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Gitter cells • Microglia function as phagocytes and likely part of the monocyte phagocytic system. They are chiefly perivascular in white matter and perivascular and perineuronal in gray matter. • If inactive, the microglia contain small, round or rod-shaped hyperchromatic nuclei. If active and phagocytic, the cytoplasm becomes foamy due to phagocytosis if lipid and water. These larger foamy or vacuolated cells are termed " gitter cells" or " compound granule cells ". Proliferation of microglia in some viral diseases results in small nodules called glial nodule. These cells, not oligodendroglia, may indulge in neuronophagia of degenerate neurons. 1 Gitter cells 2 Gitter cell, Myelin basic protein IHC 3 Neuronophagia 4 Microglial nodule 5 6 Ependymal cells and undifferentiated glial cells- prominent in newborn animals 7 Ependymal cells • Ependymal cells line the ventricles, choroid plexuses and central canal. Production and flow of CSF are modified by ependymal cells. • Inflammation (ventriculitis or choroid plexitis) or neoplasia can result in CSF disturbances of pressure and/or volume. • Granular ependymitis 8 9 Extragranular layer10 Perivascular lymphocytic cuffing • There is a space between the CNS parenchyma and stroma and the blood vessels with limited supporting framework. • This is the perivascular space causing perivascular lymphocytic infiltrations or " cuffing". 11 • Virchow-Robin space (Perivascular space) • Neuroectoder mal and mesodermal derivation 12 Perivascular lymphocytic cuffing 13 Perivascular eosinophilic cuffing 14 Neuronal necrosis • Neurons are very susceptible to inadequate nutrients and oxygen and degeneration and necrosis result. • The order of sensitivity to lack of oxygen is : neurons, oligodendroglia, astrocytes, and microglia. • Some neurons are more susceptible to hypoxia than others, e.g. neocortical neurons have a 5 minute survival, basal nuclei- 10 minutes. 15 Necrosis of neuron groups • Focal or laminar • Focal necrosis may result from vascular compromise (infarction). Neurons and glia are both involved usually. • Focal necrosis of specific nuclei may occur with some toxicities, e.g. pallidonigral necrosis with yellow star thistle poisoning of horses. • Causes of neuron necrosis include: cardiac arrest, cerebral embolism and thrombosis and ruptured aneurysm which lead to infarction, and toxins (lead, mercury, plant toxins). 16 17 Laminar cortical necrosis • Occurs due to the extreme susceptibility of the second and third layers of the cerebral cortex to hypoxia. • Causes of laminar cortical necrosis include: – – – – Carbon monoxide poisoning Hypoglycemia Salt poisoning in swine Thiamine deficiency in cattle and sheep 18 19 Laminar cortical necrosis, Polioencephalomalacia (PEM), B1 deficiency in cattle 20 21 Laminar cortical necrosis, salt poisoning in pigs 22 Malacia • If larger areas undergo necrosis, the gross change is termed malacia. This is liquefactive necrosis. • The sequence of events is as follows: – 2-5 days: grossly softened and discolored yellow – Liquefaction in 7-14 days – If the area of necrosis is large, there is a cavity lined by glia; if small, the space may be obliterated by gliosis – Large numbers of macrophages or gitter cells may be present 23 24 Peripheral nerve damage and repair 25 Wallerian degeneration • When a nerve fiber is severed or damaged, the breakdown of the axon and its myelin sheath is termed Wallerian degeneration. The process is termed degeneration although the axon and myelin are really destroyed or die. • Causes of Wallerian degeneration: – Compression and crushing by trauma, abscesses or neoplasms – Transection – Stretching – Intoxication (lead, mercury, arsenic) 26 Multiple digestion chambers (arrows) containing axonal fragments and macrophages 27 28 Function of myelin sheath • Increase the velocity of impulse conduction. • Protect the portion of the nerve cell it surrounds. • Relate the nutrition of the nerve cell. • Necessary for repair and regeneration. 29 Demyelination • Disorders of oligodendroglia or schwann cells can produce myelin sheath defects. Although the axon is initially intact, it is eventually altered and destroyed secondary to myelin defects. Whether demyelination or axonal degeneration occurs first in some diseases is not clear and there is some overlap. • There are two categories of myelin disease: – Demyelinating (myelinoclastic) – Dysmyelinogenesis disorders of myelin formation such as leukodystrophies • Demyelination stimulates glial proliferation. • Demyelinated nerves may regenerate but most demyelinating diseases are progressive. 30 31 Demyelination of cerebellum, canine distemper 32 Demyelination, LFB-CEV 33 GFAP 34 35 Axonal degeneration • Axonal degeneration affects the entire neuron but degeneration usually begins at the distal end of the neuron and proceeds toward the cell body. This is called "dying back". • Schwann cell proliferation in the area of axonal degeneration occurs but less than in Wallerian degeneration. Regeneration and recovery are possible if the degeneration process is stopped in time. 36 Alterations of Neurons, glial cells and other components in the nervous system 37 Neurons • • • • • • Central chromatolysis VS peripheral chromatolysis Neuronophagia Acute necrosis Laminar cortical necrosis Intranuclear or cytoplasmic inclusion body Vacuolar change: BSE, Scrapie • Abnormal accumulations: lipofuscin, storage disease • Deposition of extraneous pigment: hematin pigment, ferrugination or iron incrustation • Axonal degeneration • Hytrophic changes: Bi- or multinucleated neuron • Wallerian degeneration (axonal alteration) • Axonal balls 38 Astrocytes • • • • • • • Hypertrophic astrocytes (Gemistocytes) Rothensal fibers Gliosis (astrocytic gliosis) Viral inclusion: CD Corpora amylacea Chronic degenerative change: lipofuscin Abnormal accumulations: mucopolysaccharidiosis 39 Oligodendrocytes • • • • Satellitosis Viral inclusions: papovavirus Acute swelling (hydropic change) of the cytoplasm-- autolytic change Convert to astrocytes and participate in glial scar formation 40 Microglia • • • “Gitter” (=lattice in German) cells and “Compound granular corpuscles” (French) Microglial nodule Neuronophagia 41 Ependymal cells • Granular ependymitis 42 Other alterations • Malacia • Infarct • Perivascular lymphocytic cuffing • Demyelination • Vascular endotheliumhypertrophy (HC), viral inclusions (ICH, canine parvoviral infection) • • • • Hemorrhage Edema Abscess- bacterial infection Granuloma- mycotic infection • Primary tumors or metastasizing tumors 43 Thanks for joining the lecture. In coming issue….. Comparative Pathology and Emerging Zoonosis 44