Avian Pathology最新文献

Research highlights: ARV strains of the same genotype had distinct pathogenic and transmission traits.LambdaC, muB, and sigmaC genes made a difference.SigmaC-based genotyping obscures pathogenicity differences.

Live attenuated chicken embryo origin (CEO) vaccines against infectious laryngotracheitis virus (ILTV) are commonly used in long-lived chickens in Australia and generally provide good protection when administered by eye drop (ED). Although vent brush (VB) vaccination provides excellent protection, the associated immune responses are not well characterized. This study compared vaccine-mediated protection conferred by SA2 ILTV vaccine strain administered via ED or VB to 4-week-old layer chicks against a virulent (class 9) challenge 2 weeks after vaccination. No significant differences in ILTV DNA in choanal swabs were observed between vaccinated-challenged and non-challenged groups from 4-11 days post challenge (DPC), indicating that both VB and ED vaccination prevented increases in viral load after challenge, although neither prevented infection. Both vaccination routes resulted in high protection indices against clinical signs after challenge (VB, 99%; ED, 90%) and pathological lesion scores in conjunctiva (VB, 83%; ED, 74%) and trachea (VB, 78%; ED, 69%). The non-vaccinated challenged group exhibited significant over-expression of complement component 5a receptor 1, interleukin 1 beta, interleukin 6, myxovirus resistance 1 (MX1), and signal transducer and activator of transcription 1 (STAT1) in both conjunctiva and trachea at DPC 4, whereas ED- and VB-vaccinated challenged groups displayed similar gene expression profiles, resembling those of vaccinated non-challenged group except for elevated MX1 expression at DPC 4 and 7, and STAT1 expression at DPC 4 in the trachea. In conclusion, VB and ED vaccination conferred equivalent clinical protection with gene expression profiles similar to vaccinated, non-challenged chickens, indicating comparable immunological efficacy.

Condemnations in slaughterhouses are a recurring cause of losses for the poultry industry. This study aimed to evaluate the involvement of avian reovirus (ARV) in arthritis-related condemnations in a broiler slaughterhouse under Brazilian Federal Inspection. A total of 150 pelvic limbs condemned for arthritis were collected from the inspection line at the time of condemnation, originating from 30 flocks not vaccinated against ARV. For the detection of ARV, real-time polymerase chain reaction following reverse transcription (RT-qPCR) was performed on a pool of five gastrocnemius tendons from each flock using the primers ReoS-F1, ReoS-R1, ReoS-F2, and ReoS-R2, followed by Sanger sequencing of the σC gene. For macroscopic and histopathological analyses, the gastrocnemius, digital flexor, and extensor tendons, as well as the articular cartilage of the tibiotarsometatarsal joint, were evaluated. Injuries were classified into four degrees, ranging from G0 (no changes) to G3 (highest degree of injury). Macroscopic injury scores revealed a higher percentage of injuries in the gastrocnemius tendon compared to the extensor and flexor tendons. Histological changes were observed in the peritendon and muscles adjacent to the tendons, including infiltration of heterophils, macrophages, lymphocytes, plasma cells with lymphoid aggregates, haemorrhage, and fibrinous exudate in the gastrocnemius, flexor, and digital extensor tendons. ARV was detected in 50% of the flocks by RT-qPCR, with no correlation to increased arthritis condemnations (P > 0.05). The sequence analysis identified the cluster as lineage VI, a strain not present in Brazil's commercial vaccination programmes. The study concludes that half of the investigated flocks were positive for ARV, identifying a cluster absent in current Brazilian vaccination programmes.

Heat shock protein 90 alpha (HSP90α), a conservative chaperone protein, is closely involved in signal transduction and virus proliferation, but how it engages the lifecycle of fowl adenovirus serotype 4 (FAdV-4) remains unknown. Here, we demonstrated that the expression of HSP90α was significantly upregulated in Leghorn male hepatoma (LMH) cells infected with FAdV-4. Functional study revealed that overexpression of HSP90α promoted FAdV-4 replication in vitro, whereas knockdown of HSP90α exerted the opposite effect. Subsequently, co-immunoprecipitation (Co-IP) assay showed that HSP90α, particularly the truncated HSP90α variant encompassing amino acid residues 286-542, interacted with hexon protein of FAdV-4. These findings collectively identify HSP90α as a critical host factor that modulates FAdV-4 replication through direct interaction with the viral hexon protein (via its 286-542 amino acid domain), thereby providing novel insights into the molecular crosstalk between FAdV-4 and host cells.

Research highlights: An emerging highly virulent S. Gallinarum strain caused uncommon respiratory and intestinal lesions.The intranasal route of challenge caused a more severe and systemic disease, with broader organ involvement.The emerging strain targeted novel organs including larynx, trachea, bursa of Fabricius, and bone marrow.

Low pathogenic avian influenza viruses (LPAIVs) are typically associated with subclinical or mild disease in poultry. However, recent outbreaks involving atypical LPAIV strains, including H3N1 strains like A/chicken/Belgium/460/2019, have demonstrated severe clinical outcomes despite low intravenous pathogenicity index (IVPI) scores. These findings challenge current classification systems and raise questions about alternative markers of virulence, such as loss of a neuraminidase (NA) glycosylation site linked to plasminogen-binding and haemagglutinin (HA) cleavage. This study compared the pathogenicity of a wild-type H3N1 strain (wtH3N1), isolated from a disease outbreak in Belgium, with a genetically modified, loss-of function variant (mH3N1) carrying a single amino acid substitution (S122N) in NA that blocks plasminogen-dependent cleavage of HA in chickens. Four-week-old pullets and cockerels, and 30-week-old laying hens were inoculated with either wtH3N1 or mH3N1 and clinical signs, egg production, viral replication, post-mortem and tissue pathology were evaluated. Adult hens infected with wtH3N1 showed a complete cessation of egg production, systemic viral replication, and histopathological lesions in the reproductive tract, brain, and kidneys. In contrast, birds infected with mH3N1 displayed only mild, transient reductions in egg production and minimal viral detection. No mortality was observed in any group. All young chickens exhibited subclinical infections. Overall, the S122N mutation significantly attenuated viral virulence and tissue tropism. The study provides functional evidence that position 122 on NA contributes to increased virulence in H3N1 AIV. These findings support the role of molecular markers in risk assessment of non-H5/H7 LPAIVs and highlight the limitations of the current IVPI-based classification system.

Highly pathogenic Avian Influenza (HPAI) viruses, especially the newly discovered H5N8 clade 2.3.4.4b strain, are the world's biggest concern. The HPAI virus challenge in broilers is a significant issue, especially for short-lived commercial broiler chickens. This study examined H5 inactivated vaccine regimens. Phylogenetic analysis was used to compare the genetic sequences of vaccination seeds, the challenge virus (H5N8 clade 2.3.4.4 strain), and the circulating HPAI H5N8 strain. Following this, a field investigation evaluated various vaccination schedules using the H5 inactivated vaccine against the HPAI virus in early-challenged commercial broilers with maternal immunity against the AIV-H5N8 virus. Three vaccination regimens were planned: a prime-boost regimen (days 1 and 9) in group 1 (G1), a single dose 1.5 times the manufacturer-recommended dosage on day 7 in group 2 (G2), and the routinely recommended single dose on day 7 in group 3 (G3). Weekly AI-H5 humoral immune response antibody titers were measured. Both vaccinated and unvaccinated positive controls were challenged with HPAI H5N8 virus clade 2.3.4.4b on day 28 of age. Clinical signs, Survival, and virus shedding were monitored for 10 days post-challenge. After three weeks post-vaccination (WPV), prime-boost antibody titers were significantly higher than those in single-dose groups. After the challenge, G2 and G3 had high survival rates (91.7%) but a noticeably high shedding rate following the early challenge (3-WPV), while G1 had 100% survival and negligible viral shedding. HPAI H5N8 virus protection increased with prime-boost vaccination in early challenge. These findings highlight the importance of implementing optimal vaccination programs to mitigate HPAI virus risks in commercial chicken production.Research Highlights: A phylogenetic study has proven vaccine genetic match with circulating H5N8 strains.Prime-boost vaccine regimen provided 100% survival in H5N8-challenged broilers.Enhanced immunity observed in prime-boost groups, with minimal viral shedding⁣.Single-dose groups achieved 91.7% survival and showed higher viral shedding.

Research highlights: Not all Clostridium perfringens (Cp) strains can reproduce severe necrotic enteritis (NE) in turkeys.The developed NE reproduction model caused 80% mortality.A reliable NE reproduction model is crucial to investigate pathogenic Cp strains.

Research highlights: Dietary supplementation with phytogenic and prebiotic blend (PPB) effectively mitigated Eimeria spp. infection in broilers.PPB and salinomycin reduced oocyst excretion.Oocyst excretion was highest in the infected group.PPB was as effective as salinomycin.

Research highlights: Natural HPAIV H5N1 infection causes mortality and pathology in Humboldt penguins.Molecular analysis identified the aetiology as a novel H5N1 clade 2.3.4.4b genotype.Immunohistochemical analysis demonstrated infection of endothelial cells, macrophages and reticular cells in lymphoid tissue.