Chicken astrovirus (CAstV) was recently indicated as the factor of the "white chicks" condition associated not only with increased embryo/chick mortality but also with weakness and white plumage of hatched chicks. In February 2014, organ samples (livers and kidneys) from dead-in-shell embryos, as well as 1-day-old whitish and normal chicks, were delivered from one hatchery in Poland for disease diagnosis. The samples originated from the same 30-week-old breeder flock in which the only observed abnormal signs were 4-5% decrease in the number of hatched chickens and the presence (about 1%) of weaker chicks with characteristic whitish plumage among normal ones. CAstV was detected in submitted samples and was then isolated in 10-day-old embryonated specific pathogen free (SPF) chicken eggs. We also reproduced an infection model for the "white chicks" condition in SPF layer chickens using the isolated PL/G059/2014 strain as the infectious agent. Results of experimental reproduction of the "white chicks" condition were somewhat more serious than field observation. The administration of the CAstV material into the yolk sac of 8-day-old SPF chicken eggs caused delay and prolongation of hatching, as well as death of embryos/chicks, and also a change of plumage pigmentation. Only two chicks of a total of 10 inoculated SPF eggs survived and were observed for 2 months. A gradual elimination of the CAstV genome was noted in this period. Moreover, a few contact-naive SPF chicks, which had been placed in the same cage, were infected with CAstV. Molecular characterization of detected CAstV was performed by nucleotide sequencing of the full ORF2 region encoding the capsid precursor protein gene. Phylogenetic studies showed that the PL/G059/2014 isolate clustered in the subgroup Aiii of CAstV. In the light of the new classification rules, the Polish PL/G059/2014 CAstV isolate could be assigned to a new species of the Avastrovirus genus.
Variants assigned to GI-23 lineage of infectious bronchitis virus (IBV), formerly called Var2, have circulated for nearly 20 years only in countries of the Middle East. Strains of this lineage were first identified in Israel in 1998. More severe form of the virus appeared in 2006, when the second wave of Var2 epidemic has spread over the Middle East region. The present study describes the detection and detailed genetic characterization of the GI-23 viruses in Poland. The full-length genome of gammaCoV/Ck/Poland/G052/2016 strain consists of 27596 nucleotides and has typical organization for IBV (UTR5'-POl-S-3a-3b-E-M-4b-4c-5a-5b-N-UTR3'). The phylogenetic analysis of the complete sequence showed that it formed separate branch distinct from all of the full-length genome sequences analyzed in this study. Recombination analyses with other gammacoronaviruses revealed that Polish GI-23 strain may originate from recombination events and potential donors of build-in sequences are IBV of GI-1, GI-13 and G-19 lineages (Mass-, 793B- and QX-like strains, respectively). The 1a, 1b and N genes were involved in these recombination events. The source of virus introduction to the chicken population in Poland is unknown.
In April/May 2013, four outbreaks of avian influenza virus (AIV) infections caused by H9N2 subtype were diagnosed in Poland in fattening turkey flocks exhibiting a drop in feed and water intake, depression, respiratory signs and mortality. The subsequent serological survey carried out on samples collected between June 2012 and September 2013 from 92 poultry flocks detected positive sera in two additional meat turkey flocks located in the same province. The analysis of amino acids in the haemagglutinin and neuraminidase glycoproteins revealed that the detected H9N2 viruses possessed molecular profiles suggestive of low pathogenicity, avian-like SAα2,3 receptor specificity and adaptation to domestic poultry. Phylogenetic studies showed that these H9N2 AIVs grouped within the Eurasian clade of wild bird-origin AIVs and had no relationship with H9N2 AIV circulating in poultry in the Middle East and Far East Asia over the past decade. Experimentally infected SPF chickens with the index-case H9N2 virus remained healthy throughout the experiment. On the other hand, ten 3-week-old commercial turkeys infected via the oculonasal route showed respiratory signs and mortality (2/10 birds). Additional diagnostic tests demonstrated the consistent presence of DNA/RNA of Ornithobacterium rhinotracheale, Bordetella avium and, less frequently, of astro-, rota-, reo-, parvo- and adenoviruses in turkeys both from field outbreaks and laboratory experiment. Although no microbiological culture was performed, we speculate that these secondary pathogens could play a role in the pathogenicity of the current H9N2 infections.
Infectious bursal disease virus (IBDV) is a non-enveloped, bisegmented double-stranded RNA virus included into the Birnaviridae family (Delmas et al., 2019). This virus was first described in the United States in 1962 and linked as aetiological agent of a highly contagious chicken immunodeficiency disorder known as Gumboro disease (Cosgrove, 1962). The initial classical IBDV strains were widely spread across the world, and the outbreaks caused by this type of strains were successfully controlled by application of vaccination policies. However, in the late 80s the epidemiological situation concerning IBDV suddenly changed and the scientific community was facing the emergence of very virulent IBDV (vvIBDV) strains, that caused severe economic losses in poultry, mainly due to an increase in the mortality of the infected animals up to 60% (Berg, Gonze, & Meulemans, 1991). Notoriously, the emergence of vvIBDV strains resulted from a reassortment event in which the new viral pathogenic fitness was initiated by the acquisition of a 'very virulent'
Infectious bursal disease virus (IBDV) is one of the most important immunosuppressive viral agents in poultry production. Prophylactic vaccinations of chicken flocks are the primary tool for disease control. Widely used immunoprophylaxis can, however, provide high pressure which contributes to the genetic diversification of circulating viruses, e.g. through reassortment of genome segments. We report the genetic and phenotypic characterization of a field reassortant IBDV (designated as Bpop/03) that acquired segment A from very virulent IBDV and segment B from classical attenuated D78-like IBDV. Despite the mosaic genetic make-up, the virus caused high mortality (80%) in experimentally infected SPF chickens and induced lesions typical of the acute form of IBD. The in vivo study results are in contrast with the foregoing experimental investigations in which the natural reassortants exhibited an intermediate pathotype, and underline the complex nature of IBDV virulence.
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