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C O N F E R E N C E 21 13 April 2016 Joint Pathology Center Veterinary Pathology Services WEDNESDAY SLIDE CONFERENCE 2015-2016 C o n f e r e n c e 21 13 April 2016 Jey Koehler, DVM, PhD, DACVP Director, Histopathology Core Laboratory Department of Pathobiology Auburn University College of Veterinary Medicine CASE I: 1888-15 (JPC 4070542). grey matter of the cerebrum, cerebellum and brainstem, are numerous intense Signalment: 6-year-old castrated male inflammatory foci that often coalesce. Yorkshire terrier dog (Canis familiaris) Inflammatory cells are comprised of large numbers of macrophages, lymphocytes, with History: Per history provided, Milo is a 6- fewer plasma cells and neutrophils. The year-old castrated male Yorkshire terrier macrophages often appear epithelioid cells dog that was diagnosed with tra- and form granulomatous foci that efface and cheobronchitis for the past month and was replace neuropil. Within neuropil adjacent to placed on antibiotic therapy. The dog granulomatous foci are large numbers of developed sudden onset of hindlimb glial cells (gliosis) and reactive gemistocytic weakness and was unable to walk on both astrocytes. Both lymphocytes and ma- hind limbs. He collapsed acutely, failed to crophages are arranged in dense and often revive when administered cardiopulmonary whirling, perivascular cuffs. Mitoses in the resuscitation, and was submitted for macrophage population are present at 1-3 necropsy. per high power field (400x) in areas of perivascular cuffs. Endothelium associated Gross Pathology: There were no with the perivascular cuffing is reactive, and significant gross findings noted. lined by plump and hypertrophied endothelial cells, and vessel walls are Laboratory Results: N/A infiltrated by the mononuclear cells described above. Histopathologic Description: Brain: Multi- focally, expanding the meninges and Spinal cord: Diffusely expanding meninges Virchow-Robins space primarily within the and multifocally replacing white and grey white matter and less severely affecting the matter of the spinal cord are similar 1 Cerebrum, dog. In cross sections from the cerebrum and cervical spinal cord, the vessels (especially at the interface of the grey and white matter) are accentuated by a perivascular inflammatory infiltrate. (HE, 5X) inflammatory cells as those described above system of predominantly young to middle- for the brain sections. Perivascular gran- aged, small toy breed dogs, although age ulomatous, lymphocytic cuffs are present in and breed of affected dogs can vary vastly.3,4 neuropil and meninges. The disease was first reported in 1978, and represents 5-25% of central nervous system disease of dogs.3 A higher incidence of this Contributor’s Morphologic Diagnosis: disease may be seen in females, and affected Brain: 1. Severe, multifocal to coalescing dogs are typically mature.2 The disease is lymphohistiocytic encephalitis almost always progressive and is associated 2. Severe, diffuse lymphohistiocytic clinical signs include ataxia, non- meningitis ambulation, paresis, paralysis, as well as a Spinal cord: 1. Severe, multifocal lymp- wide range of other neurological signs.2 hohistiocytic myelitis Dogs with GME may develop neutrophilic 2. Severe, diffuse lymphohistiocytic leukocytosis, with increased protein and meningitis cellularity in CSF fluid.2 While the disease is normally progressive and prolonged, some 2 Contributor’s Comment: This dog had dis- affected dogs can die spontaneously. seminated granulomatous men- Grossly, the lesions of GME can be hard to identify, and affected white matter may ingoencephalomyelitis (GME) that affected 4 the brain and spinal cord (and optic nerve, appear as small foci of malacia. The disease not included on slide). GME is an idiopathic tends to affect white matter of cerebrum and disease that affects the central nervous cerebellum, and occasionally occurs in the 2 optic nerve and spinal cord. Histological variable and may be steroid dependent.3 findings of prominent perivascular cuffing Definitive diagnosis of the disease is based of mononuclear cells and discrete gran- on brain biopsy.3 Treatment for GME is ulomatous aggregates are distinctive features largely based on immunosuppression with of the disease.4 corticosteroid therapy, and azathioprine, cy- tosine arabinoside, procarbazine, cy- GME can be classified as focal, dis- 3 closporine and radiation therapy have more seminated (multifocal) and ocular. The recently been attempted in treatment focal type is characterized by coalescing regime.3 granulomas that form a space-occupying In general, prognosis of dogs with lesion and associated clinical signs, and are GME is poor. Considering the clinical more common in the cerebrum and history of tracheobronchitis in this dog and 3 the nature of inflammatory cells, the brainstem. The disseminated form affects differential diagnosis includes canine more than one of the following sites: cer- distemper (Morbillivirus) infection. There ebrum, brainstem, spinal cord, cerebellum, 3 were no intranuclear or intracytoplasmic meninges and optic nerves. The ocular form viral inclusions present in any of the is associated with optic neuritis and oc- sections examined to further support a viral casionally uveitis, retinal hemorrhage or 3 etiology in this case. Ancillary testing using retinal detachment. The exact etiology of immunohistochemistry to label viral antigen GME is unknown, although infectious in the brain sections would be useful to causes and immune-mediated disease have definitively rule out canine distemper in this been proposed. Antemortem diagnosis of case. Fungal or protozoa infection are lower GME is typically based on CSF analysis, on the differential list as organisms were not characterized by increased leukocyte count, observed in any of the examined sections. mononuclear pleocytosis and increased 3 protein content. However, changes can be Cerebrum, dog. Virchow-Robins spaces are filled by various combinations of histiocytes and lymphocytes (black arrow). Some vessels have a predominantly histiocytic infiltrate (green arrow). (HE, 81X) 3 pathogenesis of GME (and NME), and the JPC Diagnosis: Brain, cerebrum, brainstem; phenomenon of molecular mimicry has also spinal cord: Meningoencephalomyelitis, been implicated. Infectious agents have not lymphohistiocytic, chronic, multifocal, been identified via light microscopy or marked. culture and molecular techniques have failed to identify a viral agent; however, molecular Conference Comment: In addition to techniques have identified Mycoplasma granulomatous meningoencephalitis (GME), canis (an agent not typically associated with other idiopathic inflammatory conditions CNS disease) in cases of both GME and that affect the nervous system include NME. To date, the precise role of M. canis necrotizing meningoencephalitis (NME) in the pathogenesis of GME and NME (see case 2 of this conference) and remains unclear.1 Aside from explanations necrotizing leukoencephalitis (NLE). Each involving an infectious agent and immune of these entities has unique features with dysregulation, it has also been postulated reference to breed predilection, histologic that GME may represent a lymph- lesions, anatomic location and clinical oproliferative disorder.7 Overall, the presentation. While NME and NLE are common view is that this condition is mul- associated with specific dog breeds, GME is tifactorial with a complex pathogenesis not. CD3-positive T-cells appear to play an involving genetic factors, immune dy- important role in development of lesions, sregulation and environmental factors (i.e. particularly in GME. CD163-positive pathogens).1,7 macrophages also play an important role in GME where they exhibit a unique, 5 The conference histologic description predominantly perivascular distribution. mirrored the contributor’s description above. Histologic findings in GME include Additional features described include mild granulomatous foci composed of primarily rarefaction and vacuolation of the neuropil macrophages and lymphocytes, with fewer adjacent to inflammatory aggregates, and plasma cells and neutrophils, located in the microgliosis (in addition to the astrocytosis cerebral white matter, subcortical region, noted above). Although many of the cerebellum, and midbrain. In GME, astrocytes appear hypertrophied/reactive, the interleukin 17 (IL-17) levels are often majority have not yet reached the elevated within inflammatory cells characteristic gemistocytic stage. Low (primarily macrophages / microglia) and numbers of necrotic neurons are also may contribute to the development of the present, although this is not a prominent associated lesions. IL-17 is a component of feature. Perivascular cuffs consist primarily the Th17 immune response and is produced of lymphocytes, while most of the in some autoimmune conditions, such as histiocytes are localized to the neuropil rheumatoid arthritis and Crohn’s disease, adjacent to perivascular cuffs. The among others. It has been postulated that moderator noted that the distinct asymmetric GME may be represent a delayed type nature of the lesions, particularly within the hypersensitivity reaction and that mast cells perivascular cuffs, is a characteristic feature may play a role in development of early 6 of GME. She also pointed out the vas- lesions. culocentric nature of the meningeal inflammation and how it is not evenly Aside from (or in conjunction with) an distributed, which is another common autoimmune disorder, infectious agents have feature of this entity. Conference long been suspected to be involved
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