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Winter 2007 Newsletter

Granulomatous meningo encephalomyelitis
Ovine Progressive Pleuropneumonia
Porcine Circovirus Associated Diseases
Potomac Horse Fever


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Final diagnosis: Granulomatous meningoencephalomyelitis

History:  A reportedly 3-year-old, spayed female rat terrier dog was submitted to the ADDL for necropsy.  This dog originally presented to the referring veterinarian with a history of ataxia and pelvic limb paraparesis.  Clinical signs progressed over the next two weeks with the development of tetraparesis, hyperesthesia, loss of anal tone, and hemorrhagic diarrhea.  Lower motor neuron reflexes were present in the pelvic and thoracic limbs.  Following treatment, clinical signs improved slightly over the next five days with the recurrence of anal tone, increased alertness, and increased mobility in the forelimbs; however, clinical signs subsequently worsened the following week-end resulting in death.

Gross findings:  On gross examination, the spinal cord was soft and swollen, filling the vertebral canal.  No other significant lesions were observed in the brain or other body systems.

Histologic findings:  Along the entire length of the spinal cord, the meninges were markedly expanded by a pleomorphic inflammatory infiltrate, predominantly consisting of macrophages and lymphocytes with fewer plasma cells and neutrophils.  Epitheloid macrophages were often arranged in concentric layers forming granulomas which were often oriented around small vessels.  Inflammatory cells extended from the meninges into the white, and sometimes, grey, matter, effacing and rarefying the neuropil.  There was marked lymphocytic perivascular inflammation which was predominantly in the white matter.

  In the cerebrum, macrophages, lymphocytes, and plasma cells expanded the meninges, occasionally extending into and effacing adjacent neuropil.  Foci of predominantly perivascular necrosis and granulomatous inflammation, consisting of epitheloid macrophages, lymphocytes, and fewer neutrophils and plasma cells, were scattered throughout the cerebrum, primarily in the white matter.  Similar foci of necrosis and inflammation were present in the pons and ventral cerebellum.  Special stains, including Gram, periodic acid-Schiff (PAS), and Giemsa stains were performed on sections of spinal cord in order to identify potential infectious agents; however, no organisms were identified.

Discussion:  Granulomatous meningo-encephalomyelitis (GME) is an inflammatory disease of unknown etiology, characterized by predominantly perivascular, granulomatous inflammation in the meninges and white matter of the central nervous system.  Lesions may be focal, multifocal, or disseminated, affecting the cerebrum, cerebellum, brainstem, spinal cord, or optic tracts. Granulomatous meningoencephalomyelitis occurs in many breeds of dog and can occur both in males and females; however, small breed dogs, poodles, terriers, and female dogs have been shown to have an increased incidence of disease. The age of onset is usually between one and nine years; however, animals may be affected at any age.  Affected animals usually present with an acute onset of disease, which progresses over days to months.  The clinical presentation is variable, reflecting the distribution of lesions, but may include intermittent fever, lethargy, depression, convulsions, head tilt, circling, cervical pain, hyperesthesia, conscious proprioceptive deficits, paresis, or paralysis.

  Clinical diagnosis of GME is based on clinical signs and cerebral spinal fluid analysis, which is characterized by pleocytosis, increased protein, and normal to increased pressure in the absence of infectious agents.  A definitive diagnosis of GME is based on characteristic histopathologic lesions. Including primarily perivascular granulamatous inflammation in meninges and white matter with no associated infectious agents.  Immunosuppressive therapy, primarily consisting of corticosteroids, has been the principle treatment modality for GME and, in some cases, can result in long term improvement of clinical signs; however, GME is a continuously progressive disease, often resulting in recurrence and progression of clinical signs, especially when immunosuppressive therapy is discontinued.  Radiation therapy has also been used with some success, particularly in the presence of focal disease.  In general, due to its progressive nature, GME is associated with a poor prognosis.  However, in one study, animals with focal disease had longer median survival times as compared to those with multifocal disease.  Currently, the cause of granulomatous meningoencephalomyelitis is unknown, and GME has not been associated with any infectious agents.  Based on the predominance of CD3+ T-cells and MCH II+ macrophages, one study has proposed that GME may be a T-cell mediated autoimmune disorder; however, additional studies have not been performed to support or refute this hypothesis.

Perivascular granu-lomatous inflammation in cerebral white matter 20X

Perivascular granu-lomatous inflammation in cerebral white matter 40X

by Dr. Joshua Webster, ADDL Graduate Student


  1. Baumgärtner, KA, Vogl C, Gaedke K, Wellman M: 1998.  Immunohistochemical characterization of inflammatory cells in brains of dogs with granulomatous meningoencephalitis.  Vet Pathol 35: 43-52.

  2. LeCouteur Ra, Grandy JL: 2005. Diseases of the spinal cord In: Textbook of Veterinary Internal Medicine: Diseases of the Dog and Cat, 6th ed.  Ettinger SJ, Feldman EC, eds. Elsevier, St. Louis MO.  1: 842-887.

  3. Munana KR, Luttgen PJ: 1998.  Prognostic factors for dogs with granulomatous meningoencephalo-myelitis: 42 cases (198201996). JAVMA 212: 1902-1906

  4. Zachary JF: 2006.  Nervous system In: Pathologic Basis of Veterinary Disease, 4th edition.  McGavin MD, Zachary JF, eds.  Elsevier, St. Louis MO. Pp 833-971.



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