VETERINARY MEDICINE : LAGOMORPHA
 

Leporidae

• Lepus
• Lepus europaeus (European hare) : Francisella tularensis, Yersinia enterocolitica, Yersinia pseudotuberculosis


•  Oryctolagus
• Oryctolagus cuniculus (rabbit) : Taenia serialis, Taenia pisiformis, Taenia taeniaeformis,Otobius lagophilus, Yersinia pestis, Francisella tularensis, monkeypox virus, Mycobacterium avium subsp. paratuberculosis (Johne's disease / chronic dysentery of cattle / paratuberculosis), Pasteurella multocida (hemolytic septicemia : transmitted primarily by direct contact, although aerosol transmission may also occur; rhinitis, otitis media et interna, pneumonia, abscesses, reproductive tract infections, torticollis, nystagmus, conjunctivitis), Bordetella bronchiseptica (asymptomatic), Staphylococcus aureus, Pseudomonas aeruginosa, Listeria monocytogenes, Microsporum canis, Trichophyton mentagrophytes, Sarcoptes scabiei (sarcoptic mange : back, head, limbs and genitalia)
• stools : Salmonella enterica serotype Typhimurium, Salmonella enterica, Yersinia pseudotuberculosis
• urine : Encephalitozoon cuniculi (even asymptomatic)
Other nontransmissible diseases :
• Shope rabbit fibroma virus (SFV)
• myxoma virus (MYX) is a poxvirus that causes a benign cutaneous fibroma in Sylvilagus brasiliensis and Sylvilagus bachmani  rabbits in South America which is transmitted mechanically by mosquitoes. In the European rabbit, Oryctolagus, which is a pest in Australia and England, the virus from Sylvilagus produces myxomatosis, a generalized fibromatosis (edema of face, eyelids, and anogenital region and pseudotumors of ears, nose, footpads) with systemic immunosuppression that is lethal in 50%. Myxomatosis was deliberately introduced into Australia in 1950 and into Europe in 1952 : the rabbit flea Spilopsyllus cuniculi is not an effective vector for myxoma in Australia, but is the principal vector in Britain. It was at first spectacularly successful in controlling the rabbit pest, but biological adjustments occurred in the virulence of the virus and the genetic resistances of rabbits. After 30 years of interaction, natural selection has resulted in a balance at a fairly high level of viral virulence. This may have occurred more rapidly in hot climates, as high ambient temperatures increase the survival rate of infected rabbits. Resistant rabbits are less effective transmitters of the virus and this may encourage the emergence of more virulent virus strains. Myxomatosis is endemic in the UK's fauna. The disease prevails also in several other European countries, but some countries have reportedly managed to eradicate it^ref. Myxoma virus infection of primary mouse embryo fibroblasts elicits Erk signaling, which is integrated to IRF3 activation and type I interferon induction. Erk inactivation or disruption of interferon signaling mediated by the transcription factor STAT1 breaks the cellular blockade to myxoma virus multiplication. Moreover, STAT1 deficiency renders mice highly susceptible to lethal myxoma virus infection. Thus, the Erk–interferon–STAT1 signaling cascade elicited by myxoma virus in nonpermissive primary mouse embryo fibroblasts mediates an innate cellular barrier to poxvirus infection^ref. During 2004, the disease was reportedly present in the following European countries: Belgium, Czech Republic, Denmark, Estonia, France, Germany, Hungary, Ireland, Malta, Poland Portugal, Russia, Slovnia, Spain, Switzerland and UK. Rabbits were introduced into Britain by invading Roman legions 2000 years ago. The population, estimated at 37.5 million, is at its highest for half a century. Myxomatosis was 1st observed in laboratory rabbits in Uruguay in 1896. It was tolerated by South American rabbits but proved lethal to their European cousins. The disease was deliberately introduced into Australia to devastating effect in 1950. In the autumn of 1953, it arrived in Britain. Ministry of Agriculture officials tried to contain it but failed. 2 years later, 99% of Britain's wild rabbits were dead. It was alleged that some farmers had spread the disease deliberately, as rabbits had been blamed for the destruction of vast swathes of crops. The Pests Act of 1954 criminalized intentional transmission, but few prosecutions followed. The rabbit population has now grown to half of what it was before the disease spread. The high cost of vaccination -- between 10 to 20 GBP [17 to 34 USD] per rabbit -- is helping to spread the disease. Responsible pet owners already vaccinate their rabbits twice a year. Your average person will buy rabbits for their kids and then just leave them at the bottom of the garden when the family gets bored
• rabbit hemorrhagic disease virus (RHDV) => rabbit hemorrhagic disease (RHD) / viral hemorrhagic disease (VHD) of rabbits : a highly infectious viral disease of the European rabbit (Oryctolagus cuniculus). This is the species from which all U.S. domestic and commercial rabbits are derived. American cottontail rabbits and jackrabbits are not susceptible to infection. RHD is not known to harm humans or other animals.  Once the disease is introduced into a rabbitry, it can spread rapidly, causing a high percentage of the rabbits to die. There is no treatment for the disease. RHD damages the liver, intestines, and lymphatic tissue and causes terminal massive blood clots. The incubation period is about 24 to 48 hours.  Predominantly, young adult and adult rabbits die suddenly within 6 to 24 hours of the onset of fever with few clinical signs. ever may be as high as 105 F (40.5 C) but often is not detected until rabbits show terminal clinical signs. Most animals appear depressed or reluctant to move in the final hours and may show a variety of neurologic signs, including excitement, incoordination, paddling, and opisthotonos (abnormal position of the head due to spasms of the muscles at the top and back of the neck). Some affected rabbits may have a foamy nasal discharge. The death rate for RHD ranges from 50 to 100%. RHD is caused by a highly contagious virus.  The disease can be transmitted by contact with infected rabbits, rabbit products, rodents, and contaminated objects, such as cages, feeders, and clothing.  The virus also may be carried short distances through moisture in the air.  The risk of spread of RHD is higher when confined rabbits are in close contact with each other. Infected rabbits that recover may become carriers of the virus and may shed virus for at least 4 weeks. To protect against introducing RHD into the U.S. rabbit population, owners and producers should avoid contact between their rabbits and imported rabbit meat, pelts, or other possibly contaminated objects from RHD-affected countries. To prevent the spread of the disease if it enters the USA, rabbit owners should prevent contact between healthy rabbits and infected rabbits and contaminated objects (e.g., cages, feeders, and clothing). Rabbits that appear healthy can be in the early stage of disease and later spread the disease. Recovered rabbits also appear healthy but can be carriers for at least 4 weeks and spread the disease to other rabbits. Owners should be cautious and isolate new rabbits and rabbits returning from shows for at least 5 days.  If rabbits were exposed to RHD, isolation may help prevent spread to other rabbits. Clinical disease usually will be noticeable within 48 hours of infection. If RHD is suspected, to prevent spread of the virus, rabbit owners should clean and disinfect all equipment. After thorough cleaning, rabbit breeders should use one of the following disinfectant solutions on equipment to inactivate the virus: 2% 1-Stroke Environ (Steris Corporation, St. Louis, MO), 0.5% sodium hypochlorite, or 10% household bleach. No vaccine is legally available for use in the USA. Vaccine has been used in other countries. Vaccination often reduces the number of rabbits dying from RHD, but will not eradicate the disease. Rabbits vaccinated against RHD may become infected but not show signs of disease, thereby allowing spread of the virus as a carrier^ref.

There is no definitive proof that a rabbit surviving the disease can act as a carrier of the virus for 4 weeks. If an animal is able to survive (5-25% of the infected), it is because there was a quick and efficient immune response. After 5-6 days post infection, a consistent immune response can be observed; no more viral circulating particles will be detected in the bloodstream using traditional diagnostic tests (i.e. ELISA), and the residual virions can be detected in a complex form only in the liver and spleen. What is surely true is that the virus is highly resistant in the environment and can persist at an infectious level for a very long time (several months). Therefore, even convalescent rabbits can act as vectors of the disease if, for example, their fur had been contaminated during the acute phase of the disease. It is true that there is no specific treatment, but the use of hyper-immune serum in the initial phases of the disease can stop the infection. This is due to the fact that humoral immunity is most important in protecting rabbits from infection. 3) For the same reason, vaccination is absolutely effective in preventing both the infection and the disease. If animals are correctly vaccinated, there is no infection at all, and the virus is fully neutralized. In our experience, by applying a regular and correct vaccination plan, it is possible to prevent the diffusion of the disease in industrial farms, and it is also possible to obtain a full eradication in those infected units. Therefore, we believe that the "carrier" status of vaccinated/infected rabbits does not exist. Indeed, it could be important and interesting to determine which viral strain is responsible for the outbreak and to check whether the available vaccine has been prepared with the same strain. In fact, it is known that there is at least one major antigenic variant of the virus -- called RHDVa^ref -- that indeed was also responsible for the 1st outbreak in USA in 2000. This viral variant present some major antigenic changes in neutralizing epitopes, and therefore, even if there is quite a good level of cross immunity induced by the "classical" vaccine, the overall level of protection could be lower. What is especially interesting is that the OIE laboratory clarifies how the contaminated fur of a convalescing rabbit may be the source of infection for other rabbits. The USDA website does not make that clarification. The vaccine mentioned above does not appear to have approval in the USA.
It is an acute infectious disease of wild and domestic rabbits and hares. Contact with infected rabbits, rabbit products, rodents, and contaminated objects, such as cages, feeders, and clothing can spread the disease. Infected droplets may spread the virus short distances through the air. The risk of spread of RHD is higher when confined rabbits are in close contact with each other. Infected rabbits that recover may become carriers of the virus and may shed virus for at least 4 weeks. RHD has an incubation time of 24 to 48 hours and damages the liver (necrotizing hepatitis), intestines, and lymphatic tissue and causes terminal massive blood clots. Young adult and adult rabbits suddenly die, within 6 to 24 hours of the onset of hyperacute fever, with few clinical signs (lethargy, tachypnea, and cyanosis). Fever may be as high as 105°F (40.5°C) but often is not detected until rabbits show terminal clinical signs. Animals appear depressed or reluctant to move in the last hours and may show a variety of neurologic signs, including excitement, incoordination, paddling, and an abnormal position of the head due to spasms of the muscles at the top and back of the neck (opisthotonos). Some affected rabbits may have a foamy nasal discharge. The death rate for RHD ranges from 50 to 100%. Vaccination is available for domestic rabbits in some countries. RHD was first released illegally into New Zealand in 1997. Rabbit hemorrhagic disease was first recognized in China in the mid-1980s. It occurs in Korea, is widespread in Australia and New Zealand, and has been reported in most of Europe. The domestic rabbit and the European rabbit are susceptible, and it appears as though other lagomorphs are not. The disease has a high mortality rate, so it is of some consequence. Although not reported previously from South America, Cuba and the United States have had significant outbreaks, and the disease has been eradicated from Mexico since 1992. Both the United States and Mexican outbreaks had some association with infected meat imported from China, so I would like to know if Uruguay imports any rabbit meat from China and, if so, whether there any association with this new outbreak. A farmer (not the government!) in New Zealand intentionally introduced the virus as a biocontrol tool after great frustration with rabbit control policies. In 1997 the government changed the law. The RHDVa variant was first identified in Europe, in 1997. In Italy, it is slowly replacing the original RHDV strain in the field. The RHDV identified in the USA in 2000 and in Uruguary in 2004 was also the RHDVa variant. Under experimental conditions, the vaccine produced with the original RHDV strain protects rabbits exposed to RHDVa. However, if we consider that the antigenic drift that led to RHDVa involves an epitope that is important for protection from infection, it might be better to use a vaccine produced using the RHDVa strain. Control measures:
• culling of sick rabbits;
• disinfection of premises and equipment;
• spraying of insecticide;
• control of rodents and birds;
• burning and burying of dead rabbits, feedstuff, skins and faeces;
• recommendations have been issued aimed at preventing gatherings of rabbit producers and related persons;
• vaccination: arrangements are being made to import vaccine; vaccination is due to be applied in at-risk areas and establishments where the disease has not been registered but will not be applied in commercial rabbit farms unless necessary;
• control of the movements of people, animals, and vehicles; ban on the movement of rabbits to other establishments and slaughterhouses;
• exports of rabbits and by-products were immediately suspended.
RHD is a highly contagious and acute fatal disease of wild and domestic European rabbits, 1st reported in 1984 in the People's Republic of China. Currently, it is endemic in East Asia, Europe (including the UK) and Oceania. Outbreaks have also been recorded in Central America (Mexico and Cuba), USA, Saudi Arabia, West and North Africa. The disease is one (B353) of the 3 lagomorph diseases reportable to the OIE. Chinese authorities assert that this was associated with importation of Angora rabbits from Germany. There is significant debate about its origins. There are numerous reports of a non-pathogenic virus circulating in Europe before the discovery of rabbit calicivirus disease in China. In 1996 a non-pathogenic rabbit calicivirus closely related to rabbit calicivirus was described^ref. Rabbit calicivirus is now established in > 40 countries. In 1989 Australian authorities commenced their investigations into the potential of rabbit calicivirus for control of European rabbits. The Australian Agricultural Council and the former Council of Nature Conservation Ministers (CONCOM) recommended that rabbit calicivirus disease virus be examined as a potential biological control agent for rabbits. After some preliminary studies, a 3 year laboratory investigation of rabbit calicivirus was carried out in the biocontainment facilities at CSIRO Australian Animal Health Laboratory (AAHL). To ensure the virus would be safe under Australian and New Zealand conditions, a list of animals for testing was developed by a national working party with animal welfare and conservation representation. 28 species were chosen to represent a range of Australian and New Zealand fauna. 5 other species were tested later. When testing non target-species, AAHL used 4 animals from each species.They were tested by applying a large number of tests and test systems to each animal, looking for any sign that the virus was capable of replicating in the non-target species. The dose used was 1,000 LD₅₀'s, sufficiently large to present a realistic challenge, but not large enough (in most animals) to induce an antibody response to the inert virus protein - that is why it was chosen. When testing non target-species, AAHL used 4 animals from each species. They were tested by applying a large number of tests and test systems to each animal, looking for any sign that the virus was capable of growing in the non-target species. A typical regime was :
• clinical observation
• serology for detecting antibodies on samples at days 0, 7 and 14 (using indirect and competition ELISA's)
• virus detection by PCR on days 1, 2, 7, 14
• gross pathology at post mortem on day 14
• histological examination of tissues taken at post mortem from heart, lung, liver, kidney, spleen
• several histopathology tests on samples from the same organs
• virus detection PCR on the samples from the same organs
• a sentinel rabbit was kept with the test animals and subjected to a similar test regime.
If animals died, if a test provided an ambivalent result, or if there was any suspicion of infection then further tests were conducted. Rabbit calicivirus did not replicate in any of the 33 non-target species tested. Antibodies to RCD were found in several species, this was caused by an immune response to injection of foreign material and further testing clearly showed the virus was not growing in the animals. In 1996, Australia's Biological Control Authority (BCA) independently assessed CSIRO's work and concluded that 'the range of tests used would be expected to find evidence of infection of any of the species tested.  There was no evidence of infection of any of the non-target species tested. There was no evidence of infection of any of the non-target species tested. The Biological Control Authority (BCA) also noted that throughout the world, 43 different animal species had been tested for susceptibility to rabbit calicivirus. The virus did not replicate in any of them. After the testing at AAHL had demonstrated the safety of the virus, State and Commonwealth agencies determined that more study was required about its potential effectiveness in the field.  They established the Australia and New Zealand Rabbit Calicivirus Disease Program (ANZRCDP) to take responsibility for the program, including field trials on an island. A consortium of different organisations make up this program. The virus appeared on the mainland in October 1995. While the mechanisms of transmission of the virus are well documented, we may never know what combination of methods led to the escape of the virus. Both Australian and overseas research into rabbit calicivirus disease was independently assessed by the BCA in 1996. Their report has been published. The authority considered the scientific evidence and issues raised in 472 public submissions (including several from international scientists) received in response to national press advertisements and gazette notices. Concern for public health was raised in some of the submissions. In response to this, a Rabbit Calicivirus Disease Human Health Study group was formed. It consisted of representatives from the Bureau of Resource Sciences, Department of Health and Family Services and independent infectious disease experts. Information collected from 47 organisations that were working with rabbit calicivirus disease in 16 countries, and a survey on Australians with occupational exposure to rabbit calicivirus disease confirmed that infection or ill effects are not known to occur in people who have worked closely with this virus. Rabbit calicivirus has been vigorously assessed by Australian authorities. The BCA considered the requirements of the Biological Control Act 1984, and concluded that the requirements for recommending declarations of rabbits as target organisms and rabbit calicivirus disease virus as agent organisms were met^{ref1, ref2, ref3}
• Schmorl's disease : necrobacillosis in rabbits and rats, characterized by abscesses and areas of necrosis on the body, head, and interior of the mouth.
• penicillin enterotoxemia
• enteropathogenic Escherichia coli (EPEC) O109 (watery diarrhoea)
• Clostridium piliforme (Tizzer's bacillus) : watery diarrhea (Tizzer's disease)
• Treponema paraluiscuniculi
• Eimeria stiedae (hepatic coccidiosis)
• Eimeria flavescens, Eimeria intestinalis, Eimeria irresidua, Eimeria magna, Eimeria neoleporis (intestinal coccidiosis)
• Passalurus ambiguus (enterocolitis or asymptomatic)
• Graphidium strigosum (gastroenteritis)
• Trichuris spp.
• Psoroptes cuniculi (rabbit ear mite : psoroptic or auricular mange : otitis externa => media)
• Cheyletiella parasitovorax (rogna : dermatitis with right plaques and alopecia in dorsal neck)
• Demodex cuniculi (demodectic mange)
• myasis
• rabbit syphilis / vent disease : a venereal disease of rabbits consisting of lesions with scabs around the external genitalia, and sometimes elsewhere on the body, caused by infection with Treponema paraluiscuniculi

•  Sylvilagus
• Sylvilagus audubonii (desert cottontail, jack rabbit) : Yersinia pestis, Anaplasma phagocytophilum

monkeypox virus

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