipment, contaminated delivery pipe of feed vehicles, boots or birds.
It can be spread by flies, mice, birds and dogs.
Stress resulting from change of feed may precipitate.
Poor sanitation and wet pens enhance the disease.
Overcrowding.
It is a major disease in the growing pig but the breeding female can become a carrier for a long period of time and therefore acts as a potential source of infection to other pigs.
Diagnosis
This is based on the history, the clinical picture, post-mortem examinations, laboratory tests on faecal smears and the isolation and identification of S. hyodysenteriae by serological and biochemical tests and DNA analysis. Identification requires specialised procedures which are not available in every laboratory.
Post-mortem examinations show that the lesions are confined to the large bowel and sometimes the greater curvature of the stomach.

The disease has to be distinguished from colitis caused by other spirochetes, non-specific colitis, PIA and bloody gut (PHE), acute salmonella infections and heavy infections of the whip worm, trichuris.

Swine Fevers; African, Classical, Hog Cholera
Swine fever is one of the most important virus diseases of pigs. It is notifiable in most countries of the world. .
The pig is the only natural host. The virus is spread from infected or carrier pigs via discharges from the nose, mouth, urine and faeces or infected semen and it is highly contagious. The virus survives in frozen carcasses for long periods of time

Control is by slaughter or as a last resort by vaccination. African swine fever (ASF) and Classical Swine fever are caused by very similar viruses which are only distinguishable by laboratory testing.

Symptoms
Piglets
Huddled.
Chilled.
Vomiting.
Diarrhoea.
Incoordination.
Conjunctivitis.
High fever.
Death sudden.
Piglet malformations.
Very weak piglets at birth showing trembling (congenital tremor).
Sows
When first introduced into the breeding herd it causes inappetence and high fevers.
The virus can cross the placenta to invade the foetuses.
Returns 18 23 days.
Foetal death with mummification.
Embryo death.
Dog sitting position.
Nervous signs
Abortions.
Increases in stillbirths.
Convulsions may occur with death within a few hours.
Sows may lose the use of their legs.
The disease in the acute form will have dramatic effects on reproduction through abortions and embryo and foetal deaths.
Weaners & Growers
Pigs dejected - hang their heads.
Not eating.
Pigs chilled - huddled together.
Diarrhoea.
Eye discharge - heavy.
High persistent fever.
Nervous signs - Incoordination, swaying on the legs.
Blue discoloration of the skin.
High mortality.
Call your veterinarian immediately if you have the above symptoms.

Diagnosis
CSF is a rapid spreading disease with high mortality. There are characteristic post-mortem changes with haemorrhagic lymph nodes, dead patches in the spleen, multiple small haemorrhages in the kidneys and so-called "button ulcers" in the gut.

Laboratory tests include the identification of viral antigen, isolation of the virus and the presence of antibodies in serum. In most countries CSF is notifiable.

Swine Influenza Virus (SI), Flu
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MaxiVac®-FLU
PRV/Marker Gold-MaxiVac FLU
Swine influenza is caused by a number of closely related influenza A viruses that are noted for their ability to change their antigenic structure and create new strains.
Each serotype is identified by surface proteins referred to as "H" and "N". The three common strains that affect the pig are described as H1 N1, H1 N2 and H3 N2. There are also different strains within these serotypes with differing pathogenicity (capacity to produce disease).

The incubation period of the disease is very short, as little as 12-48 hours and the onset is usually rapid and dramatic.

It is virtually impossible to maintain a population of pigs that is influenza virus free.

SI in large herds may become endemic with intermittent bouts of disease and infertility and different strains may also sequentially infect the herd. Immunity to influenza viruses is often short lived (6 months) and the immunity profile in the breeding herd varies considerably with time.



 
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Symptoms
Piglets
It would be unusual to see any signs of swine flu in the sucking pig unless disease entered the herd for the first time.
Colostrum may prevent infection during the sucking period.
Coughing.
Pneumonia.
Fever.
Sows
High temperatures which cause abortions.
Widespread coughing.
Pneumonia
When the virus first enters the herd two or three animals may be observed sick for the first two days, followed by:
A rapid explosive outbreak of inappetence and clinically very ill pigs.
The effects on the reproductive system follow the sudden onset of a rapid spreading respiratory disease with coughing, pneumonia, fevers and inappetence.
Acute respiratory distress persists over a period of 7-10 days (depending on the amount of contact between groups of sows).
At a herd level the following may also be seen:
A sudden and rapid onset of acute illness in sows.
Coughing and pneumonia spreading rapidly.
A return to clinical normality over 7-10 days.
Delayed returns to heat after weaning.
Increased repeats at 21 days.
Increased repeats outside the normal cycle.
Increased numbers of sows coming through not in-pig.
Increased numbers of abortions, particularly late term.
Increased numbers of stillbirth rates and slow farrowings.
Premature farrowings.
Occasionally an increase in mummified pigs.
During the phases of high temperatures other diseases present in the herd may be triggered off. A typical example would be an increase in abortions associated with leptospira infection.
Weaners & Growers
Acute disease:

Classically the pigs suddenly become prostrate.
Breathing heavily.
Severe coughing.
Most of them look as if they are going to die but most of them survive without treatment unless the herd already has a respiratory disease problem.
SI causes severe pneumonia on its own but when it is combined with other infections such as App, EP and PRRS an intractable chronic respiratory disease syndrome can develop. Severely affected individuals or groups of pigs are therefore best given antibiotic cover to prevent secondary pneumonias developing.
Endemic disease:
Here the virus remains in the herd, affecting small groups of pigs often weaners. It may be responsible for continuing respiratory diseases with symptoms as in acute disease but less dramatic.
Causes / Contributing factors
SI can be introduced by:
Infected animals including people, pigs and birds.
Carrier pigs.
Probably on the wind although this has not been proved.
Birds particularly water fowl, are reservoirs of infection.
Secondary bacterial infections.
Fluctuating temperatures.
Stress.
Wet bedding and floor surfaces.
Poor nutrition.
Diagnosis
This can often be made reliably on clinical grounds with acute disease because there are no other diseases that are so dramatic in their onset and clinical effects. No other disease affects so many pigs so quickly. Blood samples taken at the time of onset of disease from affected sows and repeated 2-3 weeks later show rising levels of antibody to the specific virus. SIV can be readily grown from nasal and throat swabs and identified in the laboratory. This is often the best approach to confirm the diagnosis.
In acute disease the spread is so dramatic across all ages that little else can be confused with it. In endemic disease however differentiation from other viral infections can be difficult, but PRRS, PRCV, AD and also erysipelas should be considered.

Swine Pox
This is a disease caused by the swine pox virus which can survive outside the pig for long periods of time and is resistant to environmental changes. It is a vesicular disease.
Symptoms
All Pigs
Small circular red areas 10-20mm in diameter that commence with a vesicle containing straw-coloured fluid in the centre.
After two to three days the vesicle ruptures and a scab is formed which gradually turns black.
The lesions may be seen on any part of the body but are common along the flanks, abdomens and occasionally the ears.
A secondary dermatitis may occur.
Unusual in piglets.
Causes / Contributing factors
It can be spread by lice or mange mites.
Skin abrasions.
Fighting and mixing of pigs.
Diagnosis
It can be confused with localised greasy pig disease, pustular dermatitis and the allergic form of mange. Close examination shows swine pox lesions.

Swine Vesicular Disease (SVD)
(549) Although the virus which causes swine vesicular disease (SVD) virus is different from that causing foot-and-mouth disease (FMD) it produces a disease in pigs that is clinically indistinguishable from FMD. So if you are concerned about SVD in your pigs read also the FMD section.
Should you be concerned about SVD?

If your pig farm is in the UK, mainland Europe or S.E. Asia you should be aware of the possibility of it becoming infected with SVD, however low the risk might be. The herd will probably be slaughtered if it gets infected.

If your pig herd is in Ireland, where SVD has never occurred and which does not import pig meat products, the risk is extremely low. It is just conceivable that it could be brought in on an inadequately disinfected pig lorry returning from mainland Europe where the virus periodically circulates.

If you farm in North or South America, or Australia or New Zealand, the risk of your pig farm becoming infected with SVD or FMD is virtually nil.

Importance of SVD

Although clinically SVD is similar to FMD it causes little impact on productivity. Often it can be so mild that the pigs do not appear lame particularly if they are on straw bedding. What is more, it is strictly a disease of pigs and does not infect cattle, goats, sheep or other species. Why then is it regarded as so important that governments, such as those in the EU, bring in costly slaughter and eradication policies? It is for the very reason first stated, namely, that it is clinically indistinguishable from FMD. They are afraid that if SVD became widespread in the pig populations of FMD free and fringe areas that pig farmers and pig veterinarians may become accustomed to seeing vesicles on pigs noses and feet and not report them or even consider FMD.

One could argue that an expensive slaughter policy is unnecessary, that SVD could be made notifiable (i.e. any pigs with vesicles would have to be reported to the authorities) and that accurate rapid tests (e.g. ELISAs and PCRs) could be available in all diagnostic laboratories, but such an argument would be academic. The fact is that most governments in free and fringe areas would adopt a slaughter and eradication policy if there were a risk of contamination. If you farm in such an area you have to live with such a policy.

Clinical signs

SVD does not infect or affect cattle, sheep, goats or any species other than the pigs. So, unlike FMD, if you keep other livestock they will not be affected.

Clinical signs of SVD are much the same as FMD so read that section.

If there is no slaughter policy and pigs are not killed some may lose the claws off some of their toes. SVD does not usually cause abortion and boars are not sufficiently lame to stop serving sows. Mortality among all age groups is low.

The pigs recover completely in 2-3 weeks but you may see bruises under the claws which gradually move down under the horn as it grows (about 2mm per week). See chapter 10.

In fringe areas (e.g. in the EU) it is a serious problem because the herd will almost certainly be compulsorily slaughtered and although compensation is likely to be paid, the farm cannot be restocked for at least three months. This is twice as long as for FMD because the SVD virus is much tougher and survives longer. Furthermore, after that time small numbers of susceptible pigs may have to be introduced onto the farm to act as sentinels. If there is still residual virus in the premises these sentinels are likely to come down with disease and the farm will have to be emptied and disinfected again.

The pig farm is a long time out of production even if the sentinels do not develop disease but if they do it is even longer with all the financial hardship that this will cause. So-called recrudescences on farms which had been slaughtered out, disinfected and later restocked, were a major problem in the early days of the SVD eradication programmes in Europe.

Diagnosis

This is the same as for suspected FMD. Read the FMD section. SVD cannot be distinguished from FMD on clinical grounds so to confirm the presumptive diagnosis, samples have to be sent without delay to an appropriate laboratory.

Management control and prevention

Vaccination - There is only one main serotype of SVD and theoretically it should be possible to produce an effective vaccine but in endemic areas the disease is too mild to warrant it. Vaccination is not allowed in fringe areas because it might mask the disease and go undiagnosed.
Other precautions
Countries in free and fringe areas apply strictly-enforced national preventative measures against the introduction of SVD. The main features of these measures are control over the importation of pigs and of pig meat products from counties in which SVD occurs. Pig meat products are particularly dangerous because, unlike the FMD virus, SVD virus is tough and survives rigor mortis. If infected pig meat gets into the food chain there is a risk of uncooked waste being eaten by pigs which could trigger off an outbreak. To prevent this many countries have brought in cooked waste feed policies which forbid the feeding of animal products to pigs unless they have been processed through a licensed processing plant.
If the disease does enter a free or fringe area, a slaughter policy is implemented similar to that described for FMD. All diseased and in-contact pigs are slaughtered. A standstill on animal movement is usually imposed and tracings are carried out to check possible spread of the disease through previous contacts.
If you farm in the EU which is an SVD-risk region you should keep in mind the possibility (small though it may be) of contamination of your herd and you should take simple appropriate precautions.
The greatest risk is from contaminated pig lorries returning from Italy where the disease is still present. The virus survives well in lorries and pigs can become infected by mouth or via skin abrasions. The lorry collecting your pigs for slaughter is the obvious danger.
You should not feed pig meat products.
Windborne spread does not occur in SVD so the simple precautions outlined later in this chapter should be effective.

Teat Necrosis
Teat necrosis is a condition in which rubbing the end of the teat causes the teat tip to die (necrosis) and slough off. It is of no consequence in commercial herds which are buying in replacement gilts but it is very important where breeding females are being produced.
It first becomes evident 12 to 24 hours after birth. The teats in front of the umbilicus are the ones at risk because these have the greatest contact with the floor during sucking.

Commercially the condition is not important but it is if gilts are reared for breeding.

Symptoms
Piglets
The teat end appears bright red gradually becoming black.
The damage can be severe resulting in a blind or inverted teat.
Sows
Teats may show permanent damage from trauma at birth.
More common in the teats in front of the navel.
Weaners & Growers
N/A
Causes / Contributing factors
Trauma to the teats occurs on all floor surfaces but to a lesser extent on those that are well bedded with shavings or straw.
Diagnosis
Examine teats 8 - 24 hours after birth for red or black teat sphincters.

.

Teschen Disease
Also called Talfan disease, benign enzootic paresis or poliomyelitis suum.
Teschen disease is caused by a porcine enterovirus, serotype 1, of which there are highly virulent and mildly virulent variants. The virus probably exists throughout the world wherever pigs are kept but most infections are sub-clinical and outbreaks of clinical disease are rare.

The name Teschen disease is traditionally used for the most severe form of the disease, large outbreaks of which were reported many years ago near the borders of Germany and Poland and in Madagascar. Since then smaller, generally milder, outbreaks have occurred from time to time in other regions of the world. These milder outbreaks have usually been called by other names such as Talfan disease (Talfan is a hill in Wales where an outbreak occurred) to evade the application of a slaughter policy. Most countries in the western world had erroneously made Teschen disease notifiable very early on before it was realised that the virus was so widespread. Teschen disease was quietly removed from the EU lists of notifiable diseases several years ago.

When cases occur these days they are usually in weaned and young growing pigs. The disease does not often progress to full paralysis probably because the pigs have a level of immunity or because it is a milder strain of the virus.

It is an infection of the motor nerves only and not the sensory nerves. The pig still has sensation and can feel pin pricks.

The virus multiplies in the intestines and is shed in large quantities in the faeces. It is relatively tough, can survive outside the body, and is highly infectious requiring only a small dose of infected faeces to be ingested to establish infection in the intestines.

Within a herd the virus cycles in the weaner and follow-on accommodation. It is prevented from multiplying in the intestines of suckled piglets by the sow's lactogenic immunity, i.e. the secretory antibodies present in her milk. After the pig has been weaned the lactogenic immunity ceases to be supplied and the virus is able to multiply in the intestines but it cannot get to the nervous system (CNS) because whenever it escapes from the gut it is neutralised by the sow's colostral antibodies which are still circulating in the pig's blood stream. The virus multiplies in the intestines harmlessly for several weeks until the pig has developed an active immunity which stops it from multiplying. The pig is then immune and virus free. If its a young gilt which is retained later for breeding it will in turn pass on its antibodies to its piglets.

The virus can only reach the central nervous system (CNS), multiply in the nerves and cause damage when there are no circulating specific antibodies or when they are at too low a level. It can then be carried in the blood stream to the CNS. This situation may arise if the mother has never been infected with the virus, if the newborn piglet didn't get enough colostrum, or if the virus enters a naive herd for the first time.

Symptoms
All Pigs
Partially loses the use of its lower back legs, and then its thighs and then the rear end of its body.
The partial loss may progress to a total paralysis.
Initially the pig may be slightly off its feed and a little depressed for a day but after that it is otherwise fine with a good appetite and normal temperature.
The pig develops a drunken swaying gait from which many may recover spontaneously.
Its only problem is that it can't walk around very well and in severe cases can't rise from a dog-sitting position.
Incoordination.
In the severe form of the disease the motor nerves are totally destroyed and the disease is irreversible.
Causes / Contributing factors
Poor hygiene i.e. dirty floor surfaces, water contamination.
Environmental contamination from one pen to another i.e. boots, brushes, shovels, clothing etc.
Spread between herds through the movement of young sub-clinical carrier pigs.
Mechanical means via faeces and contaminated equipment, lorries etc.
Contaminated boots and clothing.
Vehicles.
Diagnosis
The clinical signs are suggestive but not conclusive. Serum samples can be taken to demonstrate rising antibodies in paired blood samples taken from a group of pigs at the start of the disease and 10-14 days later. Single blood samples are no good because sub-clinical infection is fairly common and so positive blood samples are also common even when no disease has been observed.
Microscopic examination of the brains and spinal cord of pigs which have been killed will show changes typical of any virus disease but they are not specific for Teschen disease.

Tetanus
Tetanus is caused by the bacterium Clostridium tetani which produces toxins that affect the central nervous system. The organism, which can form spores, lives in the large intestines and faeces of many mammals and in certain soils. This disease can be a problem in outdoor pigs. The incubation period is from 1 to 10 weeks. It would be uncommon to see disease in the sucking piglet under 2 weeks of age.
Symptoms
All Pigs
Hypersensitive.
Fits.
Shows stiffness of legs and muscles.
An erect tail.
Muscular spasms of the ears and face.
High mortality.
Causes / Contributing factors
The bacteria must enter through a dirty abrasion or a cut.
In the sucking pig the most common source is castration - unhygienic methods.
Diagnosis
This is based on the clinical symptoms.

Thin Sow Syndrome
The thin sow syndrome develops over a period of months and one or two pregnancy cycles, with gradual declining body condition until 10 to 30% of the animals have a condition score of 1 or 2. During lactation the sow is unable to maintain her body condition due to an insufficient intake of energy combined with increasing milk output. This process continues over successive lactations.
In sows kept permanently outdoors the stockman should ensure that all the sows have a high body score before the start of cold weather.

Symptoms
Piglets, Weaners & Growers
N/A
Sows
Thin emaciated sows.
Body condition decreases with each successive pregnancy.
Infertility.
Anoestrus.
Abortions
Cystitis - blood in urine.
Causes / Contributing factors
The syndrome arises due to:

Inadequate nutrition.
Poor quality feeds.
Damp floors or draughts will increase the energy requirement of the dry sow.
Fluctuating temperatures.
It is exacerbated in sows kept outdoors in cold weather.
Heavy worm burdens.
Specific diseases e.g. cystitis.
Poor management.
Diagnosis
This is by clinical signs. Select at least twelve faeces samples from thin sows. Submit them to a laboratory for examination to eliminate parasites and blood (from gastric ulcers). Eliminate specific individual diseases such as kidney infections and chronic infections.

 

Thrombocytopaenic Purpura, Bleeding
This is an uncommon condition seen only in young piglets from approximately 7 to 21 days of age. Disease commences 7 to 10 days after the intake of colostrum.
The piglet dies through the failure of normal blood clotting mechanisms. The disease is very sporadic but up to half the litter may be affected.

Symptoms
Piglets
Clinical signs can be sudden.
Good pigs found dead.
Look closely at the skin of these and you will see haemorrhages and blue areas wherever there has been bruising, teeth marks or trauma.
Haemorrhages are evident throughout all body tissues.
Sows, Weaners & Growers
N/A
Causes / Contributing factors
It arises when the sows colostrum contains antibodies that destroy the piglets blood platelets (thrombocytes) which are responsible for the clotting of blood.
The immune system of the sow during the period of pregnancy recognises the platelets as foreign protein and produces antibodies against them.
The formation of these antibodies is also related to the boar that is used.
Diagnosis
Seek veterinary advice and post-mortem examinations. Can be confused with swine fever.

Torsion of the Stomach and the Intestines
Torsion of the stomach or the small intestine is a main cause of sudden death in adult breeding stock. The twist can involve the stomach, the spleen, part of the liver or the intestine.
Symptoms
Piglets
Uncommon but symptoms as in sow.
Sows
Bloated abdomen.
Blue skin.
Sudden death: Often within 2 3 hours of feeding..
Anaemia.
Weaners & Growers
Usually none but sudden death.
Grossly distended abdomen.
The carcass is fresh but the pig is very pale.
Causes / Contributing factors
Deaths are usually sporadic although they can be of significance where, for example, whey is being fed and bloat occurs.
Over-feeding and abnormal fermentation of the contents of both the small and large intestine result in gas formation, increased pressure and torsion.
Prolonged over excitement at feeding may predispose.
Overeating liquid feed.
Large amounts of feed eaten during lactation will predispose.
Diagnosis
Post-mortem examination shows the small and large intestines heavily congested and full of blood. The intestinal tract in the pig is suspended from a common point and this makes it liable to rotate and twist.

Transmissible Gastro Enteritis, TGE
TGE is a very important and highly infectious disease caused by a coronavirus. The virus is killed by sunlight within a few hours but will survive for long periods outside the pig in cold conditions. It is very susceptible to disinfectants particularly iodine based ones, quaternary ammonia and peroxygen compounds.
Disease will persist in the farrowing houses over a period of 3 to 4 weeks until sows have developed sufficient immunity to protect the piglets.

In herds of less than 300 sows the virus is usually self eliminating provided there are good all-in, all-out procedures in farrowing houses and grower accommodation. In larger herds however the virus will persist in the growing herd because piglets at weaning, still under the influence of the maternal antibody, move into houses where the virus still persists. Once the lactogenic immunity in the sow's milk is no longer being taken in the pigs become infected allowing the virus to multiply. The pigs then shed the virus, contaminating the weaner rooms and infecting pigs being weaned after them. TGE can become endemic in herds in a mild form with high morbidity but low mortality.

This disease in the weaning and the growing pig is clinically indistinguishable from porcine epidemic diarrhoea. In small grower-finisher units the virus is likely to disappear from the population. In large finishing units in which susceptible pigs are being brought in frequently, the virus is maintained indefinitely in the population by repeated infection of the newcomers.

Symptoms
Weaners & Growers
When the virus is introduced into a finishing herd for the first time there is rapidly spreading, vomiting and a watery diarrhoea, eventually affecting almost all the animals.
Disease disappears spontaneously over a 3 to 5 week period.
Mortality is usually low.
The main effect on the individual growing pig is dehydration which is resolved in about a week.
Nevertheless the disease may increase the slaughter age by 5-10 days.
Piglets
In the sucking piglet the disease is very severe.
Acute watery diarrhoea.
Almost 100% mortality within 2 to 3 days in piglets under 7 days of age due to severe dehydration and electrolyte imbalance.
There is no response to antibiotic therapy.
The most striking feature is the wet and dirty hairy appearance of all the litter due to the profuse diarrhoea.
Sows
In acute outbreaks the most striking feature is the rapidity of spread.
Vomiting.
Diarrhoea.
Adult animals show varying degrees of inappetence and usually recover over a 5 to 7 day period.
Causes / Contributing factors
The virus is shed in large numbers in the faeces.
Pig faeces therefore are the major source of transmission either directly through the purchased carrier pig or indirectly through mechanical transmission.
Poor pen floors.
Poor pen hygiene associated with bad drainage
Poor hygiene procedures, between pens
Environmental contamination from one pen to another i.e. boots, brushes, shovels clothing etc.
Feeder pipes and feed bins. This is a high risk source for the spread of enteric diseases.
Dogs may shed the virus in their faeces for 2 to 3 weeks.
Birds and in particular starlings may transmit the disease.
Contaminated feed.
Continual use of buildings without all-in, all-out may perpetuate disease.
Continual purchase of naive weaners.
Diagnosis
The clinical picture in acute disease is almost diagnostic. There are no other enteric diseases that spread so rapidly across all pigs. The ultimate diagnosis of TGE must be made in the laboratory from the intestine of a fresh dead pig using fluorescent antibody tests (FAT's). Isolation of the virus is also carried out.
Porcine epidemic diarrhoea (PED) could give a similar picture but it would be less acute and with less mortality in sucking pigs.

Tuberculosis
Tuberculosis affects mammals, including people, and birds. The causal organism, Mycobacterium tuberculosis, is sub-classified into types, human, bovine and avian. The avian type is referred to as M. avium or more often the avian/intracellulare complex because it is not a uniform species. M. avium itself infects mainly birds but is also found in the environment along with M. intracellulare which is predominantly saprophytic or free living. Pigs are rarely infected by the human or bovine types but are commonly infected by the avian/intracellulare complex.
The avian/intracellulare complex also causes sub-clinical non-progressive infection in healthy people. The main concern is that it could cause more serious disease in immuno-suppressed people and people with AIDS.

In most countries if lesions are found in the neck at slaughter the whole head is condemned and if they are found in the mesenteric lymph nodes which drain the intestines the offals are condemned. If they are more widespread in the body, which is rare, the whole carcass may be condemned or cooked. If small lesions are missed by the meat inspector normal kitchen cooking destroys the organism.

Symptoms
All Pigs
It causes small nodules in the lymph nodes of the neck and those that drain the small intestine.
In the great majority of cases the lesions are non-progressive, they do not spread through the body, do not make the pig ill and are not excreted.
There are no clinical symptoms and there is no difference in performance between infected and non-infected pigs.
Causes / Contributing factors
The disease does not spread between pigs and should be regarded as an environmental infection. It is rarely diagnosed in living pigs.
Paddocks that have been treated with poultry manure up to one year previously, (or, in the case of bovine TB, which have been grazed by infected cattle or badgers).
Avian TB as the name implies is found in wild birds. The organism is shed in large numbers via droppings and therefore food, grain or bedding contaminated by birds becomes a potent source.
Peat often contains M. intracellulare. Peat is used both for bedding and gut stimulation in the young piglets. It should only be used if it as been pasteurised.
Water contaminated by M. avium/intracellulare is often a source.
Diagnosis
In living pigs diagnosis is by the skin tuberculin test but usually it is brought to the farmer's attention by high condemnation rates at slaughter

Udder Oedema, Failure of Milk Let Down
This presents itself as a failure of milk let down associated with excess fluid in the mammary tissues and is a condition seen in both gilts and sows. The oedema or fluid can be both in the skin and deep in the udder tissue. The pressure produced in the glands once farrowing has ceased prevents a good milk flow and there is a reduction in both the quantity and quality of the colostrum which means a lowered immune status of the piglet. Severe oedema, particularly in the rear glands may result in poor accessibility of teats at sucking time. Such glands often dry off. When piglets eventually find the teat they will not thrive but waste away.
Usually there is a history on the farm of poor milking amongst all ages and one or two pigs per litter having to be fostered at around 5 to 7 days of age due to poor growth. Scouring problems can sometimes be related back to udder oedema and a poor intake of colostrum.

Symptoms
Sows
It is characterised by a clinically normal animal with no fever or loss of appetite.
The distinguishing features are a firmness and swellings of all the glands, discomfort on high pressure but no actual pain.
Mastitis may develop.
Palpitation of the udder shows fluid either just beneath the skin or deep in the gland and often extending between the legs towards the vulva. The vulva is also often involved.
No milk.
Constipation.
Piglets, Weaners, Growers
N/A
Causes / Contributing factors
High levels of feed 7 to 10 days before farrowing, particularly high energy levels.
Constipation associated with a reduction in fibre intake
Breed of sow.
Lack of exercise.
Low intake of water.
Diagnosis
This is based on the demonstration of oedema of the udder, by appearance and palpation and the appearance of the litter. Oedema and congestion can lead to mastitis.

Vesicular Exanthema
The virus of vesicular exanthema of swine (VES) is different from those causing foot-and-mouth disease (FMD) and swine vesicular disease (SVD) but it produces a disease in pigs that are clinically indistinguishable from FMD and SVD. Unlike FMD it only effects pigs.
Symptoms
All Pigs
VES does not affect cattle, sheep, goats or any species other than the pigs and sea mammals. So, unlike FMD, if you keep other livestock they will not be affected.
Mortality is low but there may be some deaths in sucking piglets.
Salivation.
Inappetance.
Vesicles around the mouth, nose, tongue and feet.
Causes / Contributing factors
Feeding uncooked garbage/pork scraps to pigs.
Diagnosis
This is the same as for suspected FMD and SVD and requires laboratory tests to identify it.

Vesicular Stomatitis
This disease occurs mainly in South and Central America, occasionally in the USA and rarely as epidemics extending as far North as Canada and as far South as Argentina.
The VS virus produces a disease in pigs that is clinically indistinguishable FMD, SVD and VES. Most often however infection of pigs is subclinical.

Symptoms
All Pigs
Drooling saliva.
Foot lesions and lameness.
May be a reduction in growth rate.
Rise in body temperature to 40-41°C (106-107°F).
Clinical signs are so closely similar to those of FMD, that they need not be repeated in detail here.
Like FMD, the most striking feature is the appearance of vesicles (blisters) up to 30mm diameter on the nose, lips, and teats and around the coronets of the feet which may make the pigs lame.
Mortality is usually low and most pigs recover in one to two weeks.
One difference from FMD is the relatively small proportion of pigs in a herd outbreak that show vesicles. Another difference from FMD is that usually when an outbreak occurs in a pig herd it rarely if ever spreads to cattle and horses on the same farm and vice versa.
Causes / Contributing factors
The virus is spread mechanically by a variety of insects and has been isolated from face flies, black flies, eye gnats, sand flies, leaf hoppers and mosquitoes.
The virus may multiply in some of these insects and can pass vertically through the ovaries to the offspring.
Insects are therefore thought to act as reservoirs, perpetuating the virus in the enzootic regions.
It is thought that in the spread between pigs in epizootic regions insects get the virus on their mouth parts from feeding on the lesions left after the vesicles have burst and carry it mechanically to other pigs in the same herd or in neighbouring herds. It is unlikely that they get infected from sucking the pigs' blood.
The virus can also spread between pigs by direct contact particularly when pigs are tightly packed together, for example, during transport or when pigs fight after mixing
The virus can also be carried from herd to herd through the movement of pigs.
Diagnosis
VS is notifiable in most epizootic areas, i.e. if you suspect it in the herd you or your veterinarian have to report it to the authorities.
The clinical signs of VS are similar to those of FMD and SVD both of which are subject to government slaughter and eradication policy in Canada, the USA, Mexico, Chile, South Brazil, and Argentina. It is therefore crucial to reach a fast accurate diagnosis. This can only be done by delivering samples to a laboratory equipped and capable of doing the appropriate tests. The aim is to eliminate the possibility of the disease being FMD or SVD (or in California VES).

The best samples to submit are vesicular fluid, if available, which has high concentrations of virus and/or vesicular tissue (e.g. the thin superficial skin layer over the vesicle) which also contains virus. If these samples are from pigs or cattle the authorities will probably only allow you to send them to a designated FMD laboratory in case the disease is FMD. If they are from a horse then they cannot be FMD (horses do not get FMD, SVD, or VES) and you may be allowed send them to other laboratories (e.g. in the USA, the USDA-NVSL at Ames or other State laboratories).

The possibility of the disease being FMD or SVD (or in California VES) should be eliminated and an accurate identification of the VS virus made. The first of these, namely, elimination of FMD, SVD and VES can probably only be done in the designated FMD laboratories. Other diagnostic laboratories may be able to do the second, namely, identification of the VS virus in samples from horses. This is done by demonstrating the presence of the VS virus in the vesicular fluid or tissue first by ELISA which is rapid giving an answer in a few hours time.

Paired blood samples (i.e. one sample taken during the early stage of the disease and one 10-14 days later) may also be taken. The authorities will probably allow these to be tested in non FMD-designated laboratories (e.g. in the USA, State laboratories). The tests used are generally ELISAs with back-up neutralisation and complement fixation tests. In horses, rising antibody levels to the VS virus have to be demonstrated in the blood samples to be sure that an active VS infection has taken place. This is because in epizootic regions some old horses may have positive antibodies from the last outbreak. Pigs generally do not live so long so single positive samples would be strongly indicative of active infection.

Unfortunately blood sampling and serology may mean a delay of at least two weeks which is too long.

Vice
Vice can be a major problem with considerable economic loss. Why do pigs mutilate each other? Poor environmental conditions and poor stockmanship cause aggravation and aggression. Stand for a few minutes and observe pigs that are either tail biting or ear chewing and you will see that there is one overriding feature, the pigs give the impression of being very unhappy. If you notice that only one pig appears to be the aggressor, remove it from the pen.
Vice in the dry sow is confined to vulval biting particularly in the last 3 to 4 weeks of pregnancy. This can be a major problem in loose-housed sows and in badly managed systems there may be 80% of all sows in a herd with the vulva completely bitten off. Severely traumatised vulvas heal with scar tissue and this can cause constrictions and difficulties at farrowing.

Types of Vice
The weaned pig
Penis / navel sucking..
Prepuce sucking.
Ear sucking..
Tail biting.
Growers
Tail biting.
Ear necrosis.
Chewing feet.
Flank biting.
Sows
Vulval biting See disease listing
Piglets
Prepuce sucking
Symptoms
Weaners & Growers
Evident by trauma and infection of the skin - Dermatitis.
Lameness.
Mortality.
Piglets
N/A
Sows (See Vulval Biting)
Swollen / torn vulva.
Evidence of blood on the skin and noses of the sows highlight the possibility of this condition.
Severe haemorrhage with loss of life in a few animals.
Low grade infections.
Ascending womb infections.
Increased repeats.
Scar tissue.
Causes / Contributing factors
Weaners, Growers & Piglets

Management factors
A change in the diet.
A very humid environment.
Long tails.
Aggressive breeds.
Draughts.
No bedding.
Fluctuating temperatures.
Trauma.
High air speed
Uncomfortable conditions.
High stocking densities.
Unhappy pigs.
Shortage of trough space.
Water shortage.
Ammonia levels > 20ppm.
Wet pens.
Automatic feeding and little human/pig empathy.
High hydrogen sulphide levels > 10ppm.
Pigs too small for the environment.
Bad pen designs - badly sited feeders.
High carbon dioxide levels > 3000ppm.
Nutritional factors
Low salt in the diet.
Inadequate nutrition.
Diet changes.
Poor feed availability.
Feeding pellets.
Rations with small particle sizes.
Disease factors
Colitis.
Greasy pig disease.
New concrete and skin trauma.
Parasites.
Pneumonia.
PRRS skin lesions.
Skin trauma.
Swine pox.
Wet eczema.
Diagnosis
Based on observations and skin lesions.

Vomiting, Wasting Disease, Ontario Encephalitis
This is caused by a coronavirus which is widespread in the pig populations of North America and Europe but clinical disease is rare. This is because although the virus can infect susceptible pigs at any age it only causes clinical disease in newborn piglets. Most sows have been infected and are immune. They pass their immunity to their piglets in colostrum which protects them through the vulnerable period.
There is a variation in virulence between strains resulting in two different disease syndromes. Both start at around 4 days of age, are sudden in onset and affect whole litters

Symptoms
Sows, Weaners & Growers
N/A
Piglets
Huddled.
Hairy.
Vomit bright green-yellow vomitus.
Constipated.
In the typical vomiting and wasting disease syndrome piglets lose their ability to suck or swallow, become very thirsty and stand with their heads over water but are unable to drink.
They waste away, become severely emaciated and die.
In the typical encephalitis or brain infected syndrome they:
Froth and champ at the mouth.
Develop blueing of their extremities.
Abdomens become bloated.
Tremble.
Stilted gait which rapidly progresses to partial paralysis of the legs.
They lie down.
Go into convulsions.
Roll their eyes.
Die within four days of onset.
Causes / Contributing factors
Lack of immunity from sows to piglets via colostrum.
Diagnosis
The clinical and pathological picture is diagnostic of the disease. If you open up their abdomens you will find gas in the stomach and intestine but no food, only some brightly coloured liquid. You will also see brightly coloured crystals in the kidneys. A blood test is available. There is no treatment.

Vulval Biting
This is a common condition in sows loose housed in the last 5 - 6 weeks of pregnancy.
Sows bite at the vulva, which has become swollen with advancing pregnancy, particularly when access to food fed on the floor is poor. A sow bites the vulva to gain access to feed. The trauma causes haemorrhage, infection and the development of scar tissue which may inhibit the farrowing process.

Symptoms
Sows
Acute:

Blood on the noses of sows.
Blood around the vulva of the affected sow.
Haemorrhage.
Swollen red torn infected vulva.
Occasionally inappetence.
Chronic:
Scar tissue.
Abscesses.
Low grade infections.
Ascending womb infections discharges.
Repeats in some badly affected sows.
Piglets, Weaners & Growers
N/A
Causes / Contributing factors
Group behavioural abnormalities.
Vulval biting is much more common in pens that are long and narrow rather than those that are wide. There is less competition at feeding time in a wide pen.
Vulva biting is also common when electronic feeder systems are used. It requires careful stockmanship and good pen design to prevent it.
There is a relationship between vulva biting and feed intake, the size of the feed pellet, the type of floor surface and the bedding used. Many cases occur in the last 3 - 4 weeks of pregnancy.
High stocking densities predispose.
Diagnosis
Made from the symptoms, examine the vulva for trauma.

May be confused with cystitis

Vulval discharge syndrome
Since 1985 there has been a gradual reduction in farrowing rates in many herds associated with increased repeats in sows. A survey carried out at that time indicated that up to 24% of herds may have had previously unrecognised problems with this disease.
A discharge from the vulva post-service does not automatically mean there has been a pregnancy failure, but it will in most cases indicate infection. Discharges can arise from the rectum, the vulva, the vagina, the cervix and the uterus. Discharges can also arise from infection of the kidneys (pyelonephritis) or the bladder (cystitis) with pus being passed in the urine. It is important to record the time when discharges are first seen, their colour and composition and effects on the sow.

Vulval discharges are common within 3-4 days of farrowing when a thick viscous material may be excreted. If the sow is healthy, the udder is normal and there is no mastitis, ignore it.

A heavy smelling bloody discharge may indicate a retained piglet or afterbirth.

Discharges are important between 14-21 days post-service. The lips of the vulva of each sow should be parted daily and any tackiness or small discharge noted. The sow should be marked and if she repeats a problem may be developing. Discharging sows may be pregnant and always pregnancy test before culling.

Discharges in healthy sows are normal up to 5 days post farrowing at mating and 3 - 5 days post mating - only if slight.

Symptoms
Piglets, Weaners & Growers
N/A
Sows
Vulval discharges are common within 3-4 days of farrowing when a thick viscous material may be excreted. This is normal.
If the sow is healthy, the udder is normal and there is no mastitis, ignore it. It is common practice to inject such sows, but this is not necessary under these circumstances.
A heavy smelling bloody discharge may be from a retained piglet or afterbirth.
Sow may be ill.
Mastitis.
Increases in returns at 18 - 23 days post service with discharge.
Increases in returns >23 days post service with discharge.
Increases in sows not in pig.
Reduced farrowing rates by 10 - 20%.
Increased negative or doubtful pregnancy tests at 30 days post service.
Litter size normal.
Embryo death.
Abortion.
Anoestrus.
The table below gives the times discharges might be seen and their likely significance.

INSERT TABLE


Causes / contributing factors
Infection can be caused in a number of ways:

Vulval discharges arise from opportunist bacteria in the anterior vagina that cause a womb infection or endometritis. These include:
- Actinomyces pyogenes
- Chlamydia
- E. coli *
- A. suis
- Erysipelothrix
- Klebsiella *
- Leptospira bratislava / muenchen
- Pasteurella
- Proteus
- Pseudomonas
- Staphylococci *
- Streptococci * (* Common causes)
Herds with high numbers of old sows.
A short lactation length (14-21 days).
Multiple matings. Cross mating boars.
Handling the prepuce at mating and squeezing the preputial sac.
No supervision at mating.
Matings towards the end of the oestrus period.
Wet, dirty boar pens. Poor drainage. Continual use.
Dirty, wet sow mating pens and continual use without cleaning.
Small stalls where the sow adopts a dog sitting posture with heavy contamination of the vulva.
Housing maiden gilts in stalls.
Heavy vulval contamination, for example in maiden gilts housed on slats where slurry spills over.
Early embryo mortality.
Re-mating discharging sows.
Using old boars on young sows.
Using young boars on older sows.
Diagnosis
Diagnosis is considered in three parts:

Studying records.
Observations on vulvas 14 - 21 days post service.
Bacteriological examinations of swabs from the prepuce and vagina from all boars and 10 problem sows and post mortem examinations on the uteri of affected sows.
Cultures are carried out on the swabs and the predominating bacteria determined. Sensitivity tests identify antibiotics that could be used.
The main organisms associated with endometritis and vulval discharges are opportunist invaders. In some herds no specific organism can be identified, although bacteriological tests may show one or more bacteria predominating either in the prepuce or vagina. A precise diagnosis can be difficult.

Further Reading

Yersina Infection
Two species of this bacterium occur in the pig's intestine, Y. pseudotuberculosis and Y. enterocolitica. They normally cause no disease but have been associated with minor problems in weaned pigs. The bacteria are often found in the tonsils. It can cause diarrhoea in people.
Symptoms
Weaners & Growers
Y. enterocolitica causes inflammation of the small and large intestines with diarrhoea and
Y. pseudotuberculosis causes small tiny abscesses throughout the carcass.
Inappetence.
Mild fever.
Sows
N/A
Piglets
Rare
Causes / Contributing factors
This is a faeces spread disease.
Diagnosis
The main significance of the organisms is cross reactions that occur when blood tests are carried out for brucellosis. Pigs carrying the organism are likely to react positively. If this is the case it is necessary to determine the point in the rearing system when exposure takes place and break the cycle by management control. Yersinia are easily grown in the laboratory.

Though this subject is old, I find this educational to a newbie like me. Thank you sir for sharing.God bless.