consist of the microbiota, mucin layer, epithelium, gut motility, local immune cells and peyer’s patches as well as several enzymes and proteins incl IgAs. In the small intestine the epithelium forms long villi and deep crypts, all designed to increase the surface area to maximise absorption of nutrients. Cells replicate at the bottom of the crypts and them migrate and mature to the top of the villi where they are shed and digested. Generally this takes around 7 days. The cell population will change to one that is most suitable for the digestion of the diet. For this reason all diets changes should always happen gradually.

several changes can take place in the gut. The microbiota, cell population and maturity (and thus function), mucin layer are all likely to be affected. This will have an impact on secretion, absorption, permeability and will likely cause an immune response incl inflammation. As a result the breakdown of the diets is impaired, absorption will be reduced (cell maturity and villi length), which will cause bacterial overgrowth and increased bacterial by-products, which in turn cause damage to the intestine etc etc.

Not all cases of gut disease are evidenced by loose faeces. Most often it shows as unevenness, resulting in more feeding days for the batch as a whole or more “lights” being sold in the case of AI/AO systems. Sometimes the carcass qualities can be affected as indicated by the P2 measurements. The FCR will be affected, but unless accurate and current monitoring systems are in place, this can easily be lost amongst the “big data”. 

Most commercial units wean piglets at (an average of) 28 days of age (minimum weaning age in the EU). Weaning is an abrupt process and piglets experience major changes – removal from the sow, change of housing, change of feed type and source, mixing with piglets from other litters and a requirement to locate the water supply. These factors have a major impact on the small intestinal villi, causing villus atrophy. The villi can become reduced in height by 50% or more as compared with their pre-weaning height.

This causes a reduction in the absorptive capacity of the small intestine and piglets might suffer diarrhoea as a direct result. Also, piglets suffer a loss of the protective effects of secretory IgA that they had whilst sucking the sow (from sow’s milk) and this can lead to an upsurge in enteropathogenic infections after weaning, mainly enterotoxigenic E.coli. 

• -   Achieving good weaning weights with a spread of <20% within litters.

• -   Use a top quality starter ration that is highly palatable, for the first few days after weaning.

• -   Introduced small quantities of the starter ration before weaning.

• -   Group piglets according to size retaining litter groups where possible.

• -   Ensure the weaning accommodation is suitable, dry and warmed to the correct

  temperature before moving the piglets from the sow.

• -   Maintain even environmental temperatures and prevent drafts. Outdoor huts must be well-

  insulated and bedded, with plastic flaps over the doors to prevent wind-chill.

• -   Ensure (clean!) feed and water are readily accessible to minimise the period of starvation

  after weaning.

• -  All in-all-out systems with thorough washing, cleaning and disinfecting pens between

  groups help to minimise post-weaning enteric infections. Outdoor huts should be moved to fresh ground between batches. 

0. Aetiology: Pathogenic enteric E.coli belong to a restricted number of serogroups. Serotypes which cause enteric colibacillosis are 

   called enterotoxigenic E.coli (ETEC).

   
   

   Pathogenesis: ETEC adhere to the mucosa of the small intestine by means of one or more of the fimbrial adhesins K88, K99, 987P, F41 and F18. They colonise the small intestine and produce one or more enterotoxins. Both neonatal and post-weaning colibacillosis are most commonly caused by ETEC producing heat labile toxin (LT) or vero-toxigenic E. coli (VTEC) producing heat stable toxins (STa/Stb). Both types of toxin act totally in the gut and stimulate hypersecretions of mucin and electrolytes resulting in acute diarrhoea and dehydration. 

0. Epidemiology: Infection of newborn pigs is by faecal-oral route. Lack of colostrum and management factors such as low ambient temperatures reduce the vigour and feed intake of piglets leading to increased susceptibility to diarrhoea. Age and genetics determine susceptibility. Pigs are resistant to F18+ E.coli at birth but become susceptible after several weeks whereas K99 or 987P resistance is more or less complete by two weeks.
   

0. Watery diarrhoea, dehydration, metabolic acidosis, vomiting and depression or sudden death. Most common in pigs 0 - 4 days of age and can appear as early as 2-3 hours after birth. Single piglets or whole litters may be affected.

   
   Pathology: Few specific lesions are seen on post mortem. The small intestine is congested, the contents yellow and watery throughout. Histology shows coliform attachment to small intestinal villi.
   

0. Based on clinical signs, bacteriology/serotyping and histopathology.
   

0. Treatment: Should consist of oral rehydration fluids and antibiotics. See Table 05/1: Oral antibiotic treatments for piglets
   
   

   Prevention: Maternal vaccination (see Table 05/2) is effective (if sufficient colostrum of good quality is consumed within the first few hours of life) but good management, hygiene, ensuring adequate ambient temperature and colostrum intakes are also very important. Selective breeding for resistance to K88+ and perhaps F18 could have a significant effect. 

Aetiology: Seven sero-groups of rotaviruses have been reported, four of which (A,B,C,E) affect pigs.
Pathogenesis: Rotaviruses replicate predominantly in the cytoplasm of differentiated small intestinal epithelial cells. It results in small intestinal villous atrophy and severe enteritis.

Epidemiology: Rotavirus is ubiquitous on pig farms and pigs become infected between 7 and 40 days of age, via the faecal-oral route. However, adequate colostrum and milk-intake will provide the newborn piglets with maternal antibodies that persist for 3-4 weeks. Contaminated environment and adult animals serve as sources of infection. Rotavirus is stable at extreme environmental conditions and is resistant to commonly used disinfectants. 

Clinical Signs: Range from mild diarrhoea and dehydration to severe fatal diarrhoea. Diarrhoea affects piglets mainly between 5-14 days of age and lasts from 2-5 days. The younger the animal, the longer the diarrhoea will persist, as the time needed for the restoration of morphologically normal villi shortens with age. Subclinical infections are also common.
Pathology: The small intestines are thin-walled, pale, flacid and dilated with a large volume of watery, yellow or grey fluid. The caecum and colon are likewise dilated with similar contents.

Diagnosis: Detection of rotavirus in faecal samples using PAGE (polyacrylamide gel electrophoresis). Faecal samples should be collected in the acute phase of the disease: highest concentrations of porcine rotavirus are shed during the first 24 hours after the start of the diarrhoea. Histopathology of small intestine shows an acute viral-type enteropathy in the early stages.

Treatment: Should consist of electrolyte/fluid replacement.

Prevention: The prevention and control of rotavirus infection depends on excellent hygiene and disinfection of the farrowing house. Peroxygen disinfectant (Virkon S) is effective. Colostal protection is very important. Another strategy that has been used successfully is to move sows and piglets into a different cleaned and disinfected farrowing crate at 4 – 5 days post-farrowing. This reduces the level of virus challenge from the environment and this appears to be sufficient to prevent the onset of diarrhoea. Rotavirus vaccines for pigs are not available in the UK. 

Aetiology: Isospora suis is the most important protozoa in pigs. Prevalence in the UK is unknown. Eimeria species infecting pigs appear to be non-pathogenic.
Pathogenesis: After ingestion of sporulated oocysts, the sporozoites leave the oocyst, penetrate the epithelial cells in the small intestine and multiplication takes place. From 5 days post-infection oocysts can be detected in the faeces. The oocysts sporulate within 48 hours at temperatures between 20C and 37C.
Epidemiology: Newborn piglets, in a contaminated environment become infected via the faecal-oral route from sow faeces and environmental contamination.

Yellowish to greyish diarrhoea of varying consistency, piglets thinner and hairier. Morbidity is high (although not all piglets within a litter are equally affected). Concurrent bacterial, viral or other parasitic infections can lead to a higher mortality (and complicate diagnosis). Piglets that recover from I.suis infection develop immunity. When challenged they will shed no or very few oocysts (in contrast to the initial infection). Colostral antibodies against I.suis do not protect piglets from clinical coccidiosis.

Pathology: Lesions may not be apparent macroscopically. A fibrinonecrotic membrane in the jejunum and ileum is only seen in severely infected piglets. Histopathology shows degeneration of intestinal epithelium associated with colonisation by coccidial forms. Villus atrophy and necrotic enteritis occurs in more severe cases. Restoration will take 5-10 days. 

Confirmation of the diagnosis in live piglets is difficult because the coccidial stages are immature and mostly intracellular when piglets are most severely affected with diarrhoea. Post mortem examination and histopathology of several small intestine sites (especially ileum) are required to detect the infection. Examination for I.suis oocysts in

faeces can be done in piglets that are recovering (at approx 7 days after the onset of diarrhoea).

Treatment: When outbreaks of coccidiosis occur, piglets should be treated with toltrazuril orally at 3 – 5 days of age (see table 12/7). Repeat treatment might be required 4 – 5 days later. Alternatively sulpha-trimethoprim injections can be given at these times. Electrolyte solutions should be used to combat dehydration.

Prevention: Control depends on the maintenance of good hygiene, thorough washing and disinfection of farrowing pens between litters. The disinfectant of choice is Oocide (Antec International). 

Clostridium Perfringens type C enteritis

Aetiology: C.perfringens type C.
Pathogenesis: The bacteria attach to the epithelial cells of the jejunum and produce toxins; the necrotising beta-toxin is the most important factor in the pathogenesis. Death results from the effects of the intestinal damage and toxaemia.
Epidemiology: Faecal-oral route of infection. Fatal necrotic enteritis occurs mostly in piglets from 12 hours to 7 days. Beta-toxin is very sensitive to trypsin. Trypsin-secretion is absent in pigs of less than 4 days of age. Clinically affected animals usually die. Morbidity varies, according to the immune status of the sows. Introduction of the disease onto a farm: buying in carrier sows or contaminated clothing/footwear. C.perfringens type C can persist in the environment as a vegetative organism or in the spore form. Spores can persist for at least a year in contaminated buildings.

Clostridium perfringens type c enteritis clinical signs 

Clinical Signs: Clinical signs vary accordingly to the immune status and the age of the piglets. Piglets may be found dead within 12-36 hours of birth. If noticed ill, watery/haemorrhagic diarrhoea is profuse, the rectal temperature falls to 35C and the animal dies. Less acute cases may survive 2 days: the reddish-brown liquid faeces contains shreds of necrotic debris. Piglets that suffer from the subacute/chronic form have intermittent or persistent non-haemorrhagic diarrhoea and die after 1 or more weeks. They remain alert but become progressively more emaciated.

Pathology of peracute cases shows intensely haemorrhagic small intestines and blood stained fluid in the abdominal cavity. On microscopy, the villi in the affected part of the jejunum are necrotic and covered by large gram-positive bacilli. Pathology of (sub)acute cases is less dramatic.

Diagnosis: A presumptive diagnosis can be made on the basis of the clinical signs and the gross pathology in peracute/acute and subacute cases. Histopathology and demonstration of the beta-toxin in the intestinal contents confirms the diagnosis. Isolation of C.perfringens type C alone is not sufficient to make a diagnosis since the organism can be found as a secondary agent colonising lesions caused by, for example, rotavirus.

Treatment: Once clinical signs are present, treatment generally will not be successful. Penicillin injections can be used during outbreaks to try and minimise losses.
Prevention: Prevention of the disease is based on vaccination of the sow with a vaccine containing C.perfringens type C toxoid. 

Aetiology: A small coccidian parasite Cryptosporidium parvum.
Pathogenesis: Infection is by the faecal-oral route. The parasites attach to the brush border of the small intestine and multiply. Diarrhoea occurs from approximately 3 days post infection. Oocysts appear in faeces approx 8 – 9 days post infection. Immunity develops fairly rapidly. Cryptosporidium is a zoonotic infection.

Clinical signs: Watery yellow-brown diarrhoea usually from 7 days of age or more and persists for several days with piglets showing dehydration and weight loss.
Pathology: The gross findings are similar to piglets with rotavirus infection. Histopathology shows many cryptosporidia closely associated with villi in the jejunum. Damage to the villus epithelium and villus atrophy can be seen in piglets that have been affected for several days. 

PM and histopathology of freshly dead or euthanased piglets should confirm the presence of infection. Examination of faeces for oocysts can be done in recovering piglets (at approx 10 days post infection).

Treatment: Electrolyte solutions should be used to combat dehydration.

Prevention: Thorough cleaning and disinfection of farrowing pens between litters and maintaining good hygiene of farrowing pens during occupancy are very important. A number of disinfectants are effective including hypochlorite, and Oocide (Antec). Cryptosporidial oocysts can survive in faeces for 45 days and can be carried by rats, mice and humans. Vermin control and personal hygiene of farm workers are important.