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H U Bertschinger

Publications and source records attributed to H U Bertschinger.

At least 19 recordsLinked to original sources
PubMed2005

Inheritance of the F4ab, F4ac and F4ad E. coli receptors in swine and examination of four candidate genes for F4acR.

Susceptibility to enterotoxigenic Escherichia coli with fimbriae F4ac is dominantly inherited in the pig. A three-generation pedigree was created to refine the position of F4acR on chromosome 13 comprising 202 pigs: eight parents, 18 F1 and 176 F2 pigs. The 17-point analysis indicates that F4acR lies between Sw207 and S0283. Recombinant offspring specify that the most probable order is Sw207-S0075-F4acR-Sw225-S0283. We observed six phenotypes for the three fimbrial variants F4ab, F4ac and F4ad. The two missing phenotypes F4abR-/F4acR+/F4adR+ and F4abR-/F4acR+/F4adR- indicate that pigs susceptible to F4ac are always susceptible to F4ab. Furthermore, a weak and a strong adhesion of F4ab and F4ad bacteria was observed. The weak receptor F4abR (F4abRw) was present only in pigs devoid of the receptor F4acR (F4abR+/F4acR-). In contrast, in pigs with the phenotype F4abR+/F4acR+, F4ab bacteria adhered to the majority of enterocytes. F4abRw constitutes a frequently observed phenotype whose inheritance is still unclear. Strong adhesion of F4ab and F4ac bacteria is most likely influenced by the same receptor that we name F4bcR. The number of F4ad bacteria that adhered to enterocytes was very variable in the adhesion test. Moreover, expression of F4adR was independent of age. Our segregation analyses indicated a dominant inheritance of F4adR, although the number of susceptible pigs was smaller than expected. We examined four genes as candidates for the F4acR locus: the transferrin receptor gene (TFRC) and three genes members of the glucosyl/galactosyltransferase family (B3GnT5, B3GALT3 and B4GALT4). Comparison of sequences from resistant and homozygous susceptible F4ac pigs did not reveal any causative single nucleotide polymorphism in the four genes. Two silent mutations at the positions 295 (C/T) and 313 (T/C) in B3GALT3 were found. Using the somatic cell hybrid panel, B3GnT5 and B3GALT3 were assigned to the chromosomal region SSC13q23-q41. No mutations were found in the cDNA sequences of these genes associated with the F4acR genotypes.

Animals↗
PubMed2002

Fine-mapping of the intestinal receptor locus for enterotoxigenic Escherichia coli F4ac on porcine chromosome 13.

The aim of this study was to refine the localization of the receptor locus for fimbriae F4ac. Small intestinal enterocyte preparations from 187 pigs were phenotyped by an in vitro adhesion test using two strains of Escherichia coli representing the variants F4ab and F4ac. The three-generation pedigree comprised eight founders, 18 F1 and 174 F2 animals, for a total of 200 pigs available for the linkage analysis. Results of the adhesion tests on 171 F2 pigs slaughtered at 8 weeks of age show that 23.5% of the pigs were adhesive for F4ab and non-adhesive for F4ac (phenotype F4abR+/F4acR-; R means receptor). Pigs of this phenotype were characterized by a weak adhesion receptor for F4ab. No pigs were found expressing only F4acR and lacking F4abR. Receptors for F4ab and F4ac (F4abR+/F4acR+) were expressed by 54.5% of the pigs. Animals of this phenotype strongly bound both F4ab and F4ac E. coli. In the segregation study, the serum transferrin (TF) gene and 10 microsatellites on chromosome 13 were linked with F4acR (recombination fractions (theta) between 0.00 and 0.11 and lod score values (Z) between 11.4 and 40.4). The 11-point analysis indicates the F4acR locus was located in the interval S0068-Sw1030 close to S0075 and Sw225, with recombination fractions (theta) of 0.05 between F4acR and S0068, 0.04 with Sw1030, and 0.00 with S0075 and Sw225. The lack of pigs displaying the F4abR-/F4acR+ phenotype and the presence of two phenotypes for F4abR (a strong receptor present in phenotype F4abR+/F4acR+ and a weak receptor in phenotype F4abR+/F4acR-) led us to conclude that the receptor for F4ac binds F4ab bacteria as well, and that it is controlled by one gene localized between S0068 and Sw1030 on chromosome 13.

Animals↗
PubMed2000

Microencapsulated enterotoxigenic Escherichia coli and detached fimbriae for peroral vaccination of pigs.

The feasibility of peroral immunisation with microencapsulated Escherichia coli and detached fimbriae to prevent enterotoxigenic E. coli infections in pigs was examined. For this E. coli and fimbriae were microencapsulated into poly(lactide-co-glycolide) microspheres by spray-drying. Various microsphere formulations designed to deliver priming and booster doses were fed to new-born and weaned pigs. The pigs were challenged 19 days after the booster dose by peroral administration of an infective dose of the homologous E. coli. Serum IgA antibody titres and excretion of challenge E. coli, as indicators for colonisation, were determined. The data showed that no significant serum antibodies were induced, and E. coli colonisation was not reduced by the peroral administration of the various antigen-loaded microspheres. These results are in contradiction to some of the previously published experiments typically in rats or rabbits, where model antigens or unpractical immunisation procedures have frequently been used.

Administration, Oral↗
PubMed2000

Structural analysis of F18 fimbriae expressed by porcine toxigenic Escherichia coli.

The F18 fimbriae expressed by porcine toxigenic Escherichia coli strains are 1- to 2-mm-long filaments that mediate the adhesion of the bacteria to enterocytes. The backbone of these fimbriae is built from a major structural 15.1-kDa protein, FedA. The structure of isolated negatively stained F18 fimbriae imaged by dark-field scanning transmission electron microscopy (STEM) was resolved to approximately 2 nm. Analyzing their helical symmetry showed the axially repeating units to alternate in a "zigzag" manner around the helical axis with an axial rise of 2.2 nm. Two repeating units give rise to the observed 4.3-nm helical repeat, which is practically identical to the pitch of the one-start helix formed. Additionally, an axially repeating pattern with a 27-nm spacing was found on rotary-shadowed fimbriae. Mass-per-length determination of unstained F18 fimbriae by STEM revealed the axially repeating unit to have a molecular mass of 25.4 kDa, indicating that it is a FedA monomer, with the difference in mass arising from the minor subunits, FedE and FedF. The presence of the latter two proteins might cause the observed 27-nm axial pattern.

Animals↗
PubMed2000

A DNA polymorphism influencing alpha(1,2)fucosyltransferase activity of the pig FUT1 enzyme determines susceptibility of small intestinal epithelium to Escherichia coli F18 adhesion.

The alpha(1,2)fucosyltransferases (FUT1 and FUT2) contribute to the formation of blood group antigen structures, which are present on cell membranes and in secretions. In the present study we demonstrate that both FUT1 and FUT2 are expressed in the pig small intestine. FUT1 polymorphisms influence adhesion of F18 fimbriated Escherichia coli (ECF18) to intestinal mucosa, and FUT2 is associated with expression of erythrocyte antigen 0. The FUT1 polymorphisms result in amino acid substitutions at positions 103 (Ala-->Thr) and 286 (Arg-->Glu). Tightly controlled expression of the FUT2 gene results in either an abundance or an absence of mRNA in small intestinal mucosa. ECF18-resistant animals were shown to be homozygous for threonine at amino acid 103 of the FUT1 enzyme. Susceptibility to ECF18 adhesion appeared to be solely dependent on the activity of FUT1 in intestinal epithelia. In intestinal mucosae of ECF18-resistant pigs which expressed FUT1 but not FUT2 RNA, the levels of alpha(1,2)fucosyltransferase activity were significantly lower (28- to 45-fold, P<0.001) than in susceptible pigs. Moreover, lysates of CHO cells transfected with FUT1 constructs encoding threonine at amino acid position 103 also showed significantly reduced enzyme activity compared with constructs encoding alanine at this position. Our genetic and enzymatic studies support the hypothesis that the FUT1 enzyme, and particularly the amino acid at position 103, is likely important in the synthesis of a structure that enables adhesion of ECF18 bacteria to small intestinal mucosa.

Animals↗
PubMed2000

Active oral immunization of suckling piglets to prevent colonization after weaning by enterotoxigenic Escherichia coli with fimbriae F18.

Immunoprophylaxis of porcine oedema disease and post-weaning diarrhoea caused by strains of Escherichia coli expressing fimbriae F18 is an unsolved problem. The study was designed to examine whether vaccination with a live F18ac vaccine of unweaned pigs born to sows with F18ac antibody in the colostrum requires preformed fimbriae in the vaccine, and whether protection against the heterologous fimbrial variant F18ab is induced as well. Genetically susceptible pigs were vaccinated orally on three consecutive days, beginning 10 days before weaning with 10(11) CFU of an F18ac culture. Challenge with a dose of 10(7) CFU of E. coli F18 on three consecutive days was initiated 9 or 11 days after weaning. Eighteen pigs given the fimbriated F18ac vaccine and challenged with a strain of the homologous fimbrial variant were protected against colonization; mean faecal viable counts of the challenge strain were >3 log10 lower than those from the 17 non-vaccinated control pigs. The vaccinated pigs developed a significant rise of F18ac IgA serum antibodies. The 23 pigs which had received the non-fimbriated vaccine showed no significant protection and exhibited much lower serum F18ac IgA ELISA reactivities. Eighteen pigs vaccinated with the fimbriated F18ac and challenged with an F18ab strain had faecal viable counts nearly as high as those from 16 non-vaccinated control pigs. It is concluded that only oral vaccines having preformed fimbriae induce protection limited to the homologous fimbrial variant.

Administration, Oral↗
PubMed2000

[Main virulence factors in Escherichia coli isolates from swine over two weeks old with edema disease and/or E. coli diarrhea].

The OK antigens and the fimbriae F4 of E. coli with haemolysis isolated from 113 cases of oedema disease and/or diarrhoea were identified serologically. The genes for F18 and for enterotoxins LT, STIa and STII as well as Shigatoxin Stx2e were determined by PCR. Fimbrial variants F18ab and F18ac were distinguished by means of indirect immunofluorescence on smears prepared from the intestinal mucosa and from cultures grown under appropriate conditions. Adhesive fimbriae were detected with every case or isolate, respectively, by means of at least one out of the techniques mentioned above. The serogroup O149:K91 with fimbriae F4ac (K88ac) and genes for the enterotoxins LT and STII was most prevalent. Serogroup O139:K12 with fimbriae F18ab and the gene for Stx2e was second, whereas serogroups O141ab and O141ac with fimbriae F18ac and genes for Stx2e, STII and often LT were much less prevalent. The serogroup O147:K89 with fimbriae F18ac, and genes for STIa and STII was detected for the first time in Switzerland.

Animals↗
PubMed1997

Biological relationship between F18ab and F18ac fimbriae of enterotoxigenic and verotoxigenic Escherichia coli from weaned pigs with oedema disease or diarrhoea.

Comparative fimbrial expression and adhesion studies were made on enterotoxigenic and verotoxigenic E. coli (ETEC and VTEC) strains isolated from cases of porcine postweaning diarrhoea or oedema disease. F107(F18ab) fimbriae--monitored by polyclonal and monoclonal antibodies and by electron microscopy--were poorly expressed on most VTEC strains. In contrast, 2134P(F18ac) fimbriae were more readily detected on most ETEC strains. The F18ac strains adhered in vivo to ligated intestinal loops in weaned pigs while the F18ab strains did not adhere or adhered weakly. Similarly, the F18ac strains adhered to isolated intestinal brush borders in weaned pigs but the F18ab strains (except for the F107 reference E. coli) did not adhere or adhered weakly in vitro. Neither the F18ab nor F18ac strains adhered to brush borders from newborn pigs. In vitro adhesion of F18ab and F18ac strains was mannose resistant and receptors for F18 seemed to differ from receptors for K88(F4). It is concluded that the antigenic variants of F18 fimbriae (F18ab and F18ac) are biologically distinct. F18ab fimbriae are expressed poorly both in vitro and in vivo and are frequently linked with the production of SLT-IIv and serogroup O139, while F18ac are more efficiently expressed in vitro and in vivo and most often are linked with enterotoxin (STa, STb) production, and serogroups O141, O157.

Animals↗
PubMed1997

Fimbrial colonisation factors F18ab and F18ac of Escherichia coli isolated from pigs with postweaning diarrhea and edema disease.

During the last 5 years at least four new types of colonisation factors have been described in association with porcine postweaning diarrhea and edema disease strains of E. coli. Recently, evidence was presented that these fimbrial factors are closely related to each other, and therefore the common denomination F18 was proposed. Until now, two variants F18ab and F18ac were identified that can be distinguished by serology. Alternatively, to circumvent elaborate growth conditions for the optimal expression of F18 fimbriae in vitro, PCR and subsequent restriction enzyme digestion of the amplification product can be used to differentiate F18ab from F18ac positive isolates. Reports that studied the prevalence of F18 positive E. coli show that this factor is present in about 30% to more than 50% of the PWD or ED strains negative for F4, F5, F6 or F41. Susceptibility of pigs to colonisation depends on the availability of intestinal receptors, and is under the control of a chromosomal locus. In young pigs susceptibility increases with age. Intestinal infection with F18 positive E. coli induces protection against repeated colonisation with E. coli bearing the homologous or the heterologous fimbrial variant of F18. Finally, preliminary passive protection studies suggest that F18 antibodies inhibit the colonisation of the pig's intestine by F18ab and F18ac positive strains.

Age Factors↗
PubMed1997

Two alpha(1,2) fucosyltransferase genes on porcine chromosome 6q11 are closely linked to the blood group inhibitor (S) and Escherichia coli F18 receptor (ECF18R) loci.

The Escherichia coli F18 receptor locus (ECF18R) has been genetically mapped to the halothane linkage group on porcine Chromosome (Chr) 6. In an attempt to obtain candidate genes for this locus, we isolated 5 cosmids containing the alpha (1,2)fucosyltransferase genes FUT1, FUT2, and the pseudogene FUT2P from a porcine genomic library. Mapping by fluorescence in situ hybridization placed all these clones in band q11 of porcine Chr 6 (SSC6q11). Sequence analysis of the cosmids resulted in the characterization of an open reading frame (ORF), 1098 bp in length, that is 82.3% identical to the human FUT1 sequence; a second ORF, 1023 bp in length, 85% identical to the human FUT2 sequence; and a third FUT-like sequence thought to be a pseudogene. The FUT1 and FUT2 loci therefore seem to be the porcine equivalents of the human blood group H and Secretor loci. Direct sequencing of the two ORFs in swine being either susceptible or resistant to adhesion and colonization by F18 fimbriated Escherichia coli (ECF18) revealed two polymorphisms at bp 307 (M307) and bp 857 (M857) of the FUT1 ORF. Analysis of these mutations in 34 Swiss Landrace families with 221 progeny showed close linkage with the locus controlling resistance and susceptibility to E. coli F18 adhesion and colonization in the small intestine (ECF18R), and with the locus of the blood group inhibitor S. A high linkage disequilibrium of M307-ECF18R in Large White pigs makes the M307 mutation a good marker for marker-assisted selection of E. coli F18 adhesion-resistant animals in this breed. Whether the FUT1 or possibly the FUT2 gene products are involved in the synthesis of carbohydrate structures responsible for bacterial adhesion remains to be determined.

Adhesins, Escherichia coli↗
PubMed1997

Role of fimbriae F18 for actively acquired immunity against porcine enterotoxigenic Escherichia coli.

Enterotoxigenic (ETEC) and enterotoxaemic (ETEEC) Escherichia (E.) coli that express F18 (F107) fimbriate colonize the small intestine and cause diarrhoea and/or oedema disease in weaned pigs. So far, two antigenic variants of F18 can be distinguished with a common antigenic factor designated 'a' and two specific factors called 'b' and 'c'. In this study the existence of crosswise anti-colonization immunity between E. coli strains that express F18ab or F18ac fimbrial variants, respectively, was demonstrated. Weaned pigs of susceptible genotype with respect to susceptibility to adhesion of E. coli with fimbriae F18 were inoculated with E. coli strains 3064STM (0157:K-:H-:F18ab; resistant to streptomycin) and 8199RIF (0141ab:K-:H4:F18ac; resistant to rifampicin). The faecal shedding was compared subsequent to immunization and homologous or heterologous challenge. An enzyme-linked immunosorbent assay (ELISA) was applied to measure IgA, IgM and IgG antibodies against the F18ab and F18ac antigens in saliva, faeces, serum and intestinal wash samples. About 8 log CFU/g of the inoculated strains were found in faeces of all pigs following immunization as well as in non-immunized controls after challenge. Bacterial counts of the inoculated strains after challenge were between 2 and 5 log lower, without any difference between homologous and heterologous challenge. Intestinal colonization with fimbriated E. coli resulted in production of significantly increased levels of anti-fimbrial antibodies, especially IgA, in serum and intestinal wash samples. There were higher levels of homologous than of heterologous anti-fimbrial antibodies. Production of antibodies against F18a or against another common fimbrial antigen is probably responsible for crosswise anti-colonization immunity between E. coli strains with F18ab and F18ac fimbrial variants. Serum F18-specific IgA may be a useful indicator of a mucosal immune response directed against F18 fimbriae.

Animals↗
PubMed1997

Reduced intestinal colonisation with F18-positive enterotoxigenic Escherichia coli in weaned pigs fed chicken egg antibody against the fimbriae.

Newly weaned pigs were fed a basal diet containing either egg antibody against fimbriae F18 at a high or low level, control egg powder or no egg, and challenged with enterotoxigenic Escherichia coli with fimbriae F18. The challenge was repeated after termination of the antibody treatment. Antibody-containing egg powder was produced by vaccination of hens with semi-purified fimbriae of the two variants F18ab and F18ac. Pigs eating egg powder with antibody against the same fimbrial variant were fully protected, even if the vaccine for the hens was produced with a different serotype devoid of enterotoxins. The effect was dose-dependent. The high dose of antibody against the heterologous variant of fimbriae F18 reduced colonisation at a level which was not significant. Ingestion of egg antibody partially suppressed the build-up of anti-colonisation immunity. Oral application of egg antibodies offers a promising approach for the prevention of infectious diseases of the digestive tract.

Animal Feed↗
PubMed1997

[A molecular test for the detection of E. coli F18 receptors: a breakthrough in the struggle against edema disease and post-weaning diarrhea in swine].

Oedema disease and post-weaning diarrhoea in swine are associated with the colonization of the intestine with toxigenic Escherichia (E.) coli bacteria of various serotypes. Colonization depends on specific binding between adhesive fimbriae and receptors on the enterocytes. The demonstration of these receptors allows the identification of susceptible and resistant pigs. Direct sequencing of the alpha (1,2) fucosyltransferase gene (FUT1) in swine being either susceptible or resistant to adhesion by F18 fimbriated E.coli revealed a mutation at basepair 307 (M307). Analysis of the mutation in Swiss Landrace and Large White families showed close linkage with the locus controlling resistance and susceptibility to E.coli F18 adhesion (ECF18R). The FUT1 (M307) mutation is a good marker for selection of E.coli of F18 adhesion resistant animals. The mutation is found with variable frequencies in Duroc, Hampshire and Pietrain pigs as well.

Animals↗
PubMed1996

Genes specifying receptors for F18 fimbriated Escherichia coli, causing oedema disease and postweaning diarrhoea in pigs, map to chromosome 6.

The study comprised 236 pigs selected for resistance or susceptibility to oedema disease. The susceptibility to colonization of the small intestine by an Escherichia coli strain causing oedema disease was determined: (1) by monitoring faecal excretion of weaned pigs orally inoculated with E. coli strain O139:K12(B):H1:F18ab serotype; and (2) by an in vitro adhesion assay using an F18ab positive E. coli strain and small intestinal enterocyte preparations. Susceptibility to adhesion by these bacteria was shown to be controlled by a dominant (B) allele of the ECF18R locus and resistance by the alternative recessive allele (b). Pigs were typed for 14 blood group systems, 11 biochemical polymorphisms and the polymorphism at nucleotide 1843 of the RYR1 locus. Linkage was demonstrated between the locus for F18 E. coli receptors and the loci S, RYR1, GPI, EAH, A1BG and PGD (Z > 20). The most likely gene orders are: S-ECF18R-RYR1-GPI-PGD or GPI-RYR1-ECF18R-S-PGD. The recombination frequencies between ECF18R-S and ECF18R-RYR1 were estimated to be theta = 0.5% and 3.1%, respectively.

Adhesins, Bacterial↗
PubMed1995

Designations F18ab and F18ac for the related fimbrial types F107, 2134P and 8813 of Escherichia coli isolated from porcine postweaning diarrhoea and from oedema disease.

The relatedness of the fimbriae produced by eight E. coli strains including type strains with F107 fimbriae, 2134P pili and colonization factor 8813 (preliminary F18), was examined. These strains had been isolated principally from pigs which were affected with postweaning diarrhoea or with oedema disease. The fimbriae were analyzed by means of electron microscopy, slide agglutination, immunofluorescence, immunogold labelling, immuno-diffusion, immunoelectrophoresis and western blot, molecular genetic techniques, and in vitro adhesion. The fimbriae of all the strains were long flexible filaments with a diameter not larger than 4.6 nm showing a zig-zag pattern. Results obtained by the serological techniques confirmed that the fimbriae possessed a common antigenic determinant designated 'a' in addition to a variant-specific determinant designated 'b' or 'c'. Immunoelectron microscopy demonstrated that the determinants 'a' and 'b' or 'a' and 'c' were localized along the same fimbrium. In immunoelectrophoresis, fimbrial extracts of selected strains yielded a single precipitation line towards the cathode. One single major subunit of approximately 15 kDa was recognised in western blots by antisera against the common antigenic determinant and the variant specific determinants. All strains possessed sequences related to gene fedA, coding for the major subunit of fimbriae F107. Two types of fedA-related subunit genes were differentiated, corresponding to the 'ab' and 'ac' types of fimbriae as defined by serological methods. The results demonstrated that F107 fimbriae, 2134P pili and colonization factor 8813 are related, and that two serological variants can be distinguished. We propose designations F18ab (for F107), and F18ac (for 2134P and 8813) in analogy to the nomenclature of F4 fimbriae.

Animals↗
PubMed1994

Prevalence of F107 fimbriae on Escherichia coli isolated from pigs with oedema disease or postweaning diarrhoea.

The study comprises fifty 4 to 12 weeks old pigs that died from oedema disease or severe diarrhoea. Smears were prepared from the mucosa of duodenum, jejunum and ileum, and by immunofluorescence F107 fimbrial antigens were detected. E. coli strains were isolated from the intestines and were characterised by slide agglutination (serogroup and F107 fimbriae production), by their cytotoxicity for Vero cells, and by gene amplification (genes coding for the major F107 subunit FedA, the toxin causing oedema disease SLT-IIv, and enterotoxins LTI, STIa and STII). F107 fimbriae were demonstrated in association with E. coli of serogroups O139:K12 and O141:K85a,b but not of serogroup O149:K91:F4a,c. Expression in culture of F107 fimbriae by some isolates gave additional evidence for production of these fimbriae by ETEC strains. The genetic determinant of SLT-Ilv was found in association with F107, and could not be detected in serogroup O149:K91:F4a,c. Gene fedA was demonstrated in two isolates which were devoid of SLT-IIv. Most isolates from cases of oedema disease belonged to serogroup O139:K12 and did not contain enterotoxin genes. Isolates from pigs that suffered from diarrhoea were serotyped O141:K85a,b or O149:K91:F4a,c, and carried at least two enterotoxin genes in their genomes. In a small proportion of the cases F107 antigens were demonstrated in intestinal smears although gene fedA was not detected in the corresponding isolates. The results confirm the importance of F107 fimbriae as virulence factor in oedema disease E. coli strains, but also demonstrate that F107 fimbriae can be found in association with postweaning diarrhoea isolates. In these latter strains enterotoxins were always demonstrated, irrespective of the presence of toxin SLT-IIv.

Animals↗
PubMed1994

[Diarrheal diseases in 1 to 4 week old suckling piglets from problem herds: microbial spectrum, histology, enzyme histochemistry].

Postmortem investigation was performed on 54 scouring (soon after onset of diarrhea) and 23 healthy suckling piglets. The animals were 1 to 4 weeks of age and were collected from 27 herds. In 21 herds diarrhea had been observed for a long time in piglets in this age group. Coccidia were found in 34 piglets, rotavirus in 2, cryptosporidia in 2, enterotoxigenic E. coli in 6, attaching and effacing E. coli in 1, Cl. perfringens type C in 1, Campylobacter coli in 53 and C. hyointestinalis in 8 piglets. Some of these microorganisms were isolated from healthy piglets as well. TGE- and PED-Virus antigen, as well as Salmonella were not recovered from any of the pigs. Results of the histopathological and enzyme histochemical investigations were in agreement with data from the literature. They confirmed and emphasized the role of coccidia as enteropathogenic agents in the animals examined. On the other hand evidence was shown, that C. coli is non-pathogenic. The role of C. hyointestinalis could not be fully elucidated. At least one sort of enteropathogenic agent was detected in about 68% (n = 37) of the scouring pigs or was present in 81% (n = 17) of the herds, respectively.

Animals↗