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Background Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) continues to be a major economic issue for the swine industry worldwide, not only due to acute outbreaks but also endemic infections. PRRS disease severity and consequently financial losses can vary greatly between endemically infected farms and estimation of damage is challenging. This study aimed to assess the economic effect of PRRS in a systematic way at individual farm-level for endemically infected herds, using a PRRS cost simulation tool. In total 21 German sow herds with endemic PRRSV infection were investigated. Data on health and production performance, farm management and environment to be fed into the calculator was collected on each farm, and blood samples taken to confirm the PRRSV status. Results All study farms experienced a significant loss attributable to PRRS. The median farm budget across all farms was − 31 € per sow and year, compared to a median simulated farm budget of 248 € if these farms had been PRRSV negative. The median total loss attributable to PRRS was 74,181 € per farm per year, corresponding to a median total loss per sow and year of 255 €. The impact of PRRS on farm profits was − 19.1% on average and − 41% in the worst case. Conclusions The calculated losses give a good hint of the economic damage due to PRRS for the pig industry. Even in endemically infected farms, farmers face a non-negligible damage and profit from a concerted PRRS control. The calculator has proven itself in the field to render a valid estimation of losses due to PRRS in endemically infected farms.

The duration of birth is an important factor influencing the survival of piglets and the health of sows. A prolonged parturition is usually treated with oxytocin, even though several undesirable side effects are described. Therefore, the aim of this study was to evaluate the safety and efficacy of Prostaglandin E2 (PGE2) of different concentrations as an intravaginal applied gel after the birth of the fourth piglet in sows. Twelve sows were randomly allocated to one of four treatment groups: Group I (control group) application of placebo gel; Group II application of 0.5 mg; Group III application of 1.0 mg PGE2; Group IV PGE2 application of 2.0 mg PGE2. Total duration of parturition (time between first piglet and last placenta), piglet interval before and after treatment and placenta expulsion duration (time between first and last placenta) were recorded, and each piglet was scored for meconium staining and vitality. Furthermore, stillborn piglets were categorized into ante-partum and intra-partum deaths.A significant dose-dependent effect of PGE2 after the fourth piglet in a linear regression model with group I, II and III on the total duration of parturition and the placenta expulsion duration was detected. An increase of the PGE2 dosage from 0 to 1 mg significantly reduced the total duration of parturition (group I: 553.7 ± 114.2; group II:456 ± 167.9; group III: 284.7 ± 40.5; p-value: 0.02) and placenta expulsion duration (group I: 364 ± 120; group II: 289 ± 144.1; group III: 119 ± 46.13; p-value: 0.03). Although no further significant differences between the groups using ANCOVA and a linear regression model including all groups were detected, severe meconium staining in more than 10% of piglets was observed in group II and IV. Moreover, piglets of group IV showed oedematous and haemorrhagic umbilical cords, lethargy and anoxia after treatment, and intra-partum deaths were recorded.The best outcome for the sows and piglets was achieved using the 1 mg PGE2 dosage, whereas the other dosages showed more negative side effects, impairing the health and welfare of the animals. The results of this study can be used for further studies with larger sample sizes.

Background: The Swiss pig population enjoys a favourable health situation. To further promote this, the Pig Health Service (PHS) conducts a surveillance program in affiliated herds: closed multiplier herds with the highest PHS-health and hygiene status have to be free from swine dysentery and progressive atrophic rhinitis and are clinically examined four times a year, including laboratory testing. Besides, four batches of pigs per year are fattened together with pigs from other herds and checked for typical symptoms (monitored fattening groups (MF)). While costly and laborious, little was known about the effectiveness of the surveillance to detect an infection in a herd. Therefore, the sensitivity of the surveillance for progressive atrophic rhinitis and swine dysentery at herd level was assessed using scenario tree modelling, a method well established at national level. Furthermore, its costs and the time until an infection would be detected were estimated, with the final aim of yielding suggestions how to optimize surveillance. Results: For swine dysentery, the median annual surveillance sensitivity was 96.7 %, mean time to detection 4.4 months, and total annual costs 1022.20 Euro/herd. The median component sensitivity of active sampling was between 62.5 and 77.0 %, that of a MF between 7.2 and 12.7 %. For progressive atrophic rhinitis, the median surveillance sensitivity was 99.4 %, mean time to detection 3.1 months and total annual costs 842.20 Euro. The median component sensitivity of active sampling was 81.7 %, that of a MF between 19.4 and 38.6 %. Conclusions: Results indicate that total sensitivity for both diseases is high, while time to detection could be a risk in herds with frequent pig trade. From all components, active sampling had the highest contribution to the surveillance sensitivity, whereas that of MF was very low. To increase efficiency, active sampling should be intensified (more animals sampled) and MF abandoned. This would significantly improve sensitivity and time to detection at comparable or lower costs. The method of scenario tree modelling proved useful to assess the efficiency of surveillance at herd level. Its versatility allows adjustment to all kinds of surveillance scenarios to optimize sensitivity, time to detection and/or costs.

Background Diabetes insipidus (DI) is a rare disease in humans and animals, which is caused by the lack of production, malfunction or dysfunction of the distal nephron to the antidiuretic effect of the antidiuretic hormone (ADH). Diagnosis requires a thorough medical history, clinical examination and further laboratory confirmation. This case report describes the appearance of DI in five Duroc boars in Switzerland. Case presentation Two purebred intact Duroc boars at the age of 8 months and 1.5 years, respectively, with a history of polyuric and polydipsic symptoms had been referred to the Swine Clinic in Berne. Based on the case history, the results of clinical examination and the analysis of blood and urine, a tentative diagnosis of DI was concluded. Finally, the diagnosis was confirmed by findings from a modified water deprivation test, macroscopic examinations and histopathology. Following the diagnosis, three genes known to be involved in inherited DI in humans were analyzed in order to explore a possible genetic background of the affected boars. Conclusion The etiology of DI in pigs is supposed to be the same as in humans, although this disease has never been described in pigs before. Thus, although occurring only on rare occasions, DI should be considered as a differential diagnosis in pigs with polyuria and polydipsia. It seems that a modified water deprivation test may be a helpful tool for confirming a diagnosis in pigs. Since hereditary forms of DI have been described in humans, the occurrence of DI in pigs should be considered in breeding programs although we were not able to identify a disease associated mutation.

BACKGROUND: This study was aimed at evaluating the clinical protection, the level of Porcine circovirus type 2 (PCV2) viremia and the immune response (antibodies and IFN-γ secreting cells (SC)) in piglets derived from PCV2 vaccinated sows and themselves vaccinated against PCV2 at different age, namely at 4, 6 and 8 weeks. The cohort study has been carried out over three subsequent production cycles (replicates). At the start/enrolment, 46 gilts were considered at first mating, bled and vaccinated. At the first, second and third farrowing, dams were bled and re-vaccinated at the subsequent mating after weaning piglets. Overall 400 piglets at each farrowing (first, second and third) were randomly allocated in three different groups (100 piglets/group) based on the timing of vaccination (4, 6 or 8 weeks of age). A fourth group was kept non-vaccinated (controls). Piglets were vaccinated intramuscularly with one dose (2 mL) of a commercial PCV2a-based subunit vaccine (Porcilis® PCV). Twenty animals per group were bled at weaning and from vaccination to slaughter every 4 weeks for the detection of PCV2 viremia, humoral and cell-mediated immune responses. Clinical signs and individual treatments (morbidity), mortality, and body weight of all piglets were recorded. RESULTS: All vaccination schemes (4, 6 and 8 weeks of age) were able to induce an antibody response and IFN-γ SC. The highest clinical and virological protection sustained by immune reactivity was observed in pigs vaccinated at 6 weeks of age. Overall, repeated PCV2 vaccination in sows at mating and the subsequent higher levels of maternally derived antibodies did not significantly interfere with the induction of both humoral and cell-mediated immunity in their piglets after vaccination. CONCLUSIONS: The combination of vaccination in sows at mating and in piglets at 6 weeks of age was more effective for controlling PCV2 natural infection, than other vaccination schemas, thus sustaining that some interference of MDA with the induction of an efficient immune response could be considered. In conclusion, optimal vaccination strategy needs to balance the levels of passive immunity, the management practices and timing of infection.

BACKGROUND A discrete time, stochastic, compartmental model simulating the spread of within a batch of industrially raised pigs was developed to understand infection dynamics and to assess the impact of a range of husbandry practices. A 'disease severity' index was calculated based on the ratio between the cumulative numbers of acutely and chronically diseased and infectious pigs per day in each age category, divided by the length of time that pigs spent in this age category. This is equal to the number of pigs per day, either acutely or chronically infectious and diseased, divided by the number of all pigs per all days in the model. The impact of risk and protective factors at batch level was examined by adjusting 'acclimatisation of gilts', 'length of suckling period', 'vaccination of suckling pigs against ', 'contact between fattening pigs of different age during restocking of compartments' and 'co-infections in fattening pigs'. RESULTS The highest 'disease severity' was predicted, when gilts do not have contact with live animals during their acclimatisation, suckling period is 28 days, no vaccine is applied, fatteners have contact with pigs of other ages and are suffering from co-infections. Pigs in this scenario become diseased/infectious for 26.1 % of their lifetime. Logistic regression showed that vaccination of suckling pigs was influential for 'disease severity' in growers and finishers, but not in suckling and nursery pigs. Lack of contact between gilts and other live pigs during the acclimatisation significantly influenced the 'disease severity' in suckling pigs but had less impact in growing and finishing pigs. The length of the suckling period equally affected the severity of the disease in all age groups with the strongest association in nursery pigs. The contact between fatteners of different groups influenced the course of infection among finishers, but not among other pigs. Finally, presence of co-infections was relevant in growers and finishers, but not in younger pigs. CONCLUSION The developed model allows comparison of different prevention programmes and strategies for controlling transmission of .

Background Mycoplasma hyopneumoniae is the etiologic agent of enzootic pneumonia mainly occurring in fattening pigs. It is assumed that horizontal transmission of the pathogen during nursery and growing phase starts with few suckling pigs vertically infected by the sow. The aim of the present study was the exploration of the herd prevalence of M. hyopneumoniae infections in suckling pigs followed by an investigation of various herd specific factors for their potential of influencing the occurrence of this pathogen at the age of weaning. Results In this cross-sectional study, 125 breeding herds were examined by taking nasal swabs from 20 suckling pigs in each herd. In total, 3.9% (98/2500) of all nasal swabs were tested positive for M. hyopneumoniae by real-time PCR. Piglets tested positive originated from 46 different herds resulting in an overall herd prevalence of 36.8% (46/125) for M. hyopneumoniae infection in pigs at the age of weaning. While the herds were epidemiologically characterized, the risk for demonstration of M. hyopneumoniae was significantly increased, when the number of purchased gilts per year was more than 120 (OR: 5.8), and when the number of farrowing pens per compartment was higher than 16 (OR: 3.3). In herds with a planned and segregated production, where groups of sows entered previously emptied farrowing units, the risk for demonstration of M. hyopneumoniae in piglets was higher in herds with two or four weeks between batches than in herds with one or three weeks between batches (OR: 2.7). Conclusions In this cross-sectional study, several risk factors could be identified enhancing the probability of breeding herds to raise suckling pigs already infected with M. hyopneumoniae at the time of weaning. Interestingly, some factors (farrowing rhythm, gilt acclimatisation issues) were overlapping with those also influencing the seroprevalences among sows or the transmission of the pathogen between older age groups. Taking the multifactorial character of enzootic pneumonia into account, the results of this study substantiate that a comprehensive herd specific prevention programme is a prerequisite to reduce transmission of and disease caused by M. hyopneumoniae.