Verminous Arteritis Due to Crassicauda sp. in Cuvier's Beaked Whales (Ziphius Cavirostris).

The vascular system of Cuvier's beaked whales (CBW) (Ziphius cavirostris; family Ziphiidae), an extremely deep, prolonged-diving cetacean, is increasingly receiving anatomic and physiologic study due to possible anthropogenic interactions; however, vascular pathology rarely has been reported in this species. Thirteen CBW stranded in the Canary Islands from June 2008 to June 2014 were autopsied. A careful dissection of the thoracic and abdominal vasculature was performed on these animals. All had moderate to severe and extensive chronic fibrosing arteritis with aneurysms, hemorrhages, and thrombosis primarily involving the mesenteric and gastroepiploic arteries and the thoracic and abdominal aorta. Microscopically, the lesions varied from subacute subintimal hemorrhages and severe neutrophilic, eosinophilic, and histiocytic dissecting arteritis with intralesional nematode larvae to marked, chronic, fibrosing arteritis with thickening and distortion of the vascular wall with calcification and occasional cartilage metaplasia. In addition, adult nematodes in renal arteries and veins, renal parenchyma and/or ureter were identified morphologically as Crassicauda sp. Nucleic acid sequenced from renal nematodes from 2 animals yielded closest nucleotide identity to C. magna The pathogenesis is proposed to involve a host response to larval migration from the intestine to the kidney through the mesenteric arteries, abdominal aorta, and renal arteries. Severe consequences for such lesions are possible and could vary from reduced vascular compliance to chronic renal disease and predisposition to the development of disseminated intravascular coagulation and multiorgan failure. Severe chronic arteritis in CBW is associated with renal parasitism by Crassicauda spp.

Streptozotocin-induced diabetes, and the optic nerve blood barrier.

OBJECTIVE: To study the features of the endoneurial micro-vessels of the optic nerve in streptozotocin-induced diabetic animals. METHODS: Optic nerves from control and streptozotocin-induced diabetic animals were studied by light and transmission electron microscopy. Patency was determined by indirect immunofluorescence albumin detection. The expression of major histocompatibility complex class II molecules was performed by direct immunofluorescence. The endoneurial vessels were counted, and the endothelial cell, the basement membrane, and the surface of the transverse section of the nerve were measured. RESULTS: Vessels of diabetic rats showed vessel wall thickening, preservation of pericytes, an increase in endothelial cell transcytosis, and an increased number of perivascular macrophage cells. It may be concluded that the effects of hyperglycaemia on the inner vessels of the optic nerve are more similar to the cerebral diabetic vessels than to the retinal vessels in diabetic animals.

High-grade astrocytoma (Glioblastoma Multiforme) in an Atlantic spotted dolphin (Stenella frontalis).

This report describes the gross, microscopical and immunohistochemical features of a high-grade astrocytoma (glioblastoma multiforme) in an adult male Atlantic spotted dolphin (Stenella frontalis). On necropsy examination, a 5 × 2.5 × 2 cm, poorly demarcated, red, friable and locally expansile mass effaced the thalamus and the left periventricular region and extended to the left lateral ventricle of the brain. Microscopically, the mass consisted of haphazardly arranged bundles and rows of interweaving polygonal to spindle-shaped cells. These often palisaded along serpentine foci of necrosis and were surrounded by prominent vessels. Immunohistochemically, the neoplastic cells expressed glial fibrillary acidic protein, but not vimentin, S100 protein, neuron-specific enolase or neurofilament protein. A diagnosis of high-grade astrocytoma was made and this represents the first description of a glioma in a cetacean species.

[Epileptic crisis and multiple sclerosis: anatomo-clinical correlation]. / Crisis convulsiva y esclerosis múltiple: correlación anatomoclínica.

INTRODUCTION: The prevalence of epilepsy in multiple sclerosis (MS) is low and the occurrence of an epileptic seizure as a first sign of this illness is even more infrequent. The relationship between both these illnesses is not clear; as epilepsy is a common condition, a coincidental association only could exist between the two diseases. OBJECTIVE: To establish a nexus of causality between epilepsy an MS. Clinical case. We present one case of epileptic seizures as the first manifestation of MS. The patient was a woman of 25 years old. The only result of the clinical examination was a right homonymous inferior cuadrantanopsy. The patient presented a high Tibbling index, lesions of demyelination in the subcortical occipital region and semioval centrum in the MRI and a pathological electroencephalogram; also, the visual and auditory evoked potential latency were delayed. CONCLUSIONS: We related he results of the neuroimaging, the clinical examination and the complementary tests of the patient. The appears to be a causal association between epilepsy and MS.

Ultrastructural analogies between intimal alterations in veins from diabetic patients and animals with STZ-induced diabetes.

The aim of this study was to document similarities and differences between veins from human diabetic patients and an experimentally induced diabetic animal model. The saphenous vein and posterior tibial vein from diabetic patients and the femoral vein from rats were studied. An increase in the extracellular matrix with migration of smooth muscle cells and endothelial alterations were observed in the intima of all specimens. These findings demonstrate that there is a high degree of similarity between the pathological changes in the venous wall during human diabetes mellitus and streptozotocin (STZ) induced-diabetes. This finding validates STZ induced-diabetes in rats as a model for further experimental study to clarify the fate of the diabetic venous wall when used as a graft.

Immunohistochemical and ultrastructural study of microvessels in diabetic veins.

The aim of this study was to examine the localization and features of the intramural microvessels in the wall of inferior limb veins in diabetic patients. The study was conducted in a group of 10 insulin-dependent diabetic patients, who had suffered inferior limb amputation as a consequence of chronic limb ischemia. Sections of long saphenous and posterior tibial veins were investigated by light and transmission electron microscope. The von Willebrand factor and albumin were detected by immunohistochemical techniques. The results show the presence of numerous microvessels in the intima and inner third of the media layer of the venous wall of the sections studied. These microvessels present morphological and functional modifications in relation to those observed in the control veins. They also showed the presence of endothelial cells migrating from the lumen. The authors conclude that the venous wall of inferior limbs in amputated diabetic patients presents a neovascularization process. Some of the endothelial cells of the venous lumen can also have a role in the angiogenesis.

Diabetes-induced structural changes of venous and arterial endothelium and smooth muscle cells.

The structural alterations of endothelium and smooth muscle cells of the hind limb and heart veins and arteries were investigated in Golden Syrian hamsters subjected to streptozotocin induced diabetes. Animals were examined at 5, 10, and 15 weeks after induction of diabetes. At each time point body weight and plasma glucose concentrations were recorded. Anesthetised animals were washed out of blood, fixed in situ, and the femoral vein and artery, saphenous vein and artery, and heart veins and coronaries were dissected out, and processed for electron microscopical examination. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The endothelial localization of von Willebrand factor was carried out by immunocytochemistry. The results showed that induction of experimental diabetes generated morphological changes of the endothelium and smooth muscle cells of both hind limb and heart vessels. The common alterations developed in endothelial cells of venous and arterial origin consisted in: 1) the development of a secretory phenotype, enriched in biosynthetic and degradative organelles; 2) the abundance of cytoskeletal elements, especially intermediary filaments; 3) the increase in number of fused plasmalemmal vesicles and transendothelial channels, and 4) the hyperplasia of the basal lamina. In contradistinction to the arterial endothelium, the peculiarities of the venous endothelium in the diabetic hamsters examined were: 1) the uniform distribution of the anionic sites exposed on the luminal plasma-lemma (as in normal animals), and 2) the increased number of copies of Weibel-Palade bodies (up to 13 copies per endothelial cell in the hind limb). Von Willebrand factor was immunodetected in Weibel-Palade bodies, Golgi cisternae and some vesicles of normal and diabetic hamsters. With time, and especially pronounced at 15 weeks of diabetes, the smooth muscle cells of veins and arteries examined exhibited a characteristic secretory phenotype, and were surrounded by a reticulated basal lamina and a hyperplasic extracellular matrix (especially pronounced in arteries). These data indicate that diabetes affects both heart and hind limb veins and arteries, producing structural changes of the endothelium and smooth muscle cells which may account, at least in part, for the specific vascular complications.