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

The efficacy of respiratory support devices has been compromised by respiratory infection possibly related to the support mechanism itself. Differentiation between airway contamination (tracheobronchitis) and parenchymal infection (pneumonitis) is clinically significant, as is the differentiation of respiratory infection from other foci of sepsis in the complicated surgical patient. Serial quantitative tracheal cultures provide excellent objective measures of the presence, progression, and/or resolution of respiratory infection with few false positive or negative observations. Indeed, such observations often allow earlier definitive diagnosis of infection than can be achieved with conventional clinical, chemical, or roentgenographic studies. The method represents a useful supplement to the care of the patient requiring respiratory support when infection is a realistic possibility.
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PMID:Quantitative tracheal cultures in surgical patients requiring mechanical ventilatory assistance. 116 13

Nine adult patients from three community teaching hospitals had bronchospasm unresponsive to standard therapy. Bronchoscopic, cytologic, histopathologic, and virologic studies confirmed that necrotizing and exudative tracheobronchitis was due to herpes simplex virus. No patient had a history of previous chronic lung disease; most were not immunocompromised. Three patients never had intubation during hospitalization. All patients were successfully treated with intravenous acyclovir. Herpetic tracheobronchitis may be a commoner clinical syndrome than generally assumed. In an elderly patient with unresolving acute bronchospasm, herpesvirus infection of the lower respiratory tract should be considered in the differential diagnosis. In the immunocompetent host, antiviral therapy can successfully treat herpesvirus respiratory infection, with reversal of clinical, virologic, and pathologic findings. A prompt and accurate diagnosis is crucial.
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PMID:Herpetic tracheobronchitis. 283 59

The most important lower respiratory infection is pneumonia, the fourth leading cause of death. Most cases of bronchitis are of viral etiology and are not major problems. Empyema can present an important problem in management. Although the diagnosis of pneumonia is usually relatively straightforward, the specific etiologic diagnosis remains a major problem. Availability of empyema fluid or a positive blood culture result can be helpful in making the etiologic diagnosis, but these are unavailable in most patients. Screening of sputum Gram stains under 100 X magnification is very important; there should be fewer than 10 squamous epithelial cells, more than 25 polymorphonuclear leukocytes, or both per field of this size. The major causes of pneumonia are Streptococcus pneumoniae, Mycoplasma pneumoniae, anaerobic bacteria, Staphylococcus aureus, various gram-negative aerobic or facultative bacilli and Legionella. However, many other organisms are capable of causing pneumonia, even in the immunocompetent host. Further adding to the problem is the fact that a number of different organisms are manifesting increasing resistance to antimicrobial agents. Our study with ticarcillin plus clavulanic acid included seven patients with pneumonia, one with empyema, and one with purulent tracheobronchitis. Organisms recovered from pleural fluid, transtracheal aspiration and sputum or tracheostomy aspirate included multiple anaerobes, pneumococci, S. aureus, Hemophilus influenzae, Klebsiella pneumoniae, K. ozaenae, Pseudomonas aeruginosa, Acinetobacter, Enterobacter cloacae, Proteus mirabilis, beta-hemolytic streptococci, Neisseria meningitidis and Branhamella catarrhalis. Several of the organisms were ticarcillin resistant. Eight of the patients had cures and the other patient showed improvement. Only minor side-effects were encountered--Coombs' positivity (without hemolysis), eosinophilia, drug fever and one case of questionable neutropenia.
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PMID:Lower respiratory tract infection. 407 97

Epidemiologic characteristics of childhood tracheobronchitis occurring over a 104-month period in Chapel Hill, NC, were ascertained and compared to those of other pediatric lower respiratory illness (LRI) syndromes. Tracheobronchitis accounted for 40% of all LRI seen at the community's only pediatric practice. Tracheobronchitis incidence was highest during the first two years of life, through the ratio of tracheobronchitis incidence to total LRI incidence increased with age. A viral pathogen or Mycoplasma pneumoniae was isolated from 23% of tracheobronchitis cases; the agents most commonly isolated were parainfluenza viruses, influenza viruses, respiratory syncytial virus, and M. pneumoniae. Influenza virus, particularly type B, was isolated more commonly in tracheobronchitis than in other LRI syndromes. Over all age groups, peak incidence of tracheobronchitis, like that of pneumonia and bronchiolitis, occurred during the winter months. In school-age children, however, tracheobronchitis incidence was more likely than that of other syndromes to be elevated in late winter or early spring, when several influenza B outbreaks occurred in Chapel Hill. Available evidence suggests that risk of chronic respiratory disease is related inversely to age at which acute respiratory infection first occurs, and that a component of wheezing may not be required to confer such risk. These considerations, coupled with the high incidence of tracheobronchitis early in life, warrant further description of this syndrome and assessment of its implications.
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PMID:The epidemiology of tracheobronchitis in pediatric practice. 679 94

"Kennel cough" in dogs in animal shelters is readily transmissible, reduces adoption rates, and commonly leads to the euthanasia of affected dogs. In cats, tracheobronchitis, conjunctivitis, and pneumonia have been associated with Bordetella bronchiseptica infection-but most cases of upper-respiratory infection (URI) probably are caused by herpesvirus and calicivirus, and many B. bronchiseptica culture-positive cats are clinically normal. Our prospective observational study was undertaken to document the contribution of B. bronchiseptica to disease in cats and dogs from two animal shelters undergoing outbreaks of canine kennel cough, to evaluate whether cross-species transmission might have occurred, and to determine if the presence of infected cats represented a risk to dogs. Clinically defined cases of kennel cough in dogs and URI in cats were investigated in two shelters by calculating clinical-disease incidence, alveolar-lavage cytological examination, bacterial and viral cultures, antibiotic-susceptibility testing, and molecular fingerprinting by pulsed-field gel electrophoresis. In a 40-cat and 40-dog "no-kill" shelter, the prevalences of culture positivity were 47% for B. bronchiseptica and 36% for calicivirus at the same time as two resident dogs demonstrated clinical cough. When no dogs had kennel cough 3 months later, 10% of cats were B. bronchiseptica-culture-positive and 63% calicivirus positive. In a large traditional shelter, the incidence of kennel cough in dogs increased over 12 weeks to a maximum of 19 cases/week/120 dogs, during which time the culture prevalence was 23% for B. bronchiseptica in dogs and 47% in cats. Three to 6 months before the kennel-cough epidemic, no dogs or cats were B. bronchiseptica positive. Very little genetic variability was detected in isolates from these shelters; all isolates except one corresponded to a single strain type which was identical to the pattern in a vaccine used in these shelters. Isolates from other cats, a horse, a llama, and a sea otter were genetically distinct from the shelter isolates. There was widespread resistance to cephalosporins and ampicillin, but low or no resistance to amoxicillin/clavulanate, trimethoprim-sulfamethoxazole, tetracycline, and enrofloxacin. Greater percent resistance was observed in the traditional shelter than in the no-kill shelter and feline isolates were more likely to be resistant than canine isolates.
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PMID:Molecular epidemiology of feline bordetellosis in two animal shelters in California, USA. 1206 77

Infectious tracheobronchitis (ITB), also known as the kennel cough, is a respiratory syndrome of dogs and usually appears to be contagious among dogs housed in groups. Etiologic agent of ITB is multiple and sometimes complex. In the present study, 68 household dogs showing clinical signs of respiratory infection were examined, and 20 dogs (29.4%) were found to be positive for either of following agents. Bordetella bronchiseptica (B.b.) was most frequently detected from nasal and oropharynx sites of 7 dogs (10.3%). Among the viruses examined, canine parainfluenza virus (CPIV) was detected with the highest frequency (7.4%). Other pathogens included in the order of frequency group 1 canine coronavirus (4.4%), canine adenovirus type 2 (2.9%), group 2 canine respiratory coronavirus (1.5%), and canine distemper virus (1.5%). Only 2 cases showed mixed infections. Neither influenza A virus nor canine bocavirus (minute virus of canines) was found in any dogs examined. These results indicate that both B.b. and CPIV are likely to be the principal etiologic agents of canine ITB in Japan, and they may be considered as the target for prophylaxis by vaccination.
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PMID:Etiologic study of upper respiratory infections of household dogs. 1862 96

Twelve normal monkeys inoculated on the mucous membranes of the nose or nose and mouth with a strain of Bacillus influenzae; originally isolated in pure culture from the pleural exudate of a case of empyema following influenzal pneumonia in man and subsequently raised in virulence by animal passage, developed an acute self-limited respiratory disease of from 3 to 5 days duration, characterized by sudden onset with profound prostration, the development of rhinitis and tracheobronchitis, with sneezing, cough, and the outpouring of a scanty mucoid, or mucopurulent exudate, a variable febrile reaction, and either a leucopenia or no significant change in the leucocyte count. This disease was complicated in five instances by purulent sinusitis of one or both antra, in three by bronchopneumonia. Bacillus influenzae was recovered at autopsy from the lesions of the disease either in pure culture or in association with organisms that are normal inhabitants of the upper respiratory tract of monkeys. Of ten normal monkeys injected intratracheally with the same strain of Bacillus influenzae, seven developed bronchopneumonia, two developed tracheobronchitis without pneumonia, and one resisted infection. The general symptoms and duration of the disease were similar to those of the preceding group. There were a severe cough and accelerated respirations. Bacillus influenzae was recovered in pure culture from the lungs, bronchi, or trachea in the animals killed during the active stage of the disease. It disappeared promptly from the respiratory tract with recovery. The significance of the first series of experiments in which monkeys were inoculated in the upper respiratory tract is twofold. First, they establish the fact that Bacillus influenzae can initiate in monkeys an acute infection of the normal mucous membranes of the upper respiratory tract; that is, it can act as a primary incitant of respiratory infection without the assistance of a preceding or concomitant contributing cause. In this respect it differs radically from the pneumococcus and Streptococcus haemolyticus, since experiments previously reported(2, 4) have shown that neither of these organisms possesses the property of initiating an infection of the normal mucous membranes of the upper respiratory tract of monkeys, even though the strains used were incalculably more virulent for monkeys than the strain of Bacillus influenzae used in the foregoing experiments. Secondly, the experiments show that Bacillus influenzae infection of the mucous membranes of the upper respiratory tract may spread by continuity to the paranasal sinuses, setting up an acute sinusitis, that it spreads readily to the lower respiratory tract, producing a tracheobronchitis and permitting the ready invasion of secondary bacteria, and that it may penetrate as far as the terminal bronchioles, alveolar ducts, atria, and alveoli, there setting up a bronchiolitis and true bronchopneumonia. In these respects it likewise differs radically from the pneumococcus and Streptococcus haemolyticus which do not possess these pathogenic properties as previous experiments have shown.(2, 4) The bearing of these facts on the possible etiologic relation of Bacillus influenzae to influenza is important, since they show that Bacillus influenzae possesses certain definite primary pathogenic properties which distinguish it and therefore separate it from the group of recognized secondary organisms in influenzal complications, of which the pneumococcus and the streptococcus are the most frequent. The possible etiologic relation of Bacillus influenzae to influenza is further supported by the character of the respiratory disease that occurred in the monkeys. The sudden onset with profound prostration, the absence of leucocytosis or often a leucopenia, the congestion of the mucous membranes of the respiratory tract, the development on the 2nd or 3rd day of an irritative cough due to an inflammatory tracheitis or tracheobronchitis, the brief self-limited course of the infection, and the irregular febrile reactions are all characteristic of influenza. Many of these symptoms were in striking contrast with the symptoms and course of pneumococcus or streptococcus infections in monkeys in which there were no prostration at onset, invariable leucocytosis, and infrequent cough developing only late in the disease. While all the above features of the disease produced in monkeys are characteristic of influenza in man, none are pathognomonic and, in fact, it is doubtful whether uncomplicated influenza possesses any pathognomonic features by which it may be diagnosed certainly in the absence of an epidemic. Even during epidemic times many respiratory infections arise which, though presumably influenza, it is impossible to diagnose as such with certainty. Nor does pathology help in this respect, since there would appear to be no established distinctive lesions of uncomplicated influenza in man, nor for that matter of the complications of influenza, apart from the complications which have been ascribed by Pfeiffer,(5) MacCallum,(6) Wolbach,(7) and others to infection with Bacillus influenzae because of the association of Bacillus influenzae in pure culture with these complications. For these reasons, although the disease produced in monkeys appears to be essentially identical with influenza in man with respect to its clinical course and complications, it is impossible to determine certainly whether it is actually so. The experiments are advanced, therefore, as evidence in favor of the etiologic relation of Bacillus influenzae to influenza, though they do not permit of a definite conclusion in this respect. Their bearing upon the relation of Bacillus influenzae to certain of the complications of influenza would appear to be reasonably conclusive. The recovery of Bacillus influenzae in pure culture at autopsy from the antra, from the trachea and bronchi, and from the lungs in some of the animals developing sinusitis, bronchiolitis, and a characteristic type of bronchopneumonia confirms by animal experiment the etiologic relation of Bacillus influenzae to these complications of influenza, which hitherto has rested solely upon the frequent association of the influenza bacillus with these lesions in man. The production of tracheobronchitis and the same type of bronchopneumonia by the intratracheal injection of Bacillus influenzae in the second series of experiments serves as additional confirmation of this, but has no direct bearing on the etiologic relation of Bacillus influenzae to uncomplicated influenzae.
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PMID:STUDIES ON EXPERIMENTAL PNEUMONIA : IX. PRODUCTION IN MONKEYS OF AN ACUTE RESPIRATORY DISEASE RESEMBLING INFLUENZA BY INOCULATION WITH BACILLUS INFLUENZAE. 1986 70

Intubated patients are at risk of bacterial colonization and ventilator-associated respiratory infection (VARI). VARI includes tracheobronchitis (VAT) or pneumonia (VAP). VAT and VAP caused by multidrug-resistant (MDR) pathogens are increasing in the United States and Europe. In patients with risk factors for MDR pathogens, empiric antibiotics are often initiated for 48 to 72 hours pending the availability of pathogen identification and antibiotic sensitivity data. Extensive data indicate that early, appropriate antibiotic therapy improves outcomes for patients with VAP. Recognizing and treating VARI may allow earlier appropriate therapy and improved patient outcomes.
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PMID:Diagnosis of ventilator-associated respiratory infections (VARI): microbiologic clues for tracheobronchitis (VAT) and pneumonia (VAP). 2186 22

One of the fundamental elements of therapy in patients hospitalised in the Intensive Care Unit (ICU) is mechanical ventilation (MV). MV enables sufficient gas exchange in patients with severe respiratory insufficiency, thus preserving the proper functioning of organs and systems. However, clinical and experimental studies show that mechanical ventilation may cause severe complications, e.g. lung injury (VALI, VILI), systemic inflammatory response syndrome (SIRS), and, on rare occasions, multiple organ failure (MOF). Mechanical ventilation and especially endotracheal intubation are associated also with higher risk of infectious complications of the respiratory system: ventilator-associated respiratory infection (VARI) and ventilator-associated pneumonia (VAP). The complications of the MV listed above have a significant influence on the length of treatment and also on the increase of the costs of therapy and mortality of patients who stay in an ICU. These negative effects of supported breathing are the reasons for intensive research to find new biological markers of inflammation and lung injury, more sensitive and specific diagnostic instruments, more effective methods of therapy, and programs of prevention. The purpose of this article is the presentation of current knowledge concerning VAP-related infections, to allow pulmonologists and general practitioners to become more familiar with the problem. Basic and the most important data concerning the definition, epidemiology, pathophysiology, microbiology, diagnostics, treatment, and prevention of VAP have been included. Additionally, ventilator-associated tracheobronchitis (VAT) was discussed.
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PMID:[Ventilator-associated pneumonia and other infections]. 2513 17

Bacterial pneumonia and tracheobronchitis are diagnosed frequently following lung transplantation. The diseases share clinical signs of inflammation and are often difficult to differentiate based on culture results. Microbiome and host immune-response signatures that distinguish between pneumonia and tracheobronchitis are undefined. Using a retrospective study design, we selected 49 bronchoalveolar lavage fluid samples from 16 lung transplant recipients associated with pneumonia (n = 8), tracheobronchitis (n = 12) or colonization without respiratory infection (n = 29). We ensured an even distribution of Pseudomonas aeruginosa or Staphylococcus aureus culture-positive samples across the groups. Bayesian regression analysis identified non-culture-based signatures comprising 16S ribosomal RNA microbiome profiles, cytokine levels and clinical variables that characterized the three diagnoses. Relative to samples associated with colonization, those from pneumonia had significantly lower microbial diversity, decreased levels of several bacterial genera and prominent multifunctional cytokine responses. In contrast, tracheobronchitis was characterized by high microbial diversity and multifunctional cytokine responses that differed from those of pneumonia-colonization comparisons. The dissimilar microbiomes and cytokine responses underlying bacterial pneumonia and tracheobronchitis following lung transplantation suggest that the diseases result from different pathogenic processes. Microbiomes and cytokine responses had complementary features, suggesting that they are closely interconnected in the pathogenesis of both diseases.
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PMID:Looking Beyond Respiratory Cultures: Microbiome-Cytokine Signatures of Bacterial Pneumonia and Tracheobronchitis in Lung Transplant Recipients. 2669 65


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