Swine Dysentery (SD)

Occurrence: Worldwide, many herds free.
Age affected: Weaners, growers/ finishers (all ages).
Causes: Bacterium - Serpulina hyodysenteriae; poor hygiene; stress.
Effects: Diarrhoea with mucus and sometimes blood, weight loss, reduced feed conversion, death.


Swine dysentery is caused by the spiral bacterium Brachyspira (formerly Serpulina or Treponema) hyodysenteriae and its close relative, B. hampsonii. B. hyodysenteriae is 6-10 microns long, flexible and active, with a central pointed cylinder wrapped in 7-14 flagellae overlapping centrally within an outer envelope.

The organism grows on blood agar and forms colonies 1 mm in diameter surrounded by ß-haemolysis after 48 hours’ incubation in anaerobic conditions. B hyodysenteriae is distinguished from other spirochaetes by its haemolysis, biochemically, using monoclonal antibody and by it nucleic acids. There are at least 11 serogroups which can be sub-divided further. It is sensitive to drying and acid pH <6.0 and is readily destroyed by heat but survives in water or faeces for days or weeks. Infection with B. hyodysenteriae is oral.

The organism reaches the large intestine, colonises the mucosa, multiplies in the crypts, invades epithelial cells and damages or disrupts them with its haemolysins. Inflammation results in loss of tissue and blood, the colonic epithelium fails to re-absorb chloride and sodium ions. Diarrhoea containing blood and mucus develops and death by dehydration or ion imbalance results. Serum antibody develops within 7-10 days. Local lesions persist for 40-50 days after clinical recovery and animals remain carriers for up to 90 days.

Mode of transmission

Infection is solely oral. Pigs can become infected after ingesting infective faeces or water and feed contaminated by infected faeces. Sucking piglets may be infected from carrier sows, but the clinical disease rarely develops until after weaning and mixing. Indirect infection can occur from contaminated pen furniture, clothing, implements, and in transport. Mice can become colonised and may represent reservoirs of infection for pigs and other animals, such as flies, birds and farm dogs, may also carry the organism and spread it within a farm. Spread between farms is usually in carrier pigs, but can be by indirect means, on boots, in transport and by means of rodents.

Clinical signs

Early cases develop twitching of the tail, abdominal discomfort, hollowing of the flanks, slight reddening of the skin and slight inappetence. Diarrhoea develops and persists throughout the course of the disease. Blood, mucus and, later, pieces of necrotic material appear in the faeces which are yellowish in colour at first and later become brownish-red, liquid in consistency and foul-smelling. There is a rapid loss of bodily condition and pigs are thin with sunken eyes, hollow flanks and prominent ribs and backbones. The coat may be rough, the tail limp and the perineum (hindquarters) stained with faeces. Affected pigs show a variable reduction in appetite but all continue to drink. Permanently stunted pigs may pass khaki liquid faeces.

Pigs of all ages are affected although the peak incidence is in weaned pigs of 6-12 weeks of age. The disease can be particularly severe in sows at farrowing or mid-lactation. The disease spreads in a farm by pig movement and with drainage. Production depression extends the rearing time from birth – 100 kg by up to 30 days. The presence of immunity, treatment of inadequate duration or level and, where they are still used, the use of some growth promoters may all reduce the severity of the clinical signs.

Swine dysentery is diagnosed on the basis of the clinical signs and the post-mortem findings followed by laboratory confirmation of the presence of B. hyodysenteriae. The presence of a slowly-spreading diarrhoeic condition on a farm with diarrhoea containing fresh blood and mucus and causing loss of condition and some deaths suggests the presence of swine dysentery. Post-mortem examination provides further evidence. Carrier animals must be identified by culture as serological tests are not widely available.

A pig with SD. The animal has a grey-ish diarrhoea.
Foto: RBI - Ruben Keestra.

Postmortem lesions

Pigs which have died from swine dysentery are usually in poor bodily condition. Changes are confined to the large intestine which is flaccid with fluid, foul smelling brownish red contents containing mucus, undigested food and necrotic material. In early cases the mucosa is swollen and congested, later becoming covered with blood-streaked mucus and patches of fibrinous diphtheritic material.

There is an extensive layer of necrotic material in older lesions and this may become dislodged in patches to expose the bleeding mucosa. B. hyodysenteriae can be demonstrated in smears made from the mucosa using fluorescence microscopy, cultured using selective media such as spectinomycin blood agar or identified by its nucleic acids using the Polymerase Chain Reaction (PCR). B. hyodysenteriae must be distinguished from other spirochaetes present in diarrhoea, such as B. pilosicoli, which causes spirochaetal colitis, a much milder disease. Lesions of other diseases such as salmonellosis may also be present.

Treatment and prevention

Treatment is best administered in the drinking water, but individual severely affected animals should be treated by injection. This is particularly important if feed medication is to be used. All animals in drainage contact should be treated at the same time and disinfection of pens or a move to clean pens after treatment gives best results. Tiamulin (injectable, water and feed), valnemulin and aivlosin (feed) and lincomycin (injection, water and feed) are all effective. Dimetridazole and ronidazole (water and feed) are no longer available in many countries. Swine dysentery can be controlled by medication, treating groups of pigs at weaning and moving to clean accommodation, or at entry to clean, dry, disinfected all-in, all-out accommodation.

Control in continuously stocked accommodation relies on rigorous hygiene, courses of treatment and prompt treatment of nay clinical disease. Slatted floors, solid partitions between pens, control of flies and rodents and lowering of slurry levels all reduce the spread of the disease. Spread from house to house can be reduced by disinfecting pathways and by using disinfectant foot dips and separate implements. Vaccines are not available widely. Swine dysentery can be eradicated by medication or depopulation and restocking and kept out by isolation and use of clean breeding stock.