Age affected: Weaners, growers/finishers.
Causes: Dietary problems; bacteria – spirochaetes, Yersinia, Bacteroides, Clostridium, E. coli
Effects: Diarrhoea, stunting.
Colitis can be caused by nutrition or by infection and is often caused by both. Both can allow undigested feed components to reach the colon as a result of poor digestibility of the feed (oligosaccharides, caramelised carbohydrates and poorly-digestible proteins), antitryptic agents, intestinal hurry, and villous atrophy resulting from infection. The undigested food components ferment and reduce or abolish the ability of the colon to absorb water and cause the diarrhoea or pasty faeces. Nutritional factors known to affect digestion include some wheats, pelleting, the trypsin inhibitors in peas, beans and raw soya and the effects of poor quality fat. A wide range of infections occurs from weaning onward, depending upon exposure and the immune status of the pig. Rotaviruses, Porcine Epidemic Diarrhoea and enteroviruses, E. coli, salmonella, Lawsonia intracellularis, cryptosporidiosis and some Eimeria infections may all reduce small intestinal digestion. Torovirus, enterovirus, some rotaviruses, Brachyspira hyodysenteriae, B. pilosicoli, salmonellae, Yersinias, campylobacter, Bacteriodes fragilis, parasites such as Oesophagostomum and Trichuris suis and some Eimeria species may affect the large intestine directly. Cryptosporidia are often present in the intestines of affected pigs. Both Balantidium coli and Tritrichomonas spp may colonise lesions. Clostridium perfringens type A can initiate a syndrome resembling some forms of colitis.
The individual infectious agents which cause this syndrome are transmitted from pig to gig by the routes described under the individual conditions. Colitis is most common when the predisposing dietary factors described above are present. The condition occurs in successive batches of pigs from the same source, fed on the same ration and housed and managed in the same way. Only exhaustive investigation can determine the precise mode of transmission (if any) in an outbreak.
Colitis is most common in the 8-10 week age group but can occur later. Affected pigs are hairy, hollow-flanked, dirty and restless. The faeces are usually soft and may occasionally contain mucous. Diarrhoea can also develop, but it is featureless and smooth with no blood or necrotic tissue. The faeces of affected pigs may froth and bubble immediately after they have been passed. Individual pigs may be affected for 3-20 days, but the faecal changes persist for longer in the group. Growth rates are usually depressed and feed conversion may be affected. Affected pigs recover eventually and there are no deaths. Colitis often occurs in pigs on an individual farm receiving a particular feed and the disease often disappears when that feed is replaced. In many cases the use of this ‘suspect’ feed on other farms is not associated with the syndrome. Disease often occurs on pelletised rations and less commonly on meal. Fever and clinical signs of specific diseases such as swine dysentery are absent.
Diagnosis is based on the clinical signs of pasty faeces or fermentative diarrhoea and growth depression and the absence of fever, mortality and diseases such as swine growth depression and absence of fever, mortality and disease such as swine dysentery, spirochaetal diarrhoea, salmonellosis which produce recognisable clinical signs. There may be a history of association with a particular ration and especially with pelleting. The presence of known predisposing nutrients in the feed may provide further evidence. Untreated soya, some peas, some wheats, high levels of fat are particularly important.
Post-mortem examination can provide additional information. In classic ‘colitis’ only the large intestine is affected. The contents are fluid, contain bubbles and sometimes have an oily sheen. In early cases the mucosa appears to be normal even microscopically, even by scanning electron microscopy which provides high magnifications. The only changes may be the local loss of absorptive microvilli from colonic epithelial (lining) cells. In some cases there may be more obvious colonic lesions. Diagnosis can only be confirmed by exclusion of infections with agents known to cause enteric disease. The large intestinal lining may show evidence of swine dysentery or worm infections and proliferative enteropathy may be present in the small intestine. Laboratory examination for disease-causing viruses, bacteria and parasites should be negative.
Specific causes of mild diarrhoea and colitis such as spirochaetal diarrhoea should be identified and treated or controlled. In cases where spirochaetal diarrhoea has been identified, tiamulin, valnemulin, aivlosin, lincomycin or tylosin have been used successfully. Where C. perfringens type A is important, some growth promoters have had a dramatic effects, but are now rarely available. Ampicillin, amoxicillin or trimethoprim sulphonamide treatment may be of value. Where Lawsonia intracellularis (proliferative enteropathy) or Yersinia enterocolitica are present, tetracyclines may be of value. Accommodation should be cleaned and all-in, all-out housing adopted. Nutritional colitis can be eliminated in some cases by changing pelleted feed for meal (but not for reground pellets) or by using a diet specifically formulated to prevent the condition. Such ‘colitis’ diets have been formulated to eliminate or reduce antitryptic factors (for example by inactivating thoroughly those present in soya meal) and indigestible carbohydrates. The use of some varieties of wheats or peas may be avoided. These diets are available commercially in the UK, but may not be available in all countries. It may be difficult to prepare them where home mixing is practised. Diseases or other body systems such as pleuropneumonia, which contribute to growth depression in this age group should be eliminated.