tetano
Editor, Senior Moderator
Avian Dis. 2016 May;60(1 Suppl):279-85. doi: 10.1637/11141-050815-Reg.
[h=1]Histopathologic Characterization and Shedding Dynamics of Guineafowl (Numida meleagris) Intravenously Infected with a H6N2 Low Pathogenicity Avian Influenza Virus.[/h] Dimitrov KM[SUP]1,[/SUP][SUP]2[/SUP], Zarkov IS[SUP]3[/SUP], Dinev I[SUP]4[/SUP], Goujgoulova GV[SUP]1[/SUP], Miller PJ[SUP]2[/SUP], Suarez DL[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Guineafowl of different ages were inoculated intravenously with a H6N2 wild waterfowl-origin low pathogenicity avian influenza virus (LPAIV). No clinical disease was observed. The infected birds had atrophy of the spleen, thymus, and cloacal bursa when compared with the noninfected control groups. The central and peripheral lymphoid tissues presented either lymphoproliferative or degenerative lesions that increased in intensity from 14 to 21 days postinoculation (DPI). Lymphoid depletion was present in the bursa, thymic lobes, and spleen T-dependent zone. In contrast, lymphoid proliferation was observed in liver, pancreas, and spleen B-dependent zone. Bronchus associated lymphoid tissue hyperplasia was observed in the lungs of the birds at 14 and 21 DPI. The virus was detected by virus isolation and reverse transcription PCR from both oropharyngeal and cloacal swabs with higher isolation rates from the latter. Most birds from the LPAIV inoculated groups shed virus up to 7 DPI. The virus was infrequently isolated from lung, kidney, liver, bursa, or spleen of infected birds until 14 DPI and from two samples (kidney and spleen, 1-yr-old birds) at 21 DPI. These data indicate that the wild bird-origin LPAIV used in this study caused pantropic infection in guineafowl when inoculated intravenously.
[h=4]KEYWORDS:[/h] H6N2; LPAI; avian influenza; guineafowl; histopathology; rRT-PCR; shedding
PMID: 27309068 [PubMed - in process]
[h=1]Histopathologic Characterization and Shedding Dynamics of Guineafowl (Numida meleagris) Intravenously Infected with a H6N2 Low Pathogenicity Avian Influenza Virus.[/h] Dimitrov KM[SUP]1,[/SUP][SUP]2[/SUP], Zarkov IS[SUP]3[/SUP], Dinev I[SUP]4[/SUP], Goujgoulova GV[SUP]1[/SUP], Miller PJ[SUP]2[/SUP], Suarez DL[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Guineafowl of different ages were inoculated intravenously with a H6N2 wild waterfowl-origin low pathogenicity avian influenza virus (LPAIV). No clinical disease was observed. The infected birds had atrophy of the spleen, thymus, and cloacal bursa when compared with the noninfected control groups. The central and peripheral lymphoid tissues presented either lymphoproliferative or degenerative lesions that increased in intensity from 14 to 21 days postinoculation (DPI). Lymphoid depletion was present in the bursa, thymic lobes, and spleen T-dependent zone. In contrast, lymphoid proliferation was observed in liver, pancreas, and spleen B-dependent zone. Bronchus associated lymphoid tissue hyperplasia was observed in the lungs of the birds at 14 and 21 DPI. The virus was detected by virus isolation and reverse transcription PCR from both oropharyngeal and cloacal swabs with higher isolation rates from the latter. Most birds from the LPAIV inoculated groups shed virus up to 7 DPI. The virus was infrequently isolated from lung, kidney, liver, bursa, or spleen of infected birds until 14 DPI and from two samples (kidney and spleen, 1-yr-old birds) at 21 DPI. These data indicate that the wild bird-origin LPAIV used in this study caused pantropic infection in guineafowl when inoculated intravenously.
[h=4]KEYWORDS:[/h] H6N2; LPAI; avian influenza; guineafowl; histopathology; rRT-PCR; shedding
PMID: 27309068 [PubMed - in process]