Distribution of α-2,3 and α-2,6 receptors in the digestive tract of falcons demonstrated by means of MAAII and SNA lectin histochemistry.

<p><b>A.</b> Proventriculus stained by MAAII lectin. <b>B.</b> Duodenum stained by MAAII lectin. <b>C.</b> Rectum stained by MAAII lectin. <b>D.</b> Proventriculus stained by SNA lectin. <b>E.</b> Duodenum stained by SNA lectin. <b>F.</b> Rectum stained by SNA lectin.</p

Oral shedding from experimentally infected falcons with avian influenza virus.

<p>Viral RNA shedding detected by RRT-PCR in oropharyngeal swabs of falcons infected via the feeding route or via the nasochoanal route. Ct, cycle of threshold. <b>A.</b> Falcons infected with A/<i>Anas plathyrhynchos</i>/Spain/1877/2009 (H7N2) LPAI virus and euthanized at 11 dpi. <b>B.</b> Falcons infected with A/Great crested grebe/Basque Country/06.03249/2006 (H5N1) HPAI virus.</p

Brain tissue from an experimentally H5N1 HPAI virus-inoculated falcon dead at 5 dpi.

<p><b>A.</b> Focal area of malacia in the cortex (HE stain). <b>B.</b> Immunohistochemical staining of influenza A virus antigen in brain tissue.</p

Experimental design of the study.

<p>LPAI, low pathogenic avian influenza; HPAI, highly pathogenic avian influenza; PBS, phosphate buffer saline; EID₅₀, 50% egg infectious dose; ELD₅₀, 50% egg lethal dose.</p><p>LPAI virus was A/<i>Anas plathyrhynchos</i>/Spain/1877/2009 (H7N2); HPAI virus was A/Great crested grebe/Basque Country/06.03249/2006 (H5N1).</p

Distribution of α-2,3 and α-2,6 receptors in the respiratory tract of falcons demonstrated by means of MAAII and SNA lectin histochemistry.

<p><b>A.</b> Nasal turbinates stained by MAAII lectin. <b>B.</b> Trachea stained by MAAII lectin. <b>C.</b> Lung stained by MAAII lectin. <b>D.</b> Nasal turbinates stained by SNA lectin. <b>E.</b> Trachea stained by SNA lectin. <b>F.</b> Lung stained by SNA lectin.</p

Average distribution of nucleoprotein antigen, as determined by immunohistochemistry, in tissues sampled from falcons infected via the nasochoanal route with A/Great crested grebe/Basque Country/06.03249/2006 (H5N1) HPAI virus.

<p>− = no positive cells; + = single positive cells; ++ = scattered groups of positive cells; +++ = widespread positivity.</p><p>NSL, no significant lesions; nd, not determined.</p

Spatiotemporal Phylogenetic Analysis and Molecular Characterisation of Infectious Bursal Disease Viruses Based on the VP2 Hyper-Variable Region

<div><p>Background</p><p>Infectious bursal disease is a highly contagious and acute viral disease caused by the infectious bursal disease virus (IBDV); it affects all major poultry producing areas of the world. The current study was designed to rigorously measure the global phylogeographic dynamics of IBDV strains to gain insight into viral population expansion as well as the emergence, spread and pattern of the geographical structure of very virulent IBDV (vvIBDV) strains.</p><p>Methodology/Principal Findings</p><p>Sequences of the hyper-variable region of the VP2 (HVR-VP2) gene from IBDV strains isolated from diverse geographic locations were obtained from the GenBank database; Cuban sequences were obtained in the current work. All sequences were analysed by Bayesian phylogeographic analysis, implemented in the Bayesian Evolutionary Analysis Sampling Trees (BEAST), Bayesian Tip-association Significance testing (BaTS) and Spatial Phylogenetic Reconstruction of Evolutionary Dynamics (SPREAD) software packages. Selection pressure on the HVR-VP2 was also assessed. The phylogeographic association-trait analysis showed that viruses sampled from individual countries tend to cluster together, suggesting a geographic pattern for IBDV strains. Spatial analysis from this study revealed that strains carrying sequences that were linked to increased virulence of IBDV appeared in Iran in 1981 and spread to Western Europe (Belgium) in 1987, Africa (Egypt) around 1990, East Asia (China and Japan) in 1993, the Caribbean Region (Cuba) by 1995 and South America (Brazil) around 2000. Selection pressure analysis showed that several codons in the HVR-VP2 region were under purifying selection.</p><p>Conclusions/Significance</p><p>To our knowledge, this work is the first study applying the Bayesian phylogeographic reconstruction approach to analyse the emergence and spread of vvIBDV strains worldwide.</p></div

Pancreatic macroscopic lesions from a falcon experimentally infected with highly pathogenic avian influenza virus H5N1.

<p>Multifocal hemorrhagic necrosis in the pancreas of a falcon infected via the nasochoanal route with A/Great crested grebe/Basque Country/06.03249/2006 H5N1 HPAI virus (5 dpi).</p

Viral RNA in tissues of falcons infected with A/Great crested grebe/Basque Country/06.03249/2006 (H5N1) HPAI virus.

<p>Ct, cycle of threshold; CNS, central nervous system; undet, not detected by RRT-PCR.</p

Average distribution of nucleoprotein antigen, as determined by immunohistochemistry, in tissues sampled from falcons infected via the feeding route with A/Great crested grebe/Basque Country/06.03249/2006 (H5N1) HPAI virus.

<p>− = no positive cells; + = single positive cells; ++ = scattered groups of positive cells; +++ = widespread positivity.</p><p>NSL, no significant lesions; nd, not determined.</p