Abstract
Rabbit hemorrhagic disease (RHD), also known as rabbit calicivirus disease (RCVD), is caused by a calicivirus in the genus Lagovirus. RHD was first reported in captive domestic rabbits (Oryctolagus cuniculus) in China in 1984, and subsequently spread throughout Asia, Africa, and Europe.1-3 Although primarily reported in captive rabbits, it has also occurred in wild rabbits in Europe7 and feral rabbits in Australia and New Zealand1,3. RHD was first reported in the Western Hemisphere in Mexico in 1988, where disease was introduced by importation of infected frozen rabbit carcasses from China.1,2 There have been several reported outbreaks in the United States, the first in Iowa in April 20001,4 and a second in Utah in August 2001 (with shipment of rabbits from the Utah facility to Illinois resulting in cases in that state)5,6. The origin of infection in the Iowa and Utah outbreaks was not determined.
The disease is not zoonotic and only affects domestic and wild European rabbits (Oryctolagus cuniculus) and not the North American cottontail rabbit (Sylvilagus floridanus), black-tailed jackrabbit (Lepus californicus),or volcano rabbit (Romerolagus diazi).1-3 Transmission is by direct contact with contaminated feces, secretions, fomites (i.e., cages, clothing) that have been in contact with contaminated rabbits, or by aerosol transmission. The disease causes high mortality with death shortly after infection. Animals of all ages are susceptible to infection; however, serious disease resulting in death generally affects animals older than 5–7 wk of age. Sudden death with no premonitory clinical signs is often the case. Clinical signs in acute cases are generally nonspecific but can include anorexia, depression, constipation, and diarrhea. CNS signs such as paddling, ataxia, convulsions or opisthotonos may be seen and are due to cerebral microinfarctions. Gross necropsy lesions may be subtle but usually include hepatic necrosis, splenomegaly, pulmonary congestion, tracheal serous to blood-tinged transudate and sometimes a catarrhal enteritis. The most marked histologic lesion is diffuse, acute, peripheral lobular hepatic necrosis and occasional visceral microthrombi and infarction, particularly in the kidneys. Rabbits that survive infection may shed virus for 4 wk or more postinfection.1-3
Between 1 and 9 December 2001, three domestic rabbits housed at the Queens Zoo in Queens, New York died with little or no premonitory clinical signs (index cases). Based upon gross and histologic lesions, RHD infection was suspected and samples were sent to the Foreign Animal Disease Diagnostic Laboratory (FADDL), Plum Island, New York, where RHD infection was confirmed. The United States Department of Agriculture (USDA) classifies RHD as a foreign animal disease. Therefore, depopulation of the remaining five rabbits (contacts) at the park was required by the USDA and conducted on 10 December 2001. The contacts were anesthetized, bled, and humanely euthanatized with a concentrated pentobarbital sodium solution (Beuthanasia-D Special, Schering-Plough Animal Health, Union, NJ, USA).
The index cases had very subtle gross lesions. Lesions included serosanguinous nasal discharge, pulmonary or tracheal edema, congestion or hemorrhage, and the livers were light brown/red and mildly friable. Nephritis, gastritis, splenomegaly, or rectal hemorrhage were also seen, but were mild and not consistent between cases. The contacts had only incidental findings, not consistent with RHD. Significant histologic lesions referable to RHD were found in the livers of all index cases. These included severe, diffuse, acute, massive peracute hepatic necrosis with chromatolysis, chromatin margination, dissociation of hepatic cords, and few intranuclear inclusion bodies. The spleen showed moderate, diffuse, periarteriolar, lymphoid necrosis with chromatin margination and few intranuclear inclusion bodies. Mild, multifocal congestion and hemorrhage were seen in the lungs. None of the contacts demonstrated lesions consistent with RHD.
Upon diagnosis of RHD, the USDA mandated quarantine and euthanasia of the remaining rabbits and enclosure decontamination per USDA guidelines. Areas where the rabbits had been housed or transported, and potentially contaminated objects, were cleaned with one of the following: 0.5% sodium hypochlorite solution (10% solution of household bleach), 2% phenolic disinfectant (1 Stroke Environ, Calgon Vestal Laboratories, Inc., St. Louis, MO, USA), or steam sterilization. Substrate and enclosures were cleaned again 24 h later. Bedding was disposed of by incineration and materials used for euthanasia were disposed of by standard biomedical waste procedures. Staff cleaning potentially contaminated areas wore disposable coveralls. An investigation performed by the USDA was unsuccessful in identifying the origin of RHD. All collection rabbits originated from public donations of unknown source. Frozen rabbit carcasses are regularly purchased from a commercial source and are fed to carnivores at the zoo. The specific origin of rabbit carcasses purchased and fed prior to the outbreak could not be determined. However, the supplier's inventory included rabbits imported from China. Testing of remaining frozen rabbit carcasses from the zoo, and purchased from this vendor, were negative for RHD. A carrier collection rabbit, an infected frozen rabbit carcass that resulted in cross-contamination or fomite transmission, or a visitor to the zoo may have introduced the infection. There is no commercially available RHD diagnostic test and no licensed RHD vaccine available in the United States.1 Although RHD is considered exotic to the United States, it may be underdiagnosed. Suspected cases should be reported to state or federal animal health authorities.
Acknowledgments
The authors thank members of the Queens Zoo Animal Department, especially Kimm Koocher, for assistance.
Literature Cited
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