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)

Two patients had pulmonary infections with atypical mycobacteria superimposed on mineral oil pneumonia. In both cases, long-standing laxative use and neurological disorders led to development of the lipid pneumonia. The pathogenicity of the rapidly growing mycobacteria causing infection in the two patients is apparently enhanced by the presence of mineral oil, a relationship supported by experimental studies. The clinical diagnosis of both atypical mycobacterial infection and mineral oil pneumonia may be difficult, but the presence of one should suggest the possibility of occurrence of the other.
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PMID:Atypical mycobacterial infection complicating mineral oil pneumonia. 67 64

The pulmonary lesions were studied in 24 autopsy cases of Japanese patients with AIDS. The major pathological findings were opportunistic infections, which were the major clinical symptoms in some patients. The pathogens identified were as follows; Pneumocystis carinii (PC) in 10, cytomegalovirus (CMV) in 14, atypical mycobacterium in 5, cryptococcus in 2, candida in 2, and nocardia in 1. PC pneumonia was prominent in 8 cases and was the cause of death. In such patients, the lung were heavy and appeared parenchymatous. Histological examination revealed numerous protozoa in the foamy material in the alveolar spaces, associated with swelling of the alveolar lining cells and edematous thickening of the alveolar septa. In some cases, only hyaline membrane formation was prominent without foamy material in the alveolar spaces. Immunostaining with anti-PC monoclonal antibody or in-situ hybridization with oligopeptide demonstrated pathogens in the hyaline membranes. Many cases with PC pneumonia had concomitant opportunistic infections such as CMV, Herpes simplex virus, and atypical mycobacterium. Extrapulmonary infection of PC was seen in only one case. CMV infection was found in 14 cases; 7 had innumerable inclusion bodies, and in some cases the lesions were most prominent around the bronchioles. Of the 5 cases of atypical mycobacterial infection, 2 were caused by M. kansaii (MK) and 3 by M. avium intracellulare (MAI). Both lesions of MK infection showed necrosis and cavitation. One of three cases of MAI infection showed cavitation. Around the cavitary lesions, numerous cytomegalic inclusion bodies were identified in the mesenchymal cells, which may have been the cause of necrosis and cavitation of the lesions. MAI infection was systemic and pronounced in the lymph nodes, spleen, and intestinal mucosa. Neoplastic lesions comprised 2 cases of Kaposi's sarcoma and 4 of extranodal non-Hodgkin lymphoma in other organs. Lung involvement was seen in only one case of Kaposi's sarcoma although very small in size. The lesion was situated along the pulmonary vein and appeared hemorrhagic macroscopically. Pulmonary lesions in AIDS are complicated, and many of opportunistic pathogens were identified in single patients.
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PMID:[Pulmonary lesions of acquired immunodeficiency syndrome--analysis of 24 Japanese autopsy cases with AIDS]. 163 37

Chronic eosinophilic pneumonia is a relatively uncommon condition associated with fever, malaise, weight loss, dyspnea, and hypoxia. The chest radiograph displays peripheral air-space consolidation, often referred to as the negative of pulmonary edema. The characteristic pathologic findings in the lung include marked accumulation of eosinophils in the alveolar spaces, often with the formation of eosinophilic abscesses. We report the history and pathologic findings in a patient who fit the clinical, radiologic, and pathologic features of chronic eosinophilic pneumonia, but who went on to develop cavitary atypical mycobacterial infection and died. We believe that this case represents an unusual response to an atypical mycobacterial infection.
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PMID:Eosinophilic pneumonia and atypical mycobacterial infection. 683 57

Middle lobe syndrome (MLS) is an uncommon lung disorder involving the right middle lobe and/or lingula and is characterized by a spectrum of clinical and pathological lesions ranging from recurrent atelectasis or pneumonias to bronchiectasis. Despite several series reporting the clinical features of MLS, histopathological descriptions are rare. We reviewed the clinical characteristics and pathological findings in 21 patients with MLS who underwent surgical resections. Six male and 15 female patients between the ages of 5 and 80 years (mean, 47 years) were studied. All patients were symptomatic and complained of chronic cough (8), hemoptysis (6), chest pain (4), dyspnea (3), or fever (2). The right middle lobe was involved in 11 patients, the lingula in four patients, and both right middle lobe and lingula in six patients. Chest radiographs, bronchograms, and/or computed tomography scans were available for review in 19 patients and showed consolidation (8), bronchiectasis (9), patchy infiltrates (5), and atelectasis (4) in various combinations. Pathological findings included bronchiectasis in 10 patients, chronic bronchitis/bronchiolitis with lymphoid hyperplasia in seven, patchy organizing pneumonia in six, atelectasis in five, granulomatous inflammation in five, and abscess formation in four. Three patients with granulomatous inflammation had associated atypical mycobacterial infection. Broncholithiasis was confirmed by pathological examination in one patient. No pathological cause for bronchial obstruction was identified in the remaining 20 patients, although one was thought to have had broncholithiasis on the basis of preoperative bronchoscopy. The presence of bronchiectasis, bronchitis or bronchiolitis, organizing pneumonia, or atelectasis in specimens from the right middle lobe or of lingula in the absence of an identifiable cause of bronchial obstruction should suggest a diagnosis of MLS.
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PMID:Middle lobe syndrome: a clinicopathological study of 21 patients. 789 Feb 82

We report the case of a nonimmunocompromised female patient, who developed exogenous lipoid pneumonia with Mycobacterium fortuitum infection at diagnosis, later followed by Aspergillus fumigatus infection. The association of exogenous lipoid pneumonia with atypical mycobacterial infection is uncommon but well-recognized, but, to our knowledge, association with A. fumigatus infection has not previously been reported.
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PMID:Exogenous lipoid pneumonia complicated by Mycobacterium fortuitum and Aspergillus fumigatus infections. 883 51

The T cell-derived macrophage-activating lymphokine, interferon-gamma (IFN-gamma), is the most broadly acting antimicrobial-inducing and host defense-enhancing cytokine thus far identified in experimental models of infectious diseases. The activity induced by IFN-gamma encompasses all classes of non-viral pathogens including intracellular and extracellular parasites, fungi and bacteria. In man, treatment with immuno-enhancing doses of IFN-gamma is safe, well-tolerated and stimulates the antimicrobial mechanisms of blood monocytes, circulating neutrophils and tissue macrophages. Aerosol administration activates alveolar macrophages in a compartmentalized fashion. Monocytes from IFN-gamma-treated patients with cancer, leprosy, and AIDS all respond with the activated phenotype, and suppressed monocyte HLA-DR expression in trauma patients can be up-regulated by IFN-gamma therapy. Thus far, IFN-gamma has been recognized as effective in the prophylaxis of chronic granulomatous disease and as adjunctive treatment in at least one systemic intracellular infection, visceral leishmaniasis. Additional trials suggest beneficial effects as prophylaxis in trauma and as treatment in leprosy, cutaneous leishmaniasis, and HIV- and non-HIV-related disseminated atypical mycobacterial infection. IFN-gamma is also being tested as a prophylaxis in patients with burns and advanced HIV infection and as an adjunct in drug-resistant tuberculosis. Future antimicrobial applications for IFN-gamma include: a) long-term prophylaxis in T cell-deficient states, b) short-term prophylaxis in patients with a reversible host defense defect such as granulocytopenia or immune response suppression induced by trauma or burn injury, and c) adjunctive treatment along with conventional antibiotic therapy for i) nosocomial pneumonia (aerosol administration), ii) opportunistic infections in general, iii) infections which typically respond poorly to available treatment and iv) for infections which require prolonged therapy for cure. In the latter, the addition of IFN-gamma may accelerate the response to conventional therapy and permit a clinically important reduction in the duration of treatment while preserving efficacy.
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PMID:Current and future clinical applications of interferon-gamma in host antimicrobial defense. 892 89