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

Infectious bronchitis virus (IBV) associated with a catarrhal tracheitis, sudden decline in egg production, and reduced shell quality was isolated from an Indiana White Leghorn breeder flock. It was found to be serologically different from Massachusetts, Connecticut, Iowa 97, Iowa 609, Florida, Arkansas 99, JMK, Holte, Gray and SE 17 IBV serotypes. Two different Massachusetts vaccine strains protected chickens from respiratory signs but not against virus infection using the isolant for challenge in laboratory trials. The isolant was passed through a 0.22 mu. filter. It was heat (56 C), acid pH (3.0), ether and chloroform labile. In embryos it produced deaths or lesions of infectious bronchitis in one to five days after inoculation. It is suggested that this IBV isolant be designated Indiana-type.
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PMID:Variant infectious bronchitis virus isolated from Indiana chickens. 18 40

Mass prophylactic vaccinations have radically chaugned the clinical syndrome, pathogenesis, and morphological picture of the Newcastle disease: clinically it is manifested with respiratory troubles, and morphologically--with tracheitis. The method for isolating the virus on chick embryos from immune birds have proved undependable: the higher the immunity of birds, the lower the probability of virus isolation. Following the vaccination of birds after the adopted prophylactic programme and at the three-fold vaccination with a lentogenic La Sota strain and four-fold vaccination with a mesogenic Komarov strain precipitating antibodies have been detected in single serum samples only. In the presence of respiratory troubles in immune birds the rise of antiheamagglutination titers and the mass manifestation of precipitating antibodies in the blood serum is said to be an indication of the presence of a field of velogenic virus, while HI and AGPT are suitable methods for the detection of immune carriers of Newcastle disease. These can be used also for the differential diagnosis of the latent forms of infectious bronchitis, infectious laryngotracheitis, the diphtheroid form of pox, and CRD. In order to restrict and do away with the velogenic field strains of the Newcastle disease virus a suggestion is made to kill all birds that have shown respiratory troubles and positive results in virologic and serologic examinations through HI and AGPT.
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PMID:[Comparative studies of methods for the detection of immune carriers of the Newcastle disease virus in poultry]. 37 31

The development of therapeutic bronchoscopy into diagnostic bronchoscopy is described. Based on a personal experience of more than 35,000 bronchoscopies, attention is given to some important points in diagnosis and therapy. In diagnosis, these factors include: 1) color of mucosa, 2) structure of cartilage, 3) minimal tissue changes (nodules, vessels, folds), 4) tonus, 5) secretion, 6) miscellaneous peculiarities. Therapeutic studies involve: 1) recanalisation (from secretion to foreign body and tumor), 2) scrubbing (in treatment of fibrinous bronchitis and tracheitis, 3) bougies, 4) irrigation, 5) washing (for status asthmaticus, aspiration of gastric contents, etc.), 6) tamponade for persistent hemoptysis.
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PMID:[Diagnostic and therapeutic applications of bronchoscopy (author's transl)]. 91 63

Escherichia coli numbers and histopathological changes were studied in the respiratory tract of line 151 chickens intranasally inoculated with infectious bronchitis virus (IBV) and/or virulent E. coli; this line is highly susceptible to IBV. Chickens inoculated with IBV alone showed increased numbers of E. coli in the trachea and had tracheitis, airsacculitis, and bronchiolitis. One of 17 chickens inoculated with IBV alone died with fibrinopurulent serositis. Chickens inoculated with IBV and E. coli had more severe and persistent respiratory lesions than those inoculated with IBV alone. E. coli was isolated from tracheas of chickens inoculated with IBV and E. coli more frequently than from chickens inoculated with IBV alone. In this group, 14 of 27 chickens died with tracheal plugs or with fibrinopurulent serositis. There was neither increased numbers of E. coli nor significant lesions in the respiratory tract of the group inoculated with E. coli alone. These results suggest that IBV may facilitate E. coli invasion into the lower respiratory tract of the chicken.
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PMID:Escherichia coli multiplication and lesions in the respiratory tract of chickens inoculated with infectious bronchitis virus and/or E. coli. 133 61

Severe economic loss due to high mortality and condemnation rates occurred on two commercial broiler facilities. Chickens had moderate-to-severe airsacculitis, pericarditis, perihepatitis, tracheitis, and synovitis. Pasteurella gallinarum was isolated from 16 of 18 pericardia, four of 14 livers, 11 of 16 air sacs, six of seven joints and one of 28 tracheas in pure culture. In addition, Mycoplasma synoviae was isolated from trachea and air sac. Lesions were suggestive of an Escherichia coli septicemia, but E. coli was isolated from only four of 28 tracheas and one of 14 livers in pure culture. A coronavirus was isolated from trachea and lung. Whether this coronavirus represented a vaccine or field strain of infectious bronchitis was not determined. These findings suggested that the severe lesions were due to a concomitant infection with an atypical strain of P. gallinarum.
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PMID:Severe mortality in broiler chickens associated with Mycoplasma synoviae and Pasteurella gallinarum. 141 18

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

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

A bronchofibroscopy study of cases with histologic investigation of the bronchi and pulmonary mucous biopsy of 29 asbestos-textile workers, revealed diffuse bilateral endo-bronchitis (DBE) with concomitant tracheitis at different stages. No correlation was found between the endoscopy pictures and the clinical manifestations of asbestosis and dust bronchitis. The asbestosis diseased patients displayed pulmonary fibrosis++ without granulomatous inflammation in the asbestos dusts zone. In some cases, bronchial epithelium diffuse metaplasia was diagnosed with some dysplasia elements, as well as papillomatosis and malignant tumours in the lungs. Dust bronchitis++ and asbestosis can perform precancerous conditions in the lungs, what should be taken into account in cancer prevention measures for asbestos industry workers.
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PMID:[Endoscopic and morphological characteristics of the bronchi and lungs in asbestosis and dust-induced bronchitis in asbestos-textile industry workers]. 221 Apr 23

Avian urolithiasis syndrome was diagnosed in 14-to-25-week-old chickens from a multiple-age caged-layer complex housing more than 2.5 million chickens. Losses from this syndrome ranged from 0.5 to 1.0% per week. Seven-to-14-week-old pullets from this facility had multifocal renal tubular necrosis leading to interstitial fibrosis, tophus formation, and tubular dilation. A coronavirus was isolated in embryos inoculated with pooled samples of trachea, kidney, and cecal tonsil of 4-week-old pullets. This virus, identified as 85-209, was related to infectious bronchitis virus strain Florida 88 by hemagglutination-inhibition assay. Day-old specific-pathogen-free chicks were inoculated with fifth-embryo-passage amnioallantoic fluid containing this virus. These chicks developed histologic lesions of tracheitis at 5 to 7 days postinoculation. Half the chicks inoculated by eyedrop developed renal tubular necrosis after 7 days. Urolithiasis in the flock investigated was attributed to renal damage by this strain of infectious bronchitis virus occurring in 4-to-7-week-old pullets and progressing to segmental atrophy, hyperplasia, and ureteral stone formation in 14-to-25-week-old chickens.
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PMID:Studies of avian urolithiasis associated with an infectious bronchitis virus. 282 78

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


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