Enteric Escherichia coli infections are a highly relevant cause of disease and death in young pigs. Breeding genetically resistant pigs is an economical and sustainable method of prevention. Resistant pigs are protected against colonization of the intestine through the absence of receptors for the bacterial fimbriae, which mediate adhesion to the intestinal surface. The present work aimed at elucidation of the mode of inheritance of the F4ad receptor which according to former investigations appeared quite confusing. Intestines of 489 pigs of an experimental herd were examined by a microscopic adhesion test modified in such a manner that four small intestinal sites instead of one were tested for adhesion of the fimbrial variant F4ad. Segregation analysis revealed that the mixed inheritance model explained our data best. The heritability of the F4ad phenotype was estimated to be 0.7±0.1. There are no relations to the strong receptors for variants F4ab and F4ac. Targeted matings allowed the discrimination between two F4ad receptors, that is, a fully adhesive receptor (F4adRFA) expressed on all enterocytes and at all small intestinal sites, and a partially adhesive receptor (F4adRPA) variably expressed at different sites and often leading to partial bacterial adhesion. In pigs with both F4ad receptors, the F4adRPA receptor is masked by the F4adRFA. The hypothesis that F4adRFA must be encoded by at least two complementary or epistatic dominant genes is supported by the Hardy–Weinberg equilibrium statistics. The F4adRPA receptor is inherited as a monogenetic dominant trait. A comparable partially adhesive receptor for variant F4ab (F4abRPA) was also observed but the limited data did not allow a prediction of the mode of inheritance. Pigs were therefore classified into one of eight receptor phenotypes: A1 (F4abRFA/F4acR+/F4adRFA); A2 (F4abRFA/F4acR+/F4adRPA); B (F4abRFA/F4acR+/F4adR−); C1 (F4abRPA/F4acR−/F4adRFA); C2 (F4abRPA/F4acR−/F4adRPA); D1 (F4abR−/F4acR−/F4adRFA); D2 (F4abR−/F4acR−/F4adRPA); E (F4abR−/F4acR−/F4adR−).

Single-locus disorders in domesticated animals were among the first Mendelian traits to be documented, and to be included in early linkage maps. The use of linkage maps and comparative genomics has been essential to the identification of the causative genes for disorders. A DNA marker for selection of resistance to F18+ E. coli in the pig is available since several years. The use of this marker decreases mortality due to post-weaning diarrhoea and/or oedema disease. For more than 100 disorders the molecular lesion has been identified and hence for which a DNA test is available. However, for most diseases such as Porcine Reproductive and Respiratory Syndrome (PRRS) and Porcine Circovirus Associated Diseases (PCVAD), resistance is a complex and polygenic trait. Novel technologies such as gene microarrays and advanced bioinformatics are being used to analyse health data. Lagging behind, however, is availability of large DNA data sets from pedigreed populations with accurately measured health phenotypes that are needed to identify associations between markers and health traits. As the pig genome is sequenced to a great extent and ten thousands of markers can be analysed at a reasonable price, genomic selection for health traits is possible.

The objectives of this study were a description of the practical implementation of the painless castration under inhalational anaesthesia with an objective assessment of animal welfare, workplace safety and time exposure. 600 questionnaires were sent to farmers all over Switzerland and 100 farms were visited during castration under inhalation anaesthesia. 44 % of the visited farmers administered analgetics during anaesthesia or less than 10 minutes before castration. 14 % of the piglets were insufficiently anaesthetised (moving or vocalising) and 18 % showed stronger bleeding tendency after castration. The mortality rate was less than 0.1 %. 22 % of the swine farmers reported headache or dizziness during or after castration work. The Isoflurane level on 2 farms was above the Swiss safety limits. The time needed for castration was with 4.3 minutes clearly above the time necessary without anaesthesia. The additional financial costs and time are at the moment not adequately compensated to the farmers.

In Switzerland postweaning multisystemic wasting syndrome (PMWS), caused by porcine circovirus type 2, was detected for the first time in 2001. To comprise the PMWS epizooty in 2003 - 2006 retrospectively, individual animals were diagnosed according to internationally accepted criteria and temporal and regional patterns of the epizooty were reconstructed. Occurrence of PMWS was predominantly in regions with a high frequency of swine farms (central and eastern Switzerland). Apparently it was spread to other, less affected regions, through trade of infected fattening pigs. Concurrently, disease was found in different establishments of production. Affected were mainly weaners or fattening pigs. In 40 % of the breeding farms and in 25 % of the fattening farms mortality rate was higher than 5 %. Starting in 2003, also a higher frequency of porcine dermatitis and nephropathy syndrome (PDNS) diseased pigs was diagnosed. In the years 2004 to 2006 they accounted for about 10 % of the diagnosed PCV2-associated diseases. Besides the characteristic skin- and kidney lesions approximately half of the PDNS cases showed wasting and lymphoid lesions with high quantities of PCV2 antigen. We termed these mixed forms PMWS-PDNS-hybrid forms.

Porcine circovirus type 2 (PCV2) is the obligate infectious agent in postweaning multisystemic wasting syndrome (PMWS) of pigs. To control PMWS, we vaccinated dams at 4 and 2 weeks before pregnancy and again in the 12th week of gestation with an inactivated PCV2 vaccine (Circovac). Two producer farms run under the control of Swiss Swine Health Organization were selected for the experiment. Previously, in one farm PMWS was diagnosed on pigs after weaning, whereas in the other farm, pigs wasted during the fattening period. For the experiments 113 dams were randomly vaccinated, and 111 dams were sham injected. Vaccination increased serum antibodies in dams 3-to 9-fold, accompanied by serum antibody titer increases in their offspring. In the sixth week of life, progeny from vaccinated dams had about the same IgG antibody titers as progeny of unvaccinated dams at the third day of life. In sera of vaccinated dams only low concentrations of PCV2 DNA were detected, and no progeny developed PMWS. Interestingly, at day 56 four progeny of unvaccinated dams tested positive for anti-PCV2 IgM antibodies, indicating a primary infection with PCV2. Of economic importance is the observation that progeny of vaccinated dams had a significantly higher daily weight gain in the fattening period (farm X, +51 g/day; farm Y, +30 g/day) and thus a shortened fattening period of about 6 days compared to progeny of controls. To our knowledge this is the first demonstration of subclinical circovirus infection and its effects on growth performance of fattening pigs by vaccination of dams.

Based on Directive (EC) No 99/2003, monitoring programs on the development of antimicrobial resistance in bacteria from livestock are implemented in many European countries. The aim of the present study was (i) to establish comprehensive baseline data on the antimicrobial resistance situation in Escherichia coli isolates obtained from healthy pigs (pooled fecal samples) originating from 60 Swiss pig-breeding farms, and (ii) to analyze differences in the resistance frequency between Escherichia coli isolates from weaned pigs and sows. Susceptibility testing (disc diffusion method) was performed on 429 isolates from weaned pigs and 431 isolates from sows. Overall, 17.7% of the isolates from weaned pigs and 22.5% of the Escherichia coli isolates from sows were susceptible to all antibiotics tested. Low resistance prevalence was found for amoxicillin, amoxicillin/clavulanic acid, ampicillin, cefquinome, ciprofloxacin, colistin, florfenicol, and gentamicin. The most frequently found resistances were against streptomycin (60.6% of the isolates from weaners and 64.3% of the isolates from sows), sulfonamide (51.5% and 26.9%), tetracycline (35.2% and 22.0%), and trimethoprim (27.5% and 11.1%). With exception of colistin, most resistances were found for those antibiotics commonly used on the farms. Except for ciprofloxacin and streptomycin, isolates from weaned pigs showed higher resistance prevalence than those from sows. This difference was significant for cefquinome, florfenicol, sulfonamide, tetracycline, and trimethoprim (p<0.05).

In boars, scrotal haemangiomas have been described frequently, but intratesticular haemangiomas are rare. Of 12 boars with scrotal haemangiomas, three animals also had testicular tumours, as follow: testicular haemangioma (TH) (n=1); TH with intratubular germ cell tumour (ITGT) (n=1); TH with intratubular germ cell-like tumour (ITGLT) and Sertoli cell tumour (n=1). In the nine remaining boars, no testicular tumours were found. Immunohistochemical examination of scrotal and testicular haemangiomas revealed labelling of endothelial cells for vimentin and factor VIII-related antigen. Labelling of smooth muscle actin was occasionally observed in the walls of neoplastic vessels. In the ITGT, no labelling was produced by any of the antibodies used. The Sertoli cell tumour was strongly positive for S-100. Sperm granulomas and degeneration of seminiferous tubules were also observed.

The cause of porcine congenital progressive ataxia and spastic paresis (CPA) is unknown. This severe neuropathy manifests shortly after birth and is lethal. The disease is inherited as a single autosomal recessive allele, designated cpa. In a previous study, we demonstrated close linkage of cpa to microsatellite SW902 on porcine chromosome 3 (SSC3), which corresponds syntenically to human chromosome 2. This latter chromosome contains ion channel genes (Ca(2+), K(+) and Na(+)), a cholinergic receptor gene and the spastin (SPG4) gene, which cause human epilepsy and ataxia when mutated. We mapped porcine CACNB4, KCNJ3, SCN2A and CHRNA1 to SSC15 and SPG4 to SSC3 with the INRA-Minnesota porcine radiation hybrid panel (IMpRH) and we sequenced the entire open reading frames of CACNB4 and SPG4 without finding any differences between healthy and affected piglets. An anti-epileptic drug treatment with ethosuximide did not change the severity of the disease, and pigs with CPA did not exhibit the corticospinal tract axonal degeneration found in humans suffering from hereditary spastic paraplegia, which is associated with mutations in SPG4. For all these reasons, the hypothesis that CACNB4, CHRNA1, KCNJ3, SCN2A or SPG4 are identical with the CPA gene was rejected.

Postweaning multisystemic wasting syndrome (PMWS) is a disease caused by porcine circovirus type 2 (PCV-2). The disease was present as early as 1986 in Spain, 1989 in Japan and 1993 in Thailand. In view of this, we considered it possible that the disease may also have been present in Switzerland prior to its first description in 2001. A retrospective investigation was performed on paraffin-embedded lymphoid organs and ileum from 496 pigs aged 5–13 weeks collected between 1976 and mid-2001. The sections were investigated immunohistochemically using a monoclonal antibody specific for PCV-2 capsid antigen encoded by ORF2. Virus antigen was detected in tissue samples of 39 pigs from 28 farms. The earliest positive sample originated from 1986. After 1989, positive pigs were found almost every year among the 20–40 cases investigated annually. These results indicate that PCV-2 has been present in Switzerland for some time, and at least since 1986.