Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Orthotopic liver transplantation was performed in a 29-year-old woman because of increasing decompensation of HBs-antigen positive post-hepatitic cirrhosis. Postoperatively she developed a mild rejection reaction and diabetes mellitus. Thirteen months after the transplant she conceived twins. This high risk pregnancy was complicated by a febrile viral infection with purulent tracheobronchitis at 9 weeks and a threatened abortion at 11 weeks. At 33 weeks there was a sudden drop in haemoglobin due to a minor uterine rupture which necessitated cesarean section. The female infants--of development in keeping with the dates--showed no clinical or ultrasound evidence of any malformations. Apart from initial difficulties--asphyxia (second twin), fluctuating glucose and calcium levels, an episode of neonatal jaundice which required phototherapy, reluctance to suck and hypotonia--the further development of both twins proceeded normally. The maternal diabetes disappeared after delivery, HBs-antigen remained negative and the HBs-antibody titre rose. The patient has remained in good condition, both mentally and physically.
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PMID:[Twin pregnancy after liver transplantation]. 235 62

A 37-year-old female patient reported marked weight loss, prolonged alopecia, recurrent infections and watery diarrhoea. Examination revealed Salmonella infection, candidiasis and immunological signs of previous toxoplasmosis. Between 1978 and 1981, the patient had had close sexual relations to a patient with haemophilia A. Due to this fact, AIDS was suspected. Serological tests for HIV were not available at the time. The findings in DNA image cytometry (nuclear DNA inclusion bodies, polyploid lymphocyte nuclei and binuclear lymphocytes) suggested a viral infection of the lymphoid cells. Electron microscopy revealed in hepatocytes and cerebral cells intranuclear inclusion bodies whose size and contents were not compatible with an infection caused by cytomegalovirus, herpes virus or Epstein-Barr virus. In autopsy, infections of various organ systems such as pneumonia, tracheobronchitis, urocystitis, pyelonephritis, Candida oesophagitis and enteritis were found.
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PMID:[AIDS in a woman having had sexual relations with a patient with hemophilia A. Characteristic findings in DNA image cytometry]. 379 20

We report the case of a 52 year-old homosexual AIDS patients suffering from Herpes simplex virus type II infection of the esophagus and the bronchial system. The chest radiograph revealed a homogeneous, well-defined consolidation of the right upper lobe. Gastroscopy showed an ulcer of the esophagus and gastritis of the antrum. Bronchoscopically, marked necrotizing tracheobronchitis and an exophytic tumour causing complete blockage of the apical segment of the right upper lobe were demonstrated. Histological examination of the biopsy specimens of the esophagus and of the bronchus revealed Herpes simplex virus type II infection of both organs. The patient was treated by acyclovir for 2 weeks. 6 weeks after the diagnosis of acute Herpes simplex virus type II infection had been established, the patient died as a result of a highly malignant non-Hodgkin's lymphoma of the cerebellum. Autopsy showed no remaining endobronchial tumour. Histological examination of the bronchus showed no evidence of viral infection or non-Hodgkin's lymphoma. An endobronchial tumour caused by Herpes simplex virus type II infection has not been described up to now.
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PMID:[Herpes simplex virus type II infection as an exophytic endobronchial tumor]. 761 Jun 61

Genetic reassortment of H5N1 highly pathogenic avian influenza viruses (HPAI) with currently circulating human influenza A strains is one possibility that could lead to efficient human-to-human transmissibility. Domestic pigs which are susceptible to infection with both human and avian influenza A viruses are one of the natural hosts where such reassortment events could occur. Virological, histological and serological features of H5N1 virus infection in pigs were characterized in this study. Two- to three-week-old domestic piglets were intranasally inoculated with 10(6) EID(50) of A/Vietnam/1203/04 (VN/04), A/chicken/Indonesia/7/03 (Ck/Indo/03), A/Whooper swan/Mongolia/244/05 (WS/Mong/05), and A/Muscovy duck/Vietnam/ 209/05 (MDk/VN/05) viruses. Swine H3N2 and H1N1 viruses were studied as a positive control for swine influenza virus infection. The pathogenicity of the H5N1 HPAI viruses was also characterized in mouse and ferret animal models. Intranasal inoculation of pigs with H5N1 viruses or consumption of infected chicken meat did not result in severe disease. Mild weight loss was seen in pigs inoculated with WS/Mong/05, Ck/Indo/03 H5N1 and H1N1 swine influenza viruses. WS/Mong/05, Ck/Indo/03 and VN/04 viruses were detected in nasal swabs of inoculated pigs mainly on days 1 and 3. Titers of H5N1 viruses in nasal swabs were remarkably lower compared with those of swine influenza viruses. Replication of all four H5N1 viruses in pigs was restricted to the respiratory tract, mainly to the lungs. Titers of H5N1 viruses in the lungs were lower than those of swine viruses. WS/Mong/05 virus was isolated from trachea and tonsils, and MDk/VN/05 virus was isolated from nasal turbinate of infected pigs. Histological examination revealed mild to moderate bronchiolitis and multifocal alveolitis in the lungs of pigs infected with H5N1 viruses, while infection with swine influenza viruses resulted in severe tracheobronchitis and bronchointerstitial pneumonia. Pigs had low susceptibility to infection with H5N1 HPAI viruses. Inoculation of pigs with H5N1 viruses resulted in asymptomatic to mild symptomatic infection restricted to the respiratory tract and tonsils in contrast to mouse and ferrets animal models, where some of the viruses studied were highly pathogenic and replicated systemically.
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PMID:Domestic pigs have low susceptibility to H5N1 highly pathogenic avian influenza viruses. 1861 94

We describe an oligosymptomatic patient with Good syndrome (thymoma and hypogammaglobulinemia) in who a follow-up chest computed tomography showed circumferential tracheobronchial wall thickening. Bronchoscopy demonstrated tracheobronchitis with necrotic, vesicular and blister areas. The histopathological and immunohistochemical findings were compatible with herpes simplex virus infection. The therapeutical response to oral acyclovir was satisfactory.
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PMID:[Tracheobronchial wall thickening secondary to herpesvirus infection in a patient with Goods syndrome]. 1876 47

We report a complication of the novel H1N1 influenza A viral infection not yet described during this 2007-2009 pandemic. Pulmonary hemorrhage is a known complication of influenza pneumonia, including well documented reports from previous pandemics. A 57-year-old African American female presented with fevers, progressive shortness of breath, and cough. After being admitted with an initial diagnosis of myocardial infarction, hemoptysis developed. Nasopharyngeal swabs rapid testing was negative for influenza A and B antigen, but a polymerase chain reaction test for influenza A type H1N1 was positive. A fiberoptic bronchoscopy for ongoing hemoptysis demonstrated diffuse erythema and bleeding, and bronchoalveolar lavage was consistent with alveolar hemorrhage. Progressive hypoxemic respiratory failure ensued, eventually leading to her demise. Our case highlights one of the more feared complications that may have been more common in prior outbreaks, such as the 1918 "Spanish Flu." Autopsy studies from the 1918 influenza pandemic found severe tracheobronchitis (oftentimes hemorrhagic), septal edema, necrotizing bronchiolitis, alveolitis, and extensive hemorrhage, as opposed to the more benign laryngitis and tracheobronchitis that is commonplace in other influenza infections. Similar pathology appearances, including pulmonary hemorrhage, have also been described in H5N1 outbreaks in China and Thailand. It is crucial for pandemic preparedness planning that additional careful and complete autopsy study of this present pandemic influenza infection be performed and reported to answer questions regarding the natural history, pathology, and pathogenesis of this novel H1N1 influenza.
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PMID:Novel H1N1 influenza A viral infection complicated by alveolar hemorrhage. 2042 Jul 34

Twenty autopsy cases with 2009 pandemic influenza A (2009 H1N1) virus infection, performed between August 2009 and February 2010, were histopathologically analyzed. Hematoxylin-eosin staining, immunohistochemistry for type A influenza nucleoprotein antigen, and real-time reverse transcription-PCR assay for viral RNA were performed on formalin-fixed and paraffin-embedded specimens. In addition, the D222G amino acid substitution in influenza virus hemagglutinin, which binds to specific cell receptors, was analyzed in formalin-fixed and paraffin-embedded trachea and lung sections by direct sequencing of PCR-amplified products. There were several histopathological patterns in the lung according to the most remarkable findings in each case: acute diffuse alveolar damage (DAD) with a hyaline membrane (four cases), organized DAD (one case), acute massive intra-alveolar edema with variable degrees of hemorrhage (three cases), neutrophilic bronchopneumonia (five cases) and tracheobronchitis with limited histopathological changes in alveoli (four cases). In two cases, the main findings were due to preexisting disease. Influenza virus antigen was only detected in the respiratory tract in 10 cases by immunohistochemistry. The antigen was detected in type II pneumocytes (three cases) in the epithelial cells of the trachea, bronchi and glands (six cases), and in the epithelial cells in both of the above (one case). The four cases with acute DAD presented with antigen-positive type II pneumocytes. In one case, the D222G substitution was detected in the lung as a major sequence, although 222D was prominent in the trachea, suggesting that selection of the viral clones occurred in the respiratory tract. In five cases, the pathogenesis of 2009 H1N1 was confirmed to be viral infection in pneumocytes, which caused severe alveolar damage and fatal viral pneumonia. Further studies on both host and viral factors in autopsy or biopsy materials will be essential to elucidate the other pathogenic factors involved in influenza virus infection.
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PMID:Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection. 2187 12

SARS-CoV-2, the etiologic agent of COVID-19, is a global pandemic with substantial mortality dominated by acute respiratory distress syndrome. We systematically evaluated lungs of 68 autopsies from 3 institutions in heavily hit areas (2 USA, 1 Italy). Detailed evaluation of several compartments (airways, alveolar walls, airspaces, and vasculature) was performed to determine the range of histologic features. The cohort consisted of 47 males and 21 females with a median age of 73 years (range 30-96). Co-morbidities were present in most patients with 60% reporting at least three conditions. Tracheobronchitis was frequently present, independent from intubation or superimposed pneumonia. Diffuse alveolar damage (DAD) was seen in 87% of cases. Later phases of DAD were less frequent and correlated with longer duration of disease. Large vessel thrombi were seen in 42% of cases but platelet (CD61 positive) and/or fibrin microthrombi were present at least focally in 84%. Ultrastructurally, small vessels showed basal membrane reduplication and significant endothelial swelling with cytoplasmic vacuolization. In a subset of cases, virus was detected using different tools (immunohistochemistry for SARS-CoV-2 viral spike protein, RNA in situ hybridization, lung viral culture, and electron microscopy). Virus was seen in airway epithelium and type 2 pneumocytes. IHC or in situ detection, as well as viable form (lung culture positive) was associated with the presence of hyaline membranes, usually within 2 weeks but up to 4 weeks after initial diagnosis. COVID-19 pneumonia is a heterogeneous disease (tracheobronchitis, DAD, and vascular injury), but with consistent features in three centers. The pulmonary vasculature, with capillary microthrombi and inflammation, as well as macrothrombi, is commonly involved. Viral infection in areas of ongoing active injury contributes to persistent and temporally heterogeneous lung damage.
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PMID:COVID-19 pulmonary pathology: a multi-institutional autopsy cohort from Italy and New York City. 3287 13