Severe leukopenia and liver biochemistry changes in adult rabbits after calicivirus infection

• Published in: Research in veterinary science 2006-04, Vol.80 (2), p.218-225
• Main Authors: Ferreira, P.G., Costa-e-Silva, A., Oliveira, M.J.R., Monteiro, E., Cunha, E.M, Águas, A.P.
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; biomarkers; blood cell counts; blood composition; Caliciviridae; Caliciviridae Infections - complications; Caliciviridae Infections - pathology; Caliciviridae Infections - physiopathology; Caliciviridae Infections - veterinary; Cholestasis; disease course; epidemiology; Hemorrhagic Disease Virus, Rabbit - pathogenicity; Hemorrhagic Disease Virus, Rabbit - physiology; Hepatic transaminases; histopathology; Hypoglycemia; leukopenia; Leukopenia - blood; Leukopenia - complications; Leukopenia - metabolism; Leukopenia - pathology; liver; Liver - enzymology; Liver - pathology; Liver - virology; Liver Failure, Acute - enzymology; Liver Failure, Acute - physiopathology; Liver Failure, Acute - virology; mechanism of action; pathogenesis; rabbit diseases; Rabbit hemorrhagic disease virus; Rabbits; reaction kinetics; RHD; Time Factors; Ultrastructure; Veterinary medicine; viral diseases of animals and humans
• ISSN: 0034-5288; 1532-2661
• DOI: 10.1016/j.rvsc.2005.05.007

Calicivirus infection is the major cause of the severe decrease in the stocks of wild and farm rabbits that has occurred worldwide during the last two decades. Adult rabbits (10-weeks-old) were experimentally infected with a calicivirus inoculum that killed all animals by causing rabbit haemorrhagic disease (RHD) within 24–62 h of infection. The rabbits were used to evaluate blood cell numbers and serum biochemistry every 6 h, starting 12 h after the inoculation of the caliciviruses. No significant changes in blood parameters were observed in most of the rabbits up to 18 h of infection. Severe leukopenia was seen 6 h before death of the infected rabbits; both heterophils and lymphocytes contributed to the decrease in circulating white blood cells. Platelets were also severely decreased in number. Marked enhancement in liver enzymes was seen 6–12 h before death of the infected rabbits. There was also evidence both for cholestasis, as expressed by the elevated levels of direct (conjugated) bilirubin, and for hypoglycemia, an alteration that it is likely to contribute for the seizures that rabbits show during the late stages of RHD. Liver ultrastructure of rabbits that died from RHD revealed extensive hepatocyte vacuolization, severe changes in mitochondrial structure, and depletion of glycogen granules. We conclude that: (i) severe leukopenia characterizes the final hours of calicivirus-induced RHD; (ii) hypoglycemia and cholestasis precede death of rabbits from RHD; (iii) the kinetics of liver enzymes allows an accurate prediction of the time of death of rabbits from calicivirus-induced RHD.