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1.
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.  相似文献   

2.
The objective of this investigation was to determine whether or not herpesvirus (herpes-), adenovirus (adeno-), or canine parvovirus DNA is present in the brains of dogs with necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalitis (GME). Paraffin-embedded brain specimens from 12 histopathologically confirmed dogs with NME, 3 with NLE, and 7 with GME were screened for viral DNA with degenerate herpes- and adenovirus polymerase chain reaction (PCR) and a canine parvovirus-specific PCR. Positive-control specimens included genomic viral DNA and paraffin-embedded tissues from dogs with confirmed herpes-, adeno-, or canine parvovirus infections. Herpes-, adeno-, or canine parvovirus DNA was amplified by PCR from the corresponding positive-control specimens. Negative controls included 7 dogs with various brain disorders and produced no viral amplicons. The 22 dogs with NME, NLE, and GME were negative for viral DNA. Additional studies testing for other viruses or inherited genetic mutations are warranted to gain insight into the etiologies of NME, NLE, and GME. We discuss potential etiologies and provide a clinical and histopathologic overview of these common canine encephalitides.  相似文献   

3.
Necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE) and granulomatous meningoencephalomyelitis (GME) are common idiopathic inflammatory central nervous system (CNS) diseases with unknown etiology in dogs. We previously showed that IgG autoantibodies in the cerebrospinal fluid (CSF) of NME cases reacted to unknown brain proteins as well as to glial fibrillary acidic protein (GFAP). In the present report, we evaluated the autoantibodies against transglutaminase2 (TG2) in the canine CNS diseases. CSF samples obtained from dogs with NME (n=19), NLE (n=7), GME (n=11) and miscellaneous CNS diseases (n=12) were subjected. CSFs from 20 healthy dogs were used as controls. Indirect fluorescent antibody test on the canine cerebrum revealed astrocyte-binding IgG in the CSF of NME. After absorption of the CSF with bovine GFAP, the CSF still possessed the reactivity to astrocytes. Double-color staining showed clear colocalization of the autoantibodies and anti-human TG2 rabbit polyclonal IgG. An immunoblot assay against human recombinant TG2 revealed anti-TG2 IgG in the CSF from dogs with NME, NLE and GME. The CSF of canine idiopathic encephalitis cases, notably of NME, tended to show high ELISA OD values against human recombinant TG2 compared to healthy controls. The presence of anti-TG2 autoantibodies in the CSF may contribute to the elucidation of the etiology of canine NME, NLE and GME.  相似文献   

4.
This study characterized the [(18)F]2-deoxy-2-fluoro-D-glucose positron emission tomography (FDG-PET) findings of encephalitis in dogs and assessed the role of FDG-PET in the diagnosis of meningoencephalitis. The medical records, magnetic resonance (MR), and FDG-PET images of 3 dogs with necrotizing meningoencephalitis (NME), 1 dog with granulomatous meningoencephalitis (GME), and 1 dog with meningoencephalitis of unknown etiology (MUE) were reviewed. On the FDG-PET, glucose hypometabolism was identified in the dog with NME, whereas hypermetabolism was noted in the dog with GME. The T2-weighted images (WI) and fluid attenuated inversion recovery (FLAIR) images were characterized by hyperintensity, whereas the signal intensity of the lesions on the T1-WI images was variable. The metabolic changes on the brain FDG-PET corresponded well to the hyper- and hypointense lesions seen on the MR imaging. This type of tomography (FDG-PET) aided in the differentiation of different types of inflammatory meningoencephalitis when the metabolic data was combined with clinical and MR findings.  相似文献   

5.
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.  相似文献   

6.
An acute to chronic idiopathic necrotizing meningoencephalitis was diagnosed in 5 Chihuahua dogs aged between 1.5 and 10 years. Presenting neurologic signs included seizures, blindness, mentation changes, and postural deficits occurring from 5 days to 5.5 months prior to presentation. Cerebrospinal fluid analyses from 2 of 3 dogs sampled were consistent with an inflammatory disease. Magnetic resonance imaging of the brain of 2 dogs demonstrated multifocal loss or collapse of cortical gray/white matter demarcation hypointense on T1-weighted images, with T2-weighted hyperintensity and slight postcontrast enhancement. Multifocal asymmetrical areas of necrosis or collapse in both gray and white matter of the cerebral hemispheres was seen grossly in 4 brains. Microscopically in all dogs, there was a severe, asymmetrical, intensely cellular, nonsuppurative meningoencephalitis usually with cystic necrosis in subcortical white matter. There were no lesions in the mesencephalon or metencephalon except in 1 dog. Immunophenotyping defined populations of CD3, CD11d, CD18, CD20, CD45, CD45 RA, and CD79a immunoreactive inflammatory cells varying in density and location but common to acute and chronic lesions. In fresh frozen lesions, both CD1b,c and CD11c immunoreactive dendritic antigen-presenting cells were also identified. Immunoreactivity for canine distemper viral (CDV) antigen was negative in all dogs. The clinical signs, distribution pattern, and histologic type of lesions bear close similarities to necrotizing meningoencephalitis as described in series of both Pug and Maltese breed dogs and less commonly in other breeds.  相似文献   

7.
To examine the prevalence of autoantibody in canine cerebrospinal fluids (CSFs), CSFs were collected from 14 healthy controls and 88 clinical cases with various diseases in the central nervous system (CNS), and were analyzed by an indirect fluorescence antibody test on frozen sections of the cerebrum from normal Beagle dogs. An anti-astrocyte autoantibody was detected in 31 clinical cases with titers ranging from 1:1 to >/=1:100. All tested cases with necrotizing meningoencephalitis (NME: n=22) and granulomatous meningoencephalitis (GME: n=3) possessed the anti-astrocyte autoantibody, while the autoantibody was negative in most cases with other inflammatory CNS diseases. The autoantibody was also detected in 4 of 12 cases with brain tumors. Hence, examination of the autoantibody in the canine CFS would be significant for diagnosing NME and/or GME, as well as for understanding peritumoral events in cases with brain tumors.  相似文献   

8.
Background: Vector‐transmitted microorganisms in the genera Ehrlichia, Anaplasma, Rickettsia, Bartonella, and Borrelia are commonly suspected in dogs with meningoencephalomyelitis (MEM), but the prevalence of these pathogens in brain tissue and cerebrospinal fluid (CSF) of dogs with MEM is unknown. Hypothesis/Objectives: To determine if DNA from these genera is present in brain tissue and CSF of dogs with MEM, including those with meningoencephalitis of unknown etiology (MUE) and histopathologically confirmed cases of granulomatous (GME) and necrotizing meningoencephalomyelitis (NME). Animals: Hundred and nine dogs examined for neurological signs at 3 university referral hospitals. Methods: Brain tissue and CSF were collected prospectively from dogs with neurological disease and evaluated by broadly reactive polymerase chain reaction (PCR) for Ehrlichia, Anaplasma, Spotted Fever Group Rickettsia, Bartonella, and Borrelia species. Medical records were evaluated retrospectively to identify MEM and control cases. Results: Seventy‐five cases of MUE, GME, or NME, including brain tissue from 31 and CSF from 44 cases, were evaluated. Brain tissue from 4 cases and inflammatory CSF from 30 cases with infectious, neoplastic, compressive, vascular, or malformative disease were evaluated as controls. Pathogen nucleic acids were detected in 1 of 109 cases evaluated. Specifically, Bartonella vinsonii subsp. berkhoffii DNA was amplified from 1/6 dogs with histopathologically confirmed GME. Conclusion and Clinical Importance: The results of this investigation suggest that microorganisms in the genera Ehrlichia, Anaplasma, Rickettsia, and Borrelia are unlikely to be directly associated with canine MEM in the geographic regions evaluated. The role of Bartonella in the pathogenesis of GME warrants further investigation.  相似文献   

9.
Background: The magnetic resonance imaging (MRI) characteristics of necrotizing meningoencephalitis (NME) are not well documented.
Objectives: To describe common MRI features of NME, to compare the MRI features to histopathologic findings, and to determine whether or not MRI lesions are predictive of survival time.
Animals: Eighteen Pugs with NME.
Methods: Retrospective MRI case study of Pugs identified by a search of medical records at 6 veterinary institutions. Eighteen dogs met inclusion criteria of histopathologically confirmed NME and antemortem MRI exam. MRI lesions were characterized and compared with histopathology with the kappa statistic. Survival times were compared with MRI findings by use of Mann-Whitney U -tests and Spearman's ρ.
Results: Twelve of 18 lesions were indistinctly marginated with mild parenchymal contrast enhancement. Prosencephalic (17/18) lesion distribution included the parietal (16/18), temporal (16/18), and occipital (16/18) lobes. There were cerebellar (4/18) and brainstem (3/18) lesions. Asymmetric lesions were present in both gray and white matter in all dogs. Falx cerebri shift was common (11/18), and 6 dogs had brain herniation. Leptomeningeal enhancement was present in 9/18 dogs. A moderate positive association was found between parenchymal contrast enhancement and both necrosis (κ= 0.45; P = .045) and monocytic inflammation (κ= 0.48; P = .025). Higher MRI lesion burden was correlated with longer time from disease onset to MRI ( P = .045). MRI lesion burden did not correlate to survival time.
Conclusions and Clinical Importance: Asymmetric prosencephalic grey and white matter lesions with variable contrast enhancement were consistent MRI changes in Pugs with confirmed NME. While not pathognomonic for NME, these MRI characteristics should increase confidence in a presumptive diagnosis of NME in young Pugs with acute signs of neurologic disease.  相似文献   

10.
BACKGROUND: Although the histopathologic features of necrotizing meningoencephalitis (NME) have been described previously, little information is available concerning the signalment, geographic distribution, seasonal onset, treatment, and survival of affected dogs. ANIMALS: Sixty Pugs with NME and 14 contemporaneous control Pugs with other intracranial diseases (non-NME group). METHODS: Pugs that were euthanized or died because of intracranial disease were prospectively obtained. All dogs had necropsy, histopathology, and testing for various infectious diseases and were subsequently divided into NME and non-NME groups. Signalment, geographic distribution, seasonal onset, treatment, and survival were compared between groups. RESULTS: In Pugs with NME, median age at onset of clinical signs was 18 months (range, 4-113 months). A greater proportion of female dogs were present in the NME group (40/60) compared with the control group (6/14). Pugs with NME had a significantly lower mean weight (7.81 kg) than control Pugs (9.79 kg) (P= .012). Mean survival in Pugs with NME was 93 days (range, 1-680 days), with dogs receiving any form of treatment living significantly longer than those that were not treated (P= .003). Anticonvulsive drugs were the only treatment significantly associated with longer survival (P= .003). CONCLUSIONS AND CLINICAL IMPORTANCE: NME appears to be a common cause of intracranial signs in Pugs, based on the high proportion of NME dogs reported in this population. Pugs with NME are most commonly young adult female dogs. Although further investigation is needed to determine the optimal treatment of NME, anticonvulsive drugs appear to beneficially affect duration of survival.  相似文献   

11.
Administration of immunosuppressive doses of glucocorticosteroids is the traditional primary treatment in necrotizing meningoencephalitis (NME) in dogs. However, response is variable and clinical signs often recur quickly with tapering dosage. Prognosis is poor and long-term therapy causes many complications. In the present study, we compared the long-term effects of combination (cyclosporine plus prednisolone) therapy with sole prednisolone therapy in management in dogs with NME. All NME cases in this study were examined with magnetic resonance imaging and cerebrospinal fluid analysis, and confirmed by histopathologic examination. The mean survival time of combination therapy group was 305.7 +/- 94.7 days. The mean survival time of sole prednisolone therapy group was 58.3 +/- 30.5 days. This case report demonstrates that combination treatment of cyclosporine with prednisolone is more effective in survival time than administration of only prednisolone in NME cases.  相似文献   

12.
Cerebrospinal fluids (CSFs) from 9 Pug dogs with necrotizing meningoencephalitis (NME: Pug dog encephalitis) were examined to identify the antigens for anti-astrocyte autoantibodies. Each CSF exhibited a positive reaction to the cytoplasm of cultured canine astrocytes by an indirect fluorescent antibody test. In an immunoblotting analysis on normal canine brain proteins, eight of 9 CSFs showed a common band of 52 kDa, corresponding to glial fibrillary acidic protein (GFAP), and all of 9 CSFs reacted with purified bovine GFAP. From these results, GFAP is one of the common autoantigens in Pug dogs with NME. On the other hand, the reactivity of CSFs to chymotrypsin-digested bovine GFAP fragments were variable among dogs, indicating that the antibodies in the CSFs recognized different epitopes on GFAP.  相似文献   

13.
Purpose To describe the clinical, histological, and immunohistochemical manifestations of canine necrotizing scleritis. Methods A retrospective examination of the clinical records and samples of ocular tissues from five dogs with a histological diagnosis ‘necrotizing scleritis’ was completed. Archived, formalin‐fixed, paraffin‐embedded samples and two control globes were stained with hematoxylin and eosin, Gram, periodic acid–Schiff (PAS) and Masson trichrome stains, and they were immunohistochemically labeled for CD3, CD18, and CD20. Results Of the five cases reviewed, only two could be confirmed as idiopathic necrotizing scleritis. The other three cases were retrospectively diagnosed as unilateral focal, non‐necrotizing scleritis, one as episcleritis and the third was scleritis secondary to a proptosed globe based on our retrospective clinical, histological, and immunohistochemical evaluations. In these two cases, idiopathic necrotizing scleritis manifested as a bilateral, progressive, inflammatory disease of the sclera and cornea that induces significant uveitis. Light microscopic examination confirmed collagen degeneration and granulomatous inflammation. There was no evidence for an infectious etiology based on Gram’s and PAS stainings. Immunohistochemical labeling revealed a predominance of B cells in idiopathic, bilateral necrotizing scleritis. Tinctorial staining abnormalities with Masson’s trichrome stain were present in scleral collagen of the two cases with idiopathic necrotizing scleritis as well as a case of secondary traumatic scleritis. Conclusions Based on a limited number of cases, idiopathic canine necrotizing scleritis shares similar histopathological features with non‐necrotizing scleritis and episcleritis; however, necrotizing scleritis is B‐cell‐dominated and bilateral, and significant collagen alterations manifest with Masson’s trichrome stain.  相似文献   

14.
A progressive neurological disease affecting twenty-two young adult dogs of smaller breeds is reported. The disease was most often acute in onset and the neurological signs included cervical pain, seizures, behavioural changes, ataxia, head tilt, muscle tremor and paresis. The lesions were those of a disseminated granulomatous meningoencephalomyelitis in which perivascular cuffs of macrophages and lymphoid cells were the predominant finding. Severe lesions were most often seen in the cerebral white matter although the brain stem, mid-brain and spinal cord were also commonly affected.  相似文献   

15.
To clarify the involvement of excitatory and inhibitory amino acids in canine necrotizing meningoencephalitis (NME), glutamate, aspartate, taurine and gamma-aminobutylic acid (GABA) were determined in the cerebrospinal fluids (CSF) from eight NME cases and ten healthy controls. NME dogs exhibited significantly higher concentrations of glutamate and aspartate than those in controls (p<0.001 and p<0.001, respectively), while there was no difference in taurine or GABA between the two groups. When fetal canine astrocytes were cultured for 24 hr in the presence of NME-CSF, supernatant concentrations of glutamate, aspartate and taurine were significantly elevated. Simultaneously, expression of excitatory amino acid transporter 2 (EAAT2) mRNA was significantly reduced in the astrocytes without change in EAAT1 mRNA. Hence, reduced expression of EAAT2 and impaired glutamate homeostasis may contribute to the pathogenesis of NME.  相似文献   

16.
Granulomatous meningoencephalitis (GME) is an acute, progressive, and often fatal inflammatory disease of the central nervous system, affecting mainly small and toy dog breeds. A definitive diagnosis of GME can only be achieved through histopathologic examination of samples collected after death. This retrospective study describes transcranial Doppler ultrasonography (TDS) findings in dogs with confirmed clinical histopathology of GME. Eleven dogs were selected for this study. Sonographic findings in B-mode demonstrated diffuse decreased brain parenchyma echogenicity in 9 dogs, ventriculomegaly in 8 dogs, brain atrophy in 4 dogs, and hyperechoic focal lesions in 6 dogs. Color Doppler imaging revealed more obvious vessels of the arterial circle in 10 dogs. Spectral Doppler examination was performed in 10 dogs to detect the 6 major cerebral arteries of interest. The examination showed normal and high resistive index (RI) values in the outlined arteries. The TDS findings were consistent with pathology found on postmortem examination.  相似文献   

17.
The purpose of the study was to describe magnetic resonance (MR) imaging features of histologically confirmed necrotizing encephalitis in four Pugs and to compare those findings with MR imaging characteristics of necrotizing encephalitis in other breeds. All dogs had the following common findings: lesions restricted to the forebrain, both cerebral hemispheres diffusely but asymmetrically affected, lesions affected gray and white matter resulting in loss of distinction between both, most severe lesions in occipital and parietal lobes, lesions were irregularly T2-hyperintense and T1-isointense to slightly T1-hypointense, and no cavitation. There were various degrees of contrast enhancement of brain and leptomeninges. Asymmetry of lateral ventricles and midline shift was seen in one dog each. Two dogs had brain herniation, which may have contributed to the progression of neurologic signs. Hyperintensity on T2-weighted and fluid attenuated inversion recovery images in the hippocampus and piriform lobe was consistent with excitotoxic edema, whereas similar imaging features in other forebrain areas corresponded to areas of inflammation or liquefaction on histopathology. In comparison with necrotizing encephalitis in other canine breeds, Pug dog encephalitis has some unique MR imaging features. Therefore, these characteristics cannot be applied to other breeds, nor should imaging features of necrotizing encephalitis of other canine breeds be used for interpretation of MR images in Pug dogs.  相似文献   

18.
: Granulomatous meningoencephalomyelitis (GME) is an inflammatory disease of the central nervous system in dogs that is characterised by focal or disseminated granulomatous lesions within the brain and/or spinal cord, non-suppurative meningitis and perivascular mononuclear cuffing. The aetiology of the disease remains unknown, although an immune-mediated cause is suspected. This article reviewed the typical history, clinical signs and pathology of the condition along with current opinions on pathogenesis. The potential differential diagnoses for the disease were discussed along with current treatment options.  相似文献   

19.
An 8-year-old male rhesus monkey (Macaca mulatta) died following a 6-day illness consisting of progressive depression, anorexia, labored abdominal breathing, coughing, and tachypnea. Gross necropsy findings included severe multifocal (miliary) granulomatous pneumonia, granulomatous splenitis, and multifocal cerebral abscesses. Histologic examination revealed 10-15-microm broad-based budding organisms within pyogranulomatous inflammatory lesions in the lung, tracheobronchial lymph node, brain, spleen, and liver. The distribution of extrapulmonary lesions was intermediate between that described for dogs and that described for humans. These findings were consistent with blastomycosis, which is previously unreported in nonhuman primates.  相似文献   

20.
A 4-year-old male Pekingese dog was referred to the clinic with a history of recurrent seizures and progressive abnormal gait and behavior, which did not respond to treatment. At necropsy, a large cortical defect in the right temporo-parietal cortex, malacia of subcortical white matter, right basal nuclei, and capsula interna, as well as abnormalities of the right hippocampus were observed. Histological examination of the brain revealed moderate to severe nonsuppurative meningoencephalitis in the left cerebral hemisphere and extensive infarction-like lesions with milder inflammation in the right hemisphere. In the right hippocampus, the pyramidal cells were arranged in a gyrus-like pattern and intermingled with gemistocytic and fibrillary astrocytes. The histopathological features of the inflammatory lesions were consistent with necrotizing meningoencephalitis and resembled those described in so-called Pug dog encephalitis. The hippocampal changes were interpreted as dysplasia (monolateral hippocampal cortical hamartia), unrelated to clinical signs and necrotizing inflammatory lesions.  相似文献   

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