Comparative Pathobiology of Low and High Pathogenicity H7N3 Chilean Avian Influenza Viruses in Chickens

Abstract

Chickens were intranasally inoculated with Chilean H7N3 avian influenza (AI) viruses of low pathogenicity (LP) (H7N3/LP), high pathogenicity (HP) (H7N3/HP), and a laboratory derivative (02-AI-15-#9) (H7N3/14D) from the LPAI virus to determine pathobiologic effects. All chickens inoculated with H7N3/HP AI virus became infected and abruptly died 2 or 3 days postinoculation, but a few showed moderate depression before death. The H7N3/HP AI virus produced focal hemorrhages of the comb, petechial hemorrhage at the esophageal-proventricular junction and proventricular mucosa, edema and congestion of the lung, petechiation of the spleen, and generalized decrease in body fat. Histologically, severe necrosis, hemorrhage, and inflammation were primarily identified in lungs and the lymphoid tissues. All tissues sampled from the H7N3/HP AI group were positive for the AI viral antigen, predominantly in endothelium of blood vessels throughout most tissues and less frequently in histiocytes and cellular debris of lymphoid tissues. Even less consistently, cardiac myocytes, hepatocytes, Kupffer cells, glandular epithelial cells, microglial cells, and neurons became infected. These studies suggest the Chilean H7N3/LP AI virus was poorly infectious for chickens and may have been recently introduced from a nongalliform host. By contrast, the H7N3/HP AI virus was highly infectious and lethal for chickens. The H7N3/HP AI virus had a strong tropism for the cardiovascular system, principally vascular endothelium, which is similar to the viral tropism demonstrated previously with other H5 and H7 HPAI viruses. Interestingly, the H7N3/LP AI virus on intravenous inoculation replicated in cardiac myocytes, a feature of HPAI and not LPAI viruses, which further supports the theory that the H7N3/LP AI virus was in transition from LP to HP.

H5N2 Avian Influenza Outbreak in Texas in 2004: the First Highly Pathogenic Strain in the United States in 20 Years?

“…Similar viral replication and lesion distribution have been seen in other intravenous experiments using low-pathogenicity AIVs in chickens (33,35,36). By contrast, highly pathogenic AIVs on intranasal or intravenous inoculation typically produce systemic virus infection, including viremia, with virus replication and necrobiotic lesions in multiple visceral organs, brain, and skin (8,10,18,25,40).…”

“…In the current study, the low-pathogenic parent virus did not change in virulence following passage in the 14-day-old ECE passage model system, and all the resulting derivatives had biological characteristics of low-pathogenicity AIVs, including lack of plaque formation in the chicken embryo fibroblasts in the absence of added trypsin, absence of high mortality in intravenous pathotyping tests, and virus demonstration and lesions limited to epithelial cells. However, the presence of viral antigen in some cardiac myocytes of derivative 2-inoculated chickens is a pattern seen with highly pathogenic AIVs (8,10,18). This could represent an early stage in the transition from low-to high-pathogenicity AIV.…”

Pathogenesis of highly pathogenic avian influenza A virus (H7N1) infection in chickens inoculated with three different doses

“…Remarkable findings were observed that differed from the natural disease. Firstly, fibrinous peritonitis was a usual macroscopic lesion described during the H7N1 HPAIV natural outbreak Mutinelli et al, 2003), but was not observed in the present experimental infection or in other HPAIV experimental infections (Swayne, 1997(Swayne, , 2007Perkins & Swayne, 2001;Jones & Swayne, 2004;Swayne & Beck, 2005). Fibrinous peritonitis is a very common lesion in commercial birds, associated with secondary bacterial infections (Barnes et al, 2008) and its description in a natural outbreak can reflect a simultaneous viralÁ bacterial infection (Zanella, 2003;Swayne & Halvorson, 2008).…”

Pathobiology of avian influenza virus infection in minor gallinaceous species: a review

“…Myocardial necrosis or myocarditis with IHC-positive cardiomyocytes is commonly observed in all the species mentioned above (Perkins & Swayne, 2001;Antarasena et al, 2006;Isoda et al, 2006;Bertran et al, 2011Bertran et al, , 2013, sometimes together with myocyte necrosis and positive myocytes in the skeletal muscle (Perkins & Swayne, 2001;Bertran et al, 2011Bertran et al, , 2013. The HPAIVs, especially the Eurasian H5N1 HPAIVs, are generally defined as neurotropic (Perkins & Swayne, 2001;Jones & Swayne, 2004;Swayne & PantinJackwood, 2008) and are thought to reach the central nervous system via the haematogenous route . Frequent lesions in the brain are lymphocytic meningoencephalitis with neuronal necrosis, neuronophagia, and focal gliosis (Figure 2c) (Perkins & Swayne, 2001;Isoda et al, 2006;Bertran et al, 2011Bertran et al, , 2013.…”