LET's TALK about EDEMA DISEASE
LET's TALK about EDEMA DISEASE
Podcasts to provide knowledge on this disease
Welcome to the space that deals with the consequences of V-TEC infections in the field through quick audio episodes:
EPISODE 1: What's the pathology of ED and it's virulence factors?
Let's talk about Edema Disease with:
KEN STEEN PEDERSEN, Veterinarian
Our objective is to put the focus on Edema disease, that, as you know, is a highly contagious enterotoxaemia disease causing great economic losses due to increasing mortality and productive alterations on swine farms. The etiological agent of this disease is a Verotoxin 2e, produced by certain E. coli (VTEC) that colonize the small intestine. This VT2e enters the bloodstream and damages vessel walls resulting in edema in targeted tissues. In affected animals, different clinical forms of the disease have been described.
Can you give us a quick and simple update on E.coli types and pathologies produced by E. coli?
Quick and simple (haha), nothing about E. coli is quick and simple, but let me try to give a fair overview of the jungle of porcine pathogenic E. coli. We are operating with some broad classes of pathogenic E. coli´s. We can call it different “pathotypes” based on the E. coli´s virulence mechanisms. We have the “pathotypes” ETEC (enterotoxigenic E. coli), VTEC (verotoxin-producing E. coli), EPEC (enteropathogenic) and ExPEC (extraintestinal pathogenic E. coli). Detection of virulence factors is important for the identification of pathogenic E. coli since a lot of E. coli are just normal harmless inhabitants of the intestinal tract. The combination of these factors for a particular isolate determinate which disease it can cause and also to some extent the age of pigs that can be affected. Thus, we have some ETEC causing neonatal diarrhea and preweaning “turbo”-diarrhea, and other ETEC and VTEC causing early and late post-weaning diarrhea and edema disease.
Can you explain more about ETEC and V-TEC and their virulence factors?
ETEC are characterized by the ability to produce two types of virulence factors; adhesins that promote binding to specific enterocyte receptors for intestinal colonization and enterotoxins responsible for fluid secretion. The best characterized adhesins are expressed in the context of fimbriae, such as F4, F5, F6, and F18. Once established in the pig’s small intestine, ETEC produces enterotoxins that lead to diarrhea. The enterotoxins belong to two major classes: heat-labile toxin (LT), and heat-stable toxins, that are small polypeptides named STa and STb.
VTEC are characterized by the ability to produce the cytotoxin VT2e (verotoxin). When VT2e enters the bloodstream, it damages vessel walls resulting in edema in targeted tissues. VTEC strains often possess the fimbria variant F18ab or F18ac. But pathogenic ED strains without F18 are seen in Denmark as well. Moreover, some VTEC strains have the ability to produce STa, STb and LT. So, we can see VTEC or ED strains with or without F18, Sta, STb, LT but always with verotoxin.
Let us dig deeper into edema disease. As you have described for us, the etiology is VTEC E. coli strains with or without F18, Sta, STb and LT but always with verotoxin 2e. Based on this, I have three questions: 1.What is the pathology? 2.how does the disease look in pigs? AND 3. which is the productive cost of the disease?
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