Sequential development of the liver lesions in new-born lambs infected with Rift Valley fever virus. I. Macroscopic and microscopic pathology

Ten new-born lambs were necropsied at various intervals after artificial infection with Rift Valley fever virus for the study of the sequential development of the hepatic lesions. During the late stage of the disease, the livers were slightly to moderately swollen and mottled yellow, orange-brown and red. Greyish-white foci, approximately 0,25-0,5mm in diameter, were also scattered throughout the parenchyma. Microscopically, the liver lesions progressed from sparsely distributed acidophilic bodies and hepatocytes, revealing acidophilic degeneration and necrosis 6-12h post-inoculation, to small randomly scattered primary foci of necrosis 12-24h after infection. At 30-36h, these primary foci were larger and more circumscribed. In addition, numerous acidophilic bodies and necrotic hepatocytes were dispersed throughout the markedly degenerated parenchyma. The terminal stage of the disease (48-53h after inoculation), was characterized by massive hepatic necrosis in which primary foci of necrosis could still be recognized as dense aggregates of cytoplasmic and nuclear debris.The articles have been scanned in colour with a HP Scanjet 5590; 600dpi. Adobe Acrobat XI Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format

Sequential development of the liver lesions in new-born lambs infected with Rift Valley fever virus. II. Ultrastructural findings

The macroscopic and microscopic lesions in livers of new-born lambs experimentally infected with Rift Valley fever virus and killed at various intervals between 6 - 53 h after inoculation, were described in a previous paper. This communication gives an overview of the ultrastructural changes affecting hepatocytes, sinusoids and spaces of Disse, biliary tree and portal triads as well as observations on the morphology and morphogenesis of the virus. Hepatocytes were those primarily affected, while inflammatory and architectural changes were secondary. The changes included prominent nuclear alterations, fragmentation or disintegration of necrotic hepatocytes, focal cytoplasmic degradation and sequestration, and the presence of acidophilic bodies. The ultrastructure and origin of the intranuclear inclusions are discussed.The articles have been scanned in colour with a HP Scanjet 5590; 600dpi. Adobe Acrobat XI Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format