Swine Bloody Diarrhea: Differential Diagnosis and Clinical Management in Pigs

The clinical presentation of swine bloody diarrhea represents a critical diagnostic challenge in porcine medicine, with etiologies ranging from bacterial enteropathogens to viral agents and parasitic infections. This review provides an exhaustive examination of the primary bacterial causes of hemorrhagic diarrhea in pigs, their pathophysiology, diagnostic differentiation, and evidence-based management strategies. Viral and parasitic causes are considered where they enter the differential list.

Etiologic Agents of Swine Bloody Diarrhea

Hemorrhagic diarrhea in swine is most frequently associated with spirochetal, enteric bacterial, and in some regions, protozoal infections. The predominant bacterial agents include Brachyspira hyodysenteriae, Brachyspira hampsonii, Salmonella enterica serovars, Escherichia coli pathotypes, and Lawsonia intracellularis. Viral agents such as Porcine Epidemic Diarrhea Virus (PEDV) and Transmissible Gastroenteritis Virus (TGEV) can produce watery diarrhea but less frequently frank blood, though they remain differentials [1, 2].

Brachyspira Species

Brachyspira hyodysenteriae is the classical etiologic agent of swine dysentery, a mucohemorrhagic colitis of growing and finishing pigs. The spirochete colonizes the large intestine, inducing severe inflammation, mucus hypersecretion, and capillary hemorrhage [1, 3]. A strongly hemolytic novel species, provisionally designated Brachyspira hampsonii, has been identified and is associated with clinical disease indistinguishable from classical swine dysentery [4, 5]. Molecular epidemiological studies have demonstrated relationships between genetic groups of B. hampsonii and different geographic regions and host species [4]. The fecal microbiota of pigs undergoes marked dysbiosis following B. hampsonii inoculation, with a decrease in commensal Lactobacillus populations and an increase in pathogenic taxa [6]. Experimental inoculation protocols have been refined to improve the consistency of disease induction, which is essential for pathogenesis studies and vaccine efficacy trials [7].

Dietary fiber level and type influence the clinical expression of B. hyodysenteriae infection; pigs fed diets high in insoluble fiber exhibit more severe diarrhea and poorer growth performance compared with those fed low-fiber diets [8]. This nutritional interaction affects colonic fermentation and mucus composition, modulating spirochete colonization. In gnotobiotic chick cecal models, Treponema hyodysenteriae (former nomenclature) induces diarrhea and cecal lesions, providing a surrogate model for studying pathogenicity mechanisms [9].

Salmonella enterica

Non-typhoidal Salmonella serovars, particularly Salmonella enterica serovar Typhimurium and Salmonella Choleraesuis, can cause enterocolitis with hemorrhagic diarrhea in pigs. The pathogenesis involves invasion of intestinal epithelial cells via type III secretion systems, triggering inflammatory responses that result in mucosal damage, neutrophilic infiltration, and erosion. Salmonella infection may present with or without systemic involvement, and co-infections with other enteropathogens are common.

Escherichia coli Pathotypes

Enterotoxigenic E. coli (ETEC) typically causes watery diarrhea in neonatal and post-weaning pigs, but certain pathotypes can produce hemorrhagic diarrhea. Shiga toxin-producing E. coli (STEC), including serotypes such as O157:H7 and non-O157 strains, have been isolated from pigs [10, 11]. In piglet models, E. coli O157:H7 infection results in diarrhea, and passive immunization with anti-Shiga toxin antibodies prevents fatal systemic complications [12]. A gnotobiotic piglet model has been used to evaluate the safety of antibiotics against E. coli O157:H7 infection [13]. More recently, porcine-derived hybrid E. coli strains have emerged that possess both intestinal and extraintestinal virulence determinants, complicating the clinical picture [14]. Shiga toxin-producing E. coli from swine harbor a range of antimicrobial resistance genes, including those encoding resistance to beta-lactams, tetracyclines, and sulfonamides [10].

Lawsonia intracellularis

Lawsonia intracellularis is the causative agent of porcine proliferative enteropathy (PPE), which can manifest as an acute hemorrhagic form (proliferative hemorrhagic enteropathy, PHE) typically in young adult pigs [15]. The obligate intracellular bacterium infects enterocytes of the ileum and proximal colon, causing crypt hyperplasia and adenomatous proliferation. Immunohistochemical detection of L. intracellularis in tissue sections is a standard diagnostic method [16]. The acute hemorrhagic form presents with sudden onset of bloody diarrhea, often fatal, and must be differentiated from swine dysentery [15].

Other Etiologies

Balantidium coli, a ciliated protozoan, can cause colitis and bloody diarrhea in pigs, particularly under poor sanitation conditions. Although its primary host is swine, it has zoonotic potential [2]. Clostridium perfringens type C can cause necrotic enteritis in neonatal piglets, with hemorrhagic diarrhea and high mortality. However, this review focuses on bacterial etiologies. Viral pathogens such as PEDV and TGEV produce profuse watery diarrhea but in severe cases may cause mucosal hemorrhage, thus they remain in the differential.

Clinical Presentation and Pathology

The hallmark of swine dysentery is mucohemorrhagic feces containing fresh blood and mucus, often described as "raspberry jam" consistency. Affected pigs show reduced feed intake, dehydration, and weight loss [1, 3]. In acute cases, mortality can be high, but most pigs recover after treatment, though they may become chronic shedders. Scanning electron microscopy of swine dysentery lesions reveals erosion of colonic epithelium, loss of microvilli, and heavy spirochete colonization on the luminal surface [3]. Histologically, the lesion is a diffuse catarrhal to fibrinous colitis with goblet cell hyperplasia and neutrophilic infiltration [1].

Fecal calprotectin levels are elevated in pigs following experimental colitis (e.g., Brachyspira infection) but not after enteritis, suggesting its utility as a biomarker for colonic inflammation [17].

Diagnostic Approach

Definitive diagnosis relies on detection of the causative agent. The differential list must be systematically narrowed based on age group, clinical signs, gross pathology, and laboratory findings. Table 1 summarizes key differentials for swine bloody diarrhea.

Table 1. Differential Diagnosis of Swine Bloody Diarrhea

A diagnostic workflow is illustrated in Figure 1.

graph TD
    A[Pig with bloody diarrhea], > B{Age group?}
    B, >|Neonatal| C[Consider ETEC, C. perfringens, PEDV]
    B, >|Weaner| D[Consider Brachyspira, Salmonella, STEC, PEDV]
    B, >|Grower-finisher| E[Consider Brachyspira, Lawsonia, Salmonella, Balantidium]
    B, >|Adult| F[Consider Lawsonia, Brachyspira, Salmonella]
    C, > G[Fecal culture, PCR for toxins, PEDV/TGEV PCR]
    D, > H[Fecal culture for Brachyspira, Salmonella; PCR for Brachyspira, STEC, PEDV]
    E, > I[Fecal microscopy for Balantidium; Brachyspira culture/PCR; Lawsonia PCR; Salmonella culture]
    F, > J[Fecal PCR for Lawsonia, Brachyspira; serology]
    G, > K{Results}
    H, > K
    I, > K
    J, > K
    K, > L[Confirm etiology and treat specifically]
    L, > M[Implement biosecurity and control measures]

Laboratory diagnostics include anaerobic culture for Brachyspira species, which requires selective media (e.g., blood agar with spectinomycin and rifampin). Molecular methods such as PCR are now standard for rapid detection and speciation [4, 5]. For Lawsonia intracellularis, PCR on fecal samples or immunohistochemistry on ileal tissue is highly sensitive [16]. STEC detection involves PCR targeting Shiga toxin genes stx1 and stx2 [10, 11]. Salmonella isolation requires pre-enrichment and selective plating.

Treatment and Clinical Management

Therapeutic strategies must be guided by antimicrobial susceptibility testing where possible, given the increasing concern of antimicrobial resistance. For swine dysentery caused by Brachyspira hyodysenteriae, several classes of antimicrobials have traditionally been effective, including pleuromutilins (tiamulin), macrolides (tylosin), and lincosamides (lincomycin). A specific derivative, 3-acetyl-4''-isovaleryl tylosin, has demonstrated efficacy in preventing swine dysentery under experimental conditions [18]. However, resistance is emerging; a combined approach using a zinc chelate treatment alongside adapted management measures has been shown to achieve successful eradication of B. hyodysenteriae from herds [19]. The zinc chelate, when evaluated under field conditions, reduced clinical scores and improved growth performance in pigs with clinical swine dysentery [20].

For Salmonella infections, antimicrobial therapy is often reserved for systemic cases, and fluoroquinolones or ceftiofur may be used, but resistance patterns must be monitored. STEC infections in pigs are often self-limiting but supportive therapy including fluid and electrolyte replacement is critical [13, 12]. Ionophores and other growth promoters are not recommended for STEC control due to resistance concerns [10].

PPE due to Lawsonia intracellularis responds well to macrolides (tylosin, tulathromycin) and pleuromutilins. Vaccination with an avirulent live vaccine is available in some regions for prevention [15]. Balantidium coli infections are treated with antiprotozoal agents such as metronidazole or paromomycin, combined with improved sanitation [2].

Supportive care is essential for all cases of hemorrhagic diarrhea: provision of clean water, electrolyte supplementation, and in severe cases, parenteral fluid therapy. Affected pigs should be isolated to reduce within-herd transmission.

Control and Prevention

Biosecurity measures are paramount. Swine dysentery is introduced through carrier pigs; therefore, all-in/all-out management, thorough cleaning and disinfection, and quarantine of new stock are critical. Eradication protocols combining antimicrobial treatment, zinc chelate therapy, and depopulation-repopulation strategies have been successful [19]. For Lawsonia intracellularis, vaccination of replacement gilts and growing pigs reduces clinical outbreaks.

Dietary manipulation can influence disease severity. For Brachyspira infections, reducing insoluble fiber in the diet may minimize colonization and clinical signs [8]. Probiotics and prebiotics that promote a healthy gut microbiota are being explored, but their efficacy remains to be rigorously validated.

Conclusion

Swine bloody diarrhea is a multifactorial syndrome requiring systematic differential diagnosis. Bacterial agents such as Brachyspira hyodysenteriae, Salmonella spp., STEC, and Lawsonia intracellularis are the primary etiologies, with viral and parasitic causes playing lesser but important roles. Accurate diagnosis relies on age-specific presentation, lesion distribution, and laboratory confirmation using culture, PCR, and immunohistochemistry. Treatment must be tailored to the specific pathogen and guided by antimicrobial susceptibility, with an emphasis on supporting the animal's hydration and nutritional status. Integrated control strategies combining biosecurity, vaccination, dietary modulation, and judicious antimicrobial use are necessary to reduce the burden of hemorrhagic diarrhea in swine herds.

References

[1] Burrough ER. Swine Dysentery. Vet Pathol. 2017. [URL: https://pubmed.ncbi.nlm.nih.gov/27288432/]

[2] Schuster FL, Ramirez-Avila L. Current world status of Balantidium coli. Clin Microbiol Rev. 2008. [URL: https://pubmed.ncbi.nlm.nih.gov/18854484/]

[3] Kennedy GA, Strafuss AC. Scanning electron microscopy of the lesions of swine dysentery. Am J Vet Res. 1976. [URL: https://pubmed.ncbi.nlm.nih.gov/131500/] *** 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.

[4] Mirajkar NS, Bekele AZ, Chander YY, et al. Molecular Epidemiology of Novel Pathogen "Brachyspira hampsonii" Reveals Relationships between Diverse Genetic Groups, Regions, Host Species, and Other Pathogenic and Commensal Brachyspira Species. J Clin Microbiol. 2015. [URL: https://pubmed.ncbi.nlm.nih.gov/26135863/]

[5] Chander Y, Primus A, Oliveira S, et al. Phenotypic and molecular characterization of a novel strongly hemolytic Brachyspira species, provisionally designated "Brachyspira hampsonii". J Vet Diagn Invest. 2012. [URL: https://pubmed.ncbi.nlm.nih.gov/22914820/]

[6] Costa MO, Chaban B, Harding JC, et al. Characterization of the fecal microbiota of pigs before and after inoculation with "Brachyspira hampsonii". PLoS One. 2014. [URL: https://pubmed.ncbi.nlm.nih.gov/25166307/]

[7] Parra-Aguirre JC, Nosach R, Fernando C, et al. Improving the consistency of experimental swine dysentery inoculation strategies. Vet Res. 2023. [URL: https://pubmed.ncbi.nlm.nih.gov/37328906/]

[8] Lee GI, Skou Hedemann M, Borg Jensen B, et al. Influence of infection with Brachyspira hyodysenteriae on clinical expression, growth performance, and digestibility in growing pigs fed diets varying in type and level of fiber. J Anim Sci. 2022. [URL: https://pubmed.ncbi.nlm.nih.gov/35255495/]

[9] Sueyoshi M, Adachi Y. Diarrhea induced by Treponema hyodysenteriae: a young chick cecal model for swine dysentery. Infect Immun. 1990. [URL: https://pubmed.ncbi.nlm.nih.gov/2205578/]

[10] Galarce N, Sánchez F, Fuenzalida V, et al. Phenotypic and Genotypic Antimicrobial Resistance in Non-O157 Shiga Toxin-Producing Escherichia coli Isolated From Cattle and Swine in Chile. Front Vet Sci. 2020. [URL: https://pubmed.ncbi.nlm.nih.gov/32754621/]

[11] Gannon VP, Gyles CL, Friendship RW. Characteristics of verotoxigenic Escherichia coli from pigs. Can J Vet Res. 1988. [URL: https://pubmed.ncbi.nlm.nih.gov/3048621/]

[12] Sheoran AS, Chapman-Bonofiglio S, Harvey BR, et al. Human antibody against shiga toxin 2 administered to piglets after the onset of diarrhea due to Escherichia coli O157:H7 prevents fatal systemic complications. Infect Immun. 2005. [URL: https://pubmed.ncbi.nlm.nih.gov/16040972/]

[13] Zhang Q, Donohue-Rolfe A, Krautz-Peterson G, et al. Gnotobiotic piglet infection model for evaluating the safe use of antibiotics against Escherichia coli O157:H7 infection. J Infect Dis. 2009. [URL: https://pubmed.ncbi.nlm.nih.gov/19125676/]

[14] Pan X, Liu J, Chen Z, et al. Emergence of porcine-derived hybrid Escherichia coli with dual-disease manifestations in intestinal and extraintestinal niches. Virulence. 2025. [URL: https://pubmed.ncbi.nlm.nih.gov/40602993/]

[15] Wilson JB, Pauling GE, McEwen BJ, et al. A descriptive study of the frequency and characteristics of proliferative enteropathy in swine in Ontario by analyzing routine animal health surveillance data. Can Vet J. 1999. [URL: https://pubmed.ncbi.nlm.nih.gov/10572667/]

[16] Szczotka A, Stadejek T, Zmudzki J, et al. Immunohistochemical detection of Lawsonia intracellularis in tissue sections from pigs. Pol J Vet Sci. 2011. [URL: https://pubmed.ncbi.nlm.nih.gov/22439321/]

[17] Barbosa JA, Rodrigues LA, Columbus DA, et al. Experimental infectious challenge in pigs leads to elevated fecal calprotectin levels following colitis, but not enteritis. Porcine Health Manag. 2021. [URL: https://pubmed.ncbi.nlm.nih.gov/34429170/]

[18] Jacks TM, Judith FR, Feighner SD, et al. 3-Acetyl-4''-isovaleryl tylosin for prevention of swine dysentery. Am J Vet Res. 1986. [URL: https://pubmed.ncbi.nlm.nih.gov/3789492/]

[19] Vangroenweghe FACJ. Successful Brachyspira hyodysenteriae Eradication Through a Combined Approach of a Zinc Chelate Treatment and Adapted Management Measures. Pathogens. 2025. [URL: https://pubmed.ncbi.nlm.nih.gov/41598985/]

[20] Vangroenweghe F, Allais L, Van Driessche E, et al. Evaluation of a zinc chelate on clinical swine dysentery under field conditions. Porcine Health Manag. 2020. [URL: https://pubmed.ncbi.nlm.nih.gov/31969985/]