Swine dysentery (Brachyspira hyodysenteriae)
Swine Dysentery and Spirochaetal Colitis
(Brachyspira [previously Serpulina and Treponema] hyodysenteriae and Brachyspira pilosicoli)
Swine dysentery (SD) is a severe, infectious disease characterized by mucohemorrhagic diarrhea and marked inflammation limited to the large intestine (cecum and/or colon). Spirochaetal colitis (SC) causes milder colitis in young -pigs.
Swine dysentery (SD) occurs only in swine although the etiologic agent infects and persists in rodents. All ages of swine may have SD although it seldom is apparent in piglets less than three weeks old. The disease occurs more frequently during the growing/finishing periods. Swine dysentery occurs worldwide in the major swine-raising countries and can cause very significant economic losses on affected herds. In the United States, SD now occurs only occasionally because of successful eradication and/or effective manure removal techniques. Outbreaks occur throughout the year, more often in late summer and early fall. With the increased interest in niche pork production (e.g. organic, antibiotic free) in the US, there has been an increase in incidence of SD in these systems.
Spirochaetal colitis associated with Brachyspira pilosicoli also has worldwide distribution, causing a milder, non-hemorrhagic colitis.
Swine dysentery was first reported in 1921. Subsequently it was reported from many swine-raising countries throughout the world. The etiology remained unknown until 1971. Much of the extensive research on the disease was reported during the 1970s and 1980s. Spirochaetal colitis associated with Brachyspira pilosicoli was described subsequent to SD.
Prior to the discovery of organic arsenicals as an effective treatment and preventative, SD caused disastrous losses among swine herds. Improved methods of control have markedly reduced losses in the US, although SD is still an important disease in some parts of the world. Methods of elimination of SD from swine herds have been well described and the establishment of a national eradication program has been considered, but lack of a sensitive monitoring test remains a problem.
Brachyspira (previously, Serpulina or Treponema) hyodysenteriae, a spirochete, is the etiologic agent. It has axial filaments, is Gram-negative, anaerobic and the most pathogenic strains are strongly beta-hemolytic. There are a few avirulent or weakly beta-hemolytic Brachyspira strains that are predominantly nonpathogenic. Other organisms in the large intestine, especially anaerobes, may facilitate colonization and lesion formation. Brachyspira hyodysenteriae has the ability to survive under a wide range of environmental conditions but is susceptible to heat, ultraviolet (UV) light, and desiccation, as well as soaps and disinfectants. Other spirochetes, especially B. innocens and B. pilosicoli are found in the large intestine of many swine and are easily mistaken for B. hyodysenteriae.
While considering a diagnosis of swine dysentery, one should be aware of recent work in describing a nonfatal, non-bloody, diarrheal disease in swine caused by Brachyspira (Serpulina) pilosicoli. This agent appears to be common in swine populations and is an occasional cause of catarrhal colitis in young growing swine. Virtually all statements related to B. hyodysenteriae are also true for B. pilosicoli with the exception that disease caused by the latter is much milder.
Transmission of B. hyodysenteriae is by ingestion of infectious feces. It can persist in lagoon water for at least two months, moist feces for two months, and soil for 18 days. Mice have been reported to shed B. hyodysenteriae for 180 days and dogs for 13 days. The organism can be transmitted by birds, flies, and fomites. Carrier swine can transmit the agent for at least 90 days. Clinically normal, purchased carriers, including breeding stock, often are the source of initial exposure. Carrier sows often transmit to their piglets. Infected mice on premises may also be a source of infection.
Brachyspira hyodysenteriae is ingested with clinical signs developing 5-21 days later; incubation period is dependent upon dose but the infective dose is quite small. The organism reaches the large intestine where it colonizes, proliferates, penetrates the mucus layer and becomes closely associated with epithelial cells. Invasion may not be essential for lesion production. The exact mechanism of tissue destruction is not known but lipopolysaccharide in the organism probably is involved. Also, B. hyodysenteriae producestwo known toxins and a hemolysin that may play roles. In typical lesions the organisms can be seen within epithelial cells and occasionally in the lamina propria. Lack of lesions at other sites suggests the entire pathogenesis is associated with the cecal and colonic lesions. B. pilosicoli appears to exert pathogenic effect by attachment to enterocytes and microerosion of epithelium.
Systemic effects presumably are the result of fluid and electrolyte imbalance caused by colitis. Fluid imbalance is the result of failure of the colon to absorb fluid, much of it from endogenous secretions, and explains the progressive dehydration and deaths that occur. Peracute deaths occasionally occur, perhaps caused by the toxins.
Diarrhea, usually with gray to yellow, mucoid feces often is the first sign noticed. With SD, diarrhea continues and quickly becomes mucohemorrhagic, with excess mucus and fresh blood apparent. In a small percent of the pigs, diarrhea may be preceded by tail twitching or a humped, gaunt appearance. Fresh, red blood in mucus-containing feces often is profuse and the perineal area may become blood stained. Signs that follow prolonged diarrhea are those associated with dehydration. These include sunken eyes, marked weakness, hollow flanks and weight loss. In advanced cases, appetite is erratic but the animals continue to drink. Advanced cases remain unthrifty, even with treatment. Occasionally, sudden death is observed. In untreated herds morbidity is high and mortality can approach 50%.
Spirochaetal colitis is generally seen as a mild persistent diarrhea with mucus. Affected pigs may be less thrifty but effects on growth performance may not be overtly obvious.
Lesions are limited to large intestine, except for dehydration and the nonspecific reddening of the gastric mucosa. The mesentery and serosa are edematous and the serosa is rather opaque. Any or all parts of the large intestine (cecum, spiral colon, rectum) may be affected. It is heavy, thick walled, congested and edematous. The mucosa is thrown into folds and is covered, diffusely or in patches, with a layer of fibrin, necrotic debris and mucus. There often are flecks of blood in the mucus or on uncovered mucosa. The colon contains fibrinonecrotic debris and excessive mucus, often mixed with blood.
In acute cases the mucosa of the affected large intestine is reddened, edematous and swollen. There may be only small amounts of fibrin but excessive mucus. Blood usually can be seen in the feces. Pigs that die suddenly may be in surprisingly thrifty condition although lesions in the large intestine are extensive.
Microscopically, there is moderate nonsuppurative colitis and typhlitis, mucosal metaplasia, edema, and superficial epithelial necrosis. Spiral-shaped organisms can be demonstrated within crypts, enterocytes, and debris by silver stain.
Lesions of spirochaetal colitis are milder, with mild hyperemia and excess mucus observed on the mucosa of large intestine. Microscopically, there may be abundant spiral-shaped organisms colonizing epithelium, accompanied by mild nonsuppurative inflammation.
A field diagnosis of SD often can be made on the basis of clinical signs and typical gross lesions. A simple aid in diagnosis is the demonstration of many spirochetes in stained smears made from colonic scrapings. Brachyspira hyodysenteriae is weakly Gram-negative so organisms are best demonstrated with crystal violet or Victoria blue 4-R stains. Other spirochetes are easily mistaken for B. hyodysenteriae, so it is advisable to get laboratory confirmation of the diagnosis, especially if the outbreak is an initial one or there is doubt about the diagnosis. B. hyodysenteriae often can be cultured and identified from rectal swabs or colonic scrapings from acutely affected, unmedicated pigs. Biochemical differentiation of pathogenic and nonpathogenic strains can be challenging. Polymerase chain reaction (PCR) techniques are available for detection of the organism and provide differentiation to the species level; their use is encouraged.
Several diarrheal diseases of swine must be differentiated from SD. These include proliferative enteritis, whipworm infestation, gastric ulcers, spirochaetal colitis (B. pilosicoli), and salmonellosis. Severe whipworm infections mimic mucohemorrhagic SD and worms are not grossly visible until three to four weeks after infestation. Salmonellosis lesions usually are not confined to the large intestine, as are swine dysentery lesions. Lesions of salmonellosis tend to extend deeper into the mucosa as ulcers and may be patchy in distribution with less mucus. Necropsy of several pigs and microscopic study of the colon often are helpful in separating the two diseases. Dual infections can occur. Spirochaetal colitis is best diagnosed by necropsy of acutely affected pigs, histopathology, isolation of the weakly beta-hemolytic causative organism, and definitive identification biochemically or by PCR.
Preventing the introduction of B. hyodysenteriae to negative herds is a high priority. Additions to the herd should be only from herds known to be free of swine dysentery. They should be added only after a quarantine period of 30-60 days. Some veterinarians recommend treating high-risk animals with tiamulin or carbadox during quarantine to reduce the possibility of carriers being introduced.
Three methods are used to eliminate swine dysentery and have been quite successful in the US. Early weaned piglets (< three weeks) taken to a clean site and raised there usually remain free of B. hyodysenteriae. Meanwhile, the infected herd can be marketed, and the facilities cleaned and disinfected. This method allows one to retain valuable genetic stock. Segregated rearing with all in/all out production techniques has been quite successful in eliminating SD.
A second method relies on medication. Reduction of a herd to a minimal number of animals, followed by intensive treatment of those retained, is often used. Debilitated animals must be disposed of since they may not consume enough medicated feed or water. Prolonged, intensive treatment is expensive so numbers of swine to be treated should be minimized. Three widely used therapeutic agents include carbadox, lincomycin and tiamulin. Directions for their use should be followed carefully and every animal must be treated.
The third method of complete depopulation may be useful on premises with endemic swine dysentery where biosecurity and sanitation are difficult to implement. Depopulation should be done during warm, dry weather. During depopulation all facilities and equipment should be thoroughly cleaned and disinfected. The premises should be left vacant for at least two weeks, depending on the weather and level of achievable sanitation. Brachyspira hyodysenteriae usually will not survive for more than two weeks in soil or grass pens kept dry and relatively free of feces during dry, warm weather. Repopulation should be made with swine free of SD.
Any effort to eradicate SD requires an initial accurate diagnosis of SD, a commitment from the owners, and initial agreement on a protocol for accomplishing eradication and ongoing veterinary supervision. The eradication effort should be made during the warmest time of the year. A professionally-managed rodent control program is essential. Eradication must be coordinated with pig flow so that thorough cleaning and disinfection can be accomplished when the premises are vacant or the population minimal. If infected animals must be retained during the effort, a barrier system must be set up to separate clean from potentially contaminated areas.
Producers trying to control, but not eliminate infection with endemic swine dysentery can use preventive and therapeutic levels of antibiotics administered in feed and/or water. Those herds often can be treated intermittently to advantage. Although several products are FDA-approved for swine dysentery, carbadox, lincomycin, and tiamulin seem to be most effective. Antibiotic resistance is an increasing problem with this organism, making control programs (as opposed to elimination) a poor long term strategy. Vaccination has not proved to be reliably effective in control or elimination programs.
Control of B. pilosicoli should follow the same principals of sanitation and husbandry. The disease usually responds favorably to the antimicrobials listed for swine dysentery