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Query: UMLS:C0040584 (tracheitis)
 384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of Parker's Rat Coronavirus (PRCV) was studied in axenic CD rats. Three to four 9 to 10 week old rats were euthanized daily for eight days after intranasal inoculation. Rats remained free of clinical disease. Virus was recovered from the nasopharynx and trachea after twenty-four hours and from the lung by day three but was not detected in respiratory tract after seven days. Viral antigen was detected by indirect immunofluorescence in the mucosal epithelium of upper respiratory tract and in pulmonary alveolar septae from day two to six postinoculation. Acute rhinitis developed by day two and was associated with mild focal necrosis of respiratory mucosal epithelium. Mild nonsuppurative tracheitis and multifocal interstitial pneumonia appeared by day five and persisted through day eight. Dacryoadenitis did not occur, sialoadenitis was detected in only three rats and virus was recovered from only one submaxillary salivary gland. This experiment indicates that PRCV can be a primary pathogen for the respiratory system of adult rats. In contrast to sialodacryoadenitis (SDA) virus the tropism of PRCV for salivary and lacrimal glands is low.
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PMID:Experimental infection of adult axenic rats with Parker's rat coronavirus. 90 78

Respiratory organs of newborn rats inoculated intranasally with broth culture of Myc. hominis were studied by the histological, histochemical and immunofluorescence methods. Tracheitis and development of purulent and interstitial pneumonia with a hemorrhagic component were revealed 24 hours after the infection. These changes were observed up to the 7th day of the experiment. At the same period a specific fluorescence of the Myc. hominis antigen was found by the antibody fluorescent test. The present study pointed to the pathogenicity of the Myc. hominis for the respiratory tract of the newborn rats.
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PMID:[Mycoplasma hominis as an agent of respiratory tract diseases]. 91 95

Immunocompetent and cyclophosphamide-immunosuppressed ferrets were intranasally infected with canine parainfluenza virus (CPIV) and observed for clinical signs, histopathologic lesions, the immunocytochemical demonstration of CPIV antigen in the respiratory tract and scanning electron microscopic alterations of the tracheal epithelium until 36 days post infection (p.i.). In both groups, clinical signs were minimal, restricted to the upper respiratory tract and consisted of cough elicited by tracheal compression between 3 and 7 days p.i. Microscopically, inflammatory and degenerative lesions were observed in the trachea and less frequently in the nasal cavity; bronchiolitis or interstitial pneumonia was not demonstrated. By immunocytochemistry, CPIV antigen was demonstrated in tracheal epithelial cells, whereas nasal cavity, bronchi, bronchioles and lung were devoid of viral antigen. Ferrets given CPIV alone developed a minimal lymphocytic tracheitis with minimal loss of cilia and CPIV antigen was observed only 4 days p.i. 17 days p.i., normal epithelial organization and ciliary reappearance was reestablished. Ferrets treated with cyclophosphamide and infected with CPIV exhibited mild to moderate histological lesions as above with similar scanning electron microscopic changes until 36 p.i. Tracheal lesions consisted of intraepithelial and submucosal infiltration of lymphocytes and macrophages, focal epithelial hyperplasia and multifocal loss of cilia. In addition, mild and transient neutrophilic infiltration was observed. In immunosuppressed ferrets, viral antigen expression was prominent and demonstrated 4 and 8 days p.i. These data suggest that ferrets are susceptible to aerosol CPIV infection.
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PMID:Intranasal infection of ferrets (Mustela putorius furo) with canine parainfluenza virus. 166 81

Fourteen juvenile (15- to 20-month-old) green sea turtles (Chelonia mydas), representative of a group of sea turtles with clinical signs of respiratory tract disease, were euthanatized and submitted for necropsy. Macroscopically, lesions included periglottal necrosis, tracheitis with intraluminal caseous and laminated necrotic debris, and severe pneumonia. Several turtles had caseous conjunctival exudate covering the eyes. Microscopically, the turtles had fibrinonecrotic inflammation around the glottal opening, tracheitis, and severe bronchopneumonia and interstitial pneumonia. In multifocal areas, periglottal and tracheal epithelial cells adjacent to areas of necrosis had hypertrophic nuclei with amphophilic intranuclear inclusions. A mixed population of primarily gram-negative microorganisms was isolated from the tracheal and glottal lesions. Attempts at viral isolation in cultures of green sea turtle kidney cells resulted in the development of cytopathic effects characterized by giant cell formation and development of intranuclear inclusions. Using electron microscopy, intranuclear viral particles (88 to 99 nm in diameter) were seen in inclusion-containing tracheal and glottal epithelial cells and infected green sea turtle kidney cells; particles were consistently seen enveloping from nuclear membranes, and mature particles (132 to 147 nm) were found in the cytoplasm. On the basis of size, conformation, location, and presence of an envelope, the particles most closely resembled those of herpes-viruses.
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PMID:Conjunctivitis, tracheitis, and pneumonia associated with herpesvirus infection in green sea turtles. 285 69

Six- to eight-week-old gnotobiotic F344/N rats were inoculated intranasally with 10(5.0) colony-forming units of Mycoplasma pulmonis or were sham inoculated, then one week later were given 10(0.2) 50% tissue culture infective doses of Sendai virus or sterile medium. Groups of rats were killed immediately after virus inoculation and three, five, ten, and 20 days later. Lesions in nasal passages, middle ears, larynxes, tracheas, and lungs from half of the rats in each group were subjectively scored. Organs from the other rats were quantitatively cultured for M. pulmonis and for Sendai virus. Rats given Sendai virus alone had mild, patchy, necrotizing rhinitis, laryngitis, tracheitis, and bronchitis, but not bronchiolitis or interstitial pneumonia. M. pulmonis alone induced mild lesions of murine respiratory mycoplasmosis including mild to moderate suppurative rhinitis, otitis media, laryngitis, and tracheitis with submucosal lymphoid accumulation and epithelial hyperplasia, but not lung lesions. Rats given M. pulmonis and Sendai virus had severe lesions characteristic of advanced mycoplasmal disease throughout the respiratory tract, including suppurative bronchitis with extensive lymphoid accumulations and epithelial hyperplasia; some rats also had suppurative pneumonia and bronchiectasis. Larger numbers of M. pulmonis colony-forming units were in rats given Sendai virus, but there was no statistically significant difference in Sendai virus infectious units between rats also given M. pulmonis and those given virus only.
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PMID:Exacerbation of murine respiratory mycoplasmosis in gnotobiotic F344/N rats by Sendai virus infection. 298 78

Conventionally raised male Holstein calves, 1 month of age, were infected by intranasal and intratracheal inoculation with bovine respiratory syncytial virus. Viral antigen was identified by fluorescence microscopy most commonly in the cytoplasm of tracheal and bronchial epithelial cells 3 to 5 days after inoculation. Cytoplasmic viral antigen was identified also in nasal, nasopharyngeal, bronchiolar, and alveolar epithelial cells and in alveolar macrophages. Bronchitis and tracheitis, characterized in part by epithelial necrosis, formation of syncytial epithelial cells and epithelial hyperplasia, were the most common lesions observed histologically. Rhinitis, bronchiolitis, and interstitial pneumonia were observed less frequently. Alterations were not detected in the numbers of cells recovered by bronchoalveolar lavage after inoculation. An increase in the phagocytic rate of latex beads occurred in macrophages 5 days after inoculation. Viral-induced lesions were resolved by 30 days after inoculation. The results indicated that bovine respiratory syncytial virus inoculation of calves results in reversible alterations in airway epithelial structure and in the phagocytic function of alveolar macrophages.
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PMID:Experimental bovine respiratory syncytial virus infection in conventional calves: light microscopic lesions, microbiology, and studies on lavaged lung cells. 399 21

Herpes simplex virus (herpesvirus) was isolated from autopsy lung specimens of 20 patients with clinical, roentgenographic, and histologic evidence of pneumonia. Mucocutaneous herpesvirus infection preceded the onset of pneumonia in 17. Twelve patients had focal pneumonia, 10 of whom had concomitant herpetic tracheitis, esophagitis, or both. Eight patients had diffuse interstitial pneumonia, six of whom had dissemination of herpesvirus to the other organs. Of the eight lung isolates available for typing, seven were herpesvirus-1 and one, herpesvirus-2. A high prevalence of herpesvirus antibody in serum samples obtained before pneumonia and identical restriction endonuclease patterns between mucosal and lung isolates in individual patients indicated that, in most cases, herpesvirus pneumonia was due to endogenous reactivation of virus. Focal herpesvirus pneumonia appeared to result from contiguous spread of herpesvirus to lung parenchyma, whereas diffuse interstitial pneumonia appeared to be a manifestation of hematogenous dissemination of virus.
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PMID:Herpes simplex virus pneumonia: clinical, virologic, and pathologic features in 20 patients. 629 56

Ten strains of adenovirus representing 10 serotypes were administered intratracheally to 3-week-old specific-pathogen-free chickens, which also received 2.9 X 10(5) colony-forming units of a pathogenic Escherichia coli intranasally. One group was given only E. coli, and one was retained as an uninoculated control. Gross pathologic alterations post-mortem were minimal and limited to multiple scattered, pale areas in the lungs of an occasional chicken in various groups. Histopathologic changes in the lungs were those of multifocal, interstitial, and occasionally diffuse pneumonia. Moderate to marked interstitial pneumonia was incited by adenovirus strains 75-1A, B-3 A-2, C-2B, and X-11; Ind-C, Stein, Tipton, J-2, and T-8 caused similar but milder lesions. Strains 75-1A, A-2, C-2B, T-8, and X-11 incited moderate to marked multifocal pneumonia; Ind-C, Stein, Tipton, J-2, and B-3 caused mild multifocal pneumonia. In all groups, the pneumonic lesions were more severe 5 days postinoculation than 12 days postinoculation. Bronchiolitis and tracheitis lesions also varied in severity with serotype. A mild hepatitis was seen with serotypes T-8 and 75-1A. Neither the uninoculated control group nor the group inoculated with only E. coli exhibited gross or histopathologic alterations.
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PMID:Pathogenicity of various adenovirus serotypes in the presence of Escherichia coli in chickens. 632 35

Mitogenic preparations of nonviable lysed cells and purified membranes of Mycoplasma pulmonis induced interstitial pneumonia and tracheitis after intranasal administration to pathogen-free rats. The pneumonia, characterized by peribronchial, perivascular, and alveolar wall infiltration by lymphocytes, was indistinguishable from that produced by viable M. pulmonis. Both pathologic and mitogenic effects were significanlty reduced by prior treatment of membranes with heat or proteolytic enzyme. Intranasal administration of the thymus-derived-cell mitogen, concanavalin A, produced interstitial pneumonia but not tracheitis. These results indicate a correlation of mitogenicity and pathogenicity and suggest that activation of thymus-derived lymphocytes is the major cause of the pneumonia resulting from infections with M. pulmonis.
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PMID:Mitogenicity and pathogenicity of Mycoplasma pulmonis in rats. I. Atypical interstitial pneumonia induced by mitogenic myeoplasmal membranes. 678 4

A free-living adult female Atlantic bottlenose dolphin (Tursiops truncatus) found dead near Panama City, Florida (USA), had necrotizing and ulcerative tracheitis, suppurative and hemorrhagic pneumonia, and necrotizing myocarditis; fungal hyphae were present in these lesions. Additionally, lungs had multifocal proliferative interstitial pneumonia with occasional syncytial cells. Some syncytial cells and type II pneumocytes contained eosinophilic intranuclear or intracytoplasmic inclusion bodies, or both. Based on an immunoperoxidase technique, there was morbilliviral antigen within cytoplasm and nuclei of type II pneumocytes and syncytial cells: antigen also occurred in trachea, skin, liver, stomach, intestine, and uterus. Based on pathologic and immunocytochemical findings, the dolphin had morbillivirus-induced disease. This is the first report of morbilliviral disease in a marine mammal from the Gulf of Mexico.
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PMID:Morbilliviral disease in an Atlantic bottlenose dolphin (Tursiops truncatus) from the Gulf of Mexico. 776 Apr 93


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