Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fucosidosis is caused by a deficiency of the lysosomal enzyme alpha-L-fucosidase (ALF) leading to an accumulation of glycoproteins in a variety of cells. Infants and young children with this disorder are prone to recurrent sinus and pulmonary infections and often die of pneumonia. We studied the mucociliary and systemic immune function in a 6 year old girl with fucosidosis and recurrent respiratory infections. All measurements of systemic immune function were normal. Sweat chloride was normal when measured on angiokeratotic skin but was greater than 65 mg/L on uninvolved areas. During the placement of tympanic ventilation tubes, tracheal mucus was gently aspirated and a mucosal biopsy was taken. Tracheal mucus transport was not measured. The biopsy material was examined under phase contrast microscopy and revealed ciliated cells with apparently normal beating. TEM of these cells showed a characteristic pattern of vacuoles in the cytoplasm as described in other tissues from patients with fucosidosis. Ciliary ultrastructure was normal. Mucus viscoelasticity was measured in a magnetic microrheometer. The loss tangent was 2 SD above the mean for normal mucus and mechanical impedance was about 2 SD below the mean. These changes are similar in direction but double in magnitude to what has been described with methacholine administration in dogs. The high compliance of the mucus may be due to incomplete assembly of mucus glycoprotein or to decreased secretion of glycoproteins in respiratory secretions. This leads to mucus that is abnormally watery and thus difficult to clear from the airway.
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PMID:Recurrent respiratory infections in a child with fucosidosis: is the mucus too thin for effective transport? 189 42

The detection of TATC may inform about the presence of thrombin generation and, and hence of a pre-thrombotic status. An ELISA test (Enzygnst TAT) has been developed here in order to evaluate the predictive role played by TATC, and it was applied on 182 patients who distributed in 14 with cirrhosis of the liver, 11 with sepsis, 17 with chronic arterial insufficiency, 55 with neoplasms, 9 with thrombosis, 15 in postoperative period, 15 with pneumonia, 16 with disseminated intravascular coagulation (DIC), 14 with multiple injuries and 16 with pancreatitis. TATC levels were significantly increased in all groups with regard to the control group. Patients with thrombosis, sepsis, multiple injuries, DIC and in the postoperative period showed especially high TATC figures. No correlation between TATC and fibrinogen, platelet count, activated partial thromboplastin time or prothrombin complex assay was found in the post-operative patient-group. It was concluded that TATC are a good indicator of hypercoagulability.
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PMID:[Detection of thrombin-antithrombin complexes in hypercoagulability conditions. Analysis of 182 cases]. 229 Nov 47

113 lung specimens from rats and mice were observed under both LM and TEM, after inhalation of gonidiospores of Beauveria bassiana for 18 months 78.8% of the 113 cases developed chronic interstitial pneumonia (IP). There were desquamative pneumonitis mainly with macrophage; granuloma with multinucleate giant cells or fibrosis, and localized pulmonary edema. These lesions were firstly described to be caused by the spores here. It was considered that IF lesions might be related to types III, IV hypersensitivity reaction. The authors emphasized that these lesions might be similar to those observed in farmer's lung or extrinsic allergic alveolitis (EAA).
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PMID:[Experimental study on farmer's lung-like lesions caused by Beauveria bassiana]. 258 46

Piperacillin is one of the new generation of semisynthetic penicillins which can be administered intravenously or intramuscularly. It has a broad spectrum of activity against Gram-positive and Gram-negative aerobic and anaerobic bacteria. Although piperacillin has shown greater activity against beta-lactamase-producing organisms than the other penicillins, it is hydrolysed by the plasmid-mediated beta-lactamases (TEM-1). Activity against Pseudomonas aeruginosa is better than that of ticarcillin, carbenicillin and mezlocillin. Although only limited controlled studies have been reported, in those which have been conducted and in a larger number of open studies piperacillin was effective in the treatment of complicated urinary tract infections and lower respiratory tract infections, particularly pneumonia, caused by Gram-negative bacilli. Favourable clinical results have been obtained in patients with infections caused by mixed aerobic/anaerobic organisms (such as intra-abdominal infections) but the relatively average in vitro activity of piperacillin against Bacteroides fragilis may not indicate its usage in situations where this organism is the suspected or proven pathogen. Piperacillin in combination with an aminoglycoside or a 'third generation' cephalosporin gave encouraging results in the treatment of infections in immunocompromised patients, whilst its penetration into the diseased central nervous system and lack of toxicity indicate a potential value in the treatment of neonatal Gram-negative bacillary meningitis, particularly where the causative organism is Pseudomonas aeruginosa. Whether piperacillin alone is appropriate therapy for conditions usually treated with aminoglycosides (other than pseudomonal infections) needs additional clarification, but if established as equally effective in such conditions it has the advantages of its apparent lack of serious adverse effects and freedom from the need to undertake plasma concentration monitoring. These advantages would not, however, apply when considering one of the new (third generation) cephalosporins as alternative therapy in non-pseudomonal infections. Generally, however, it is still considered necessary to treat serious and complicated infections with combination therapy, either a cephalosporin, or in cases of resistance to P. aeruginosa an aminoglycoside.
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PMID:Piperacillin. A review of its antibacterial activity, pharmacokinetic properties and therapeutic use. 639 88

Using TAT and ELISA, 50 samples of pleural effusion and sera from patients infected with non-Legionella pneumophila were detected for antibodies against Legionella pneumophila serogroups 1 and 6, respectively. The average titre and upper limit value (99%, mean + 2.326S) calculated. In addition, a pleural effusion and a serum from a patient with Legionnaire's pneumonia were also detected by TAT and ELISA. The result showed that the titre of this antibody in his pleural effusion was not only over the upper limit, but also higher than that in his serum.
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PMID:[Detection of antibodies against Legionella pneumophila from pleural effusion--a case report of Legionnaire's pneumonia with pleural effusion]. 783 96

Legionellosis is an important cause of severe pneumonia in the community. Inadequate therapy will lead to respiratory distress syndrome, disseminated intravascular coagulation (DIC) and finally fatal multiple organ failure. We encountered a rare case in which early manifestation included septic shock and DIC complicated by acute myocardial infarction (AMI) suspected to be derived from Legionnaires' disease. A 54-year-old healthy female complained of lumbago, high fever and dry cough 10 days after visiting a hot spring spa. She was emmergently admitted due to shock. Physical examination demonstrated hypotension, high fever, course creakle in the right lower lung. Hepatosplenomegaly, lymphadenopathy and eruption were not found. WBC count was 34600/microliters with nuclear shift. CRP elevated. FDP, D dimer and TAT also elevated CPK elevated with dominance of the MB isozyme. Chest roentogenography revealed congestive heart failure, pleural effusion and obscure pneumonic shadow and EKG showed ST segment elevation in leads I, II, III, aVF, V4, V5, and V6. The patient was diagnosed as having septic shock, DIC and AMI. She was treated with gabexate mesilate, high dose methyl prednisolone and dopamine hydrochloride as well as piperacillin, meropenem, isepamycin and fluconzaole. Despite intensive care, the blood pressure fell again and pneumonia had progressed on the 8th hospital day. These antibiotics appeared to be ineffective. Erythromycin was then administered and a dramatic effect. was obtained as the patient recovered. Serum titer of Legionella pneumophila (serogroup 1) rose to 128-fold 2 weeks after the onset. Other serum titers such as Chlamydia psittaci, Rickettsia, Mycoplasma were all negative. Cultures obtained from the sputum, throat swab, urine and blood did not yield any microorganisms. Although the diagnosis could not be confirmed because the titer did not elevate over 256-fold of 4-fold within 2 weeks after the onset, Legionella infection was highly suspected from the clinical features. This is a rare case in which septic shock and DIC with AMI preceded pulmonary symptoms in a non-immunocompromised patient.
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PMID:[Early manifestation of septic shock and disseminated intravascular coagulation complicated by acute myocardial infarction in a patient suspected of having Legionnaires' disease]. 958 3

A 60-year-old woman was admitted in June 1993, because of anemia and purpura and given a diagnosis of acute myelogenous leukemia with trilineage dysplasia. She entered partial remission (PR) after three courses of low-dose Ara-C and G-CSF, but never reached complete remission (CR) in spite of additional chemotherapy. In October 1994, the number of leukocytes, myeloblasts, and erythroblasts in the patient's peripheral blood increased, and her clinical condition deteriorated. The disease was resistant to other therapy. The patient had pneumonia and died of septic shock in December 1994. A chromosomal analysis performed on admission showed 46,XX,t(3;5) (q21;q31) [9/9]. As an additional chromosomal abnormality, deletion of the X chromosome was observed in January, 1994. Analysis of the p53 gene by the polymerase chain reaction-single strand conformation polymorphism method showed one base transposition, from TAT to TGT (Tyr to Cys), at codon 220 of exon 6. Karyotype evolution and p53 gene mutation were observed during the disease course and may have been related to progression of the disease.
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PMID:[t(3;5) (q21;q31) chromosomal abnormality in a patient with acute myelogenous leukemia with trilineage myelodysplasia]. 979 99

Respiratory infections are the most frequent reason for primary health care consultation. The main causes of respiratory tract infections in children are viruses and the most common types are upper respiratory tract infections: common cold, pharyngitis, otitis media and sinusitis. Pneumonia is much more serious. As well as viruses, bacteria are often involved in respiratory tract infections. Three bacterial species are most commonly isolated: Streptococcus pneumoniae, non-encapsulated Haemophilus influenzae and Moraxella (Branhamella) catarrhalis. The most common bacterial cause of pharyngitis is Streptococcus pyogenes. Bacteria isolated from community-acquired infection usually are sensitive to the majority of suitable drugs, but during the past two decades, significant antibiotic resistance has emerged. Resistance to penicillins has spread among H. influenzae and S. pneumoniae. The mechanism of penicillin resistance in H. influenzae is mainly by production of beta-lactamases TEM-1 and ROB-1, whereas in S. pneumoniae resistance is an effect of the changes in penicillin binding proteins. Among respiratory pathogens, resistance to tetracyclines, macrolides, trimethoprim-sulphamethoxazole and fluoroquinolones has also appeared. Several mechanisms depending on changes in target, active efflux and modifying enzymes are involved.
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PMID:Epidemiological aspects of antibiotic resistance in respiratory pathogens. 1173 35

TEM- or SHV-type extended-spectrum beta-lactamases (ESBLs) are of clinical concern in Europe and the United States, whereas bacterial strains producing such types of ESBLs have not been reported in Japan. We report here two cases of infection due to Klebsiella pneumoniae resistant to extended-spectrum cephalosporins in Japan. A ceftadizime-resistant K. pneumoniae strain (minimum inhibitory concentration; 32 &mgr;g/ml) was isolated transiently from the sputum of an 87-year-old woman with acute myocardial infarction and pneumonia (patient 1). Ceftadizime-susceptible and -resistant (minimum inhibitory concentration; >/=8 &mgr;g/ml) K. pneumoniae strains were isolated over a month from the blood, ascites, and feces of a 44-year-old man after bone marrow transplantation for acute lymphoblastic leukemia (patient 2); this patient died of K. pneumoniae sepsis and peritonitis followed by multiple organ failure. These isolates produced penicillinase, which was inhibited by clavulanic acid. A polymerase chain reaction (PCR) study showed that both isolates carried the SHV or LEN genes, but not the TEM, Toho-1, and IMP-1 genes. The pulsed-field gel electrophoresis profile of the strain isolated from patient 1 was genetically distinguishable from the profiles of the strains isolated from patient 2. It appeared that mutation of the beta-lactamase gene may have occurred in the body of patient 2, since the genotypes of the ceftadizime-susceptible and -resistant isolates from this patient were identical. Another 12 strains of K. pneumoniae, isolated from other patients in the same wards during the period in which the K. pneumoniae strains were isolated from patients 1 and 2, did not produce ESBLs and showed different genotypes. The results suggest that these isolates of resistant K. pneumoniae did not spread by cross transmission in the hospital and that the two cases were sporadic. Surveillance of these types of resistant bacteria is necessary, since they may well be present in other hospitals in Japan. Although the organisms are suspected to produce SHV-type ESBLs or LEN-1 variant beta-lactamases, further studies are necessary to specify the resistance genes.
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PMID:Two sporadic cases of infections due to Klebsiella pneumoniae resistant to expanded-spectrum cephalosporins in Japan. 1181 Apr 97

Enterobacter cloacae has been associated with several outbreaks, usually involving strains that overproduce chromosomal beta-lactamase or, uncommonly, strains expressing extended-spectrum beta-lactamases (ESBL). Only sporadic cases of ESBL-producing E. cloacae have been identified in our hospital in recent years. We describe the epidemiology and clinical and microbiological characteristics of an outbreak caused by ESBL-producing E. cloacae in a cardiothoracic intensive care unit (CT-ICU). Prospective surveillance of patients with infection or colonization by ESBL-producing E. cloacae among patients admitted to the CT-ICU was performed during the outbreak. Production of ESBL was determined by decreased susceptibility to expanded-spectrum cephalosporins and a positive double-disk test result. Clone relatedness was determined by pulsed-field gel electrophoresis (PFGE). From July to September 2005, seven patients in the CT-ICU with ESBL-producing E. cloacae were identified (four males; median age, 73 years; range, 45 to 76 years); six patients had cardiac surgery. Four patients developed infections; three had primary bacteremia, one had ventilator-associated pneumonia, and one had tracheobronchitis. ESBL-producing E. cloacae showed resistance to quinolones and aminoglycosides. PFGE revealed two patterns. Five isolates belonged to clone A; two carried a single ESBL (pI 8.2 and a positive PCR result for the SHV type), and three carried two ESBLs (pIs 8.1 and 8.2 and positive PCR results for the SHV and CTX-M-9 types). Isolates belonging to clone B carried a single ESBL (pI 5.4 and a positive PCR result for the TEM type). Review of antibiotic consumption showed increased use of cefepime and quinolones during June and July 2005. The outbreak was stopped by the implementation of barrier measures and cephalosporin restriction. ESBL production could be increasingly common in nosocomial pathogens other than Escherichia coli or Klebsiella pneumoniae.
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PMID:Nosocomial outbreak due to extended-spectrum-beta-lactamase- producing Enterobacter cloacae in a cardiothoracic intensive care unit. 1758 32


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