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•We evaluated swine influenza A transmission virus in piglets with different MDA statuses after a single-dose vaccination.•The transmission rate of the challenge strain was found 3.6 time greater in MDA-positive than in MDA-negative pigs.•Estimated parameters were unsed to feed a mechanistic model of SwIAV transmission in a farrow-to-finish pig farm.•An extended SwIAV within-farm persistence was observed when both sows and piglets were batch-to-batch vaccinated.•Alternative vaccination schemes need to be tested, accounting for population dynamics and hosts’ immune statuses. Swine influenza A virus (swIAV) is a major pathogen affecting pigs with a huge economic impact and potentially zoonotic. Epidemiological studies in endemically infected farms permitted to identify critical factors favoring on-farm persistence, among which maternally-derived antibodies (MDAs). Vaccination is commonly practiced in breeding herds and might be used for immunization of growing pigs at weaning. Althoughinterference between MDAs and vaccination was reported in young piglets, its impact on swIAV transmission was not yet quantified. To this aim, this study reports on a transmission experiment in piglets with or without MDAs, vaccinated with a single dose injection at four weeks of age, and challenged 17 days post-vaccination. To transpose small-scale experiments to real-life situation, estimated parameters were used in a simulation tool to assess their influence at the herd level. Based on a thorough follow-up of the infection chain during the experiment, the transmission of the swIAV challenge strain was highly dependent on the MDA status of the pigs when vaccinated. MDA-positive vaccinated animals showed a direct transmission rate 3.6-fold higher than the one obtained in vaccinated animals without MDAs, estimated to 1.2. Vaccination nevertheless reduced significantly the contribution of airborne transmission when compared with previous estimates obtained in unvaccinated animals. The integration of parameter estimates in a large-scale simulation model, representing a typical farrow-to-finish pig herd, evidenced an extended persistence of viral spread when vaccination of sows and single dose vaccination of piglets was hypothesized. When extinction was quasi-systematic at year 5 post-introduction in the absence of sow vaccination but with single dose early vaccination of piglets, the extinction probability fell down to 33% when batch-to-batch vaccination was implemented both in breeding herd and weaned piglets. These results shed light on a potential adverse effect of single dose vaccination in MDA-positive piglets, which might lead to longer persistence of the SwIAV at the herd level.

Edema disease (ED), a fatal disease in weaned piglets, is caused by Shiga toxin-producing Escherichia coli (STEC). The increasing emergence of antibiotic-resistant E. coli strains has necessitated the exploration of alternatives such as bacteriophage therapy. Using a porcine model, this study evaluated the prophylactic effect of bacteriophage P-GXEC-L2P5 administered by oral gavage against ED. The novel phage P-GXEC-L2P5 was isolated using a multidrug-resistant (MDR) STEC strain GXEC-STL2 as the host. P-GXEC-L2P5 was identified as a member of Caudoviricetes , Dhillonvirus , with an 88,607 base pair (bp) genome, and it possessed a short latent period (10 min), moderate pH stability (5–10), and appropriate thermal tolerance (4–60 ℃). Piglets pretreated with P-GXEC-L2P5 showed no apparent clinical signs (e.g., eyelid edema or neurological symptoms) after challenge with GXEC-STL2. B-scan ultrasound revealed no significant hydronephrosis. Necropsy showed only mild intestinal congestion, with no other gross pathological lesions noted. Histopathology demonstrated no significant differences in features compared with noninfected controls. Phage treatment significantly reduced fecal STEC shedding ( P < 0.05) and significantly decreased Stx2e concentrations in serum, cerebral cortex, kidney, and small intestine ( P < 0.01). The messenger RNA (mRNA) expression of Gb4 (Stx2e receptor) was significantly lower in these tissues ( P < 0.05). Concurrently, vascular endothelial cells exhibited increased FITC-labeled wheat germ agglutinin (FITC-WGA) fluorescence intensity and increased mRNA expression of endothelial integrity factors (connexin43, vinculin, and zonula occludens-1; P < 0.05). In addition, phage treatment preserved jejunal microbiota diversity and abundance. In conclusion, P-GXEC-L2P5 effectively prevented STEC-induced ED by reducing STEC load and Stx2e levels, while mitigating increased vascular permeability.

Actinobacillus pleuropneumoniae is a Gram-negative bacterium that belongs to the family Pasteurellaceae. It is the causative agent of porcine pleuropneumonia, a highly contagious respiratory disease that is responsible for major economic losses in the global pork industry. The disease may present itself as a chronic or an acute infection characterized by severe pathology, including hemorrhage, fibrinous and necrotic lung lesions, and, in the worst cases, rapid death. A. pleuropneumoniae is transmitted via aerosol route, direct contact with infected pigs, and by the farm environment. Many virulence factors associated with this bacterium are well characterized. However, much less is known about the role of biofilm, a sessile mode of growth that may have a critical impact on A. pleuropneumoniae pathogenicity. Here we review the current knowledge on A. pleuropneumoniae biofilm, factors associated with biofilm formation and dispersion, and the impact of biofilm on the pathogenesis A. pleuropneumoniae. We also provide an overview of current vaccination strategies against A. pleuropneumoniae and consider the possible role of biofilms vaccines for controlling the disease.

Porcine edema disease (ED) is caused by infection with Shiga toxin type 2 e variant (Stx2e)-producing Escherichia coli (STEC). To develop a new ED vaccine, we engineered a fusion protein, in which the Stx2e B subunit (Stx2eB) was fused to the five-stranded α-helical coiled coil domain of cartilage oligomeric matrix protein (COMP), based on our recent finding that the coiled coil strongly stabilizes the B subunit pentamer of Stx2 (Tamaki Y, Harakuni T, Arakawa T. Shiga toxin type 2 B subunit protects mice against toxin challenge when leashed and bundled by a stable pentameric coiled-coil molecule. Vaccine. 2024 Mar 7;42(7):1757–1767). Purified Stx2eB–COMP fusion protein administered to mice conferred complete protection against a lethal dose of Stx2e. However, unfused Stx2eB conferred only 10 % protection. Furthermore, when Stx2eB was fused to a trimeric or tetrameric coiled coil, a marked reduction in protective efficacy was observed, indicating the importance of “five-to-five” fusion stoichiometry. Next, we immunized weaned piglets twice with 100 μg or 10 μg of the Stx2eB–COMP fusion protein, and then orally challenged the animals with a lethal dose of STEC. The piglets immunized with the high dose were almost completely free from clinical symptoms of ED, whereas three of the six piglets administered adjuvant-only died, and the remaining surviving piglets exhibited severe ED symptoms. Although all piglets immunized with the low dose survived, they exhibited mild to moderate ED symptoms. Our findings indicate that Stx2eB is highly protective only when bundled and molecularly stabilized by the coiled coil molecule. •Shiga toxin type 2e (Stx2e) was fused to cartilage oligomeric matrix protein (COMP).•Fusion was between the Stx2eB subunit and the COMP pentameric α-helical coiled coil.•Stx2eB–COMP fusion protein, expressed in E. coli inclusion bodies, refolded in vitro.•Only the “five-to-five” chimera was protective in mice against Stx2e challenge.•Fusion protein protected piglets against orally infected Stx2e-producing E. coli.

Porcine cysticercosis is caused by a zoonotic tapeworm, Taenia solium, which causes serious disease syndromes in human. Effective control of the parasite requires knowledge on the burden and pattern of the infections in order to properly direct limited resources. The objective of this study was to establish the spatial distribution of porcine cysticercosis in Mbulu district, northern Tanzania, to guide control strategies. This study is a secondary analysis of data collected during the baseline and follow-up periods of a randomized community trial aiming at reducing the incidence rate of porcine cysticercosis through an educational program. At baseline, 784 randomly selected pig-keeping households located in 42 villages in 14 wards were included. Lingual examination of indigenous pigs aged 2-12 (median 8) months, one randomly selected from each household, were conducted. Data from the control group of the randomized trial that included 21 of the 42 villages were used for the incidence study. A total of 295 pig-keeping households were provided with sentinel pigs (one each) and reassessed for cysticercosis incidence once or twice for 2-9 (median 4) months using lingual examination and antigen ELISA. Prevalence of porcine cysticercosis was computed in Epi Info 3.5. The prevalence and incidence of porcine cysticercosis were mapped at household level using ArcView 3.2. K functions were computed in R software to assess general clustering of porcine cysticercosis. Spatial scan statistics were computed in SatScan to identify local clusters of the infection. The overall prevalence of porcine cysticercosis was 7.3% (95% CI: 5.6, 9.4; n = 784). The K functions revealed a significant overall clustering of porcine cysticercosis incidence for all distances between 600 m and 5 km from a randomly chosen case household based on Ag-ELISA. Lingual examination revealed clustering from 650 m to 6 km and between 7.5 and 10 km. The prevalence study did not reveal any significant clustering by this method. Spatial scan statistics found one significant cluster of porcine cysticercosis prevalence (P = 0.0036; n = 370). In addition, the analysis found one large cluster of porcine cysticercosis incidence based on Ag-ELISA (P = 0.0010; n = 236) and two relatively small clusters of incidence based on lingual examination (P = 0.0012 and P = 0.0026; n = 241). These clusters had similar spatial location and included six wards, four of which were identified as high risk areas of porcine cysticercosis. This study has identified local clusters of porcine cysticercosis in Mbulu district, northern Tanzania, where limited resources for control of T. solium could be directed. Further studies are needed to establish causes of clustering to institute appropriate interventions.

Background Edema disease (ED) and post-weaning diarrhea (PWD) are major health and economic challenges in the swine industry, primarily caused by F18 + Shiga toxin-producing Escherichia coli (STEC). These diseases typically occur within 1–2 weeks after weaning and are associated with high morbidity and mortality, resulting in substantial economic losses worldwide. The pathogenesis of ED is largely mediated by bacterial adhesion via F18 fimbriae, particularly the FedF adhesin, and systemic toxemia induced by Shiga-like toxin IIe (SLT-IIe). Although passive or active immunization with SLT-IIe toxoids or detoxified variants can provide some protection, their immunogenicity is often limited and may be accompanied by adverse effects. Currently, no commercial vaccines are available, and reliance on antibiotics has accelerated the emergence of multidrug-resistant E. coli. Therefore, the development of safe and effective vaccines targeting both F18 fimbrial adhesion and SLT-IIe-mediated toxemia is urgently needed. Results Recombinant rSF toxoid (fusion of SLT-IIe B subunit and FedF adhesin) mixed with Ee strain formed a novel rSF toxoid bacterin-inactivated vaccine. Compared to conventional bacterin-inactivated vaccine, the rSF vaccine group showed significantly higher protection efficacy against F18+ SLTEC challenge, with reduced histological scores, attenuated inflammation, decreased creatinine levels, and minimized kidney damage, alongside increased average daily gain and nitric oxide levels. Conclusion rSF toxoid addition safely enhances protection efficacy against F18+ SLTEC and alleviates renal pathology.

Porcine edema disease (ED) is an enterotoxaemia that frequently occurs in 4–12 week-old piglets and results in high mortality. ED is caused by Shiga toxin 2e (Stx2e), produced by host-adapted Shiga toxin-producing Escherichia coli (STEC) strains. We constructed a recombinant protein in which the B subunit of Stx2e (Stx2eB) was linked to Cartilage Oligomeric Matrix Protein (COMP)’s pentameric domain to enhance antigenicity to induce neutralizing antibodies against Stx2e. We evaluated the efficacy of this antigen as a vaccine on the farm where ED had occurred. The suckling piglets were divided into two groups. The pigs in the vaccinated group were intramuscularly immunized with the vaccine containing 30 µg/head of Stx2eB-COMP at 1 and 4 weeks of age. The control pigs were injected with saline instead of the vaccine. The neutralizing antibody titer to Stx2e, mortality, clinical score, and body weight was evaluated up to 11 weeks after the first vaccination. In the vaccinated group, the Stx2e neutralizing antibody was detected 3 weeks after the first vaccination, its titer increased during the following weeks. The antibody was not detected in the control group during the test period. The STEC gene was detected in both groups during the test period, but a typical ED was observed only in control pigs; the mortality and clinical score were significantly lower in the vaccinated group than in the control group. These data indicate that the pentameric B subunit vaccine is effective for preventing ED and offers a promising tool for pig health control.

The goal of this study was to evaluate survival of important viral pathogens of livestock in animal feed ingredients imported daily into the United States under simulated transboundary conditions. Eleven viruses were selected based on global significance and impact to the livestock industry, including Foot and Mouth Disease Virus (FMDV), Classical Swine Fever Virus (CSFV), African Swine Fever Virus (ASFV), Influenza A Virus of Swine (IAV-S), Pseudorabies virus (PRV), Nipah Virus (NiV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), Swine Vesicular Disease Virus (SVDV), Vesicular Stomatitis Virus (VSV), Porcine Circovirus Type 2 (PCV2) and Vesicular Exanthema of Swine Virus (VESV). Surrogate viruses with similar genetic and physical properties were used for 6 viruses. Surrogates belonged to the same virus families as target pathogens, and included Senecavirus A (SVA) for FMDV, Bovine Viral Diarrhea Virus (BVDV) for CSFV, Bovine Herpesvirus Type 1 (BHV1) for PRV, Canine Distemper Virus (CDV) for NiV, Porcine Sapelovirus (PSV) for SVDV and Feline Calicivirus (FCV) for VESV. For the remaining target viruses, actual pathogens were used. Virus survival was evaluated using Trans-Pacific or Trans-Atlantic transboundary models involving representative feed ingredients, transport times and environmental conditions, with samples tested by PCR, VI and/or swine bioassay. SVA (representing FMDV), FCV (representing VESV), BHV-1 (representing PRV), PRRSV, PSV (representing SVDV), ASFV and PCV2 maintained infectivity during transport, while BVDV (representing CSFV), VSV, CDV (representing NiV) and IAV-S did not. Notably, more viruses survived in conventional soybean meal, lysine hydrochloride, choline chloride, vitamin D and pork sausage casings. These results support published data on transboundary risk of PEDV in feed, demonstrate survival of certain viruses in specific feed ingredients (“high-risk combinations”) under conditions simulating transport between continents and provide further evidence that contaminated feed ingredients may represent a risk for transport of pathogens at domestic and global levels.

Human influenza A viruses are classic examples of antigenically variable pathogens that have a seemingly endless capacity to evade the host's immune response. The viral hemagglutinin (HA) and neuraminidase (NA) proteins are the main targets of our antibody response to combat infections. HA and NA continuously change to escape from humoral immunity, a process known as antigenic drift. As a result of antigenic drift, the human influenza vaccine is updated frequently. The World Health Organization (WHO) coordinates a global influenza surveillance network that, by the hemagglutination inhibition (HI) assay, routinely characterizes the antigenic properties of circulating strains in order to select new seed viruses for such vaccine updates. To facilitate a quantitative interpretation and easy visualization of HI data, a new computational technique called “antigenic cartography” was developed. Since its development, antigenic cartography has been applied routinely to assist the WHO with influenza surveillance activities. Until recently, antigenic variation was not considered a serious issue with influenza vaccines for poultry. However, because of the diversification of the Asian H5N1 lineage since 1996 into multiple genetic clades and subclades, and because of the long-term use of poultry vaccines against H5 in some parts of the world, this issue needs to be re-addressed. The antigenic properties of panels of avian H5N1 viruses were characterized by HI assay, using mammalian or avian antisera, and analyzed using antigenic cartography methods. These analyses revealed antigenic differences between circulating H5N1 viruses and the H5 viruses used in poultry vaccines. Considerable antigenic variation was also observed within and between H5N1 clades. These observations have important implications for the efficacy and long-term use of poultry vaccines.

Hepatitis E virus (HEV) is the causative agent of hepatitis E in humans, an emerging zoonosis mainly transmitted via food in developed countries and for which domestic pigs are recognised as the main reservoir. It therefore appears important to understand the features and drivers of HEV infection dynamics on pig farms in order to implement HEV surveillance programmes and to assess and manage public health risks. The authors have reviewed the international scientific literature on the epidemiological characteristics of HEV in swine populations. Although prevalence estimates differed greatly from one study to another, all consistently reported high variability between farms, suggesting the existence of multifactorial conditions related to infection and within-farm transmission of the virus. Longitudinal studies and experimental trials have provided estimates of epidemiological parameters governing the transmission process (e.g. age at infection, transmission parameters, shedding period duration or lag time before the onset of an immune response). Farming practices, passive immunity and co-infection with immunosuppressive agents were identified as the main factors influencing HEV infection dynamics, but further investigations are needed to clarify the different HEV infection patterns observed in pig herds as well as HEV transmission between farms. Relevant surveillance programmes and control measures from farm to fork also have to be fostered to reduce the prevalence of contaminated pork products entering the food chain.