scholarly journals Microsatellite loci in Japanese quail and cross-species amplification in chicken and guinea fowl

2002 ◽  
Vol 34 (2) ◽  
pp. 233 ◽  
Author(s):  
Boniface Kayang ◽  
Miho Inoue-Murayama ◽  
Takuya Hoshi ◽  
Koji Matsuo ◽  
Hideaki Takahashi ◽  
...  
2003 ◽  
Vol 74 (4) ◽  
pp. 255-259 ◽  
Author(s):  
Boniface Baboreka KAYANG ◽  
Miho INOUE-MURAYAMA ◽  
Hideaki TAKAHASHI ◽  
Mitsuru MINEZAWA ◽  
Masaoki TSUDZUKI ◽  
...  

2017 ◽  
Vol 91 (21) ◽  
Author(s):  
Kateri Bertran ◽  
Dong-Hun Lee ◽  
Mary J. Pantin-Jackwood ◽  
Erica Spackman ◽  
Charles Balzli ◽  
...  

ABSTRACT In 2014 and 2015, the United States experienced an unprecedented outbreak of Eurasian clade 2.3.4.4 H5 highly pathogenic avian influenza (HPAI) virus. Initial cases affected mainly wild birds and mixed backyard poultry species, while later outbreaks affected mostly commercial chickens and turkeys. The pathogenesis, transmission, and intrahost evolutionary dynamics of initial Eurasian H5N8 and reassortant H5N2 clade 2.3.4.4 HPAI viruses in the United States were investigated in minor gallinaceous poultry species (i.e., species for which the U.S. commercial industries are small), namely, Japanese quail, bobwhite quail, pearl guinea fowl, chukar partridges, and ring-necked pheasants. Low mean bird infectious doses (<2 to 3.7 log10) support direct introduction and infection of these species as observed in mixed backyard poultry during the early outbreaks. Pathobiological features and systemic virus replication in all species tested were consistent with HPAI virus infection. Sustained virus shedding with transmission to contact-exposed birds, alongside long incubation periods, may enable unrecognized dissemination and adaptation to other gallinaceous species, such as chickens and turkeys. Genome sequencing of excreted viruses revealed numerous low-frequency polymorphisms and 20 consensus-level substitutions in all genes and species, but especially in Japanese quail and pearl guinea fowl and in internal proteins PB1 and PB2. This genomic flexibility after only one passage indicates that influenza viruses can continue to evolve in galliform species, increasing their opportunity to adapt to other species. Our findings suggest that these gallinaceous poultry are permissive for infection and sustainable transmissibility with the 2014 initial wild bird-adapted clade 2.3.4.4 virus, with potential acquisition of mutations leading to host range adaptation. IMPORTANCE The outbreak of clade 2.3.4.4 H5 highly pathogenic avian influenza (HPAI) virus that occurred in the United States in 2014 and 2015 represents the worst livestock disease event in the country, with unprecedented socioeconomic and commercial consequences. Epidemiological and molecular investigations can identify transmission pathways of the HPAI virus. However, understanding the pathogenesis, transmission, and intrahost evolutionary dynamics of new HPAI viruses in different avian species is paramount. The significance of our research is in examining the susceptibility of minor gallinaceous species to HPAI virus, as this poultry sector also suffers from HPAI epizootics, and identifying the biological potential of these species as an epidemiological link between the waterfowl reservoir and the commercial chicken and turkey populations, with the ultimate goal of refining surveillance in these populations to enhance early detection, management, and control in future HPAI virus outbreaks.


2016 ◽  
Vol 9 (3) ◽  
pp. 200-206 ◽  
Author(s):  
Sajid Umar ◽  
Sajjad Asif ◽  
Muhammad Usman ◽  
Muhammad Atif ◽  
Shahzad Ali ◽  
...  

Avian influenza (H9N2) virus infection is an emerging respiratory problem and its prevalence varies significantly among different species of birds. The current knowledge about virus shedding parameters in terrestrial birds is limited. With this in mind, the present study was conducted in different domestic and wild terrestrial birds to investigate species-related differences in infectivity and pattern of viral shedding associated with H9N2 AI virus. Groups of terrestrial birds (domestic Guinea Fowl Numida meleagridis, Japanese Quail Coturnix coturnix japonica, House Sparrows Passer domesticus, House Crows Corvus splendens and Bank Myna Acridotheres ginginianus) were inoculated intra-nasally with A/chicken/Pakistan/10RS3039-284-48/2010 (H9N2) AI virus (106 EID50) and then examined for infectivity and virus shedding patterns. With the exception of House Crows, all infected birds showed clinical signs of different severity, showing the most prominent disease signs in Japanese Quail. All infected birds showed positive results for virus shedding, however, the pattern of virus shedding was different among wild terrestrial birds. Japanese Quail showed the highest levels of virus shedding while samples collected from House Crows revealed only very low levels. Interestingly, virus shedding was observed predominantly via the gastrointestinal tract in House Sparrows and Bank Myna and via the buccal cavity route in Guinea Fowl and Japanese Quail. Here we investigated that the novel genotype of H9N2 AI virus circulating in Pakistan causes clinical disease signs in domestic and wild terrestrial birds. The results of this study suggest that virus shedding varies between different related avian species and highlights the potential role of Guinea Fowl, Japanese Quail, House Sparrows and Bank Myna as mixing bowls for the transmission and maintenance of H9N2 AI viruses between premises.


1999 ◽  
Vol 30 (3) ◽  
pp. 195-199 ◽  
Author(s):  
S. W. Y. Pang ◽  
C. Ritland ◽  
J. E. Carlson ◽  
K. M. Cheng

2007 ◽  
Vol 10 (8) ◽  
pp. 1195-1199 ◽  
Author(s):  
C. Amirinia ◽  
H. Emrani ◽  
M.A. Radjaee Arbabe ◽  
R.Vaez Torshizi ◽  
A. Nejati Javaremi

2017 ◽  
Vol 8 (16) ◽  
pp. 172-176
Author(s):  
Oreynab Looch Maleki ◽  
Ali Hashemi ◽  
Ghorban Elyasi Zarringhabaie ◽  
Mohammad Farhadian ◽  
Zahra Erfaniasl

2006 ◽  
Vol 58 (3) ◽  
pp. 291-298 ◽  
Author(s):  
N.R.S. Martins ◽  
A.C. Horta ◽  
A.M. Siqueira ◽  
S.Q. Lopes ◽  
J.S. Resende ◽  
...  

Since 2000, Macrorhabdus ornithogaster "megabacteriosis" has been diagnosed in the avian diseases laboratory in a diversity of avian species and varied spectrum of disease. The disease in some species (chickens, turkeys, guinea fowls) was clinically characterized by emaciation, prostration, loss of appetite, cachexia and death, with a typically chronic course. A more acute disease was observed in finches (canary-Serinus and zebra-Taeniopygia) and budgerigars (Melopsittacus undulatus). The large rod shaped organism, visible from 100 times magnification, with and without staining, could be detected in sick and also in reasonably normal individuals of some species, such as chickens, turkeys, quails and pigeons. In rheas (Rhea americana), ostriches (Struthio camelus), canaries, zebra-finches, guinea-fowl (Numida meleagris) and budgerigars. The disease was severe, causing to up to 100% mortality. The infection could be detected in some species along with other infectious or disease problems, such as endoparasites (helminths, coccidia) and ectoparasitism (order Mallophaga or/and order Acarina). The cultivation of M. ornithogaster was successfully achieved in solid and liquid media, originated from chickens (four isolates), guinea fowl (1 isolate), chuckar partridge (1 isolate) and canary (1 isolate). A very interesting finding at microscopy was motility of M. ornithogaster, as detected both in cultures obtained on agar for pathogenic fungi and passaged into thioglycolate broth, as well as on samples observed in wet preparations from in vivo. Differences in colony aspects were noted among the isolates. Experimental infections were attempted in chicken and japanese quail, using a chicken isolate, allowing the detection of the organism in the proventriculus and liver in apparently normal birds. One chicken isolate was injected intraperitoneally in Balb/c mice and resulted in 100% mortality.


2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Kateri Bertran ◽  
Mary J. Pantin-Jackwood ◽  
Miria F. Criado ◽  
Dong-Hun Lee ◽  
Charles L. Balzli ◽  
...  

Abstract In the 2014–2015 Eurasian lineage clade 2.3.4.4A H5 highly pathogenic avian influenza (HPAI) outbreak in the U.S., backyard flocks with minor gallinaceous poultry and large commercial poultry (chickens and turkeys) operations were affected. The pathogenesis of the first H5N8 and reassortant H5N2 clade 2.3.4.4A HPAI U.S. isolates was investigated in six gallinaceous species: chickens, Japanese quail, Bobwhite quail, Pearl guinea fowl, Chukar partridges, and Ring-necked pheasants. Both viruses caused 80–100% mortality in all species, except for H5N2 virus that caused 60% mortality in chickens. The surviving challenged birds remained uninfected based on lack of clinical disease and lack of seroconversion. Among the infected birds, chickens and Japanese quail in early clinical stages (asymptomatic and listless) lacked histopathologic findings. In contrast, birds of all species in later clinical stages (moribund and dead) had histopathologic lesions and systemic virus replication consistent with HPAI virus infection in gallinaceous poultry. These birds had widespread multifocal areas of necrosis, sometimes with heterophilic or lymphoplasmacytic inflammatory infiltrate, and viral antigen in parenchymal cells of most tissues. In general, lesions and antigen distribution were similar regardless of virus and species. However, endotheliotropism was the most striking difference among species, with only Pearl guinea fowl showing widespread replication of both viruses in endothelial cells of most tissues. The expression of IFN-γ and IL-10 in Japanese quail, and IL-6 in chickens, were up-regulated in later clinical stages compared to asymptomatic birds.


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