Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We experienced three cases of lower respiratory tract infections worsened after Rhinovirus infection. Case 1: A 42-year-old male with diffuse panbronchiolitis was admitted to our hospital with the complaint of dyspnea on November 21, 1988. Rhinovirus was isolated from nasal washing and P. aeruginosa was cultured from transtracheal aspiration (TTA). Case 2: A 67-year-old male, whose underlying disease was pulmonary asbestosis, was admitted to our hospital complaining of pyrexia on June 12, 1990. Rhinovirus was isolated from TTA and H. influenzae and others were cultured from TTA. Case 3: A 64-year-old male with pulmonary emphysema was admitted to our hospital with a complaint of dyspnea on August 11, 1989. On December 17, 1989 the patient developed rhinorrhea and complained of purulent sputum, pyrexia and dyspnea after five days. Rhinovirus was isolated from nasal washing and TTA and S. nonhaemolyticus and others were cultured from TTA. As indicated in this report, it is interesting to study the relationship between viral infection of the upper respiratory tract and bacterial infection of the lower respiratory tract.
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PMID:[Three cases of lower respiratory tract infection worsened after rhinovirus infection]. 133 Dec 64

Choosing appropriate antimicrobial therapy for patients with pneumonia requires knowledge of the etiologic agents seen in specific kinds of patients at specific times and places. For community-acquired pneumonia, there is an important difference in the agents seen in the normal and the compromised host. The normal host most often presents with viral, mycoplasmal, or pneumococcal pneumonia. The exact place of Chlamydia pneumoniae is still under study. A normal host who aspirates is at risk of anaerobic pneumonia. Normal hosts with influenza may acquire superinfection with Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus. Under specific epidemiologic conditions, community-acquired pneumonia may be due to Legionella species, Yersinia pestis, Francisella tularensis, Coxiella burnetii, Chlamydia psittaci, a mycotic agent, or tuberculosis. Patients with chronic bronchitis and emphysema are predisposed to H. influenzae, Moraxella catarrhalis, and S. pneumoniae infections. HIV-infected patients are likely to have Pneumocystis carinii pneumonia and pneumonia due to cytomegalovirus, S. pneumoniae, and H. influenzae. Patients with diabetes, nursing-home patients, hospitalized patients, immuno-compromised patients, and patients with recent antibiotic therapy are predisposed to pneumonia due to Gram-negative aerobic bacilli of enteric and environmental origin. Initial therapy should be directed at the likely organism or organisms based on hospital susceptibility surveillance. In the normal host with community-acquired pneumonia, the therapy will often be penicillin G or erythromycin. In the patient predisposed to Gram-negative pneumonia, a third-generation cephalosporin with or without an aminoglycoside is the usual choice.
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PMID:Pneumonia. Patient profiles, choice of empiric therapy, and the place of third-generation cephalosporins. 173 Jan 86

Bacterial infections is one of the most important complications in the patients with pulmonary tuberculosis. We reported the causative microorganisms in these cases with special reference to various clinical features and presented the recommended treatment and prophylaxis against respiratory bacterial infections in the patients with pulmonary tuberculosis sequelae. In 1988 and 1989, 63 patients with tuberculosis sequela were demonstrated to have been infected with respiratory pathogenic bacteria by the quantitative sputum culture method (greater than or equal to 10(7)/ml) in Tokyo National Chest Hospital. The male/female ratio of these patients was 3.5, and their average age was 62.5 years. Causative microorganisms of the secondary infections in the patients with tuberculosis sequela were essentially similar in those with other lower respiratory tract infections, i.e., chronic bronchitis, bronchiectasis, diffuse panbonchiolitis, chronic pulmonary emphysema, etc. Pseudomonas aeruginosa, other glucose-nonfermentative Gram-negative bacilli (GNF-GNB), and glucose-fermentative Gram-negative bacilli (GF-GNB) were the major pathogenic bacteria responsible for the chronic respiratory failure and/or fatal outcome in the post-tuberculous patients. Patients with complications, including aspergillosis, atypical mycobacteriosis, bronchial asthma, and so forth, showed no specific causative microorganism for the secondary infections except frequent isolation of Haemophilus influenzae. Our clinical observations clearly demonstrated that there were differences between the causative microorganisms in patients hospitalized during 1988 to 1989 and those in patients without admission. Gram-negative bacilli, including P. aeruginosa, GNF-GNB and GF-GNB, and Staphylococcus aureus were predominant in hospitalized patients. On the contrary, Streptococcus pneumoniae, H. influenzae, and Branhamella catarrhalis were major pathogenic bacteria in patients without hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tuberculosis sequelae: secondary bacterial infections]. 207 64

Clinical evaluation and kinetics in serum of cefoperazone (CPZ) in patients with lower respiratory tract infections have been conducted as a multicenter trial participated by 20 institutions in Kyushu area during a period of 8 months from October 1984 to May 1985. Mean serum CPZ levels up to 4 hours following the end of intravenous infusion of either 1 or 2 g CPZ remained higher than the MIC80 of CPZ against major causative organisms of lower respiratory tract infections such as H. influenzae, P. aeruginosa, K. pneumoniae, and S. pneumoniae. Serum half-lives of CPZ following intravenous infusion were prolonged in the elderly and in patients who showed moderate liver or kidney dysfunction, but did not exceed twofold of normal value. Clinical efficacy rates of CPZ were 82.9% (34/41) against pneumonia, 80% (4/5) against lung abscess, 88.9% (32/36) against acute exacerbation of chronic bronchitis, 66.7% (2/3) against panbronchiolitis, 100% (1/1) against acute bronchitis, and 85.7% (12/14), 64.3% (9/14) and 70.0% (7/10) against infections concurrent to chronic respiratory diseases, pulmonary emphysema and bronchiectasis, respectively. The overall efficacy rate was 81.5% (101/124). Bacteriological eradication rates against P. aeruginosa, H. influenzae and S. pneumoniae were 60% (6/10), 88.9% (8/9) and 100% (3/3), respectively. The overall eradication rate including polymicrobial infection was 67.5% (27/40). The clinical efficacy rate of CPZ in patients with underlying diseases such as lung cancer, pulmonary tuberculosis, and pneumoconiosis, etc. was not significantly different from the efficacy rate in patients without these underlying diseases. Of 20 patients who failed to respond to previous antibiotic treatments, 13 were effectively treated by CPZ. Adverse reactions occurred in 6.7% (11/164) of the patients, and consisted primarily of rash, fever, diarrhea and loose stool. Laboratory abnormalities were seen in 5 patients during the study. These included elevations of S-GOT and S-GPT, eosinophilia and neutropenia. CPZ is a very useful drug in the treatment of lower respiratory tract infections because of its excellent clinical efficacy and rare incidence of abnormal accumulations in sera following the recommended 2-4 g/day administration even in the elderly.
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PMID:[Clinical evaluation of cefoperazone in lower respiratory tract infections]. 354 33

Respiratory infections of 19 subjects of advanced age and/or with underlying respiratory disease were treated with cefoperazone (CPZ) and its clinical effects were studied. Sixteen subjects suffered from respiratory tract infection and 3 subjects had pneumonia. The age of the subjects ranged from 39 to 77 years with the mean of 63.8, 7 of them being more than 70 years of age. The underlying respiratory diseases included chronic pulmonary emphysema in 6 subjects, diffuse panbronchiolitis in 3, bronchiectasis in 3, silicosis in 2 and one each of chronic bronchitis, pulmonary fibrosis, lung cancer and old pulmonary tuberculosis. One case, 75 years of age, had renal insufficiency. The daily dose of CPZ was 4 grams in 18 of the 19 subjects and the duration of administration ranged 5 to 22 days. The remaining 1 subject received 2 g of CPZ daily for 6 days. Clinical effects were judged from the changes in fever, cough, amount of sputum, dyspnea, rales, cyanosis, chest X-ray, white blood cell counts, CRP, erythrocyte sedimentation rates and results of sputum culture. Clinical effects were good in 16 subjects, fair in 1, and poor in 2. Bacteriological follow-up was carried out in 13 subjects. Infecting bacteria were eliminated from 5 subjects, reduced in 2 and, in 4 subjects, they were replaced by other bacteria. In 1 subject, P. aeruginosa was isolated from sputum even after the treatment with CPZ, and in another subject H. influenzae relapsed immediately after the cessation of the CPZ treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of cefoperazone on respiratory infections of patients of advanced age and/or with underlying respiratory diseases]. 373 62

Respiratory infections of 10 subjects with underlying respiratory diseases were treated with cefmetazole (CMZ) and its clinical effects were studied. Five subjects of them were respiratory tract infection, 3 subjects were pneumonia and 2 subjects were pneumonia followed by empyema. The underlying diseases were chronic pulmonary emphysema in 4 subjects, diffuse panbronchiolitis in 3, chronic bronchitis in 2 and bronchial asthma in 1. The doses of CMZ were 4 to 8 grams per day and the durations of administration ranged 3 to 39 days. The clinical effects were judged from the changes of fever, cough, amount of sputum, dyspnea, rale, chest X-ray, white blood cell counts, erythrocyte sedimentation rates, sputum culture and PaO2. The clinical effects of 6 subjects were evaluated as good, those of 3 were fair and that of 1 was poor. In 3 subjects H. influenzae in the sputum was eliminated and in 1 subject both H. aphrophilus and alpha-Streptococcus found in the pleural effusion were eliminated. In 1 subject Klebsiella in the sputum was eliminated and replaced by Enterobacter. No side effects were observed. We conclude that CMZ is considerably useful in the treatment of respiratory infections of the patients with underlying respiratory diseases.
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PMID:[Clinical evaluation of the efficacy of cefmetazole in respiratory tract infections of patients with underlying respiratory diseases]. 658 38

Isolated pathogenic bacteria from sputum of the patients with pulmonary emphysema who were admitted in our hospital from 1984 to 1994 were examined to elucidate the relationship between isolated bacteria from sputum and pulmonary functions including vital capacity (VC), forced expiratory volume (FEV1.0), PaO2 and PaCO2. VC of the patients from whom MSSA (methicillin-sensitive Staphylococcus aureus) or Enterococcus faecalis (E. faecalis) were isolated was significantly lower than that of the patients from whom Streptococcus pneumoniae (S. pneumoniae), Branhamella catarrhalis (B. catarrhalis) or Haemophilus influenza (H. influenza) were isolated. FEV1.0 had a similar tendency as VC in terms of isolated organisms from the patients with emphysema. Similarly, PO2 of the patients from whom MSSA or E. cloacae were isolated was significantly lower than that of the patients from whom S. pneumoniae, B. catarrhalis or H. influenzae were isolated, and PCO2 of the patients from whom S. pneumoniae, B. catarrhalis or H. influenza were isolated. There was also impaired respiratory function in the patients from whom MSSA, Escherichia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa), Xanthomonas maltophilia (X. maltophilia) or Enterobacter cloacae (E. cloacae) were isolated, compared with those in the patients from whom S. pneumonia, B. catarrhalis or H. influenzae were isolated. These results suggest that isolated pathogenic bacteria are shifted from S. pneumoniae, B. catarrhalis or H. influenza to MSSA, E. coli, P. aeruginosa, X. maltophilia or E. cloacae in the course of impairment of respiratory function in pulmonary emphysema. The treatment and prophylaxis for acute exacerbation in pulmonary emphysema should be based on these results.
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PMID:[Pathogenic bacteria isolated from the sputum of the patients with pulmonary emphysema]. 870 5

In order to determine the presence and distribution of Haemophilus influenzae in lung tissue sections, we obtained lung explants from 49 lung transplant recipients with cystic fibrosis (CF) (n = 16), chronic obstructive pulmonary disease (COPD) including emphysema (n = 16), bronchiectasis (n = 5), pulmonary hypertension (n = 9), Langerhans cell histiocytosis (n = 1), and idiopathic pulmonary fibrosis (n = 2). Analysis was done by selective culturing, immunoperoxidase (IP) staining, and by polymerase chain reaction (PCR). H. influenzae was cultured from specimens of the lung explants from one CF and one COPD patient. IP staining of tissue sections was positive in 24 patients (10 CF patients, eight COPD patients, two bronchiectasis patients, and four patients with noninfectious pulmonary diseases). IP-positive tissue sections were PCR-positive, and IP-negative sections were PCR-negative. H. influenzae was more frequently detected in tissue sections of lung explants from CF and COPD patients than from patients with bronchiectasis or noninfectious pulmonary diseases. H. influenzae was diffusely present in the epithelium, the submucosa of the bronchi, the bronchioles, the interstitium, and the alveolar epithelium. H. influenzae was localized extracellularly alone and in bacterial clusters, and was also associated with macrophages in CF patients. The results of this study demonstrate that H. influenzae is often present in the lungs of patients with end-stage pulmonary disease, especially CF and COPD patients. H. influenzae is diffusely present in the respiratory epithelium and subepithelial layers of the lungs of these patients.
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PMID:Haemophilus influenzae in lung explants of patients with end-stage pulmonary disease. 951 16

Chronic obstructive pulmonary disease (COPD) comprises a spectrum of conditions including chronic bronchitis, emphysema, asthma, and bronchiectasis. It has a prevalence in the United States of 5.1% to 5.4% in the middle-aged to elderly population, with a lower rate in nonsmoking individuals. Moreover, COPD is complicated by frequent and recurring acute exacerbations of chronic bronchitis (AECB). Overall, COPD represents the fourth leading cause of mortality in the United States and is the second leading cause of work disability. This condition is also associated with high morbidity and health care expenditures. Despite the controversy over the need to prescribe antibiotics for patients with AECB, high-risk patients have been identified who will benefit from this therapy.These include, patients with a history of repeated infections (>4 per year), comorbid illnesses (such as diabetes, asthma, coronary heart disease), or marked airway obstruction. Furthermore, a bacterial cause is shown in approximately 50% of AECB episodes, and primarily includes Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae. Additionally, resistance among community-acquired respiratory pathogens in the United States has risen dramatically, with beta-lactamase production evident in 40% of H. influenzae and greater than 95% of M. catarrhalis isolates, and with approximately 10% of pneumococci highly resistant to penicillin and simultaneously resistant to macrolide antibiotics. The criteria used to make choices for antibiotic use in patients with AECB should include knowledge of the frequencies of pathogen resistance and patients' clinical characteristics. An effective antibiotic, however, must be able to rapidly resolve the acute infection with the least patient morbidity and need for hospitalization. Although there remains controversy as to when to initiate antibiotic therapy in patients with AECB, several guidelines have been published.
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PMID:Antibiotic therapy in acute exacerbations of chronic bronchitis. 1105 24

Nontypeable Haemophilus influenzae (NTHi) commonly causes otitis media, chronic bronchitis in emphysema, and early airway infections in cystic fibrosis. Long-term, low-dose azithromycin has been shown to improve clinical outcomes in chronic lung diseases, although the mechanism of action remains unclear. The inhibition of bacterial biofilms by azithromycin has been postulated to be one mechanism mediating these effects. We hypothesized that subinhibitory concentrations of azithromycin would affect NTHi biofilm formation. Laboratory strains of NTHi expressing green fluorescent protein and azithromycin-resistant clinical isolates were grown in flow-cell and static-culture biofilm models. Using a range of concentrations of azithromycin and gentamicin, we measured the degree to which these antibiotics inhibited biofilm formation and persistence. Large biofilms formed over 2 to 4 days in a flow cell, displaying complex structures, including towers and channels. Subinhibitory concentrations of azithromycin significantly decreased biomass and maximal thickness in both forming and established NTHi biofilms. In contrast, subinhibitory concentrations of gentamicin had no effect on biofilm formation. Furthermore, established NTHi biofilms became resistant to gentamicin at concentrations far above the MIC. Biofilm formation of highly resistant clinical NTHi isolates (azithromycin MIC of > 64 microg/ml) was similarly decreased at subinhibitory azithromycin concentrations. Clinically obtainable azithromycin concentrations inhibited biofilms in all but the most highly resistant isolates. These data show that subinhibitory concentrations of azithromycin have antibiofilm properties, provide mechanistic insights, and supply an additional rationale for the use of azithromycin in chronic biofilm infections involving H. influenzae.
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PMID:Subinhibitory concentrations of azithromycin decrease nontypeable Haemophilus influenzae biofilm formation and Diminish established biofilms. 1795 87


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