The control of Newcastle disease (ND) highly relies on vaccination. Immunity provided by a ND vaccine can be characterized by measuring the level of clinical protection and reduction in challenge virus shedding. The extent of shedding depends a lot on the characteristics of vaccine used and the quality of vaccination, but influenced also by the genotype of the challenge virus. We demonstrated that vaccination of SPF chicks with recombinant herpesvirus of turkey expressing the F-gene of genotype I ND virus (rHVT-ND) provided complete clinical protection against heterologous genotype VII.1.1 ND virus strain and reduced challenge virus shedding significantly. 100% of clinical protection was achieved already by 3 weeks of age, irrespective of the challenge route (intra-muscular or intra-nasal) and vaccination blocked cloacal shedding almost completely. Interestingly, oro-nasal shedding was different in the two challenge routes: less efficiently controlled following intra-nasal than intra-muscular challenge. Differences in the shedding pattern between the two challenge routes indicate that rHVT-ND vaccine induces strong systemic immunity, that is capable to control challenge virus dissemination in the body (no cloacal shedding), even when it is a heterologous strain, but less efficiently, although highly significantly (p < 0.001) suppresses the local replication of the challenge virus in the upper respiratory mucosa and consequent oro-nasal shedding.

The aim of this study is to follow the gp production in IBDV-vaccinated and challenged birds. The progress of IBDV infection was monitored using anti-VP2 immunocytochemistry, light and transmission electron microscopy. In the medulla of the bursal follicle, the Movat pentachrome staining discovered an extracellular glycoprotein (gp) produced by bursal secretory dendritic cells (BSDCs). The secretory granules of BSDCs either discharge resulting in extracellular gp or fuse together forming intracellular corpuscles. The double fate of granules suggests a dual function of BSDCs: (a.) For the discharged granules, gp contributes to the medullary microenvironment (ME). (b.) The intracellular corpuscles may be the sign of BSDC transformation to a macrophage-like cell (Mal). Infectious bursal disease virus (IBDV) infection accelerates the BSDC transformation to Mal. The decreased number of BSDCs is feedback for the precursor cells of BSDCs lodging in the cortico-medullary epithelial arches (CMEA), where they proliferate. Opening the CMEA, the precursor cells enter the medulla, and differentiate to immature BSDCs. The virus uptake in the corpuscles prevents the granular discharge resulting in the absence of gp and alteration in ME. In vaccine-take birds, the mitotic rate of BSDC precursor cells cannot restore the precursor pool; therefore, in the case of IBDV challenge, the number of newly formed BSDCs is too low for outbreak of clinical disease. The BSDCs, as a primary target of IBDV, may contribute to the long-lasting immunosuppressive status of IBDV-infected chickens.

To investigate the immunogenic cross reactivity between goose parvovirus (GPV) and Muscovy duck parvovirus (MDPV), cross-neutralization was carried out with serum samples collected from birds after infection with one of the two waterfowl parvoviruses. The significantly higher virus neutralization titer obtained against the homologous virus than against the heterologous one suggests important differences between the GPV and MDPV antigenic make up that affects the induced protective virus-neutralizing antibody specificity. This was further confirmed by cross-protection studies carried out in waterfowl parvovirus antibody-free Muscovy ducks immunized at one day of age with whole-virus inactivated oil-emulsion vaccines containing either GPV or MDPV as a monovalent vaccine, or both viruses as a bivalent vaccine. Protection against the clinical disease (growth retardation and feathering disorders) provided by the monovalent vaccine was complete against homologous virus challenge at 2 weeks post-vaccination, while the protection against the heterologous virus challenge was significantly lower (p < 0.001). Only the bivalent vaccine containing both goose and Muscovy duck parvoviruses in an inactivated form protected the birds (90–100%) against both waterfowl parvoviruses that can cause disease in Muscovy ducks. Both the cross-neutralization and cross-protection results indicated that adequate protection in Muscovy ducks against the two waterfowl parvoviruses could be achieved only with a vaccine containing both goose and Muscovy duck parvoviruses. Our results showed that the inactivated vaccine applied at one day of age could induce fast immunity (by 2 weeks post-vaccination), providing complete clinical protection in maternal antibody-free birds. It was also demonstrated that day-old vaccination of ducks with maternal antibodies with bivalent vaccine induced active immunity, resulting in 90 to 100% protection by 3 weeks of age, after the decline of maternal antibodies. A booster vaccination administered at 3 weeks of age following the day-old vaccination resulted in a strong and durable immunity against the clinical disease during the susceptible age of the birds.

There are two types of secretory cells in the chicken bursa of Fabricius (BF): (a) interfollicular epithelial cells (IFE), and (b) bursal secretory dendritic cells (BSDC) in the medulla of bursal follicles. Both cells produce secretory granules, and the cells are highly susceptible to IBDV vaccination and infection. Before and during embryonic follicular bud formation, an electron-dense, scarlet-acid fuchsin positive substance emerges in the bursal lumen, the role of which is unknown. In IFE cells, IBDV infection may induce rapid granular discharge, and in several cells, peculiar granule formation, which suggests that the glycosylation of protein is injured in the Golgi complex. In control birds, the discharged BSDC granules appear in membrane-bound and subsequently solubilized, fine-flocculated forms. The solubilized, fine-flocculated substance is Movat-positive and can be a component of the medullary microenvironment, which prevents the medullary B lymphocytes from nascent apoptosis. Vaccination interferes with the solubilization of the membrane-bound substance, resulting in: (i) aggregation of a secreted substance around the BSDC, and (ii) solid lumps in the depleted medulla. The non-solubilized substance is possibly not “available” for B lymphocytes, resulting in apoptosis and immunosuppression. In IBDV infection, one part of the Movat-positive Mals fuse together to form a medullary, gp-containing “cyst”. The other part of Mals migrate into the cortex, recruiting granulocytes and initiating inflammation. During recovery the Movat-positive substance appears as solid, extracellular lumps between the cells of FAE and Mals. Possibly the Mals and Movat-positive extracellular lumps glide into the bursal lumen via FAE to eliminate cell detritus from the medulla.

Background/Objectives: Effective control of Newcastle disease (ND) requires a reduction in virus shedding and transmission. While recombinant herpesvirus of turkey vectored Newcastle disease (rHVT-ND) vaccines induce strong systemic immunity, their ability to generate early mucosal immunity and limit transmission may not be optimal when used alone. Methods: Day-old layer chicks with maternally derived antibodies were vaccinated with the rHVT-ND vaccine alone or in combination with conventional live ND vaccines administered either at hatch or in a booster program. Birds were challenged with a genotype VII.2 velogenic ND virus strain at 3, 4 or 6 weeks of age. Humoral immune responses, clinical protection, challenge virus shedding and transmission to vaccinated contact groupmates were assessed. Results: All vaccination programs provided strong clinical protection (85–100%); however, combined vaccination strategies induced earlier immunity and reduced virus shedding more efficiently than the rHVT-ND vaccine alone. Booster vaccination further accelerated the onset of immunity and decreased shedding. By 6 weeks of age, differences among vaccination regimens had mainly disappeared, with all vaccinated groups showing minimal or no challenge virus shedding. Transmission to vaccinated contact birds was significantly reduced in the combined vaccinated groups, whereas unvaccinated controls efficiently spread the challenge virus and consequently caused high mortality in the contact groupmates. Conclusions: Both the rHVT-ND vaccine alone and in combination with live ND vaccines provided similar clinical protection against genotype VII.2 NDV challenge; however, combined vaccination programs accelerated immunity and more effectively reduced virus shedding and transmission, supporting their use for improved ND control, particularly in endemic regions.