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Feline spongiform encephalopathy (FSE) is a fatal, degenerative neurological disease of domestic cats, associated with the accumulation of an abnormal isoform of the prion protein called PrPsc. The disease was first identified in Britain in 1990 and experimental data have suggested an association with BSE. Affected cats with FSE show neurological signs including behavioural changes and movement disorder not easily distinguishable from other feline neurological conditions. Diagnosis can be achieved only by histopathological examination of brain tissue and identification of typical spongiform changes. A surveillance system of FSE is set up in Italy to find cases of spongiform encephalopathy in the feline population. In this project 61 cat brains with neurological signs have been examined and no evidence of FSE has been proved on the basis of histopathology and immunohistochemistry but this research had allowed to identified other neurological disease of cats.
FELINE SPONGIFORM ENCEPHALOPATHY: RESULTS OF
Introduction:SCC is a malignant tumor of squamous epithelial cells in which the cells show differentiation to keratinocytes. It is relatively common, locally invasive and occasionally metastatic neoplasm of domestic animals .The tumor is uncommon in sheep and the most sites reported are frontal and ear, however in any species this tumor may arise from any site.
Materials and Methods:In may-2004 a skin biopsy specimen from middle part of right side of thoracic area of a 4 - year- old native ewe was submitted to the Pathology Department of, Faculty of Veterinary Medicine, University of Tehran. On the basis of history, the lesion was seen from 1 month ago. The tumor was growing slowly, heamorrhagic and infected with bacteria which caused discharge of pus. The dimensions of mass was12×12×5 cm and grossly appeared cauliflower like with dark gray color.The tissue sample was processed routinely and stained with H&E.
Results: Histopathologically neoplastic cells with pleomorphic and hyperchromatic nuclei and high mitotic figures were seen and a few horn pearls were present. There was also invasion of neoplastic cells to blood vessels and lymphatics and adjacent tissues.
Conclusion:there is reported at least 2 cases of SCC from frontal site in sheep from shahrekord which is very high altitude region in Iran. In this unusual case tumor was aroused from a part of skin which is densely covered with moderate pigmented and dense wool.
A
CASE REPORT OF SQUAMOUS CELL CARCINOMA(SCC)
IN SHEEP FROM
S
HAHREKORD(I
RAN)
23rdMeeting of the European Society of Veterinary Pathology 9393 Javaheri Abbas, Mardjanmehr Seyed Hosein , Dehghan Mohammad Mehdi.
Tavasoly Abbas , Ashrafi Helan Javad ,
University of Semnan, Faculty of veterinary Medicine, Department of Pathology, Semnan,Iran.
e-mail: [email protected]
Proceedings of the 23 Meeting of the European Society of Veterinary Pathology
23rdMeeting of the European Society of Veterinary Pathology 94
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Introduction:The most important subject of this study is to survey the Histopathologic changes of corpus luteum after administration of corticosteroid in animals, which have been treated with PGF2α and cattle with normal estrous cycle.
Material and method:In this research estrous cycle of 14 heifers were synchronized by two intramuscularly injection of PGF2α (25 mg PGF2 , upjohn, co) at 14 days interval.
These animals were divided into 5 groups. (Control, A, B, C, D). No drug was administrated in 2 heifers in control group. PGF2α was administrated in 4 heifers in- group A and 3 heifers in group D on 9th day of estrous cycle. Four heifers in-group B received 4 mg Dexamethason on 8th day and 25 mg PGF2α on 9th day of estrous cycle.
Dexamethason was injected to one heifer (group c). Corpus luteum removed via laparatomy on day 11 of cycle in all animals except group D (in 12) and then these tissues fixed in 10% buffered formalin solution. The samples were sectioned with 7micron thickness and stained with H & E.
Results: Few lymphocytes were observed in corpus luteum of animal's in-group C and control group (average 2.75 lymphocyte in each field of microscope in x400 magnification). Leukocyte aggregated foci were not seen in these groups but a lot of similar foci were diagnosed in-group A and D which were treated with PGF2α (average 10.57 in each cm2 of tissue section). Numerous leukocytes contain lymphocyte;
macrophages and plasma cells in each of foci were seen (13.55, 6.5, 3.5) respectively.
Leukocyte aggregated foci were not seen at group B which received dexamethason and PGF2α. But few lymphocyte (average 4.75 lymphocyte in each field of microscope in X400 magnification) were observed. Many luteal cells had characteristics of necrotic cells. The corpus luteum of cows at group D was similar to group A, but the fibroblasts moderately were increased.
Conclusion:the research revealed that administration of dexamethason decreased the number of leukocytes in corpus luteum and also inhibit to produce the leukocyte aggregated foci which forms normally after administration of PGF2α. For this reason dexamethason inhibit or decrease the luteolytic affection of PGF2α in corpus luteum of ovary.
H
ISTOLOGICAL CHANGES OF BOVINE CORPUS LUTEUM AFTER ADMINISTRATION OFD
EXAMETHASONTavasoly Abbas, Javaheri Abbas, Mohammad Sadegh Majid Pathology Dept. Semnan University, Semnan , Iran..
Ab_javaheri @ Yahoo. Com
Proceedings of the 23 Meeting of the European Society of Veterinary Pathology
Previous studies have identified a C→A-transversion in exon 29 of the feline PKD1 gene resulting in a premature stop codon. In this survey a of sample persian cats in Germany was scanned for the prevalence of this mutation.
137 persian cats including four families were examined for polycystic kidney disease using ultrasonography or pathological examination. The described mutation causes a new restriction site. Therefore, PCR products of mutated and normal alleles can be differentiated by RFLP analysis.
None of the 71 cats without renal cysts but 94 % of the 62 Persian cats with renal cysts displayed the mutation. In all positive cases the mutation was found in the heterozygous state. The mutation was absent in 6 % of the affected persian cats. The ultrasonographic examination and the genetic testing are concordant in 97 %.
These data support the assumption that the stop mutation causes most cases of feline PKD. The distribution of the mutation within the families agrees with the autosomal dominant mode of inheritance. In homocygous cats the mutation seems to be a lethal factor. Not all cats with multiple renal cysts have the investigated mutation. In these cases the disease might be caused by another mutation or another pathogenesis.
P
OINT MUTATION IN THEPKD1
GENE:
MAIN CAUSE OF POLYCYSTIC KIDNEY DISEASE OF PERSIAN CATS IN
G
ERMANY23rdMeeting of the European Society of Veterinary Pathology 9595 Kappe, Eva Christina1, Hecht, Werner1, Gerwing, Martin2, Michele, Ursula2, Reinacher, Manfred1
1Institut für Veterinär-Pathologie, Justus-Liebig-Universität, Frankfurter Str. 96, 35392 Giessen, Germany
2Klinik für Kleintiere, Chirurgie, Justus-Liebig-Universität Giessen, Germany [email protected]
Proceedings of the 23 Meeting of the European Society of Veterinary Pathology
23rdMeeting of the European Society of Veterinary Pathology 96
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Introduction:A 15 year old, neutered domestic short hair male cat presented with severe hyperproteinemia and neurological symptoms presumably of cerebral origin. Post- mortem examination showed a multiple myeloma involving the bone marrow, liver and spleen, an intraventricular psammomatous meningioma and pronounced senile neuronal lipofuscinosis.
Results: The spleen and liver were slightly enlarged. Multiple scattered subcapsular hemorrhages, measuring 0.1-1.0 cm, were observed in both organs. The spleen had a lighter than normal, fleshy cut surface. There was a diffuse yellowish discolouration of the brain parenchyma and the nerve roots of the spinal cord. Situated in the plexus choroideus/tela choroidea, close to the hippocampus, a nodular, well-circumscribed mass measuring 0.8 cm in diameter was found, compressing the underlying brain parenchyma.
The bone marrow was homogenously red and firmer than normal.
Microscopically, infiltration of neoplastic plasma cells was observed in the bone marrow, the splenic red pulp and the hepatic sinusoids. The neoplastic cells were well differentiated, only slightly pleomorphic, closely resembling normal plasma cells.
Occasional binucleated cells were observed.
The intraventricular mass was a psammomatous meningioma made up of neuroid, spindle-shaped mesenchymal cells growing in streaks and concentrically arranged around calcium deposits.
Severe lipofuscin deposits were found in neurons of the cerebrum and spinal cord, in the Purkinje cells and in ganglion cells of the spinal nerve roots.
Discussion: Based on the severe hyperproteinemia and the pronounced infiltration of neoplastic plasma cells in the bone marrow, spleen and liver, a diagnosis of multiple myeloma was made. A hyperviscosity syndrome, caused by the high protein content of the plasma, manifested as dementia-like neurological signs, can occur in multiple myeloma and thus may contributed to the symptoms in the reported case. However, the meningioma probably had the greatest influence on the clinical picture as it was intraventricularly located and caused a clearly visible compression of the surronding brain parenchyma. Senile lipofuscinosis is a common finding in aged animals, normally not considered clinically relevant, but as the lipofuscin deposits were unusually heavy in this case, they may not be a neglectable finding.