Hemorrhagic septicemia (HS) is an acute septicemic disease principally affecting cattle and buffaloes caused by specific serotypes B:2 and E:2 of Pasteurella multocida in Asia and Africa, respectively. Despite continuing researches on pathogenesis of P. multocida for several decades, the mechanisms by which these bacteria develop the diseases are poorly understood. Although the involvement of the nervous system in the disease progress of HS is rare under natural conditions, few reports indicated the involvement of the nervous system in outbreaks of HS in cattle and buffaloes. Additionally, recent pathogenesis studies in both mouse and buffalo experimental models reported the involvement of nervous system due to P. multocida B:2, with bacteriological and histopathological evidences. In this review, we summarized and discussed the updates on the involvement of the nervous system in pathogenesis of HS focusing on clinical signs, pathological and pathophysiological changes. [J Adv Vet Anim Res 2015; 2(3.000): 252-262]

Neuromuscular and cardiovascular effects of atracurium, a nondepolarizing neuromuscular blocking agent, were evaluated in 10 halothane-anesthetized adult horses. Hind limb digital extensor tension (hoof twitch) was measured with a strain gauge to quantitate the muscle relaxant effects of atracurium. Response of facial muscles was compared with hoof twitch. Five injections of atracurium were given. Initial mean (+/- SEM) dosage of 0.07 +/- 0.01 mg of atracurium/kg of body weight caused 98.6 +/- 0.8% reduction of the preinjection hoof twitch. Subsequent dosages of 0.04 +/- 0.003 mg/kg induced a degree of relaxation similar to that induced by the initial dose. Duration of paralysis from maximal effect to 10% recovery of twitch was 12.2 +/- 1.5 minutes for the first injection. This was significantly (P less than 0.05) different from subsequent paralysis periods, which lasted approximately 7 miutes. The 10% to 75% recovery time after all injections was similar--approximately 16 minutes. The facial muscles were less affected objectively by atracurium than was the hind limb. Atracurium did not cause cardiovascular changes. When the hoof twitch had recovered to 95% of its tension before atracurium administation, 0.5 mg of edrophonium/kg, was given to antagonize neuromuscular blockage. Within 5 minutes of edrophonium administration, twitch tension exceeded that measured before atracurium administrations. Within 2 minutes of edrophonium administration blood pressure began to increase and continued to increase approximately 10 mm of Hg above the value measured before edrophonium administration. Heart rate was not affected by edrophonium. Other muscarinic side effects of edrophonium were not observed. Of the 10 horses, 9 had good, unremarkable recovery to standing position. One horse had a violent recovery period.

Toxocara canis, cynomolgus macaques (exper.), visceral larva migrans, hematologic and serologic changes, neurologic signs, diminished growth rates, diagnostic antibody titers in enzyme-linked immunosorbent assay, severe granulomatous hepatitis and encephalomyelitis, no ocular lesions, basis for clinical interpretation and diagnosis in humans

sarcocystosis causing death in calf immediately after birth, rosette and palisade configurations of merozoites in schizonts observed in histologic sections of gray and white matter from cerebrum; encephalitis, to lesser extent meningitis, and necrosis of cerebrum, cerebellum, and brain stem; calf's dam probably was exposed to infective cysts in feed or water contaminated by feces from carnivores

This study was carried out to nvestigate the NPY-immunohistochemical characteristics of the olfactory bulb in the striped field mouse(Apodemus agrarius). The animals were anesthesized with thiopental sodium and perfused with 4% paraformaldehyde through left ventricle and aorta. Brains were removed and tranfered 10%, 20% and 30% sucrose. Sections were then cut on a cryostat into 40 micro meter-thick. The tissue immunostained with avidin-biotinylated complex method. The main olfactory bulb consisted of seven circumferential laminae: and olfactory nerve fiber layer, a glomerular layer with glomeruli surrounding by periglomerular cells, an external plexiform layer having granule and tufted cells, a mitral cell layer, a narrow internal plexiform layer, a granule cell layer forming several cell rows and alayer of white matter. The accessory olfactory bulb had four layers: an olfactory or vomeronasal nerve fiber layer, a glomerular layer consisting of small glomeruli, a mixed layer not distinguishing the external plexiform/mitral cell/granule cell layers and a granule cell layer. Most of NPY-immunoreactive(NPY-IR) neurons in main olfactory bulb were localized in the deeper portion of granule cell layer, white matter and anterior olfactory nucleus. In addition, some NPY-IR neurons were identified in the external plexiform layer. The shape of NPY-IR neurons of all olfactory bulb were predominant round or oval, sometime multipolar in shape. And most NPY-IR processes were parallel to long axis of white matter. In accessory olfactory bulb, NPY-IR neurons were not found in all region.

Ultrastructural examination of optic nerve capillaries in the canine lamina cribrosa revealed many spherical, membrane-bound, electron-dense inclusions that closely resembled Weibel-Palade bodies, in pericytes and endothelial cells of preglaucomatous, early, moderately, and advanced affected Beagles with hereditary primary open-angle glaucoma. This ultrastructural difference between the laminar capillary endothelial cells of normal and glaucomatous Beagles could represent a functional vascular disorder, because Weibel-Palade bodies are associated with microcirculatory abnormalities.

Scanning electron microscopy of vascular corrosion casts of the optic nerve region in normal and glaucomatous Beagles demonstrated that the blood supply to the laminar optic nerve is derived from short posterior ciliary arteries, cilioretinal arteries, and longitudinal pial vessels. The short posterior ciliary arteries formed a ring of striated pillars around the scleral canal. The central retinal artery was not present in the dog. Differences between the casts in normal and glaucomatous dogs were not detected.