Swine Dysentery (Bloody Scours); Recognition and Awareness, Diagnosis, Transmission and Clinical Signs
Swine dysentery (SD or bloody scours), once one of the most expensive swine diseases, largely disappeared in North America in the 1990’s with three site production and improved hygiene, among other changes in swine industry structure. However, since the early 2000s, SD has re-emerged in swine operations in portions of the U.S. and several Canadian provinces. SD is an intestinal bacterial disease that is very expensive to treat and control medically. It is very difficult to completely eliminate once pigs and facilities are contaminated. SD can be spread by infected swine, rodents and other animals in contact with infected swine as well as any fecal material on equipment or clothing. Biosecurity practices are effective at reducing the exposure risks and, when properly implemented, will prevent or slow the spread of this disease (and other diseases) between farms. Please see the Pork Information Gateway Factsheet, “Steps for Treatment, Control and Elimination of Swine Dysentery” for more information.
- Increase producer awareness that swine dysentery is an economically significant disease threat
- Review disease characteristics to help recognize clinical signs and the key steps for diagnosis
- Review transmission methods of disease and biosecurity measures to prevent or decrease its spread
Long before Porcine Reproductive and Respiratory Syndrome (PRRS), swine dysentery was the major “profit robber” disease for swine producers. Between 1970 and 1990, swine dysentery cost the U.S. swine industry at least $64 million annually. The disease was present in over a third of Iowa swine herds and was widespread globally. The bacterial cause of swine dysentery, Treponema hyodysenteriae, was identified in 1971 (Harris et al., 1972), with subsequent name changes (Serpula, Serpulina) before its current classification as Brachyspira hyodysenteriae (Hampson and Burrough, 2019). After the discovery of this organism, better understanding of its transmission and environmental survival led to new treatment, control, prevention and elimination strategies. These strategies along with improved facility design, industry consolidation, health and improved genetics caused clinical SD to virtually disappear from farms during the 1990s. Although the disease appears to have reduced in prevalence, it is not fully eradicated and is now re-emerging. Producer and veterinary awareness of distinguishing this economically significant disease from a similar enteric disease, ileitis caused by Lawsonia intracellularis, makes awareness paramount.
Swine dysentery has been re-emerging in North America since 2007 according to data from the Iowa State University Veterinary Diagnostic Laboratory (ISU VDL) (Burrough, 2013). The frequency of Brachyspira hyodysenteriae detection in samples from grow-finish pigs submitted to the ISU VDL has risen from three positive cases in 2005 to forty-three cases from multiple states in 2019. Recognition of re-emergence early on was complicated by clinical similarity to other diseases such as porcine proliferative enteritis (ileitis) caused by Lawsonia intracellularis, and relying on very precise diagnostic testing, which failed to detect the emergence of two additional species, Brachyspira hampsonii and Brachyspira suanatina (Mushtaq et al., 2015; Mirajkar et al., 2016b). So far, only B. hyodysenteriae and B. hampsonii have been detected in North America.
The increased frequency of SD in the Midwest has corresponded with the importation of infected pigs to Iowa for finishing. Currently 25-26% of U.S. market hogs are finished in Iowa and a majority of those pigs originate from outside of Iowa (Plain and Lawrence, 2003). Trailers, buying station, packing plants and contaminated by healthy looking infected (subclinically infected) pigs are potential sources of infection. All are potentially infective to other pigs until appropriate cleaning and disinfection procedures take place.
The cost of SD is both in the expense of frequent or continuous medication administration and in loss of production efficiencies. In 1994, it was estimated that the total financial cost of swine dysentery in the U.S. alone was approximately $115.2 million. The treatment and ongoing control costs using antimicrobials adds $4-8 per pig marketed, which when coupled with decreased gain, impact on feed efficiency, and increased mortality and culls, is variously estimated to cost $9-15 per pig. Antimicrobial resistance is well-documented and is an increasing concern globally for loss of efficacy of available antimicrobials (Hidalgo et al., 2011; Mirajkar et al., 2016a), particularly since control of SD relies on frequent or continuous use of antimicrobials. In addition, there is increased scrutiny of routine antimicrobial use in food animals, with emphasis on decreasing antimicrobial use.
Clinical Signs and Diagnosis of Swine Dysentery
- Soft to watery feces with or without gelatinous mucus are common first signs, progressing to diarrhea usually with varying amounts of mucus and blood (Figure 1).
- Uneven pig growth, increased mortality and significantly reduced feed efficiency are common as disease progresses, especially in untreated pigs.
- Appropriate laboratory testing is needed to differentiate swine dysentery from other causes of diarrhea, some of which may be present concurrently.
SD most often affects pigs from 8 weeks-of-age through marketing, but can occur in naïve adults or pigs as young as 3 weeks-of-age. SD causes diarrhea with variations in consistency, color (gray, yellow or reddish brown) and composition (feces often contain mucus or blood) (Table 1). Signs of SD are typically observed in a few pigs 7-10 days after initial infection as soft, yellow-to-gray feces (Hampson and Burrough, 2019). Variation in clinical signs from a low-grade diarrhea to obvious clinical SD may occur (Figure 2). The clinical signs may spread slowly within a barn, or rapidly, depending on the causative organism and exposure dosage as there is variation in virulence within and among potential agents of SD. Antimicrobials can mask the presence and severity of Brachyspira infections, particularly in the nursery phase.
Groups of pigs will grow unevenly leading to variation in weights within or between pens. Variation in growth may not be easily recognized, but is a costly consequence of infection. This variation in growth needs to be noted and addressed, otherwise SD may go undiagnosed. As SD progresses, mucus, flecks of whitish fibrin and variable amounts of blood are found in the feces. Diarrhea staining may appear around and below the rectum or uncontrolled bowel movements may be noted and will need a laboratory diagnosis for confirmation of SD (Figure 3). If left untreated, mortalities may occur. Careful observation is required to identify potential SD infections, particularly in constantly infected herds where some degree of immunity exists.
Tips for early identification of the signs of SD – if you see any of these signs, INVESTIGATE:
- Walk pens first thing in the morning when pigs are more active and before feces are pushed through the slats.
- Look for individually affected pigs that may be gaunt, have fecal staining below the rectum, or blood and/or mucus in the feces.
- Observe the flooring for fresh feces with special attention to consistency, color and composition characteristics. If you see abnormal stools, collect samples immediately as they may not be there later in the day.
Any abnormal feces containing mucus and/or blood or affected pigs should be investigated by a veterinarian. Your veterinarian may make a presumptive clinical diagnosis, but more often will need to investigate further with necropsy, evaluation of tissue abnormalities and usually laboratory testing. Accurate diagnosis is critical, particularly for definitive diagnosis, since the clinical signs are similar for many gastrointestinal infections including other Brachyspira spp., Salmonella, proliferative ileitis (Lawsonia), whipworms and gastric ulcers.
Specific Considerations for Definitive Diagnosis of Swine Dysentery
- Swine dysentery is an important differential diagnosis for grow-finish diarrheas
- Isolation of typical, strongly beta-hemolytic Brachyspira colonies by culture of the large intestine or feces is the gold standard to confirm the diagnosis
- There is no available antibody (blood) test in the U.S.
- There are other species of Brachyspira, often with weak hemolytic colonies when cultured, that can cause grow-finish diarrhea and colon inflammation but not SD
- There are non-Brachyspira causes of grow-finish diarrhea and colon inflammation that should be investigated concurrently
- Accurate diagnosis requires veterinary involvement and often requires necropsy and/or laboratory testing
A diagnosis of SD cannot be confirmed by the appearance of feces alone. Relying on fecal appearance only may lead to a misdiagnosis of salmonellosis, ileitis, whipworms or gastric ulcer as SD can appear similar to these other diseases at various stages. Since SD clinical signs resemble those of other enteric infections, your swine veterinarian can assist in an accurate determination the cause of the diarrhea. It is important to obtain an early diagnosis to start on treatment, control and elimination strategies. It is important to investigate with laboratory tests, including one or more of the following: 1. Bacterial (anaerobic) culture of feces or colon; 2. Diagnostic testing (molecular testing via PCR) performed on oral fluids, feces or colon scrapings; 3. Microscopic examination (histopathology) to confirm the diagnosis and rule out other co-infections or causes (Burrough, 2017). Accurate diagnosis is necessary for appropriate treatment and control strategies to be selected and implemented. Diagnostic tools for ongoing surveillance or monitoring of herds or production sites exist and are quite useful. Veterinarians trained in disease diagnosis, along with disease prevention and control can provide valuable information about causes and solutions to the production team.
Transmission of Swine Dysentery
- Infected (carrier) pigs shedding Brachyspira in their feces are primary sources of infection
- Brachyspira can survive in feces, manure, lagoons, manure storage areas and handling equipment as long-term sources of infection
- Fecal contamination of fomites (transport vehicles, handling equipment, tools, boots, etc.) can transfer infection to new locations
- Mice can carry and shed hyodysenteriae for up to a year after infected pigs are removed
An important characteristic of the bacteria causing SD is their ability to survive in feces-contaminated environments for long periods of time. In general, Brachyspira survive well in moist, cool feces or organic material, or on feces-contaminated inanimate objects (fomites). Fomites include boots, clothing, transport vehicles, farm equipment, tools and manure disposal equipment – anything that can be contaminated with swine feces, all of which can be a potential source of infection to previously unaffected populations. A pig affected with SD can shed millions of organisms per day and one teaspoon of contaminated feces contains enough organisms to infect large numbers of additional pigs, each of which will then amplify the bacteria and spread it within a herd. Transmission is not only by pigs. Feces-contaminated fomites, transport vehicles, manure handling equipment and service vehicles that travel between farms or markets may and often are sources of introduction of SD into a previously healthy herd.
Appropriate, widely accepted and effective biosecurity assures that practices and procedures are in place to prevent the introduction of disease to a herd or production site. When herds cannot be closed, it is essential to prevent introduction through breeding stock. Pigs that travel back and forth to exhibitions are a high risk for introduction of new diseases, including SD to a herd. With SD, limiting swine exposure to any outside source of pig manure is essential. Rodents, specifically mice, can carry the bacteria and shed viable organisms for at least 200 days (Harris, 1984). A strong rodent control program should be established (Joens and Kinyon, 1982) and maintained, which is particularly important for elimination from a premises. Cats, dogs and birds are potential short-term carriers of Brachyspira spp.; swine barns should be constructed to prevent entry of dogs, cats, birds and other wildlife. The organism can survive in manure, including lagoon water, for extended periods (Schwartz et al., 2012) and waterfowl are another risk factor for spread between farms (Martínez-Lobo et al., 2013). Exposure to previously infected manure puts the entire herd at risk for infection.
Accurate diagnosis of intestinal disease in growing and finishing swine is very important because the clinical signs of several important infectious diseases are similar. Swine dysentery (bloody scours) can be difficult to differentiate from proliferative ileitis (Lawsonia), salmonellosis, whipworms, gastric ulcers or other intestinal disturbances without laboratory assistance. If SD is in your herd, it may cost more than any of these other enteric pathogens. Hence, SD is a disease to avoid because of the high costs of treatment, control and production losses, and hardiness of the causative bacteria, Brachyspira, within the environment. Preventing strongly beta-hemolytic colonies of Brachyspira spp. from entering your herds and contaminating your facilities is by far the preferred strategy. Your swine veterinarian is a key information source for development of prevention and biosecurity plans, and essential for accurate diagnosis, treatment, control and elimination should this disease enter you herd. For more information on treatment, control and elimination strategies for SD, please refer to the Pork Information Gateway’s Factsheet on, “Steps for Treatment, Control and Elimination of Swine Dysentery”.
References and Citations
Burrough, E. R. 2013. Swine dysentery – re-emergence in the United States and Canada. In: 6th International Conference on Colonic Spirochaetal Infections in Animals and Humans, Guildford, UK. p 55-56.
Burrough, E. R. 2017. Swine dysentery: etiopathogenesis and diagnosis of a reemerging disease. Vet Pathol 54(1):22-31. doi: 10.1177/0300985816653795.
Hampson, D. J., and E. R. Burrough. 2019. Swine Dysentery and Brachyspiral Colitis. In: J. J. Zimmerman, L. A. Karriker, A. Ramirez, K. J. Schwartz, G. W. Stevenson and J. Zhang, editors, Diseases of Swine. Wiley-Blackwell, Hoboken, NJ. p. 951-970.
Harris, D. L. 1984. The epidemiology of swine dysentery as it relates to the eradication of the disease. Compendium on Continuing Education for the Practicing Veterinarian 6(2):S83-S88.
Harris, D. L., R. D. Glock, C. R. Christensen, and J. M. Kinyon. 1972. Inoculation of pigs with Treponema hyodysenteriae (new species) and reproduction of the disease. Vet Med Small Anim Clin 67(1):61-64.
Hidalgo, Á., A. Carvajal, B. Vester, M. Pringle, G. Naharro, and P. Rubio. 2011. Trends towards lower antimicrobial susceptibility and characterization of acquired resistance among clinical isolates of Brachyspira hyodysenteriae in Spain. Antimicrobial agents and chemotherapy 55(7):3330-3337. (Research Support, Non-U.S. Gov’t) doi: 10.1128/AAC.01749-10.
Joens, L. A., and J. M. Kinyon. 1982. Isolation of Treponema hyodysenteriae from wild rodents. J Clin Microbiol 15(6):994-997.
Martínez-Lobo, F. J., Á. Hidalgo, M. García, H. Argüello, G. Naharro, A. Carvajal, and P. Rubio. 2013. First identification of “Brachyspira hampsonii” in wild European waterfowl. PLoS One 8(12):e82626. (Research Support, Non-U.S. Gov’t) doi: 10.1371/journal.pone.0082626.
Mirajkar, N. S., P. R. Davies, and C. J. Gebhart. 2016a. Antimicrobial susceptibility patterns of Brachyspira species isolated from swine herds in the United States. J Clin Microbiol 54(8):2109-2119. doi: 10.1128/JCM.00834-16.
Mirajkar, N. S., N. D. Phillips, T. La, D. J. Hampson, and C. J. Gebhart. 2016b. Characterization and recognition of Brachyspira hampsonii sp. nov., a novel intestinal spirochete that is pathogenic to pigs. J Clin Microbiol 54(12):2942-2949. doi: 10.1128/JCM.01717-16.
Mushtaq, M., S. Zubair, T. Råsbäck, E. Bongcam-Rudloff, and D. S. Jansson. 2015. Brachyspira suanatina sp. nov., an enteropathogenic intestinal spirochaete isolated from pigs and mallards: genomic and phenotypic characteristics. BMC microbiology 15:208. doi: 10.1186/s12866-015-0537-y.
Plain, R. L., and J. D. Lawrence. 2003. Swine production. Vet Clin North Am Food Anim Pract 19(2):319-337. doi: 10.1016/s0749-0720(03)00025-2.
Schwartz, T., J. S. Pittman, J. M. Kinyon, and M. Hammer. 2012. Effect of waste environment on survival of Brachyspira hyodysenteriae. In: 43rd Annual Meeting of the American Association of Swine Veterinarians, Dencer, CO. p 85-89.
Wood, E. N., and R. J. Lysons. 1988. Financial benefit from the eradication of swine dysentery. Vet Rec 122(12):277-279. doi: 10.1136/vr.122.12.277.
Table 1: Diarrhea & The 3 Cs of swine dysentery
|Color||Grey||Yellowish, greenish-yellow||Dark or bright red|
Moist and glistening
Dry mucus particles
Fresh blood, small flecks
Blood mixed with mucus
Blood mixed uniformly with feces
White or tan ‘strings’
Pieces of sloughed tissue
Specks of sloughed tissue
Table 2: Survival of Brachyspira hyodysenteriae in different conditions
|Location||Condition||Temperature (F)||Survival time|
|Hog Lots||Sun-dried Manure||65||7 days|
|Hog Lots||Cold or frozen||45||Until temp increases|
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