Tenosynovitis In Chickens Research Articles

Avian Reovirus σA Protein Inhibits Type I Interferon Production by Abrogating Interferon Regulatory Factor 7 Activation.

Type I interferon (IFN) response is the first line of host-based innate immune defense against viral infections. However, viruses have developed multiple strategies to counter host IFN responses, so they may continue infecting hosts via effective replication. Avian reovirus (ARV), an RNA virus, causes viral arthritis or tenosynovitis in chickens. Previous studies have shown that ARV is highly resistant to the antiviral effects of IFN. However, the underlying mechanisms that enable ARV to block the IFN pathway remain unclear. In this study, we found that ectopic expression of ARV protein, σA, significantly inhibited the production of IFN-β induced by melanoma-differentiation-associated gene 5 (MDA5) and poly(I·C). Knockdown of σA during ARV infection enhances the IFN-β response and suppresses viral replication. ARV σA inhibited the MDA5-mediated IFN-β activation by targeting interferon regulatory factor 7 (IRF7). Further studies demonstrated that σA interacts with IRF7, thereby blocking IRF7 dimerization and nuclear translocation, finally leading to the inhibition of IFN-β production. These findings reveal a novel mechanism that allows ARV to evade host antiviral immunity. IMPORTANCE ARV, the causative agent of viral arthritis or tenosynovitis in chickens, has a significant economic impact as it results in poor weight gain and increased feed conversion ratios. The MDA5-mediated IFN-β signal pathway plays an important role in host antiviral defense. Therefore, RNA viruses have developed mechanisms to counter this signaling pathway and successfully establish infection. However, the strategies adopted by ARV to block MDA5-IRF7 signaling remain unclear. In the current study, we demonstrated that ARV σA inhibits this pathway by binding to IRF7, which blocked IRF7 dimerization and nuclear translocation. Our findings may provide insights into how avian reovirus counteracts the innate antiviral immunity of the host to ensure viral replication.

Assessing the Impact of Antistress Pharmacologic Agents on Serological Status to Prevent Tenosynovitis in Chickens

Assessing the Impact of Antistress Pharmacologic Agents on Serological Status to Prevent Tenosynovitis in Chickens

Pathogenesis of experimental reovirus tenosynovitis in chickens: Influence of the route of infection

Four groups of specific pathogen-free, day-old chicks were infected experimentally with an avian arthrotropic reovirus strain R2 by four different routes: oral, subcutaneous, foot-pad and intra-articular. These groups were followed sequentially to study: pathological changes in the hock joints and liver; cloacal virus shedding and the presence of virus in hock joints; serological responses as determined by enzyme linked immunosorbent assay (ELISA), agar gel precipitation (AGP) and virus neutralization tests. All 4 infected groups developed arthritis or tenosynovitis with synovial hyperplasia and lymphocytic infiltration. Foot-pad and intra-articular routes of infection were found to advance the disease process by 2 to 3 weeks after infection and the more severe pathological responses seen after infection by these routes were associated with superficial degenerative changes in articular cartilage. Antibodies were detected at 2 to 3 weeks p.i. by all 3 methods, but there were no significant differences between the patterns of serological response in the infected groups. Injection into the foot-pad appears to be the most convenient and effective parenteral route of experimental infection.

Reovirus‐induced tenosynovitis in chickens: The effect of breed

The effect of breed of chicken on infection with an arthrotropic avian reovirus strain R2 was studied by oral or footpad inoculation of 1-day-old chicks of the following breeds: (1) specific pathogen-free (SPF) light-hybrid, (2) commercial White Leghorn egg-layer, and (3) commercial Ross I broiler, and observed to 12 weeks of age. Although most inoculated birds of all three breeds developed swelling of one or both legs below the hock joint at 3 to 4 weeks of age, gross lesions of tenosynovitis became progressively more severe and extended above the joints only in broilers, whereas in most orally-infected SPF and commercial light chickens gross lesions were intermittently severe and regressed with time. Cloacal virus shedding continued up to 2 weeks in the lighter breeds and 3 weeks after infection in broilers. From a small proportion of infected chickens, reovirus was also reisolated from heart, pancreas and caecal tonsils. In all breeds, the tissue in which virus persisted longest was the hock joint/tendon. There was a poor correlation between isolation of virus and the presence of gross lesions in chickens of 12 weeks of age, especially in broilers. Virus-neutralisation tests demonstrated that seroconversion in the lighter breeds occurred predominantly at 3 weeks and in broilers at 4 weeks after infection. In all three breeds the footpad infection gave significantly lower growth rates than were found in the control and oral-infection groups. Oral infection had no apparent effect on growth rates. The greater susceptibility of broilers to reovirus infection is discussed.

Reovirus‐induced tenosynovitis in chickens the influence of age at infection

Groups of specific pathogen-free (SPF) light hybrid chickens were infected with an arthrotropic reovirus at 1 day old, or at 2, 4, 6 or 9 weeks of age. In each group, approximately 20 were infected orally and 6 via the footpad. For each age group clinical signs of tenosynovitis, gross and microscopic lesions in the legs, virus excretion in the faeces, virus persistence in the joints, and precipitin response to reovirus were observed over a period of 9 weeks post infection (p.i.). For both routes of infection an age-limited susceptibility was shown, the most serious effects, both in numbers of affected birds and severity of gross lesions including tendon rupture, being seen in the youngest group. Gross lesions were rarely seen after oral infection of 6- and 9-week-old chickens. Footpad inoculation of virus had a more severe effect overall, and extended the age susceptibility, mild leg swellings being seen in some birds infected at 6 and 9 weeks of age. After oral infection, higher virus titres in the faeces and a more prolonged persistence in the gut and hock joint were recorded in chicks infected at 1 day old compared with the other age groups. Also, compared with the older groups, a delayed precipitin response was found in those infected at 1 day old. Footpad inoculation provoked earlier virus replication in the gut and a more rapid precipitin response.

Experimental infection of chickens with an adenovirus isolated from tenosynovitis, following infection with either (1) an arthrotropic reovirus, or (2) infectious bursal disease virus

In an attempt to show arthrotropic activity for an adenovirus isolated from tenosynovitis in chickens, but which did not cause tenosynovitis on its own, two dual infections were conducted. In the first, specific pathogen-free (SPF) chicks were infected with a tenosynovitis-inducing reovirus at 1-day-old, and the adenovirus was given 3 days later. In both cases viruses were administered orally or via the footpad. The adenovirus did not exacerbate reovirus-induced lesions of tenosynovitis. There was an indication that lesions regressed more rapidly in dually-infected chickens. Neither virus appeared to influence the persistence of the other in joints or the gut. In a second experiment, infectious bursal disease virus (IBDV) was inoculated onto the conjunctiva of 1-day-old SPF chicks and 6 days later they were infected with the adenovirus by either route. No tenosynovitis occurred, although preinfection with IBDV caused a more prolonged shedding of adenovirus, and in a greater proportion of the birds than those infected with adenovirus alone. In neither experiment did the dual infection cause the adenovirus to become pathogenic for the hock joints. It is considered that there is no evidence that adenoviruses are important agents of hock disorders in the chicken.

Experimental infection of chickens with adenoviruses isolated from tenosynovitis

Two adenoviruses isolated as the only viruses from the hock joints of chickens in outbreaks of tenosynovitis were tested for their ability to cause experimental tenosynovitis in chickens. It was previously shown that they were capable of growth in tendon organ cultures. One strain, designated 92, was used for infection of specific pathogen-free light hybrid chicks either in ovo at 17 days incubation or at 1-day-old orally or via the footpad. It was also used for infection of commercial broiler chicks at 1-day-old via the oral or footpad routes. The other virus, strain PS, was similarly used for infection of broiler chicks via the same routes. In none of the experiments did clinical signs or lesions of tenosynovitis develop other than transient inflammatory changes in the tissues and there was no evidence of prolonged virus persistence in hock joints. Of the tissues examined for virus, persistence was greatest in the gut.

Organ culture studies on adenoviruses isolated from Tenosynovitis in chickens

Five strains of adenovirus isolated from tenosynovitis in chickens were examined for their ability to grow in vitro in pieces of explanted tendon from 20-day-old chicken embryos from light or heavy breeds. Replicate tendon organ cultures (TOCs) were infected with three concentrations of each strain of virus and supernatant fluids were assayed for virus at intervals after infection up to 11 days. Two strains grew well in TOC, one moderately well, and the other two failed to grow. A strain of Newcastle disease virus (NDV), an agent not associated with tenosynovitis, also failed to grow. TOC from broiler embryos seemed slightly more susceptible to the two actively growing viruses than explants from a light breed. Growth of the adenovirus was demonstrated by immuno-fluorescence staining of sections of TOC but the appearance of stained antigen was dependent on virus titre. One of the strains which showed no activity in TOC grew in tracheal organ cultures (TrOC), as did one which multiplied in tendon, and NDV. In a more prolonged experiment, one of the viruses was found to persist in TOC at high titre for at least 37 days. The likelihood of the in vitro behaviour of these adenoviruses reflecting that occurring in vivo in tendon tissue of infected chickens is discussed.

TENOSYNOVITIS IN CHICKENS

An adenovirus was isolated from the tendon fluid of broilers and meat breeders with clinical tenosynovitis. The viral infection was in many cases accompanied by a staphylococcal infection. The significance of the adenovirus is not yet known, although initial transmission studies indicate that it may play a role in the tendon thickening process.