Liver Enzymes and Ultrastructure in Rabbit Haemorrhagic Disease (RHD)

• Published in: Veterinary research communications Vol. 30; no. 4; pp. 393 - 401
• Main Authors: Ferreira, P.G, Costa-e-Silva, A, Monteiro, E, Oliveira, M.J.R, Águas, A.P
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01-05-2006
• Subjects: alanine transaminase; analytical methods; Animals; aspartate transaminase; Bilirubin - blood; biochemistry; blood serum; Caliciviridae Infections - enzymology; Caliciviridae Infections - virology; Calicivirus; cell biology; diagnostic techniques; disease course; electron microscopy; endoplasmic reticulum; enzyme kinetics; Hemorrhagic Disease Virus, Rabbit - ultrastructure; hepatocytes; Hepatocytes - ultrastructure; Hepatocytes - virology; liver; Liver - enzymology; Liver - ultrastructure; liver diseases; Liver Diseases - enzymology; Liver Diseases - veterinary; Liver Diseases - virology; mitochondria; Mitochondria - ultrastructure; Mitochondria - virology; rabbit diseases; rabbit hemorrhagic disease; Rabbit hemorrhagic disease virus; Rabbits; tissue degeneration; Transaminases - metabolism; ultrastructure; viral diseases of animals and humans
• ISSN: 0165-7380; 1573-7446
• DOI: 10.1007/s11259-006-3297-1

Rabbit haemorrhagic disease (RHD) is caused by a calicivirus infection that kills most adult rabbits 24-72 h after viral inoculation. Two liver enzymes (AST, aspartate aminotransferase, and ALT, alanine aminotransferase) were monitored in blood samples of calicivirus-infected rabbits during the short course of RHD. Values of AST were used to differentiate three stages of hepatocellular degeneration in RHD: mild (up to 20-fold increase in AST), moderate (150-200-fold elevation of AST) and severe (more than 1000-fold elevation in AST). Liver samples of rabbits from these three biochemical stages of hepatocellular degeneration of RHD were studied by transmission electron microscopy to define the fine structure of the hepatocytes. In the mild hepatocellular degeneration there was proliferation (microvesiculation) of the smooth endoplasmic reticulum and swelling of mitochondria into spheroid bodies with loss of cristae. In moderate hepatocellular degeneration, vacuolization of cytoplasm and mitochondrial damage continued to be present, and there was also formation of autophagic vesicles. In the severe hepatocellular degeneration of RHD, the altered mitochondria also showed loss of density of their matrix; rupture of cytoplasmic vacuoles led to the formation of large vesicles. Marked depletion of liver glycogen was also found in this late stage of RHD. These data offer a correlation between biochemical and cytological features of the liver during the hepatocellular degeneration of RHD.