Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040584 (tracheitis)
 384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A chronic 90-day inhalation of polyethylsiloxane fluid at a concentration of 10 and 2 mg/m3 produced local irritation and general toxic effect on rats. Local irritation induced catarrhal-desqueamative tracheitis that was accompanied by a microfocal interstitial process in the lungs. The general toxic effect gave rise to interstitial myocarditis that was followed by focal cardiosclerosis and dystrophic lesions of vascular walls and areas of liver parenchyma. Changes in the thymus-lymph system and adrenal structure suggested prolonged protective tension of the animal body. A chronic 90-day inhalation of polyethylsiloxane at a concentration of 0.2 mg/m3 brought about no pathological lesions in the microstructure of animal organs.
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PMID:[Pathomorphologic changes in the organs of rats following chronic inhalation exposure to liquid polyethylsiloxane]. 97 25

The outbreak of the disease occurred in a large multiple-age farm with about 50,000 meat turkeys, where groups of 6-8000 one-day-old birds were stalled up every 14 days. All the turkey poults housed were affected mostly in the 1.-3. week of the life. The respiratory disease spread rapidly within the flocks and were characterised clinically by inclination of huddle, ruffled feathers, anorexia, stunted growth, swelling of the infraorbital sinus and nasal discharge. The clinical apparent disease lasted 3 to 4 weeks on the average in the affected flocks and were associated with a mortality from 7-20 percent. The main pathoanatomical lesions were catarrhal-fibrinopurulent rhinitis, sinusitis, tracheitis, bronchopneumonia and air sacculitis as well as atrophy of the thymus. Fibrinous adhesive peri- and epicarditis, perihepatitis, miliary necrotic foci in the liver and diarrhea have been found less frequently. The results of cultural and serological examinations of moribund and dead turkey poults of 6 different flocks indicate that Bordetella avium and Chlamydia psittaci are the primary inciting agents of the respiratory disease. However, the following severe course of the disease were mainly caused by concurrent infections with Klebsiella pneumoniae subsp. pneumoniae, Escherichia coli and Pseudomonas fluorescens. In some cases coccidiosis with lesions in ceca were additionally diagnosed. Campylobacter jejuni could be always isolated culturally from the liquid cecal content of diseased birds.
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PMID:[Multicausal infectious respiratory tract disease of young fattening turkeys]. 155 65

Inclusion body hepatitis (IBH) was diagnosed in 15 broiler flocks supplied by one breeder in the South Island of New Zealand. The affected flocks suffered mortality up to 30%. Malaise and slightly increased mortality were noticed by growers from about day 12 post-hatch; mortality peaked in the fourth week, and, in most flocks, declined to normally accepted levels from day 33 on. Gross signs seen at necropsy usually included bone-marrow aplasia, atrophy of the bursa of Fabricius and the thymus, and swollen hemorrhagic livers with focal necrosis. Jaundice was seen in many surviving birds. In some flocks, there was also proventricular hemorrhage, mild tracheitis, and airsacculitis. Downgrading and condemnation rates were increased in all flocks. Eosinophilic intranuclear inclusion bodies were seen in hepatocytes of some affected birds. An adenovirus was isolated from a number of cases investigated. The disease in broilers was preceded by production drops associated with feed refusal and increased mortality in the breeder stock.
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PMID:A primary epidemic of inclusion body hepatitis in broilers. 255 99

To determine whether consumption of colostrum with high levels of serum neutralizing antibody to bovine herpesvirus 1 would protect neonatal calves from the frequently fatal multisystemic form of infectious bovine rhinotracheitis, Holstein calves were fed for 48 h after birth with either pooled colostrum from seropositive vaccinated cows or colostrum from seronegative unvaccinated cows. The serum neutralizing antibody achieved in the former calves was between 64 and 256 and the titer in the latter calves was below 8. At 48 h of age the calves were challenged by aerosolization with bovine herpesvirus 1. All five seronegative calves died or were euthanized in a moribund state between days 5 and 7 of the trial, whereas all five seropositive animals remained healthy throughout the study. Twice daily clinical examination revealed significantly lower scores in the seronegative group from 60 h postinfection. Relative lung weights were greater in the seronegative group, associated with a severe acute necrotizing bronchiolitis with fibrin exudation. The seronegative group of calves also demonstrated an acute necrotizing rumenitis, pharyngitis, glossitis, esophagitis, laryngitis and tracheitis. The seropositive animals had only small areas of subacute necrotizing fibrinopurulent rhinitis. Bovine herpesvirus 1 virus was isolated from all nasal passages of all calves but isolation of virus in the seronegative calves was made from the trachea (5/5), lung (4/5), bronchial lymph nodes (4/5), spleen (4/5), thymus (3/5), liver (2/5), rumen (2/5) and brain (1/5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection of newborn calves against fatal multisystemic infectious bovine rhinotracheitis by feeding colostrum from vaccinated cows. 283 76

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

The bird examined was a 10-week-old female Gouldian finch (Chloebia gouldiae) from an aviary that had housed about 100 Gouldian finches, which had nasal discharge, dyspnoea, anorexia, depression and a very high mortality (50%) in both adult and young birds. Gross and histopathology revealed moderate to severe lymphoid depletion in the bursa of Fabricius and thymus, and sinusitis/rhinitis, tracheitis, bronchopneumonia, myocarditis, nephritis and splenitis. Circovirus infection was diagnosed in the Gouldian finch based on finding characteristic globular intracytoplasmic inclusion bodies containing 15 to 18 nm virus particles in the mononuclear cells of the bursa of Fabricius by transmission electron microscopy and by demonstrating circovirus DNA in the cytoplasm of mononuclear cells of the bursa of Fabricius by in situ hybridization using a circovirus-specific DNA probe. The Gouldian finch was also affected by concurrent bacterial and adenovirus infections. This is the first report of circovirus infection in a Gouldian finch.
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PMID:Circovirus infection in a Gouldian finch (Chloebia gouldiae). 1554 33

Thirty-nine 4- to 5-week-old broiler chickens from an outbreak of Newcastle disease (ND) in Japan were examined pathologically. The causative agent was identified as a mesogenic strain of ND virus. Predominant gross lesions included haemorrhage in the lungs, congestion of the trachea, splenomegaly, atrophy of the thymus and bursa of Fabricius, and whitish discolouration of the brain. Microscopically, there was mild haemorrhagic pneumonia, catarrhal tracheitis, lymphoid necrosis in the spleen, thymus, bursa of Fabricius and caecum and diffuse non-suppurative encephalitis. Lesions associated with encephalitis were characterized by multifocal perivascular cuffing, malacia, demyelination and proliferative vasculitis. Malacic lesions occurred in the hyperstriatum, neostriatum, subleptomeningeal and periventricular regions of the cerebrum, whereas demyelination was seen mainly in the brain stem. The morphological changes that occurred in the brain in these cases were distinctive and the lesions in the lymphoid tissues were related to concurrent infection with infectious bursal disease virus.
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PMID:Brain lesions in young broiler chickens naturally infected with a mesogenic strain of Newcastle disease virus. 1867 Nov 35

Infectious bronchitis virus (IBV) Cal99 variant was isolated from the kidneys of seven 2-5-mo-old game chickens with nephritis and respiratory disease. IBV Cal99 variant is usually associated with respiratory disease in broiler chickens in California. Macroscopically, the majority of the birds had moderately to severely enlarged and mottled pale kidneys, with increased urates in the ureters. Microscopically, most of the birds had acute nephrosis and interstitial nephritis. The birds also had sinusitis, tracheitis, bronchopneumonia, airsacculitis, salivary gland adenitis, and lymphoid depletion in the thymus and bursa of Fabricius. Immunohistochemistry was strongly positive for IBV antigen in the cytoplasm of tubular epithelial cells in the kidneys and also in the epithelium of the respiratory tract, salivary glands, proventriculus, intestine, and bursa of Fabricius. Infectious bronchitis virus was isolated from the trachea, lungs, kidneys, and cecal tonsils. Sequencing of the hypervariable region of the S1 gene of the kidney IBV isolate, designated IBV/CA99variant/07, revealed that the virus was 98% homologous to the Cal99 serotype of IBV.
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PMID:Nephritis associated with infectious bronchitis virus Cal99 variant in game chickens. 2201 40

The pathogenicity of Newcastle disease (ND) virus, isolated from ND outbreak in vaccinated chickens, was evaluated through experiments. The pathogenicity indexes (mean death time (MDT); 58 hr, intracerebral pathogenicity index (ICPI); 1.7 and intravenous pathogenicity index (IVPI); 2.51) indicated that the ND virus was velogenic. The ND virus caused lymphocytic necrosis in the spleen with fibrinous exudation and proliferation of macrophages, sinusoidal fibrin exudation in the liver, proliferation of macrophages in the lung, lymphocytic necrosis and depletion in the bursa of Fabricius, cecal tonsils and thymus, necrosis of bone marrow, tracheitis, conjunctivitis and necrosis of feather epithelial cells in specific-pathogen-free chickens. Immunohistochemically, ND virus antigens were seen in the lesions mentioned above. The ND virus could not induce the encephalitis and pancreatitis that were observed in the natural case of ND in vaccinated chickens. There was no clinical disease in vaccinated chickens after the challenge of the ND virus. In diluted ND vaccine experiments, chickens vaccinated with a high dilution of vaccine and then challenged with the ND virus showed clinical sign and mortality with pancreatic focal necrosis. Vaccine diluted with fresh tap water had no effect on protection against the challenge of the ND virus. This study suggests that improper vaccination may be involved in outbreaks of ND in vaccinated chickens.
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PMID:Pathogenesis of Newcastle disease in vaccinated chickens: pathogenicity of isolated virus and vaccine effect on challenge of its virus. 2396 12

In this study, commercial broilers were experimentally infected with single (classical IBV, variant IBV or AIV-H9N2) or mixed AIV-H9N2 with classical, variant or vaccine strains of IBV. Birds were monitored for clinical and pathological outcomes and virus shedding for 10days post infection (DPI). Clinical signs were limited to the respiratory tract in all challenged groups and varied from mild to moderate mouth breathing to severe respiratory signs with snorting sound and extended head. Mortalities were only recorded in mixed AIV-H9N2/variant IBV challenge group. AIV-H9N2 challenge caused tracheal petechial hemorrhage that progressed to tracheal congestion and caseation. In mixed AIV-H9N2/IBV vaccine challenge, severe tracheitis with bronchial cast formation was observed. In mixed AIV-H9N2/variant IBV challenge severe congestion of the tracheal mucosa and excessive exudates with a tendency to form tubular casts were observed. Kidney ureate deposition was only observed in variant IBV challenge group. Histopathologically, tracheal congestion, severe degeneration, and deciliation were noticed in all groups of mixed infection. Interestingly, hemorrhage and atrophy were observed in thymus gland of birds challenged with single AIV-H9N2 or mixed AIV-H9N2/IBV. There was no difference in the tracheal shedding level of variant IBV between single and mixed infected groups while classical IBV shedding increased in mixed infection group. Interestingly, the AIV-H9N2 showed constantly high shedding titers till 7DPI with variant or vaccine IBV co-infection. In conclusion, co-infection of IBV and AIV-H9N2 induced severe clinical outcome and high mortality. Also, IBV co-infection increased the shedding of AIV-H9N2 in experimentally infected birds.
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PMID:Experimental co-infection of infectious bronchitis and low pathogenic avian influenza H9N2 viruses in commercial broiler chickens. 2869 24


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