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

Squirrel monkeys (Saimiri sciureus) inoculated intratracheally with 10(4.2)-10(8.2) egg median infectious doses (EID50) of type A influenza virus (H3N2) responded with clinical illness including such signs as fever, sneezing or coughing, coryza, and increased respiratory rates. Necropsy studies performed six days after inoculation revealed bronchopneumonia in addition to a mild tracheitis. Squirrel monkeys given 10(5)-6 x 10(8) colony-forming units (cfu) of Streptococcus pneumoniae intratracheally died four to six days later after developing severe illness characterized by fever, bacteremia, lethargy, anorexia, coughing, labored breathing, and bronchopneumonia. Monkeys given 770 cfu of S. pneumoniae responded with less severe symptoms and survived. Four squirrel monkeys inoculated with 10(8.2) EID50 of virus and then 102 hr later with 770 cfu of S. pneumoniae developed severe disease; three of the four animals died within 40 hr. At necropsy these monkeys had more extensive and severe bronchopneumonia than was seen in monkeys infected with either organism alone.
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PMID:Influenza alone and in sequence with pneumonia due to Streptococcus pneumoniae in the squirrel monkey. 2215 62

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

To evaluate the efficacy of a commercial bacterial vaccine in protecting Strain 13 guineapigs against fatal Bordetella bronchiseptica pneumonia, it was necessary to establish the infectivity and disease pathogenesis induced by virulent organisms. When guineapigs were exposed to small-particle aerosols of varying concentrations of virulent B. bronchiseptica, a spectrum of disease was produced that ranged from inapparent illness to fulminant bronchopneumonia. Clinical signs began by day 4 after exposure, and were evidenced by anorexia, weight loss, respiratory distress and serous to purulent nasal discharge. Pathological alterations were limited to the respiratory system. Moribund animals exhibited a suppurative necrotizing bronchopneumonia and necrotizing tracheitis. In animals that survived the challenge, the bacteria were eliminated from the lungs by day 28 but continued to persist in the laryngeal area and the trachea. The median infectious dose and the median lethal dose were estimated to be 4 colony-forming units (CFU) and 1314 CFU respectively. These data suggest that the guineapig will be a valuable model system in which to study interactions between Bordetella species and host cells as well as to evaluate potential B. bronchiseptica immunogens.
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PMID:Airborne-induced experimental Bordetella bronchiseptica pneumonia in strain 13 guineapigs. 362 70

Beginning at the end of March 1999, a syndrome characterized by severe depression, anorexia, fever, and respiratory and enteric symptoms appeared in flocks of turkeys and, to a lesser extent, of chickens in the densely populated poultry-rearing regions of northeast Italy. The disease was characterized by sinusitis, tracheitis, peritonitis, and pancreatitis. The mortality varied between 5% and 90%. The disease was diagnosed as low pathogenic avian influenza, H7N1 serotype. After a summer period of declining cases, the disease reappeared in autumn exclusively in turkeys. Since the middle of December 1999, many farms of chickens, turkeys, and guinea fowl were abruptly affected by a highly pathogenic H7N1 virus, with very severe depression and mortality up to 100% in a few days. By the end of March 2000, nearly 500 farms, representing over 15 million birds, were affected or depopulated. To date, control measures have focused on improved biosecurity measures. Vaccine was not allowed, but its use was debated.
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PMID:Avian influenza epidemic in Italy due to serovar H7N1. 1133 92

In March 1999 a syndrome characterized by depression, anorexia, fever, and respiratory and enteric signs appeared in many flocks of turkeys and, to a lesser extent, chickens in the densely populated poultry-rearing regions of Northeastern Italy. Initially the disease was characterized by sinusitis, tracheitis, peritonitis, and pancreatitis. The responsible agent was identified as low-pathogenicity (LP) avian influenza (AI) of H7N1 subtype. Concerning the light layers, the mortality was variable, from 1.7% to 9.5%, whereas egg production decreased by 10% to 40%. According to the epidemiologic data, chickens seemed to be less sensitive to the virus than were turkeys. Nine months later, the AI virus changed to a highly pathogenic (HP) AI virus and affected, besides turkeys, a great number of pullet and layer flocks, with high mortality (80%-100%) in a few days. However, the course of disease was more prolonged in pullets. Within 3 1/2 mo, over 100 outbreaks were reported. Following the HPAI outbreaks, in late 2000 and early 2001, LPAI reemerged, but only one flock of layers was affected.
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PMID:Avian influenza attributable to serovar H7N1 in light layers in Italy. 1457 37

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

Low pathogenic avian influenza subtype H9N8 was diagnosed on a Korean native chicken farm in Gyeonggi province, South Korea, in late April 2004. Clinical signs included moderate respiratory distress, depression, mild diarrhoea, loss of appetite and a slightly elevated mortality (1.4% in 5 days). Pathologically, mucopurulent tracheitis and air sacculitis were prominently found with urate renal deposition. The isolated A/chicken/Kr/164/04 (H9N8) had an Ala-Ser-Gly-Arg (A/S/G/R) motif at the cleavage site of haemagglutinin, which has been commonly found in H9N2 isolated from Korean poultry. Phylogenetic analysis of the haemagglutinin and neuraminidase genes of the H9N8 avian influenza virus (AIV) isolate showed that reassortment had occurred. Its haemagglutinin gene was similar to that of Korean H9N2 AIVs, but its neuraminidase gene was closely related to that of A/WBF/Kr/KCA16/03 (H3N8) isolated from the faeces of wild birds in Korea. The pathogenicity of the isolate was tested on 6-week-old specific pathogen free chickens. The inoculated virus (H9N8) was recovered from most tested organs, including the trachea, lung, kidney, spleen, and caecal tonsil. This is the first report of an outbreak of low pathogenic avian influenza in chickens caused by AIV subtype H9N8.
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PMID:An outbreak of avian influenza subtype H9N8 among chickens in South Korea. 1712 32

A novel herpesvirus infection in nine Bourke's parrots (Neopsephotus bourkii, formerly Neophema bourkii) housed in an outdoor aviary comprised of multiple species of birds was diagnosed based on histopathology, electron microscopy and polymerase chain reaction (PCR). Clinical signs in the parrots included anorexia, ruffled feathers, depression, loss of weight and respiratory distress. The most common gross lesions were moderately congested and oedematous lungs and a mild fibrinous exudate in the air sacs and lumen of the trachea. Histological examination revealed mild to severe bronchopneumonia and airsacculitis with syncytial cells containing eosinophilic intranuclear inclusion bodies in most birds. Other less frequent changes included tracheitis, syringitis, sinusitis, rhinitis, otitis media and conjunctivitis. Attempts to culture the virus in chicken embryos and chicken embryo liver cells were unsuccessful. Examination by transmission electron microscopy of syncytial cells from the lungs of two birds revealed intranuclear virus particles typical of the family Herpesviridae. DNA from a novel herpesvirus was amplified from lung tissue by PCR using degenerate primers derived from conserved avian herpesvirus sequences. The virus belongs in the genus Iltovirus of the Alphaherpesvirinae subfamily. It is not closely related to Psittacid herpesvirus 1 that causes Pacheco's disease but does group phylogenetically with a clade of herpesviruses that cause respiratory disease in a number of avian species. The proposed name for this herpesvirus is Psittacid herpesvirus 3.
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PMID:A novel herpesvirus associated with respiratory disease in Bourke's parrots (Neopsephotus bourkii). 2323 65

Mortality of 20% of a flock of 1000 chukar partridge chicks occurred over a 6-week period in Northern California from August to September 2012. Affected birds were 2 to 42 days old and died without premonitory clinical signs or after showing ruffled feathers and anorexia for 24 to 72 hours. Three carcasses were submitted for necropsy, 2 birds had hemorrhagic tracheitis grossly, and all 3 had lymphoplasmacytic and histiocytic myocarditis with myocardial necrosis microscopically. The differential diagnoses and the diagnostic workup to achieve a final diagnosis are discussed. The detection of 2 zoonotic agents in these birds makes this an interesting case from a public health perspective.
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PMID:Diagnostic exercise: High mortality in a flock of chukar partridge chicks (Alectoris chukar) in California. 2468 86

Circumstantial evidence has linked a new group of nidoviruses with respiratory disease in pythons, lizards, and cattle. We conducted experimental infections in ball pythons (Python regius) to test the hypothesis that ball python nidovirus (BPNV) infection results in respiratory disease. Three ball pythons were inoculated orally and intratracheally with cell culture isolated BPNV and two were sham inoculated. Antemortem choanal, oroesophageal, and cloacal swabs and postmortem tissues of infected snakes were positive for viral RNA, protein, and infectious virus by qRT-PCR, immunohistochemistry, western blot and virus isolation. Clinical signs included oral mucosal reddening, abundant mucus secretions, open-mouthed breathing, and anorexia. Histologic lesions included chronic-active mucinous rhinitis, stomatitis, tracheitis, esophagitis and proliferative interstitial pneumonia. Control snakes remained negative and free of clinical signs throughout the experiment. Our findings establish a causal relationship between nidovirus infection and respiratory disease in ball pythons and shed light on disease progression and transmission.
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PMID:Respiratory disease in ball pythons (Python regius) experimentally infected with ball python nidovirus. 2932 83


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