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Neuropathological Findings in the Brain of Cattle with Clinical Neurological Signs in Slovenia Since the Year 2000
J. Comp. Path. 2017, Vol. 156, 54e141
ESVP and ECVP Proceedings 2016
109
CANINE BRACHIAL PLEXUS NEURITIS S. Nesic *, Z. Loncar y and M. Jovanovic* *Faculty of Veterinary Medicine, University of Belgrade and yPrivate Veterinary Clinic ‘Novak’, Belgrade, Serbia Introduction: Brachial plexus neuritis (neuropathy) is rare condition in domestic animals with very few published reports in dogs, cats and cows. This entity is a rare tumour-like, chronic inflammatory, focal or multifocal, mainly demyelinating neuropathy of unknown origin, most frequently involving some nerves of the brachial plexus. Material and Methods: The surgical specimen of the musculocutaneous nerve from the brachial plexus of a 10-year-old male Bichon Frise dog that had shown right forelimb weakness was submitted for histopathology. Tissues were fixed in 10% neutral buffered formalin, processed routinely and embedded in paraffin wax. Sections were stained with HE, Luxol fast blueecresyl violet and Massons’s trichrome technique. Results: Gross findings included striking thickening, haemorrhagic discolouration and fibrosis. Histopathological studies revealed extensive inflammation and axon degeneration in the musculocutaneous nerve. The changes included marked inflammation and proliferation of the epineurial and perineurial nerve sheaths. The surrounding tissue and nerve fascicles were oedematous and infiltrated extensively by lymphocytes, macrophages and plasma cells and sustained great loss of nerve fibres. In some fascicles all component nerve fibres appeared degenerate, in others a part of the nerve fibre population was spared. Some nerve fascicles contained necrotic foci. Segmental myelin loss was evident in the infiltrated areas. Often demyelination was associated with invading macrophages. Conclusions: In some studies brachial plexus neuritis has been compared with neuritis of the cauda equina in horses and to the GuillaineBarre syndrome in man. An immunological pathogenetic mechanism has been suspected to underlie all three forms of neuropathy.
GUT MICROBIOTA MODULATION ENHANCES AMYLOID-B UPTAKE BY MACROPHAGES OF AN ALZHEIMER’S DISEASE TRIPLE TRANSGENIC MOUSE MODEL S. Scarpona *, S. Berardi *, A.M. Eleuteri *, J. Suchodolski y, A. Gavazza *, M. Bordicchia z and G. Rossi* *School of Biosciences and Veterinary Medicine, University of Camerino, Italy, y Department of Small Animal Clinical Sciences, Texas A&M University, TX, USA and zUniversity Veterinary Teaching Hospital, University of Sydney, NSW, Australia Introduction: Microglia constitute the first line of defence against invading pathogens or other types of brain tissue injury. Apart from resident microglia, monocyte-derived macrophages (MDMs) play a phagocytic role and are implicated in the presentation of antigen to T cells. Studies have shown that MDMs are able to efficiently eliminate amyloid and confer neuroprotection by secretion of growth factors. In Alzheimer’s disease, microglia play a controversial role: on the one hand activation seems to be neuroprotective in early stages of the disease, but later loses its protective effects. On this basis, the MDM arises as a key immune cell to compensate for the altered functions of resident microglia. Amyloid phagocytosis by macrophages is induced by Toll-like receptor 4 (TLR4), which should be overexpressed to enhance such phagocytosis, and the gut plays an important role in this mechanism. Materials and Methods: We investigated whether gut microbiome modulation by administration of probiotics (SLAB51) to 3 TG-AD mice is able to activate macrophages. Two different in-vitro assays regarding macrophage activity were used to assess phagocytosis and the respiratory burst. Results: There was higher phagocytic activity in the treated group (+40%) versus placebo and a real activation of macrophage binding capability toward generic and specific antigens (1-42 Ab). The respiratory burst was less impressive (0.150/0.103 OD), but still indicated a positive trend in terms of increased macrophage oxidative metabolism. Conclusions: In conclusion, for peripheral macrophages we can assume that gut microbiota modulation is able to promote the oxidative activity and phagocytosis in Alzheimer’s disease.
NEUROPATHOLOGICAL FINDINGS IN THE BRAIN OF CATTLE WITH CLINICAL NEUROLOGICAL SIGNS IN SLOVENIA SINCE THE YEAR 2000 P. Juntes, I. Zdovc and P. Hostnik University of Ljubljana, Veterinary Faculty, Ljubljana, Slovenia Introduction: The importance of passive surveillance in cattle expressing neurological clinical signs declined along with the beginning of the active surveillance of bovine spongiform encephalopathy (BSE), and other neuropathology has been often neglected. We examined the brains of such clinical cases, not just for BSE, but also for other lesions. Materials and Methods: Whole brain histopathology of 378 cattle with neurological signs of all ages was performed from the years 2000 to 2015 (347 fallen stock from farms, 31 emergency slaughtered or sick ante-mortem from abattoirs). All were examined for BSE by histopathology and from the beginning of 2001 with the rapid post-mortem tests. All were tested for rabies by the immunofluorescence test (IF) and were cultured for Listeria monocytogenes. Whole brain histopathology was performed for the lesions related to these three diseases and for other neuropathology. Results: All samples from the passive surveillance were negative for BSE, 66 (17.5%) had morphological lesions consistent with listeriosis, two (0.5%) were positive for rabies, 21 (5.6%) had lesions consistent with malignant catarrhal fever, 29 (7.7%) with other undetermined viral infections and 22 (5.8%) with other bacterial infections, 23 (6.1%) revealed cerebrocortical necrosis (polioencephalomalacia), five (1.3%) tumours, 31 (8.2%) metabolic or toxicity related lesions and 179 (47.3%) only non-specific lesions. Conclusions: Neuropathology of the brains collected during passive surveillance for BSE did not reveal any positive BSE cases, but was important for the diagnosis of some other infectious, metabolic and neoplastic diseases in almost half of the examined animals with neurological signs.
CORRELATED IMAGING FINDINGS IN MENINGEAL PATHOLOGIES OF THE SPINE S. H€ ogler *, A. Probst y, I. Walter y and S. Kneisslz *Institute of Pathology, yInstitute of Anatomy, Histology and Embryology and z Diagnostic Imaging, University of Veterinary Medicine Vienna, Austria Introduction: To improve understanding of the lesionemyelon interface and verify a presumed extradural, intraduraleextramedullary or intramedullary pathology on CT/MR images, correlated macroscopical and microscopical sections were acquired. Materials and Methods: Four cats and three dogs with inflammatory or neoplastic disease, seen on CT (n 5 1) or 1.5 TMR images (n 5 6), were humanely destroyed. Sections from fresh cadavers were cut and photographed in the same level and plane as best documented on CT/MR images. Tissues were fixed in formalin, decalcified with EDTA for 60 to 80 days, embedded in paraffin wax, sectioned (2e3 mm) and stained with HE. Results: On CT/MR images all patients had primary extramedullary disease, two had presumed intraduraleextramedullary and two presumed intramedullary extension. CT/MR features of lesion location correlated well with microscopical images. However, in two cases, soft tissue oedema, seen on CT/MR images, was not noticed on macroscopical sections before feedback from the radiologist. Histology confirmed CT/MR classification as either inflammatory or neoplastic disease. One dog and one cat showed meningitis and one dog and one cat showed meningitis and myelitis, respectively. In two cats, primary neoplasia and in one dog metastatic neoplastic disease were evident in the spine. In three cases microscopical evidence of mild meningeal infiltration could not be seen on MR images before feedback from the pathologist. Conclusions: Compared with pathological sections, MR imaging is superior in detecting oedema; however, depiction of meningeal pathologies is limited on MR images by patient size, microchip-associated susceptibility artefacts, selected imaging plane and experience of the observer.
ESVP and ECVP Proceedings 2016
109
CANINE BRACHIAL PLEXUS NEURITIS S. Nesic *, Z. Loncar y and M. Jovanovic* *Faculty of Veterinary Medicine, University of Belgrade and yPrivate Veterinary Clinic ‘Novak’, Belgrade, Serbia Introduction: Brachial plexus neuritis (neuropathy) is rare condition in domestic animals with very few published reports in dogs, cats and cows. This entity is a rare tumour-like, chronic inflammatory, focal or multifocal, mainly demyelinating neuropathy of unknown origin, most frequently involving some nerves of the brachial plexus. Material and Methods: The surgical specimen of the musculocutaneous nerve from the brachial plexus of a 10-year-old male Bichon Frise dog that had shown right forelimb weakness was submitted for histopathology. Tissues were fixed in 10% neutral buffered formalin, processed routinely and embedded in paraffin wax. Sections were stained with HE, Luxol fast blueecresyl violet and Massons’s trichrome technique. Results: Gross findings included striking thickening, haemorrhagic discolouration and fibrosis. Histopathological studies revealed extensive inflammation and axon degeneration in the musculocutaneous nerve. The changes included marked inflammation and proliferation of the epineurial and perineurial nerve sheaths. The surrounding tissue and nerve fascicles were oedematous and infiltrated extensively by lymphocytes, macrophages and plasma cells and sustained great loss of nerve fibres. In some fascicles all component nerve fibres appeared degenerate, in others a part of the nerve fibre population was spared. Some nerve fascicles contained necrotic foci. Segmental myelin loss was evident in the infiltrated areas. Often demyelination was associated with invading macrophages. Conclusions: In some studies brachial plexus neuritis has been compared with neuritis of the cauda equina in horses and to the GuillaineBarre syndrome in man. An immunological pathogenetic mechanism has been suspected to underlie all three forms of neuropathy.
GUT MICROBIOTA MODULATION ENHANCES AMYLOID-B UPTAKE BY MACROPHAGES OF AN ALZHEIMER’S DISEASE TRIPLE TRANSGENIC MOUSE MODEL S. Scarpona *, S. Berardi *, A.M. Eleuteri *, J. Suchodolski y, A. Gavazza *, M. Bordicchia z and G. Rossi* *School of Biosciences and Veterinary Medicine, University of Camerino, Italy, y Department of Small Animal Clinical Sciences, Texas A&M University, TX, USA and zUniversity Veterinary Teaching Hospital, University of Sydney, NSW, Australia Introduction: Microglia constitute the first line of defence against invading pathogens or other types of brain tissue injury. Apart from resident microglia, monocyte-derived macrophages (MDMs) play a phagocytic role and are implicated in the presentation of antigen to T cells. Studies have shown that MDMs are able to efficiently eliminate amyloid and confer neuroprotection by secretion of growth factors. In Alzheimer’s disease, microglia play a controversial role: on the one hand activation seems to be neuroprotective in early stages of the disease, but later loses its protective effects. On this basis, the MDM arises as a key immune cell to compensate for the altered functions of resident microglia. Amyloid phagocytosis by macrophages is induced by Toll-like receptor 4 (TLR4), which should be overexpressed to enhance such phagocytosis, and the gut plays an important role in this mechanism. Materials and Methods: We investigated whether gut microbiome modulation by administration of probiotics (SLAB51) to 3 TG-AD mice is able to activate macrophages. Two different in-vitro assays regarding macrophage activity were used to assess phagocytosis and the respiratory burst. Results: There was higher phagocytic activity in the treated group (+40%) versus placebo and a real activation of macrophage binding capability toward generic and specific antigens (1-42 Ab). The respiratory burst was less impressive (0.150/0.103 OD), but still indicated a positive trend in terms of increased macrophage oxidative metabolism. Conclusions: In conclusion, for peripheral macrophages we can assume that gut microbiota modulation is able to promote the oxidative activity and phagocytosis in Alzheimer’s disease.
NEUROPATHOLOGICAL FINDINGS IN THE BRAIN OF CATTLE WITH CLINICAL NEUROLOGICAL SIGNS IN SLOVENIA SINCE THE YEAR 2000 P. Juntes, I. Zdovc and P. Hostnik University of Ljubljana, Veterinary Faculty, Ljubljana, Slovenia Introduction: The importance of passive surveillance in cattle expressing neurological clinical signs declined along with the beginning of the active surveillance of bovine spongiform encephalopathy (BSE), and other neuropathology has been often neglected. We examined the brains of such clinical cases, not just for BSE, but also for other lesions. Materials and Methods: Whole brain histopathology of 378 cattle with neurological signs of all ages was performed from the years 2000 to 2015 (347 fallen stock from farms, 31 emergency slaughtered or sick ante-mortem from abattoirs). All were examined for BSE by histopathology and from the beginning of 2001 with the rapid post-mortem tests. All were tested for rabies by the immunofluorescence test (IF) and were cultured for Listeria monocytogenes. Whole brain histopathology was performed for the lesions related to these three diseases and for other neuropathology. Results: All samples from the passive surveillance were negative for BSE, 66 (17.5%) had morphological lesions consistent with listeriosis, two (0.5%) were positive for rabies, 21 (5.6%) had lesions consistent with malignant catarrhal fever, 29 (7.7%) with other undetermined viral infections and 22 (5.8%) with other bacterial infections, 23 (6.1%) revealed cerebrocortical necrosis (polioencephalomalacia), five (1.3%) tumours, 31 (8.2%) metabolic or toxicity related lesions and 179 (47.3%) only non-specific lesions. Conclusions: Neuropathology of the brains collected during passive surveillance for BSE did not reveal any positive BSE cases, but was important for the diagnosis of some other infectious, metabolic and neoplastic diseases in almost half of the examined animals with neurological signs.
CORRELATED IMAGING FINDINGS IN MENINGEAL PATHOLOGIES OF THE SPINE S. H€ ogler *, A. Probst y, I. Walter y and S. Kneisslz *Institute of Pathology, yInstitute of Anatomy, Histology and Embryology and z Diagnostic Imaging, University of Veterinary Medicine Vienna, Austria Introduction: To improve understanding of the lesionemyelon interface and verify a presumed extradural, intraduraleextramedullary or intramedullary pathology on CT/MR images, correlated macroscopical and microscopical sections were acquired. Materials and Methods: Four cats and three dogs with inflammatory or neoplastic disease, seen on CT (n 5 1) or 1.5 TMR images (n 5 6), were humanely destroyed. Sections from fresh cadavers were cut and photographed in the same level and plane as best documented on CT/MR images. Tissues were fixed in formalin, decalcified with EDTA for 60 to 80 days, embedded in paraffin wax, sectioned (2e3 mm) and stained with HE. Results: On CT/MR images all patients had primary extramedullary disease, two had presumed intraduraleextramedullary and two presumed intramedullary extension. CT/MR features of lesion location correlated well with microscopical images. However, in two cases, soft tissue oedema, seen on CT/MR images, was not noticed on macroscopical sections before feedback from the radiologist. Histology confirmed CT/MR classification as either inflammatory or neoplastic disease. One dog and one cat showed meningitis and one dog and one cat showed meningitis and myelitis, respectively. In two cats, primary neoplasia and in one dog metastatic neoplastic disease were evident in the spine. In three cases microscopical evidence of mild meningeal infiltration could not be seen on MR images before feedback from the pathologist. Conclusions: Compared with pathological sections, MR imaging is superior in detecting oedema; however, depiction of meningeal pathologies is limited on MR images by patient size, microchip-associated susceptibility artefacts, selected imaging plane and experience of the observer.