Disseminated granulomatous meningoencephalomyelitis in a dog

A 6-year-old, intact, female miniature Doberman pinscher was evaluated for lethargy, intermittent back pain, and unstable gait. Physical and neurological findings included bradycardia, hypothermia, hyperesthesia, progressive and ascending ataxia, and proprioceptive deficits in all limbs. Laboratory findings and magnetic resonance imaging were consistent with disseminated granulomatous meningoencephalomyelitis, confirmed later by microscopy.     

Treatment of granulomatous meningoencephalomyelitis in a dog

The clinical work-up, diagnosis and follow-up of an 8-year-old, female-spayed Shih Tzu with diffuse, granulomatous meningoencephalomyelitis (GME)-causing visual deficits is reported. The use of cytosine arabinoside as an alternative treatment for GME is discussed.     

Protothecal granulomatous meningoencephalitis in a dog

A case of central nervous system protothecosis in a dog is reported. A three-year-old male Maremma sheepdog was referred with a two month history of diarrhoea associated with progressive tetraparesis, depression and right circling. Stupor, severe proprioceptive deficits, bilateral decreased thoracic limb flexor reflexes and bilateral deficit of the menace reaction were detected on neurological examination and a multi-focal neurological localisation was suspected. Histopathological evaluation revealed multi-focal granulomatous foci in the thalamus, hippocampus and caudal brainstem containing numerous oval-rounded organisms with a thick, periodic acid-Schiff-positive and Gomori's methenamine silver-positive cell wall, a basophilic cytoplasm and one nucleus. Scattered sporangia containing two to four endospores were also observed. Morphological features were consistent with Prototheca species. Ultrastructurally, numerous degenerated algae were present within macrophages mainly lacking nuclei and cytoplasmic organelles. Generally, protothecosis in dogs is characterised by systemic signs because of a multi-organ involvement, and haemorrhagic colitis or ophthalmologic signs are the most frequent presenting signs. However, protothecosis should be added, also in Europe, to the list of the differential diagnoses in adult dogs with a multi-focal neurological localisation even in absence of other clinical signs.     

A comparative pathological study on canine necrotizing meningoencephalitis and granulomatous meningoencephalomyelitis

Canine necrotizing meningoencephalitis (NME) and granulomatous meningoencephalomyelitis (GME) were compared pathologically. Gross observation exhibited lateral ventricular dilation and discoloration, malacia and/or cavitation of the cerebrum in NME. On the contrary, gross changes were milder in GME, except for occasional visible granulomatous mass formation. Histopathologically, the lesions of NME were distributed predominantly in the cerebral cortex and various degrees of inflammatory and necrotic changes were observed according to clinical stages. Besides, microscopic lesions of GME were mainly distributed in the white matter of the cerebrum, cerebellum and brainstem, which are characterized by perivascular cuffing, multiple granulomas and leptomeningeal infiltrates. Although macrophages and lymphocytes were predominant in the inflammatory lesions of both disorders, macrophages in GME transformed into epithelioid cells and exhibited more massive infiltration. Although lectin RCA-1-reactive cells were numerous in both disorders, lysozyme immunoreactive cells in NME were fewer than that in GME. Parenchymal infiltration of MAC387-positive cells was common in GME and limited in NME. The number of CD3-positive lymphocytes in the GME lesions tended to be greater than in NME, though the difference was not statistically significant. Morphological and immunohistochemical differences of the lesions, in particular, the characteristics of infiltrative macrophages may reflect these different pathogeneses of the two disorders.     

Adipsia and hypernatraemia in a dog with focal hypothalamic granulomatous meningoencephalitis

A 7-year-old Doberman was presented with a history of progressive neurological disease of 4 weeks duration. Initially there were episodes of aimless wandering and uncharacteristic aggression, however, the dog was obtunded at presentation. Serum biochemical analysis revealed profound hypernatraemia and moderate hyperproteinaemia. Despite correction of the hypernatraemia by the infusion of hypotonic fluids, the dog continued to periodically exhibit pacing and head pressing. A patchy, ill-defined contrast-enhancing area was evident in the ventral midbrain on computed tomography of the brain. Analysis of the cerebrospinal fluid revealed a mild increase in protein concentration, positive Pandy's test and mild pleocytosis. Because of the poor prognosis, euthanasia and necropsy were performed. Histopathological analysis of the brain revealed a severe focal meningoencephalitis affecting hypothalamic nuclei and mammillothalamic tracts. Destruction of osmoreceptors in the hypothalamus responsible for recognition of thirst is believed to have resulted in adipsia and subsequent hypernatraemia.     

Focal granulomatous meningoencephalomyelitis in a pup

Granulomatous meningoencephalomyelitis (GME) was diagnosed in an 8-month-old Maltese with signs of CNS disease. Serum immunoglobulin (Ig) G concentration was decreased, and CSF analysis revealed high concentrations of mononuclear WBC and IgG. Initial improvement of the pup's signs in association with prednisolone treatment and postmortem examination of CNS tissues confirmed GME. Granulomatous meningoencephalomyelitis occurs rarely in young dogs and the abnormal Ig concentrations in this pup's serum and CSF suggest that immune responses may have a role in the cause and/or pathogenesis of GME.     

Cerebellar focal granulomatous meningoencephalitis in a dog: clinical findings and MR imaging

The authors encountered a dachshund dog, presenting vestibular disorder. On magnetic resonance (MR) imaging, a mass showing isointensity on the T1- and T2-weighted images and enhanced by contrast medium, was observed in the right cerebellum. In addition, the periphery of the mass showed isointensity on the T1-weighted image and hyperintensity on the T2-weighted image, suggesting sever oedema. Although the dog underwent surgery, it died. The mass was diagnosed pathologically as a granulomatous meningoencephalitis.     

犬瘟热病毒与犬瘟热的预防免疫

犬瘟热(Canine Distemper,CD)是由犬瘟热病毒(Canine Distemper.Virus,CDV)感染引起的急性、高度接触性传染病.它常引起大批犬、貂、狐等动物发病,病死率达30%～80%.是当前对我国养犬业、毛皮动物养殖业和野生动物保护业危害最大的疫病之一.因此提高对犬瘟热的预防和控制也是当前值得关注的问题.     

Differential diagnosis of tenesmus in the dog

Tenesmus refers to severe straining due to abnormalities in or around the lower alimentary or urinogenital systems. Differential diagnosis is based on (a) history; (b) visual inspection of the perineum (where painful lesions leading to dyschezia are often located); (c) abdominal palpation, possibly followed by catheterization; (d) rectal examination; (e) radiography including contrast studies; (f) proctoscopy and possibly biopsy; (g) laparotomy in unresolved cases. The incidence of alimentary and urinary tenesmus is illustrated in a select series. The forms of tenesmus in 110 dogs were as follows: urinary (53 cases), alimentary (38), urinary and alimentary (14), unknown cases (5).     

Comprehensive immunohistochemical studies on canine necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalomyelitis (GME)

In dogs, there are several idiopathic meningoencephalitides, such as necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalomyelitis (GME). Although they are often assumed to be immune mediated, the etiology of these diseases remains elusive. In this study, the histopathology of the lesions caused by these conditions and the inflammatory cell populations produced in response to them were examined among dogs affected with GME, NME, or NLE to understand their pathogeneses. The brain tissues of dogs with NME (n = 25), NLE (n = 5), or GME (n = 9) were used. The inflammatory cells were identified by immunohistochemistry using antibodies against CD3, IgG, CD20, CD79acy, and CD163. In NME and NLE, malacic changes were located in the cerebral cortex, as well as the cerebral white matter and thalamus, respectively. The distribution of the brain lesions in NME and NLE was breed specific. In GME, granulomatous lesions that were mostly composed of epithelioid macrophages were observed in the cerebral white matter, cerebellum, and brainstem. Although the proportions of IgG-, CD20-, and CD79acy-positive cells (B cells) were not significantly different among the GME, NME, and NLE lesions, that of CD3-positive cells (T cells) was increased in GME. In NME and NLE, CD163-positive cells (macrophages) had diffusely infiltrated the cerebral cortex and white matter, respectively. However, in GME, CD163-positive cells accumulated around the blood vessels in the cerebral and cerebellar white matter. The distributions of these lesions were quite different among GME, NME, and NLE, whereas there were no marked differences in the proportions of inflammatory cells.     

Ischaemic encephalopathy and focal granulomatous meningoencephalitis in the cat

Three cats were presented with neurological deficits compatible with cerebral disease. Two of the cats had temporal lobe infarction diagnosed as ischaemic encephalopathy; one cat had granulomatous inflammation, diagnosed as focal granulomatous meningoencephalitis. In all three cases the lesions were characterized by necrotic, cavitated areas. Vascular insult was the cause of the ischaemic encephalopathy and the focal granulomatous meningoencephalitis may have been caused by feline infectious peritonitis (FIP) virus. An infectious aetiology, possibly FIP virus, is proposed for the ischaemic encephalopathy. A relationship between these two neurological diseases may exist.     

Hepatozoonosis in a dog with skeletal involvement and meningoencephalomyelitis

Abstract: A 15‐month‐old, female mongrel dog was presented with a 6‐week history of inappetence, weight loss, and tetraparesis. Physical examination revealed weakness, poor body condition, mild fever, pale mucous membranes, and diffuse muscle atrophy. The right hind limb was painful and edematous, with large ecchymoses. The femur was irregular on palpation and moderate popliteal lymphadenopathy was evident. Results of a CBC showed severe anemia with mild regeneration, an inflammatory leukogram with 90% of neutrophils parasitized by Hepatozoon sp. gamonts, and moderate thrombocytopenia. A bone marrow aspirate had myeloid hyperplasia and contained a few extracellular Hepatozoon meronts and a few intracellular gamonts within neutrophils. Serum chemistry abnormalities included hypoalbuminemia, hyperglobulinemia, hypoglycemia, hypercalcemia, hyperphosphatemia, and elevated alkaline phosphatase activity. Radiologic findings of the right femur included periosteal bone proliferation and lesions compatible with osteomyelitis. A fine needle aspirate specimen from the bone lesion had neutrophilic inflammation; 36% of the neutrophils contained Hepatozoon gamonts. Results of cerebrospinal fluid analysis included a protein concentration of 37 mg/dL and marked mononuclear pleocytosis (243 cell/μL) with a predominance of lymphocytes. An ELISA was positive for Hepatozoon canis and PCR results with DNA sequencing confirmed infection with this organism. A diagnosis of hepatozoonosis with skeletal involvement and meningoencephalomyelitis was made. The dog recovered almost completely neurologically and had no gamonts in the blood after 60 days of therapy with imidocarb dipropionate and prednisone. This is an unusual case of canine hepatozoonosis involving neurologic signs and a periosteal reaction more typical of H. americanum infection and rarely reported in dogs infected with H. canis.     

Characteristics of magnetic resonance images of granulomatous meningoencephalomyelitis in 11 dogs

The characteristics of magnetic resonance imaging (mri) of the brains and spinal cords of 11 dogs with histologically confirmed granulomatous meningoencephalomyelitis (gme) were determined. The lesions were in the brain of eight of the dogs, in the brain and spinal cord of two, and in the spinal cord alone in one dog. A single lesion was present in four of the dogs and multiple lesions were found in six. In one dog with intracranial signs, no visible lesions could be detected on mri. No meningeal enhancement was detected in T1-weighted images post-contrast, or in fluid attenuation inversion recovery (flair) images, but there were histological lesions in the meninges in nine of the dogs. The T2-weighted images and flair sequences were characterised in all cases by hyperintensity, whereas the signal intensity of the lesions on T1-weighted images was variable. After the administration of paramagnetic contrast, some of the lesions showed no enhancement, but others showed marked patterns of enhancement. The lesions in 10 of the dogs were easily identifiable by mri and the images had several unifying characteristics, but they could not be considered disease-specific.     

Clinical evaluation of rabies virus meningoencephalomyelitis in a dog

A 6-month-old, female, mixed-breed dog presented for acute, progressive, flaccid paraplegia and bilateral pelvic-limb hyperesthesia. A lymphocytic pleocytosis with 366 mg/dL protein was found on cerebral spinal fluid (CSF) evaluation. Electromyography (EMG) demonstrated positive sharp waves and fibrillations in the left pelvic limb; the M wave of the left sciatic nerve was not obtainable by nerve stimulation. Seizures and dementia began during recovery from anesthesia. Six days after onset of paralysis, the dog was euthanized. Direct fluorescent antibody testing of the brain was positive for raccoon rabies virus. This case demonstrates clinical evaluation, CSF analysis, and EMG in an animal with rabies meningoencephalomyelitis.     

Streptococcal meningoencephalitis in a dog.

A 5.5-year-old French bulldog was presented with acute neck pain and a short history of central vestibular syndrome. A marked neutrophilic pleocytosis and numerous gram-positive cocci were evident on cerebrospinal fluid (CSF) cytology. Streptococcus pneumoniae, a pathogen of humans, was isolated upon CSF microbiological culture. Treatment consisted of intravenous antibiotics, supportive care, and anticonvulsants for the generalized seizures which developed shortly after admission. The dog responded to therapy and two years later exhibited only a mild, residual head tilt. The pathogenesis and treatment of bacterial meningoencephalitis in dogs are reviewed.     

A comparative pathological study on granulomatous meningoencephalomyelitis and central malignant histiocytosis in dogs

Histiocytic proliferative disorders in canine central nervous system (CNS) including granulomatous meningoencephalomyelitis (GME) and malignant histiocytosis were compared pathologically. Lesions of GME mainly existed in the white matter of the cerebrum, brainstem and cerebellum and consisted of characteristic perivascular cuffing, parenchymal granuloma and leptomeningeal infiltrates of mononuclear cells. In malignant histiocytosis, there were two histological patterns, diffuse proliferation of neoplastic histiocytes through the leptomeninges and neoplastic nodule formation in the parenchyma. Neoplastic histiocytes exhibited mild to severe cellular atypia and high ability of invasion into the brain parenchyma. Mitotic and phagocytic figures were also observed. Several histiocytic markers, including lysozyme, alpha1-antitrypsin and lectin RCA-1, revealed histiocytic origin of both inflammatory and neoplastic cells, however, those were not determinative for the discrimination between GME and malignant histiocytosis. CD3- and PCNA-positive cells existed in the lesions of both diseases. The number of CD3-positive cells in GME tended to be greater than in malignant histiocytosis, while the difference was not statistically significant.     

Correlation between the clinical course of granulomatous meningoencephalomyelitis in dogs and the extent of mast cell infiltration

The data from 20 dogs with histopathologically confirmed granulomatous meningoencephalomyelitis were reviewed in an attempt to identify clinical signs and morphological and cellular parameters, particularly the infiltration of mast cells, which might be associated with the clinical course of the disease. Thirteen of the dogs had the acute form of the disease and seven had the chronic form. Young to middle-aged, small breed female dogs were over-represented. Central vestibular signs were observed in six of the dogs with the acute disease. Analyses of cerebrospinal fluid revealed moderate to severe pleocytosis and high protein concentrations in all cases. Histopathological investigations revealed disseminated perivascular cuffs, large confluent granulomata, tissue necrosis, infiltration with neutrophils and a large number of mitotic cells in the dogs with either of the clinical forms of the disease. Tryptase-positive mast cells were observed in all the cases, but there were significantly larger numbers in the dogs with the acute form.