Impairment of Renal Function and Electrolyte Balance in Rabbit Hemoorhagic Disease

Abstract

ABSTRACT. Rabbit hemorrhagic disease virus (RHDV) induced viral fulminant hepatitis in adult rabbits. We investigated the damage of renal function and electrolyte balance in experimentally infected rabbit by measuring the related serum parameters to elucidate the pathogenesis of RHDV as an index for medical treatment. Nineteen New Zealand White rabbits, ten females and nine males, were each intramuscularly inoculated with 0.5 ml 50% rabbit lethal dose (RLD 50 ) rabbit hemorrhagic disease virus. Blood samples were collected at 0 hr post inoculation (HPI) and every 6 hr from 18 HPI repeatedly through 66 HPI. After virus inoculation, serum blood urea nitrogen (BUN), creatinine (CREA) and sodium (Na + ) were elevated to a highly significant level (p<0.0001), whereas serum potassium (K + ) was moderately elevated to a significant level (p<0.05). Hypoglycemia developed highly significantly (p<0.0001). Serum chloride ion (Cl -) was the only parameter which did not change significantly (p=0.077). No significant sexual difference was observed among these parameters. Renal insufficiency progressed from 36 hr, as indicated by the increases in BUN and CREA; significant changes in electrolytes resulting in the increased osmolality of extracellular fluid that induced flow disturbance which consequently destroy the homeostasis in cells. Therefore, the later impairments in renal function and electrolyte balance might be an important threat for rabbits which might have survived from acute fulminant hepatitis in RHD. KEY WORDS: electrolyte balance, rabbit hemorrhagic disease virus, renal insufficiency, serum.J. Vet. Med. Sci. 70(9): 951-958, 2008 Rabbit hemorrhagic disease (RHD) was first reported in 1984 in the People's Republic of China [12] and widespread worldwide to Europe, Australia, Mexico, North Africa and New Zealand in the following years. In 1994, RHD was first recognized in Taiwan by Dr. Y. S. Lu through serological tests and was characterized by hemagglutination, electron microscopic examination, viral protein analysis and RT-PCR in 1998 [20]. The characteristic pathological signs for RHD were hemorrhages in the respiratory system, liver, spleen, cardiac muscle, and occasionally in the kidneys. Incubation period in rabbits is 2 to 3 days, morbidity approaches 100%, and mortality is sometimes over 90% in adults. The high morbidity and mortality rates have made RHD a big threat for rabbit industry and also a biological control tool for wild rabbit population. The causative virus, rabbit hemorrhagic disease virus (RHDV), was classified into the family Caliciviridae. This single-stranded nonenvelope RNA virus has a 7.5-kb genome and a 2.2 kb subgenome well packaged in a 27 to 35 nm (in diameter) icosahedral capsid with a major structural protein of about 60 kDa (VP60), and 10 peripheral cup-shaped depressions [12,20]. The ability to agglutinate human erythrocytes of group O, A, B and AB were reported [12,15,20].Detection by reverse transcriptase-polymerase chain reaction (RT-PCR) in a rabbit inoculation model showed t...

Clinicopathologic findings of naturally occurring Rabbit Hemorrhagic Disease Virus 2 infection in pet rabbits

“…This reflects abnormalities in the extrinsic and intrinsic coagulation pathways, respectively, associated with deficient hepatic synthesis of these factors by the diseased liver and consumption in association with the hemorrhagic diathesis and marked thrombocytopenia . Interestingly, systemic thrombosis, a typical lesion in classic RHD (especially in the kidneys) was not observed in the histopathologic examination of rabbit 1, although hemorrhagic diathesis was present . The liver is the primary source of protease coagulation factors, anticoagulants, and other critical hemostatic proteins deficiencies; therefore, hepatic disease can be associated with various combinations of procoagulant and anticoagulant proteins.…”

“…Additionally, the short half‐life of AST and ALT in rabbits (approximately 5 hours) could contribute to the fact the results were low by the time the rabbits were presented to the practice, even if they had been initially increased . The shorter disease course of classic RHD (with death typically in 2‐4 days post inoculation as compared with 3‐9 days in RHDV2) could explain why low AST and ALT were not detected in experimental studies. Anorexia and a decreased liver biosynthetic ability could have caused the mild hypocholesterolemia (downregulation due to decreased production of cholesterol precursors) and moderate hypoalbuminemia (in contrast to classic RHDV) and the severe hypoglycemia that developed in rabbit 1 .…”

RHDV2 epidemic in UK pet rabbits. Part 1: clinical features, gross post mortem and histopathological findings

“…RHD has been investigated extensively in the laboratory where the clinical course of the disease and the pathological changes can be monitored closely after an infective dose of the virus (Ueda et al 1992, Lavazza et al 1996, Alonso et al 1998, Mikami et al 1999, Prieto et al 2000, Kimura et al 2001, Chen et al 2008, Le Gall-Reculé et al 2013, Capucci et al 2017, Dalton et al 2018, Le Minor et al 2019. The clinical course of RHD has been described as peracute, acute or chronic (Marcato et al 1991, Abrantes et al 2012, OIE 2019b.…”

Toxicological Assessment of Aqueous and Methanol Leaves Extracts of Scoparia dulcis Linn (Plantaginaceae) in Wistar Rats

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