The study of histopathological changes caused by influenza A (H5N8) viral infection in bird species is essential for the understanding of their role in the spread of this highly infectious virus. However, there are few such studies under natural conditions in minor gallinaceous species. This article describes the pathomorphological findings in Colchis pheasants infected naturally with H5N8 during an epizootic outbreak in Bulgaria. Samples of internal organs of 10 carcasses were collected for histopathological and immunohistochemical evaluation, virus isolation and identification, and nucleic acid detection. Consistent macroscopic findings were lesions affecting the intestine, heart, lung, and pancreas. Congestion and mononuclear infiltrate were common findings in the small intestine, as were necrosis and lymphoid clusters in the lamina propria of the caeca. Congestion with small focal necrosis and gliosis with multifocal nonpurulent encephalitis were observed in the brain. Myocardial interstitial oedema and degenerative necrobiotic processes were also detected. Immunohistological analysis confirmed systemic infection and revealed influenza virus nucleoprotein in all analysed organs. Variable necrosis was observed in the brain, liver, trachea, heart, small intestine, and caeca. Viral antigen was commonly found in the brain, heart, lung and trachea. Contact with migrating waterfowls was suspected as a reason for the outbreak.

Highly pathogenic avian influenza (HPAI) is caused by influenza virus A from the family Orthomyxoviridae. It is a severe, systemic disease with high mortality in avians. The mortality can be as high as 100% in a few days. On 28 February 2017, HPAI virus of H5N1 subtype was confirmed in village chickens at Kampung Pulau Tebu, Batu 5, Tunjong Kota Bharu, Kelantan. It wasthe second outbreak of HPAI in Kelantan after the first reported case at Tumpat Kelantan on 17 August 2004. Most of the dead poultry showed similar clinical signs of sudden death with high mortality, cyanosis and oedema of head, comb, wattle and snood as well as red discolouration of shanks and feet. Post-mortem was performed on dead poultry and there were generalised haemorrhages of all internal organs, congested mesenteric blood vessels andpinpoint haemorrhages on proventriculus. Histopathological examination revealed generalised pulmonary haemorrhages with moderate interstitial pneumonia, generalised hepatic haemorrhages and hepatitis with multifocal area of hepatic necrosis, generalised haemorrhagic myocarditis and generalised haemorrhagicnephritis. Confirmation test was performed using RT-PCR and viral isolation at Veterinary Research Institute, Ipoh. 36 foci wereaffected involving five districts (Kota Bharu, Tumpat, Bachok, Pasir Mas and Tanah Merah) causing depopulation of 56,953 poultryand 17,531 eggs. Surveillance and control measures were taken by Department of Veterinary Services to contain the disease from spreading to other areas.

Objective—To evaluate whether an equine-derived canine H3N8 influenza A virus was capable of infecting and transmitting disease to ponies. Animals—20 influenza virus-seronegative 12- to 24-month-old ponies. Procedures—5 ponies were inoculated via aerosol exposure with 10(7) TCID50 of A/Canine/Wyoming/86033/07 virus (Ca/WY)/pony. A second group of 5 ponies (positive control group) was inoculated via aerosol exposure with a contemporary A/Eq/Colorado/10/07 virus (Eq/CO), and 4 sham-inoculated ponies served as a negative control group. To evaluate the potential for virus transmission, ponies (3/inoculation group) were introduced 2 days after aerosol exposure and housed with Ca/WY- and Eq/CO-inoculated ponies to serve as sentinel animals. Clinical signs, nasal virus shedding, and serologic responses to inoculation were monitored in all ponies for up to 21 days after viral inoculation. Growth and infection characteristics of viruses were examined by use of Madin-Darby canine kidney cells and primary equine and canine respiratory epithelial cells. Results—Ponies inoculated with Ca/WY had mild changes in clinical appearance, compared with results for Eq/CO-inoculated ponies. Additionally, Ca/WY inoculation induced significantly lower numbers for copies of the matrix gene in nasal secretions and lower systemic antibody responses in ponies than did Eq/CO inoculation. The Ca/WY isolate was not transmitted to sentinel ponies. Conclusions and Clinical Relevance—Inoculation of ponies with the canine H3N8 isolate resulted in mild clinical disease, minimal nasal virus shedding, and weak systemic antibody responses, compared with responses after inoculation with the equine H3N8 influenza isolate. These results suggested that Ca/WY has not maintained infectivity for ponies.

Mx1 (Myxovirus resistance protein) and Oas1b (Oligoadenylate synthetase-1), induced by type 1 interferon (IFN), play a role in early antiviral innate immunity by inhibiting the replication of viruses. In mice, Mx1 and Oas1b confer resistance to the infection of orthomyxoviruses including influenza viruses and flaviviruses including West Nile viruses, respectively. Laboratory mice have been used to study the mechanisms of the pathogenesis of these virus infections; however, it is possible that they are not a suitable model system to study these viruses, since most of the inbred laboratory mouse strains lack both genes. It has been reported that feral mouse-derived inbred strains show resistance to the infection of these viruses due to the presence of intact both genes. In this study, we generated congenic strains in which the Mx or Oas locus of the MSM/Mx (MSM) mouse was introduced to the most widely used mouse strain, C57BL/6J (B6). B6.MSM-Ms mice showed resistance to the infection of influenza virus but not of West Nile virus. On the other hand, B6.MSM-Oas mice showed resistance to the infection of West Nile virus but not of influenza virus. Our results indicate that Mx1 and Oas1b show highly antiviral specificity in mice possessing the same genetic background. Therefore, these congenic mice are useful for not only infection study but also investigation of host defense mechanism to these viruses.