150 research outputs found

    Оформление конструкторской документации на печатные платы в условиях автоматизированного проектирования и подготовки производства

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    Предложен подход к оформлению чертежей печатных плат, позволяющий значительно упростить документацию, а также упорядочить документооборот

    Risk based culling for highly infectious diseases of livestock

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    The control of highly infectious diseases of livestock such as classical swine fever, foot-and-mouth disease, and avian influenza is fraught with ethical, economic, and public health dilemmas. Attempts to control outbreaks of these pathogens rely on massive culling of infected farms, and farms deemed to be at risk of infection. Conventional approaches usually involve the preventive culling of all farms within a certain radius of an infected farm. Here we propose a novel culling strategy that is based on the idea that farms that have the highest expected number of secondary infections should be culled first. We show that, in comparison with conventional approaches (ring culling), our new method of risk based culling can reduce the total number of farms that need to be culled, the number of culled infected farms (and thus the expected number of human infections in case of a zoonosis), and the duration of the epidemic. Our novel risk based culling strategy requires three pieces of information, viz. the location of all farms in the area at risk, the moments when infected farms are detected, and an estimate of the distance-dependent probability of transmission

    Highly pathogenic avian influenza subtype H5Nx clade 2.3.4.4 outbreaks in Dutch poultry farms, 2014–2018 : Clinical signs and mortality

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    In recent years, different subtypes of highly pathogenic avian influenza (HPAI) viruses caused outbreaks in several poultry types worldwide. Early detection of HPAI virus infection is crucial to reduce virus spread. Previously, the use of a mortality ratio threshold to expedite notification of suspicion in layer farms was proposed. The purpose of this study was to describe the clinical signs reported in the early stages of HPAI H5N8 and H5N6 outbreaks on chicken and Pekin duck farms between 2014 and 2018 in the Netherlands and compare them with the onset of an increased mortality ratio (MR). Data on daily mortality and clinical signs from nine egg-producing chicken farms and seven Pekin duck farms infected with HPAI H5N8 (2014 and 2016) and H5N6 (2017–2018) in the Netherlands were analysed. In 12 out of 15 outbreaks for which a MR was available, MR increase preceded or coincided with the first observation of clinical signs by the farmer. In one chicken and two Pekin duck outbreaks, clinical signs were observed prior to MR increase. On all farms, veterinarians observed clinical signs of general disease. Nervous or locomotor signs were reported in all Pekin duck outbreaks, but only in two chicken outbreaks. Other clinical signs were observed less frequently in both chickens and Pekin ducks. Compared to veterinarians, farmers observed and reported clinical signs, especially respiratory and gastrointestinal signs, less frequently. This case series suggests that a MR with a set threshold could be an objective parameter to detect HPAI infection on chicken and Pekin duck farms at an early stage. Observation of clinical signs may provide additional indication for farmers and veterinarians for notifying a clinical suspicion of HPAI infection. Further assessment and validation of a MR threshold in Pekin ducks are important as it could serve as an important tool in HPAI surveillance programs.</p

    Comparing farm biosecurity and antimicrobial use in high-antimicrobial-consuming broiler and pig farms in the Belgian-Dutch border region

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    As antimicrobial resistance is a worldwide problem, threatening both livestock and public health, understanding the drivers for resistance in different settings and countries is essential. Therefore, 30 pig and 30 poultry farms with country-specific high antimicrobial use (AMU) were recruited in the Belgian-Dutch border region. Information regarding production parameters, farm characteristics, biosecurity, and AMU was collected. On average, more biosecurity measures were implemented on Dutch farms, compared to Belgian farms in both animal species. In addition, more opportunities were found to increase the level of internal biosecurity compared to external biosecurity in both countries. AMU, quantified as treatment incidence (TI), differed marginally significant between broiler farms in Belgium and the Netherlands (median BE: 8; NL: 3), whereas in weaned piglets (median BE: 45 and NL: 14) and finishing pigs (median BE: 5 and NL: 1), there was a substantial difference in AMU between farms from both countries. Overall, Dutch farms showed less between-farm variation in TI than did Belgian farms. In both poultry and pig production, the majority of antimicrobials used were extended-spectrum penicillins (BE: 32 and 40%; NL: 40 and 24% for poultry and pigs, respectively). Compared to Belgian farms, Dutch poultry farms used high amounts of (fluoro)quinolones (1 and 15% of total AMU, respectively). None of the production parameters between broiler farms differed significantly, but in pig production, weaning age in Belgian farms (median: 23) was lower than in Dutch farms (median: 27). These results indicate considerable room for improvement in both countries and animal species. Farm-specific preventive strategies can contribute to lowering the risk for animal disease and hence the need for AMU

    Conserved developmental trajectories of the cecal microbiota of broiler chickens in a field study

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    There is great interest in identifying gut microbiota development patterns and underlying assembly rules that can inform strategies to improve broiler health and performance. Microbiota stratification using community types helps to simplify complex and dynamic ecosystem principles of the intestinal microbiota. This study aimed to identify community types to increase insight in intestinal microbiota variation between broilers and to identify factors that explain this variation. A total of 10 well-performing poultry flocks on four farms were followed. From each flock, the cecal content of nine broilers was collected at 7, 14, and 35 days posthatch. A total of two robust community types were observed using different clustering methods, one of which was dominated by 7-day-old broilers, and one by 35-day-old broilers. Broilers, 14-day-old, were divided across both community types. This is the first study that showed conserved cecal microbiota development trajectories in commercial broiler flocks. In addition to the temporal development with age, the cecal microbiota variation between broilers was explained by the flock, body weight, and the different feed components. Our data support a conserved development of cecal microbiota, despite strong influence of environmental factors. Further investigation of mechanisms underlying microbiota development and function is required to facilitate intestinal health promoting management, diagnostics, and nutritional interventions

    Analysis of chicken intestinal natural killer cells, a major IEL subset during embryonic and early life

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    Restrictions on antimicrobials demand alternative strategies to improve broiler health, such as supplying feed additives which stimulate innate immune cells like natural killer (NK) cells. The main objective of this study was to characterize intestinal NK cells in broiler chickens during embryonic and early life and compare these to NK cells in spleen, blood and bone marrow. Also T-cell subsets were determined. The majority of intestinal NK cells expressed IL-2Rα rather than 20E5 and 5C7, and showed low level of activation. Within intestinal NK cells the activation marker CD107 was mostly expressed on IL-2Rα+ cells while in spleen and blood 20E5+ NK cells primarily expressed CD107. High percentages of intestinal CD8αα+, CD8αβ+ and from 2 weeks onward also gamma delta T cells were found. Taken together, we observed several intestinal NK subsets in broiler chickens. Differences in NK subsets were mostly observed between organs, rather than differences over time. Targeting these intestinal NK subsets may be a strategy to improve immune-mediated resistance in broiler chickens.SUPPLEMENTARY MATERIAL : Table S1. Characterization of immune cells generated in broiler chickens in the present study compared to data known in layer chickens.The Dutch Research Council (NWO) and by Cargill Animal Nutrition and Health.http://www.elsevier.com/locate/desalhj2022Veterinary Tropical Disease

    A detailed analysis of innate and adaptive immune responsiveness upon infection with Salmonella enterica serotype Enteritidis in young broiler chickens

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    Salmonella enterica serotype Enteritidis (SE) is a zoonotic pathogen which causes foodborne diseases in humans as well as severe disease symptoms in young chickens. More insight in innate and adaptive immune responses of chickens to SE infection is needed to understand elimination of SE. Seven-day-old broiler chickens were experimentally challenged with SE and numbers and responsiveness of innate and adaptive immune cells as well as antibody titers were assessed. SE was observed in the ileum and spleen of SE-infected chickens at 7 days post-infection (dpi). At 1 dpi numbers of intraepithelial cytotoxic CD8+ T cells were signifcantly increased alongside numerically increased intraepithelial IL-2Rα+ and 20E5+ natural killer (NK) cells at 1 and 3 dpi. At both time points, activation of intraepithelial and splenic NK cells was signifcantly enhanced. At 7 dpi in the spleen, presence of macrophages and expression of activation markers on dendritic cells were signifcantly increased. At 21 dpi, SE-induced proliferation of splenic CD4+ and CD8+ T cells was observed and SE-specifc antibodies were detected in sera of all SE-infected chickens. In conclusion, SE results in enhanced numbers and activation of innate cells and we hypothesized that in concert with subsequent specifc T cell and antibody responses, reduction of SE is achieved. A better understanding of innate and adaptive immune responses important in the elimination of SE will aid in developing immune-modulation strategies, which may increase resistance to SE in young broiler chickens.ADDITIONAL FILE 1. Gating strategy of IELs and splenic lymphocytes in broiler chickens. Gating strategy included consecutive selection for lymphocytes (FSC-A vs SSC-A), singlets (FSC-A vs FSC-H) and viable cells (Live/Dead marker-negative) followed by selection of NK and T cell subsets in ileum and spleen. Furthermore, activation of NK and T cells was analyzed by surface expression of CD107 and intracellular expression of IFNγ. Conjugate controls are shown for IELs and splenic lymphocytes.ADDITIONAL FILE 2. Effect of SE infection on numbers of splenic NK cells in broiler chickens. A Numbers (cells/mg) of splenic IL-2Rα+ and B 20E5+ NK cells per mg spleen in uninfected (uninf) and SE-infected (SE-inf) chickens in the course of time. C Gene expression levels of NK cell lineage marker (NFIL3), IL-7Rα and perforin 1 (PRF1) by RT-qPCR in sorted IL-2Rα+ and 20E5+ NK cell subsets. Mean + SEM per treatment and time point is shown (n = 5), for uninfected chickens at 7 dpi n = 4 and for gene expression levels n = 1.ADDITIONAL FILE 3. Staining and sorting controls associated with Figure 4. A The staining controls for the gating strategy are shown. The left panel depicts splenocytes without the viability dye. The middle and right panels show splenocytes that are gated according to Figure 4A, but without the primary antibodies that bind MRC1LB and CD11, respectively. B The graphs show the gating strategy and purity of a representative sample of splenocytes that was sorted into CD11+ MRC1LB+, CD11+ MRC1LB− FSClow and CD11+ MRC1LB− FSChigh subpopulations. The splenocytes that are gated as CD11+ MRC1LB− in the upper panels are shown in the lower panels to visualize their FSC-A vs SSC-A pattern. C The absolute numbers of sorted APC subpopulations are shown.ADDITIONAL FILE 4. Phenotypic characterization of splenic APCs upon SE infection. A-B The presence (%) and C-D numbers (cells/mg spleen) of FSClow DCs and and FSChigh DCs in uninfected (uninf) and SE-infected (SE-inf) chickens were assessed over time. Mean + SEM per treatment and time point is shown (n = 5), for uninfected chickens at 0 dpi n = 3 and at 7 dpi n = 4. Statistical significance is indicated as ** p < 0.01.ADDITIONAL FILE 5. The gating strategy used to determine the activation status of the APC subsets as depicted in Figure 5. The three identified splenic APC subsets A macrophages, B FSClow DCs and C FSChigh DCs were assessed for CHIR-AB1, CD40, CD80 and MHC-II. For CHIR-AB1, CD40 and CD80, the cells expressing the respective markers were selected and expressed as a percentage. The expression of MHC-II by each subset was expressed as the geometric mean fluorescent intensity (gMFI).ADDITIONAL FILE 6. Numbers of intraepithelial and splenic γδ T cells and cytotoxic T cells expressing either CD8αα or CD8αβ in broiler chickens upon SE infection. A Numbers (cells/mg) of intraepithelial CD8αα+ γδ T cells, B CD8αβ+ γδ T cells, C cytotoxic CD8αα+ T cells and D CD8αβ+ T cells per mg ileum in uninfected (uninf) and SE-infected (SE-inf) chickens in the course of time. E Numbers (cells/mg) of splenic CD8αα+ γδ T cells, F CD8αβ+ γδ T cells, G cytotoxic CD8αα+ T cells and H CD8αβ+ T cells per mg spleen in uninfected and SE-infected chickens. Mean + SEM per treatment and time point is shown (n = 5), for uninfected chickens at 1 dpi in the IELs and spleen n = 4 due to numbers of events acquired in the gate of interest were < 100, and at 7 dpi in spleen n = 4. Statistical significance is indicated as * p < 0.05, ** p < 0.01. *** p < 0.001.ADDITIONAL FILE 7. Numbers of CD4 + T cells in the spleen of broiler chickens upon SE infection. Numbers (cells/mg) of splenic CD4+ αβ T cells per mg spleen in uninfected (uninf) and SE-infected (SE-inf) chickens in the course of time. Mean + SEM per treatment and time point is shown (n = 5), for uninfected chickens at 7 dpi n = 4.ADDITIONAL FILE 8. T cell activation in the IEL population and spleen of broiler chickens upon SE infection. A Percentages of intraepithelial CD8+ T cells expressing CD107 (including both γδ and αβ T cells) in uninfected (uninf) and SE-infected (SE-inf) chickens in the course of time. B Percentages of splenic CD8+ T cells expressing CD107 (including both γδ and αβ T cells), C CD8+ γδ T cells expressing IFNγ, D CD4+ αβ T cells expressing IFNγ and E CD8+ αβ T cells expressing IFNγ in uninfected (uninf) and SE-infected (SE-inf) chickens over time. Mean + SEM per treatment and time point is shown (n = 5), for uninfected chickens at 7 dpi in spleen n = 4 and at 1 and 3 dpi in the IELs percentages were not determined (n.d.) due to numbers of events acquired in the gate of interest were < 100.The Dutch Research Council (NWO) and by Cargill Animal Nutrition and Health.http://www.veterinaryresearch.orgpm2022Veterinary Tropical Disease

    No evidence of African swine fever virus replication in hard ticks

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    African swine fever (ASF) is caused by African swine fever virus (ASFV), a tick-borne DNA virus. Soft ticks of the genus Ornithodoros are the only biological vectors of ASFV recognized so far. Although other hard ticks have been tested for vector competence, two commonly found tick species in Europe, Ixodes ricinus and Dermacentor reticulatus, have not been assessed for their vector competence for ASFV. In this study, we aimed to determine whether virus replication can occur in any of these two hard tick species (I. ricinus and/or D. reticulatus), in comparison with O. moubata (the confirmed vector), after feeding them blood containing different ASFV isolates using an improved in vitro system. DNA quantities of ASFV in these infected hard ticks were measured systematically, for 6 weeks in I. ricinus, and up to 8 weeks in D. reticulatus, and the results were compared to those obtained from O. moubata. There was evidence of virus replication in the O. moubata ticks. However, there was no evidence of virus replication in I. ricinus or D. reticulatus, even though viral DNA could be detected for up to 8 weeks after feeding in some cases. This study presents the first results on the possible vector competence of European hard (ixodid) ticks for ASFV, in a validated in vitro feeding setup. In conclusion, given the lack of evidence for virus replication under in vitro conditions, D. reticulatus and I. ricinus are unlikely to be relevant biological vectors of ASFV.http://www.elsevier.com/locate/ttbdishb201

    Does having a cat in your house increase your risk of catching COVID-19?

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    [EN]Due to the zoonotic origin of SARS-Coronavirus 2 (SARS-CoV-2), the potential for its transmission from humans back to animals and the possibility that it might establish ongoing infection pathways in other animal species has been discussed. Cats are highly susceptible to SARS-CoV-2 and were shown experimentally to transmit the virus to other cats. Infection of cats has been widely reported. Domestic cats in COVID-19-positive households could therefore be a part of a human to animal to human transmission pathway. Here, we report the results of a qualitative risk assessment focusing on the potential of cat to human transmission in such settings. The assessment was based on evidence available by October 2021. After the introduction of SARS-CoV-2 to a household by a human, cats may become infected and infected cats may pose an additional infection risk for other members of the household. In order to assess this additional risk qualitatively, expert opinion was elicited within the framework of a modified Delphi procedure. The conclusion was that the additional risk of infection of an additional person in a household associated with keeping a domestic cat is very low to negligible, depending on the intensity of cat-to-human interactions. The separation of cats from humans suffering from SARS-CoV-2 infection should contribute to preventing further transmission.SIThis work was funded by the German Federal Ministry of Education and Research within the COVMon Project, being part of the InfectControl2020 Initiative (BMBF grant no. 03COV16D)
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