Swine Erysipelas in Pigs: Pathogen, Symptoms, and Control

Introduction

Swine erysipelas is a globally significant bacterial disease of pigs caused by Erysipelothrix rhusiopathiae, a Gram-positive rod-shaped bacterium [1, 52]. The disease manifests in acute, subacute, and chronic forms, with clinical presentations ranging from septicemia and characteristic skin lesions to vegetative endocarditis and polyarthritis [78, 85]. E. rhusiopathiae is also an occupational zoonotic pathogen, though this review focuses exclusively on its impact in swine [1, 71]. The bacterium is widespread in swine populations, with carrier animals harboring the organism in tonsils and lymphoid tissues, contributing to persistent herd infections [2, 3, 73]. Understanding the pathogen's biology, virulence mechanisms, and host interactions is essential for effective diagnosis and control [4, 5, 6].

Pathogen

Taxonomy and Morphology

Erysipelothrix rhusiopathiae belongs to the family Erysipelotrichaceae within the phylum Firmicutes [51, 54]. The genus Erysipelothrix includes several species, with E. rhusiopathiae being the primary pathogen in swine [52, 54]. E. tonsillarum is a closely related species that is generally considered non-pathogenic for pigs but can cause endocarditis in dogs [61, 69]. E. piscisicarius has been identified in fish and occasionally in pigs, with pathogenic potential under certain conditions [7]. The bacteria are slender, straight or slightly curved rods, 0.2–0.4 µm in width and 1.0–2.0 µm in length, and are non-motile, non-spore-forming, and facultatively anaerobic [1, 52]. They exhibit a characteristic "bottle-brush" growth pattern in broth culture and produce alpha-hemolysis on blood agar [94].

Genomic Features

The complete genome of E. rhusiopathiae strain SY1027, isolated from an acute outbreak in China, is approximately 1.8 Mb with a G+C content of 36–38% [45]. Comparative genomic analyses have revealed a core genome of approximately 1,500 genes and a pangenome that includes genes associated with host adaptation and antimicrobial resistance [8, 45]. The genome encodes numerous surface proteins, including the surface protective antigen A (SpaA), which is a major virulence factor and immunogen [9, 44, 63]. Genomic studies have identified a tagF homolog involved in teichoic acid biosynthesis that is essential for virulence [9]. Whole-genome sequencing of field isolates from diverse geographic regions, including Australia, China, Japan, and Poland, has revealed substantial genetic diversity and evidence of host adaptation [10, 6, 8, 43]. A highly virulent strain characterized by Zhao et al. (2024) exhibited unique genomic features associated with enhanced pathogenicity [4].

Serovars and Antigenic Diversity

E. rhusiopathiae is classified into serovars based on heat-stable somatic antigens. At least 28 serovars (1a, 1b, 2–23, and type N) have been described, with serovars 1a, 1b, and 2a being the most prevalent in swine erysipelas cases worldwide [11, 12, 80, 83]. Serovar 1a is frequently associated with acute septicemic disease, while serovar 2 is more commonly isolated from chronic cases [13, 76]. The serovar-specific antigen is determined by a chromosomal region encoding glycosyltransferases involved in polysaccharide biosynthesis [35]. A multiplex PCR-based assay has been developed for rapid serotyping, facilitating epidemiological surveillance [14]. Table 1 summarizes the major serovars and their association with disease.

Table 1. Major serovars of Erysipelothrix rhusiopathiae associated with swine erysipelas.

Virulence Factors

The pathogenesis of swine erysipelas is multifactorial, involving several surface-associated and secreted virulence determinants. SpaA is a choline-binding protein that mediates adherence to porcine endothelial cells and is essential for full virulence [37, 44, 46]. SpaA also binds plasminogen, facilitating bacterial dissemination [32]. The capsular polysaccharide (CPS) is modified with phosphorylcholine, which contributes to resistance against complement-mediated killing and enhances adherence to host cells [49]. Other surface proteins, including CbpB, have been characterized as adhesins and plasminogen-binding proteins [32, 36]. A putative transcription regulator identified in an acriflavine-resistant vaccine strain is involved in virulence attenuation [15]. Proteomic and transcriptomic analyses have revealed a repertoire of virulence-associated genes, including those encoding hemolysins, hyaluronidases, and neuraminidases [41, 51]. The bacterium also produces a neuraminidase that may facilitate tissue invasion [52]. Bacteriophage SE-I has been identified in E. rhusiopathiae and may contribute to horizontal gene transfer of virulence factors [40].

Clinical Signs and Pathogenesis

Acute Form

Acute swine erysipelas is characterized by sudden onset of fever (40–42°C), depression, anorexia, and reluctance to move [78, 85]. Within 24–48 hours, characteristic diamond-shaped skin lesions appear, particularly on the back, flanks, and thighs [78]. These lesions are erythematous, raised, and often coalesce into larger plaques. In severe cases, septicemia leads to death within 2–4 days [4, 43]. Mortality rates can reach 20–30% in untreated outbreaks [78]. The acute phase is associated with systemic vascular damage, increased vascular permeability, and disseminated intravascular coagulation [85, 90, 91]. The bacterium invades through the tonsillar crypts, exploiting cytokeratin 18-positive epithelial cells as an invasion gateway [48]. It then spreads via the bloodstream to multiple organs, including the heart, liver, spleen, and kidneys [85, 90].

Subacute Form

Subacute erysipelas presents with milder clinical signs, including transient fever, reduced appetite, and fewer skin lesions [78]. The diamond-shaped plaques may be less pronounced and resolve within a few days without treatment [78]. Some animals develop a chronic carrier state with persistent tonsillar colonization [2, 73].

Chronic Form

Chronic swine erysipelas typically follows an acute or subacute episode and is characterized by three main manifestations: vegetative endocarditis, polyarthritis, and chronic skin lesions [78, 79, 85]. Vegetative endocarditis, most commonly affecting the mitral valve, results from bacterial colonization of damaged endothelium and leads to heart failure, embolic events, and sudden death [93]. Chronic polyarthritis is characterized by non-suppurative inflammation of the joints, leading to lameness, joint swelling, and stiffness [79, 89]. The arthritis is immune-mediated, with deposition of immune complexes in the synovium [79, 89]. Chronic skin lesions may include areas of necrosis and sloughing, particularly on the ears, tail, and extremities [78].

Pathogenesis at the Cellular Level

E. rhusiopathiae adheres to and invades porcine endothelial cells, a process mediated by SpaA and phosphorylcholine [37, 46, 49]. The bacterium survives within macrophages and endothelial cells, evading host immune responses [52]. Intracellular survival is facilitated by resistance to phagolysosomal fusion and oxidative killing [52]. Transcriptional analysis of infected porcine heart tissue has revealed upregulation of genes involved in inflammation, apoptosis, and extracellular matrix remodeling [38]. The bacterium also induces production of pro-inflammatory cytokines, contributing to the systemic inflammatory response [38, 85].

Diagnosis

Clinical and Pathological Examination

Presumptive diagnosis is based on characteristic clinical signs, particularly the diamond-shaped skin lesions in acute cases [78]. Postmortem examination reveals petechial hemorrhages on serosal surfaces, splenomegaly, and vegetative lesions on heart valves in chronic cases [78, 93]. Histopathology shows vasculitis, thrombosis, and bacterial emboli in affected tissues [85, 90].

Bacteriological Culture

Definitive diagnosis requires isolation of E. rhusiopathiae from blood, skin lesions, joints, or internal organs [56, 94]. The bacterium grows on blood agar or selective media containing antibiotics such as sodium azide and crystal violet [56]. Colonies appear small, transparent, and alpha-hemolytic after 24–48 hours of incubation at 37°C [94]. Identification is confirmed by Gram staining, catalase-negative reaction, and biochemical tests [1, 52].

Molecular Detection

PCR assays targeting the 16S rRNA gene or the spaA gene provide rapid and sensitive detection of E. rhusiopathiae in clinical samples [67]. A multiplex PCR-based serotyping assay has been developed for simultaneous identification and serovar determination [14]. Real-time PCR is increasingly used for quantification of bacterial load in tissues [16]. Molecular methods are particularly useful for detecting the bacterium in tonsillar swabs from carrier animals [2, 73].

Serological Testing

Enzyme-linked immunosorbent assays (ELISAs) using SpaA or whole-cell antigens are available for detecting antibodies against E. rhusiopathiae [66]. Serology is useful for herd-level surveillance and vaccine potency testing but has limited value for individual diagnosis due to the prevalence of subclinical infections and vaccine-induced antibodies [66, 82]. The ELISA for feline leukemia virus p27 antigen detection is a different assay and not applicable here.

Differential Diagnosis

Acute swine erysipelas must be differentiated from other causes of septicemia and skin lesions in pigs, including African swine fever (ASF), classical swine fever, porcine reproductive and respiratory syndrome (PRRS), and Haemophilus parasuis infection (Glässer's disease) [16, 17, 30]. Chronic arthritis requires differentiation from Mycoplasma hyosynoviae and Streptococcus suis infections [78]. Co-infections with PRRS virus can exacerbate erysipelas severity and complicate diagnosis [18, 17].

Figure 1. Diagnostic workflow for swine erysipelas.

flowchart TD
    A["Clinical suspicion: fever, skin lesions, lameness"] --> B{Acute or chronic?}
    B -->|Acute| C[Blood culture / skin biopsy]
    B -->|Chronic| D[Joint fluid / heart valve culture]
    C --> E[Gram stain, culture on blood agar]
    D --> E
    E --> F[Biochemical identification]
    F --> G[PCR for spaA or 16S rRNA]
    G --> H[Serotyping by multiplex PCR]
    H --> I[Antimicrobial susceptibility testing]
    I --> J[Confirm diagnosis and guide treatment]
    C --> K["Serology (ELISA") for herd screening]
    K --> L[Interpret with caution due to vaccination]

Control

Vaccination

Vaccination is the cornerstone of swine erysipelas control. Both inactivated (bacterin) and live attenuated vaccines are available [53, 57, 68]. Inactivated vaccines are commonly used in breeding herds and provide protection against clinical disease, though they may not prevent tonsillar colonization [57, 82]. Live attenuated vaccines, such as the acriflavine-resistant strain, induce robust humoral and cell-mediated immunity and can be administered orally or parenterally [9, 15, 59, 74]. Cross-protection studies have demonstrated that vaccination with serovar 1a or 2 strains confers protection against challenge with multiple serovars [19, 20, 74, 77]. However, the emergence of Met-203 type SpaA variants has raised concerns about vaccine efficacy against certain field strains [39, 47]. Vaccination of sows against erysipelas has been shown to reduce the incidence of post-weaning multisystemic wasting syndrome (PMWS) in piglets co-infected with porcine circovirus type 2 (PCV2) [18]. The use of Propionibacterium avidum as an adjuvant has been explored to enhance vaccine immunogenicity [21, 70].

Antimicrobial Therapy

Penicillin is the drug of choice for treating acute swine erysipelas [52, 78]. Early administration of high-dose penicillin (20,000–40,000 IU/kg) for 3–5 days is highly effective [78]. Alternative antibiotics include amoxicillin, ceftiofur, and tylosin [5, 62]. Antimicrobial susceptibility testing is recommended due to the emergence of resistance in some regions [5, 6]. A study of Polish isolates found high susceptibility to penicillins but reduced susceptibility to tetracyclines and erythromycin [5]. In chronic cases, antimicrobial therapy may be less effective due to the immune-mediated nature of arthritis and endocarditis [78].

Biosecurity and Management

Control of swine erysipelas relies on a combination of vaccination, antimicrobial therapy, and management practices. Carrier pigs are a major source of infection, and stress factors such as overcrowding, poor ventilation, and sudden feed changes can precipitate outbreaks [78, 84]. All-in/all-out production systems, proper sanitation, and rodent control reduce environmental contamination [78]. The bacterium can survive for months in soil and organic matter, making thorough cleaning and disinfection essential [52]. Quarantine of newly introduced pigs and testing for carrier status using tonsillar swabs and PCR can prevent introduction of new strains [2, 73].

Integrated Control in the Context of Co-infections

Swine erysipelas often occurs concurrently with viral infections such as PRRS, PCV2, and ASF [16, 18, 17]. PRRS virus infection impairs immune function and increases susceptibility to E. rhusiopathiae [17]. In ASF-affected regions, differential diagnosis is critical, as skin lesions of erysipelas can mimic ASF [16]. Vaccination against erysipelas in PRRS-positive herds has been shown to reduce mortality and improve growth performance [17]. The use of live attenuated vaccines in PRRS-infected pigs is safe and effective [17]. In areas where ASF is present, strict biosecurity measures and rapid diagnostic testing are essential to differentiate erysipelas from ASF [16].

Conclusion

Swine erysipelas remains a significant economic burden to the global pig industry. The causative agent, Erysipelothrix rhusiopathiae, is a versatile pathogen with a wide range of virulence factors and serovars. Accurate diagnosis requires a combination of clinical observation, bacteriological culture, molecular detection, and serology. Control relies on effective vaccination, prudent antimicrobial use, and robust biosecurity. Ongoing genomic surveillance is necessary to monitor the emergence of new strains and antimicrobial resistance patterns. Future research should focus on developing improved vaccines that provide broader cross-protection and on understanding the mechanisms of host adaptation and persistence.

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.

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