Edema disease in pigs

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The edema disease or colienterotoxemia is a worldwide widespread and lossy infectious disease of pigs that is associated with the formation of edema. The disease is caused by shiga toxin, which is produced by a specific virotype of Escherichia coli called STEC. The Shigatoxin (Stx2e) and F18ab fimbriae act as virulence factors . O-serotypes 138, 139, 141, 147 and 157, which are mostly haemolytic , can often be detected during serotyping .

Etiology and pathogenesis

Colon cone of a diseased animal

The risk factors that are suspected of promoting an outbreak of the disease include the process of weaning from the mother sow and further feed changes in the course of rearing and fattening. Abrupt feed changes and phases of hunger with subsequent increased feed consumption are to be assessed critically. Changes in the intestine in terms of villus length and crypt depth as well as the composition of the microflora , the enzyme pattern and the formation of receptors play an important role, especially when weaning . The E. coli attach themselves to receptors in the mucous membrane of the small intestine with the help of fimbrial antigens (F18ab). They produce the Shiga toxin , which is absorbed into the bloodstream and damages the walls of the capillaries, causing fluid to escape from the vascular system into the surrounding tissue. This leads to edema in many parts of the body (bridge of the nose, forehead, eyelids, larynx, colon cone, gallbladder bed, brain). Depending on where they are located, nerves can be damaged because they are under oxygen deficiency . Shock states can also occur due to endotoxins from decomposing bacteria .

clinic

The disease usually occurs 2 to 3 weeks after weaning, but also at the end of rearing and in early and medium fattening. In some animals, edema can be seen in the head area, eyelids and bridge of the nose. Depending on the localization of the edema, the clinical signs are accompanied by sudden deaths, unspecific general disorders, central nervous symptoms ( uncoordinated movements , paralysis ), jitteriness, muscle twitching and hoarse, high-pitched screaming. Pulmonary edema causes shortness of breath . The animals do not have a fever . Diarrhea occurs in cases in which either STEC not only form Shiga toxin but also enterotoxins or when STEC and ETEC (enterotoxic Eschericha coli ) are present at the same time in a herd  .

diagnosis

Edema on the eyelids

A suspected diagnosis is made based on the clinic: Sudden deaths, edema in the head area and central nervous symptoms. The pathogens can be cultivated from fecal samples or intestinal swabs, then the virulence factors can be detected using the polymerase chain reaction and the virotype can be determined. The detection of virulence factors directly from the faeces or intestinal mucosa using qPCR (Real Time Quantitative PCR) delivers faster results, since the bacterial culture is no longer necessary, but makes the determination of the virotype more difficult. Pathology and histopathology can provide valuable information for establishing the diagnosis and differential diagnosis (e.g. streptococcus suis meningitis).

Therapy and prophylaxis

Previously, a combined therapy was attempted by adjusting the diet (lower in crude protein, richer in crude fiber, lower in energy and enriched with acid) and the administration of antibiotics and / or zinc oxide. The adjustment of the feed causes a reduction in the growth of the animals. Prophylaxis with antibiotics is already banned in many countries and therapy after an outbreak of disease is usually too late. In addition, in some cases there is already resistance. The use of zinc oxide is viewed critically as it is a heavy metal that enters the environment in this way. As a preventive measure, it is recommended that the piglets get used to solid feed and optimal weaning conditions (stress-free, optimal stall climate, sufficient fresh water, animal-feeding place ratio of 1: 1) before weaning. Commercial vaccines containing a genetically modified shiga toxin have been available for several years. Piglets can be vaccinated as early as the first week of life and develop serum-neutralizing antibodies against the (field) Shiga toxin. The effectiveness and tolerability have been confirmed in the field over the past few years. There are breeding sows and boar lines that are naturally resistant due to the lack of F18 receptors in the small intestine. If this is inherited homozygously, the offspring also show this characteristic.

literature

  • Medical microbiology, infection and epidemic theory by Rolle / Mayr, Enke Verlag, Stuttgart 2007
  • Diagnostics and health management in the pig population, Volume 1 by Elisabeth Große Beilage and Michael Wendt, Verlag Eugen Ulmer Stuttgart, 2013
  • http://www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/veterinary/medicines/002588/vet_med_000270.jsp&mid=WC0b01ac058008d7a8
  • http://www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/veterinary/medicines/004364/vet_med_000356.jsp&mid=WC0b01ac058008d7a8
  • https://porcinehealthmanagement.biomedcentral.com/articles/10.1186/2055-5660-1-6
  • http://www.ema.europa.eu/docs/de_DE/document_library/Referrals_document/Zinc_oxide_35/WC500233296.pdf