J Vet Sci.  2016 Jun;17(2):179-188. 10.4142/jvs.2016.17.2.179.

Experimental infection and pathology of clade 2.2 H5N1 virus in gulls

Affiliations
  • 1Faculty of Natural Sciences, Novosibirsk State University, Novosibirsk 630090, Russia. sharshov@yandex.ru
  • 2State Research Center of Virology and Biotechnology "Vector", Novosibirsk 630559, Russia.
  • 3Institute of Experimental and Clinical Medicine, Russian Academy of Sciences, Novosibirsk 630117, Russia.

Abstract

During 2006, H5N1 HPAI caused an epizootic in wild birds, resulting in a die-off of Laridae in the Novosibirsk region at Chany Lake. In the present study, we infected common gulls (Larus canus) with a high dose of the H5N1 HPAI virus isolated from a common gull to determine if severe disease could be induced over the 28 day experimental period. Moderate clinical signs including diarrhea, conjunctivitis, respiratory distress and neurological signs were observed in virus-inoculated birds, and 50% died. The most common microscopic lesions observed were necrosis of the pancreas, mild encephalitis, mild myocarditis, liver parenchymal hemorrhages, lymphocytic hepatitis, parabronchi lumen hemorrhages and interstitial pneumonia. High viral titers were shed from the oropharyngeal route and virus was still detected in one bird at 25 days after infection. In the cloaca, the virus was detected sporadically in lower titers. The virus was transmitted to direct contact gulls. Thus, infected gulls can pose a significant risk of H5N1 HPAIV transmission to other wild migratory waterfowl and pose a risk to more susceptible poultry species. These findings have important implications regarding the mode of transmission and potential risks of H5N1 HPAI spread by gulls.

Keyword

H5N1 virus; clade 2.2; experimental infection; pathogenicity

MeSH Terms

Animals
*Charadriiformes
Influenza A Virus, H5N1 Subtype/*physiology
Influenza in Birds/mortality/*pathology/transmission/*virology
Morbidity
Tissue Distribution
Virus Shedding

Figure

  • Fig. 1 Survival curve of experimental groups A, C and D.

  • Fig. 2 (A) Damage of the blood-brain barrier at 2 days post infection (DPI). (B) Mild lymphoplasmacytic encephalitis at 8 DPI. (C) Increasing plasmacytes number in brain at 8 DPI. H&E stain (A and B) and methyl green-pyronin stain (C). 40× (A–C).

  • Fig. 3 (A) Bleeding in the liver parenchyma at 5 DPI. (B) Locus of a lymphocytic hepatitis at 2 DPI. (C) Hemosiderosis in the liver at 8 DPI. H&E stain (A and B) and Perl's Prussian blue stain (C). 40× (A–C).

  • Fig. 4 (A) Hemorrhages in a lumen of parabronchi at 2 DPI. (B) Interstitial pneumonia at 6 DPI. (C) Secondary bacterial interstitial pneumonia at 18 DPI. H&E stain. 20× (A–C).

  • Fig. 5 (A) Mild lymphocytic myocarditis at 4 DPI. (B) Necrotizing pancreatitis at 4 DPI. (C) Heterolymphoplasmacytic serositis of the pancreas at 8 DPI. H&E stain. 40× (A–C).


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