No description available.

Call number: LD2668 .T4 1984 G57 / Master of Science

Typescript. / Digitized by Kansas Correctional Industries

Jaagsiekte is a contagious cancer affecting the lungs of sheep. Although the etiological agent is Jaagsiekte retrovirus (JSRV), two other retroviruses viz South African maedi visna virus ( SA - OMVV) and a novel Bovine retrovirus (BRV) have been associated with or implicated in the jaagsiekte disease complex. JSRV was sufficiently purified from lung rinse material using a Freon extraction, Percoll density gradient centrifugation and chranatography on a Sephacryl column, its polypeptide composition was studied by gel electrophoresis and its morphology observed electron microscopically. Monoclonal antibodies were made against purified preparations of the virus. Two hybridomas were isolated that produced MAbs which appear to be tumour cell specific. A third hybridoma, called 4A1O, produces antibodies considered to be viral specific. These MAbs have been used in the development of JS specific immunoassays. A cross reaction between JSRV and a polyclonal serum against Mason Pfizer monkey virus (MPMV) was confirmed and used in a Western blot technique to identify, monitor and differentiate JSRV from other viruses. During the study of JSRV it became apparent that another retrovirus was often present in JS infected lungs. This virus, referred to as SA - OM1V I, is a novel South African isolate of maedi visna virus (MVV). As SA - OM1V I has physicochemical characteristics similar to JSRV, it was often found in purified JSRV preparations. Being a retrovirus it is also detected by the reverse transcriptase assay which was the only method used to assay and monitor for JSRV during the early stages of our work. Using a Westen blot technique and sera against MVV and MPMV it was possible to simultaneously detect and differentiate JSRV from SA - OMVV I. A method was also developed whereby the two viruses could be separated from each other during purification. The information gained and techniques developed whilst studyiing JSRV were also used to isolate and characterize BRV. This novel virus originated from bovine cells that had been co-cultivated with white blood cells from an ox suffering from malignant catarrhal fever. Three out of four sheep inoculated with BRV developed JS. It therefore had to be· ascertained whether this virus was related to JSRV or not. The comparative study revealed that BRV was biochemically and morphologically quite different fran JSRV. Interestingly, it was shown that serum against MPMV cross reacted with a 32 kd protein of BRV indicating a serological relationship between JSRV, MPMV and BRV. The possible role of BRV in the etiology of jaagsiekte remains to be elucidated. / Thesis (Ph.D.)-University of Natal, Pietermaritzburg, 1987.

Thesis (M.Sc.)--University of Melbourne, School of Veterinary Science, 2006. / Typescript. Includes bibliographical references (leaves 181-202).

Thesis (MMedVet. (Wildlife Diseases))--University of Pretoria, 2007. / Includes bibliographical references.

Thesis (MSc (Veterinary Tropical Diseases))--University of Pretoria, 2008. / Includes bibliographical references. Also available in print format.

No description available.

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Orientador: Antonio Carlos Paes / Banca: Marcio Garcia Ribeiro / Banca: Hélio Langoni / Banca: Christian Hirsch / Banca: Osimar de Carvalho Sanches / Resumo: O estudo objetivou identificar efeitos do tratamento com ribavirina, prednisona e DMSO na cinomose; identificar a presença viral no sangue, medula óssea e líquor antes e após o tratamento, os efeitos colaterais dos fármacos experimentais e associações. Foram utilizados 60 cães apresentando sinais neurológicos da cinomose com evolução de dez dias. Animais foram internados para tratamento de suporte; avaliados diariamente e submetidos ao hemograma e dosagens bioquímicas. Os grupos 1 e 2 foram tratados com ribavirina associada ao DMSO; os grupos 3 e 4 foram tratados com DMSO e prednisona e os grupos 5 e 6 foram tratados com ribavirina e prednisona, ribavirina, prednisona e DMSO. Os animais foram anestesiados e colhidos líquor, medula óssea e sangue, antes e após o tratamento e realizada a RTPCR das amostras; as negativas foram analisadas pela técnica de hn-PCR. O vírus foi encontrado em 95% das amostras de sangue, 90% de medula óssea e 53,3% de líquor pré-tratamento. O efeito adverso da ribavirina quando associada com a prednisona foi anemia. A prednisona na dose imunossupressora causou aumento da dosagem de proteína e diminuição da celularidade liquórica, leucocitose. Já a dose antinflamatória causou diminuição de proteína no líquor. Baseado nos índices de sobrevida e melhora clínica, o tratamento mais efetivo foi o G2 (80%); seguido do G1, G5 e G3 (70%); o G6 (60%); o G4 com o pior índice (30%). Pós-tratamento, a frequência viral foi 97,7% no sangue, 86,4% na medula óssea e 27,3% no líquor / Abstract: The present study aims at the identification of ribavirin, prednisone and DMSO's treatment effects in dogs with canine distemper, at the identification of the viral presence in the blood, bone marrow and cerebrospinal fluid (CSF) before and after the treatment and also at the identification of side effects of the experimental drugs and its combinations. Sixty dogs presenting canine distemper with neurological signs about ten days evolution were observed. The animals were hospitalized for the support treatment, assessed on daily basis and subjected to blood cells count and biochemical analysis. Groups 1 and 2 were treated with ribavirin and its combination with DMSO; Groups 3 and 4 treated with prednisone and DMSO, Group 5 treated with ribavirin and prednisone, while Group 6 with ribavirin, prednisone and DMSO. The animals were anesthetized for the cerebrospinal fluid, bone marrow and blood samples collection before and after the treatment, then the RT-PCR of the samples was proceeded. The negative were analysed according to the hn-PCR technique. The canine distemper virus were found in 95% of blood samples, 90% of bone marrow and 53,3% of CSF before the treatment. The adverse effect of ribavirin and its association with prednisone was anemia. Prednisone, at its immunosuppressive dose, led to the increase of protein and decrease of cellularity in CSF, and increase of leukocytes blood count. The antiinflammatory dose led to the CSF protein concentration's decrease. Considering the survival and clinical improvement rates, the most successful treatment was the one applied to the G2 (80%); followed by G1 (70%); G5 (70%) and G3 (70%); G6 (60%); and the lowest rate G4 (30%). After the treatment, the virus frequency was 97,7% in the blood, 86,4% in the bone marrow and 27,3% in the CSF / Doutor