Intracranial germ cell tumours in two dogs

Intracranial germ cell tumours were identified in two middle-aged, male dogs. The predominant clinical signs were progressive visual and pupillary abnormalities; one dog was blind. At post mortem examination a discrete extramedullary tumour was found at the base of the brain in each dog. Expansion of the mass had produced severe destruction of the diencephalon and brain stem. Histopathological examination revealed a mixed cellular pattern, consistent with a neoplasm derived from germ cells.     

Certain cytologic features of the porcine adrenal medulla

Adrenal glands were collected from pigs of various ages under general anesthesia. Glutaraldehyde-fixed medullary tissue was postfixed with OsO4 for electron microscopy and with potassium dichromate or potassium iodate for light microscopy. Columnar epinephrine (E) cells formed cords between wide sinusoidal capillaries at the corticomedullary junction and were arranged in palisade fashion along the central vein and its major tributaries. The E cells usually were polarized, with the nuclei located away from the sinusoidal capillaries. Clusters of polygonal norepinephrine (NE) cells formed large central aggregates surrounded by E cells. Granulated vesicles were the predominant cytoplasmic feature of both E and NE cells. Round or oval E granules were bounded by a crenated membrane separated from the granule by a clear halo. The more electron-dense, elongate NE granules were bounded by a closely apposed, smooth membrane. The average longest granule axis was 270 nm for E granules and 305 nm for NE granules. Many cytoplasmic organelles were congregated in a granule-free paranuclear zone, which contained a prominent Golgi complex. Thin nonmyelinated nerve fibers (singly or in small groups) were interposed between the E and NE cells. Nerve fibers often were located close to the nucleus in a depression of the cell surface and often were wrapped by thin E or NE cell processes. The medulla of newborn pigs was composed predominantly or exclusively of NE cells. In both adults and pigs, E or NE cell cords radiated through the cortex toward the capsule, and isolated clusters of E or NE cells frequently were found in the capsule or zona glomerulosa.     

Comparison of genome segments 2, 7 and 10 of bluetongue viruses serotype 2 for differentiation between field isolates and the vaccine strain

Bluetongue (BT) virus serotype 2 (BTV 2) was first confirmed in Tunisia in February 2000 and has since spread northward and westward, infecting several other countries and islands, including Corsica, where clinical disease was reported in October 2000. BT was again reported on the Island in July 2001, some six months after a vaccination campaign against BTV 2. The molecular relationship between isolates of the BTV 2 Corsican wild-type viruses from 2000 and 2001, and the attenuated BTV 2 vaccine were determined by comparing corresponding sequences of genome segments 2, 7 and 10 with each other and with already published sequences available in the genome database. Complete genetic stability was observed between the isolates of the Corsican BTV 2. There was some divergence between the nucleotide sequences of segment 10 obtained from the wild-type and vaccine virus strains. Based on these differences, primers were selected that could be used in RT-PCR to differentiate between the wild-type and the vaccine viruses.     

Field evaluation of moxidectin/praziquantel oral gel in horses

The safety and efficacy of 2% moxidectin/12.5% praziquantel oral gel administered at a rate of 0.4 mg moxidectin and 2.5 mg praziquantel/kg was studied in client-owned horses under field use conditions. Four hundred horses (300 treated with moxidectin/praziquantel oral gel and 100 treated with vehicle) were enrolled, feces were collected, and eggs were counted. Investigators as well as horse owners were masked to treatment assignment. No adverse reactions to treatment were observed in any horses. Moxidectin/praziquantel gel reduced Anoplocephala spp by more than 99% and provided a significant (P <.05) reduction (> 98%) in the strongyle egg count of treated horses.     

16alpha-Bromo-epiandrosterone therapy modulates experimental feline immunodeficiency virus viremia: initial enhancement leading to long-term suppression

16alpha-Bromo-epiandrosterone (epiBr), a synthetic derivative of the natural hormone dehyroepiandrosterone (DHEA), was evaluated for its effects on feline immunodeficiency virus (FIV) infection in experimental cats. The rationale for this study was based on the ability of DHEA to significantly reduce the mortality to viral infections in mice. DHEA and epiBr also have demonstrable in vitro anti-viral activity for both HIV-1 and FIV. Preliminary pharmacokinetic studies in cats demonstrated that subcutaneously injected epiBr was rapidly absorbed, completely metabolized, and nontoxic. Metabolites were excreted in both urine and feces, with the latter having the most complex pattern of breakdown products. Cats were then divided into four groups; two groups were infected with FIV and two uninfected. Two groups, one infected and one uninfected were treated on 5 consecutive days of weeks 0, 4, 8, 12 and 16 with epiBr. The remaining two groups were mock treated with the drug vehicle alone. Treatment started 1 week prior to infection and extended for 4 weeks after infection. Cats were observed for 20 weeks post-FIV infection. Infected cats had identical decreases in blood neutrophil and lymphocyte counts following, regardless of whether they were treated with epiBr or vehicle alone. The CD4/CD8 T-cell ratio was decreased following FIV exposure, but was significantly more decreased for the epiBr treated animals from week 2 post-infection onward. CD4+ T cells were decreased in FIV-infected cats treated with epiBr compared to their untreated cohort, while CD8+ T cells tended to be higher in treated animals. FIV infected cats that were treated with epiBr had over one-log higher virus loads at week 2 post-infection than non-epiBr treated cohorts. In spite of this enhanced initial viremia, the subsequent levels of virus in the blood were significantly lower in epiBr treated versus untreated animals. EpiBr treated cats had significantly higher FIV-p24 antibody responses than control cats receiving vehicle alone, although primary and secondary antibody responses to a T-cell dependent non-FIV antigen, keyhole limpet hemocyanin (KLH), were unaffected. EpiBr treatment significantly decreased the expected FIV-induced suppression of IL-12 p40 mRNA levels in peripheral blood mononuclear cells (PBMCs) observed at weeks 4, 5, 8, 9 and 16 post-infection, but had no influence on FIV-induced changes in IL-4, IL-6, IL-10, IFN-gamma, MIP-1alpha and RANTES.     

Neuronal ceroid lipofuscinosis in Merino sheep

OBJECTIVE: To characterise neuronal ceroid lipofuscinosis (NCL) in Merino sheep. DESIGN: A prospective clinical, pathological, biochemical and genetic study. PROCEDURE: NCL cases were studied from a medium-wool Merino flock, the stud of origin of its replacement rams, and an experimental flock established at the University of Sydney. RESULTS: Behavioural changes and visual impairment were first detected at 7 to 12 months of age and progressed, with associated motor disturbances and at later stages seizures, to premature death by 27 months of age. At necropsy there was severe cerebrocortical atrophy associated with neuronal loss, astrocytosis and the presence in neurons of eosinophilic intracytoplasmic storage bodies with the characteristics of a lipopigment. In the retina there was progressive loss of photoreceptor cells. Storage bodies isolated from fresh brain, liver and pancreas formed electron-dense aggregates and coarse multilamellar and fine fingerprint profiles ultrastructurally, and consisted mainly of the hydrophobic protein, subunit c of mitochondrial ATP synthase. A homozygosity mapping approach localised the gene causing the disease in Merino sheep to the chromosomal region (OAR7q13-15) associated with NCL in South Hampshire sheep. CONCLUSION: NCL in Merino sheep is a subunit c-storing disease, clinically and pathologically similar to NCL in South Hampshire sheep. We propose that the disease in both breeds represents mutation at the same gene locus in chromosomal region OAR7q13-15.     

Neuronal ceroid-lipofuscinosis in Borderdale sheep

AIM: To describe the gross and histological lesions of a neurological disease in Borderdale sheep characterised clinically by blindness and circling, as a basis to its classification. METHODS: Formalin-fixed tissues were processed into paraffin wax and epoxy resin for light and electron microscopy of variously stained sections. RESULTS: Lesions were those of a lysosomal storage disease with severe neurodegeneration of the cerebral cortex. The staining reactions, autofluorescence and ultrastructure of storage material allowed the diagnosis of neuronal ceroid-lipofuscinosis associated with the accumulation of subunit-c of mitochondrial ATP synthase. CONCLUSIONS: The severity of neurodegeneration and minor differences in the ultrastructure of storage material implied that this was a different disease from other forms of ovine ceroid-lipofuscinosis that accumulate subunit-c of mitochondrial ATP synthase. An autosomal recessive mode of inheritance is considered probable. Although of only minor economic importance, this disease may be important to research into the group of ceroid-lipofuscinoses as a whole.