Intracytoplasmic eosinophilic inclusion bodies with embryonic folliculosebaceous-apocrine unit differentiation in syringocystadenoma papilliferum

2018 ◽  
Vol 45 (12) ◽  
pp. 923-926
Author(s):  
Mari Kishibe ◽  
Takeshi Iwasaki ◽  
Ichiro Takahashi ◽  
Akemi Ishida-Yamamoto
Keyword(s):  
Inclusion Bodies ◽  
Syringocystadenoma Papilliferum ◽  
Eosinophilic Inclusion

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 Herpetic esophagitis: An uncommon cause of dysphagia

2014 ◽  
Vol 05 (03) ◽  
pp. 119-120 ◽  
Author(s):  
Rinkesh K. Bansal ◽  
Piyush Ranjan
Keyword(s):  
Herpes Simplex ◽  
Inclusion Bodies ◽  
Giant Cells ◽  
Gi Endoscopy ◽  
Upper Gi ◽  
Igm Antibodies ◽  
Retrosternal Pain ◽  
Eosinophilic Inclusion ◽  
Upper Gi Endoscopy ◽  
Compromised Patients

AbstractHerpes simplex esophagitis usually occurs in immune-compromised patients. We report a case of 44 year-old lady without any immune deficient state, who presented with dysphagia and retrosternal pain. Upper GI endoscopy revealed multiple punched out ulcers in esophagus. Biopsy from these ulcers revealed intranuclear eosinophilic inclusion bodies and multinucleated epithelial giant cells suggestive of herpetic esophagitis. Serum HSV-1 IgM antibodies was positive. Dysphagia improved on treatment with acyclovir.

scholarly journals Lewy and his inclusion bodies: Discovery and rejection

2017 ◽  
Vol 11 (2) ◽  
pp. 198-201 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Marleide da Mota Gomes
Keyword(s):  
Parkinson Disease ◽  
Lewy Body ◽  
Inclusion Bodies ◽  
Lewy Bodies ◽  
Brain Nuclei ◽  
Eosinophilic Inclusion ◽  
Paralysis Agitans ◽  
Extensive Information ◽  
The Subject ◽  
Lewy Body Diseases

ABSTRACT Fritz Jacob Heinrich Lewy described the pathology of Paralysis agitans [Parkinson disease] and was the first to identify eosinophilic inclusion bodies in neurons of certain brain nuclei, later known as Lewy bodies, the pathological signature of the Lewy body diseases. In 1912, he published his seminal study, followed soon after by an update paper, and 10 years later, in 1923, by his voluminous book, where he exhaustively described the subject. The publication provided extensive information on the pathology of Paralysis agitans, and the entirely novel finding of eosinophilic inclusion bodies, which would become widely recognized and debated in the future. His discovery was acknowledged by important researchers who even named the structure after him. However, after his last publication on the issue, inexplicably, he never mentioned his histopathological discovery again. Despite several hypotheses, the reasons that led him to neglect (reject) the structure which he so preeminently described have remained elusive.

scholarly journals Outbreak of Bovine Herpetic Meningoencephalomyelitis in Southern Brazil

2018 ◽  
Vol 46 ◽  
pp. 6
Author(s):  
Julia Gabriela Wronski ◽  
Bianca Santana Cecco ◽  
Luan Cleber Henker ◽  
Marina Paula Lorenzett ◽  
Paulo Michel Roehe ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Cultures ◽  
Inclusion Bodies ◽  
Grey Matter ◽  
Plasma Cells ◽  
Clinical Signs ◽  
Sequencing Analysis ◽  
Eosinophilic Inclusion ◽  
Gross Lesions ◽  
Inflammatory Infiltrates

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells. Inflammation was also seen in a milder degree in the spinal cord, characterized by infiltrate of lymphocytes at grey matter, mainly around vessels. A herpesvirus which induced typical cytopathic effect in cell cultures was recovered from tissues. The isolated virus was typed as BoHV-5 by nucleotide sequencing analysis of the gC coding region.Discussion: The diagnosis of meningoencephalomyelitis associated to BoHV-5 was based on epidemiological, clinical, macroscopical, histological, virological and genomic findings. In the outbreak here reported, the disease occurred in young animals, with low morbidity but high lethality rates. Clinical signs on this case were consistent with previous reports on the literature. Bovines affected by BoHV-5 may display no gross lesions within the CNS; however, inflammatory and degenerative changes are frequently seen, characterized by malacia, leptomeningeal vessels hyperemia, edema and hemorrhages. Histologically, non-suppurative necrotizing meningoencephalitis is seen, with perivascular inflammatory infiltrates and, occasionally, intranuclear eosinophilic inclusion bodies in astrocytes and neurons. Similar but milder lesions were seen in the spinal cords of two of the necropsied calves, a feature which has only been previously associated to BoHV-1 infections. The identification of the implicated agent was accomplished by virus isolation in cell cultures followed by genome typing. Specific treatments for this condition are not currently available, and the number of animals that recover from clinically apparent disease is extremely low. Preventive measures are based on serological testing of herds, and segregation or elimination of seropositive calves. To avoid progression of the disease in seropositive animals, control efforts must be directed to avoid stressful conditions. Vaccination with BoHV-1 and BoHV-5 vaccines is expected to confer protection to clinical disease.

scholarly journals Eosinophilic Inclusion Bodies and Cytoplasmic Masses in Verrucae*

1951 ◽  
Vol 17 (4) ◽  
pp. 209-211 ◽  
Author(s):  
Maurice J. Strauss ◽  
Henry Bunting ◽  
Joseph L. Melnick
Keyword(s):  
Inclusion Bodies ◽  
Eosinophilic Inclusion

scholarly journals Rabies outbreak in buffaloes in Rio Grande do Sul, Brazil

2017 ◽  
Vol 47 (4) ◽  
Author(s):  
Ronaldo Michel Bianchi ◽  
◽  
Welden Panziera ◽  
Glauco José Nogueira de Galiza ◽  
Glaucia Denise Kommers ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Inclusion Bodies ◽  
Fluorescent Antibody ◽  
Clinical Signs ◽  
Rio Grande ◽  
Antibody Test ◽  
Definitive Diagnosis ◽  
Rio Grande Do Sul ◽  
Viral Antigens ◽  
Eosinophilic Inclusion

ABSTRACT: This report aimed to describe the clinical, epidemiological and pathological aspects of an outbreak of rabies in buffaloes in Rio Grande do Sul (RS), Brazil. Seven out of 41 buffaloes from the same farm became fatally ill; they showed the clinical signs of ataxia, ascending paresis, and paralysis of the limbs. During necropsy, marked hyperemia of the leptomeningeal vessels, and severe distention of the urinary bladder were noted. Histologically, there were indications of nonsuppurative meningoencephalitis and ganglioneuritis with intracytoplasmic and eosinophilic inclusion bodies in the neurons. The fluorescent antibody test was positive for rabies. Viral antigens were also detected by immunohistochemistry (IHC) in sections of the cerebellum. These results allowed for the definitive diagnosis of rabies, which is uncommonly reported in buffaloes.

THE DEVELOPMENT OF INCLUSIONS IN TISSUE CULTURES OF MONKEY KIDNEY EPITHELIAL CELLS INFECTED WITH POLIOMYELITIS VIRUS

1956 ◽  
Vol 2 (3) ◽  
pp. 298-303 ◽  
Author(s):  
A. J. Beale ◽  
Patricia F. Stevens ◽  
Norma Davis ◽  
W. Stackiw ◽  
A. J. Rhodes
Keyword(s):  
Tissue Culture ◽  
Epithelial Cells ◽  
Inclusion Bodies ◽  
Cytoplasmic Inclusion ◽  
Monkey Kidney ◽  
Tissue Cultures ◽  
Cytoplasmic Inclusions ◽  
Poliomyelitis Virus ◽  
Eosinophilic Inclusion ◽  
Cytoplasmic Inclusion Body

A cytoplasmic inclusion body has been found in the epithelial cells of monkey kidney grown in tissue culture and infected with poliomyelitis virus. This inclusion is at first closely applied to the nucleus, and later develops into a clearly demarcated structure. The nucleus is pushed to the periphery of the cell and becomes pyknotic. Finally, the cytoplasm around the inclusion becomes vacuolated, and the cell breaks up at about the time virus first appears in the fluid part of the infected tissue cultures. Multiple small intranuclear eosinophilic inclusion bodies have also been found in some cells that contain cytoplasmic inclusions.

scholarly journals Myocarditis caused by naturally acquired canine distemper virus infection in 4 dogs

2020 ◽  
Vol 33 (1) ◽  
pp. 167-169
Author(s):  
Dae Young Kim ◽  
Michael M. Zinn ◽  
Solomon O. Odemuyiwa ◽  
William J. Mitchell ◽  
Gayle C. Johnson
Keyword(s):  
Retrospective Study ◽  
Virus Infection ◽  
Inclusion Bodies ◽  
Canine Distemper Virus ◽  
Myocardial Necrosis ◽  
Canine Distemper ◽  
Eosinophilic Inclusion

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.

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