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•Effect of IBD vaccine (228E®) on S. Enteritidis infected chickens was indicated.•The recorded mortalities were higher in the 228E®+SE infected group.•The anti-S. Enteritidis antibody titres were higher in the SE infected group.•The 228E®+SE group had higher bursal lesion scores than the SE infected group.•Chickens given IBDV vaccine failed antibody response to the S. Enteritidis. Chickens infected with both infectious bursal disease virus (IBDV) and Salmonella had higher mortality. In this work, we investigated the effect of IBDV vaccine (modified live-virus bursal disease vaccine, Nobilis strain 228E®) on experimentally infected chickens with Salmonella Enteritidis (SE). Four experimental groups were included in this study, negative control group, 228E®group, 228E®+SE infected group, and SE infected group. Chickens were ocularly administrated 228E® at 12days of age and orally infected with S. Enteritidis at 13days of age. Sera, intestinal fluid, blood, cloacal swabs and tissue samples were collected at 1, 2 and 3weeks post vaccination (PV). The recorded mortalities were higher in the 228E®+SE infected group, compared to the SE infected group. The anti-S. Enteritidis serum antibody titer and the intestinal mucosal IgA level were higher in the SE infected group at 2 and 3weeks PV, compared to 228E®+SE infected group. S. Enteritidis fecal shedding and organ colonization were significantly higher in the 228E®+SE infected group than the SE infected group at 2 and 3weeks PV. The 228E®+SE group had significantly lower bursa to body weight ratios at 2 and 3weeks PV, as well as had higher bursal lesion scores than the SE infected group. IBDV vaccine depressed the specific-SE systemic and mucosal antibody responses, but did not affect the specific-SE cellular immune responses. Chickens administrated IBDV vaccine, followed by S. Enteritidis infection, could cause a significant effect on the bursa of Fabricius, resulting in failure of systemic and mucosal antibody responses to the S. Enteritidis and reduce the elimination and the clearance of S. Enteritidis.

Coinfection of farm-reared salmonids involving two viruses has been described, but there is no report on the interactions between viruses. Here we examine whether infectious pancreatic necrosis virus (IPNV) strain Sp interferes with the growth of infectious hematopoietic necrosis virus (IHNV) strain S46, a coinfected isolate from rainbow trout. When BF-2 cell culture was inoculated with S46 the infective titer of the IHNV fraction decreased by 3 log10 units compared to the growth curve of IHNV in the single infection. RT-PCR assay confirmed this reduction, which after successive passages of the co-infected sample led to a decrease in IHNV mRNA and the absence of the specific PCR product for IHNV. Flow cytometry showed that only 13% of the cells inoculated with S46 strain were infected with IHNV at 48-72 h post infection, in contrast to the 50-80% of cells that were positive for IPNV. Exposure of cells to IHNV for 24 h before infection with IPNV did not affect the infective titers of either virus or the PCR results obtained in simultaneous coinfections. Moreover IHNV was not inhibited when the IPNV inoculum was reduced. So, a multiplicity of infection dependence was demonstrated for IPNV-IHNV interference; the RT-PCR assay described here was found to be a suitable technique for identifying and studying dual viral infections.

Chickens infected with infectious bronchitis virus (IBV) and infectious bursal disease virus (IBDV) commonly develop secondary infection of the respiratory tract with Escherichia coli, resulting in significant economic losses. To understand the host factors that may contribute to the E. coli infection, we investigated macrophage-mediated E. coli phagocytosis, intracellular bacterial killing, and development of opsonizing antibody in previously uninfected chickens and in those infected with IBV, IBDV, and IBDV plus IBV. Macrophages from the peripheral blood and the respiratory tracts of chickens infected with IBV or IBDV plus IBV efficiently performed in vitro phagocytosis of E. coli in the presence of positive-control serum (i.e., E. coli antiserum produced in normal chickens). Those macrophages also had adequate bactericidal activity, indicating that IBV and IBDV infections had not affected their phagocytic activity or bactericidal function. The phagocytic activity of macrophages remained unaffected (P < 0.05) when the positive-control serum was replaced with E. coli antiserum produced in chickens infected with IBV alone. However, when E. coli antisera raised in IBDV-infected and, especially, that produced in IBDV plus IBV-infected chickens were supplemented, the percentage of phagocytosis and number of bacteria ingested per phagocyte were significantly (P < 0.05) less. These results indicate that although IBDV alone has the potential to markedly reduce opsonizing ability of antibody, this effect is significantly (P < 0.05) exacerbated by IBV infection.

The pathogenicity and persistence of Salmonella enteritidis (SE) phage type 8 and resulting egg contamination in normal and infectious bursal disease virus (IBDV)-infected white leghorn chicks were evaluated over 34 weeks and in some birds over a 64-week period. Four hundred 1-day-old specific-pathogen-free (SPF) straight-run white-leghorn chickens were allotted into four treatment groups: negative control, IBDV-infected, IBDV+SE-infected, and SE-infected. Chicks were infected with IBDV at 1 day of age and with SE phage type 8 at 2 days of age. SE persisted in the gut of more than 50% of the chicks of both SE-infected groups through 34 weeks postinoculation (PI), and SE could still be isolated from cloacal/rectal swabs taken at 64 weeks. IBDV+ SE-infected chicks had severe gross lesions and significantly (P 0.001) higher mortality (32%) than the negative control (1%), IBDV-infected (10%), and SE-infected (1%) groups. Gross lesions consisting of fibrinous pericarditis, perihepatitis, peritonitis, airsacculitis, and inspissated yolk were observed only in the IBDV+SE-infected group. SE isolations from internal organs of chickens in the IBDV+SE-infected group decreased from 83% at 8 weeks to 0% at 14 weeks PI; isolations from the SE-infected group decreased from 50% at 8 weeks to 0% at 10 weeks PI. Salmonella isolations increased from 0% to 14% in both groups at 18 weeks, corresponding with the time of sexual maturity. Of the 1,050 eggs cultured from the IBDV+SE-infected group, SE was isolated from 88 shells, five albumens, and two yolks. In contrast, of 1,258 eggs from the SE-infected group, 33 shells and none of the albumens and yolks were positive for SE. All eggs that had SE-positive contents also had SE-positive shells

Background Infectious bursal disease virus (IBDV) is a highly contagious immunosuppressive virus of chickens. Chickens acquire infection by the oral route under natural conditions. Although the histological and pathological changes after IBDV infection are well described, the alterations in serum metabolome have not been reported. In this study, SPF chickens were infected with attenuated IBDV (atIBDV) strain LM and very virulent IBDV (vvIBDV) strain LX, respectively. On the seventh day after oral infection, serum samples of experimental chickens were identified using ultra-high performance liquid chromatography-MS/MS (UHPLC-MS/MS). The serum metabolic profiles were analyzed by multivariate statistical methods. KEGG enrichment analysis was performed to evaluate the dysregulated biological pathways. Results We identified 368 significantly altered metabolites in response to both atIBDV and vvIBDV infection. The metabolic disorder of amino acid and lipid was associated with IBDV infection, especially tryptophan, glycerophospholipid, lysine, and tyrosine metabolism. The differential metabolites enriched in the four metabolic pathways were PC(20:4(5Z,8Z,11Z,14Z)/18:0), PE(16:0/18:2(9Z,12Z)), PE(16:0/22:6(4Z,7Z,10Z,13Z,16Z,19Z)), PE(18:0/20:4(5Z,8Z,11Z,14Z)), PE(18:0/20:4(8Z,11Z,14Z,17Z)), PE(18:0/22:6(4Z,7Z,10Z,13Z,16Z,19Z)), PE(20:3(8Z,11Z,14Z)/16:0), PE(22:6(4Z,7Z,10Z,13Z,16Z,19Z)/16:0), PE-NMe(20:5(5Z,8Z,11Z,14Z,17Z)/18:0), PS(20:3(5Z,8Z,11Z)/18:2(9Z,12Z)), 2-aminobenzoic acid, 4-(2-aminophenyl)-2,4-dioxobutanoic acid, N-acetylserotonin, 5-hydroxyindoleacetate, indole-3-acetaldehyde, indole-3-acetate, p -coumaric acid, L-tyrosine, homovanillin, and S-glutaryldihydrolipoamide. Conclusion The atIBDV and vvIBDV infection causes metabolic changes in chicken serum. The differential metabolites and dysregulated metabolic pathways reflect the host response to the IBDV infection.

Different infectious bursal disease virus (IBDV) live vaccines (intermediate, intermediate plus) were compared for their immunosuppressive abilities in specific-pathogen-free (SPF) layer-type chickens or commercial broilers. The Newcastle disease virus (NDV) vaccination model was applied to determine not only IBDV-induced immunosuppression but also bilateral effects between IBDV and NDV. None of the IBDV vaccines abrogated NDV vaccine–induced protection. All NDV-vaccinated SPF layers and broilers were protected against NDV challenge independent of circulating NDV antibody levels. Sustained suppression of NDV antibody development was observed in SPF layers, which had received the intermediate plus IBDV vaccine. We observed a temporary suppression of NDV antibody development in broilers vaccinated with one of the intermediate, as well as the intermediate plus, IBDV vaccines. Different genetic backgrounds, ages, and residual maternal antibodies might have influenced the pathogenesis of IBDV in the different types of chickens. Temporary suppression of NDV antibody response in broilers was only seen if the NDV vaccine was administered before and not, as it was speculated previously, at the time the peak of IBDV-induced bursa lesions was detected. For the first time, we have demonstrated that the NDV vaccine had an interfering effect with the pathogenesis of the intermediate as well as the intermediate plus IBDV vaccine. NDV vaccination enhanced the incidence of IBDV bursa lesions and IBDV antibody development. This observation indicates that this bilateral effect of an IBDV and NDV vaccination should be considered in the field and could have consequences for the performance of broiler flocks.

Acute pancreatitis is an inflammatory disease of the pancreas. Acute abdominal pain is the most common symptom, and increased concentrations of serum amylase and lipase confirm the diagnosis. Pancreatic injury is mild in 80% of patients, who recover without complications. The remaining patients have a severe disease with local and systemic complications. Gallstone migration into the common bile duct and alcohol abuse are the most frequent causes of pancreatitis in adults. About 15-25% of pancreatitis episodes are of unknown origin. Treatment of mild disease is supportive, but severe episodes need management by a multidisciplinary team including gastroenterologists, interventional radiologists, intensivists, and surgeons. Improved understanding of pathophysiology and better assessments of disease severity should ameliorate the management and outcome of this complex disease.