Meningoencephalitis Of Unknown Etiology Research Articles

Use of neurofilament light chain to identify structural brain diseases in dogs.

Neurofilament light chain (NfL) is released into the peripheral circulation by damaged axons. To evaluate the diagnostic value of serum NfL concentration in dogs with intracranial diseases. Study included 37 healthy dogs, 31 dogs with idiopathic epilepsy (IE), 45 dogs with meningoencephalitis of unknown etiology (MUE), 20 dogs with hydrocephalus, and 19 dogs with brain tumors. Cohort study. Serum NfL concentrations were measured in all dogs using single-molecule array technology. Serum NfL concentration in dogs with each structural disease was significantly higher than in healthy dogs and dogs with IE (P = .01). The area under the receiver operating characteristic curve of NfL for differentiating between dogs with structural diseases and IE was 0.868. An optimal cutoff value of the NfL 27.10 pg/mL had a sensitivity of 86.67% and a specificity of 74.19% to differentiate the dogs with IE from those with structural brain diseases. There were significant correlations between NfL concentrations and lesion size: (1) MUE, P = .01, r = 0.429; (2) hydrocephalus, P = .01, r = 0.563. Serum NfL could be a useful biomarker for distinguishing IE from structural diseases in dogs and predicting the lesion sizes of MUE and hydrocephalus.

Clinical features, treatment, and outcome of juvenile dogs with meningoencephalitis of unknown etiology.

The information relating to the outcome specifically for juvenile dogs with meningoencephalitis of unknown etiology (MUE) is lacking. To describe the clinical presentation, diagnostic findings, treatment, and outcome in a cohort of dogs with MUE <52 weeks old. Thirty-four client-owned dogs. Multicenter retrospective case series. Records from 5 referral centers were searched. Data was extracted from the medical records and referring veterinarians were contacted for survival data if this was not available from the record. The mean age was 31 weeks; the youngest dog was 11 weeks and 3 dogs were <16 weeks old. Altered mentation (71%), ataxia (44%), seizures (29%), and circling (26%) were the most common presenting complaints. Neuroanatomical localization was to the forebrain (38%), multifocal (35%), brainstem (18%), and cerebellum (12%). Corticosteroid monotherapy (n = 15) and corticosteroid plus cytosine arabinoside (n = 15) were used in equal proportions. Outcome data was available for 26 dogs, 8 (31%) were alive at the time of data collection with a follow-up range of 135 to 2944 days. Death or euthanasia was related to MUE in 17/18 dogs that died during the study period. Kaplan-Meier survival analysis demonstrated a median survival time for all-cause death of 84 days. The prognosis for MUE in this subset of dogs was considered poor.

Magnetic resonance imaging in acute meningoencephalitis of viral and unknown origin: frequent findings and prognostic potential.

Magnetic resonance imaging (MRI) findings in meningoencephalitis have mainly been described in terms of their diagnostic value rather than their prognostic potential, except for herpes simplex virus (HSV) encephalitis. The aims of our study were to describe frequency and anatomic locations of MRI abnormalities specific to limbic, circadian and motor systems in a cohort of meningoencephalitis patients, as well as to investigate the prognostic value of these MRI findings. A secondary, selective analysis of a retrospective database including all meningitis, meningoencephalitis and encephalitis cases treated between 2016 and 2018 in the University hospital of Bern, Switzerland was performed. Patients with meningitis of any cause, bacterial or autoimmune causes of encephalitis were excluded. MRI scans and clinical data from 129 meningoencephalitis cases found that the most frequent causes were tick-borne encephalitis (TBE, 42%), unknown pathogens (40%), VZV (7%), and HSV1 (5%). At discharge, median modified Rankin Score (mRS) was 3 (interquartile range, IQR, 1), 88% of patients had persisting signs and symptoms. After a median of 17 months, median Glasgow Outcome Score (GOS) was 5 (IQR 1), 39% of patients still had residual signs or symptoms. All patients with HSV, 27% with TBE and 31% of those with meningoencephalitis of unknown etiology had fluid-attenuated inversion recovery (FLAIR) and to a lesser extent diffusion-weighted imaging (DWI) lesions in their initial MRI, with highly overlapping anatomical distribution. In one fifth of TBE patients the limbic system was affected. Worse outcome was associated with presence of DWI and/or FLAIR lesions and lower normalized apparent diffusion coefficient (ADC) signal intensities. Presence of FLAIR lesions, restricted diffusion as well as the extent of ADC hypointensity in initial MRI are parameters which might be of prognostic value regarding the longterm clinical outcome for patients with meningoencephalitis of viral and of unknown origin. Although not described before, affection of limbic structures by TBE is possible as shown by our results: A substantial proportion of our TBE patients had FLAIR signal abnormalities in these regions.

Expression of sphingosine-1-phosphate receptor 1 in neuroinflammation of canine brains

Sphingosine-1-phosphate (S1P) is a signaling lipid mediator that is involved in multiple biological processes. The S1P/S1P receptor (S1PR) signaling pathway has an important role in the central nervous system. It contributes to physiologic cellular homeostasis and is also associated with neuroinflammation. Therefore, this study was performed to evaluate the expression of S1PR in dogs with meningoencephalitis of unknown etiology (MUE) and experimental autoimmune encephalomyelitis (EAE). The analysis used 12 brain samples from three neurologically normal dogs, seven dogs with MUE, and two canine EAE models. Anti-S1PR1 antibody was used for immunohistochemistry. In normal brain tissues, S1PR1s were expressed on neurons, astrocytes, oligodendrocytes, and endothelial cells. In MUE and EAE lesions, there was positive staining of S1PR1 on leukocytes. Furthermore, the expression of S1PR1 on neurons, astrocytes, oligodendrocytes, and endothelial cells was upregulated compared to normal brains. This study shows that S1PR1s are expressed in normal brain tissues and leukocytes in inflammatory lesions, and demonstrates the upregulation of S1PR1 expression on nervous system cells in inflammatory lesions of MUE and EAE. These findings indicate that S1P/S1PR signaling pathway might involve physiologic homeostasis and neuroinflammation and represent potential targets for S1PR modulators to treat MUE.

Retrospective evaluation of prognosis and survival with various immunosuppressants in 82 dogs diagnosed with meningoencephalitis of unknown etiology (2010–2021)

BackgroundMeningoencephalomyelitis of unknown etiology (MUE) is a comprehensive term for non-infectious inflammatory brain diseases of the central nervous system (CNS) caused by abnormal autoimmune responses. This study aims to compare the differences in survival and clinical response of MUE according to the adjuvant immunosuppressant use. Medical records of 82 dogs diagnosed with MUE were reviewed retrospectively.ResultsThe overall survival time was 769 days (range 14–2687 days). The median survival time for each adjunctive was: leflunomide 1035 days (range 126–2163 days), mycophenolate mofetil 865 days (range 39–2191 days), cyclosporin 441 days (range 11–2176 days), cytosine arabinoside 754 days (range 6–1898 days) and a combination of mycophenolate mofetil and cytosine arabinoside 132 days (range 23–1227 days). There was no significant difference in the incidence rate of adverse events according to the immunosuppressants, but moderate to severe anemia was confirmed in 3 patients (18.7%) in the leflunomide group.ConclusionsThe survival time and response rate of MUE dogs differed depending on which adjunctive immunosuppressants were used. Leflunomide showed a long survival time and a relatively good response rate in dogs with MUE. However, a large-scale further study with standardized doses of immunosuppressants and supportive treatment and constant monitoring interval is needed.

Diagnostic investigation of Mycoplasma hyorhinis as a potential pathogen associated with neurological clinical signs and central nervous system lesions in pigs

Mycoplasma hyorhinis (M. hyorhinis) is a commensal of the upper respiratory tract in swine with the typical clinical presentations of arthritis and polyserositis in postweaning pigs. However, it has also been associated with conjunctivitis and otitis media, and recently has been isolated from meningeal swabs and/or cerebrospinal fluid of piglets with neurological signs. The objective of this study is to evaluate the role of M. hyorhinis as a potential pathogen associated with neurological clinical signs and central nervous system lesions in pigs. The presence of M. hyorhinis was evaluated in a clinical outbreak and a six-year retrospective study by qPCR detection, bacteriological culture, in situ hybridization (RNAscope®), and phylogenetic analysis and with immunohistochemistry characterization of the inflammatory response associated with its infection. M. hyorhinis was confirmed by bacteriological culture and within central nervous system lesions by in situ hybridization on animals with neurological signs during the clinical outbreak. The isolates from the brain had close genetic similarities from those previously reported and isolated from eye, lung, or fibrin. Nevertheless, the retrospective study confirmed by qPCR the presence of M. hyorhinis in 9.9% of cases reported with neurological clinical signs and histological lesions of encephalitis or meningoencephalitis of unknown etiology. M. hyorhinis mRNA was confirmed within cerebrum, cerebellum, and choroid plexus lesions by in situ hybridization (RNAscope®) with a positive rate of 72.7%. Here we present strong evidence that M. hyorhinis should be included as a differential etiology in pigs with neurological signs and central nervous system inflammatory lesions.

Abnormal Hyperphosphorylation of Tau in Canine Immune-mediated Meningoencephalitis.

Tau is a microtubule-associated protein involved in the assembly and stabilization of microtubules. In human medicine, hyperphosphorylation of tau is associated with microtubule instability and is considered to play a role in the progression of multiple sclerosis (MS). MS is an autoimmune neurological disease that shares many characteristics, including pathological mechanisms, with canine meningoencephalitis of unknown etiology (MUE). With this background, this study investigated the presence of hyperphosphorylated tau in dogs with MUE and experimental autoimmune encephalomyelitis (EAE). In total, eight brain samples were examined from two neurologically normal dogs, three dogs with MUE, and three canine EAE models. Anti-(phospho-S396) tau antibody was used for immunohisto-chemistry, which stained hyperphosphorylated tau. In normal brain tissues, hyperphosphorylated tau was not found. In all the dogs with EAE and one of the dogs with MUE, immunoreactivity for S396 p-tau was observed in glial cell cytoplasm and the background in the periphery of the inflammatory lesion. These results suggest for the first time that tau pathology may be involved in the progression of neuroinflammation in dogs, similar to that in human MS.

Анализ структуры сопутствующих инфекционных заболеваний у госпитализированных ВИЧ-инфицированных пациентов

Objective. To analyze the frequency of concomitant pathology in HIV-infected outpatients of the Chechen Republic. Materials and methods. The study was conducted according to the data of the "Republican Clinical Center for Infectious Diseases", "Republican Center for the Prevention and Control of AIDS" of the Ministry of Health of Chechen Republic. The data of inpatient records of 378 HIV-infected outpatients (male – 64.5%, female – 35.5%) of "Republican Clinical Center for Infectious Diseases" Grozny for the period from 2013 to 2020 were analyzed. Results. As a result of the retrospective analysis, it was found that chronic viral hepatitis C leads among the causes of HIVinfected outpatients in the infectious hospital – 51% of cases. Respiratory diseases were registered in 33.2% of cases, including pneumonia without an established etiological factor in 19.3% of cases; pneumocystis pneumonia – in 10%; bronchitis of unknown etiology – in 3.9%. Acute respiratory viral infections were registered in 5.4% of cases; acute gastroenteritis – in 3.7%; meningoencephalitis of unknown etiology – in 2.2%; herpes simplex virus – in 1.2%; chronic viral hepatitis B – in 0.7%; ascariasis – in 0.4%; fever of unknown origin – 0.4%. Conclusion. The structure of secondary diseases in outpatients with HIV is dominated by chronic viral hepatitis C and pneumocystic pneumonia, while mortality is significantly higher in patients with respiratory diseases. Not timely diagnosis of various secondary diseases in the HIV-infected patient complicates treatment tactics, which increases the l unfavorable outcomes and requires optimization of diagnostic algorithms. Key words: HIV infection, Co-infection, outpatient, chronic viral hepatitis C

A Preliminary Study of Pharmacokinetics and Pharmacodynamics of Oral Fingolimod in Dogs.

Fingolimod is a sphingosine-1-phosphate receptor modulator that prevents lymphocytes egress from lymphoid organs. It has been used as a disease-modifying drug for human multiple sclerosis and has shown better therapeutic effects than other conventional therapies. Therefore, this study was performed to obtain preclinical data of fingolimod in dogs. Nine laboratory Beagle dogs were used and randomized into three groups for pharmacokinetics (PK) and pharmacodynamics (PD). The dogs were administered once with a low-dose (0.01 mg/kg, n=3), medium-dose (0.05 mg/kg, n=3), and high-dose (0.1 mg/kg, n=3) of fingolimod, orally. Samples were collected serially at predetermined time points, and whole blood fingolimod concentrations were measured using high-performance liquid chromatography-mass spectrometry. Differential counts of leukocytes over time were determined to identify immune cells' response to fingolimod. Regarding PK, the concentration of fingolimod in the blood increased in a dose-dependent manner, but it was not proportional. Regarding PD, the number of lymphocytes significantly decreased compared to baseline in all dose groups (low-dose, p=0.0002; medium-dose, p<0.0001; high-dose, p=0.0012). Eosinophils were significantly reduced in low- (p=0.0006) and medium- (p=0.0006) doses, and neutrophils were also significantly reduced in medium-(p=0.0345) and high- (p=0.0016) doses. This study provides the basis for future clinical applications of fingolimod in dogs with immune-mediated diseases, such as meningoencephalitis of unknown etiology.

Evaluation of the blood neutrophil-to-lymphocyte ratio as a biomarker for meningoencephalitis of unknown etiology in dogs.

BackgroundThe neutrophil‐to‐lymphocyte ratio (NLR) has been identified as a biomarker in several inflammatory and autoimmune diseases. Multiple sclerosis (MS) has been found to be associated with changes in the NLR in humans.ObjectivesTo examine the diagnostic value of the NLR in meningoencephalitis of unknown etiology (MUE) in dogs.AnimalsThirty‐eight MUE dogs, 20 hydrocephalic dogs, 10 brain tumor (BT) dogs, 32 idiopathic epilepsy (IE) dogs, and 41 healthy dogs.MethodsRetrospective study. Medical records were reviewed to identify dogs with a diagnosis of neurologic disease. The NLR was determined in all dogs.ResultsThe median NLR was significantly higher in MUE dogs (6.08) than in healthy (1.78, P < .001), IE (2.50, P < .05), and hydrocephalic dogs (1.79, P < .05). The area under the receiver operating characteristic curve of the NLR for differentiation between MUE and healthy dogs was 0.96, and between the MUE dogs and dogs with other forebrain diseases was 0.86. An optimal cutoff of 4.16 for the NLR had a sensitivity of 71.1% and specificity of 83.9% to differentiate the MUE dogs from the dogs with other forebrain diseases.Conclusions and Clinical ImportanceThe NLR could be a biomarker for diagnosing MUE and distinguishing it from other intracranial diseases in dogs.

Neurofilament light chain as a biomarker of meningoencephalitis of unknown etiology in dogs.

BackgroundNeurofilament light chain (NfL) is a neuron‐specific cytoskeletal protein expressed in axons. Damaged axons of the central nervous system release NfLs into the cerebrospinal fluid (CSF) and the blood. In humans with neurologic diseases, NfL is used as a biomarker.ObjectivesTo identify the potential of NfL as a supportive tool for the diagnosis, prognosis, and monitoring of meningoencephalitis of unknown etiology (MUE) in dogs.AnimalsTwenty‐six client‐owned healthy dogs, 10 normal Beagle dogs, and 38 client‐owned MUE dogs.MethodsCohort study. The concentrations of NfL in serum and CSF were measured using single‐molecule array technology.ResultsMedian NfL concentration was significantly higher in MUE dogs (serum, 125 pg/mL; CSF, 14 700 pg/mL) than in healthy dogs (serum, 11.8 pg/mL, P < .0001; CSF, 1410 pg/mL, P = .0002). The areas under the receiver operating characteristic curves of serum and CSF NfL concentrations were 0.99 and 0.95, respectively. The cut‐off values were 41.5 pg/mL (serum) and 4005 pg/mL (CSF) for differentiating between healthy and MUE dogs, with sensitivities of 89.19% and 90%, respectively, and specificities of 96.97% and 100%, respectively. The NfL concentration showed a significant decrease (pretreatment, 122 pg/mL; posttreatment, 36.6 pg/mL; P = .02) in the good treatment‐response group and a significant increase (pretreatment, 292.5 pg/mL; posttreatment, 1880 pg/mL, P = .03) in the poor treatment‐response group.Conclusions and Clinical importanceNeurofilament light chain is a potential biomarker for diagnosing MUE and evaluating response to treatment.

TBE in Denmark

Since the 1950s tick-borne encephalitis (TBE) has been known to be endemic in Denmark but only on the island of Bornholm. Bornholm is situated east of mainland Denmark, south of Sweden (Figure 3) and has a different fauna and flora from the rest of Denmark. Bornholm has about 45,000 inhabitants, but about 500,000 tourists visit the island every year. Freundt carried out a serosurvey during 1958–19621 and found TBE antibodies in 1.4% of blood donors and 30% of woodworkers on Bornholm but no antibodies in subjects living in mainland Denmark. In 1963, Freundt found that 8 of 12 patients admitted to the hospital with acute meningoencephalitis of unknown etiology during 1951–1960 had antibodies to tick-borne encephalitis (TBEV).2 In 2000, TBE was rediscovered on Bornholm, where a retrospective study covering the period 1994–2002 (7 years) identified 14 TBE cases; 2 cases were tourists and 12 were inhabitants of Bornholm, giving an incidence of 3.81 per 100,000 inhabitants.3 At least 5 patients (37.7%) got permanent sequelae. In addition, 32 forest workers on Bornholm were tested in 2000, and 20% had IgG antibodies but never symptoms. This is similar to the finding of Freundt in 1960. It was concluded that the data did not provide evidence of an increase in incidence of TBE. Ticks (Ixodes ricinus) from Bornholm were investigated for TBEV in 2000 and 2% were found to be infected.4 Since 2001 an average of 2.5 (range 1–8) TBE cases per year have been reported in Bornholm (Figure 1).

Prednisolone-induced diabetes mellitus without pancreatic islet pathology in a dog

A one-year-old, intact male Maltese was referred with dehydration, anorexia, and marked hyperglycemia. The dog had been managed due to meningoencephalitis of unknown etiology (MUE) for three months. The dog had been treated with long-term prednisolone administration. Diabetic ketoacidosis (DKA) was identified based on the blood chemistry and venous gas analyses, and intensive treatments including insulin administration were initiated. On further examinations, there was no any other disease that contributed to the occurrence of DKA. Insulin resistance resulted from the administration of prednisolone was highly suspected, but the agent could not be tapered due to managing MUE. Following resolution of DKA, the dog was discharged with life-long insulin and prednisolone therapy. Over the next two years, the dog continued to be routinely re-evaluated and was managed with permanent insulin therapy (0.8–1.4 units/kg SC 12 hourly) and medications including prednisolone (0.4–1.1 mg/kg PO 12 hourly). Because MUE severely progressed, the dog was euthanized by owner’s request. Histopathologic examination of pancreas obtained by post-mortem revealed that both endo- and exocrine pancreas was within normal limit. The case described herein showed the risk of ketoacidosis as well as hyperglycemia after long-term prednisolone administration in a dog without pancreatic islet pathology.

Low-Field Magnetic Resonance Imaging Findings in 18 Dogs With Presumed Optic Neuritis.

Canine optic neuritis has been attributed to a focal or disseminated form of granulomatous meningoencephalitis (GME) amongst other etiologies. Magnetic resonance imaging (MRI) has been proven to help differentiate the structures within the optic nerve sheath and therefore could aid the diagnosis of optic neuritis in dogs. The objectives of this study were to describe and compare the MRI abnormalities affecting the optic nerve sheath complex and optic chiasm in dogs with clinically suspected optic neuritis as a component of meningoencephalitis of unknown etiology (MUE) or as an isolated form (I-ON). Retrospective evaluation of patient details, clinical signs, cerebrospinal fluid (CSF) analysis, and MRI findings of dogs with clinically suspected optic neuritis between January 2011 and May 2018 was performed. Eighteen dogs met the inclusion criteria. MRI findings included contrast enhancement of both optic nerves (11/18) and optic chiasm (6/18), changes within the CSF volume surrounding the optic nerve (10/18), changes to the optic disc (10/18), changes of size or signal affecting the optic chiasm (10/18), changes in the Short TI inversion recovery (STIR) signal of the optic nerve (7/15), retrobulbar changes (3/18), and concurrent brain lesions (13/18). A variety of subtle MRI features may indicate optic nerve involvement and low-field MRI is a sensitive method to detect changes within the optic nerve sheath complex in dogs with optic neuritis as an isolated form (I-ON) or as an extension of MUE.

The bioavailability of cytarabine in dogs with meningoencephalitis of unknown etiology through iontophoresis and rectal delivery.

Background:Cytarabine (CA) is used to treat dogs with meningoencephalitis of unknown etiology (MUE) by subcutaneous or intravenous administration.Aim:The objective was to investigate transdermal iontophoresis and rectal administration as alternative routes of CA delivery.Methods:Two client-owned dogs with MUE were studied. The ActivaPatch® IONTOGO™ 12.0 iontophoresis drug delivery system delivered 200 mg/m2 CA transdermally. Blood samples were collected by sparse sampling technique after initiation of the device. At another visit, 100 mg/m2 CA was administered rectally. Blood samples were collected by sparse sampling technique after administration. Plasma CA concentrations were measured by high-pressure liquid chromatography. Results:The concentration of plasma CA after transdermal and rectal administration was below the limits of quantification (0.1 μg/ml) in all samples suggesting inadequate bioavailability with transdermal and rectal administration. Conclusion:Transdermal and rectal CA administration are not reasonable alternative routes of delivery.

Cerebrospinal Fluid Analysis for Viruses by Metagenomic Next-Generation Sequencing in Pediatric Encephalitis: Not Yet Ready for Prime Time?

Metagenomic next-generation sequencing offers an unbiased approach to identifying viral pathogens in cerebrospinal fluid of patients with meningoencephalitis of unknown etiology. In an 11-month case series, we investigated the use of cerebrospinal fluid metagenomic next-generation sequencing to diagnose viral infections among pediatric hospitalized patients presenting with encephalitis or meningoencephalitis of unknown etiology. Cerebrospinal fluid from patients with known enterovirus meningitis were included as positive controls. Cerebrospinal fluid from patients with primary intracranial hypertension were included to serve as controls without known infections. Cerebrospinal fluid metagenomic next-generation sequencing was performed for 37 patients. Among 27 patients with encephalitis or meningoencephalitis, 4 were later diagnosed with viral encephalitis, 6 had non-central nervous system infections with central nervous system manifestations, 6 had no positive diagnostic tests, and 11 were found to have a noninfectious diagnosis. Metagenomic next-generation sequencing identified West Nile virus (WNV) in the cerebrospinal fluid of 1 immunocompromised patient. Among the 4 patients with known enterovirus meningitis, metagenomic next-generation sequencing correctly identified enteroviruses and characterized the viral genotype. No viral sequences were detected in the cerebrospinal fluid of patients with primary intracranial hypertension. Metagenomic next-generation sequencing also identified sequences of nonpathogenic torque Teno virus in cerebrospinal fluid specimens from 13 patients. Our results showed viral detection by cerebrospinal fluid metagenomic next-generation sequencing only in 1 immunocompromised patient and did not offer a diagnostic advantage over conventional testing. Viral phylogenetic characterization by metagenomic next-generation sequencing could be used in epidemiologic investigations of some viral pathogens, such as enteroviruses. The finding of torque Teno viruses in cerebrospinal fluid by metagenomic next-generation sequencing is of unknown significance but may merit further exploration for a possible association with noninfectious central nervous system disorders.

Characteristics of Magnetic Resonance Imaging Findings in 32 Dogs Diagnosed with Meningoencephalitis of Unknown Etiology

The purpose of this retrospective study was to describe the characteristics of magnetic resonance imaging (MRI) findings in dogs with meningoencephalitis of unknown etiology (MUE), and to evaluate the usefulness of meningeal enhancement. Thirty-two dogs were included in MUE group on the basis of clinical signs, MRI findings and cerebrospinal fluid (CSF) results, and for comparison of the meningeal enhancement, twenty-three dogs with normal MRI, normal CSF and no clinical sign were included in the control group. The evaluated MRI findings included lesion site, lesion number, signal intensity of each MRI sequence, mass effect, perilesional edema, contrast enhancement, and meningeal enhancement. The MUE was most frequently associated with multiple lesions (50%) with perilesional edema (72%) in forebrain (66%) that were hyperintense (92%) in T2W and FLAIR images. Of the meningeal enhancement, there was no significant difference between the control group and the MUE groups in the pachymeningeal enhancement. However, leptomeningeal (or both) enhancement was found relatively high proportion in the MUE group than in the control group (P ＜ 0.001, Odd ratio = 10.26), and based on this result, leptomeningeal (or both) enhancement is considered to be significant finding for indicating MUE.

Investigation of astrovirus and bornavirus in the cerebrospinal fluid of dogs clinically diagnosed with meningoencephalitis of unknown etiology.

BackgroundNon‐suppurative encephalitides in a variety of species, including humans and dogs, have been linked to infection by astroviruses and bornaviruses.Hypothesis/ObjectivesTo determine whether or not ribonucleic acid of astroviruses or bornaviruses was present in the cerebrospinal fluid (CSF) of dogs with clinically diagnosed meningoencephalomyelitis of unknown etiology (MUE).AnimalsTwenty‐five client‐owned dogs evaluated by CSF analysis at a single university referral hospital.MethodsProspective case‐control study. Cerebrospinal fluid was collected from clinically diagnosed MUE and control cases and evaluated by reverse‐transcriptase polymerase chain reaction for the presence of astrovirus and bornavirus.ResultsNeither astrovirus nor bornavirus nucleic acids were identified in CSF collected from 20 clinically diagnosed MUE and 5 control cases.Conclusions and Clinical ImportanceThe negative results of this investigation suggest that astrovirus and bornavirus are not commonly detectable in CSF of dogs with MUE.

Cerebrospinal fluid lactate in dogs with inflammatory central nervous system disorders.

BackgroundCerebrospinal fluid (CSF) lactate is frequently used as a biomarker in humans with inflammatory central nervous system (CNS) disorders including bacterial meningitis and autoimmune disorders such as multiple sclerosis.HypothesisCerebrospinal fluid lactate concentrations are increased in a subset of dogs with inflammatory CNS disorders.AnimalsOne hundred two client‐owned dogs diagnosed with inflammatory CNS disease.MethodsCase series. Cases were identified both prospectively at the time of diagnosis and retrospectively by review of a CSF biorepository. Cerebrospinal fluid lactate was analyzed with a commercially available, handheld lactate monitor. Subcategories of inflammatory disease were created for comparison (eg, steroid‐responsive meningitis arteritis, meningoencephalitis of unknown etiology).ResultsCerebrospinal fluid lactate concentrations were above reference range in 47% of dogs (median, 2.5 mmol/L; range, 1.0‐11.7 mmol/L). There was no significant difference in lactate concentrations between disease subcategories (P = .48). Significant but weak correlations were noted between CSF lactate concentration and nucleated cell count (r = .33, P < .001), absolute large mononuclear cell count (r = .44, P < .001), absolute small mononuclear cell count (r = .39, P < .001), absolute neutrophil cell count (r = .24, P = .01), and protein (r = .44, P < .001). No correlation was found between CSF lactate concentration and CSF red blood cell count (P = .58). There was no significant association of CSF lactate concentration with survival (P = .27).Conclusions and Clinical ImportanceCerebrospinal fluid lactate concentrations could serve as a rapid biomarker of inflammatory CNS disease in dogs.

Long-term follow-up of optic neuritis associated with meningoencephalitis of unknown etiology in a Maltese dog

Long-term follow-up of optic neuritis associated with meningoencephalitis of unknown etiology in a Maltese dog