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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary infections are a significant cause of morbidity after liver transplantation; Gram-negative bacilli, cytomegalovirus, and Pneumocystis carinii were the usual pulmonary pathogens in the earlier studies in liver transplant recipients receiving cyclosporine. We prospectively assessed the impact of pulmonary infection in 101 consecutive liver transplant recipients receiving the new immunosuppressive agent tacrolimus (FK506). Fifteen percent (15/101) of the patients had 19 episodes of pneumonia; 58% (11/19) of the pneumonias were bacterial, 37% (7/19) were fungal, and 5% (1/19) were protozoal (Toxoplasma gondii). Twenty-seven percent of the bacterial pneumonias were due to Legionella. None of the patients had cytomegalovirus or P carinii pneumonia. Seven percent (7/10) of the study patients had fungal pneumonitis; 4% had invasive aspergillosis and 3% had cryptococcosis. Mortality was significantly higher (53%, 8/15) for patients with pneumonia than for patients without pneumonia (10%, 9/86, P = 0.0004). Only fungal pneumonias were the direct cause of death; 63% (5/8) of the deaths were in patients with fungal pneumonitis. Our data suggest a changing pattern of microbial etiologies of pneumonitis in the era of modern immunosuppressive agents. We show that P carinii pneumonia and cytomegalovirus can be effectively curtailed with appropriate prophylaxis. Fungal infections, on the contrary, not only constituted a major proportion of the pneumonia, but also carried the highest pneumonia-associated mortality. Legionella infections can be overlooked unless specialized laboratory methodology (cultured on selective media, urinary antigen) are applied routinely on all cases of pneumonia. We recommend routine culture on the water supply for Legionella in all transplant centers.
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PMID:Pulmonary infections in liver transplant recipients receiving tacrolimus. Changing pattern of microbial etiologies. 861 Mar 49

Pulmonary infection with cytomegalovirus (CMV) is a well recognised complication of AIDS. It is often possible to detect CMV-infected cells in bronchoalveolar lavage (BAL) specimens with monoclonal antibodies, but the clinical significance of their presence remains unclear. To investigate this, 24 AIDS patients were tested for CMV antigenaemia and viraemia, in addition to CMV detection in BAL. CMV was detected in the BAL of nine patients (38%), five with clinical and laboratory evidence of pulmonary infection and four without pulmonary involvement. Blood samples positive for CMV antigen were observed in two patients with CMV-positive BAL specimens and, in both cases, antigenaemia resolved without therapy. No case of viraemia was detected. Pneumocystis carinii was detected concomitantly with CMV in the BAL of four of the patients with pulmonary involvement and in one without signs of pulmonary infection. These data suggest that CMV-positive BAL results are of limited significance in the diagnosis of CMV pneumonia in AIDS patients, unless associated with high levels of antigenaemia or viraemia and compatible clinical symptoms.
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PMID:Cytomegalovirus in bronchoalveolar lavage specimens from patients with AIDS: comparison with antigenaemia and viraemia. 868 52

Increasing numbers of children with human immunodeficiency virus (HIV) infection continue to be seen in the United States. Pulmonary infections constitute a major cause of morbidity and mortality in these children Pneumoncystis carinii pneumonia, pulmonary lymphoid hyperplasia/lymphoid interstitial pneumonitis, and bacterial pneumonias, all described in high frequency in the earliest cases of pediatric acquired immunodeficiency syndrome, remain the pulmonary diseases confronted most often. Other pathogens, such as Mycobacterium tuberculosis and respiratory virus infections are now being identified in increasing numbers in HIV-infected children. Advances in our understanding of these disease processes and their clinical manifestations have allowed development of a systematic approaches to the common problem of the HIV-infected child with fever, tachypnea, and hypoxemia and an abnormal chest radiograph. These approaches, coupled with improvements in available treatment options, have led to earlier diagnosis and improved survival. Prophylaxis strategies have been developed for the most serious pulmonary infections, especially P carinii pneumonia. However, lack of identification of infants and children at risk of HIV infection has limited their effectiveness. Pulmonary infections in HIV-infected children continue to take a high toll with regard to morbidity and mortality. Only with continued advances in primary therapy to slow progression of the underlying immunodeficiency and widespread use of available prophylactic guidelines will these be reduced.
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PMID:Human immunodeficiency-virus-related pulmonary infections in children. 888 75

Pulmonary infections caused by several types of viruses and other miscellaneous organisms may cause disease in HIV infection. Evidence suggests that pulmonary conditions may result from infections of the lung by HIV itself. Other viruses, most commonly cytomegalovirus, may be primary perpetrators of pneumonitis or may contribute to diseases caused by coexisting infections. Although diagnosis and assessment of the clinical significance of these infections may be difficult, their recognition is of practical importance because potentially effective therapeutic agents are available for several of them. Miscellaneous infections such as pulmonary toxoplasmosis and pertussis are other uncommon but potentially treatable complications of HIV disease.
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PMID:Viruses and other miscellaneous organisms. 901 75

Pulmonary disease was studied in four patients with ataxia-telangiectasia. Immunodeficiency was characterized by lymphopaenia, hypo-gammaglobulinaemia and decreased T-cell response to phytohaemagglutinin stimulation in mixed lymphocyte cultures. All four patients died from respiratory failure. Autopsy revealed that all four patients suffered from bronchiolitis obliterans in all lobes. Immunohistochemical examination demonstrated expression of MHC class II antigens on bronchiolar epithelium. Pulmonary infections in ataxia-telangiectasia patients included a case of mycoplasma pneumonia, one of cytomegalovirus pneumonia and one of Pseudomonas aeruginosa infection. The aetiology and immunological background of bronchiolitis obliterans are discussed. Bronchiolitis obliterans is a characteristic finding in ataxia-telangiectasia and may be due to the underlying immune deficit.
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PMID:Bronchiolitis obliterans in ataxia-telangiectasia. 908 16

Pulmonary disease is a common presenting feature and complication of T-cell immunodeficiency. We retrospectively reviewed 15 children with severe combined immune deficiency (SCID) and 19 children with DiGeorge syndrome at the time of their first presentation to the Royal Children's Hospital in the 15-year period from 1981 to 1995. In children with SCID, pulmonary disease was a common (67%) presenting feature and the organisms identified were Pneumocystis carinii (PCP) (n = 7), bacteria (n = 4), viruses (n = 3), and a fungus (n = 1). Late pulmonary complications included lower respiratory tract infections, bronchiolitis obliterans, and lymphointerstitial pneumonitis. Pulmonary infections were common (17 occasions) and the organisms identified were bacteria (n = 7), viruses (n = 6), fungi (n = 3), and Mycobacterium tuberculosis (n = 1). Pulmonary complications were responsible for 5 of 9 deaths. PCP was not identified as a late complication in any child, presumably as a result of effective prophylactic therapy. Although pulmonary disease was not a major presenting feature in children with DiGeorge syndrome, pulmonary complications were common. These included recurrent bacterial and viral infections and bronchomalacia, which complicated management and predisposed to morbidity and mortality, even in those without a T-cell defect. We conclude that pulmonary disease is a common manifestation in children with SCID and DiGeorge syndrome.
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PMID:Pulmonary diseases in children with severe combined immune deficiency and DiGeorge syndrome. 940 65

Pulmonary infections with formation of bacterial granules are rare. We reviewed the clinical and pathologic data from 18 cases diagnosed using surgical specimens in our department during the last 10 years. Three clinicopathologic forms were observed: endobronchial infections complicating tuberculous sequelae or bronchiectases (n = 7), tumor-like lesions (n = 8), and diffuse pneumonia (n = 3). The two latter forms contrasted with the former by a male predominance, association with general debilitating conditions and inflammatory syndrome, and pathologically by smaller granules often located in parenchymal abscesses or excavations. The pathologic examination of the bacteria forming the granules permitted the diagnoses of actinomycosis (n = 10), botryomycosis (n = 7), or nocardiosis (n = 1). The latter case corresponded to an endobronchial infection. Both actinomycosis and botryomycosis were encountered in every clinicopathologic form. At present, pulmonary actinomycosis and related infections rarely seems to present with chest wall invasion. On the contrary, purely endobronchial forms represented a large proportion of our cases. Cultures are often difficult and the clinical appearance is not specific. However, pathologic examination with special stains must indicate the type of involved microorganism.
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PMID:Actinomycosis and other bronchopulmonary infections with bacterial granules. 1019 85

A 72 year old female with rheumatoid arthritis was treated with methotrexate for nine months. Four days before admission she complained of dyspnea NYHA III. Chest-X-ray revealed diffuse interstitial pneumopathy. Pulmonary infection was excluded by several microbiological samples. A pulmonary manifestation of rheumatoid arthritis is usually more chronic. Methotrexate-induced pneumonitis remained the most probable diagnosis. We halted methotrexate and initiated therapy with glucocorticoids. This treatment led to rapid clinical improvement and complete resolution of radiological changes.
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PMID:[Methotrexate pneumonitis]. 1023 32

Pulmonary infection due to Pseudomonas aeruginosa has emerged as a leading cause of mortality. A vigorous host response is required to effectively clear the organisms from the lungs. This host defense is dependent on the recruitment and activation of neutrophils and macrophages. A family of chemotactic cytokines (chemokines) has been shown to participate in this protective response. In this study, we assessed the role of the ELR(+) (glutamic acid-leucine-arginine motif positive) CXC chemokines and their CXC chemokine receptor (CXCR2) in lung antibacterial host defense. The intratracheal administration of Pseudomonas to mice resulted in the time-dependent influx of neutrophils to the lung, peaking at 12 to 24 h after inoculation. The influx of neutrophils was associated with a similar time-dependent expression of the ELR(+) CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolysaccharide-induced CXC chemokine (LIX). Selective neutralization of MIP-2 or KC resulted in modest changes in neutrophil influx but no change in bacterial clearance or survival. However, neutralization of CXCR2 resulted in a striking increase in mortality, which was associated with a marked decrease in neutrophil recruitment and bacterial clearance. Conversely, the site-specific transgenic expression of KC resulted in enhanced clearance of bacteria after Pseudomonas challenge. This study indicates that ELR(+) CXC chemokines are critical mediators of neutrophil-mediated host defense in Pseudomonas pneumonia.
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PMID:CXC chemokine receptor CXCR2 is essential for protective innate host response in murine Pseudomonas aeruginosa pneumonia. 1085 47

Pulmonary infection leading to pneumonia is a significant cause of morbidity and mortality worldwide. Airborne particles have been associated with pneumonia through epidemiological research, but the mechanisms by which particles affect the incidence of pneumonia are not well established. The purpose of this review is to examine the potential of animal models to improve our understanding of the mechanisms by which inhaled particles might affect the incidence and resolution of pulmonary infection. The pathogenesis of pneumonia in most animal models differs from that in humans because humans frequently have underlying diseases that predispose them to infection with relatively low doses of pathogens. Normal, healthy animals lack the underlying pathology often found in humans and clear bacteria and viruses rapidly from their lungs. To overcome this, animals are administered large inocula of pathogens, are treated with agents that cause mucosal lesions, or are treated with immunosuppressive drugs. Alternatively, pathogenic bacteria are protected from phagocytosis by encasing them in agar. No one animal model will replicate a human disease in its entirety, and the choice of model depends upon how well the animal infection mimics the particular human response being examined. The advantages and disadvantages of animal models in current use for bacterial and viral infections important in the etiology of human pneumonia are reviewed in detail. Considerable data indicate that prior exposure to particles compromises the ability of experimental animals to resolve a subsequent infection. In addition, information is available on the effects of particle exposure on various portions of respiratory defense including phagocytic function, ciliary movement, inflammation, and antibody response in the absence of infection. In contrast, little research to date has examined the consequences of particle exposure on the host defense mechanisms of animals already infected or on their ability to resolve their infection.
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PMID:Animal models of pulmonary infection in the compromised host: potential usefulness for studying health effects of inhaled particles. 1098 65


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