Avian Diseases最新文献

Hepatosplenitis or inclusion body disease is a fatal disease in owls caused by Columbid alphaherpesvirus 1 (CoHV-1). A few old case reports describe it worldwide. In Italy, knowledge regarding virus circulation and disease development is lacking. Four Eurasian eagle-owls (Bubo bubo), two adults and two juveniles, were submitted for postmortem examination showing aspecific clinical signs a few hours before death. Grossly disseminated petechial hemorrhages on serosal surfaces (n = 4), hepatic and splenic necrosis (n = 3), bilateral and symmetric necrosis of pharyngeal tonsils (n = 2), and diffuse and bilateral dark-red discoloration and firmness in lungs (n = 2) were seen. Tissues were sampled for histology, bacteriology, molecular testing, and transmission electron microscopy (TEM). On histology, disseminated petechial hemorrhages (n = 4) and necrosis of liver (n = 3) and spleen (n = 3) were seen, as well as lympho-histiocytic interstitial pneumonia and meningoencephalitis (n = 2). Intranuclear inclusion bodies (INIBs) were detected in one case. A panherpesviral PCR led to positive results in one case, identified in sequencing as CoHV-1. On TEM, intranuclear and intracytoplasmic virions with herpesviral morphology were seen in the same case. For the other three birds, the lack of PCR positivity, INIBs, and TEM detection could be linked to a possible reduction of the virus to undetectable levels. Death possibly occurred secondarily to bacterial infections, supposedly established during the acute phase of CoHV-1 infection. This paper reports the presence of CoHV-1in Italy and the development of a fatal form of the disease in a Eurasian eagle-owl.

Avian orthoreoviruses are causative agents of tenosynovitis and viral arthritis in both chickens and turkeys. Current commercial reovirus vaccines do not protect against disease caused by emerging variants. Custom-made inactivated reovirus vaccines are commonly utilized to help protect commercial poultry against disease. Antibody epitopes located on the viral attachment protein, σC, involved in virus neutralization, have not been clearly identified. In this study, the S1133 vaccine strain (Genetic Cluster 1 [GC1], a GC1 field isolate (117816), and a GC5 field isolate (94826) were determined to be genetically and serologically unrelated. In addition, chickens were vaccinated with either a commercial S1133 vaccine, 117816 GC1, or 94826 GC5, and sera were used in peptide microarrays to identify linear B-cell epitopes within the σC protein. Specific-pathogen-free (SPF) chickens were vaccinated twice with either: 1) live and live, 2) inactivated and inactivated, or 3) a combination of live and inactivated vaccines. Epitope mapping was performed on individual serum samples from birds in each group using S1133, 117816, and 94826 σC sequences translated into an overlapping peptides and spotted onto microarray chips. Vaccination with a combination of live and inactivated viruses resulted in a greater number of B-cell binding sites on the outer-capsid domains of σC for 117816 and 94826, but not for S1133. In contrast, the S1133-vaccinated birds demonstrated fewer epitopes, and those epitopes were located in the stalk region of the protein. However, within each of the vaccinated groups, the highest virus-neutralization titers were observed in the live/inactivated groups. This study demonstrates differences in antibody binding sites within σC between genetically and antigenically distinct reoviruses and provides initial antigenic characterization of avian orthoreoviruses and insight into the inability of vaccine-induced antibodies to provide adequate protection against variant reovirus-induced disease.

Avian reoviruses have sole or partial responsibility for a wide range of conditions that are of economic concern to the poultry industries in the United States. It is difficult, however, to determine the exact cost of reoviral-induced disease to this industry for several reasons. Avian reoviruses are ubiquitous in commercial poultry operations, but vary greatly in their ability to cause disease. Many reovirus isolates are not pathogenic, and this contributes to the difficulty in determining their role in production losses or whether they are merely coincidental findings of little or no importance. Results of infection with this virus can be difficult to measure in a commercial setting, aside from morbidity, mortality, or loss of finished product in a processing plant due to condemnation or trim. The fact that there is a relatively high morbidity rate, and at the same time a low mortality rate, makes it extremely difficult to accurately estimate the economic impact of infection with this virus. Variations in the pathogenicity of the virus, the extent of infection within a flock, the blending of progeny from different breeder source flocks into a broiler house, and the lack of separation of infected birds from uninfected birds at processing makes evaluation of economic variables, such as feed conversion and weight gain, very difficult to ascertain. The broiler and turkey industries have been surveyed on the importance of this virus in their respective operations and the results will be consolidated here to consider the economic impact to the poultry industries in the United States.

Reoviral-induced tenosynovitis/viral arthritis is an economically significant disease of poultry. Affected birds present with lameness, unilateral or bilateral swollen hock joints or shanks, and/or reluctance to move. In severe cases, rupture of the gastrocnemius or digital flexor tendons may occur, and significant culling may be necessary. Historically, vaccination with a combination of modified live and inactivated vaccines has successfully controlled disease. Proper vaccination reduced vertical transmission and provided maternal-derived antibodies to progeny to protect against disease, at an age when they were most susceptible. Starting in 2011-2012, an increased incidence of tenosynovitis/viral arthritis was observed in chickens and turkeys. In chickens, progeny from reovirus-vaccinated breeders were affected, suggesting commercial vaccines did not provide adequate protection against disease. In turkeys, clinical disease was primarily in males, although females can also be affected. The most significant signs were observed around 14-16 wks of age and include reluctance to move, lameness, and limping on one or both legs. The incidence of tenosynovitis/viral arthritis presently remains high. Reoviruses isolated from clinical cases are genetically and antigenically characterized as variants, meaning they are different from vaccine strains. Characterization of the field isolates reveals multiple new genotypes and serotypes that are significantly different from commercial vaccines and each other. In 2012, a single prevalent virus was isolated from a majority of the cases submitted to the Poultry Diagnostic and Research Center at the University of Georgia. Genetic characterization of the σC protein revealed the early isolates belonged to genetic cluster (GC) 5. Soon after the initial identification of the GC5 variant reovirus, many broiler companies incorporated these isolates from their farms into their autogenous vaccines and continue to do so today. The incidence of GC5 field isolates has decreased significantly, likely because of the widespread use of the isolates in autogenous vaccines. Unfortunately, variant reoviruses belonging to multiple GCs have emerged, despite inclusion of these isolates in autogenous vaccines. In this review, an overview of nomenclature, sample collection, and diagnostic testing will be covered, and a summary of variant reoviruses isolated from clinical cases of tenosynovitis/viral arthritis over the past 10 yrs will be provided.

Prevention of tenosynovitis/viral arthritis caused by variant avian reoviruses within commercial broiler production has become increasingly more challenging because of the lack of protection afforded by the current commercially available vaccines. Avian reoviruses isolated from clinical cases of tenosynovitis/viral arthritis in recent years are antigenically distinct from nearly all of the commercially licensed modified live and inactivated biologics available in the United States. The emergence of new variants is likely shaped by a lack of homologous protection coupled with selection pressure influences and results in antigenically diverse populations of avian reoviruses. One tool available to the poultry industry is the use of autogenous (custom) vaccines. Although these can be effective, isolation, characterization, and screening of isolates from clinical cases is paramount for the selection of isolates to include in these vaccines. With no treatment options, control can only be attained via prevention of infection. To achieve this goal, commercially licensed products with antigenic applicability and broadly cross-protective vaccine strains are needed.

The success of treatments for, or prophylaxis of, coccidiosis with classical anticoccidial feed additives or alternative treatments can be measured with a variety of metrics. Three important metrics are body weight or body weight gain (BW or BWG), lesion scores (LS), and oocyst shedding (OS). A meta-analysis of floor-pen experiments was performed to determine if using LS and OS would lead to systematically different assessments compared to the use of BW at the end of the experiment, and to what degree changes in LS and OS are correlated with BW. We also investigated if there were days postinfection on which one could expect larger ratios between untreated control groups and treated groups for LS and OS as an aid to selecting sampling days. A total of 38 experiments from 37 articles in peer-reviewed journals were included. Data sets containing experiments that investigated LS or OS in addition to BW or BWG to assess anticoccidial feed additives or alternative treatment were tested for the effectiveness of the intervention either by univariate meta-analyses for each metric or by robust variance estimation multivariate meta-analysis combining BW with LS or BW with OS. The results did not show evidence that the inclusion of LS and OS in experimental designs to assess the effect of conventional and alternative feed additives with assumed anticoccidial activity systematically changed the conclusions drawn from an experiment, but there was no significant correlation between the LS and OS ratios of untreated and treated groups determined during the experiments with the ratios of the BW at the end of the experiment for each experiment. There was also no discernible relationship between LS or OS ratios and days postinfection.

Dietary, environmental, and hereditary causes were reported as causative agents of angel wing syndrome in waterfowl. Since 2017, several Muscovy duck flocks at Behira governorate were found to exhibit this syndrome associated with the clinical symptoms of goose parvovirus (GPV) infection. Four strains of goose parvovirus named HS1-HS4 were isolated and identified from diseased ducks at some of these flocks. Phylogenetic analysis revealed clustering of these strains together and within a distinct monophyletic group in relation to GPV strains of Derzsy's disease and short beak and dwarfism syndrome (SBDS). Nucleotide identities with goose parvovirus strain B of Derzsy's disease were 95.7%-96.6%, and with the strain JS1603 of SBDS they were 96.8%-97.4%. However, nucleotide identities with Muscovy duck parvovirus strain FM were 74.1%-74.6%. The disease was reproduced experimentally via oral-route artificial infection with HS1 strain, and both clinical symptoms of goose parvovirus and angel wing syndrome were observed in the artificially infected Muscovy ducks, but with less severity in geese. This study demonstrated clear evidence for induction of angel wing syndrome, at least partially, with GPV infection in Muscovy duck. To the authors' knowledge, this is the first work to mention a viral cause of angel wing syndrome in waterfowl.