Pathogenesis of pancreatic atrophy by avian influenza a virus infection

Abstract

Specific-pathogen-free (SPF), 2-day-old chicks were inoculated with type A influenza virus (A/whistling swan/Shimane/499/83/(H5N3)) into their caudal thoracic air sac. The original isolate of the virus was of low virulence (ICPI 0. 20 to 0.40), and was passaged 10 times through the respiratory organs of SPF chicks. Most of the chicks inoculated with the passaged virus (strain 499) showed respiratory and alimentary signs. Three of 30 chicks died on days 2, 6 and 7 post-inoculation (p.i.). Almost half of the infected chicks showed poor growth, and the variation of body size in the flock became prominent from day 10 p.i. Infected chicks consistently had pathological changes in the pancreas, liver, kidneys and respiratory tracts, and occasionally in the brain, duodenum and bone marrow. Positive immunoreaction to avian influenza virus (AIV) antigen and recovery of the virus persisted for longer period in the pancreas than in other organs. The pancreatic lesions were caused by a direct, lytic virus infection of the acinar cells and contributed to poor growth of the chicks.

Enhanced Neuropathogenicity of Avian Influenza A Virus by Passages through Air Sac and Brain of Chicks.

“…Genomic comparison of the 4e and 24a5b revealed multiple mutations in the HA gene and the description on the details of these mutations will appear elsewhere. Viral infection in the vascular endothelial cells and astrocytes of the brain was found in chicks inoculated with the strain 10a [24], but was not present in chicks inoculated with the original isolate. Incidence and quantity of viral antigen and the severity of brain lesions increased in chicks inoculated with 18a, 24a and 24a5b strains.…”

“…Mortalities of 4e, 10a [24], 18a, 24a and 24a5b were 0%, 50%, 67% and 100%, respectively. The pathogenicity to visceral organs such as the liver, kidneys, pancreas, and lungs was intensified by passages of the strains through the air sac.…”

“…In our previous report [24], low virulent (ICPI 0.20 to 0.40) AIV caused pancreatic atrophy and poor growth of chicks after 10 times passages of the virus through the chicken air sacs. The strain aggravated in pathogenicity to chicks infected the brain and induced mild, nonsuppurative encephalitis.…”

“…The same volume was given in group 2 with sterile chorioallantoic fluid via the same route. At regular intervals of 6,12,18,24,27,30,36,42 and 48 hr PI, 1 to 4 moribund or dead chicks of group 1 were necropsied. Two or one chicks from groups 2 or 3 were necropsied at the same time Subtypes H5 and H7 of type A influenza virus (AIV) have the possibility to mutate into highly virulent AIV [7,17].…”

Primary target cells of virulent strains of type A influenza virus in chicken embryos

“…All tissue samples were embedded in paraffin, sections taken and stained with haematoxyli n and eosin. For the detection of avian influenza virus (AIV) antigen in the tissues, all sections were stained with a streptoavidin-biotin immunoperoxidase complex method (Histofine SAB-PO kit; Nichirei Corp., Tokyo, Japan) using anti-AIV antibody (rabbit anti-strain 499 hyperimmune serum at a dilution of 1:1000; Shinya et al, 1995).…”