1,721,014 research outputs found

    Neuropathology of Canine Hemangioblastoma

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    Hemangioblastoma is a benign, slow-growing, highly vascular human neoplasm (WHO grade I). The tumor most commonly arises in the cerebral hemispheres and cerebellum, where it is more frequently observed in patients with von Hippel-Lindau disease. Only 7.5 to 25% of all hemangioblastomas occur in the spinal cord, and cases of extraneural localization are exceedingly rare. In veterinary medicine, hemangioblastoma has only been described in the central nervous system of dogs and in the skin of a lamb. Cases of canine hemangioblastoma have been reported in the spinal cord (5 cases), forebrain (1 case), and brainstem (1 case). Dogs treated surgically had a good prognosis. Our study aimed to characterize the neuropathological features of 6 cases of canine spinal cord hemangioblastoma and one case of sciatic nerve localization. The dogs were 4 males and 3 females aged between 6 and 12 years. The histological staining panel included H&E, Luxol Fast Blue, and Goldner trichrome staining; immunohistochemistry included the following markers: NSE, VIM, factor-VIII, GFAP, inhibin-α, carbonic anhydrase IX (CAIX), and Ki67. The tumor was composed of numerous, haphazardly arranged capillaries lined by plump endothelium and interstitial fusiform to stellate stromal cells with slightly eosinophilic cytoplasm, occasionally containing small lipid vacuoles. Mitotic activity was low. Frequently, surrounding the capillaries were moderate to prominent perivascular aggregates composed of plasma cells and fewer lymphocytes. Immunohistochemically, the stromal cells were strongly immunolabeled with NSE and were negative for factor-VIII in all cases. Inhibin-α was negative, whereas stromal cells expressed CAIX in most cases. Although the predominant location of canine hemangioblastoma is the spinal cord, its morphological and immunohistochemical features are comparable to the human counterpart. This is the first report of peripheral nerve hemangioblastoma in animals

    Emerging arthropod-borne viral diseases: Equine encephalosis

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    Equine encephalosis (EE) is a viral vector borne disease carried by hematophagous midges of the genus Culicoides sustained by an Orbivirus of the family Reoviridae. The first isolation of the virus (EEV) occurred in South Africa in 1967 from the blood of a mare affected by neurological symptoms. EEV can infect all equines and, rarely, elephants; in any case, horses are the most susceptible species. Several epizootics were subsequently reported in South Africa and Botswana followed by periods of absence of disease or sporadic outbreaks. The highest number of cases was reported in 1983. Seven non-cross reactive serotypes have been identified so far. EEV infection is frequently sub-clinical, but has been also associated with acute or hyperacute illness. The most common observed clinical signs are fever, anorexia accompanied by increased respiratory distress and congestion of mucosal membranes. Some pregnant mares may abort during the first period of gestation. Less frequently, affected horses can show facial swelling, epistaxis, congiuntival petechiae, and signs of chronic heart failure. Neurological signs, including ataxia, convulsions, hyperexcitability have been described in severe cases. At post-mortem examination it can be observed pulmonary edema, hydropericardium, hepatomegaly, splenomegaly, petechial haemorrhages on serous membranes, hyperemia of glandular stomach, brain edema and congestion. Microscopic examination of liver specimens shows hydropic and fatty degeneration of hepatocytes and in CNS perivascular infiltration of lymphocytes in the periventricular areas of the midbrain and thalamus can be observed. Clinical diagnosis is not easy, due to frequent subclinical course. For this reason, the disease is probably underdiagnosed. Between 2008 and 2009 EE was reported for the first time in Israel. The question of how and when the virus arrived in Israel still remains unanswered. This was the first time in which the virus had been reported outside Africa and this finding is a warning bell for other areas of the Mediterranean basin

    A case of narcolepsy-cataplexy associated with distemper encephalitis

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    Narcolepsy associated with localized brain lesions is described in a 10-month-old Argentine Dogo. Neurological examination and MRI study suggested an inflammatory lesion of the left frontal lobe. Postmortem examination revealed diffuse encephalitis in the forebrain and marked necrotic lesions in the ventral pontine area. Immunohistochemistry for distemper virus antigen showed positive staining of the cytoplasm of many neurones of the pons and cerebral cortex. The pathological pattern was suggestive of post-vaccinal distemper encephalitis and the localization of the lesions was consistent with the neurological syndrome shown by the animal. At any event, the possibility of coincidental findings of distemper encephalitis and idiopathic narcolepsy must be accounted for

    SOSPETTA NEURITE MONOLATERALE DEL PLESSO LOMBOSACRALE IN UN CANE

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    Gli Autori riferiscono riguardo un cane meticcio femmina di 15 anni di età con monoparesi posteriore sinistra ingravescente. Nonostante la terapia medica con prednisone abbia determinato un parziale miglioramento, si è proceduto ad un approfondimento diagnostico mediante esecuzione di EMG e biopsia muscolo-nervosa. l'EMG ha evidenziato riduzione della VCM e della VCS del nervo sciatico mentre la biopsia del nervo sciatico sx e del muscolo semitendinoso sx hanno evidenziarto rispettivamente un quadro di neuropatia demielinizzante e atrofia muscolare neurogena. Gli Autori hanno avanzato il sospetto diagnostico di esito di neurite focale al plesso lombo-sacrale sinistro. Dopo tre mesi il cane è migliorato quasi del tutto pur rimanendo segni riferibili ad atrofia neurogena

    Juvenile neuronal ceroid lipofuscinosis (Batten's disease) in a Poodle dog

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    Clinical and pathological findings consistent with neuronal ceroid-lipofuscinosis were evaluated in a 2.5-year-old purebred standard Poodle dog. Progressive visual loss and neurological deficits were observed since 2 years of age. Computed tomography and postmortem examination revealed brain atrophy with dilatation of the ventricular system. Deposition of autofluorescent granular material throughout the central nervous system, the retina, and other organs was observed. The storage material consisted of membrane-bound fingerprint bodies. Results were compared to the cases of canine neuronal ceroidlipofuscinosis reported in the literature

    Polyarteritis Nodosa in a Cat with Involvement of the Central and Peripheral Nervous Systems

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    An 18-month-old neutered male domestic shorthair cat was referred with a history of pyrexia, polyuria and polydypsia, and transient episodes of bilateral hindlimb paralysis. Cardiac evaluation revealed severe systemic hypertension and severe concentric hypertrophy of the left ventricle. One month later the cat had a new episode of hindlimb paralysis with recurrent seizures, and died in status epilepticus. At necropsy examination, the coronary arteries, arcuate renal arteries and common iliac arteries showed marked thickening with nodules segmentally located along the vessels and consequent narrowing of the lumina. Histologically, acute and chronic inflammatory infiltration of the vascular walls was associated with necrosis of the muscular layer. Lesions were consistent with polyarteritis nodosa and involved the small, medium and large arteries of the heart, kidneys, small and large intestine, mesentery, liver and thyroid. Multifocal meningeal vasculitis associated with focal infarction of the frontal lobe and necrotizing vascular polyneuropathy were detected. Involvement of the central and peripheral nervous systems in polyarteritis nodosa is a novel finding in cats
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