Differential Viral Genome Diversity of Healthy and RSS-Affected Broiler Flocks.

The intestinal virus community contributes to health and disease. Runting and stunting syndrome (RSS) is associated with enteric viruses and leads to economic losses in the poultry industry. However, many viruses that potentially cause this syndrome have also been identified in healthy animals. To determine the difference in the virome of healthy and diseased broilers, samples from 11 healthy and 17 affected broiler flocks were collected at two time points and analyzed by Next-Generation Sequencing. Virus genomes of Parvoviridae, Astroviridae, Picornaviridae, Caliciviridae, Reoviridae, Adenoviridae, Coronaviridae, and Smacoviridae were identified at various days of poultry production. De novo sequence analysis revealed 288 full or partial avian virus genomes, of which 97 belonged to the novel genus Chaphamaparvovirus. This study expands the knowledge of the diversity of enteric viruses in healthy and RSS-affected broiler flocks and questions the association of some viruses with the diseases.

Investigation of avian rotavirus infections in broiler chicks from commercial flocks with different performance efficiency indexes.

The aim of this study was to investigate and compare the frequency of occurrence of avian rotavirus (AvRV) in poultry flocks according to its Performance Efficiency Index (PEI) scores. A total of 256 individual intestinal content samples of small sized-chicks (runts) with clinical signs of Runting Stunting Syndrome (RSS) and 24 clinically healthy chicks (control) were collected from twelve flocks in southern Brazil with different PEI scores: good (n = 4, PEI mean = 365); moderate (n = 4, PEI mean = 342) or poor (n = 4, PEI mean = 319). Silver-stained polyacrylamide gel electrophoresis (ss-PAGE) was used to detect and identify the AvRV species followed by RT-PCR and sequencing of the partial VP6 gene for species confirmation. AvRV was detected in 83% (10/12) of the flocks and 23.4% (60/256) of the chicks. The electrophoretic migration patterns of viral dsRNA segments were compatible with AvRV species A (AvRV- A), D (AvRV-D) and F (AvRV-F) in 9 (15%), 18 (30%), and 33 (55%) of the positive chicks fecal samples, respectively. The AvRV species identified by ss-PAGE were confirmed by RT-PCR and partial sequence analysis of the VP6 gene. The AvRV detection rate was statistically higher (p = 0.007) in chicks from flocks with poor PEI when compared to those with good PEI. The occurrence of AvRV-D and AvRV-F was statistically higher in 7 to 9 days old chicks, while AvRV-A was detected only in 13 to 14 days old animals.

Runting Stunting Syndrome in Broiler Chickens Is Associated with Altered Intestinal Stem Cell Morphology and Gene Expression.

Runting stunting syndrome (RSS) in broiler chickens is characterized by altered intestinal morphology and gene expression and stunted growth. The objective of this study was to conduct a retrospective study of gene expression in stem and differentiated cells in the small intestine of RSS chicks. Two different models of RSS were analyzed: broiler chicks that were experimentally infected and broiler chicks that were naturally infected. Experimentally infected chicks were exposed to litter from infected flocks (RSS-litter chicks) or infected with astrovirus (RSS-astrovirus chicks). Intestinal samples from naturally infected chicks showing clinical signs of RSS were acquired from commercial farms in Georgia and were brought into a poultry diagnostic lab (RSS-clinical-GA) and from farms in Brazil that had a history of RSS (RSS-clinical-BR). The RSS-clinical-BR chicks were separated into those that were positive or negative for gallivirus based on DNA sequencing. Intestinal morphology and intestinal cell type were identified in archived formalin-fixed, paraffin-embedded tissues. In situ hybridization for cell-specific mRNA was used to identify intestinal stem cells expressing olfactomedin 4 (Olfm4), proliferating cells expressing Ki67, absorptive cells expressing sodium glucose cotransporter 1 (SGLT1) and peptide transporter 1 (PepT1), and goblet cells expressing mucin 2 (Muc2). RSS-litter and RSS-clinical-GA chicks showed 4% to 7.5% cystic crypts, while gallivirus-positive RSS-clinical-BR chicks showed 11.7% cystic crypts. RSS-astrovirus and gallivirus-negative RSS-clinical-BR chicks showed few cystic crypts. RSS-litter and gallivirus-positive RSS-clinical-BR chicks showed an increase in crypt depth compared to control or gallivirus-negative chicks, respectively. There was no expression of Olfm4 mRNA in the stem cells of RSS-litter and RSS-clinical-GA chicks, in contrast to the normal expression of Olfm4 mRNA in RSS-astrovirus and RSS-clinical-BR chicks. All chicks regardless of infection status showed normal expression of Ki67 mRNA in crypt cells, Muc2 mRNA in goblet cells, and SGLT1 or PepT1 mRNA in enterocytes. These results demonstrate that RSS, which can be induced by different etiologies, can show differences in the expression of the stem cell marker Olfm4.

El síndrome del enanismo infeccioso en pollos de engorde se asocia con alteración de la morfología de las células madre intestinales y la expresión de genes. El síndrome del enanismo infeccioso (con las siglas en inglés RSS) en pollos de engorde se caracteriza por alteraciones en la morfología intestinal y en la expresión de genes, además de retraso en el crecimiento. El objetivo de este estudio fue realizar un estudio retrospectivo de la expresión genética en células madre y células diferenciadas en el intestino delgado de pollitos con el síndrome del enanismo infeccioso. Se analizaron dos modelos diferentes del síndrome del enanismo infeccioso: en pollos de engorde que fueron infectados experimentalmente y en pollos de engorde infectados naturalmente. Los pollitos infectados experimentalmente se expusieron a la cama de parvadas infectadas (RSS-litter chicks), o infectados con astrovirus (RSS-astrovirus chicks). Se adquirieron muestras intestinales de pollitos infectados naturalmente que mostraban signos clínicos del síndrome del enanismo infeccioso de granjas comerciales en Georgia y se llevaron a un laboratorio de diagnóstico avícola (RSS-Clinical-GA) y de granjas en Brasil que tenían antecedentes del síndrome del enanismo infeccioso (RSS-Clinical-BR). Los pollitos de granjas de Brasil (RSS-Clinical-BR) se separaron en aquellos que fueron positivos o negativos para gallivirus de acuerdo con la secuenciación del ADN. Se identificaron la morfología intestinal y el tipo de células intestinales en tejidos archivados fijados con formalina e incluidos en parafina. La hibridación in situ para ARNm específico de células se utilizó para identificar células madre intestinales que expresan olfactomedina 4 (Olfm4), células en proliferación que expresaban Ki67, células absorbentes que expresan el cotransportador 1 de glucosa y sodio (SGLT1) y el transportador de péptidos 1 (PepT1), y células caliciformes que expresan mucina 2 (Muc2). Los pollos expuestos a cama infectada (RSS-litter) y los infectados naturalmente de Georgia (RSS-clinical-GA) mostraron entre un 4% y un 7.5% de criptas quísticas, mientras que los pollos infectados de granjas de Brasil (RSS-clinical-BR) que eran positivos para gallivirus mostraron un 11.7% de criptas quísticas. Los pollos infectados con astrovirus (RSS-astrovirus chicks) y los pollos de Brasil (RSS-clinical-BR) que eran negativos para gallivirus mostraron pocas criptas quísticas. Los pollos expuestos a cama infectada (RSS-litter chicks) y los pollos infectados de Brasil (RSS-clinical-BR) que eran positivos para gallivirus mostraron un aumento en la profundidad de las criptas en comparación con los pollos control o negativos para el gallivirus, respectivamente. No se observó expresión de ARNm de Olfm4 en las células madre de pollitos expuestos a cama infectada (RSS-litter chicks) ni en pollos infectados de Georgia (RSS-clinical-GA), en contraste con la expresión normal de ARNm de Olfm4 en pollitos infectados con astrovirus (RSS-astrovirus chicks) y en pollitos infectados de Brasil (RSS-clinical-BR). Todos los pollos, independientemente del estado de infección, mostraron una expresión normal de ARNm para Ki67 en las células de la cripta, de ARNm para Muc2 en las células caliciformes y ARNm de SGLT1 o PepT1 en los enterocitos. Estos resultados demuestran que el síndrome del enanismo infeccioso, que puede ser inducido por diferentes etiologías, puede mostrar diferencias en la expresión del marcador para células madre Olfm4.

Molecular Biology and Pathological Process of an Infectious Bronchitis Virus with Enteric Tropism in Commercial Broilers.

Infectious bronchitis virus (IBV) induces respiratory and urogenital disease in chickens. Although IBV replicates in the gastrointestinal tract, enteric lesions are uncommon. We have reported a case of runting-stunting syndrome in commercial broilers from which an IBV variant was isolated from the intestines. The isolate, CalEnt, demonstrated an enteric tissue tropism in chicken embryos and SPF chickens experimentally. Here, we determined the full genome of CalEnt and compared it to other IBV strains, in addition to comparing the pathobiology of CalEnt and M41 in commercial broilers. Despite the high whole-genome identity to other IBV strains, CalEnt is rather unique in its nucleotide composition. The S gene phylogenetic analyses showed great similarity between CalEnt and Cal 99. Clinically, vent staining was slightly more frequent in CalEnt-infected birds than those challenged with M41. Furthermore, IBV IHC detection was more evident and the viral shedding in feces was overall higher with the CalEnt challenge compared with M41. Despite underlying intestinal lesions caused by coccidiosis and salmonellosis vaccination, microscopic lesions in CalEnt-infected chickens were more severe than in M41-infected chickens or controls, supporting the enteric tropism of CalEnt. Further studies in SPF chickens are needed to determine the pathogenesis of the virus, its molecular mechanisms for the enteric tropism, and its influence in intestinal health.

Emerging new avian reovirus variants from cases of enteric disorders and arthritis/tenosynovitis in Brazilian poultry flocks.

1. The objective of this study was to characterise circulating Brazilian avian reovirus (ARV) strains by genetic analysis of the σC protein encoded by segment 1 of the viral genome and compare these with those of viral strains used for immunising commercial poultry.2. The analysis detected the presence of ARV genomes by quantitative reverse transcriptase PCR (RT-qPCR) in the enteric samples and the joint tissues (JT) of birds with signs of viral arthritis/tenosynovitis. Nucleotide sequencing used 16 strains (three commercial vaccines, 10 from enteric tissues and three from JT). The results indicated high variability in the amino acid sequences of 13 wild strains, showing between 40% and 75% similarity compared with the vaccine strains (S1133 and 2177).3. The sequences were grouped into three well-defined clusters in a phylogenetic tree, two of these clusters together with previous Brazilian σC ARV sequences, and one cluster (VII) that was novel for Brazilian strains. Antigenic analysis showed that there were amino acids within putative epitopes located on the surface of the receptor-binding region of the σC protein with a high degree of variability.4. The study confirmed the presence of ARV genetic variants circulating in commercial birds in Brazil, and according to the antigenic prediction, the possibility of antigenic variants appears to be high.

Chicken Astrovirus (CAstV) Molecular Studies Reveal Evidence of Multiple Past Recombination Events in Sequences Originated from Clinical Samples of White Chick Syndrome (WCS) in Western Canada.

In this study, we aimed to molecularly characterize 14 whole genome sequences of chicken astrovirus (CAstV) isolated from samples obtained from white chick syndrome (WCS) outbreaks in Western Canada during the period of 2014-2019. Genome sequence comparisons showed all these sequences correspond to the novel Biv group from which no confirmed representatives were published in GenBank. Molecular recombination analyses using recombination detection software (i.e., RDP5 and SimPlot) and phylogenetic analyses suggest multiple past recombination events in open reading frame (ORF)1a, ORF1b, and ORF2. Our findings suggest that recombination events and the accumulation of point mutations may have contributed to the substantial genetic variation observed in CAstV and evidenced by the current seven antigenic sub-clusters hitherto described. This is the first paper that describes recombination events in CAstV following analysis of complete CAstV sequences originated in Canada.

Viral metagenomic analysis of chickens with runting-stunting syndrome in the Republic of Korea.

BACKGROUND AND AIMS: Runting-stunting syndrome (RSS) in chickens, also known as malabsorption syndrome, which is characterized by mild to severe enteritis and diagnosed through typical histopathologic examination as well as clinical signs, results in considerable economic losses. Despite the many studies carried out over decades to determine the etiologic agents of RSS involved in the disease, several outbreaks remained without the elucidation of, potentially multiple, etiologies involved. METHODS: We performed comparative analysis of viral metagenomes from four chicken flocks affected with RSS using next-generation sequencing. Primers for the detection of chicken enteric viruses were designed from the sequencing data obtained with metagenomics. Multiplex reverse transcription-polymerase chain reaction (PCR) and PCR were performed to detect a variety of etiological agents previously described in natural cases of RSS. RESULTS: The most abundant viral families identified in this study were Astroviridae, Picornaviridae, Parvoviridae, Caliciviridae, Reoviridae and Picobirnaviridae. Chicken astrovirus sequences were present in all four samples, suggesting an association between chicken astrovirus and RSS and chicken astrovirus as a candidate pathogen responsible for RSS. Picobirnavirus and the newly identified chapparvovirus were found in chickens in the Republic of Korea for the first time, and the genetic diversity of enteric viruses and viral communities was showed. CONCLUSIONS: Chicken astrovirus was consistently detected in broilers affected with RSS and the result of this study may contribute to knowledge of enteric diseases and viruses in chickens.

Intestinal Tropism of an Infectious Bronchitis Virus Isolate Not Explained by Spike Protein Binding Specificity.

An infectious bronchitis virus (IBV) with an unusual enteric tropism (CalEnt) was isolated from a California broiler flock exhibiting runting-stunting syndrome. IBV was detected in the small intestine, but not in the respiratory tract or kidney. During virus isolation in embryos, it did not replicate in chorioallantoic membrane (CAM) but could be recovered from intestines. Its S1 protein showed 93% amino acid sequence identity to a California variant isolated in 1999 (Cal99). Intestinal lesions were reproduced following ocular/nasal inoculation of specific-pathogen-free chickens, but respiratory signs and lesions were also present. The virus was detected in both respiratory and intestinal tissues. To determine whether the novel tropism of IBV CalEnt was due to an increased ability of its S1 protein to bind to the intestinal epithelium, we compared the binding of soluble trimeric recombinant S1 proteins derived from CalEnt and Cal99 to chicken tissues. Contrary to expectations, the CalEnt S1 protein did not bind to small intestine and, unlike Cal99 S1, did not bind to the respiratory epithelium or CAM. Using only the CalEnt S1 N-terminal domain or including the S2 ectodomain (lacking membrane and cytoplasmic domains), which have been shown to improve ArkDPI S1 protein binding, did not lead to detectable binding at the standard protein concentration to any tissue tested. Our results indicate no/poor binding of the CalEnt spike protein to both respiratory and intestinal tissues and thus do not support better attachment to intestinal epithelial cells as a reason for CalEnt's extended tropism. These results might reflect shortcomings of the assay, including that it does not detect potential contributions of the S1 C-terminal domain to attachment. We used bioinformatic approaches to explore the possibility that the unique tropism of CalEnt might be a result of functions of the S protein in cell-entry steps subsequent to attachment. These analyses suggest that CalEnt's S2 coding region was acquired through a recombination event and encodes a unique amino acid sequence at the putative recognition site for the protease that activates the S protein for fusion. Thus, S2 activation by tissue-specific proteases might facilitate CalEnt entry into intestinal epithelial cells and compensate for poor binding by its S1 protein.

Tropismo intestinal de un aislamiento del virus de la bronquitis infecciosa con una especificidad de unión a la proteína espícula inusual. Se aisló un virus de la bronquitis infecciosa (IBV) con un tropismo entérico inusual (CalEnt) de una parvada de pollos de engorde de California que presentaba síndrome de retraso en el crecimiento. Se detectó al virus de bronquitis en el intestino delgado, pero no en el tracto respiratorio o en el riñón. Durante el aislamiento del virus en huevos embrionados de pollo, no se replicó en la membrana corioalantoidea (CAM), pero pudo recuperarse de los intestinos. Su proteína S1 mostró una identidad de secuencia de aminoácidos del 93% con una variante de California aislada en el año 1999 (Cal99). Las lesiones intestinales se reprodujeron después de la inoculación ocular/nasal de pollos libres de patógenos específicos, pero también hubo signos y lesiones respiratorias. El virus se detectó en los tejidos respiratorios e intestinales. Para determinar si el nuevo tropismo de este virus de la bronquitis infecciosa CalEnt se ocasionaba por una mayor capacidad de su proteína S1 para unirse al epitelio intestinal, se comparó la unión a los tejidos de pollo de las proteínas S1 recombinantes triméricas solubles derivadas de los virus CalEnt y Cal99. Contrariamente a lo esperado, la proteína CalEnt S1 no se unió al intestino delgado y a diferencia del virus Cal99 S1, no se unió al epitelio respiratorio o CAM. Mediante el uso de solo el dominio N-terminal de la proteína S1 del virus CalEnt o por la inclusión del ectodominio S2 (que carece de dominios de membrana y citoplasmáticos), que se ha demostrado mejora la unión de la proteína S1 del serotipo Arkansas DPI, no se observó una unión detectable a ningún tejido analizado a la concentración de proteína estándar. Estos resultados indican una unión nula o deficiente de la proteína de la espícula del virus CalEnt a los tejidos respiratorios e intestinales y por lo tanto, no respaldan la preferencia de la unión a las células epiteliales intestinales como una razón para el tropismo extendido del virus CalEnt. Estos resultados pueden reflejar las deficiencias del ensayo, incluyendo el hecho de que no detecta posibles contribuciones del dominio C-terminal de la proteína S1 en la unión. Se utilizaron enfoques bioinformáticos para explorar la posibilidad de que el tropismo único del virus CalEnt podría ser el resultado de las funciones de la proteína S en los pasos de entrada a las células posteriores a la unión. Estos análisis sugieren que la región de codificación S2 del virus CalEnt se adquirió a través de un evento de recombinación y codifica una secuencia de aminoácidos única en el supuesto sitio de reconocimiento de la proteasa que activa la proteína S para la fusión. Por lo tanto, la activación de S2 por proteasas específicas de tejido podría facilitar la entrada del virus CalEnt en las células epiteliales intestinales y compensar la unión deficiente por su proteína S1.

Avian parvovirus: classification, phylogeny, pathogenesis and diagnosis.

Poultry parvoviruses identified during the early 1980s are found worldwide in intestines from young birds with enteric disease syndromes as well as healthy birds. The chicken parvovirus (ChPV) and turkey parvovirus (TuPV) belong to the Aveparvovirus genus within the subfamily Parvovirinae. Poultry parvoviruses are small, non-enveloped, single-stranded DNA viruses consisting of three open reading frames, the first two encoding the non-structural protein (NS) and nuclear phosphoprotein (NP) and the third encoding the viral capsid proteins 1 (VP1 and VP2). In contrast to other parvoviruses, the VP1-unique region does not contain the phospholipase A2 sequence motif. Recent experimental studies suggested the parvoviruses to be the candidate pathogens in cases of enteric disease syndrome. Current diagnostic methods for poultry parvovirus detection include PCR, real-time PCR, enzyme linked immunosorbent assay using recombinant VP2 or VP1 capsid proteins. Moreover, sequence-independent amplification techniques combined with next-generation sequencing platforms have allowed rapid and simultaneous detection of the parvovirus from affected and healthy birds. There is no commercial vaccine; hence, the development of an effective vaccine to control the spread of infection should be of primary importance. This review presents the current knowledge on poultry parvoviruses with emphasis on taxonomy, phylogenetic relationship, genomic analysis, epidemiology, pathogenesis and diagnostic methods.

Chicken astrovirus as an aetiological agent of runting-stunting syndrome in broiler chickens.

Despite descriptions of runting-stunting syndrome (RSS) in broiler chickens dating back over 40 years, the aetiology has not yet been described. A novel chicken astrovirus (CkAstV) was isolated in an LMH liver cell line from the intestines of chickens affected with RSS. Clinical RSS is characterized by retarded growth and cystic crypt lesions in the small intestine. In 1-day-old broiler chickens infected with the CkAstV isolate, virus was only detected in the intestinal epithelial cells during the first few days after infection. Notably, the preferred host cells are the crypt epithelial cells following initial replication in the villous epithelial cells, thus implying viral preference for immature intestinal cells. Nevertheless, the CkAstV isolate did not induce remarkable pathological changes, despite the presence of the virus in situ. Serial chicken-to-chicken passages of the virus induced increased virulence, as displayed by decreased weight gain and the presence of cystic lesions in the small intestine reproducing clinical RSS in chickens. The analysis of the full-length genome sequences from the isolated CkAstV and the CkAstV from the bird-to-bird passages showed >99 % similarity. The data obtained in this study suggest that the CkAstV isolate is capable of inducing RSS following serial bird-to-bird passages in broilers and is as an aetiological agent of the disease.

Chicken parvovirus viral loads in cloacal swabs from malabsorption syndrome-affected and healthy broilers.

Chicken parvovirus (ChPV) has been associated with malabsorption syndrome (MAS) in broilers. However, the participation of this virus in such syndrome is unclear, since it may be detected in diseased and healthy chickens. In the course of these studies, it was argued whether ChPV genome loads might be correlated to the occurrence of MAS. To check such a hypothesis, a SYBR green-based quantitative polymerase chain reaction was developed to detect and quantify ChPV genomes. Cloacal swabs from 68 broilers with MAS and 59 from healthy animals were collected from different poultry farms. Genomes of ChPV were detected in all samples, regardless of their health status. However, viral genome loads in MAS-affected broilers were significantly higher (1 × 105 genome copies per 100 ng DNA) than in healthy animals (1.3 × 103 GC/100 ng DNA). These findings indicate that there is an association between high ChPV genome loads and the occurrence of MAS in broilers.

Chicken parvovirus and its associations with malabsorption syndrome.

Malabsorption syndrome (MAS) is a multifactorial syndrome which is characterized by enteric disorders and reduced growth rates of broilers. Such condition is responsible for significant economic losses to the poultry industry. A possible association between chicken parvovirus (ChPV) infections and the occurrence of MAS has been proposed. However, such association has not to date been elucidated in view that ChPV has been detected in healthy as well as in MAS-affected chickens. This study aimed to detect and quantify ChPV loads in sera and tissues of MAS-affected, as well as in healthy broilers. Fifty nine, 39-day-old broilers (50 diseased, 9 healthy birds), obtained from the same flocks, were examined. The highest ChPV DNA loads were detected in MAS-affected broilers, particularly in fecal samples and intestinal tissues (~5500 genomic copies/300ng of total DNA). The average viral genome load in serum in MAS-affected birds was 1134copies/mL, whereas no viral DNA was found in sera and thymus tissues from healthy animals. These findings reveal that MAS-affected broilers consistently carry ChPV DNA is serum, whereas healthy animals do not. In addition, viral loads in tissues (bursa of Fabricius, spleen, intestine and liver) of MAS-affected birds were significantly higher in comparison to the same tissues from healthy broilers. Although preliminary, the results obtained here indicate an association between the detection of ChPV DNA in serum, in addition to high ChPV viral loads in tissues, and the occurrence of MAS in broilers. Further experiments should be performed to confirm such results.

Detection of enteric viruses in pancreas and spleen of broilers with runting-stunting syndrome (RSS) / Detecção de vírus entéricos em pâncreas e baço de frangos com a síndrome de nanismo e raquitismo (RSS)

Enteric disease is a multifactorial problem in chickens, which causes gastrointestinal alterations, elevated feed conversions and impairment. In the last years, several enteric viruses were implicated in enteric disease; case reports have shown their presence alone or in concomitant infections during outbreaks and have suggested that they might be determining factors in the aetiology of enteric disease. This study shows high detection rates of enteric viruses in the pancreas and spleen in samples from an outbreak of enteritis and malabsorption in 16 chicken flocks (n=80 broilers). Avian nephritis virus (ANV) was the most ubiquitous virus, present in 75% of the flocks followed by avian rotavirus group A (ART-A) with 68.75%, and by chicken astrovirus (CAstV) and chicken parvovirus (ChPV) in 43.75% of samples. Viruses were present in the pancreas of positive flocks at extremely high rates: 100% for ART-A, 91.7% for ANV, 100% for CAstV and 57.14% for ChPV. By contrast, only 16.7% and 57.14% of intestine samples were positive for ANV and CAstV, respectively. Avian reovirus (AReo) and avian adenovirus group 1 (FAdV-1) were not detected. These results suggest that high viral detection rates in pancreas samples may be a result of viremia during enteric disease, with subsequent damage of the exocrine pancreas, leading to runting-stunting syndrome (RSS).(AU)

A doença entérica é um problema multifatorial em galinhas que causa alterações gastrointestinais, conversão alimentar elevada e deficiência de crescimento. Nos últimos anos, os vírus entéricos foram associados à doença entérica; casos reportados mostraram a infecção de um único vírus e também infecções concomitantes durante os surtos sugerindo a presença de múltiplos fatores etiológicos nas doenças entéricas. Este estudo mostra uma alta taxa de detecção dos vírus entéricos em amostras de pâncreas e baço de um surto de enterite e má-absorção em 16 lotes de frangos (n=80 frangos). O vírus de nefrite aviária (ANV) foi o vírus mais detectado, estando presente em 75% dos lotes seguido pelo rotavírus aviário grupo A (ART-A) em 68,75% dos casos, e pelo astrovirus (CAstV) e parvovírus aviários (ChPV), ambos em 43,75% das amostras. Os vírus estavam presentes no pâncreas dos lotes positivos em percentuais elevados: 100% para ART-A e CAstV; 91,7% para ANV, e em 57,14% para ChPV. Em contraste, somente 16,7% e 57,14%, em amostras de intestino, foram positivos para ANV e CAstV, respectivamente. Reovírus aviário (AReo) e o adenovírus do grupo 1 (FAdV-1) não foram detectados. Estes resultados sugerem que os elevados percentuais de vírus detectados em amostras de pâncreas podem estar associados à viremia durante a doença entérica, com subsequente lesão no pâncreas exócrino das aves levando ao desenvolvimento da síndrome de nanismo e raquitismo.(AU)

A metagenomic comparison of endemic viruses from broiler chickens with runting-stunting syndrome and from normal birds.

Runting-stunting syndrome (RSS) in broiler chickens is an enteric disease that causes significant economic losses to poultry producers worldwide due to elevated feed conversion ratios, decreased body weight during growth, and excessive culling. Of specific interest are the viral agents associated with RSS which have been difficult to fully characterize to date. Past research into the aetiology of RSS has implicated a wide variety of RNA and DNA viruses however, to date, no individual virus has been identified as the main agent of RSS and the current opinion is that it may be caused by a community of viruses, collectively known as the virome. This paper attempts to characterize the viral pathogens associated with 2-3-week-old RSS-affected and unaffected broiler chickens using next-generation sequencing and comparative metagenomics. Analysis of the viromes identified a total of 20 DNA and RNA viral families, along with 2 unidentified categories, comprised of 31 distinct viral genera and 7 unclassified genera. The most abundant viral families identified in this study were the Astroviridae, Caliciviridae, Picornaviridae, Parvoviridae, Coronaviridae, Siphoviridae, and Myoviridae. This study has identified historically significant viruses associated with the disease such as chicken astrovirus, avian nephritis virus, chicken parvovirus, and chicken calicivirus along with relatively novel viruses such as chicken megrivirus and sicinivirus 1 and will help expand the knowledge related to enteric disease in broiler chickens, provide insights into the viral constituents of a healthy avian gut, and identify a variety of enteric viruses and viral communities appropriate for further study.

An unusual case of concomitant infection with chicken astrovirus and group A avian rotavirus in broilers with a history of severe clinical signs.

A molecular study of intestinal samples from 21 broiler flocks with a history of enteritis revealed that 23.8% and 14.3% were positive for chicken astrovirus (CAstV) and avian rotavirus (ARV), respectively. CAstV and group A ARV were simultaneously detected in only one broiler flock. Birds in this group developed the significant intestinal lesions characterized by frothy contents, paleness, and thin intestinal walls. In this report we present an unusual case of runting stunting syndrome (RSS) with a history of high mortality and growth retardation in broiler chickens. We also make the first identification of CAstV and group A ARV in broiler chickens in Korea.

An unusual case of concomitant infection with chicken astrovirus and group A avian rotavirus in broilers with a history of severe clinical signs

A molecular study of intestinal samples from 21 broiler flocks with a history of enteritis revealed that 23.8% and 14.3% were positive for chicken astrovirus (CAstV) and avian rotavirus (ARV), respectively. CAstV and group A ARV were simultaneously detected in only one broiler flock. Birds in this group developed the significant intestinal lesions characterized by frothy contents, paleness, and thin intestinal walls. In this report we present an unusual case of runting stunting syndrome (RSS) with a history of high mortality and growth retardation in broiler chickens. We also make the first identification of CAstV and group A ARV in broiler chickens in Korea.