Different ideas on the pathogenesis and treatment of swine edema-disease

Although literature data associate the reason of swine edema-disease with certain serotypes of Escherichia coli bacteria, the authors assume that the primary cause of edema is more different. Susceptible agents and factors, mostly of feed compound are involved. During the digestion of some feed-origin protein opiate-like metabolites, exorphins arise, simultaneously arrest the release of acetylcholine. Consequences of acetylcholine shortage are spasm of sphincters (mostly pylorus), intestine-dilatation, contraction of bladder-sphincter, and urine retention. The endorphins and exorphins intensify the insulin release from the pancreas, hypoglycemia evolves, which is associated with loss of balance. According to the authors in edema-disease piglet dies because of hypoglycemia.

Effect of Edema Disease Vaccination on Mortality and Growth Parameters in Nursery Pigs in a Shiga Toxin 2e Positive Commercial Farm

Diseases caused by Escherichia coli are recognized as major problems in the swine industry, one of them being edema disease (ED). Importantly, the current decrease in antibiotic use may cause difficulties in controlling the disorders caused by E. coli. Therefore, this study assessed the efficacy of a commercial vaccine against ED in nursery pigs from a farm with previous history of ED. A total of 1344 pigs were monitored; half of them were randomly assigned to a vaccinated group (VG) and the other half to a non-vaccinated group (NVG). The vaccine was administered at 7 days of age. Animals received a pre-starter feed with 2500 ppm of zinc oxide (ZnO) for 2 weeks and a starter feed without ZnO for another 3 weeks. Pen-group weights were recorded at 28 (weaning), 42 (end of pre-starter phase), and 63 days of life (end of nursery phase). Death/culling rates, average daily gain (ADG), and average daily feed intake (ADFI) were calculated for each group at each phase. The overall relative risk of dying/being culled for a pig in the NVG was 5 times higher than that of the VG group but increased to 12 times higher during the starter period. ADG and ADFI were also significantly higher in the VG group for that period. Vaccination against ED significantly reduced pig losses and improved ADG and ADFI, particularly when ZnO was not used.

Shiga Toxin-Producing Escherichiacoli in Feces of Finisher Pigs: Isolation, Identification and Public Health Implications of Major and Minor Serogroups

Shiga toxin-producing Escherichia coli (STEC) are major foodborne human pathogens that cause mild to hemorrhagic colitis, which could lead to complications of hemolytic uremic syndrome. Seven serogroups, O26, O45, O103, O111, O121, O145 and O157, account for the majority of the STEC illnesses in the US. Shiga toxins 1 and 2, encoded by stx 1 and stx 2, respectively, and intimin, encoded by eae gene, are major virulence factors. Our objectives were to use culture method to isolate and identify major and minor serogroups of STEC in finisher pig feces. Shiga toxin genes were subtyped to assess public health implications of STEC. Fecal samples (n=598) from finisher pigs, collected from 10 pig flows, were enriched in E. coli broth and tested for stx 1, stx 2, and eae by PCR assay. Samples positive for stx 1 or stx 2 gene were subjected to culture methods, with or without immunomagnetic separation and plating on selective or nonselective media, for isolation and identification of stx- positive serogroups. The culture method yielded a total of 178 strains belonging to 23 serogroups and the three predominant serogroups isolated were O8, O86, and O121. The 178 STEC strains included 26 with stx 1a and 152 strains with stx 2e subtypes. Strains with stx 1a, particularly in association with eae , have the potential to cause severe human infections. All stx 2 strains carried stx 2e, a subtype that causes edema disease in swine, but rarely involved in human infections. A number of strains were also positive for genes that encode for enterotoxins, which are involved in neonatal and postweaning diarrhea in swine. In conclusion, our study showed that healthy finisher pigs harbored and shed a number of serogroups of E. coli carrying virulence genes involved in neonatal diarrhea, postweaning diarrhea, and edema disease, but prevalence of STEC of public health importance was low.

Structural Insights into Escherichia coli Shiga Toxin (Stx) Glycosphingolipid Receptors of Porcine Renal Epithelial Cells and Inhibition of Stx-Mediated Cellular Injury Using Neoglycolipid-Spiked Glycovesicles

Shiga toxin (Stx) producing Escherichia coli (STEC) cause the edema disease in pigs by releasing the swine-pathogenic Stx2e subtype as the key virulence factor. Stx2e targets endothelial cells of animal organs including the kidney harboring the Stx receptor glycosphingolipids (GSLs) globotriaosylceramide (Gb3Cer, Galα1-4Galβ1-4Glcβ1-1Cer) and globotetraosylceramide (Gb4Cer, GalNAcβ1-3Galα1-4Galβ1-4Glcβ1-1Cer). Since the involvement of renal epithelial cells in the edema disease is unknown, in this study, we analyzed the porcine kidney epithelial cell lines, LLC-PK1 and PK-15, regarding the presence of Stx-binding GSLs, their sensitivity towards Stx2e, and the inhibitory potential of Gb3- and Gb4-neoglycolipids, carrying phosphatidylethanolamine (PE) as the lipid anchor, towards Stx2e. Immunochemical and mass spectrometric analysis revealed various Gb3Cer and Gb4Cer lipoforms as the dominant Stx-binding GSLs in both LLC-PK1 and PK-15 cells. A dihexosylceramide with proposed Galα1-4Gal-sequence (Gal2Cer) was detected in PK-15 cells, whereas LLC-PK1 cells lacked this compound. Both cell lines were susceptible towards Stx2e with LLC-PK1 representing an extremely Stx2e-sensitive cell line. Gb3-PE and Gb4-PE applied as glycovesicles significantly reduced the cytotoxic activity of Stx2e towards LLC-PK1 cells, whereas only Gb4-PE exhibited some protection against Stx2e for PK-15 cells. This is the first report identifying Stx2e receptors of porcine kidney epithelial cells and providing first data on their Stx2e-mediated damage suggesting possible involvement in the edema disease.