By D. L. Hank Harris, DVM, Ph.D.,
Founder and President of Harrisvaccines
Swine Dysentery (SD), commonly known as bloody scours, is a troublesome disease which had been virtually eliminated through scientific breakthroughs in the 1970s and 1980s.
But today, likely due to changes in production practices, it has begun to re-emerge and again cause disease and death in hogs.
SD is too costly a disease to live with. When an infection is suspected, it is important to get as early and accurate a diagnosis as possible. In many cases, if strong biosecurity measures are in place, the disease may be prevented from entering a farm in the first place.
SD was first described in 1921 in the Midwestern United States. By the early 1970s, the disease was prevalent in up to 38 percent of U.S. herds (1) and was estimated to cost the industry some $130 million annually.
In 1971, the work of my research team at Iowa State University resulted in the discovery and naming of the cause of swine dysentery, Treponema hyodysenteriae, now called Brachyspira hyodysenteriae (2,3). At about the same time, and unknown to our team, researchers at Cambridge University made the same discovery, helping to validate our research (5).
B. hyodysenteriae – photo: D.L. Harris
Due to this breakthrough discovery and subsequent research by many worldwide, swine dysentery became a disease of the past by the 1980s and had been mostly forgotten until its re-emergence at the turn of this century.
Recently, however, swine dysentery – also known as bloody scours – has been making resurgence. Typically affecting weaned/grower pigs, symptoms include severe diarrhea with blood and mucus.
SD was first described in 1921 in the Midwestern United States. This devastating disease caused widespread disease and death loss in swine herds worldwide
In 1971, my research team at Iowa State University discovered and named the cause Treponema hyodysenteriae,
In the 1950s and 60s, swine dysentery caused economic havoc worldwide. In the U.S., the spread of the disease was exacerbated by the common movement of 30- to 50-pound feeder pigs into Iowa from small farrowing operations in the south.
These farrowing operations were unknowingly infected with B. hyodysenteriae and apparently healthy feeder pigs were placed in finisher buildings, subsequently breaking with swine dysentery a few weeks after placement.
Pigs in farrow-to-feeder operations and even small purebred breeders were infected with B. hyodysenteriae but the disease went undetected because there is a good immunity in adult animals once recovered from the disease.
Only when young pigs and young breeding animals were transported and co-mingled did the disease emerge with a vengeance, resulting in severe diarrhea containing blood and mucus with death rates reaching as high as 40 percent in some groups of pigs.
The discovery of B. hyodysenteriae set off a decade of intense research and epidemologic investigations. Individual herd disease eradication strategies were created and methods were developed for controlling swine dysentery without the need for depopulation.
Based on serologic prevalence studies in the early 1970s, the incidence of the disease on Midwestern farms was as high as 38 percent. By the early 1980s, the disease appeared to be of little significance worldwide. Numerous patents describing vaccines for prevention of swine dysentery have been granted – most are now expired – and a commercial vaccine was sold in the U.S. for a time but has since been removed from the market.
I first became aware of the re-emergence of swine dysentery in 2004 when I was asked to investigate an outbreak in a large integrated operation in Spain. I was in Germany attending the International Pig Veterinary Society meeting when contacted by the owners of the operation. Of note, there were no presentations on swine dysentery at the 2004 IPVS meeting.
Since 2004, reports of swine dysentery occurrence in the U.S. and Canada appear to have increased.
In my opinion, two facts play heavily in the re-emergence of SD:
- Mice are a known reservoir for B. hyodysenteriae, which affects mice without causing disease so they can remain infected for more than a year; and
- Single-site farrow-to-isowean pigs operations appear to be uninfected due to B. hyodysenteriae immunity in the sow herd and colostral immunity in suckling pigs, making it difficult to detect infected farms. The large increase in movement of three-week-old isowean pigs from apparent subclinically affected farms has increased the occurrence of swine dysentery-positive isowean pigs entering wean-to-finish units in the Midwest.
Other factors include difficulties in eradicating the B. hyodysenteriae from pits due to the difficulty in effectively cleaning and disinfecting all areas of the pit. Animals exposed to pit or lagoon water can be infected by the organisms still present.
In addition, research in Australia has indicated that dietary components can influence whether clinical signs of SD are easily recognizable (4).
The organism also survives in feces for 60 days at refrigerator temperature, so it can remain viable throughout the colder periods of the year.
SD effects pigs of all ages, but is most frequent in eight- to 14-week-old pigs. With a one- to three-week incubation period, SD infection results in sunken flanks and depression, diarrhea of loose to watery consistency with blood and mucus evident in the feces.
Pig exhibiting SD symptoms – photo: D.L. Harris
Feces contain blood and mucus – photo: D.L. Harris
Microscopically, lesions are restricted to the large intestine, cecum, colon and rectum, edematous mesentery and intestinal wall. The colon contains mucus, fibrin and blood.
The most accurate determination of SD is to post pigs with clinical signs. A complete necropsy is recommended and tissues should be submitted to a diagnostic lab for accurate diagnosis. Cultures of intestinal material from pigs with lesions of SD are both specific and sensitive for confirmation of the diagnosis.
Cultures of rectal swab samples are not a good way to diagnose SD. While they are very specific if the organism can be detected, they lack sensitivity. Using rectal swab material in the qPCR test can give misleading results due to a lack of both sensitivity and specificity.
Identification of SD infections
SD is often subclinically present in sow herds, providing maternal antibody immunity to baby pigs until they are weaned then the disease breaks when they are moved to grow-finish barns.
The best indicator of whether a sow farm is subclinically infected is whether Isowean pigs break with SD soon after placement in wean-finish barns.
In wean-finish barns, SD will occur if no drugs are present in feed or water to mask the disease.
Depopulation vs. elimination vs. living with SD
Based on costs in the 1980s, it was more economically feasible to eliminate the disease without depopulation rather than live with it or conduct a total depopulation (see table). Currently, depopulation may be a viable option if additional diseases can be eradicated simultaneously.
Polson, Marsh, Harris – 1992
Several drugs used in the 1980s for prevention, treatment, and elimination are no longer available. Drugs currently approved for treatment and/or prevention can be found at http://www.accessdata.fda.gov/scripts/animaldrugsatfda/. Research is ongoing to determine if any of these drugs can be used at approved levels for elimination without depopulation programs. Consult a veterinarian for assistance in developing effective control programs
Control of swine dysentery in the future will depend on improved methods for detecting asymptomatically affected sow farms with the disease and the development of vaccines to prevent swine dysentery in growing pigs.
Immunity to SD
Research has shown that pigs which have recovered from SD without medication are immune to re-challenge, making vaccine therapy a viable option for controlling SD.
Further, pregnant gilts recovered from SD transmitted B. hyodysenteriae to their suckling pigs. These pigs did not show signs of SD while nursing, but became ill with the disease after weaning.
A commercial subunit vaccine previously approved by USDA has been removed from the market. An RNA Particle-based vaccine is now in development at Harrisvaccines and expected to be available soon.
The disease is difficult to diagnose definitively. If clinical signs and lesions are observed, intestinal tissue samples should be sent to a diagnostic lab for examination.
SD is too costly a disease to live with and biosecurity measures can prevent it from entering a farm in the first place. Though difficult, the disease can be eliminated via isowean pigs in multiple isolated site production practices.
1. Egan, I. T., D. L. Harris, and H. T. Hill. 1982. Prevalence of Swine Dysentery, Transmissible Gastroenteritis, and Pseudorabies in Iowa, Illinois and Missouri Swine. Proceedings 86th U. S. Annual Health Assoc. Meeting 497-502.
2. Glock, R. D. and D. L. Harris. 1972. Swine dysentery – II. Veterinary Medicine/Small Animal Clinician 67:65-68.
3. Harris, D. L., R. D. Glock, C. R. Christensen, and J. M. Kinyon. 1972. Swine Dysentery – I Inoculation of Pigs with Treponema hyodysenteriae (new species) and Reproduction of the Disease. Veterinary Medicine/Small Animal Clinician 67:61-64.
4. Pluske, J. R., P. M. Siba, D. W. Pethick, Z. Durmic, B. P. Mullan, and D. J. Hampson. 1996. The Incidence of Swine Dysentery in Pigs Can Be Reduced by Feeding Diets That Limit the Amount of Fermentable Substrate Entering the Large Intestine. American institute of Nutrition 126:2920-2933.
5. Taylor, D. J. and T. J. L. Alexander. 1971. The Production of Dysentery in Swine by Feeding Cultures Containing a Spirochaete. Br. vet. J. 127:lviii-lxi.