Introduction

The predominant signs, i.e. diarrhoea, anorexia, pyrexia, vomiting, dysentery and tenesmus, make the clinical diagnosis of gastroenteric disease fairly straightforward. The clinician will find the age of the pig and any other history, e.g. an alteration to diet, helpful in trying to establish causality. Faeces samples rather than rectal swabs, which are not normally sufficient, are likely to be vital. The ultimate mode of diagnosis may have to be a series of post-mortems.

Mode of Infection

Many enteric organisms and parasites are very resistant to desiccation and disinfection, particularly if this does not follow thorough cleaning. Pet or smallholder pigs are likely to become infected by faeces on visitors’ boots. Because of this, commercial pig-men, however well meaning, should be kept away from backyard pigs. Commercial pigs are particularly vulnerable to incoming stock and transport lorries. These lorries may include those delivering feed or bedding. They may be vehicles collecting dead stock. The lorries may be collecting pigs for sale; weaners, fatteners or cull sows and boars may also be a risk. All transport lorries should stay outside the farm gates and be loaded and unloaded there.

Prevention

Pig farms should avoid bringing live pigs on to the farm. The advantages of having a closed herd are many. For fattening herds, having an ‘all-in all-out’ policy is vital. All outgoing pigs should be taken and loaded outside the perimeter in special facilities. Equally, all dead pigs should be either incinerated on-farm or taken outside the perimeter for collection. All visitors have to be ‘pig free’ for 3 days before entry. All visitors should wear boots and overalls provided by the farm at the gates (veterinarians particularly should remember to uphold strict biosecurity). All visitors should leave their vehicle outside the farm gates. A visitors’ book should be kept recording all visitors’ names. The company or practice they work for should be recorded, as well as the last pig farm they have visited and the date of that visit. The reason for the visit should be noted. Pig farmers should try to limit the number of visits by outsiders to a minimum.

Causes of Enteric Disease

Enteric Diseases Caused by Viruses and Their Treatment

Epidemic diarrhoea

This is caused by a coronavirus. The disease is also called porcine epidemic diarrhoea (PED). It shows clinical signs very similar to TGE (see below). Both conditions are now rare but TGE was common in the UK in the 1960s. Epidemic diarrhoea was first recorded in the UK in 1972. Historically it was less common than TGE. There are two forms of the disease. Both have a high morbidity like TGE but a reduced mortality. One type occurs in piglets less than 5 weeks old. It causes profuse watery diarrhoea. Some young piglets may vomit. The only sign seen in older pigs is a transitory anorexia with evidence of abdominal pain. The second type causes diarrhoea in the entire herd with a few deaths in the neonatal piglets. The two types can only be differentiated on clinical signs. However there is a specific monoclonal antibody test available to differentiate epidemic diarrhoea from TGE. There is no specific treatment available. Extra warmth and the provision of electrolytes are helpful. There is no vaccine available.

Rotavirus infection

This is a very common condition in baby pigs. Rotaviruses occur in many species of farmed livestock, including birds. The rotavirus which normally infects piglets is from the Group A type of viruses. Groups B, C and E are also found. The virus is very stable and can survive in the environment for several months. When the virus infects very young piglets there is a high morbidity and a high mortality. The piglets are depressed, anorexic and reluctant to move. They may vomit. These signs are followed by profuse yellow diarrhoea. This will continue for a few days. The piglets will become less ill quite soon provided they are kept warm. The diarrhoea may continue for up to 2 weeks. However if piglets are over 1 week of age when they contract the disease, the mortality is much reduced particularly if there is good temperature control and electrolytes are provided. Older pigs are more resistant and often the disease is subclinical. It is usually only found in conjunction with another pathogen. Some authorities advise removing the diarrhoeic piglets from the sow. In the author’s experience this is not worthwhile, as the piglets become weak and die. Antibiotics and anti-protozoal drugs should be given if there is evidence of concurrent infections. Diagnosis is by isolation of the virus in a faeces sample using electron microscopy and a fluorescent antibody test (FAT). Antigens and antibodies can be confirmed with an enzyme-linked immunosorbent assay (ELISA). Serology of a few of the herd will confirm the disease retrospectively. A post-mortem will show a typical milk-filled intestine with dehydration. Histology of the small intestine will show villous atrophy. The disease spreads relatively slowly. An ‘all-in all-out’ regime in the farrowing houses is well worthwhile with thorough cleaning and disinfection. There is no vaccine available.

Transmissible gastroenteritis

This highly contagious disease is caused by a coronavirus. There has not been a major outbreak in the UK for over 30 years. The incidence of the virus is very low on mainland Europe. The disease is widespread in the USA. The virus which causes TGE is very similar to the virus which causes PED (see above). It may be that there is some cross-immunity so that low levels of PED virus prevent widespread TGE.

Vomiting wasting disease

This disease is caused by a coronavirus, the haemagglutinating encephalomyelitis virus. It was first recorded in Canada in 1962. It occurs in the UK; clinical signs are rare although serological studies indicate that the virus is very widespread. The virus is spread by the oro-nasal route. The incubation period is within 3–5 days. It affects piglets between 5 and 20 days of age. As the name suggests, they vomit, slowly lose weight and die. They have a raised rectal temperature and are constipated. They are depressed and anorexic. A very few piglets may show neurological signs of ataxia and difficulty in swallowing. Not all the piglets in a litter will be affected. The healthy piglets will look very different from the poor wasted infected piglets, which will often be very hairy. Sows rarely show any clinical signs except a brief fever and anorexia for 12 h. Gross post-mortem findings are not helpful. Twenty-five per cent of cases will show an encephalomyelitis on CNS histopathology. There is some colostral immunity. The bigger pigs will get an active immunity. This is not a disease of outdoor pigs as the virus is readily killed by ultraviolet light. Diagnosis is by virus isolation or FAT on the faeces. A retrospective diagnosis can be made with serology. There is no treatment and euthanasia is indicated. There is no vaccine available. Passive colostral immunity will protect the piglets from disease.

Enteric Diseases Caused by Bacteria and Their Treatment

Campylobacter enteritis

This is a complex condition as Campylobacter spp. are ubiquitous but rarely are clinical signs linked to the presence of an organism. The main organism is Campylobacter coli but other Campylobacter spp., e.g. C. jejuni, C. hyointestinalis subsp. hyointestinalis or subsp. lawsonii, C. mucosalis, C. hyoilei, C. lari or C. lanienae, may be involved. Campylobacter spp. classically cause a mucoid creamy diarrhoea or even dysentery in piglets less than 3 weeks of age. They will also cause mucoid diarrhoea in weaned piglets which are not immune.

In piglets the incubation period is 3 days. They will have a slight rise in rectal temperature before the diarrhoea, which will continue for a few days. There is a sharp loss of condition but death is rare. Piglets contract the infection from sows. Some will then become carriers. Therefore diagnosis can only be confirmed if there is a definite profuse growth of the organism or from a post-mortem showing massive enlargement of the lymphoid tissue in the terminal ileum. Neomycin or tetracyclines are the preferred antibiotics given by the oral route.

Clostridial diarrhoea

There are other Clostridium spp. which cause enteric problems in pigs. Clostridium difficile has been isolated from pigs and shown to cause acute haemorrhagic diarrhoea or a more chronic scouring. These isolates have been found in North America and France but not in the UK. Both A and B toxins have been found. It must be remembered that the organism is zoonotic. In piglets under 1 week of age it causes abdominal distension followed by diarrhoea. There is marked dehydration with sunken eyes. There is scrotal oedema. This unusual sign is pathognomonic for the condition. These animals will not recover and should be euthanased. There is both high morbidity and mortality. On post-mortem there is marked large bowel pathology but no small bowel pathology. This is another pathognomonic finding. Diagnosis with ELISA or polymerase chain reaction (PCR) can be made from the large bowel. Rarely mastitis has been reported in sows. Fluoroquinolones are suggested as treatment in sows. Treatment of piglets is rarely rewarding but tylosin has been suggested. There is no vaccine or antiserum available. Vancomycin and metronidazole are not licensed for pigs. They should not be used in pigs but should be reserved for human treatment.

Pigs will get tetanus caused by Clostridium tetani. It is extremely rare and in the normal course of pig husbandry, pigs do not require any preventive measures e.g. vaccination or antiserum. The one exception is when piglets, normally pet pigs, are castrated in a stable which has been used for horses. In these circumstances, it is advisable to give them 2 ml of tetanus antiserum (TAT). As in other species infection with C. tetani can follow wounds other than castration wounds, but in pigs this is extremely rare.

Pigs will show some slight stiffness in gait and have a straight tail and pricked ears. This may progress to recumbency and opisthotonos with all the limbs rigid and pointing backwards. As death normally follows, euthanasia must be advised. However, in many cases recumbency does not occur and the pigs with or without treatment with penicillin and TAT will recover.

Clostridium novyi type B will affect pigs and cause sudden death in adults and large fattening pigs. C. novyi type A may also cause similar deaths. Both organisms seem to produce very powerful toxins after multiplication in the pig’s liver. This is thought to occur if the liver does not receive sufficient oxygen as a result of chronic pneumonia. C. novyi infection may also follow any enteritis caused by another organism. Diagnosis can be made on post-mortem. The carcass will show rapid putrefaction with submandibular swelling, pulmonary oedema and an excess of pericardial and peritoneal fluid, which is often blood tinged. The pathognomonic sign is the famous ‘Aero liver’. FAT or PCR techniques can be used to confirm the diagnosis.

Clostridium septicum has been isolated from pigs which have shown gangrenous swelling of the limbs. These cases are normally fatal and euthanasia is advised.

Escherichia coli diarrhoea

This is a disease of the neonatal piglet. It normally starts with diarrhoea but quickly progresses to a septicaemia and death if there is no treatment. Escherichia coli will cause disease conditions in older pre-and post-weaned piglets. These will be described separately. In the neonatal piglet there are certain specific strains of E. coli involved, particularly those with the ‘O’, ‘K’, ‘H’ and ‘F’ antigens. The disease is often called colisepticaemia. It is the most common cause of enteritis in the pig not only in the UK but also worldwide. The bacteria are found in the intestines of normal healthy adult animals. They will infect the small intestine of the non-immune piglet and produce a toxin. The piglet will have diarrhoea and will rapidly become very ill. This may occur within a few hours of birth. They may die so quickly with convulsions that the clinician may be misled and consider neurological conditions or poisoning. Post-mortem may reveal meningitis. E. coli will be able to be grown in pure culture from heart blood, liver and spleen. Laboratory confirmation is important for the strain, so that the appropriate vaccine can be given to the sow, and the sensitivity, so that the appropriate antibiotic can be given to the piglets.

The disease may not be peracute but just acute with watery diarrhoea. The piglets will be visibly dehydrated but may continue to suck. Death will occur in 48 h. However some may recover and regain condition. Electrolytes as well as antibiotics are vital for treatment. The outbreak will continue until the sows and gilts coming to the farrowing quarters have been vaccinated. There will be lateral spread from neighbouring litters. The infection will follow inadequately cleaned farrowing pens. Post-mortem will reveal a dehydrated piglet with milk in its stomach. Infarctions in the wall of the stomach are not pathognomonic but very suggestive of E. coli