company news about The truth about swine edema disease revealed: An article explaining the genetic code of Stx2e-producing E. coli and the

Edema disease is a multifactorial disease caused by a specific pathotype of Escherichia coli that produces Shiga toxin 2e (Stx2e). It commonly affects piglets 4-12 weeks after weaning, with an acute onset and a short course, often resulting in high mortality.

Research Highlights

· The virulence profile of O139:H1 STEC has been revealed for the first time: the pW1316-2 plasmid carries a hemolytic adhesion kit, available in a "group purchase" alongside Shiga and Salmonella plasmids and drug resistance kits, enabling a single-click upgrade in virulence and drug resistance.

· Oral fluid collected using cotton rope revealed that over 60% of pig farms harbor Stx2e, regardless of the weaning period. Indoor pens fed with homemade high-energy feed are the most susceptible to the disease.

· Feed changes, free-range feeding, and monthly qPCR can mitigate the potential risk of edema disease in pigs in advance, transforming it from a "sudden death nightmare" to one that is preventable and controllable.

Recent studies on Escherichia coli (E. coli) have found that pathogenic strains often carry F18 or AIDA pili and produce multiple virulence factors. Upon entry, these strains damage the vascular endothelium, causing edema, hemorrhage, necrosis, and neurological symptoms, often manifesting as eyelid swelling, motor impairment, and coma. Diagnosis primarily relies on autopsy and molecular testing, with edema of the greater curvature of the stomach, mesentery, and gallbladder common. Due to limited treatment efficacy, prevention and control rely on full-in, full-out strategies, feed optimization, environmental improvements, and vaccination.

Research has shown that the occurrence of edema disease is not only related to strain virulence, but also influenced by factors such as feed composition, maternal antibodies, and co-infections. The prevalence of Stx2e positivity is high in European and Asian pig herds, which is related to farm type and feed source. Some strains carry plasmids similar to those of Shigella and Salmonella, harboring virulence and resistance genes, suggesting that their pathogenicity may be enhanced through horizontal gene transfer.

Introduction

Eedema disease is a typical bacterial toxin-induced disease characterized by complex pathogenic mechanisms, widespread prevalence, and difficulty in prevention and control. Strengthening pathogen monitoring, improving animal husbandry practices, and standardizing biosafety management, combined with genetic research findings, will help more effectively control disease outbreaks and reduce industry risks.

Research Results

1. Genome Magnifier: Virulence "Hidden" in Plasmids

An Italian team performed a whole-genome scan of 53 strains of O139:H1 STEC and found an overwhelming prevalence of plasmid pW1316-2 (approximately 70% carry it).

Figure 1. Seven reference plasmids were identified among 53 Italian STEC strains, with pW1316-2 being the most common (69.8%). The remaining plasmids had lower detection rates.

· It combines the hemolysin (hlyA/B), adhesin (aidA-I, faeE), and the regulatory "master switch" H-NS/Hha, achieving a single chain of "adhesion-colonization-hemolysis" trifecta.

· Even more strikingly, some strains harbor a Shigella flexneri 2a-like plasmid, directly upgrading their regulatory network. Others harbor a pB71-like plasmid with the tetA/tetC tetracycline resistance cassette—a single package of virulence and resistance, enabling rapid lateral transmission.

Conclusion: EDEC's virulence is not solely due to chromosomes, but rather to multiple plasmids, and signs of antibiotic resistance have emerged.

2. Field Reconnaissance: Oral Fluid Testing of 37 Pig Farms in Slovenia

· Using the non-invasive "bite-rope + FTA card" method, with 5-minute sampling and direct qPCR detection of stx2e, farm compliance was 100%.

Table 1. RT-PCR Analysis Results of Oral Fluid Samples from Pigs Aged 5-6, 7-8, 12, and 14 Weeks

· Results: Stx2e was detected in 64.9% of pig farms, comparable to the data from the US and Germany pig farms; however, the age distribution showed an outbreak across all stages, disproving the notion that it only occurs 4-12 weeks after weaning.

· Risk Signals:

Complete indoor rearing vs. outdoor + indoor rearing, OR = 0.13 (p < 0.001), indicating a significant reduction in risk with the outdoor model.

Homemade feed vs. commercial feed, OR = 4.7 (p < 0.001), indicating a high starch and protein content combined with a lack of fiber, creating a breeding ground for EDEC.

Only 12% of farms vaccinate piglets against edema, leaving a significant gap in herd immunity.

Conclusion: Rearing practices, feed formulation, and a lack of vaccines are three potential risks; oral fluid qPCR can proactively detect them.

3. Understanding at a Glance | The "Dark Trio" of Virulence Plasmids

pW1316-2 → Adhesion + Hemolysis
Shigella-like Plasmid → Regulatory Hook
pB71 → Virulence + Tetracycline Resistance

Figure 1. The "Dark Trio" of Virulence Plasmids for Swine Edema Disease STEC O139:H1

Red: Hemolysis + Adhesion | Yellow: Enhanced Regulation | Purple: Virulence/Resistance

4. 3-Step Action List for Pig Farmers

· Feed Change: Reduce protein by 5-8%, add 15-20% fiber, and switch to restricted/frequent feeding.

· Pen Change: Allow pigs to "venture" if conditions permit to reduce stress and bacterial load.

· Monitoring: Monthly oral fluid qPCR "physical examinations," immediate grouping of positive groups, and urgent vaccination booster.

Summary

Two studies provide a thorough understanding of swine edema disease from both a genetic and farm perspective. Genome sequencing revealed that E. coli O139:H1 carries three key advantages: hemolytic adhesion, Shigella-like regulation, and a resistance plasmid, suggesting that virulence and resistance may be transmitted across species in a coordinated manner. A survey of Slovenian farms revealed that over 60% of pigs harbor latent Stx2e, not only during the weaning period but also in confinement with high-energy feed. However, the risk can be mitigated by adjusting feed, improving the environment, and conducting regular qPCR testing. The former identifies the pathogen's genetic "arsenal," while the latter provides key points for field control. Together, these studies provide a comprehensive framework for understanding the mechanisms and practical prevention and control of edema disease.