Clinical features and rapid plasma reagin antibody titers in spontaneous and experimental rabbit syphilis

Rapid plasma reagin (RPR) titers were periodically examined during and after treatment in three rabbits clinically diagnosed with rabbit syphilis. RPR titers remained positive after clinical recovery and then gradually declined. Of the two rabbits inoculated experimentally, one showed clinical signs of the disease, while the other did not. RPR titers were also periodically evaluated before and after inoculation in these two rabbits. The trends in RPR titers reflected the course of infection, both in the spontaneous and in the experimental cases. An inapparent case and cases without clinical signs after clinical recovery showed low titers for long period of time. Useful information for interpretation of RPR titers measured clinically was obtained by this survey.     

RPR test for serological survey of rabbit syphilis in companion rabbits

Since the RPR (rapid plasma regain) test was found to be useful for the diagnosis of rabbit syphilis, serological survey by this test has been carried out in Japanese companion rabbits. A hundred virgin household rabbits kept alone and without signs and history of syphilis were examined by RPR test from April 2001 to March 2002, in Tokyo, Japan. The test was positive in 35 cases and negative in 65 cases. RPR negative rabbits should be selected for breeding to prevent the spread of rabbit syphilis in companion rabbits in Japan.     

Lethal encephalitozoonosis in cyclophosphamide-treated rabbits

Encephalitozoonosis is an opportunistic infection in animals and humans. Its clinical form is observed in immunosuppressed hosts. We studied the occurrence of the manifest form of rabbit microsporidiosis under cyclophosphamide immunomodulation in 40 New Zealand rabbits. The experimental animals were intraperitoneally infected with 5 x 10(7) Encephalitozoon cuniculi spores. Two weeks after infection the animals were treated intraperitoneally with cyclophosphamide, first with 50 mg/kg and then with 15 mg/kg weekly during the 12-week experimental period. Positive controls were either E. cuniculi-infected or cyclophosphamide-immunosuppressed animals. The negative control rabbits remained untreated. Both clinical signs of encephalitozoonosis and depression of peripheral blood cell count developed between weeks 4 and 6 in the experimental animals which died during week 6 of the experiment. No clinical signs compatible with encephalitozoonosis were observed in any of the controls. The results suggest that immunosuppression induced by cyclophosphamide can give rise to a lethal form of encephalitozoonosis.     

Rabies in two privately owned domestic rabbits

Two privately owned domestic rabbits (Oryctolagus cuniculus) in Maryland were found to be infected with the raccoon variant of the rabies virus in 1998. Both rabbits had an acute onset of anorexia and paralysis or paresis of the left forelimb; 1 also developed head tremors and a head tilt. One of the rabbits became ill 25 days after being attacked by a raccoon (Procyon lotor) and was euthanatized 3 days after onset of illness. The other rabbit, which was housed in an outdoor hutch, died 4 days after onset of clinical signs; the source of infection in that rabbit remains unknown. Currently, there is not a rabies vaccine approved for use in rabbits; thus, the only way to prevent the infection in rabbits is to prevent exposure. Veterinarians in rabies-enzootic areas should be familiar with the clinical signs of rabies in rabbits and should caution rabbit owners about the need to protect their pets from contact with wildlife.     

MALIGNANT CATARRHAL FEVER IN FARMED RUSA DEER (CERVUS TIMORENSIS): 2. Animal Transmission and Virological Studies

SUMMARY A disease with clinical signs and histological lesions similar to malignant catarrhal fever in cattle was transmitted from Rusa deer (Cervus timorensis) to rabbits. This was accomplished on 3 separate occasions, and the disease was serially passaged in rabbits up to 11 times. The clinical signs in affected rabbits were pyrexia, depression, anorexia, mucopurulent conjuctivitis, nasal discharge and diarrhoea. These signs were seen in 27 of 38 inoculated rabbits with the mean incubation period being 12 days (range 8 to 20 days). Histologically, affected rabbits exhibited mononuclear perivascular cuffing and vasculitis in the brain, heart, liver and kidney. Lymph nodes and spleen showed destruction and loss of mature lymphocytes and lymphoid follicles and an increased number of large lymphoblastoid cells. These clinical signs and lesions were not detected in control rabbits. The disease was not transmitted to cattle, sheep, guinea pigs or mice, nor was an agent isolated in cattle, deer or rabbit tissue cultures, or in chicken embryos.     

Fatal toxoplasmosis in domestic rabbits in the USA.

Three rabbits from two sources died after an acute illness characterized by fever, lethargy and diarrhea in one rabbit and no clinical signs in two rabbits. The most striking lesion in all three rabbits was foci of necrosis of the spleen and liver associated with massive presence of multiplying Toxoplasma gondii tachyzoites. The diagnosis was confirmed by specific staining with anti-T. gondii serum in an avidin-biotin complex immunohistochemical stain.     

Pathogenesis of canine parvovirus enteritis: the importance of viremia

The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.     

Experimental infection of young rabbits with a rabbit enteric coronavirus.

The clinical signs and lesions caused by the rabbit enteric coronavirus (RECV) were studied in young rabbits orally inoculated with a suspension containing RECV particles. The inoculated animals were observed daily for evidence of diarrhea. Fecal samples and specimens from the small intestine and from the gut associated lymphoid tissue (GALT) were collected from 2 h to 29 days postinoculation (PI) and processed for immune electron microscopy (IEM) and light microscopy. Coronavirus particles were detected in the cecal contents of most inoculated animals from 6 h to 29 days PI. Lesions were first observed 6 h PI and were characterized by a loss of the brush border of mature enterocytes located at the tips of intestinal villi and by necrosis of these cells. At 48 h PI, short intestinal villi and hypertrophic crypts were noted. In the GALT, complete necrosis of the M cells as well as necrosis of the enterocytes lining the villi above the lymphoid follicules with hypertrophy of the corresponding crypts were observed in all the animals. Five inoculated rabbits had diarrhea three days PI. The presence of RECV particles in the feces of the sick animals and the microscopic lesions observed in the small intestine suggested that the virus was responsible for the clinical signs. A few inoculated rabbits remained free of diarrhea. Fecal material collected at postmortem examination contained RECV particles. The results suggest that the virus could also produce a subclinical infection.     

Benzimidazole Toxicosis in Rabbits: 13 Cases (2003 to 2011)

The objective of this study was to evaluate both clinical and histologic anomalies associated with suspected benzimidazole toxicosis in rabbits. Histopathologic records were reviewed from rabbit cases that were diagnosed with suspected benzimidazole toxicosis at 2 specialty pathology services. Medical records were also solicited from veterinarians who treated rabbits with suspected benzimidazole toxicosis. In all, 13 cases were included in this retrospective study. Histologically, presumed radiomimetic lesions of benzimidazole toxicosis were noted in 3 cases. An additional 10 cases exhibited lesions suggestive of benzimidazole toxicosis. Common clinical signs observed in the study of rabbits included inappetence, lethargy, hemorrhage, and death. One rabbit with suspected benzimidazole toxicosis survived. Benzimidazoles should be used judiciously in rabbits at published doses only after the owners are knowledgeable of the potential health risks associated with this class of drugs. The prognosis for rabbits with suspected benzimidazole toxicosis is poor, but supportive care resulted in the survival of 1 suspected case in this study.     

Lymphoma with cutaneous involvement in three domestic rabbits (Oryctolagus cuniculus)

Three domestic rabbits ( Oryctolagus cuniculus ) with cutaneous lymphoma are described. Two rabbits were young (7 weeks and 1 years) and were euthanized within 1 week of showing clinical signs. Lymphoma was found in the skin and internal organs. The third rabbit was 9.5 years of age, and lived for more than 1 year after diagnosis. No response was seen to either 2 months of alpha-interferon administration or a 2.5-week course of isotretinoin treatment. After 1 year the rabbit died suddenly; the owner refused necropsy. Immunologic stains of the tumour in all three rabbits showed T cells to be the lymphoma cell type.     

The first appearance of infectious hemorrhagic disease of rabbits in Austria

In three Austrian rabbit units (two in the west, one in the east) heavy losses occurred in April/May 1989. The clinical course (deaths in adult animals, haemorrhagic diathesis) of the disease was indicative for an infection with the RHD-virus. Necropsy confirmed the suggestive clinical diagnosis as bleeding of the nostrils, hyperaemia in the respiratory tract, spleen tumor, partly decolorized livers, hyperaemia of kidneys with rare petechias could be observed. Histologic examination revealed centrolobular liver necrosis, lung bleeding and edema, tumor of spleen and atrophy of spleen follicles. Rabbits infected with organ suspensions died within 48 hours. The organ suspensions and the suspensions of the already necropsied animals showed a haemagglutination titer for above 1:100. This reaction could be inhibited with a specific RHD-antiserum. The intramuscular application of a RHD-reference strain in one hare, two wild rabbits and a rabbit did not induce clinical disease or death of the leporids during a six week observation period. The rabbit died within 48 hours post infection. However the hare and wild rabbits showed high antibody titers by ELISA at the end of the observation period. Before infection the two wild rabbits were serologically negative.     

Canine Ehrlichiosis in Six Dogs with Persistently Increased Antibody Titers

Chronic ehrlichiosis was diagnosed in six dogs on the basis of increased immunofluorescent antibody titers to Ehrlichia canis. Although clinical signs varied, all six dogs were anemic, hyperglobulinemic, and an IgG monoclonal gammopathy was documented in five dogs in which serum protein electrophoreses were performed. All dogs were treated with tetracycline for at least 14 days; four dogs also received immunosuppressive drugs. Clinical signs resolved within 1 week, hematologic abnormalities resolved in 1 to 5 months, and increased globulin concentrations normalized in 1 to 15 months; however, E. canis antibody titers remained increased for 15 to 31 months after initiation of treatment. Results of this study show that increased E. canis titers can persist in dogs with ehrlichiosis for many months after clinical recovery.     

Nasal Mucosal Adenocarcinoma in a Pet Rabbit

A 6-year-old male rabbit (Oryctolagus cuniculus) presented with upper respiratory disease that was nonresponsive to antibiotic therapy. Computed tomography revealed a severe space-occupying lesion of the right nasal cavity, deviation of the nasal septum to the left, and narrowing of the left nasal cavity. An exploratory rhinostomy was performed for the purposes of diagnostic sample collection and to improve airflow as clinical signs of dyspnea were becoming more pronounced. The histopathologic disease diagnosis from the biopsy samples was nasal mucosal adenocarcinoma. Palliative rhinostomy provided only temporary improvement in airflow, and the patient was euthanized 3 days later. On necropsy, neoplasia was found to extend into the rhinopharynx. This is the first reported case of nasal mucosal adenocarcinoma in rabbits. This important differential diagnosis should be considered for any rabbit with clinical signs of upper respiratory disease that is nonresponsive to medical therapy.     

Natural parvovirus infection in laboratory rabbits

Laboratory rabbits from various commercial and private sources were found to have high serum antibody titers specific for lapine parvovirus (LPV). By both immunofluorescence and hemagglutination inhibition assays, 75% of these sera were positive for LPV. This finding, together with the recovery of LPV from kidneys of neonatal rabbits, suggested that LPV infection is common in commercially available rabbits in the United States. It was concluded that use of infected rabbits could interfere with research in which rabbit cell cultures or in vitro immunologic assays are used.     

The immune response of rabbits to 3 strains of Mycoplasma agalactiae var. bovis isolated from mastitic bovine udders.

Rabbits were given 3 serologically-related trains of mycoplasma isolated from mastitic bovine udders. Growth inhibiting antibodies were not found. High-titered sera from each rabbit immunized with each strain developed at least 4 precipitin lines to each organism and at least one line of identity was demonstrated between the organisms. Significant indirect hemagglutination titers were found in all rabbits in 1 week, with titers reaching 1.0 X 10(5) to 3.3 X 10(5) in 4 to 6 weeks but despite continued intravenous antigenic stimulation, titers quickly fell to low levels thereafter.     

Response of congenitally immune chicks to viscerotropic velogenic Newcastle disease virus.

Separate groups of chicks of hen hyperimmune to viscerotropic velogenic Newcastle disease virus (VVNDV) were challenge-exposed to VVNDV by intraocular route at 1 day and 34 days old. Their response was evaluated by clinical symptoms, hemagglutination-inhibition (HI) titers, and virus isolations. Chicks exposed at 1 day old excreted VVNDV from the vent for up to 60 days; their active mean HI titers remained low (10-40); and deaths from VVNDV occurred early (5-16 days) and late (28-55 days). Chicks challenge-exposed at 34 days old excreted virus from the vent for 10 days; active HI titers developed quickly and remained high (891-1177); and deaths and signs of VVNDV occurred early (5-13 days).     

Host response in rabbits to infection with Pasteurella multocida serogroup F strains originating from fowl cholera

Although Pasteurella multocida serogroup F has been described as an avian-adapted serogroup, it was recently found in rabbit nests in the Czech Republic. Therefore, the ability of 2 avian P. multocida serogroup F strains to induce disease in rabbits was investigated. Two groups of 18 Pasteurella-free rabbits were intranasally challenged with strains isolated from chickens and turkeys. Half of the animals in each challenge group were immunosuppressed using dexamethasone. All of the challenged rabbits exhibited clinical signs of peracute septicemic disease, ending with shock, and died or were euthanized in the terminal stages of the disease 1 to 2 d post-infection. Gross pathological changes included systemic vascular collapse and vascular leak syndrome. Hyperemia, hemorrhage, edema, inflammatory cell infiltrates, focal necrosis, and degenerative changes were observed histologically in parenchymatous organs. This is the first study directly demonstrating that avian P. multocida serogroup F strains are highly virulent in rabbits and that avian hosts cannot be excluded as a possible source of rabbit infection with serogroup F.