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)

A multivariate analysis of 3334 Escherichia coli strains originating from different clinical materials revealed that 50.2% of isolates belonged to the most common 12 (O1, O2, O4, O6, O7, O8, O15, O18, O45, O75, O78, O83) out of 133 serogroups. Haemolysin (Hly) production, mannose resistant haemagglutinating activity for human erythrocytes (MRHA) and colicinogenicity (Col) were recorded in 30, 30 and 36%, respectively. Antigens K1 and K5 were present in 11% and 6.6%, respectively. Association were found among certain serotypes and virulence markers (O1, H-, H7, K1, MRHA, Col; O2, H-, Kl, Col; O4, H-, H5, MRHA, Hly; O6, H-, H1, MRHA, Hly; O6, K5, MRHA, Col; O7, H-, H4, K1, MRHA, Col; O18ac, H7, K1, Col; O18ac, H-, K5, MRHA, Hly; O78, H-, Col (V-type); O83, H-, K1, Col). There were associations among clinical specimens, age of patients, nosocomial group of diseases, serogroups and virulence markers, too (cerebrospinal fluid-CSF-O7, O18ac, O45, O83-K1-newborn meningitis; O78-ColV-meningitis, sepsis, inflammations diseases of premature babies; CFS-O6, MRHA, Hly-adult-meningitis, sepsis, urinary tract infection-UTI-, pneumonia, other inflammatory diseases; blood-O2, O4, O6, O18ac, ONT, K5, MRHA, Hly-sepsis, UTI, hepatic diseases; urine-O1, O2, O4, O6, O18ac, O75, virulence markers fall to differ among upper and lower UTI; faeces-O1, O4, O6, O18ac, O78, virulence markers rare). Associations were also found among animal pathogenicity tests, specimens, serogroups and virulence factors: highly virulent group strains (i.e. LD50 below 10(6)) belonged to serogroups O2, O6, O18ac, possessed antigen K1 (less frequently the presence of MRHA, Hly, K5) and originated mainly from CSF. With mouse lung toxicity test correlations of serogroups (O4, O6, O18ac), antigen K5, MRHA, Hly and specimens (blood) were also shown. However, association was found between the lack of virulence factors and phage insensitivity and also between K5 positivity and sensitivity to phages 16, 17, there were no correlations between serogroups and phage patterns. On the basis of the above-described associations one can find correlations among virulence markers, serotype, and nosological group of diseases. Animal pathogenicity tests give additional data in understanding the pathomechanism of diseases. Correlations between phage patterns and serogroups reveal certain epidemiological relatedness and also virulence of strains.
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PMID:Computerized complex typing of Escherichia coli strains from different clinical materials. 819 67

A 32-year-old man developed a rash on his body and extremities following acute fever of a few days duration, and also noticed pain and spontaneous tingling sensations in his lower extremities. Because severe pneumonia with dyspnea and low arterial blood oxygen concentration were found on examination, he was admitted and treated. After recovering from pneumonia in two months, he complained of abdominal symptoms, such as constipation, nausea and vomiting, spontaneous tingling sensations in the lower extremities, and orthostatic dizziness and fainting. On neurological examination, a mild to moderate muscle weakness was found in the distal muscles of both extremities. The ankle jerk was absent. Both superficial and deep sensations were moderately to severely decreased in the feet with positive Romberg's sign. Constipation and vomiting with nausea were noted. Clinical and laboratory examinations revealed marked orthostatic hypotension and hypohidrosis. Motor and sensory conduction studies indicated the presence of axonal degeneration and segmental demyelination and remyelination in the limbs nerves. CSF examination indicated that protein was 150 mg/dl and the cell count to be 18/mm3. Titer of antibody to rubella virus was significantly elevated. There were no other abnormalities to indicate the cause of motor, sensory and autonomic neuropathies. Therefore, the diagnosis of acute polyradiculoneuropathy with autonomic disturbances after rubella infection, which is rare in the literature, was made.
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PMID:[A case of acute polyradiculoneuropathy with autonomic disturbances following rubella infection]. 826 90

A 56 year old female patient treated with carbimazole for hyperthyroidism developed agranulocytosis complicated by pneumonia. She was treated by sc administration of 6 micrograms/kg rhGM-CSF for 10 days. The first neutrophils appeared in the peripheral blood on the 4th day and normal numbers are reached on the 7th day of treatment. This was accompanied by a rapid resolution of fever. The use of growth factors may be justified in cases of drug-induced agranulocytosis.
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PMID:Recovery of carbimazole-induced agranulocytosis following recombinant granulocyte-macrophage colony stimulating factor (rhGM-CSF) administration. 831 63

To investigate the mechanism of eosinophilia in patients with eosinophilic pleural effusions, we measured the activities of eosinophil colony-stimulating factor (Eo-CSF) and stimulating factor for eosinophil survival in the eosinophilic pleural fluids of six patients (two with tuberculous pleuritis, two with drug allergy, and one each with chronic eosinophilic pneumonia and pleuritis associated with rheumatoid arthritis). The number of eosinophil colonies formed by the pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of control patients with noneosinophilic pleural effusions (7.5 +/- 1.9 colonies/10(5) bone marrow cells, n = 6, versus 0.3 +/- 0.1 colonies/10(5) bone marrow cells, n = 6, P < 0.01). Similarly, eosinophil survival evaluated on day 4 of culture with pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of patients with noneosinophilic pleural effusions (83.9 +/- 9.8% versus 46.1 +/- 11.2%, P < 0.001). Both activities were inhibited mainly by anti-IL-5 antibody and partially by anti-GM-CSF antibody and anti-IL-3 antibody. Mononuclear cells obtained from eosinophilic pleural fluid released the activities of Eo-CSF and stimulating factor for eosinophil survival in vitro. These findings suggest that GM-CSF, IL-5, and IL-3 are important to eosinophil accumulation in pleural cavity as stimulators of proliferation and survival of eosinophils.
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PMID:Factors that stimulate the proliferation and survival of eosinophils in eosinophilic pleural effusion: relationship to granulocyte/macrophage colony-stimulating factor, interleukin-5, and interleukin-3. 832 45

Use of growth factors to augment hematopoietic recovery after cytotoxic therapy is a useful method for dose intensification. We wanted to evaluate the clinical and cost-effectiveness of granulocyte-macrophage colony stimulating factor (GM-CSF; Leucomax) in patients undergoing autologous bone marrow transplantation (ABMT) for Hodgkin's disease. Twenty-four patients with Hodgkin's disease were treated with high-dose chemotherapy and ABMT. Patients were then randomized in a double-blind manner to receive GM-CSF intravenously (10 micrograms/kg) over 6 h or placebo until the absolute neutrophil count (ANC) was greater than 1000/mm3 for 3 days. The study medication was stopped after 30 days. Patients treated with GM-CSF (n = 12) had shorter periods of neutropenia (median duration of an ANC of less than 1000 cells/mm3, 16 versus 27 days on placebo; p = 0.23), shorter periods of platelet-transfusion dependency (median duration, 13.5 versus 21 days on placebo; p = 0.03), shorter hospitalizations (median hospital stay, 32 versus 40.5 days on placebo; p = 0.0004). Other clinical outcomes, such as frequency and severity of toxicities, development of pneumonia or infection, in-hospital death, and response rate were similar in the two groups. Actuarial long-term disease free survival was 58% for patients treated with GM-CSF and 50% for patients who received placebo after 38 months of follow up (p = 0.6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of granulocyte-macrophage colony stimulating factor (GM-CSF) after autologous bone marrow transplantation for Hodgkin's disease. 834 51

Four weeks after an attack of pneumonia of unknown aetiology a 40-year-old woman was hospitalized because of a nonpurulent, predominantly basal meningoencephalitis and infratentorial abscesses. She had dysarthria, mild right-sided motor hemiparesis and central paresis affecting the 7th cranial nerve. An area of fluctuating resistance, about 3 cm in diameter, was noticed over the left thigh. Serology indicated inflammatory disease, but there was no immunodeficiency. The CSF showed lymphocytic pleocytosis with mild protein increase but no evidence of infective agent. As tubercular meningitis was suspected she was treated with rifampicin (300 mg i.v. twice daily), isoniazid (300 mg i.v. once daily), streptomycin (800 mg i.m. once daily), cefotaxime (2.0 g i.v. three times daily), fluconazole (200 mg i.v. once daily) and dexamethasone (16-8-8 mg i.v.). She suddenly died two days after admission, probably as the result of central regulatory failure. Generalized nocardiosis involving lung, subcutaneous tissue and brain was revealed at autopsy. Although nocardiosis occurs predominantly in patients under immunosuppression, this infection should be considered in the differential diagnosis of treatment-resistant pneumonia and meningoencephalitis without obvious predisposition.
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PMID:[Generalized nocardiosis with meningoencephalitis in a nonimmunosuppressed female patient]. 837 98

An orbitozygomatic infratemporal approach for the removal of large neoplasms involving the lateral skull base is described. This approach, involves a unilateral frontotemporal incision extended inferiorly to the neck, a lateral facial flap reflected anteriorly. Transection of the zygoma is followed by its reflection inferolaterally with the temporalis muscle. This exposure provides excellent visualization of both the intradural and extradural aspects of the anterior portion of the cavernous sinus, allowing an aggressive resection of neoplasms in this region. Experience with this procedure in the management of 15 patients is reported here. There was one postoperative death due to pneumonia and septicemia. The morbidities included wound infection, meningitis, CSF leakage and cranial nerve palsy. All the surviving patients, are living independently and have returned to their previous occupations.
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PMID:Orbitozygomatic infratemporal approach to lateral skull base tumors. 839 73

Recombinant human (rh) granulocyte-macrophage colony-stimulating factor (GM-SCF) is currently being tested in clinical trials for the treatment of acute myeloid leukemias with two main intentions: reduction of neutropenia and recruitment of leukemic blasts into cell cycle to enhance cytarabine (ara-C) mediated cytotoxicity. We report a case of a fatal spleen rupture in a patient with acute monocytic leukemia (AML M5b) who was treated according to a clinical phase I/II protocol with rh GM-CSF priming and standard induction chemotherapy TAD 9 (thioguanine/ara-C/daunorubicin). During treatment we observed rapidly rising peripheral blast counts and the development of an acute abdomen. Ultrasound examination revealed splenomegaly due to diffuse cellular infiltration and spleen rupture. The patient died 17 days later due to pneumonia and renewed spleen hemorrhage. Bone marrow progenitor assays before treatment showed exclusive growth of monocytoid blast cell colonies (CFU-L). Colony growth could be stimulated with rh GM-CSF and blocked dose-dependently by a monoclonal anti-GM-CSF antibody. CFU-L proliferation also increased after stimulation with rh interleukin-3 (rh IL-3) and supra-additively with rh granulocyte colony-stimulating factor (rh G-CSF) combined with rh GM-CSF. Furthermore, rh GM-CSF induced surface marker expression of CDw 65 and CD 11b on isolated CFU-L blasts. After short-term suspension culture, rh GM-CSF enhanced the expression of CD 29- and CD 11b-adhesion molecules on peripheral blast cells. In summary, this case represents a fatal spleen rupture occurring during rh GM-CSF priming and induction chemotherapy for acute monocytic leukemia. Although the etiology of this spleen rupture remains uncertain, in view of our data we suggest special caution, when further testing this therapy protocol in acute leukemias with monocytic subtype and high peripheral blast cell counts.
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PMID:Fatal spleen rupture during induction chemotherapy with rh GM-CSF priming for acute monocytic leukemia. Clinical case report and in vitro studies. 845 Jun 76

Infections due to nontuberculous mycobacteria (NTM) are especially common in patients with AIDS. Meningitis due to NTM, however, is rare. A search for CSF cultures positive for NTM over the past 11 years at our hospital yielded 16 cases. Of these, 15 were caused by Mycobacterium avium-intracellular (MAI), and one was caused by M fortuitum. All patients with MAI infection had widespread dissemination and at least one risk factor for AIDS. Clinical features included weight loss, altered mentation, and seizures. Analysis of cerebrospinal fluid revealed a mildly elevated leukocyte count with lymphocyte predominance and normal protein and glucose values. All direct smears were negative for acid-fast bacilli. In-hospital mortality was 67%. The patient with infection due to M fortuitum had a preexisting diagnosis of AIDS and had a right upper lobe pneumonia and headaches. Cranial CT showed an enlarged infundibulum of the pituitary gland. Results of CSF analysis were essentially normal, and direct smears were negative. He left the hospital against medical advice. Our study indicates that the finding of MAI in the CSF in patients with AIDS is associated with an in-house mortality of 67% indicating a very poor prognosis.
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PMID:Nontuberculous mycobacterial infection of the central nervous system in patients with AIDS. 850 83

Recently the incidence of infectious diseases caused by penicillin-resistant Streptococcus pneumoniae (PRSP) is increasing. Patients with meningitis caused by PRSP have been reported with high mortality especially in the field of pediatrics, and it is crucial to treat with accurate and precise choice of antibiotics. We report the first adult case of bacterial meningitis caused by PRSP in Japan. A 32-year-old male without immunological abnormalities developed acute pneumococcal meningitis. Empiric therapy with ampicillin and cefotaxime was not effective and the S. pneumonia from CSF showed resistance to multiple antibiotics such as penicillin and cefotaxime. He was treated successfully with the combination of panipenem/betamipron, vancomycin, and chloramphenicol. We assume that panipenem/betamipron is recommended to be added to empiric therapy of bacterial meningitis, considering an increasing incidence of PRSP infection.
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PMID:[An adult case of bacterial meningitis caused by penicillin-resistant Streptococcus pneumoniae]. 856 45


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