Disease Checklist:

[mikey]

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.

[mikey]

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.

[mikey]

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).

[mikey]

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!

[mikey]

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

[mikey]

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.

[mikey]

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

[mikey]

Enzootic Pneumonia (EP)
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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

[mikey]

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).

[mikey]

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.

[mikey]

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.

[mikey]

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.

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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).

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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.

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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.