Oral administration of Lactobacillus plantarum Lq80 and Megasphaera elsdenii iNP‐001 induces efficient recovery from mucosal atrophy in the small and the large intestines of weaning piglets

Weaning causes atrophy of intestinal mucosa and a drop of IgA protection in piglets which increases vulnerability to pathogenic infections. Probiotic lactobacilli may support recovery from such weaning stresses. Butyrate‐produce bacteria may support the growth of colonic mucosa. Megasphaera elsdenii, a lactate‐utilizing butyrate producer, may help butyrate production particularly when combined with lactobacilli. Weaned piglets (Experiment 1: 20 days old, Experiment 2: 28 days old) were orally dosed once a day with either (L) 10¹⁰ (cell/dose) L. plantarum Lq80, or (LM) 10¹⁰ (cell/dose) Lq80 with 10⁹ (cell/dose) M. elsdenii iNP‐001. Lq80 was contained in capsules resistant to gastric digestion. M. elsdenii was contained in capsules resistant to gastric and intestinal digestion. An untreated control (C) was also prepared. After 2 weeks of administration, L. plantarum enhanced the recovery from the villous atrophy in both experiments. The rectal and colonic IgA tended to be higher in L and LM than in C in Experiment 1. Colonic butyrate was higher in LM than in the others in Experiment 1. The thickness of the colonic mucosa was greater in LM than in the others in Experiment 1. In early weaned piglets, the effects of L. plantarum and M. elsdenii were clear.     

In vitro inhibition of ETEC K88 adhesion by pea hulls and of LT enterotoxin binding by faba bean hulls

Enterotoxigenic Escherichia coli (ETEC) expressing K88 (F4) adhesins are associated with post‐weaning diarrhoea in piglets. Different grain fractions from pea (Pisum sativum) and faba bean (Vicia faba) were tested in vitro for their capacity to counteract aetiological factors, which contribute to the development of diarrhoea. In detail, adhesion of E. coli O149:K91:K88ac (ETEC K88ac) to grain legume products, intended to impair the colonization of the host, was studied as well as interference with receptor binding of the pathogen’s heat‐labile enterotoxin LT, intended to reduce toxin‐inflicted gut cell damage. When comparing different pea and faba bean products tested for their binding capacity of ETEC K88ac, especially pea hulls, but also whole pea meal, starch‐enriched and protein‐enriched pea meal, and digestion‐resistant pea hull and meal fractions showed a higher binding of ETEC K88ac than faba bean products. In contrast to the ETEC K88ac adhesion results, bean hulls proved more effective than pea hulls in preventing GM1 receptor binding of LT. Previous small intestinal segment perfusion experiments we performed with ETEC K88ac‐challenged piglets indicated that both pea and bean hulls have the potential for successful application in diarrhoea prophylaxis and treatment, which is in agreement with and refined by our detection of their different modes of functioning.     

Genetic variation at the alpha‐1‐fucosyltransferase (FUT1) gene in Asian wild boar and Chinese and Western commercial pig breeds

Escherichia coli F18 bacteria producing enterotoxins and/or shigatoxin (ETEC/STEC) are main pathogens that cause oedema disease and postweaning diarrhoea in piglets, and alpha‐1‐fucosyltransferase (FUT1) gene has been identified as a candidate gene for controlling the expression of ETEC F18 receptor. The genetic variations at nucleotide position 307 in open reading frame of FUT1 gene in one wild boar breed and 20 western commercial and Chinese native pig breeds were investigated by polymerase chain reaction–restriction fragment length polymorphism. The results showed that the genetic polymorphisms of the FUT1 locus were only detected in western pig breeds and the Chinese Taihu (including Meishan pig, Fengjing pig and Erhualian pig), Huai and Lingao pig breeds; only Duroc and Pietrain possessed the resistant AA genotype, while the wild boar and other Chinese pig breeds only presented the susceptible genotype GG. The results indicated that Chinese native pig breeds lack genetic factors providing resistance to ETEC F18 bacteria. The resistant allele to ETEC F18 might originate from European wild boar. It was inferred that oedema and postweaning diarrhoea caused by ETEC F18 have close relationship with the growth rate, which can explain why on the contrary Chinese native pig breeds have stronger resistance to oedema and postweaning diarrhoea in piglets compared with western pig breeds.     

Effects of Lactobacillus plantarum on the intestinal morphology,intestinal barrier function and microbiota composition of suckling piglets

This study investigated the effect of Lactobacillus plantarum strain 299v on gut health in suckling piglets. Sixty newborn piglets were assigned to control and probiotic treatments, with three litters per treatment (ten piglets/litter). From days 1 to 20 of life, piglets were orally administered a placebo of 0.1% peptone or 1.0 ×  10¹⁰ CFU L. plantarum 299v daily. Six piglets per treatment were sacrificed on day 20, and intestinal tissues (including duodenum, jejunum, ileum and colon) and the intestinal contents from colon segments were collected. The results demonstrated that piglets treated with L. plantarum 299v had a lower diarrhoea incidence than the controls. L. plantarum 299v administration significantly increased the ratio of the villus height to the crypt depth in the jejunum and ileum, as well as the mRNA expression of jejunal occludin and ileal zonula occludens 1 (ZO‐1). The L. plantarum treatment also increased the mRNA abundance of porcine β‐defensin 2 (pBD2) and pBD3 in the jejunum and ileum and of toll‐like receptors (TLRs), such as TLR2, TLR4, TLR6 and TLR9 in the ileum, and significantly upregulated the mRNA abundances of ileal pBD1 and colonic TLR4. Additionally, the L. plantarum 299v treatment significantly changed the structure of the colonic microbiota, as evidenced by the obvious increases in the relative abundances of the phyla Firmicutes and Actinobacteria and of the genus Lactobacillus. Our findings indicate that L. plantarum 299v facilitates the gut health of suckling piglets, probably by improving the intestinal morphology and intestinal barrier function and by modifying the structure of the gut microbiota.     

Isolation of Escherichia coli from piglets in South Korea with diarrhea and characteristics of the virulence genes

Escherichia coli was isolated from the feces of 122 piglets with diarrhea on 55 farms in Korea. The virulence genes of each isolate were characterized by polymerase chain reaction (PCR). Of the 562 isolates, 191 carried 1 or more of the virulence genes tested for in this study. Of the 191 isolates, 114 (60%) carried 1 or more of the genes for enterotoxigenic E. coli (ETEC) fimbriae F4, F5, F6, F18, and F41 and ETEC toxins LT, STa, and STb, 57 (30%) carried 1 or more of the genes for the Shiga-toxin-producing E. coli (STEC) toxins Stx1, Stx2, and Stx2e, and 21% and 37% carried the gene for enteropathogenic E. coli intimin and for enteroaggregative E. coli toxin, respectively. Collectively, our results indicate that other pathotypes of E. coli as well as ETEC can be strongly associated with diarrhea in piglets. In addition, detection of the genes for Stx1 and Stx2 indicates that pigs are reservoirs of human pathogenic STEC.     

The preventive effect of Bacillus subtilus strain DB9011 against experimental infection with enterotoxcemic Escherichia coli in weaning piglets

Porcine edema disease (ED) is caused by Shiga toxin 2e‐producing Escherichia coli (STEC). Post‐weaned piglets often suffer from ED as a result of intestinal infection with STEC, which causes impaired growth performance and high mortality. Antimicrobial therapy is a curative treatment for piglets infected with STEC, but the emergence of antimicrobial‐resistant STEC has become a serious problem for Japanese pig farmers. Therefore, an alternative strategy other than antimicrobial therapy is needed for the prevention or treatment of ED. In this study, we evaluated the effect of oral administration of Bacillus subtilis DB9011 (DB9011) to prevent the experimental infection of STEC in weaning piglets. Eight 21‐day‐old piglets were divided into two groups: STEC challenge with the basal diet, and STEC challenge with DB9011 supplemented diet. The challenge was carried out when the animals were 25, 26 and 27 days old using STEC contained in capsules resistant against gastric digestion. All pigs were euthanized at 36 days of age. DB9011 improved the symptoms of ED and decreased the number of STEC in the ileal digesta and feces. Accordingly, oral administration of DB9011 in weaned piglets prevents ED through the suppression of the growth of STEC in the ileum.     

Host genotype and amoxicillin administration affect the incidence of diarrhoea and faecal microbiota of weaned piglets during a natural multiresistant ETEC infection

Enterotoxigenic Escherichia coli (ETEC) is the aetiological agent of postweaning diarrhoea (PWD) in piglets. The SNPs located on the Mucine 4 (MUC4) and Fucosyltransferase 1 (FUT1) genes have been associated with the susceptibility to ETEC F4 and ETEC F18, respectively. The interplay between the MUC4 and FUT1 genotypes to ETEC infection and the use of amoxicillin in modifying the intestinal microbiota during a natural infection by multiresistant ETEC strains have never been investigated. The aim of this study was to evaluate the effects of the MUC4 and FUT1 genotypes and the administration of amoxicillin through different routes on the presence of diarrhoea and the faecal microbiota composition in piglets naturally infected with ETEC. Seventy-one piglets were divided into three groups: two groups differing by amoxicillin administration routes—parenteral (P) or oral (O) and a control group without antibiotics (C). Faecal scores, body weight, presence of ETEC F4 and F18 were investigated 4 days after the arrival in the facility (T0), at the end of the amoxicillin administration (T1) and after the withdrawal period (T2). The faecal bacteria composition was assessed by sequencing the 16S rRNA gene. We described that MUC4 and FUT1 genotypes were associated with the presence of ETEC F4 and ETEC F18. The faecal microbiota was influenced by the MUC4 genotypes at T0. We found the oral administration to be associated with the presence of diarrhoea at T1 and T2. Furthermore, the exposure to amoxicillin resulted in significant alterations of the faecal microbiota. Overall, MUC4 and FUT1 were confirmed as genetic markers for the susceptibility to ETEC infections in pigs. Moreover, our data highlight that group amoxicillin treatment may produce adverse outcomes on pig health in course of multiresistant ETEC infection. Therefore, alternative control measures able to maintain a healthy faecal microbiota in weaners are recommended.     

Effects of dietary supplementation of lipid‐encapsulated zinc oxide on colibacillosis,growth and intestinal morphology in weaned piglets challenged with enterotoxigenic Escherichia coli

This study was aimed to evaluate the effect of dietary supplementation of lipid‐encapsulated (coated) zinc oxide ZnO on post‐weaning diarrhea (colibacillosis) in weaned piglets challenged with enterotoxigenic Escherichia coli (ETEC). Thirty‐two 35‐day‐old weaned piglets were orally challenged with 3 × 10¹⁰ colony forming units of ETEC K88 while eight piglets received no challenge (control). Each eight challenged piglets received a diet containing 100 ppm ZnO (low ZnO), 2500 ppm ZnO (high ZnO) or 100 ppm of lipid (10%)‐coated ZnO (coated ZnO) for 7 days; control pigs received the low ZnO diet. Daily gain, goblet cell density in the villi of the duodenum, jejunum and ileum, and villus height in the jejunum and ileum, which decreased due to the challenge, were equally greater in the coated ZnO and high ZnO groups versus low ZnO group. Fecal consistency score, serum interleukin‐8 concentration, subjective score of fecal E. coli shedding, and digesta pH in the stomach, jejunum and ileum, which increased due to the challenge, were equally low in the coated ZnO and high ZnO groups versus low ZnO. Results suggest that a low level of coated ZnO might well substitute for a pharmacological level of native ZnO in dietary supplementation to alleviate colibacillosis of weaned piglets.     

Synbiotics suppress the release of lactate dehydrogenase,promote non‐specific immunity and integrity of jejunum mucosa in piglets

The aim of our experiment was to study how synbiotics are able to deal with the problems of post‐weaning piglets. Lactobacillus plantarum – Biocenol^TM LP96 (CCM 7512), Lactobacillus fermentum – Biocenol^TM LF99 (CCM 7514) and flaxseed (rich in n‐3 polyunsaturated fatty acids) were administered to 36 conventional piglets from a problematic breed with confirmed presence of enterotoxigenic Escherichia coli and Coronavirus. The experimental piglets were supplied with probiotic cheeses and crushed flax‐seed in the period starting 10 days before weaning and lasting up to 14 days post‐weaning. Piglets in the control group were supplied only control cheese. The impact of such additives on the release of lactate dehydrogenase (LDH; spectroscopic and electrophoretic assay), alteration of immunity (index of metabolic activity), jejunum histology (light microscopy), and health of conventional piglets from a problematic breed (monitoring of hematology, consistency and moisture of feces and body temperature) were examined. We found significant decrease in LDH leakage in the blood serum and tissue extracts, indicating better cell membrane integrity in the individual organs of animals. Probiotics and flaxseed applied together seem to be a good source of nutrients to improve the immune status and the integrity of jejunum mucosa during infection. © 2015 Japanese Society of Animal Science     

Early supplementation with Lactobacillus plantarum in liquid diet modulates intestinal innate immunity through toll-like receptor 4-mediated mitogen-activated protein kinase signaling pathways in young piglets challenged with Escherichia coli K88

This study was conducted to investigate the effects of early supplementation during 4 to 18 d of age with Lactobacillus plantarum (LP) in liquid diets on intestinal innate immune response in young piglets infected with enterotoxigenic Escherichia coli (ETEC) K88. Seventy-two barrow piglets at 4 d old were assigned to basal or LP-supplemented liquid diet (5 × 10¹⁰ CFU·kg⁻¹). On day 15, piglets from each group were orally challenged with either ETEC K88 (1 × 10⁸ CFU·kg⁻¹) or the same amount of phosphate-buffered saline. The intestinal mucosa, mesenteric lymph node (MLN), and spleen samples were collected on day 18. Here, we found that LP pretreatment significantly decreased the mRNA relative expression of inflammatory cytokines (interleukin [IL]-1β, IL-8, and tumor necrosis factor-α), porcine β-defensin 2 (pBD-2), and mucins (MUC1 and MUC4) in the jejunal mucosa in piglets challenged with ETEC K88 (P < 0.05). Moreover, LP significantly decreased the ileal mucosa mRNA relative expression of IL-8 and MUC4 in young piglets challenged with ETEC K88 (P < 0.05). Furthermore, the piglets of the LP + ETEC K88 group had lower protein levels of IL-8, secretory immunoglobulin A, pBD-2, and MUC4 in the jejunal mucosa than those challenged with ETEC K88 (P < 0.05). Besides, LP supplementation reduced the percentage of gamma/delta T cells receptor (γδTCR) and CD172a⁺ (SWC3⁺) cells in MLN and the percentage of γδTCR cells in the spleen of young piglets after the ETEC K88 challenge. Supplementation with LP in liquid diets prevented the upregulated protein abundance of toll-like receptor (TLR) 4, phosphorylation-p38, and phosphorylation-extracellular signal-regulated protein kinases in the jejunal mucosa induced by ETEC K88 (P < 0.05). In conclusion, LP supplementation in liquid diet possesses anti-inflammatory activity and modulates the intestinal innate immunity during the early life of young piglets challenged with ETEC K88, which might be attributed to the suppression of TLR4-mediated mitogen-activated protein kinase signaling pathways. Early supplementation with LP in liquid diets regulates the innate immune response, representing a promising immunoregulation strategy for maintaining intestinal health in weaned piglets.     

Plasma metabolomic profiles and immune responses of piglets after weaning and challenge with E. coli

Background

The processes of weaning and exposure to pathogenic bacteria induce stress responses, which may alter the metabolism. In this study, we investigated the changes in plasma metabolites and immune responses in piglets in response to the stress induced by weaning and Escherichia coli challenge.

Results

Fecal dry matter decreased (P = 0.003) and nearly half (44.4%) the piglets developed diarrhea on day 2 and 3 postweaning. The concentration of plasma immunoglobulin A was higher (P < 0.001) on day 11 postweaning than on day 0 or 4 postweaning. The levels of white blood cells increased continuously (P < 0.001) from day 0 to day 11 postweaning. Differences in the percentages of neutrophils (P = 0.029) and lymphocytes (P = 0.022) were seen, but the neutrophil/lymphocyte ratio did not differ in the period after weaning. A clear separation of the metabolomic profile data for day 0 and day 4 postweaning was observed with a principal components analysis (PCA) scores plot, and the data for day 11 were located between those for day 0 and day 4 postweaning. The plasma levels of proline, taurine, and carnitine were higher, whereas those of betaine, creatine, L-arginine and acetylcarnitine were lower on day 4 postweaning than on day 0. Levels of lysophosphatidylcholine and phosphatidylcholine were either higher or lower after weaning, depending on the chain lengths or characters of these metabolites.

Conclusions

Our results show a clear separation in the plasma metabolomic profiles of piglets that corresponded to the fecal responses to stress on the piglets induced by weaning or exposure to a pathogen (E. coli). These plasma metabolite profiles suggest that the challenges induced proinflammatory responses in the piglets, resulting in postweaning diarrhea, which was associated with higher concentrations of IgA in the plasma.     

Effects of the Administration of Lactobacilli,Maltodextrins and Fructooligosaccharides upon the Adhesion of <Emphasis Type="Italic">E. coli</Emphasis> O8:K88 to the Intestinal Mucosa and Organic Acid Levels in the Gut Contents of Piglets

The influence of the administration of Lactobacillus plantarum, maltodextrin Maldex 150 and Raftifeed IPX fructooligosaccharides on the inhibition of adhesion of E. coli O8:K88 to the mucosa of the jejunum, ileum and colon as well as on the organic acid levels was investigated in 33 conventional piglets. The counts of E. coli K88 adhering to the jejunal mucosa were significantly decreased (p < 0.05) in Lact. plantarum + Maldex 150 and Lact. plantarum + Maldex 150 + Raftifeed IPX groups. The counts of E. coli K88 adhering to the colonic mucosa of Lact. plantarum + Maldex 150 + Raftifeed IPX and Lact. plantarum + Raftifeed IPX groups were significantly lower (p < 0.05) than in Lact. plantarum and Lact. plantarum + Maldex 150 animals. The acetic acid levels in the ileum and colon of the Lact. plantarum + Maldex 150 + Raftifeed IPX group and Lact. plantarum + Raftifeed IPX group were significantly higher (p < 0.05) than in the Lact. plantarum and Lact. plantarum + Maldex 150 group. The combination of Lact. plantarum, maltodextrin Maldex 150 and Raftifeed IPX proved to be the most effective one to inhibit the counts of E. coli O8:K88 adhering to the intestinal mucosa of the jejunum and colon of conventional piglets.     

An investigation into the association between cpb2-encoding Clostridium perfringens type A and diarrhea in neonatal piglets

To investigate the possible role of cpb2-positive type A Clostridium perfringens in neonatal diarrheal illness in pigs, the jejunum and colon of matched normal and diarrheic piglets from 10 farms with a history of neonatal diarrhea were examined grossly and by histopathology, and tested for C. perfringens, for C. perfringens beta2 (CPB2) toxin, as well as for Clostridium difficile toxins, Salmonella, enterotoxigenic Escherichia coli, rotavirus, transmissible gastroenteritis (TGE) virus, and coccidia. Clostridium perfringens isolates were tested using a multiplex real-time polymerase chain reaction (PCR) to determine the presence of cpa, consensus and atypical cpb2, and other virulence-associated genes. The numbers of C. perfringens in the intestinal contents were lower in diarrheic piglets (log₁₀ 5.4 CFU/g) compared with normal piglets (log₁₀ 6.5 CFU/g) (P < 0.05). The consensus cpb2 was present in 93% of isolates in each group, but atypical cpb2 was less common (56% healthy, 32% diarrheic piglets isolates, respectively, P < 0.05). The presence of CPB2 toxin in the intestinal contents of normal and diarrheic piglets did not differ significantly. Clostridium difficile toxins and rotavirus were each detected in 7 of the 21 (33%) diarrheic piglets. Rotavirus, C. difficile toxins, Salmonella, or enterotoxigenic E. coli were concurrently recovered in different combinations in 4 diarrheic piglets. The cause of diarrhea in 8 of the 21 (38%) piglets on 6 farms remained unknown. The etiological diagnosis of diarrhea could not be determined in any of the piglets on 2 of the farms. This study demonstrated that the number of cpb2-positive type A C. perfringens in the intestinal contents was not a useful approach for making a diagnosis of type A C. perfringens enteritis in piglets. Further work is required to confirm whether cpb2-carrying type A C. perfringens have a pathogenic role in enteric infection in neonatal swine.     

Several enteropathogens are circulating in suckling and newly weaned piglets suffering from diarrhea in the province of Villa Clara, Cuba

Intestinal contents of suckling (n?=?45) and newly weaned (n?=?45) piglets, suffering from diarrhea in the province of Villa Clara in Cuba, were tested for viral, bacterial, and parasitic enteropathogens from May to June 2008. At least one enteropathogen was identified in 53.3 % of piglets and enterotoxigenic Escherichia coli (ETEC; 25.6 %) was the major pathogen; mostly STa⁺/STb⁺ or F4⁺/STa⁺/STb⁺ ETEC were isolated. The overall occurrence of the rest of pathogens was 10 % for transmissible gastroenteritis virus (TGEV) and Cryptosporidium parvum, 6.7 % for rotavirus A and Isospora suis, 5.6 % for α-toxigenic Clostridium perfringens, 3.3 % for verotoxigenic E. coli (VTEC), and 2.2 % for Salmonella enterica subspecies enterica serovar Newport. TGEV and α-toxigenic C. perfringens were only identified in suckling piglets, while Salmonella Newport and VTEC were only detected in weaned pigs. Porcine epidemic diarrhea virus (PEDV), β-toxigenic C. perfringens, Eimeria spp., and helminths were not identified. Eight kinds of mixed infections were detected in 25 % of enteropathogen positive piglets. ETEC was present in 10 of 12 mixed infections, and TGEV infections were never combined. This survey demonstrates that several enteropathogens are circulating in piggeries located in the province of Villa Clara in Cuba, and that is necessary to improve surveillance, prevention, and control of enteric infections in order to increase production efficiency.     

Expression of Putative Escherichia coli Heat-labile Enterotoxin (LT) Receptors on Intestinal Brush Borders from Pigs of Different Ages

Many strains of enterotoxigenic Escherichia coli (ETEC) that cause diarrhoea in young piglets secrete a heat-labile enterotoxin (LTp) that binds to specific glycoconjugates on porcine intestinal epithelial cells. Binding of LTp to an appropriate glycoconjugate facilitates the uptake and trafficking of the toxin into the cell, where it stimulates intracellular changes that promote fluid secretion and diarrhoea. The objective of the current study was to identify the LTp-binding glycoconjugates on porcine intestinal epithelial cells, the natural target cells for LTp. We found that LTp binds, in an age-correlated manner, to an acidic glycosphingolipid (GSL) that co-migrated with GM1 on thin-layer chromatography (TLC), a small acidic GSL that appears to be a sulphatide, a neutral GSL that co-migrated with neolactotetraglycosylceramide (nLc4) on TLC, and two glycoproteins (36 and 205 kDa). Of these potential LTp receptors, the GM1-co-migrating GSL was detected most intensely in young animals, while the other four LTp-binding glycoconjugates were detected most intensely in older pigs (54 weeks). Since ETEC primarily cause disease in young piglets, the GM1-co-migrating GSL is the most likely candidate for a functional LTp receptor.     

Significance of β2‐Toxigenic Clostridium perfringens Infections in Animals and Their Predisposing Factors – A Review

The novel β2‐toxin of Clostridium perfringens has recently been described as the cause of enteric diseases in animals. The biological activity of β2‐toxin is similar to that of the β1‐toxin with a possibly weaker cytotoxic activity. However, the production of β2‐toxin in vitro is not seen in all β2‐toxin‐gene (cpb2)‐positive C. perfringens strains, and to deduce a clinical importance solely from the detection of cpb2 is difficult. Detection of cpb2‐positive C. perfringens from various animal species with and without enteric diseases demonstrates the wide distribution of cpb2 in nature, and the presence of cpb2 gene is therefore not considered a risk by itself. Predisposing factors like low trypsin activity in the intestinal tract, antibiotic and/or antiphlogistic treatment or changes in diet can result in the selection of β2‐toxigenic C. perfringens which may lead to enteritis or enterotoxaemia.     

Clostridium perfringens epsilon toxin inhibits the gastrointestinal transit in mice

Epsilon toxin produced by Clostridium perfringens type B and D is a potent toxin that is responsible for a highly fatal enterotoxemia in sheep and goats. In vitro, epsilon toxin produces contraction of the rat ileum as the result of an indirect action, presumably mediated through the autonomic nervous system. To examine the impact of epsilon toxin in the intestinal transit, gastric emptying (GE) and gastrointestinal transit (GIT) were evaluated after intravenous and oral administration of epsilon toxin in mice. Orally administered epsilon toxin produced a delay on the GIT. Inhibition of the small intestinal transit was observed as early as 1 h after the toxin was administered orally but the effects were not observed after 1 week. Epsilon toxin also produced an inhibition in GE and a delay on the GIT when relatively high toxin concentrations were given intravenously. These results indicate that epsilon toxin administered orally or intravenously to mice transitorily inhibits the GIT. The delay in the GIT induced by epsilon toxin could be relevant in the pathogenesis of C. perfringens type B and D enterotoxemia.     

Prevalence of enterotoxigenic <Emphasis Type="Italic">Escherichia coli</Emphasis> virulence genes from scouring piglets in Zimbabwe

World-wide, enterotoxigenic Escherichia coli (ETEC) and verotoxigenic E. coli (VTEC)-induced diarrhea are economically important for porcine producers. Our aim was to investigate the prevalence of toxin and fimbrial genes among E. coli isolated from diarrheic piglets from randomly selected piggeries in Zimbabwe.We used multiplex PCR for screening STa, STb, LT, and Stx-2e toxins. Subsequently F4, F5, F6, F18 and F41 fimbriae genes were screened in toxin positive isolates. Toxin positive strains lacking tested fimbriae genes were characterized using transmission electron microscopy, agglutination and agglutination inhibition tests. Approximately 32% of the 1,984 isolates tested positive for STa, STb, LT or Stx-2e genes. Of these, approximately 81% had F4, F5, F6, F18 or F41 fimbriae genes. The remaining toxin positive strains lacked tested fimbriae genes and appeared to either express F1-like fimbriae, or lacked fimbriae. The data constitute an important framework for implementation of prevention measures, such as using relevant fimbriae-based vaccines against ETEC induced diarrhea or VTEC-induced edema.     

The effect of supplementation of flax-seed oil on interaction of Lactobacillus plantarum--Biocenol™ LP96 and Escherichia coli O8:K88ab:H9 in the gut of germ-free piglets

We investigated the influence of administration of flax-seed oil on interaction of Lactobacillus plantarum – Biocenol? LP96 and Escherichia coli O8:K88ab:H9 in the gut of germ-free piglets. When compared to animals supplemented with L. plantarum, the counts of lactobacilli in the jejunal and ileal mucosa and in the intestinal content were significantly higher in LMK group (p < 0.0001). Inter-groups comparison of the counts of E. coli K88 adhering to the jejunal and ileal mucosa revealed a significantly decrease in LMK animals (p < 0.001; p < 0.05).     

Effect of added dietary threonine on growth performance,health, immunity and gastrointestinal function of weaning pigs with differing genetic susceptibility to Escherichia coli infection and challenged with E. coli K88ac

Threonine (Thr) is important for mucin and immunoglobulin production. We studied the effect of added dietary Thr on growth performance, health, immunity and gastrointestinal function of weaning pigs with differing genetic susceptibility to E. coli K88ac (ETEC) infection and challenged with ETEC. Forty‐eight 24‐day‐old weaned pigs were divided into two groups by their ETEC susceptibility using mucin 4 (MUC4) gene as a marker (2 MUC4^?/?, not‐susceptible, and 2 MUC4^+/+, susceptible, pigs per litter). Within genotype, pigs were fed two different diets: 8.5 (LThr) or 9.0 (HThr) g Thr/kg. Pigs were orally challenged on day 7 after weaning and slaughtered on day 12 or 13 after weaning. Before ETEC challenge, HThr pigs ate more (p < 0.05). The diet did not affect post‐challenge growth, but HThr tended to increase post‐challenge feed efficiency (p = 0.087) and overall growth (p = 0.087) and feed efficiency (p = 0.055). Before challenge, HThr pigs excreted less E. coli (p < 0.05), while after challenge, diet did not affect the number of days with diarrhoea and ETEC excretion. MUC4^+/+ pigs responded to the challenge with more diarrhoea, ETEC excretion and anti‐K88 IgA in blood and jejunal secretion (p < 0.001). HThr pigs had a higher increase of anti‐K88 IgA values in jejunal secretion (p = 0.089) and in blood (p = 0.089, in MUC4^+/+ pigs only). Thr did not affect total IgA and IgM values, morphometry of jejunum, goblet cells count in colon, total mucin from jejunum and colon, but varied jejunal goblet cells counts (p < 0.05). In the first two post‐weaning weeks, 8.5 g Thr/kg diet may be not sufficient to optimize initial feed intake, overall feed efficiency and intestinal IgA secretion and to control the gut microbiota in the first post‐weaning week, irrespective of the pig genetic susceptibility to ETEC infection.