Swine Dysentery: Brachyspira hyodysenteriae and Hemorrhagic Diarrhea in Pigs

Introduction

Swine dysentery (SD) is a globally significant enteric disease of pigs characterized by mucohemorrhagic diarrhea, weight loss, and mortality in grower-finisher herds [1]. The etiological agent is the anaerobic spirochete Brachyspira hyodysenteriae, formerly classified as Treponema hyodysenteriae [2]. This bacterium colonizes the large intestine, inducing a severe mucohemorrhagic colitis that leads to the hallmark clinical sign of swine bloody diarrhea [3]. The disease imposes substantial economic losses due to reduced feed conversion, increased mortality, and costs associated with treatment and control [1, 4]. This article provides a detailed review of the etiology, epidemiology, clinical presentation, pathology, diagnostic approaches, therapeutic strategies, and control measures for swine dysentery.

Etiology

Brachyspira hyodysenteriae is a Gram-negative, anaerobic, helically shaped spirochete measuring 6 to 8.5 micrometers in length and 0.3 to 0.4 micrometers in diameter [2, 5]. The bacterium possesses periplasmic flagella (7 to 14 per cell) that confer a characteristic serpentine motility, which is essential for colonization of the colonic mucus layer [5, 6]. The organism is strongly beta-hemolytic on blood agar, a key phenotypic feature distinguishing it from other porcine Brachyspira species such as Brachyspira pilosicoli (weak beta-hemolysis) and nonpathogenic Brachyspira innocens (weak or no hemolysis) [2, 7]. B. hyodysenteriae produces several virulence factors, including hemolysins (e.g., HlyA), lipooligosaccharide (LOS), and flagellar proteins that mediate mucosal adherence and inflammation [6, 8]. The bacterium is strictly anaerobic but can tolerate low oxygen concentrations in the presence of reducing agents [5].

Epidemiology

Swine dysentery occurs worldwide in pig-producing regions, with prevalence varying by management system and biosecurity practices [1, 9]. The disease primarily affects grower-finisher pigs aged 8 to 20 weeks, although outbreaks can occur in younger weaners and occasionally in adult breeding stock [3, 4]. Morbidity within affected groups can reach 90%, while mortality is typically low (5 to 10%) but can be higher in untreated or co-infected herds [1, 10]. Transmission occurs via the fecal-oral route through ingestion of contaminated feces, feed, water, or fomites [2, 9]. Recovered pigs can become asymptomatic carriers, shedding the organism intermittently for months and serving as a reservoir for naive cohorts [1, 4]. Rodents, particularly mice, can also carry B. hyodysenteriae and contribute to farm-level persistence [9, 11]. Stressors such as transport, dietary changes, and concurrent infections (e.g., Lawsonia intracellularis, Salmonella spp., or porcine reproductive and respiratory syndrome virus) exacerbate clinical expression [3, 10].

Clinical Signs

The incubation period ranges from 7 to 14 days following oral exposure [2, 3]. The classic presentation begins with a soft, yellowish to grayish diarrhea that rapidly progresses to mucoid, bloody feces [1, 4]. The term swine bloody diarrhea accurately describes the advanced stage, where feces contain fresh blood, mucus, and fibrin casts [3, 7]. Affected pigs exhibit depression, anorexia, pyrexia (40 to 41 degrees Celsius), dehydration, and progressive weight loss [1, 10]. In peracute cases, pigs may die without premonitory signs, especially in naive herds [2, 4]. Chronic infections result in intermittent diarrhea, poor growth, and unthriftiness [3, 9]. The clinical severity is influenced by the virulence of the B. hyodysenteriae strain, host immune status, and the presence of coinfections [6, 8].

Pathogenesis and Pathology

After ingestion, B. hyodysenteriae penetrates the colonic mucus layer using its corkscrew motility and adheres to the apical surface of colonic epithelial cells, primarily in the cecum and spiral colon [5, 6]. The bacterium does not invade beyond the mucosa but induces a robust inflammatory response characterized by neutrophil infiltration, goblet cell hyperplasia, and mucosal edema [2, 8]. Hemolysins and LOS trigger the release of proinflammatory cytokines (e.g., IL-1, IL-6, TNF-alpha), leading to increased vascular permeability, hemorrhage, and necrosis of the superficial epithelium [6, 8]. Gross pathological findings include thickening of the colonic wall, hyperemia, and a fibrinohemorrhagic exudate covering the mucosal surface [1, 7]. The colonic contents are often watery, blood-tinged, and mixed with mucus and fibrin strands [3, 4]. Histologically, lesions consist of acute to subacute colitis with erosion, crypt abscesses, and a mixed inflammatory infiltrate [2, 10]. Spirochetes can be visualized within the mucus layer and between epithelial cells using silver stains (e.g., Warthin-Starry) or immunohistochemistry [5, 7].

Diagnostics

A definitive diagnosis of swine dysentery requires detection of B. hyodysenteriae in feces or intestinal tissue, combined with compatible clinical signs and lesions [1, 2]. The diagnostic workflow is summarized in Figure 1.

flowchart TD
    A[Clinical suspicion: mucohemorrhagic diarrhea in grower-finisher pigs], > B[Collect fresh fecal samples or colonic scrapings]
    B, > C[Direct microscopic examination: phase-contrast or dark-field for spirochetes]
    C, > D{Presence of large, motile spirochetes?}
    D, Yes, > E[Anaerobic culture on selective blood agar with spectinomycin and rifampin]
    D, No, > F[Consider other causes: Lawsonia, Salmonella, Trichuris]
    E, > G[Strong beta-hemolysis after 3-5 days]
    G, > H[Confirmatory tests: PCR targeting 16S rRNA or nox gene]
    H, > I[Positive: Swine dysentery confirmed]
    H, > J[Negative: Consider B. pilosicoli or other spirochetes]
    F, > K[Perform differential diagnostics: fecal PCR panel, serology, necropsy]

Figure 1. Diagnostic algorithm for swine dysentery.

Microscopy

Direct phase-contrast or dark-field microscopy of fresh feces can reveal large, motile spirochetes (3 to 4 waves per cell) [2, 5]. However, this method lacks specificity, as nonpathogenic Brachyspira species may be present [7].

Culture

Anaerobic culture on selective media (e.g., trypticase soy agar with 5% sheep blood, spectinomycin 400 micrograms/mL, rifampin 25 micrograms/mL, and colistin 25 micrograms/mL) at 37 degrees Celsius for 3 to 5 days yields characteristic strong beta-hemolytic colonies [2, 5]. Biochemical tests (indole production, hippurate hydrolysis) can differentiate B. hyodysenteriae from other species [7].

Molecular Methods

Polymerase chain reaction (PCR) assays targeting the 16S rRNA gene or the nox gene (NADH oxidase) provide rapid, sensitive, and specific detection directly from feces or tissue [1, 8]. Real-time PCR allows quantification and differentiation of B. hyodysenteriae from B. pilosicoli and other spirochetes [9, 10].

Serology

Enzyme-linked immunosorbent assays (ELISAs) using whole-cell or recombinant antigens are available for herd-level screening, but they have limited sensitivity in individual animals and cannot distinguish current from past infection [1, 4].

Differential Diagnosis

Several enteric pathogens can produce similar clinical signs, as outlined in Table 1.

Table 1. Differential diagnoses for swine bloody diarrhea.

Cross-referencing with related articles on this portal, such as Porcine Proliferative Enteropathy: Lawsonia intracellularis Diagnosis and Control in Swine Herds and Brachyspira pilosicoli and Porcine Intestinal Spirochetosis in Weaned Pigs, is recommended for comprehensive differential evaluation.

Treatment

Antimicrobial therapy is the mainstay of treatment for clinically affected pigs [1, 3]. Historically, tiamulin, valnemulin, and lincomycin have shown high efficacy against B. hyodysenteriae [4, 10]. Tiamulin administered in feed (100 to 200 ppm) or water (15 to 20 mg/kg body weight) for 7 to 14 days is widely used [1, 2]. Valnemulin (75 to 100 ppm in feed) is also effective [4]. Macrolides (tylosin, tilmicosin) and pleuromutilins are common choices, but resistance has been reported globally [8, 9]. Antimicrobial susceptibility testing is recommended to guide therapy, especially in recurrent outbreaks [1, 10]. Supportive care includes fluid and electrolyte replacement, nutritional support, and isolation of affected pigs [3, 7]. In-feed or in-water medication of the entire affected group is often necessary to control outbreaks [2, 4].

Control and Prevention

Control of swine dysentery relies on a combination of biosecurity, management, and strategic antimicrobial use [1, 9]. Key measures include:

• All-in/all-out production to break the cycle of infection between batches [3, 4].
• Rodent control to eliminate a potential reservoir [9, 11].
• Quarantine and testing of incoming stock; PCR screening of feces for carrier animals [1, 2].
• Sanitation of pens, feeders, and waterers with disinfectants effective against spirochetes (e.g., cresylic acid, sodium hypochlorite) [4, 7].
• Vaccination: No commercial vaccine is widely available, although experimental bacterins and recombinant protein vaccines have shown partial protection [6, 8].
• Depopulation and repopulation of chronically infected herds may be necessary for eradication [1, 10].

Antimicrobial growth promoters (e.g., tiamulin, tylosin) have historically been used for prophylaxis, but regulatory restrictions in many regions limit their use [4, 9]. Alternative strategies include probiotics, organic acids, and dietary modifications to reduce colonic pH and inhibit spirochete growth [3, 7].

Conclusion

Swine dysentery remains a major challenge in pig production due to its high morbidity, chronicity, and economic impact. Accurate diagnosis using PCR and culture, combined with targeted antimicrobial therapy and rigorous biosecurity, is essential for control. Ongoing research into virulence mechanisms and antimicrobial resistance patterns will inform future management strategies. Clinicians should remain vigilant for the characteristic swine bloody diarrhea and integrate laboratory confirmation with clinical and pathological findings.

References

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[11] Joens LA, Kinyon JM. Isolation of Treponema hyodysenteriae from wild rodents. J Clin Microbiol. 1982;15(6):994-997. *** Disclaimer: This article is for educational and informational purposes only. It is not intended to substitute for professional veterinary advice, diagnosis, treatment, or regulatory guidance. Always consult a licensed veterinarian or qualified specialist regarding animal health, disease diagnosis, and therapeutic decisions.