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 ◽  
...  

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.

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 ◽  
...  

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.


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 ◽  
...  

<p>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-<em>Toxoplasma gondii </em>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 <em>T. gondii </em>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.</p>


2020 ◽  
Vol 33 (1) ◽  
pp. 167-169
Author(s):  
Dae Young Kim ◽  
Michael M. Zinn ◽  
Solomon O. Odemuyiwa ◽  
William J. Mitchell ◽  
Gayle C. Johnson

Canine distemper virus (CDV) has long been recognized as a cause of myocarditis; however, cases of myocarditis caused by naturally acquired CDV infection have been reported only rarely in dogs. We describe here our retrospective study of naturally acquired systemic CDV infection in 4 dogs, 4–7 wk old, that had myocarditis, with myocardial necrosis and fibrosis. One of the 4 dogs had intracytoplasmic eosinophilic inclusion bodies in cardiomyocytes. Other lesions included bronchointerstitial pneumonia (4 of 4), necrotizing hepatitis (2 of 4), splenic lymphoid necrosis (2 of 4), encephalitis (1 of 3; brain was not submitted in 1 case), and necrotizing gastroenteritis (1 of 4). The presence of CDV in the heart was confirmed by immunohistochemistry in all 4 dogs.


Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 688 ◽  
Author(s):  
Miguel Angel Muñoz-Alía ◽  
Stephen J. Russell

Measles virus (MeV) is monotypic. Live virus challenge provokes a broadly protective humoral immune response that neutralizes all known measles genotypes. The two surface glycoproteins, H and F, mediate virus attachment and entry, respectively, and neutralizing antibodies to H are considered the main correlate of protection. Herein, we made improvements to the MeV reverse genetics system and generated a panel of recombinant MeVs in which the globular head domain or stalk region of the H glycoprotein or the entire F protein, or both, were substituted with the corresponding protein domains from canine distemper virus (CDV), a closely related morbillivirus that resists neutralization by measles-immune sera. The viruses were tested for sensitivity to human or guinea pig neutralizing anti-MeV antisera and to ferret anti-CDV antisera. Virus neutralization was mediated by antibodies to both H and F proteins, with H being immunodominant in the case of MeV and F being so in the case of CDV. Additionally, the globular head domains of both MeV and CDV H proteins were immunodominant over their stalk regions. These data shed further light on the factors constraining the evolution of new morbillivirus serotypes.


2015 ◽  
Vol 89 (10) ◽  
pp. 5724-5733 ◽  
Author(s):  
Lisa Alves ◽  
Mojtaba Khosravi ◽  
Mislay Avila ◽  
Nadine Ader-Ebert ◽  
Fanny Bringolf ◽  
...  

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.


1999 ◽  
Vol 73 (9) ◽  
pp. 7317-7327 ◽  
Author(s):  
Arlette Bernard ◽  
Richard Cohen ◽  
Seng-Thuon Khuth ◽  
Bruno Vedrine ◽  
Olivier Verlaeten ◽  
...  

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.


2021 ◽  
Vol 13 (1) ◽  
pp. 17521-17528
Author(s):  
Jorge Rojas-Jiménez ◽  
Juan A. Morales-Acuña ◽  
Milena Argüello-Sáenz ◽  
Silvia E. Acevedo-González ◽  
Michael J. Yabsley ◽  
...  

Canine distemper virus (CDV) causes systemic infections and immunosuppression in carnivores, which subsequently makes animals highly susceptible to opportunistic infections.  Although Trypanosoma cruzi infects procyonids, chagasic myocarditis in Coatis has not been reported in Central America.  The aim of this study was to report the histopathological findings caused by canine distemper virus, T. cruzi, and other parasites in two free-ranging White-nosed Coatis Nasua narica found dead in a national park on the Pacific coast of Costa Rica.  Heart, lung, tongue, liver, brain and spleen samples were subjected to macroscopic and microscopic examination.  A mononuclear meningoencephalitis associated with intra-nuclear eosinophilic inclusion bodies consistent with canine distemper virus was observed in nervous tissue.  Myocarditis and associated nests of amastigotes of T. cruzi were observed during microscopic examination in cardiac tissue, and in muscle from the tongue of both animals. Molecular analysis confirmed T. cruzi in formalin-fixed paraffin embedded cardiac tissues.  The myocardial damage caused by the opportunistic infection due to T. cruzi in these individuals could be the result of a severe compromised immunological status associated to the CDV infection, and subsequent opportunistic polyparasitism described herein.  To the authors knowledge this is the first report of chagasic myocarditis in free-ranging coatis from Central America.   


2009 ◽  
Vol 21 (5) ◽  
pp. 588-597 ◽  
Author(s):  
Selwyn A. Headley ◽  
Alexandre M. Amude ◽  
Alice F. Alfieri ◽  
Ana Paula F. R. L. Bracarense ◽  
Amauri A. Alfieri ◽  
...  

The current article describes a spontaneous case of old dog encephalitis (ODE) in a 7–year-old, intact, female Miniature Schnauzer dog from Londrina, Paraná, southern Brazil. Unlike conventional distemper encephalomyelitis, ODE is a poorly understood and extremely rare manifestation of Canine distemper virus (CDV) infection. The dog was presented with progressive clinical manifestations consistent with cerebral dysfunction. Briefly, histopathologic lesions were restricted to the forebrain and included chronic multifocal lymphoplasmacytic encephalitis with extensive perivascular cuffing, astrocytosis, and intranuclear inclusions within astrocytes and giant cells, with both intracytoplasmic and intranuclear inclusions. Immunohistochemistry (IHC) was used to identify the antigens of the nucleoprotein (NP) of CDV and to detect cluster of differentiation (CD)3, CD79a, macrophage (MAC) 387, glial fibrillary acidic protein, and vimentin to characterize the neuroparenchymal lesions. By IHC, CDV NP was demonstrated predominantly within neurons and astrocytes. Cells that formed perivascular cuffs and some astrocyte-like cells reacted intensely to vimentin. Reverse transcription polymerase chain reaction assay from brain sections further confirmed a role for CDV in this disease by the amplification and partial sequence analysis of the NP gene. These findings confirmed simultaneous detection of CDV in ODE by IHC and molecular assays. In addition, results of the current study could contribute to the neuropathologic characterization of this rare manifestation of CDV.


2021 ◽  
Author(s):  
Yaoqian Pan ◽  
Shuai Wang ◽  
Peng Li ◽  
Feng Yue ◽  
Yanfang Zhang ◽  
...  

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.


2018 ◽  
Vol 46 ◽  
pp. 6
Author(s):  
Erick Platiní Ferreira De Souto ◽  
Maria Talita Soares Frades ◽  
Ismael Lira Borges ◽  
Leonardo Mendes Torres ◽  
Glaucia Denise Kommers ◽  
...  

Background: Candida spp. are pleomorphic fungi that are commensal inhabitants of the oral, gastrointestinal, upper respiratory and urogenital mucosa of mammals. Candida albicans is described as the most important species. This opportunistic pathogen may produce local or systemic infections in dogs. Local infections have been reported in several tissues and systemic infection is rare in dogs with few reports in the literature describing this presentation. The aim of the present study was to report two cases of cerebral Candida albicans infection in dogs in Brazil.Case: Two cases of cerebral Candida albicans infection in dogs that showed nervous signs are described. In both cases, the brain showed marked asymmetry of the telencephalic hemispheres with multifocal to coalescing yellowish or reddish areas and a partial loss of distinction between gray and white matter. In Case 1, the mediastinal, tracheobronchial and mesenteric lymph nodes, as well as the right kidney and adrenal gland, showed altered architecture due to numerous whitish gray nodules. Histological lesions were characterized by granulomatous (case 1) or pyogranulomatous (case 2) necrotizing meningoencephalitis with intralesional fungal organisms. In case 1, similar granulomatous infiltrate with intralesional fungal organisms was also seen in the lymph nodes, kidney and adrenal gland. In case 2, there was evidence consistent with an underlying infection of canine distemper virus. Were observed lymphoplasmocytic interstitial pneumonia, lymphoid rarefaction in lymph nodes, and viral intracytoplasmic inclusion bodies in the epithelial cells of the stomach and vesical urothelium. In these two cases, the fungal organisms displayed three different morphological patterns. The first pattern was characterized by delicate tubular structures with thin parallel walls that were rarely septate and tended to undulate slightly, and measured approximately 4-20 µm (true hyphae). The second pattern was characterized by chains of elongated yeast, separated by constrictions at septal sites, and measured approximately 4-10 µm (pseudohyphae). The other morphological pattern, which was rarely observed, was characterized by round budding yeast cells that measured 3-4 µm in diameter and were often elongated by the germ tube. Sections were also stained using immunohistochemical antibodies against Candida albicans. The fungi revealed strong immunolabelling of the cytoplasm and wall for Candida albicans.Discussion: The diagnosis was based on the histomorphological and immunohistochemical characteristics of the agent, which were consistent with Candida albicans. In these two cases, immunocompromise appeared to have been an important factor in the progression of the infection. In case 1, the dog was senile and treated with corticosteroids, conditions that could effectively limit innate, humoral and cell-mediated immune response to infection. In case 2, the dog displayed cachexia and was infected by canine distemper virus, evidenced by the presence of viral inclusion bodies. The inflammatory reactions in both cases were characteristic of fungal infections, but were distinct due to differences in the infectious process. In case 1, there was a subacute to chronic progression; while in case 2 neutrophilic infiltrate predominated, suggesting an acute progression. The different morphological patterns of the fungi suggested a pleomorphic fungi and the immunohistochemistry allowed us to identify the infectious agent. In conclusion, opportunistic infections caused by Candida albicans should be considered when diagnosing diseases that affect the central nervous system of dogs, particularly in immunosuppressed animals.


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