Leukoencephalomyelopathy in specific pathogen-free cats

Investigations were carried out on 8 specific pathogen-free cats (5 male and 3 female) from a colony experiencing "outbreaks" of progressive hind limb ataxia in 190 of 540 at-risk animals ranging from 3 months to 3 years old. These studies identified moderate to severe bilateral axonal degeneration within white matter regions of the cervical, thoracic, and lumbar spinal cord and in the white matter of the cerebral internal capsule and peduncle, in the roof of the fourth ventricle and inferior cerebellar peduncle, and in the external arcuate and pyramidal fibres of the medulla. There were varying degrees of accompanying microgliosis, astrocytosis, and capillary hyperplasia. Such a clinicopathologic syndrome, termed feline leukoencephalomyelopathy, has previously been described in cat colonies in Britain and New Zealand, although its etiology has not been determined. The degenerative nature of the lesions and their bilateral distribution suggest possible nutritional, metabolic, or toxic causes. Although these findings provide circumstantial evidence that the exclusive feeding of a gamma-irradiated diet of reduced vitamin A content is associated with the development of the neuronal lesions, further tissue micronutrient and antioxidant analysis will be required to support this hypothesis.     

Immune response of neonatal specific pathogen-free cats to experimental infection with Bartonella henselae

The purpose of this study was to determine whether neonatal cats develop and maintain a persistent bacteremia for longer than do adult cats with a normal mature immune system, and whether neonatal cats are susceptible to infection with Bartonella henselae by oral inoculation. Neonatal specific pathogen-free (SPF) cats were inoculated with B. henselae intradermally (n = 4) or orally (n = 5) or with 0.9% NaCl (n = 2). Blood was collected periodically through 16 weeks post-inoculation (PI) for serology, bacteriology and complete blood count. Cats inoculated orally or intradermally at 3-5 days of age were bacteremic through 12-16 weeks PI, similar to what is documented for adult cats inoculated intradermally or intravenously. One cat inoculated at age 2 weeks was bacteremic through 10 weeks PI; the other was not bacteremic. Intradermally inoculated neonatal cats produced serum IgG antibodies to B. henselae but orally inoculated neonatal cats did not. Infected cats with and without serum IgG antibodies to B. henselae became blood-culture negative simultaneously, suggesting that IgG is not required to clear bacteremia.     

Pathogenesis of Newcastle disease in commercial and specific pathogen-free turkeys experimentally infected with isolates of different virulence

The pathogenesis of five different Newcastle disease virus (NDV) isolates representing all pathotypes was examined in commercial and specific pathogen-free (SPF) turkeys. Experimentally-infected birds were monitored clinically and euthanatized, with subsequent tissue collection, for examination by histopathology, by immunohistochemistry for the presence of NDV nucleoprotein, and by in situ hybridization for the presence of replicating virus. Clinically, the lentogenic pathotype did not cause overt clinical signs in either commercial or SPF turkeys. Mesogenic viruses caused depression in some birds. Turkeys infected with velogenic neurotropic and velogenic viscerotropic isolates showed severe depression, and neurologic signs. Histologic appearances for all strains had many similarities to lesions observed in chickens inoculated with the various isolates; that is, lesions were present predominantly in lymphoid, intestinal, and central nervous tissues. However, in general, disease among turkeys was less severe than in chickens, and turkeys could be considered a subclinical carrier for some of the isolates.     

Feline panleukopenia virus, feline herpesvirus-1, and feline calicivirus antibody responses in seronegative specific pathogen-free cats after a single administration of two different modified live FVRCP vaccines

Two groups of feline panleukopenia virus (FPV), feline calicivirus (FCV), and feline herpesvirus-1 (FHV-1) seronegative cats (five cats per group) were administered one of two modified live feline viral rhinotracheitis, calicivirus, and panleukopenia virus (FVRCP) vaccines and the serological responses to each agent were followed over 28 days. While all cats developed detectable FPV and FCV antibody titers; only two cats developed detectable FHV-1 antibody titers using the criteria described by the testing laboratory. For FPV and FHV-1, there were no differences in seroconversion rates between the cats that were administered the intranasal (IN) FVRCP vaccine and the cats that were administered the parenteral FVRCP vaccine on any day post-inoculation. For FCV, the cats that were administered the IN FVRCP vaccine were more likely to seroconvert on days 10 and 14 when compared to cats that were administered the parenteral FVRCP vaccine.     

Feline leukemia virus-associated myelopathy in cats

Feline leukemia virus (FeLV) infection is associated with distinct neoplastic, hematologic, and immunosuppressive diseases. Here we report on a novel neurologic syndrome in 16 cats infected with FeLV for more than 2 years. Clinical signs consisted of abnormal vocalization, hyperesthesia, and paresis progressing to paralysis. The clinical course of affected cats involved gradually progressive neurologic dysfunction invariably resulting in euthanasia. Microscopically, white-matter degeneration with dilation of myelin sheaths and swollen axons was identified in the spinal cord and brain stem of affected animals. Neither neoplastic nor hematologic diseases commonly associated with FeLV infection were present. Fungal and protozoal infection in one animal was suggestive of impaired immune competence. Immunohistochemical staining of affected tissues revealed consistent expression of FeLV p27 antigens in neurons, endothelial cells, and glial cells. Furthermore, proviral DNA was amplified from multiple sections of spinal cord as well as intestine, spleen, and lymph nodes. These findings suggest that in a proportion of chronically FeLV-infected cats, a virus evolved with cytopathic potential for cells in the central nervous system.     

Feline leukemia virus-induced thrombocytopenia and macrothrombocytosis in cats

The Kawakami-Theilen strain of feline leukemia virus (FeLV-KT), an exogenous anemia-inducing retrovirus, induced significant macrothrombocytosis and thrombocytopenia during acute infections of cats. The geometric mean platelet volumes of both freshly isolated fixed platelets and ethylenediamine tetraacetic acid-sphered platelets from infected cats were increased, but the ratio of fresh-fixed to ethylenediamine tetraacetic acid-sphered platelet volumes, an estimate of ethylenediamine tetraacetic acid-induced isovolumetric shape change, was normal. Total plasma membrane increased as the platelet volumes increased in FeLV-KT-infected cats, but estimated surface connected canalicular system surface area did not. Platelet concentrations were decreased 2 to 6 weeks after inoculation, but marked macrothrombocytosis resulted in a trend toward increased platelet mass on weeks 5 and 6 after inoculation. Thus, FeLV-KT-induced macrothrombocytosis may serve as a model of impaired platelet volume regulation. The platelet volume and platelet membrane surface area abnormalities found suggest that this model would allow studies of the megakaryocyte/platelet axis, particularly in the area of membrane formation and territorial demarcation.     

Vaccination of gnotobiotic primary specific pathogen-free pigs against Haemophilus parasuis.

Three trials were conducted to establish if young primary specific pathogen free (SPF) pigs could be protected from Glasser's disease by vaccination. Three age groups of cesarean-derived isolator-reared gnotobiotic pigs were vaccinated twice at 4 and 6, 3 and 5, and 2 and 4 wk of age respectively with a formalin killed aluminum hydroxide adsorbed bacterin prepared from three strains of Haemophilus parasuis isolated from Ontario pigs affected with Glasser's disease. When challenged two weeks later with the homologous strains of virulent bacteria, all the vaccinated pigs remained healthy, while 17/18 nonvaccinated pigs became severely sick or died between three and seven days postchallenge. The one surviving nonimmunized pig was retarded in growth. All of the nonimmunized pigs had visible lesions of polyserositis, the most common being polyarthritis (14/18). Other lesions were fibrinous meningitis, pericarditis, pleurisy and/or peritonitis. Two of the pigs died with a septicemia. Haemophilus parasuis was isolated from 15/18 nonimmunized pigs, usually from several of the affected sites. The organisms were not isolated from the immunized pigs, nor from the surviving nonimmunized pig. Attempts to detect the presence of specific antibodies against the H. parasuis strains in the sera of the immunized or exposed pigs by the passive hemagglutination test or by enzyme linked immunoassay were unsuccessful. The results of this work indicate that primary SPF pigs can be protected from Glasser's disease by vaccination as early as 2 and 4 wk of age. The nature of this protective mechanism was not established in this study.     

Feline infectious peritonitis with spinal cord involvement in two cats.

Two cats from the same household had posterior paresis and hypergammaglobulinemia. Histologic evaluation of the spinal cords revealed a pyogranulomatous reaction consistent with that reported for feline infectious peritonitis.