According to Cox, 11% of all the deaths in post-weaning are due to diarrhea. It causes the death of +/-10 million piglets every year across the world. Around half of the diarrheas are due to E. coli. And no one knows for sure how much oedema provoked by E. coli costs pig producers. In newborn piglets, severe watery diarrhea can be caused by enterotoxigenic E. coli, ETEC, producing F4 (K88), F5 (K00), F41 or F6 (P987) fibriae (colonization factor). Colibacillose in weaned piglets is the result of infection with F4+ or F18+ ETEC or F18+ verotoxigenic E. coli (VTEC). Beside fibriae, ETEC produce thermolabile (LT), thermostable a (STa) and/or b (STb) enterotoxins which induce the secretory diarrhea resulting in weight loss, growth retardation and mortality, whereas sVTEC produce the Shiga toxin STX2e that binds to globotetraosylceraminde on endothelial cells, resulting in oedema, hemorrhage and micro thrombosis leading to nervous signs and mortality.
Newborn animals can be protected via the milk by vaccination of the sow against neonatal colibacillosis. This lactogenic immunity ceases at weaning, making weaned piglets highly susceptible again for enteropathogens. Weaned piglets lack or weakly express receptors on their enterocytes for F5, F6 and F41 fimbriae, but not for F4. The latter are highly expressed in the jejunum of newly weaned piglets making them highly sensible to F4+ ETEC infections. Three serological variants of F4 had been identified.
Piglets can have receptors on their enterocytes for adhesion of one or more of these variants, but receptor expressions can also be completely absent, resulting in resistance against infection. One of those variant (F4ac) is highly immunogenic fimbria that, upon oral administration, results in a specific intestinal IgA response and a protective mucosal immunity against an infection with a virulent F4ac+ETEC strain. Regarding the F18 strains, Cox and his colleagues had investigated the genetic population around the world and had been able to prove that 96% of all the strains have the same adhesion (FedF) and the same receptors on the villous enterocytes, which give a good basis to develop a worldwide management of the disease it provokes. Scientists had identified very recently these receptors as blood group O/A sugars. This identification is very important as it opens a door to fight against the adhesion on the mucosal sites and differ from strain to strain. If the F18 are glycolipides, the F4 receptors had been identified as glycoproteins.
Receptor for F18 fimbriae are absent in newborn piglets and gradually appear at the age of one week, resulting in sufficient receptors in three-week-old piglets for colonization with the F18+ ETEC and/or VTEC strains. Piglets without stress sensitivity gen (FUT1gen) are also without those receptors, a fact that militate to a genetic investigation to decrease diarrhea sensitivity in piglets.
F18 fimbriae are not very immunogenic. Oral administration of those strains does not result in immune response. Prevention of post weaning colibacillosis is difficult and should be based on prevention of predisposing factors, high hygiene and stimulation of the immune system (for F4 challenges). Although oral vaccines are on the market in the U.S. and Canada, there is doubt on their efficacy, and there is a need for developing vaccines, which can be applied during the suckling period.
Other differences had been lightened between F4 and F18 infection; the excretion of coli is quite different. F4 is excreted very soon after infection and thus is easiest to treat on the farm.