scholarly journals Apoptotic Investigation of Brain Tissue Cells in Dogs Naturally Infected by Canine Distemper Virus

2021 ◽  
Author(s):  
Yaoqian Pan ◽  
Shuai Wang ◽  
Peng Li ◽  
Feng Yue ◽  
Yanfang Zhang ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Canine Distemper Virus ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Ependymal Cells ◽  
Lymphoid Tissues ◽  
Methyl Green ◽  
Canine Distemper ◽  
Tissue Cells ◽  
The Brain ◽  
Brain Tissues

Abstract Background Canine distemper caused by canine distemper virus that belongs to the Morbillivirus genus of the Paramyxoviridae family, is still a global epidemic significant infectious disease, especially in pet dogs in China and Seriously harm to the development of the dog industry. It has been known that Apoptosis caused by canine distemper virus can show in culture cells, lymphoid tissues and cerebellum. however, its occurrence in brain tissue cells remains unclear. In order to investigate the relationship among canine distemper infecting brain tissues, apoptosis in brain tissue cells and demyelinating pathogenesis this study was performed. Methods 16 naturally infected dogs that exhibited clinical signs of CD and tested positive for anti-CDV monoclonal antibody, as well as on six healthy dogs that served as controls were used in the research. Brain specimens were divided into cerebrum, brain stem and cerebellum that was embedded in paraffin and made the sections respectively. Approximately 5 µm-thick sections were stained by haematoxylin–eosin, methyl green pyronin, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling technique and immunohistochemistry. CDV nucleocapsid protein was detected by immune streptavidin-biotinylated peroxidase complex. Results alterations in the brain tissues of CDV-infected dogs involved both various cells and nervous fibres. CDV had varying degrees of cytotropism to all brain tissue cells; apoptosis also occurred in all kind of cells in the brain, especially in the endothelia of cerebral vessels, astrocytes, oligodendrocytes and ependymal cells, the heavier infection, the more obvious apoptosis. Serious infections also involved the pyramidal and Purkinje cells. The nervous fibres exhibited demyelinating lesions (showed small multifocal vacuole) as well as some neuron axonal atrophy and disappeared gradually (formed large vacuole). Conclusions Apoptosis in brain tissue cells was mainly related to the propagation path and cytotropism of CDV. The apoptosis of astrocytes, oligodendrocytes, and some neurons may play a significant role in the demyelinating pathogenesis in dogs with acute canine distemper. A lot of diverse nervous signs shown in clinic may be in relation to different neuron apoptosis.

scholarly journals Apoptotic investigation of brain tissue cells in dogs naturally infected by canine distemper virus

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yaoqian Pan ◽  
Shuai Wang ◽  
Peng Li ◽  
Feng Yue ◽  
Yanfang Zhang ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Canine Distemper Virus ◽  
Nerve Fibers ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Ependymal Cells ◽  
Lymphoid Tissues ◽  
Methyl Green ◽  
Canine Distemper ◽  
Tissue Cells ◽  
Brain Tissues

Abstract Background Canine distemper caused by canine distemper virus that belongs to the Morbillivirus genus of the Paramyxoviridae family is still a global epidemic significant infectious disease, especially in pet dogs in China and serious harm to the development of the dog industry. It has been known that apoptosis caused by the canine distemper virus can show in culture cells, lymphoid tissues, and the cerebellum. However, its occurrence in brain tissue cells remains unclear. To investigate the relationship among canine distemper infecting brain tissues, apoptosis in brain tissue cells, and demyelinating pathogenesis was investigated. Methods 16 naturally infected dogs that exhibited clinical signs of CD and tested positive for the anti-CDV monoclonal antibody and six healthy dogs that served as the control, were used in the research. Brain specimens were divided into the cerebrum, brain stem, and cerebellum embedded in paraffin and made the sections respectively. Approximately 5 µm-thick sections were stained by hematoxylin–eosin, methyl green pyronin, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling technique, and immunohistochemistry. CDV nucleocapsid protein was detected by immune streptavidin-biotinylated peroxidase complex. Results Alterations in the brain tissues of CDV-infected dogs involved both various cells and nerve fibers. CDV had varying degrees of cytotropism to all brain tissue cells; apoptosis also occurred in all brain cells, especially in the endothelia of cerebral vessels, astrocytes, oligodendrocytes, and ependymal cells, the more serious infection, the more obvious apoptosis. Serious infections also involved the pyramidal and Purkinje cells. The nervous fibers exhibited demyelinating lesions (showed small multifocal vacuole), and some axonal neuron atrophy gradually disappeared (formed large vacuole). Conclusions Apoptosis in brain tissue cells was mainly related to the propagation path and cytotropism of CDV. The apoptosis of astrocytes, oligodendrocytes, and some neurons may play a significant role in the demyelinating pathogenesis in dogs with acute canine distemper. A lot of diverse nervous signs shown in the clinic may be related to different neuron apoptosis.

scholarly journals Molecular evidence for vaccine-induced canine distemper virus and canine adenovirus 2 coinfection in a fennec fox

2020 ◽  
Vol 32 (4) ◽  
pp. 598-603
Author(s):  
Kenichi Tamukai ◽  
Shohei Minami ◽  
Rio Kurihara ◽  
Hiroshi Shimoda ◽  
Ikki Mitsui ◽  
...  
Keyword(s):  
Inclusion Bodies ◽  
Canine Distemper Virus ◽  
Neuronal Degeneration ◽  
Molecular Evidence ◽  
Intranuclear Inclusions ◽  
Canine Distemper ◽  
Live Virus ◽  
Bronchial Epithelial ◽  
Eosinophilic Inclusion ◽  
The Brain

A 61-d-old fennec fox ( Vulpes zerda), 11 d after receiving a multivalent, modified-live virus vaccine containing canine distemper virus (CDV), canine adenovirus 2 (CAdV-2), parainfluenza virus, parvovirus, and canine coronavirus, developed oculonasal discharge, and subsequently convulsions, and hemoptysis, and died. Microscopic changes in the cerebrum were evident, including neuronal degeneration and necrosis; intracytoplasmic eosinophilic inclusion bodies were observed in astrocytes. CDV was detected in the brain tissue by immunohistochemistry. Pulmonary lesions of multifocal necrotizing bronchopneumonia had Cowdry type A intranuclear inclusions in the bronchial epithelial cells. Electron microscopy revealed crystalline arrays of adenovirus-like particles within the intranuclear inclusions. Additionally, the hemagglutinin gene of CDV and the CAdV-2 DNA polymerase gene were detected in the fennec fox; sequence analysis showed 100% identity with those of the vaccine strain viruses. To our knowledge, vaccine-induced CDV and CAdV-2 coinfections using molecular analysis have not been reported previously. Therefore, vaccine strains should be considered prior to CDV vaccination in nondomestic carnivores.

scholarly journals Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhaoxia Liang ◽  
Luyang Han ◽  
Dianjianyi Sun ◽  
Yanmin Chen ◽  
Qi Wu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Brain Tissue ◽  
Abdominal Cavity ◽  
Behavioral Changes ◽  
Dependent Manner ◽  
Diabetes In Pregnancy ◽  
The Impact ◽  
The Brain ◽  
In Pregnancy ◽  
Brain Tissues

Abstract Background Chemerin is highly expressed in the serum, placenta tissue, and umbilical cord blood of diabetic mother; however, the impact of chemerin on cognitive disorders of offspring from mothers with diabetes in pregnancy remains unclear. Methods A diabetic phenotype in pregnant mice dams was induced by streptozocin (STZ) injection or intraperitoneal injection of chemerin. Behavioral changes in offspring of diabetic dams and nondiabetic controls were assessed, and changes in chemerin, two receptors of chemerin [chemerin receptor 23 (ChemR23) and chemokine (C-C motif) receptor-like 2 (CCRL2)], macrophages, and neurons in the brain tissue were studied to reveal the underlying mechanism of the behavioral changes. Results Chemerin treatment mimicked the STZ-induced symptom of maternal diabetes in mice along with the altered behavior of offspring in the open field test (OFT) assay. In the exploring process for potential mechanism, the brain tissues of offspring from chemerin-treated dams were observed with an increase level of macrophage infiltration and a decrease number of neuron cells. Moreover, an increased level of NOD-like receptor family pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like (Asc) protein as well as pyroptosis [characterized by increased active caspase-1 content and secretion of cytokines such as interleukin (IL) 1 beta (IL-1β) and IL-18] more activated in macrophages is also observed in the brain of these diabetic dam’s offspring, in the presence of ChemR23. In vitro, it was found that pyroptosis activation was increased in macrophages separated from the abdominal cavity of normal mice, after chemerin treatment. However, depletion of CCRL2 decreased the level of chemerin in the brain tissues of diabetic dams’ offspring; depletion of ChemR23 decreased macrophage pyroptosis, and depletion of either receptor reversed chemerin-mediated neurodevelopmental deficits and cognitive impairment of offspring of diabetic pregnant dams. Conclusions Chemerin induced diabetic pregnant disease and CCRL2 were required to enrich chemerin in the brain of offspring. Aggregation of chemerin could lead to macrophage recruitment, activation of pyroptosis, the release of inflammatory cytokines, a decrease in the number of neurons, and cognitive impairment in offspring in a ChemR23-dependent manner. Targeting CCRL2 and/or ChemR23 could be useful for treating neuropsychological deficits in offspring of dams with diabetes in pregnancy.

Infection of canine mononuclear leucocytes by measles virus: possible mechanism of protection from canine distemper

1981 ◽  
Vol 27 (10) ◽  
pp. 1128-1131 ◽  
Author(s):  
C. K. Ho ◽  
L. A. Babiuk
Keyword(s):  
Peripheral Blood ◽  
Measles Virus ◽  
Canine Distemper Virus ◽  
Lymphoid Tissues ◽  
Canine Distemper ◽  
Mononuclear Leucocytes

Measles virus was shown to be infectious to canine lymphocytes from peripheral blood as well as from different lymphoid tissues, and the same held true for canine macrophage cultures prepared from peripheral blood. The susceptibility of these leucocytes to measles virus was comparable with that of canine distemper virus. These observations supported the suggestion that interference with canine distemper virus by measles virus could be a possible mechanism of the heterotypic immunity observed in dogs.

scholarly journals SLAM- and Nectin-4-Independent Noncytolytic Spread of Canine Distemper Virus in Astrocytes

2015 ◽  
Vol 89 (10) ◽  
pp. 5724-5733 ◽  
Author(s):  
Lisa Alves ◽  
Mojtaba Khosravi ◽  
Mislay Avila ◽  
Nadine Ader-Ebert ◽  
Fanny Bringolf ◽  
...  
Keyword(s):  
Glial Cells ◽  
Measles Virus ◽  
Canine Distemper Virus ◽  
Morphological Evidence ◽  
Target Cells ◽  
Viral Fusion ◽  
Canine Distemper ◽  
Persistent Infections ◽  
Demyelinating Lesions ◽  
The Brain

ABSTRACTMeasles and canine distemper viruses (MeV and CDV, respectively) first replicate in lymphatic and epithelial tissues by using SLAM and nectin-4 as entry receptors, respectively. The viruses may also invade the brain to establish persistent infections, triggering fatal complications, such as subacute sclerosis pan-encephalitis (SSPE) in MeV infection or chronic, multiple sclerosis-like, multifocal demyelinating lesions in the case of CDV infection. In both diseases, persistence is mediated by viral nucleocapsids that do not require packaging into particles for infectivity but are directly transmitted from cell to cell (neurons in SSPE or astrocytes in distemper encephalitis), presumably by relying on restricted microfusion events. Indeed, although morphological evidence of fusion remained undetectable, viral fusion machineries and, thus, a putative cellular receptor, were shown to contribute to persistent infections. Here, we first showed that nectin-4-dependent cell-cell fusion in Vero cells, triggered by a demyelinating CDV strain, remained extremely limited, thereby supporting a potential role of nectin-4 in mediating persistent infections in astrocytes. However, nectin-4 could not be detected in either primary cultured astrocytes or the white matter of tissue sections. In addition, a bioengineered “nectin-4-blind” recombinant CDV retained full cell-to-cell transmission efficacy in primary astrocytes. Combined with our previous report demonstrating the absence of SLAM expression in astrocytes, these findings are suggestive for the existence of a hitherto unrecognized third CDV receptor expressed by glial cells that contributes to the induction of noncytolytic cell-to-cell viral transmission in astrocytes.IMPORTANCEWhile persistent measles virus (MeV) infection induces SSPE in humans, persistent canine distemper virus (CDV) infection causes chronic progressive or relapsing demyelination in carnivores. Common to both central nervous system (CNS) infections is that persistence is based on noncytolytic cell-to-cell spread, which, in the case of CDV, was demonstrated to rely on functional membrane fusion machinery complexes. This inferred a mechanism where nucleocapsids are transmitted through macroscopically invisible microfusion events between infected and target cells. Here, we provide evidence that CDV induces such microfusions in a SLAM- and nectin-4-independent manner, thereby strongly suggesting the existence of a third receptor expressed in glial cells (referred to as GliaR). We propose that GliaR governs intercellular transfer of nucleocapsids and hence contributes to viral persistence in the brain and ensuing demyelinating lesions.

scholarly journals Clinical, pathological, and immunohistochemistry characterization of toxoplasmosis in dogs with distemper in the semiarid region of Paraíba, Brazil

2015 ◽  
Vol 36 (6Supl2) ◽  
pp. 4251
Author(s):  
Maria Talita Soares Frade ◽  
Lisanka Ângelo Maia ◽  
Rachel Livingstone Felizola Soares Andrade ◽  
Rodrigo Cruz Alves ◽  
Elise Miyuki Yamasaki ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Histopathological Examination ◽  
Clinical Signs ◽  
Neurological Involvement ◽  
Semiarid Region ◽  
Histopathological Analysis ◽  
Thin Wall ◽  
Canine Distemper ◽  
Eosinophilic Inclusion ◽  
The Brain

The objective of this study was to describe the clinical, pathological, and immunohistochemistry characteristics of five cases of toxoplasmosis, an infection often associated with distemper in dogs. From January 2000 to December 2012, a retrospective study was performed analyzed dogs with distemper in the semiarid region of Paraíba. We evaluated this sample to focus on individuals who presented with concomitant structures in protozoa characteristics, and performed immunohistochemistry (IHC) tests using polyclonal anti-Toxoplasma gondii antibody. In all cases, the clinical signs were similar including digestive changes, as well as respiratory, neurological, and ocular lesions, suggesting an infection of canine distemper virus. The diagnosis of distemper was confirmed on histopathological analysis depending on the presence of intranuclear and intracytoplasmic eosinophilic inclusion bodies in different tissues. Histopathological examination also revealed the characteristic presence of parasitic cysts T. gondii in the brain in four cases, and in the lung in one case. The brain cysts were associated with multifocal areas of malacia and lung there was alveolar septa thickening due to infiltration of macrophages, lymphocytes, and plasma cells, with moderate proliferation of type II pneumocytes and coalescing multifocal areas of necrosis. These cysts are characterized by round and strongly basophilic structures, measuring approximately 5 to 70 ?m, delimited by thin wall, stained by hematoxylin and eosin, and immunomarked as brown by immunohistochemistry (IHC) using the chromogen DAB. The diagnosis of toxoplasmosis associated with infection by canine distemper virus in the five case studied was based on microscopic findings and confirmed by immunohistochemistry. Toxoplasmosis should be included in the differential diagnosis of dogs with severe progressive systemic signs, especially when respiratory and neurological involvement is suspected.

scholarly journals Alteration of the Leptin Network in Late Morbid Obesity Induced in Mice by Brain Infection with Canine Distemper Virus

1999 ◽  
Vol 73 (9) ◽  
pp. 7317-7327 ◽  
Author(s):  
Arlette Bernard ◽  
Richard Cohen ◽  
Seng-Thuon Khuth ◽  
Bruno Vedrine ◽  
Olivier Verlaeten ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Leptin Receptor ◽  
Motor Impairment ◽  
Brain Structures ◽  
Receptor Expression ◽  
Leptin Resistance ◽  
Obese Mice ◽  
Canine Distemper ◽  
New Paradigm ◽  
The Brain

ABSTRACT Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.

scholarly journals Differential Expression of mRNAs in the Brain Tissues of Patients with Alzheimer’s Disease Based on GEO Expression Profile and Its Clinical Significance

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Guowei Ma ◽  
Mingyan Liu ◽  
Ke Du ◽  
Xin Zhong ◽  
Shiqiang Gong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Differential Expression ◽  
Brain Tissue ◽  
Peripheral Blood ◽  
Bioinformatics Analysis ◽  
Venn Diagram ◽  
Ad Prevention ◽  
The Brain ◽  
Brain Tissues

Background. Early diagnosis of Alzheimer’s disease (AD) is an urgent point for AD prevention and treatment. The biomarkers of AD still remain indefinite. Based on the bioinformatics analysis of mRNA differential expressions in the brain tissues and the peripheral blood samples of Alzheimer’s disease (AD) patients, we investigated the target mRNAs that could be used as an AD biomarker and developed a new effective, practical clinical examination program. Methods. We compared the AD peripheral blood mononuclear cells (PBMCs) expression dataset (GEO accession GSE4226 and GSE18309) with AD brain tissue expression datasets (GEO accessions GSE1297 and GSE5281) from GEO in the present study. The GEO gene database was used to download the appropriate gene expression profiles to analyze the differential mRNA expressions between brain tissue and blood of AD patients and normal elderly. The Venn diagram was used to screen out the differential expression of mRNAs between the brain tissue and blood. The protein-protein interaction network map (PPI) was used to view the correlation between the possible genes. GO (gene ontology) and KEGG (Kyoto Gene and Genomic Encyclopedia) were used for gene enrichment analysis to determine the major affected genes and the function or pathway. Results. Bioinformatics analysis revealed that there were differentially expressed genes in peripheral blood and hippocampus of AD patients. There were 4958 differential mRNAs in GSE18309, 577 differential mRNAs in GSE4226 in AD PBMCs sample, 7464 differential mRNAs in GSE5281, and 317 differential mRNAs in GSE129 in AD brain tissues, when comparing between AD patients and healthy elderly. Two mRNAs of RAB7A and ITGB1 coexpressed in hippocampus and peripheral blood were screened. Furthermore, functions of differential genes were enriched by the PPI network map, GO, and KEGG analysis, and finally the chemotaxis, adhesion, and inflammatory reactions were found out, respectively. Conclusions. ITGB1 and RAB7A mRNA expressions were both changed in hippocampus and PBMCs, highly suggested being used as an AD biomarker with AD. Also, according to the results of this analysis, it is indicated that we can test the blood routine of the elderly for 2-3 years at a frequency of 6 months or one year. When a patient continuously detects the inflammatory manifestations, it is indicated as a potentially high-risk AD patient for AD prevention.

scholarly journals Immunopathogenic and Neurological Mechanisms of Canine Distemper Virus

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Otávio Valério Carvalho ◽  
Clarisse Vieira Botelho ◽  
Caroline Gracielle Torres Ferreira ◽  
Paulo Oldemar Scherer ◽  
Jamária Adriana Pinheiro Soares-Martins ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Clinical Manifestations ◽  
Specific Treatment ◽  
Viral Disease ◽  
Diagnostic Methods ◽  
Lymphoid Tissues ◽  
Canine Distemper ◽  
Worldwide Distribution ◽  
Natural Hosts ◽  
The Central Nervous System

Canine distemper is a highly contagious viral disease caused by the canine distemper virus (CDV), which is a member of theMorbillivirusgenus, Paramyxoviridae family. Animals that most commonly suffer from this disease belong to the Canidae family; however, the spectrum of natural hosts for CDV also includes several other families of the order Carnivora. The infectious disease presents worldwide distribution and maintains a high incidence and high levels of lethality, despite the availability of effective vaccines, and no specific treatment. CDV infection in dogs is characterized by the presentation of systemic and/or neurological courses, and viral persistence in some organs, including the central nervous system (CNS) and lymphoid tissues. An elucidation of the pathogenic mechanisms involved in canine distemper disease will lead to a better understanding of the injuries and clinical manifestations caused by CDV. Ultimately, further insight about this disease will enable the improvement of diagnostic methods as well as therapeutic studies.

Central nervous system lesions caused by canine distemper virus in 4 vaccinated dogs

2021 ◽  
pp. 104063872110092
Author(s):  
Gimena Feijóo ◽  
Kanji Yamasaki ◽  
Luis Delucchi ◽  
José Manuel Verdes
Keyword(s):  
Choroid Plexus ◽  
Canine Distemper Virus ◽  
Clinical Signs ◽  
Ependymal Cells ◽  
South American ◽  
Canine Distemper ◽  
Pia Mater ◽  
Naturally Occurring ◽  
Type Strains

We examined the cerebellum and cerebrum of 4 vaccinated dogs, 3–60-mo-old, that displayed clinical signs of canine distemper virus (CDV) infection, and died 7–40 d after developing neurologic signs. The main histologic lesions were demyelination, gliosis, meningitis, perivascular lymphocytic cuffing, and inclusion bodies. These lesions were similar in all 4 cases regardless of the time since vaccination, except that meningoencephalitis and gliosis were subacute in 3 dogs and chronic in 1 dog. However, these differences did not appear to be related to their vaccination status. Immunohistologically, a CDV-positive immunoreaction was seen mainly in astrocytes, neurons and their axons, lymphocytes around and in the blood vessels of the pia mater and choroid plexus, ependymal cells of each ventricle, and the cells of the choroid plexus. The histologic and immunohistologic changes were similar in the cerebellum and cerebrum. The genetic characterization of the virus strains in 2 of these naturally occurring canine distemper cases confirmed that they were South American wild-type strains (Kiki and Uy251) belonging to the EU1/SA1 lineage. These strains are not included in the commercial CDV vaccines available in Uruguay.

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