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

Groups of female New Zealand White rabbits, 8-10 weeks old, were inoculated intranasally with three different Pasteurella multocida serotypes (A:3, A:4 and A:12) or one of three Bordetella bronchiseptica strains of rabbit origin. Seven out of 18 rabbits died of experimental infection with P. multocida. B. bronchiseptica killed 3 out of the 8 animals inoculated with it. Deaths occurred between 3 and 6 days postinoculation (PI). In the rabbits that died of P. multocida inoculation, necropsy and histology revealed severe pleuritis with the accumulation of a remarkable amount of fibrinopurulent exudate in the thoracic cavity, serous rhinitis and tracheitis, acute hepatitis with necrotic foci in the parenchyma, and atrophy of the lymphoid organs and tissues. Rabbits killed 10 days PI developed only subacute serous rhinitis and hyperplasia of the lymphoid tissues. Rabbits that died of B. bronchiseptica inoculation showed acute serous rhinitis, acute catarrhal-fibrinopurulent pneumonia and mild pleuritis. As opposed to P. multocida inoculated animals, hepatitis and atrophy of the lymphoid tissues were not characteristic of these rabbits. Rabbits killed 10 days PI developed subacute purulent and necrotic pneumonia with remarkable macrophage proliferation, involving all lobes, and hyperplasia of the lymphoid tissues.
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PMID:The pathology of experimental respiratory infection with Pasteurella multocida and Bordetella bronchiseptica in rabbits. 209 6

Bobwhite quails (Colinus virginianus) were inoculated with 10(6) mean tissue-culture infective dose of quail bronchitis virus at 1, 3, 6, or 9 weeks of age by intratracheal, intraperitoneal, or subcutaneous routes. Quails developed necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia; multifocal necrotizing hepatitis; necrotizing splenitis, with or without hyperplasia of splenic mononuclear phagocytes; bursal lymphoid necrosis; and bursal atrophy. Lesions were more extensive and severe in quails inoculated at 1 or 3 weeks of age than in older quails. Large intranuclear inclusions, characteristic of adenovirus infection, were identified in trachea, lung, liver, and bursa of Fabricius. This is the first report of the histopathology of experimentally induced quail bronchitis.
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PMID:Pathology of experimentally induced quail bronchitis. 215 96

Eight clinically healthy calves were inoculated intranasally, four with either noncytopathic or four with cytopathic bovine viral diarrhea virus, and were necropsied 5 or 12 days post-inoculation. The most frequent gross lesion associated with noncytopathic or cytopathic viral infection was proximal colonic mural edema. Consistent microscopic findings were acute to subacute tracheitis, mild enterocolitis with edema, petechial hemorrhages of mesenteric lymph nodes with mild follicular lymphocytic depletion, and paracortical lymphocytic hyperplasia. At necropsy, cytopathic virus was recovered from 4/4 calves and noncytopathic virus was isolated from 2/4 calves. Neutralizing antibodies to noncytopathic bovine viral diarrhea virus were detected in the two calves from which noncytopathic virus was not recovered. Immunohistochemical analysis of lymphoid tissues demonstrated a small, randomly distributed population of mononuclear cells that contained bovine viral diarrhea viral antigen in 7/8 calves.
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PMID:Experimental primary postnatal bovine viral diarrhea viral infections in six-month-old calves. 216 64

An adenovirus (isolate 1452) associated with inclusion body hepatitis of bobwhite quails (Colinus virginianus) was characterized as a group I, serotype 1 avian adenovirus and was indistinguishable from quail bronchitis virus. Bobwhite quails were inoculated via the intratracheal or intraperitoneal route with 10(6) mean tissue-culture infective dose of isolate 1452 at 1, 3, 6, or 9 weeks of age. Lesions produced by either route of inoculation were similar to those of quail bronchitis and included necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia, and multifocal necrotizing hepatitis, necrotizing splenitis with or without hyperplasia of splenic macrophages, and lymphoid necrosis and atrophy of the bursa of Fabricius. Basophilic intranuclear viral inclusions were present in respiratory mucosal epithelium, hepatocytes and occasionally bile duct epithelium, and the mucosal epithelium overlying follicles of the bursa. Results indicate that isolate 1452 is a field isolate of quail bronchitis virus and that inclusion body hepatitis of bobwhite quails is a manifestation of quail bronchitis.
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PMID:Further characterization of an avian adenovirus associated with inclusion body hepatitis in bobwhite quails. 217 32

Fifty cranes, consisting of 46 sandhill (Grus canadensis) and four whooping cranes (Grus americana), were studied. Eighteen sandhill cranes and the four whooping cranes were naturally infected with disseminated visceral coccidiosis (DVC). The remaining sandhill cranes were chicks experimentally infected with oocysts of Eimeria reichenowi and/or E. gruis; five chicks served as controls. There were no clinical signs attributed to respiratory infection. Necropsy of naturally infected adult birds revealed nodules in many organs, including the lung, air sacs, trachea and nares. Artificially infected sandhill cranes and the whooping crane chicks that died from DVC had congestion and consolidated areas in the lung with frothy fluid in the airways. Grossly visible nodules were observed from 10 days postinoculation. Granulomatous pneumonia and tracheitis were observed with light microscopy. Lesions were associated with merogonic and gametogonic stages of eimerian coccidia. Granulomas and granulomatous foci contained parasitized large mononuclear cells. Merogonic stages were seen in lymphoid cells by ultrastructural examination. Oocysts were observed in the trachea and bronchial mucosa and admixed with exudate in the airways, indicating that crane eimerians can complete their life cycle at these sites. Of the few eimeriid coccidia that have extraintestinal stages of development in birds and mammals, only the species in cranes complete their life cycle in both the digestive and respiratory tracts.
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PMID:Pulmonary lesions in disseminated visceral coccidiosis of sandhill and whooping cranes. 281 May 53

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

Forty-eight of 134 chickens collected from a flock on a broiler farm were diagnosed pathologically and microbiologically to have colibacillosis. Both acute septicemia (seven birds, 1 to 36 days old) and subacute serositis (41 birds, 5 to 57 days old) were found. The former consisted of necrosis with fibrinous exudates in the ellipsoids and lymphoid follicles of the spleen, and fibrinous thrombi in sinusoids of the liver with occasional necrosis of hepatic cells. The latter had fibrinopurulent inflammation with granulomatous changes in the serosal tissues--including the epicardium, pericardium, and hepatic peritoneal sac--accompanied by septicemic lesions in the spleen and liver. Respiratory lesions (airsacculitis, pneumonia, and tracheitis) were noted in most chickens affected with acute septicemia and subacute serositis. Degenerative changes also were observed in the bursa of Fabricius.
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PMID:Pathology of spontaneous colibacillosis in a broiler flock. 390 13

The pathogenicity of the A4557-5 strain of infectious laryngotracheitis virus for eight-week-old chickens was investigated by aerosol route of infection; chickens were necropsied five days after infection. The virus caused mild catarrhal tracheitis, peribronchial lymphoid infiltration, and focal lymphocytic infiltration in the lung and focal lymphocytic infiltration in the air sacs of some chickens. Chickens infected with this virus developed low levels of humoral antibody and were resistant to intratracheal challenge with the virulent V154 strain. By comparison, aerosol infection with a similar dose of virulent V154 strain caused severe necrotizing laryngotracheitis with marked suppurative bronchopneumonia and airsacculitis.
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PMID:Respiratory tract lesions from infectious laryngotracheitis virus of low virulence. 630 79

Five-week-old specific-pathogen-free chickens were inoculated intravenously with one of 16 low-pathogenicity type A influenza virus isolates; 14 were of wild duck origin, and two were of turkey origin. Tubulointerstitial nephritis was the most frequent specific histopathologic change. The frequency and severity of kidney lesions were independent of the virus hemagglutinin-neuraminidase subtype or titer of the challenge virus. Influenza nucleoprotein was most frequently demonstrated in the kidney and was consistently localized to necrotic proximal and/or distal renal tubule epithelium. Common nonspecific histopathologic changes were lymphoid hyperplasia of the spleen and cecal tonsils, as well as lymphocyte depletion in the cloacal bursa. Uncommon histopathologic changes, in decreasing order of frequency, were interstitial pneumonia, lymphoid follicular hyperplasia in the myocardium, and lymphocytic tracheitis. Histopathologic changes were rare or absent in the jejunum, duodenum, pancreas, and brain. The low-pathogenicity avian-origin type A influenza virus isolates were epitheliotropic in chickens, primarily nephrotropic. Such findings were dissimilar from findings with highly pathogenic avian-origin type A influenza virus isolates both in severity and in tissue distribution of histopathologic changes and influenza viral antigen.
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PMID:Comparative pathology of intravenously inoculated wild duck- and turkey-origin type A influenza viruses in chickens. 779 94

Bobwhite quails (Colinus virginianus) were inoculated intratracheally, intraperitoneally, or subcutaneously with Indiana C adenovirus at 1, 3, 6, or 9 weeks of age. Mortality rates were 33-100% in quails inoculated at 1 or 3 weeks of age and 0-10% in quails inoculated at 6 or 9 weeks of age. Gross and histologic lesions included necrotizing tracheitis and bronchitis with pneumonia, necrotizing hepatitis and splenitis, and lymphoid depletion of the bursa of Fabricius; these were consistent with quail bronchitis. Indiana C is highly pathogenic in bobwhite quails and cannot be recommended as a vaccine to prevent quail bronchitis.
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PMID:Experimental infection of bobwhite quail with Indiana C adenovirus. 798 Feb 83


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