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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing tracheobronchitis (NTB) is an acute inflammatory lesion of the lower airway which can result in total airway obstruction. While potentially treatable, this lesion has been described predominantly in autopsy or animal studies. We observed clinical symptoms which reflect development of this lesion. Symptoms of acute airway obstruction (hypercarbia, respiratory acidosis, decreased chest wall movement) occurred in eight neonates undergoing treatment with high-frequency jet ventilation; five patients treated with HFJV were studied without signs of obstruction. Emergency bronchoscopy using a rigid bronchoscope was performed in the intensive care unit. The diagnosis of NTB was made by the observation of hyperemia, intraluminal debris, or the appearance of eschar formation. Necrotic debris was removed using forceps and/or suction as necessary. All patients survived treatment. Seven were long-term survivors, all with bronchopulmonary dysplasia. In patients who died, autopsy evaluation of the airway revealed a characteristic picture consisting of necrosis, neutrophil infiltration, epithelial erosion, and intraluminal obstruction.
Laryngoscope 1987 Sep
PMID:Necrotizing tracheobronchitis: a newly recognized cause of acute obstruction in mechanically ventilated neonates. 362 23

The effect of Bordetella bronchiseptica upper airway colonization on the clinical, radiographic, serologic, pathologic, and pulmonary function changes caused by canine parainfluenza-2 virus (CPIV-2) infection was studied in 24 purebred Beagle pups (10.5 +/- 1.4 weeks old). Eight control dogs (group I) were not colonized or inoculated with CPIV-2. Of the 12 noncolonized dogs inoculated with CPIV-2 (group II), 9 developed antibody titers to CPIV-2 and 10 had clinical signs of infectious canine tracheobronchitis (kennel cough). Group I and group II dogs did not differ in radiographic findings or pulmonary function. Four group II dogs necropsied 1 to 5 days after clinical signs developed had laryngotracheobronchitis and bronchiolar inflammation not present at necropsy on 2 group I dogs. Four dogs had B bronchiseptica upper airway colonization and were inoculated with CPIV-2 (group III). All 4 group III dogs developed positive antibody titers, had clinical signs of kennel cough, and had radiographic changes. Pulmonary dynamic compliance was lower in group III than in group I or group II animals. Respiratory rate and tidal volume did not differ among the 3 groups. The 1 group III dog that was necropsied had changes similar to group II dogs with the addition of lobar bronchopneumonia. The present study indicates that asymptomatic B bronchiseptica colonization may effect the clinical, radiographic, and pulmonary function changes produced by CPIV-2 respiratory tract infections.
Am J Vet Res 1984 Sep
PMID:Role of canine parainfluenza virus and Bordetella bronchiseptica in kennel cough. 609 51

Tracheobronchitis is an uncommon manifestation of infection due to Aspergillus species, occurring in < 7% of cases of pulmonary aspergillosis. At least 58 cases of invasive aspergillus tracheobronchitis have been described since 1962. We describe four patients with AIDS, all of whom were severely immunocompromised, who had ulcerative tracheobronchitis due to Aspergillus species demonstrated histologically. Three patients had received corticosteroids or were neutropenic at presentation. At bronchoscopy, three patients had some degree of diffuse tracheobronchitis, multiple ulcerative or "plaque-like" inflammatory lesions, and occasionally nodules involving the mainstem and segmental bronchi. The remaining patient had a single deep ulceration of the proximal trachea. Aspergillus was isolated from biopsy specimens from all four patients. There were varied degrees of invasion of the mucosa, submucosa, and cartilage on histological examination in three patients, one of whom had evidence of disseminated aspergillosis. Two patients subsequently developed pulmonary parenchymal disease due to Aspergillus. A review of aspergillus tracheobronchitis, including a discussion of airway disease in patients infected with human immunodeficiency virus, is presented.
Clin Infect Dis 1993 Sep
PMID:Ulcerative and plaque-like tracheobronchitis due to infection with Aspergillus in patients with AIDS. 788 70

Human bronchial epithelium is exquisitely sensitive to high O2 levels, with tracheobronchitis usually developing after 12 h of exposure to 100% O2. To evaluate whether this vulnerability results from inability of the bronchial epithelium to provide adequate antioxidant protection, we quantified antioxidant gene expression in bronchial epithelium of normal volunteers at baseline and after exposure to 100% O2 in vivo. After 14.8 +/- 0.2 h of 100% O2, 24 of 33 individuals had evidence of tracheobronchitis. Baseline gene expression of CuZn superoxide dismutase (SOD), MnSOD, and catalase in bronchial epithelium was very low (CuZnSOD 4.1 +/- 0.8 transcripts/cell, MnSOD 5.1 +/- 0.9, catalase 1.3 +/- 0.2), with control gamma-actin expression relatively abundant (50 +/- 6 transcripts/cell). Importantly, despite 100% O2 exposure sufficient to cause tracheobronchitis in most individuals, antioxidant mRNA transcripts/cell in bronchial epithelium did not increase (P > 0.5). Catalase activity in bronchial epithelium did not change after exposure to hyperoxia (P > 0.05). Total SOD activity increased mildly (P < 0.01) but not sufficiently to protect the epithelium. Together, the very low levels of expression of intracellular antioxidant enzymes and the inability to upregulate expression at the mRNA level with oxidant stress likely have a role in human airway epithelium susceptibility to hyperoxia.
J Appl Physiol (1985) 1993 Sep
PMID:In vivo antioxidant gene expression in human airway epithelium of normal individuals exposed to 100% O2. 822 38

Four infants and children who had tracheobronchitis or bronchiolitis by respiratory syncytial virus (RSV) reinfection were presented. Their clinical features, systemic and local immune reactions to RSV were compared with those of eleven age-matched patients who had lower respiratory tract illness with primary RSV infection. Moderate antibody activities in their nasopharyngeal secretions and sera which were comparable to those of convalescent phase of primary infection were observed within several days after onset of illness; however, their clinical symptoms, such as fever or wheezing, lasted almost as long as in primary RSV infection. These observations suggest that the higher serum and secretory antibody activity to RSV during acute phase does not always bring about clinical amelioration in RSV reinfection. The contribution of immunopathological reaction between RSV and RSV-specific antibodies might also be considered as a cause of inflammation during the acute phase of RSV reinfection.
J Infect 1997 Sep
PMID:Systemic and local immune responses of four cases with lower respiratory tract illness due to reinfection with respiratory syncytial virus. 935 58

Respiratory syncytial virus (RSV) has been reported as a cause of death among autologous peripheral blood stem cell (ASCT) and marrow recipients and recommendations for therapy with aerosolized ribavirin plus intravenous immunoglobulin (IVIG) made. This therapy is expensive, may be toxic, and causes a significant disruption of patient care. The purpose of this study was to evaluate the morbidity and mortality of RSV infections in patients with multiple myeloma undergoing ASCT without ribavirin therapy. During the months of February-April 1997, 10 consecutive patients (median age 57 years, seven males) with advanced and heavily pretreated myeloma underwent ASCT while having active RSV upper respiratory tract infection. After melphalan (200 mg/m2), all patients became neutropenic (<1000 cells/mm3) for a median of 7 days. Ribavirin was not given to any patient. No patient developed lower respiratory tract infection, required transfer to intensive care or died at a median follow-up of 8 months. One patient developed tracheobronchitis requiring oxygenation by nasal cannula. No delay in the treatment of the underlying myeloma was incurred. RSV infection may not necessarily be a contraindication for ASCT or an indication for therapy with aerosolized ribavirin. Additional studies are needed to confirm our preliminary findings.
Bone Marrow Transplant 1999 Sep
PMID:Patients with multiple myeloma may safely undergo autologous transplantation despite ongoing RSV infection and no ribavirin therapy. 1048 34

Reactive oxygen species (ROS) is increased in the airway during the inhalation of 100% O(2) or cigarette smoke and participates in the development of tracheobronchitis. We hypothesized that inhaled ROS upregulates local extracellular ROS scavenging systems or reactive molecules, e.g., nitric oxide (NO). Extracellular glutathione peroxidase (eGPx) is synthesized by airway epithelium and alveolar macrophages, secreted into the surface epithelial lining fluid, and functions as a first-line defense against inhaled ROS. NO, produced by NO synthase 2 (NOS2), combines rapidly with ROS to form reactive nitrogen species (RNS). In this study, human airway epithelial cells and alveolar macrophages from healthy individuals before and after exposure to 100% O(2) for 12 h, or from cigarette-smoking individuals, were evaluated for eGPx and NOS2 messenger RNA (mRNA) expression. Hyperoxia increased NOS2 mRNA in airway epithelial cells by 2.5-fold but did not increase eGPx mRNA. In contrast, cigarette smoke upregulated eGPx mRNA over 2-fold in airway epithelial cells and alveolar macrophages but did not affect NOS2 expression. In vitro exposure of respiratory epithelial cells to ROS or RNS also increased eGPx expression. These findings define distinct molecular responses in the airway to different inhaled ROS, which likely influences the susceptibility of the airway to oxidative injury.
Am J Respir Cell Mol Biol 2000 Sep
PMID:Differential induction of extracellular glutathione peroxidase and nitric oxide synthase 2 in airways of healthy individuals exposed to 100% O(2) or cigarette smoke. 1097 Aug 26

We present a case of a rapidly progressive pseudomembranous tracheobronchitis and pneumonia in a 52-year-old woman with severe aplastic anemia. Bacillus cereus was isolated from bronchoalveolar lavage fluids, blood cultures, and pseudomembrane biopsy specimens; despite intensive antibiotic treatment, the patient's condition deteriorated rapidly. To our knowledge, this is the first report of a B. cereus infection that has caused pseudomembranous tracheobronchitis, possibly because of the production of bacterial toxins.
Clin Infect Dis 2001 Sep 01
PMID:Pseudomembranous tracheobronchitis due to Bacillus cereus. 1148

Three hundred patients with subacute or chronic non-tuberculous bronchopulmonary disease were given aerosol therapy, chiefly penicillin and more recently penicillin combined with streptomycin. The result showed that the inhalation of these antibiotics is a useful procedure in the treatment of tracheobronchitis, either subacute or protracted, or in association with bronchial asthma, bronchiectasis or pulmonary emphysema. The method of administration is simple.
Calif Med 1950 Sep
PMID:The use of aerosol penicillin and streptomycin in bronchopulmonary infections. 1543 5

A 51-year-old female with acute myeloid leukemia was admitted to our hospital in December 2001. Though she had undergone two courses of induction chemotherapy (idarubicin hydrochloride + cytarabine), she failed to achieve a complete remission. In April 2002, while in non-complete remission, she subsequently underwent total body irradiation (TBI) and treatment with cyclophosphamide (CY) and etoposide (VP-16) before receiving an allogeneic peripheral blood stem cell transplant from her HLA-identical brother. For graft-versus-host disease (GVHD) prophylaxis, she was given tacrolimus and methotrexate. The infused CD34 positive cells provided 8.1 x 10(6) cells per kg. Engraftment was obtained on post-transplant day 14, and there was no evidence of clinical acute GVHD. The use of tacrolimus was discontinued on post-transplant day 60. As there was no occurrence of clinical acute GVHD, the patient received a donor lymphocyte infusion (CD3 cells 0.57 X 10(7) cells per kg) on post-transplant day 105. On day 132, however, she complained of coughing and fever, and on day 135, she was admitted to our hospital again for dyspnea. A CT scan demonstrated ground-glass opacity in the right pulmonary lobe. After considering her clinical course, symptoms, blood gas, CT scans, etc., we suspected interstitial pneumonia. The dyspnea progressively worsened, however, and despite the use of mechanical ventilation from day 143, the patient died on day 149. From the day she was admitted till the day she was intubated, she was unable to produce sputum. Autopsy findings revealed yellow-white tracheal pseudomembranes, as well as Aspergillus hyphae in the trachea, bronchus, and bilateral lungs. These findings are characteristic of Aspergillus tracheobronchitis. The clinical course of Aspergillus tracheobronchitis in allogeneic stem cell transplant recipients is, however, different from that of the usual invasive Aspergillus infection, and although Aspergillus tracheobronchitis is a very rare disease, attention should be paid to the possibility of its occurrence.
Rinsho Ketsueki 2004 Sep
PMID:[Acute myeloid leukemia with Aspergillus tracheobronchitis after allogeneic peripheral blood stem cell transplant]. 1551 Aug 28


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