Disease Checklist:

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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.

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Streptococcal Infections
Related Products:
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.

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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.

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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.

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Swine Dysentery
Related Products:
Aurofac / Aureomycin
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.

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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.

[mikey]

Swine Influenza Virus (SI), Flu
Related Products:
MaxiVac Excell 3
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.

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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.

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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.

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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.

.

[mikey]

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.

[mikey]

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.

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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.

 

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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.

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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.