Disease Checklist:

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Pneumonia
Related Products:
Aurofac / Aureomycin
Econor
PNEU PAC®-ER
SS Pac®
Tiamutin
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.

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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).

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Porcine Dermatitis and Nephropathy Syndrome (PDNS)
Related Products:
Circovac
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.

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Porcine Enteropathy
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.

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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.

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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.

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Porcine Reproductive & Respiratory Syndrome (PRRS)
Related Products:
Ingelvac PRRS
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.

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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.

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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.

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Post Weaning Multisystemic Wasting Syndrome (PMWS)
Related Products:
Circovac
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.

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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.

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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).

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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.

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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.

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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.