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H5N2 Highly Pathogenic Avian Influenza Viruses from the US 2014-2015 outbreak have an unusually long pre-clinical period in turkeys

View Article: PubMed Central - PubMed

ABSTRACT

Background: From December 2014 through June 2015, the US experienced the most costly highly pathogenic avian influenza (HPAI) outbreak to date. Most cases in commercial poultry were caused by an H5N2 strain which was a reassortant with 5 Eurasian lineage genes, including a clade 2.3.4.4 goose/Guangdong/1996 lineage hemagglutinin, and 3 genes from North American wild waterfowl low pathogenicity avian influenza viruses. The outbreak primarily affected turkeys and table-egg layer type chickens. Three isolates were selected for characterization in turkeys: the US index isolate from December 2014 (A/northern pintail/WA/40964/2014), and two poultry isolates from April 2015 (A/chicken/IA/13388/2015 and A/turkey/MN/12528/2015).

Results: Four week old broad-breasted white turkeys were inoculated with one of three doses (102, 104 or 106 50% egg infectious doses [EID50] per bird) of each of the isolates to evaluate infectious dose and pathogenesis. The mean bird infectious dose of A/northern pintail/WA/40964/2014 and A/turkey/MN/12528/2015 was 105 EID50 per bird, but was 103 EID50 per bird for A/chicken/IA/13388/2015, suggesting the latter had greater adaptation to gallinaceous birds. All three isolates had unusually long mean death time of 5.3–5.9 days post challenge, and the primary clinical signs were severe lethargy and neurological signs which started no more than 24 h before death (the average pre-clinical period was 4 days). Infected turkeys also shed high levels of virus by both the oropharyngeal and cloacal routes.

Conclusions: The unusually long mean death times, high levels of virus in feces, and increased adaptation of the later viruses may have contributed to the rapid spread of the virus during the peak of the outbreak.

No MeSH data available.


Related in: MedlinePlus

Histological lesions and immunohistochemical detection of viral antigen in 4-week-old turkeys intranasally inoculated with H5N2 HPAI viruses. Tissues collected at 4 days post-inoculation. Virus antigen is stained in red. Magnifications 40×. a Cerebellum. Vacuolation of the molecular and granular layers of the cerebellum with necrosis of the Purkinge neurons. Inset: viral antigen in neurons and glial cells. b Heart. Focal hyalinization and fragmentation of cardiac myocytes. Inset: viral antigen in cardiac myocytes. c Pancreas. Diffuse pancreatic necrosis. Inset: viral staining in acinar epithelium. d Adrenal gland. Confluent necrosis of corticotrophic and chromaffin cells. Inset: viral antigen in adrenal corticotrophic and cromaffin cells. e Bursa de Fabricious. Lymphoid depletion with apoptosis to necrosis in remaining lymphocytes. Inset: viral antigen in phagocytic c and necrotic cells. f Harderian gland. Viral antigen present in epithelial cells and infiltrating phagocytes. g Nasal gland. Viral antigen present in glandular epithelial cells and infiltrating phagocytes. h Proventriculus. Viral antigen present in glandular epithelial cells
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Fig3: Histological lesions and immunohistochemical detection of viral antigen in 4-week-old turkeys intranasally inoculated with H5N2 HPAI viruses. Tissues collected at 4 days post-inoculation. Virus antigen is stained in red. Magnifications 40×. a Cerebellum. Vacuolation of the molecular and granular layers of the cerebellum with necrosis of the Purkinge neurons. Inset: viral antigen in neurons and glial cells. b Heart. Focal hyalinization and fragmentation of cardiac myocytes. Inset: viral antigen in cardiac myocytes. c Pancreas. Diffuse pancreatic necrosis. Inset: viral staining in acinar epithelium. d Adrenal gland. Confluent necrosis of corticotrophic and chromaffin cells. Inset: viral antigen in adrenal corticotrophic and cromaffin cells. e Bursa de Fabricious. Lymphoid depletion with apoptosis to necrosis in remaining lymphocytes. Inset: viral antigen in phagocytic c and necrotic cells. f Harderian gland. Viral antigen present in epithelial cells and infiltrating phagocytes. g Nasal gland. Viral antigen present in glandular epithelial cells and infiltrating phagocytes. h Proventriculus. Viral antigen present in glandular epithelial cells

Mentions: Tissues were examined for microscopic lesions and viral antigen staining (Table 2 and Fig. 3). Microscopic lesions were similar among the eight birds examined, with only minor variations in severity. The most severe lesions were found in the nasal cavity, brain, heart, adrenal gland and pancreas. Moderate to severe rhinitis and sinusitis with multifocal necrosis of the nasal epithelium was common in all birds. Mild tracheitis and bronchitis, and mild to moderate interstitial pneumonia were also present. Mild to severe, randomly disseminated foci of neuronal and glial cell necrosis were observed in the cerebrum and cerebellum of all turkeys examined (Fig. 3a). Microgliosis, edema and mononuclear perivascular cuffs were also commonly observed in malacic areas of the brain. In the heart, mild to moderate multifocal myocyte necrosis was commonly observed (Fig. 3b). Moderate to severe multifocal necrosis of the pancreatic acinar epithelium was present in all birds (Fig. 2c). In the adrenal gland, mild to moderate multifocal to confluent areas of vacuolar degeneration to necrosis of corticotropic cells, and less commonly, chromaffin cells was observed in all but one turkey (Fig. 2d). Thymus, bursa and mucosa-associated lymphoid tissue had moderate to severe lymphoid depletion with apoptosis to necrosis in remaining lymphocytes (Fig. 2e). Mild to moderate depletion of the white pulp with multifocal lymphocytic necrosis was observed in the spleen. Mild to moderate necrosis of the epithelia of the Harderian glands and nasal glands was observed in most turkeys. Infrequently, the kidneys presented mild focal tubular necrosis, and the liver mild multifocal fibrinoid necrosis. Epithelial cell necrosis of the proventricular gland was observed in three turkeys. No lesions were observed in the intestine, eyelid, snood, or skeletal muscle.Table 2


H5N2 Highly Pathogenic Avian Influenza Viruses from the US 2014-2015 outbreak have an unusually long pre-clinical period in turkeys
Histological lesions and immunohistochemical detection of viral antigen in 4-week-old turkeys intranasally inoculated with H5N2 HPAI viruses. Tissues collected at 4 days post-inoculation. Virus antigen is stained in red. Magnifications 40×. a Cerebellum. Vacuolation of the molecular and granular layers of the cerebellum with necrosis of the Purkinge neurons. Inset: viral antigen in neurons and glial cells. b Heart. Focal hyalinization and fragmentation of cardiac myocytes. Inset: viral antigen in cardiac myocytes. c Pancreas. Diffuse pancreatic necrosis. Inset: viral staining in acinar epithelium. d Adrenal gland. Confluent necrosis of corticotrophic and chromaffin cells. Inset: viral antigen in adrenal corticotrophic and cromaffin cells. e Bursa de Fabricious. Lymphoid depletion with apoptosis to necrosis in remaining lymphocytes. Inset: viral antigen in phagocytic c and necrotic cells. f Harderian gland. Viral antigen present in epithelial cells and infiltrating phagocytes. g Nasal gland. Viral antigen present in glandular epithelial cells and infiltrating phagocytes. h Proventriculus. Viral antigen present in glandular epithelial cells
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Fig3: Histological lesions and immunohistochemical detection of viral antigen in 4-week-old turkeys intranasally inoculated with H5N2 HPAI viruses. Tissues collected at 4 days post-inoculation. Virus antigen is stained in red. Magnifications 40×. a Cerebellum. Vacuolation of the molecular and granular layers of the cerebellum with necrosis of the Purkinge neurons. Inset: viral antigen in neurons and glial cells. b Heart. Focal hyalinization and fragmentation of cardiac myocytes. Inset: viral antigen in cardiac myocytes. c Pancreas. Diffuse pancreatic necrosis. Inset: viral staining in acinar epithelium. d Adrenal gland. Confluent necrosis of corticotrophic and chromaffin cells. Inset: viral antigen in adrenal corticotrophic and cromaffin cells. e Bursa de Fabricious. Lymphoid depletion with apoptosis to necrosis in remaining lymphocytes. Inset: viral antigen in phagocytic c and necrotic cells. f Harderian gland. Viral antigen present in epithelial cells and infiltrating phagocytes. g Nasal gland. Viral antigen present in glandular epithelial cells and infiltrating phagocytes. h Proventriculus. Viral antigen present in glandular epithelial cells
Mentions: Tissues were examined for microscopic lesions and viral antigen staining (Table 2 and Fig. 3). Microscopic lesions were similar among the eight birds examined, with only minor variations in severity. The most severe lesions were found in the nasal cavity, brain, heart, adrenal gland and pancreas. Moderate to severe rhinitis and sinusitis with multifocal necrosis of the nasal epithelium was common in all birds. Mild tracheitis and bronchitis, and mild to moderate interstitial pneumonia were also present. Mild to severe, randomly disseminated foci of neuronal and glial cell necrosis were observed in the cerebrum and cerebellum of all turkeys examined (Fig. 3a). Microgliosis, edema and mononuclear perivascular cuffs were also commonly observed in malacic areas of the brain. In the heart, mild to moderate multifocal myocyte necrosis was commonly observed (Fig. 3b). Moderate to severe multifocal necrosis of the pancreatic acinar epithelium was present in all birds (Fig. 2c). In the adrenal gland, mild to moderate multifocal to confluent areas of vacuolar degeneration to necrosis of corticotropic cells, and less commonly, chromaffin cells was observed in all but one turkey (Fig. 2d). Thymus, bursa and mucosa-associated lymphoid tissue had moderate to severe lymphoid depletion with apoptosis to necrosis in remaining lymphocytes (Fig. 2e). Mild to moderate depletion of the white pulp with multifocal lymphocytic necrosis was observed in the spleen. Mild to moderate necrosis of the epithelia of the Harderian glands and nasal glands was observed in most turkeys. Infrequently, the kidneys presented mild focal tubular necrosis, and the liver mild multifocal fibrinoid necrosis. Epithelial cell necrosis of the proventricular gland was observed in three turkeys. No lesions were observed in the intestine, eyelid, snood, or skeletal muscle.Table 2

View Article: PubMed Central - PubMed

ABSTRACT

Background: From December 2014 through June 2015, the US experienced the most costly highly pathogenic avian influenza (HPAI) outbreak to date. Most cases in commercial poultry were caused by an H5N2 strain which was a reassortant with 5 Eurasian lineage genes, including a clade 2.3.4.4 goose/Guangdong/1996 lineage hemagglutinin, and 3 genes from North American wild waterfowl low pathogenicity avian influenza viruses. The outbreak primarily affected turkeys and table-egg layer type chickens. Three isolates were selected for characterization in turkeys: the US index isolate from December 2014 (A/northern pintail/WA/40964/2014), and two poultry isolates from April 2015 (A/chicken/IA/13388/2015 and A/turkey/MN/12528/2015).

Results: Four week old broad-breasted white turkeys were inoculated with one of three doses (102, 104 or 106 50% egg infectious doses [EID50] per bird) of each of the isolates to evaluate infectious dose and pathogenesis. The mean bird infectious dose of A/northern pintail/WA/40964/2014 and A/turkey/MN/12528/2015 was 105 EID50 per bird, but was 103 EID50 per bird for A/chicken/IA/13388/2015, suggesting the latter had greater adaptation to gallinaceous birds. All three isolates had unusually long mean death time of 5.3–5.9 days post challenge, and the primary clinical signs were severe lethargy and neurological signs which started no more than 24 h before death (the average pre-clinical period was 4 days). Infected turkeys also shed high levels of virus by both the oropharyngeal and cloacal routes.

Conclusions: The unusually long mean death times, high levels of virus in feces, and increased adaptation of the later viruses may have contributed to the rapid spread of the virus during the peak of the outbreak.

No MeSH data available.


Related in: MedlinePlus