Electron-microscope studies on the pathogenesis of infectious bursal disease after intrabursal application of the causal virus.

Intrabursal application of infectious bursal disease virus (IBDV) is of advantage in studying sequential morphological events since the time of infection of the bursa is exactly known. A highly pathogenic strain caused first clinical symptoms 12 hr postinfection (PI) and death 24-30 hr PI. These are respectively 12 and 18 hr earlier than after per-oral infection. Numerous virus particles 53-58 nm in size, arrayed in a crystalline pattern and not surrounded by a membrane, are first found 6 hr PI in the cytoplasm of normal-looking lymphoid cells and macrophages. Some of the particles are less electron-dense and obviously immature; others have no core and therefore are regarded as incomplete. However, there is no evidence for the presence of more than one type of virus particle. Seven hr PI a membrane to segregate the virus clusters is formed, finally leading to autophagic vacuoles containing virus particles and cellular remnants. Within these vacuoles virus degradation takes part, though most of the infected cells, particularly the lymphoid cells, undergo cellular lysis, release the virions, and spread the infection to other cells of the bursa. At 18 hr PI the follicles are almost depleted of lymphoid cells. The findings show that early replication of IBDV is in the lymphoid cells and macrophages. These cells represent the main areas of virus multiplication, but the virions also can replicate in heterophils, reticulum cells, and reticular epithelial cells of the bursa.