Diarrhoea or Scour

Of all the diseases in the sucking piglet, diarrhoea is the most common and probably 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 levels of mortality can rise to 7% or more and in individual untreated litters up to 100% (in TGE it may reach 100% overall) . The causes of diarrhoea are shown in Fig.8-29. Four of the agents listed in Fig.8-29 are viruses, transmittable gastro-enteritis (TGE), rotavirus, porcine epidemic diarrhoea (PED) virus and PRRS virus. The main bacterial causes are E. coli and clostridia and the main parasite is coccidia. This section deals principally with E. coli diarrhoea. Clostridial diarrhoea, coccidiosis, TGE and PED are dealt with in more detail in other sections in this chapter.

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.

Other agents such as adenoviruses, astroviruses, bredaviruses, calciviruses, toroviruses, picoburnaviruses and chlamydia, have been identified in diarrhoeic faces but their significance is mostly unknown. Adenoviruses may be involved in pneumonia and are thought sometimes to worsen other pneumonias such as enzootic pneumonia. Bredaviruses have been associated with loss of appetite, weakness, tremors and death in weaners but it is extremely rare. Chlamydia cause conjunctivitis, coughing and arthritis (and in sows have been associated with infertility and stillbirths). Non of these agents cause common diseases of any importance in pigs and are best ignored by the pig farmer.

Clinical signs

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.

Acute disease
The only sign may be a perfectly good pig found dead. Post-mortem examinations shows severe acute enteritis, so sudden that there may be no evidence of scour externally. Clinically affected piglets huddle together shivering or lie in a corner. The skin around the rectum and tail will be wet. Look around the pen for evidence of a watery to salad cream consistency scour. In many cases there is a distinctive smell. As the diarrhoea progresses the piglet becomes dehydrated, with sunken eyes and a thick 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.

Sub acute disease
The symptoms 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 manifest by a watery to thin salad cream consistency diarrhoea, often white to yellow in colour.

Diagnosis

The overall picture must be considered when making a diagnosis. Sudden outbreaks of scour involving large numbers of litters with acute diarrhoea and high mortality suggest TGE, epidemic diarrhoea or PRRS. It always helps in differentiating these infections to know whether the herd had previously been exposed to any of these diseases or not. If exposure is for the first time the outbreak is likely to be explosive.

Rotavirus diarrhoea appears in waves in individual litters or groups of litters and normally in the second half of lactation. Coccidiosis has an incubation period of 6 days and is usually involved in diarrhoea complexes 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 because they pass on poorer levels of immunity. Clostridial infections also occur at this age.

Diagnosis is based on the clinical examinations, the response to treatment (viral diseases do not respond to treatment) and laboratory examination of the scour. Submit a rectal swab or a live pig to the laboratory for cultural examinations and antibiotic sensitivity tests.

Treatment

Some antibiotics available are shown in Fig.8-30. Most of these are active against E. coliand clostridia but not the virus infections.
In severe outbreaks of E. coli disease the sows feed can be top dressed with the appropriate antibiotic daily, from entry into the farrowing house and for up to 14 days post-farrowing. This can be effective in reducing bacterial output in the sows faeces.
Observe litters for the presence of diarrhoea both night and morning.
Study the history of the disease on your farm. Is it sporadic, in one piglet in a litter, or total litters?
In the light of the history either treat the individual pig or on the first signs of disease treat the whole litter.
If a litter is badly scoured dose night and morning for a minimum of two days.
Assess the response to treatment. If there is no change within 12 hours then change to another medicine as advised by your veterinarian.
Always treat piglets less than 7 days of age by mouth.
For older pigs where the disease is less acute injections are equally effective and easier to administer.
Provide electrolytes in drinkers. These prevent dehydration and maintain body electrolyte balances.
Cover the pen, the creep area and where the pigs defecate with straw, shredded paper, shavings or sawdust.
Provide an additional lamp to provide an extra source of heat.
Use binding agents such as chalk, kaolin or activated attapulgite to absorb toxins from the gut.

Management control and prevention

Adopt procedures to prevent the spread of the scour.

– Disinfect boots between pens. – Use a disposable plastic apron when dosing piglets to prevent heavy contamination of clothing. – Wash hands after handling a scoured litter. – Disinfect brushes and shovels between pen.

Ensure that farrowing houses are only used on an all-in all-out basis with a pressure wash and disinfection between each batch.
Farrowing pens must be dry before the house is repopulated. Remember that moisture, warmth, waste food and faeces are ideal for bacterial multiplication.
Pen floors should be well maintained. Poor pen hygiene associated with bad drainage predisposes to scour.
Look carefully at the part of the pen floor where there are piglet faeces. Is this poorly drained? Do large wet patches develop? If so cover them with extra bedding daily and remove. This is a most important aspect of control.
Check nipple drinkers and feeding troughs for leakages.
Ensure that faeces are removed daily from behind the sow from the day she enters the farrowing crates until at least 7 days post-farrowing if the floors are slatted. Also remove faeces daily throughout lactation if they are solid concrete.
Maintain creep environments that are always warm and comfortable. Fluctuating temperatures are a major trigger factor to scour particularly from 7 to 14 days of age.
Do not penny-pinch on your heating costs. Many cases of scour are precipitated by attempts to save on costs of energy.
Check for high air flow and draughts. They predispose to scour.
Consider vaccinating against E. coli (make sure first that this is the cause of the problem however). E. coli vaccines only protect the piglet for the first 5 to 7 days of age.
Assess the environment of all the farrowing house. Poor environments allow heavy bacterial multiplication and a much higher bacterial challenge is likely to break down the colostral immunity.
Check the sow’s health. Animals affected with enteric or respiratory disease, lameness or mastitis predispose the litter to scour.
Avoid the use of milk replacers where possible. Their routine use, particularly if they are allowed to get stale or contaminated, may increase the incidence.
Where farrowing house floors are very poor, pitted and difficult to clean, brush them over with lime wash containing a phenolic disinfectant. See chapter 15.
Scour is more common in large litters. Split suckling should be adopted.

Colostrum management

It is vital that the piglet receives the maximum amount of colostrum within the first 12 hours of birth. High levels of antibody are only absorbed during this period. Factors such as poor teat access, poor crate design, and particularly the development of agalactia in the sow, associated with udder oedema, reduce intake.

In an outbreak of scour it is important to establish if udder oedema is present. It is more common in gilts and second parity than in older sows. If E. coli diarrhoea is a problem in younger aged females this suggests that immunity levels are low and vaccination should be considered. Inject the sow twice 2 to 4 weeks apart the second injection at least two weeks before farrowing, but these times are variable depending upon the vaccine used. With good management it should not be necessary to vaccinate the sows, only the gilts.

Eradication

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.

A summary of the management factors associated with disease is shown in Fig.8-31.