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Transmission of avian influenza virus (H3N2) to dogs.

Song D, Kang B, Lee C, Jung K, Ha G, Kang D, Park S, Park B, Oh J - Emerging Infect. Dis. (2008)

Bottom Line: The beagles shed virus through nasal excretion, seroconverted, and became ill with severe necrotizing tracheobronchitis and bronchioalveolitis with accompanying clinical signs (e.g., high fever).Consistent with histologic observation of lung lesions, large amounts of avian influenza virus binding receptor (SAalpha 2,3-gal) were identified in canine tracheal, bronchial, and bronchiolar epithelial cells, which suggests potential for direct transmission of avian influenza virus (H3N2) from poultry to dogs.Our data provide evidence that dogs may play a role in interspecies transmission and spread of influenza virus.

View Article: PubMed Central - PubMed

Affiliation: Green Cross Veterinary Products Company, Ltd., Yong-in, South Korea.

ABSTRACT
In South Korea, where avian influenza virus subtypes H3N2, H5N1, H6N1, and H9N2 circulate or have been detected, 3 genetically similar canine influenza virus (H3N2) strains of avian origin (A/canine/Korea/01/2007, A/canine/Korea/02/2007, and A/canine/Korea/03/2007) were isolated from dogs exhibiting severe respiratory disease. To determine whether the novel canine influenza virus of avian origin was transmitted among dogs, we experimentally infected beagles with this influenza virus (H3N2) isolate. The beagles shed virus through nasal excretion, seroconverted, and became ill with severe necrotizing tracheobronchitis and bronchioalveolitis with accompanying clinical signs (e.g., high fever). Consistent with histologic observation of lung lesions, large amounts of avian influenza virus binding receptor (SAalpha 2,3-gal) were identified in canine tracheal, bronchial, and bronchiolar epithelial cells, which suggests potential for direct transmission of avian influenza virus (H3N2) from poultry to dogs. Our data provide evidence that dogs may play a role in interspecies transmission and spread of influenza virus.

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Histopathologic lesions in the trachea and lungs of control (A and C) or experimentally infected (B, D–F) dogs (A/canine/Korea/01/2007 [H3N2]) at different days postinoculation (dpi). A) Control dog at 9 dpi, showing normal pseudostratified columnar epithelium lining of the trachea; original magnification ×400. Hematoxylin and eosin (HE) stain. B) Influenza-infected dog at 9 dpi, showing necrotizing tracheitis characterized by necrosis (n), squamous metaplasia (s), and hyperplasia of the epithelium and nonsuppurative inflammation (c) in the connective tissue; original magnification ×400. HE stain. C) Control dog at 3 dpi, showing normal alveoli; original magnification ×200. HE stain. D) Influenza-infected dog at 3 dpi, showing severe diffuse necrotizing bronchitis and bronchiolitis with suppurative inflammation in the lumina; original magnification ×100. HE stain. E) Influenza-infected dog at 6 dpi, showing severe necrotizing bronchiolitis; original magnification ×200. HE stain. F) Influenza-infected dog at 6 dpi (serial section of E), showing large amounts of influenza A virus antigens (red stain; arrows) in the bronchiolar epithelium and lumen. Immunohistochemistry; Red Substrate (Dako, Carpinteria, CA, USA); Mayer’s hematoxylin counterstain. G) Influenza-infected dog at 9 dpi, showing severe necrotizing alveolitis with accumulation of necrotic cells in terminal bronchioles (tb) and alveoli (a); original magnification ×200. HE stain.
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Figure 3: Histopathologic lesions in the trachea and lungs of control (A and C) or experimentally infected (B, D–F) dogs (A/canine/Korea/01/2007 [H3N2]) at different days postinoculation (dpi). A) Control dog at 9 dpi, showing normal pseudostratified columnar epithelium lining of the trachea; original magnification ×400. Hematoxylin and eosin (HE) stain. B) Influenza-infected dog at 9 dpi, showing necrotizing tracheitis characterized by necrosis (n), squamous metaplasia (s), and hyperplasia of the epithelium and nonsuppurative inflammation (c) in the connective tissue; original magnification ×400. HE stain. C) Control dog at 3 dpi, showing normal alveoli; original magnification ×200. HE stain. D) Influenza-infected dog at 3 dpi, showing severe diffuse necrotizing bronchitis and bronchiolitis with suppurative inflammation in the lumina; original magnification ×100. HE stain. E) Influenza-infected dog at 6 dpi, showing severe necrotizing bronchiolitis; original magnification ×200. HE stain. F) Influenza-infected dog at 6 dpi (serial section of E), showing large amounts of influenza A virus antigens (red stain; arrows) in the bronchiolar epithelium and lumen. Immunohistochemistry; Red Substrate (Dako, Carpinteria, CA, USA); Mayer’s hematoxylin counterstain. G) Influenza-infected dog at 9 dpi, showing severe necrotizing alveolitis with accumulation of necrotic cells in terminal bronchioles (tb) and alveoli (a); original magnification ×200. HE stain.

Mentions: Gross lesions were limited to the lungs and were characterized by multifocal to coalescing reddish consolidation. In tissues collected on 3, 6 and 9 dpi, histopathologic lesions were observed in the trachea and lungs, and extrapulmonary lesions were absent in puppies infected with the isolate (A/canine/Korea/01/2007 [H3N2]). Severe virus-induced necrosis and inflammation of the upper (trachea and bronchi) and lower (bronchiole and alveoli) respiratory tracts were noted on histologic examination. Although minor differences in the severity of the histologic findings were observed among the 9 infected dogs, all infected dogs shared the following histopathologic features regardless how long after inoculation tissues were collected: 1) moderate to severe multilobular or diffuse necrotizing tracheobronchitis with suppurative inflammation in the lumina and squamous metaplasia of the tracheobronchial epithelium (Figure 3, panel B); 2) moderate to severe multilobular or diffuse necrotizing bronchiolitis and alveolitis (i.e., bronchioalveolitis, occasionally accompanied by chronic peribronchiolar and perivascular inflammation) (Figure 3, panels D and E); and 3) mild to moderate multilobular or diffuse thickening of alveolar septa by infiltrates of inflammatory cells, such as interstitial pulmonary macrophages. At 3, 6, and 9 dpi, large amounts of influenza A virus antigen were found in bronchial and bronchiolar epithelium and lumens (Figure 3, panel F).


Transmission of avian influenza virus (H3N2) to dogs.

Song D, Kang B, Lee C, Jung K, Ha G, Kang D, Park S, Park B, Oh J - Emerging Infect. Dis. (2008)

Histopathologic lesions in the trachea and lungs of control (A and C) or experimentally infected (B, D–F) dogs (A/canine/Korea/01/2007 [H3N2]) at different days postinoculation (dpi). A) Control dog at 9 dpi, showing normal pseudostratified columnar epithelium lining of the trachea; original magnification ×400. Hematoxylin and eosin (HE) stain. B) Influenza-infected dog at 9 dpi, showing necrotizing tracheitis characterized by necrosis (n), squamous metaplasia (s), and hyperplasia of the epithelium and nonsuppurative inflammation (c) in the connective tissue; original magnification ×400. HE stain. C) Control dog at 3 dpi, showing normal alveoli; original magnification ×200. HE stain. D) Influenza-infected dog at 3 dpi, showing severe diffuse necrotizing bronchitis and bronchiolitis with suppurative inflammation in the lumina; original magnification ×100. HE stain. E) Influenza-infected dog at 6 dpi, showing severe necrotizing bronchiolitis; original magnification ×200. HE stain. F) Influenza-infected dog at 6 dpi (serial section of E), showing large amounts of influenza A virus antigens (red stain; arrows) in the bronchiolar epithelium and lumen. Immunohistochemistry; Red Substrate (Dako, Carpinteria, CA, USA); Mayer’s hematoxylin counterstain. G) Influenza-infected dog at 9 dpi, showing severe necrotizing alveolitis with accumulation of necrotic cells in terminal bronchioles (tb) and alveoli (a); original magnification ×200. HE stain.
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Figure 3: Histopathologic lesions in the trachea and lungs of control (A and C) or experimentally infected (B, D–F) dogs (A/canine/Korea/01/2007 [H3N2]) at different days postinoculation (dpi). A) Control dog at 9 dpi, showing normal pseudostratified columnar epithelium lining of the trachea; original magnification ×400. Hematoxylin and eosin (HE) stain. B) Influenza-infected dog at 9 dpi, showing necrotizing tracheitis characterized by necrosis (n), squamous metaplasia (s), and hyperplasia of the epithelium and nonsuppurative inflammation (c) in the connective tissue; original magnification ×400. HE stain. C) Control dog at 3 dpi, showing normal alveoli; original magnification ×200. HE stain. D) Influenza-infected dog at 3 dpi, showing severe diffuse necrotizing bronchitis and bronchiolitis with suppurative inflammation in the lumina; original magnification ×100. HE stain. E) Influenza-infected dog at 6 dpi, showing severe necrotizing bronchiolitis; original magnification ×200. HE stain. F) Influenza-infected dog at 6 dpi (serial section of E), showing large amounts of influenza A virus antigens (red stain; arrows) in the bronchiolar epithelium and lumen. Immunohistochemistry; Red Substrate (Dako, Carpinteria, CA, USA); Mayer’s hematoxylin counterstain. G) Influenza-infected dog at 9 dpi, showing severe necrotizing alveolitis with accumulation of necrotic cells in terminal bronchioles (tb) and alveoli (a); original magnification ×200. HE stain.
Mentions: Gross lesions were limited to the lungs and were characterized by multifocal to coalescing reddish consolidation. In tissues collected on 3, 6 and 9 dpi, histopathologic lesions were observed in the trachea and lungs, and extrapulmonary lesions were absent in puppies infected with the isolate (A/canine/Korea/01/2007 [H3N2]). Severe virus-induced necrosis and inflammation of the upper (trachea and bronchi) and lower (bronchiole and alveoli) respiratory tracts were noted on histologic examination. Although minor differences in the severity of the histologic findings were observed among the 9 infected dogs, all infected dogs shared the following histopathologic features regardless how long after inoculation tissues were collected: 1) moderate to severe multilobular or diffuse necrotizing tracheobronchitis with suppurative inflammation in the lumina and squamous metaplasia of the tracheobronchial epithelium (Figure 3, panel B); 2) moderate to severe multilobular or diffuse necrotizing bronchiolitis and alveolitis (i.e., bronchioalveolitis, occasionally accompanied by chronic peribronchiolar and perivascular inflammation) (Figure 3, panels D and E); and 3) mild to moderate multilobular or diffuse thickening of alveolar septa by infiltrates of inflammatory cells, such as interstitial pulmonary macrophages. At 3, 6, and 9 dpi, large amounts of influenza A virus antigen were found in bronchial and bronchiolar epithelium and lumens (Figure 3, panel F).

Bottom Line: The beagles shed virus through nasal excretion, seroconverted, and became ill with severe necrotizing tracheobronchitis and bronchioalveolitis with accompanying clinical signs (e.g., high fever).Consistent with histologic observation of lung lesions, large amounts of avian influenza virus binding receptor (SAalpha 2,3-gal) were identified in canine tracheal, bronchial, and bronchiolar epithelial cells, which suggests potential for direct transmission of avian influenza virus (H3N2) from poultry to dogs.Our data provide evidence that dogs may play a role in interspecies transmission and spread of influenza virus.

View Article: PubMed Central - PubMed

Affiliation: Green Cross Veterinary Products Company, Ltd., Yong-in, South Korea.

ABSTRACT
In South Korea, where avian influenza virus subtypes H3N2, H5N1, H6N1, and H9N2 circulate or have been detected, 3 genetically similar canine influenza virus (H3N2) strains of avian origin (A/canine/Korea/01/2007, A/canine/Korea/02/2007, and A/canine/Korea/03/2007) were isolated from dogs exhibiting severe respiratory disease. To determine whether the novel canine influenza virus of avian origin was transmitted among dogs, we experimentally infected beagles with this influenza virus (H3N2) isolate. The beagles shed virus through nasal excretion, seroconverted, and became ill with severe necrotizing tracheobronchitis and bronchioalveolitis with accompanying clinical signs (e.g., high fever). Consistent with histologic observation of lung lesions, large amounts of avian influenza virus binding receptor (SAalpha 2,3-gal) were identified in canine tracheal, bronchial, and bronchiolar epithelial cells, which suggests potential for direct transmission of avian influenza virus (H3N2) from poultry to dogs. Our data provide evidence that dogs may play a role in interspecies transmission and spread of influenza virus.

Show MeSH
Related in: MedlinePlus