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Journal articles on the topic 'Pulmonary infection'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 April 2023

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1

Cáceres, José. "Pulmonary infection." European Journal of Radiology 51, no. 2 (August 2004): 101. http://dx.doi.org/10.1016/j.ejrad.2004.03.006.

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2

Allie, S. Rameeza, and Troy D. Randall. "Pulmonary immunity to viruses." Clinical Science 131, no. 14 (June 30, 2017): 1737–62. http://dx.doi.org/10.1042/cs20160259.

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Mucosal surfaces, such as the respiratory epithelium, are directly exposed to the external environment and therefore, are highly susceptible to viral infection. As a result, the respiratory tract has evolved a variety of innate and adaptive immune defenses in order to prevent viral infection or promote the rapid destruction of infected cells and facilitate the clearance of the infecting virus. Successful adaptive immune responses often lead to a functional state of immune memory, in which memory lymphocytes and circulating antibodies entirely prevent or lessen the severity of subsequent infections with the same virus. This is also the goal of vaccination, although it is difficult to vaccinate in a way that mimics respiratory infection. Consequently, some vaccines lead to robust systemic immune responses, but relatively poor mucosal immune responses that protect the respiratory tract. In addition, adaptive immunity is not without its drawbacks, as overly robust inflammatory responses may lead to lung damage and impair gas exchange or exacerbate other conditions, such as asthma or chronic obstructive pulmonary disease (COPD). Thus, immune responses to respiratory viral infections must be strong enough to eliminate infection, but also have mechanisms to limit damage and promote tissue repair in order to maintain pulmonary homeostasis. Here, we will discuss the components of the adaptive immune system that defend the host against respiratory viral infections.
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3

MATO, S. "Pulmonary infections in children with HIV infection." Seminars in Respiratory Infections 17, no. 1 (March 2002): 33–46. http://dx.doi.org/10.1053/srin.2002.31685.

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4

Li, Meng, and Wanqing Liao. "Pulmonary Cryptococcocal Infection." Current Respiratory Medicine Reviews 8, no. 5 (November 1, 2012): 365–69. http://dx.doi.org/10.2174/157339812803832511.

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5

Sottile, Frank D., Donald S. Prough, Anthony G. Gristina, David J. Gower, Cherri D. Hobgood, Lawrence X. Webb, Thomas J. Marrie, and J. William Costerton. "NOSOCOMIAL PULMONARY INFECTION." Critical Care Medicine 13, no. 4 (April 1985): 300. http://dx.doi.org/10.1097/00003246-198504000-00063.

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6

SOTTILE, FRANK D., THOMAS J. MARRIE, DONALD S. PROUGH, CHERRI D. HOBGOOD, DAVID J. GOWER, LAWRENCE X. WEBB, J. WILLIAM COSTERTON, and ANTHONY G. GRISTINA. "Nosocomial pulmonary infection." Critical Care Medicine 14, no. 4 (April 1986): 265–70. http://dx.doi.org/10.1097/00003246-198604000-00001.

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7

Finegold, Sydney M. "Anaerobic Pulmonary Infection." Hospital Practice 24, no. 5 (May 15, 1989): 103–33. http://dx.doi.org/10.1080/21548331.1989.11703715.

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8

Chen, Kuan-Yu, Shiann-Chin Ko, Po-Ren Hsueh, Kwen-Tay Luh, and Pan-Chyr Yang. "Pulmonary Fungal Infection." Chest 120, no. 1 (July 2001): 177–84. http://dx.doi.org/10.1378/chest.120.1.177.

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9

Lin, Jiejian, and Richard J. Hamill. "Coccidioidomycosis pulmonary infection." Current Infectious Disease Reports 3, no. 3 (June 2001): 274–78. http://dx.doi.org/10.1007/s11908-001-0030-7.

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10

Liu, Allen T., Lil J. Miedzinski, Eric Vallieres, David C. Rayner, and Dale C. Lien. "Pulmonary Alveolar Proteinosis in an AIDS Patient without Concurrent Pulmonary Infection." Canadian Respiratory Journal 2, no. 3 (1995): 183–86. http://dx.doi.org/10.1155/1995/958415.

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Patients with acquired immunodeficiency syndrome (AIDS) are potentially at increased risk for developing secondary pulmonary alveolar proteinosis because of underlying immunosuppression and frequent opportunistic lung infections. This condition. however, has been diagnosed uncommonly in these patients and, with the exception of one previously reported case. only in the presence of concurrent pulmonary infection. The case of a 35-year-old male with AIDS who was found on open lung biopsy to have pulmonary alveolar proteinosis without evidence of associated lung infection is presented.
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11

HO, HUEI-HUANG, MENG-CHIH LIN, KUANG-HUI YU, CHIN-MAN WANG, YEONG-JIAN JAN WU, and JI-YIH CHEN. "Pulmonary Tuberculosis and Disease-Related Pulmonary Apical Fibrosis in Ankylosing Spondylitis." Journal of Rheumatology 36, no. 2 (January 22, 2009): 355–60. http://dx.doi.org/10.3899/jrheum.080569.

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Objective.We investigated the etiological association and clinical characteristics of apical pulmonary fibrosis in ankylosing spondylitis (AS).Methods.We reviewed medical records of 2136 consecutive patients diagnosed with AS at a tertiary medical center. Clinical and radiographic characteristics were analyzed for evidence of apical lung fibrosis on chest radiographs.Results.Of 2136 patients with AS, 63 (2.9%) developed apical lung fibrosis, of which chronic infections were the cause in 41 and AS inflammation predisposed the fibrosis in 22 patients. Tuberculosis (TB) infection was considered to be the cause of apical lung fibrosis in 40 patients (63.5%) including 19 with bacteriologically-proven TB and 21 with chest radiographs suggestive of TB. Two were identified as having non-TB mycobacterial infection and one as Aspergillus infection. Lung cavity lesion appeared to be a crucial differentiator (p = 0.009, odds ratio 7.4, 95% CI 1.5–36.0) between TB infection and AS inflammation-induced apical fibrosis.Conclusion.Our study suggests that TB, instead of Aspergillus, is the most common pulmonary infection in patients with AS presenting with apical lung fibrosis. AS-associated apical lung fibrosis may mimic pulmonary TB infection. Thus, bacteriological survey and serial radiological followup of lung fibrocavitary lesions are critical for accurate diagnosis and treatment.
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12

Lang-Lazdunski, Loı̈c, Catherine Offredo, Françoise Le Pimpec-Barthes, Claire Danel, Antoine Dujon, and Marc Riquet. "Pulmonary resection for Mycobacterium xenopi pulmonary infection." Annals of Thoracic Surgery 72, no. 6 (December 2001): 1877–82. http://dx.doi.org/10.1016/s0003-4975(01)03245-3.

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13

Thouvenin, Maxime, Bassam Beilouny, Edgar Badell, and Nicole Guiso. "Corynebacterium ulcerans pulmonary infection." Annales de biologie clinique 74, no. 1 (January 2016): 117–20. http://dx.doi.org/10.1684/abc.2015.1120.

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14

Kim, Seog Joon, Jung Gi Im, Chang Kyu Seong, Jae Woo Song, Kyung Mo Yeon, and Man Chung Han. "Pulmonary Infection in AIDS." Journal of the Korean Radiological Society 39, no. 5 (1998): 933. http://dx.doi.org/10.3348/jkrs.1998.39.5.933.

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15

FARBER, HARRISON W. "Human Pulmonary Dirofilarial Infection." Annals of Internal Medicine 106, no. 5 (May 1, 1987): 777. http://dx.doi.org/10.7326/0003-4819-106-5-777_2.

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16

Shulman, Stanford T. "Pulmonary Infection Still Happens." Pediatric Annals 31, no. 2 (February 1, 2002): 83–84. http://dx.doi.org/10.3928/0090-4481-20020201-03.

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17

Drobniewski, Francis. "Non-pulmonary Mycobacterial Infection." Medicine 29, no. 3 (2001): 99–101. http://dx.doi.org/10.1383/medc.29.3.99.27609.

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18

Drobniewski, Francis. "Non-pulmonary mycobacterial infection." Medicine 33, no. 5 (May 2005): 109–11. http://dx.doi.org/10.1383/medc.33.5.109.64956.

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19

Edelstein, P. H. "Pulmonary Legionella tucsonensis infection." Journal of Clinical Microbiology 28, no. 1 (1990): 163. http://dx.doi.org/10.1128/jcm.28.1.163-.1990.

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20

Baker, Emma H., David M. Wood, Amanda L. Brennan, Nicholas Clark, Deborah L. Baines, and Barbara J. Philips. "Hyperglycaemia and pulmonary infection." Proceedings of the Nutrition Society 65, no. 3 (August 2006): 227–35. http://dx.doi.org/10.1079/pns2006499.

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Pathophysiological stress from acute illness causes metabolic disturbance, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycaemia. Acute hyperglycaemia is associated with increased morbidity and mortality in patients in intensive care units and patients with acute respiratory disease. The present review will consider mechanisms underlying this association. In normal lungs the glucose concentration of airway secretions is approximately 10-fold lower than that of plasma. Low airway glucose concentrations are maintained against a concentration gradient by active glucose transport. Airway glucose concentrations become elevated if normal homeostasis is disrupted by a rise in blood glucose concentrations or inflammation of the airway epithelium. Elevated airway glucose concentrations are associated with and precede increased isolation of respiratory pathogens, particularly methicillin-resistantStaphylococcus aureus, from bronchial aspirates of patients intubated on intensive care. Markers of elevated airway glucose are associated with similar patterns of respiratory infection in patients admitted with acute exacerbations of chronic obstructive pulmonary disease. Glucose at airway concentrations stimulates the growth of respiratory pathogens, over and above the effect of other nutrients. Elevated airway glucose concentrations may also worsen respiratory disease by promoting local inflammation. Hyperglycaemia may thus promote pulmonary infection, at least in part, by an effect on airway glucose concentrations. Therapeutic options, including systemic control of blood glucose and local manipulation of airway glucose homeostasis, will be considered.
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21

Dogan, Canan, Mine Gayaf, Ayse Ozsoz, Birsen Sahin, Nimet Aksel, Isil Karasu, Zekiye Aydogdu, and Nevin Turgay. "Pulmonary Strongyloides stercoralis infection." Respiratory Medicine Case Reports 11 (2014): 12–15. http://dx.doi.org/10.1016/j.rmcr.2013.10.004.

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22

White, Dorothy A. "Drug-induced pulmonary infection." Clinics in Chest Medicine 25, no. 1 (March 2004): 179–87. http://dx.doi.org/10.1016/s0272-5231(03)00134-5.

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23

Runcie, C., and G. Ramsay. "Intraabdominal infection: Pulmonary failure." World Journal of Surgery 14, no. 2 (March 1990): 196–203. http://dx.doi.org/10.1007/bf01664873.

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24

Esteban Ronda, Violeta, José Franco Serrano, and María Luisa Briones Urtiaga. "Pulmonary Strongyloides stercoralis Infection." Archivos de Bronconeumología (English Edition) 52, no. 8 (August 2016): 442–43. http://dx.doi.org/10.1016/j.arbr.2016.06.015.

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25

Bronnert, J., A. Wulff, L. Hillejan, and I. Reiter-Owona. "Pulmonary Echinococcus granulosus infection." Infection 45, no. 4 (January 20, 2017): 571–72. http://dx.doi.org/10.1007/s15010-017-0982-7.

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26

Keynan, Yoav, Hannah Sprecher, and Gabriel Weber. "Pulmonary Nocardia nova infection." European Journal of Internal Medicine 18, no. 2 (March 2007): 164. http://dx.doi.org/10.1016/j.ejim.2006.09.012.

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27

Kham-ngam, Irin, Ploenchan Chetchotisakd, Pimjai Ananta, Prajaub Chaimanee, Phuangphaka Sadee, Wipa Reechaipichitkul, and Kiatichai Faksri. "Epidemiology of and risk factors for extrapulmonary nontuberculous mycobacterial infections in Northeast Thailand." PeerJ 6 (August 16, 2018): e5479. http://dx.doi.org/10.7717/peerj.5479.

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Background Nontuberculous mycobacterial (NTM) infection is increasing worldwide. Current epidemiological data and knowledge of risk factors for this disease are limited. We investigated the trends in and risk of NTM infection in Northeast Thailand during 2012–2016. Methods Patient demographics, infection site(s), and underlying disease or conditions from 530 suspected cases of NTM infections were retrieved from medical records, reviewed and analyzed. A diagnosis of true NTM infection was accepted in 150 cases. Risk factor analyses were done for extrapulmonary NTM infections compared to pulmonary NTM infections and for Mycobacterium abscessus compared to members of the Mycobacterium avium complex (MAC). Trend analysis among NTM species causing NTM infections was performed. Results The most common species of NTMs causing extrapulmonary (n = 114) and pulmonary (n = 36) NTM infections in Northeast Thailand were M. abscessus (25.4% of extrapulmonary infected cases and 27.8% of pulmonary cases) followed by MAC (14.9% of extrapulmonary and 13.9% of pulmonary cases). Presence of anti-IFN-γ autoantibodies was the major risk factor for extrapulmonary (odds ratio (OR) = 20.75, 95%CI [2.70–159.24]) compared to pulmonary NTM infection. M. abscessus infection was less likely (OR = 0.17; 95%CI [0.04–0.80]) to be found in patients with HIV infection than was MAC infection. The prevalence of NTM infection, especially M. abscessus, in Northeast Thailand has recently increased. Extrapulmonary NTM and complicated NTM infections have increased in concordance with the recent trend of increasing frequency of anti-IFN-γ autoantibodies in the population. Conclusions M. abscessus was the commonest NTM pathogen followed by MAC. The prevalence of NTM infections and anti-IFN-γ are showing an upward trend. Autoimmune disease due to anti-IFN-γ is the major risk factor for extrapulmonary NTM infection in Northeast Thailand.
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28

M, Ravindra Chari, Manju Rajaram, Madhusmita M, Pampa ChToi, and Sneha L. "Pulmonary Aspergillus and Mucor Co-Infection." Sultan Qaboos University Medical Journal [SQUMJ] 21, no. 3 (August 29, 2021): 495–98. http://dx.doi.org/10.18295/squmj.8.2021.126.

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Co-infections or consecutive infections of mucormycosis and aspergillosis are very rare. Additionally, distinguishing between these two infections is also difficult as both these conditions have similar clinical features. We report two similar cases from Tamilnadu, who presented to a tertiary care centre in Puducherry, India in 2017 (first case) and 2019 (second case). The first case was a 70-year-old, non-diabetic male patient who presented with haemoptysis with a prior history of pulmonary tuberculosis. Computed tomography bronchial angiography revealed an air-crescent sign and the histopathological examination showed a fungal ball (aspergillus and mucor) in the right upper lobe and foci of fungal infection in the middle lobe. The second case was a 65-year-old diabetic male patient who presented with blackish expectoration and haemoptysis. A high-resolution computed tomography scan showed a reverse-halo sign in the right upper lobe. The results of the bronchoscopy-guided biopsy were consistent with a diagnosis of mixed mucormycosis and aspergillosis with angioinvasion. Both patients responded to amphotericin B with surgical excision of the affected lobe in the first case. A high degree of clinical suspicion, early surgical intervention and antifungal therapy are essential in the treatment of this rare co-infection. Keywords: Aspergillosis; Mucormycosis; Bronchoscopy; Coinfection; Amphotericin B; Case Report; India.
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29

Conly, J., R. Hilsden, H. Deneer, I. Etches, and T. Moyana. "Primary Pulmonary Hypertension and Human Immunodeficiency Virus Infection." Canadian Journal of Infectious Diseases 8, no. 5 (1997): 290–93. http://dx.doi.org/10.1155/1997/764297.

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This report details the case of a 42-year-old homosexual Caucasian male with infection due to human immunodeficiency virus type 1 (HIV-1) who presented with a four-month history of progressive dyspnea and was found to have clinical and hemodynamic evidence of severe pulmonary hypertension. He had had no opportunistic infections, and had a T helper lymphocyte count of 200×106/L. Extensive clinical laboratory and radiological evaluations revealed no underlying cause. Microscopic examination of postmortem lung tissue revealed findings consistent with grade V pulmonary hypertension. Electron microscopic analysis and polyermase chain reaction detection of HIV-DNA from dissected pulmonary arterioles failed to provide any supportive evidence to suggest productive infection of the pulmonary arteriolar endothelial cells by HIV-1. Although HIV-1 likely plays a role in the pathogenesis of primary pulmonary hypertension, evidence for direct infection of pulmonary vessel endothelium was lacking in this case. The pathogenesis of primary pulmonary hypertension associated with HIV remains obscure.
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30

Cho, Steve Y., Steven P. Rowe, Sanjay K. Jain, Lew C. Schon, Rex C. Yung, Tariq A. Nayfeh, Clifton O. Bingham, Catherine A. Foss, Sridhar Nimmagadda, and Martin G. Pomper. "Evaluation of Musculoskeletal and Pulmonary Bacterial Infections With [124I]FIAU PET/CT." Molecular Imaging 19 (January 1, 2020): 153601212093687. http://dx.doi.org/10.1177/1536012120936876.

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Purpose: Imaging is limited in the evaluation of bacterial infection. Direct imaging of in situ bacteria holds promise for noninvasive diagnosis. We investigated the ability of a bacterial thymidine kinase inhibitor ([124I]FIAU) to image pulmonary and musculoskeletal infections. Methods: Thirty-three patients were prospectively accrued: 16 with suspected musculoskeletal infection, 14 with suspected pulmonary infection, and 3 with known rheumatoid arthritis without infection. Thirty-one patients were imaged with [124I]FIAU PET/CT and 28 with [18F]FDG PET/CT. Patient histories were reviewed by an experienced clinician with subspecialty training in infectious diseases and were determined to be positive, equivocal, or negative for infection. Results: Sensitivity, specificity, positive-predictive value, negative-predictive value, and accuracy of [124I]FIAU PET/CT for diagnosing infection were estimated as 7.7% to 25.0%, 0.0%, 50%, 0.0%, and 20.0% to 71.4% for musculoskeletal infections and incalculable-100.0%, 51.7% to 72.7%, 0.0% to 50.0%, 100.0%, and 57.1% to 78.6% for pulmonary infections, respectively. The parameters for [18F]FDG PET/CT were 75.0% to 92.3%, 0.0%, 23.1% to 92.3%, 0.0%, and 21.4% to 85.7%, respectively, for musculoskeletal infections and incalculable to 100.0%, 0.0%, 0.0% to 18.2%, incalculable, and 0.0% to 18.2% for pulmonary infections, respectively. Conclusions: The high number of patients with equivocal clinical findings prevented definitive conclusions from being made regarding the diagnostic efficacy of [124I]FIAU. Future studies using microbiology to rigorously define infection in patients and PET radiotracers optimized for image quality are needed.
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31

Tang, Leilei, Lingdi Zhang, Xuan Mei, Jiawen Yu, and Guojun Jiang. "Pulmonary infection is associated with an increased IL-6 in acute exacerbation chronic obstructive pulmonary disease." European Journal of Inflammation 21 (January 5, 2023): 1721727X2211495. http://dx.doi.org/10.1177/1721727x221149534.

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Objective Acute Exacerbation Chronic Obstructive Pulmonary Disease (AECOPD) is associated with an acute worsening of respiratory symptoms that have effects on lung function, quality of life and health economic burden. In addition, the development of pulmonary infections is a common complication of Chronic Obstructive Pulmonary Disease (COPD). In the pathophysiology of AECOPD, interleukin (IL)-6 is a pleiotropic cytokine that can be produced by inflammatory and primary lung epithelial cells in response to a variety of different stimuli. We aim to investigate the correlation between serum cytokine levels and AECOPD with pulmonary infection. Methods 37 AECOPD patients diagnosed with pulmonary infection and 33 patients diagnosed with AECOPD only were selected. All COPD patients were diagnosed according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. Serum samples for C-reactive protein (CRP) and cytokines were obtained from the patients immediately after admission. Serum concentrations of cytokines were measured using a fluorescent bead immunoassay on a flow cytometer. Logistic regression was used to identify risk factors for AECOPD co-infection of the lungs. Results Serum characterization of our cohort showed patients with AECOPD and pulmonary infection had higher levels of IL-6 and IL-10 compared with the AECOPD group, and IL-6 was independently associated with AECOPD with pulmonary infection. ROC curve analysis showed that IL-6 was a useful predictor of the incidence of pulmonary infection in AECOPD patients. Conclusions Our findings highlight the role of IL-6 in the pathogenesis of AECOPD with pulmonary infection.
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32

Tablan, Ofelia C., Walter W. Williams, and William J. Martone. "Infection Control in Pulmonary Function Laboratories." Infection Control 6, no. 11 (November 1985): 442–44. http://dx.doi.org/10.1017/s019594170006478x.

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The role of the pulmonary function (PF) laboratory and PF testing equipment in the transmission of infections has not been established. Although microorganisms have been cultured from parts of in-use pulmonary function testing equipment, a relationship between equipment contamination and transmission of infection or colonization has not been documented. Nosocomial outbreaks of respiratory infections, eg, influenza, tuberculosis, and legionellosis have been described, but transmission of the microorganisms has not been shown to be more likely in the PF laboratory or with PF testing equipment than in other areas in the hospital or with other hospital equipment. Unlike nebulizers, which have been implicated in epidemic and endemic nosocomial gram-negative bacterial infections, PF machines do not generate aerosols. PF testing equipment is thus built without provision for easy machine disassembly and disinfection, except for parts that routinely come in contact with mucous membranes or secretions (eg, mouthpieces, valves, and some tubings).
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33

Swain, Satish, Kunal Sharma, Animesh Ray, Surabhi Vyas, Gagandeep Singh, Mohit Joshi, Deepali Jain, Immaculata Xess, Sanjeev Sinha, and Naveet Wig. "Post-COVID-19-Invasive Pulmonary Mycosis." Libyan International Medical University Journal 07, no. 01 (January 2022): 007–11. http://dx.doi.org/10.1055/s-0042-1750711.

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COVID-19 has been associated with myriad manifestations as well as adverse outcomes. One of the less commonly reported consequences of COVID-19 is the occurrence of secondary infections in patients suffering acutely from COVID-19 or in those recuperating. Secondary invasive fungal infections (IFIs) have also been observed earlier in other viral infections such as influenza, parainfluenza, and respiratory syncytial virus infections. Severe lung damage and immunologic derangement resulting from SARS-CoV-2 infection predispose to superinfections. Risk factors for secondary IFI includes immunologic derangement and immunoparalysis resulting from SARS-CoV-2 infection, neutropenia, or lymphopenia, poorly controlled diabetes, structural lung disease fungal colonization, and drugs such as corticosteroids or immunomodulators given as therapies for COVID-19. Invasive aspergillosis following COVID-19 is most commonly described fungal infection but other non-Aspergillus fungal infections (including mucormycosis) has also been reported. Herein we describe two interesting cases of secondary infections developing in patients beyond the acute phase of COVID-19 who had similar presentations but with different diagnoses and requiring different management strategies. Patient in case 1 developed COVID-19-associated subacute invasive pulmonary aspergillosis (SAIA) and patient in case 2 had COVID-19 associated pulmonary mucormycosis (CAPM). We have also described the various postulated immune-pathogenesis of the super-added fungal infections in COVID-19 patients.
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Maoz, C., D. Shitrit, Z. Samra, N. Peled, L. Kaufman, M. R. Kramer, and J. Bishara. "Pulmonary Mycobacterium simiae infection: comparison with pulmonary tuberculosis." European Journal of Clinical Microbiology & Infectious Diseases 27, no. 10 (May 17, 2008): 945–50. http://dx.doi.org/10.1007/s10096-008-0522-6.

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35

Balcan, Baran, Umit Ozcelik, Aylin Ozsancakli Ugurlu, Mehtap Aydin, Serdar Nalcaci, and Feza Yarbug Karakayali. "Increased Mortality Among Renal Transplant Patients With Invasive Pulmonary Aspergillus Infection." Progress in Transplantation 28, no. 4 (September 20, 2018): 349–53. http://dx.doi.org/10.1177/1526924818800044.

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Introduction: Renal transplantation is the most effective and preferred definite treatment option in patients with end-stage renal disease. Due to long-term immunesuppressive treatment, renal transplant recipients become vulnerable to opportunistic infections, especially to fungal infections. Method: This was a single-center, retrospective observational study of 438 patients who underwent renal transplantation between 2010 and 2016. Results: Thirty-eight renal transplant recipients who had lower respiratory tract infection with median age of 41.5 years were evaluated for invasive pulmonary aspergillus (IPA). Of these, 52.6% were female and 84.2% had living donors. Eleven of 38 lower respiratory patients were found to have IPA infection, 5 with proven infection. Compared to patients who did not have fungal pulmonary infection, patients with invasive aspergillus were older and had high fever, galactomannan levels, and leukocyte counts. Mortality was also higher in those patients. Having fever at the baseline and IPA infection was significantly associated with mortality in univariate analysis and remained related in multivariate model after adjustment for age, gender, and fever. Conclusion: Invasive pulmonary aspergillus infection is highly associated with increased mortality rates in renal transplant patients. Fungal pulmonary infections in immune-suppressed patients should be diagnosed and treated immediately in order to avoid the life-threatening complications and may greatly improve prognosis.
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Wang, Shih-Min, Yu-Ting Liao, Yu-Shiang Hu, Tzong-Shiann Ho, Ching-Fen Shen, Jen-Ren Wang, Yee-Shin Lin, and Ching-Chuan Liu. "Immunophenotype Expressions and Cytokine Profiles of Influenza A H1N1 Virus Infection in Pediatric Patients in 2009." Disease Markers 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/195453.

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Background. A novel swine-origin influenza A H1N1 virus (S-OIV) caused human infection and acute respiratory illness in 2009, resulting in an influenza pandemic.Objectives. This study characterized the immune responses of S-OIV infection in pediatric patients at risk of pulmonary complications.Methods. All enrolled pediatric patients were confirmed virologically for S-OIV infection in 2009-2010, prospectively. Changes in cellular immunophenotypes were analyzed using flow cytometry. Plasma cytokine levels associated with S-OIV infection by pulmonary and without pulmonary complications were measured using cytokine cytometric bead assay kits.Results. A total of 85 patients with a mean age of 10.3 years were recruited. The level of C-reactive protein (CRP) was high in patients exhibiting pulmonary complications. The percentage of cellular immunophenotypes did not change between patients with and without pulmonary complications. The absolute numbers of peripheral blood mononuclear cells (PBMC), CD3, CD8, and CD16CD56 decreased with acute S-OIV pulmonary complications. Acute influenza infection with pulmonary complications was associated with high plasma concentrations of IL-1β, IL-6, IL-12, and IFN-γ.Conclusion. Immunophenotype studies have reported variability in immune response to the severity of S-OIV infections. Acute phase cytokine profiles of the 2009 S-OIV infection might have contributed to the pathogenesis of the pulmonary complications.
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37

Ashizawa, Kazuto. "Imaging of Pulmonary Fungal Infection." Nippon Ishinkin Gakkai Zasshi 50, no. 1 (2009): 27–32. http://dx.doi.org/10.3314/jjmm.50.27.

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38

Sakamaki, Fumio. "Pulmonary Hypertension and Inflammation/Infection." Internal Medicine 55, no. 11 (2016): 1409–10. http://dx.doi.org/10.2169/internalmedicine.55.6415.

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39

Rastogi, V., P. Purohit, BP Peters, and PS Nirwan. "PULMONARY INFECTION WITH SERRATIA MARCESCENS." Indian Journal of Medical Microbiology 20, no. 3 (July 2002): 167–68. http://dx.doi.org/10.1016/s0255-0857(21)03254-0.

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Sabapathi, Ramesh. "Vibrio vulnificus and Pulmonary Infection." Annals of Internal Medicine 109, no. 12 (December 15, 1988): 988. http://dx.doi.org/10.7326/0003-4819-109-12-988_2.

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Kim, Seon Young, Myung Shin Kim, Ho Eun Chang, Jae-Joon Yim, Jae-Ho Lee, Sang Hoon Song, Kyoung Un Park, Junghan Song, and Eui-Chong Kim. "Pulmonary Infection Caused byMycobacterium conceptionense." Emerging Infectious Diseases 18, no. 1 (January 2012): 174–76. http://dx.doi.org/10.3201/eid1801.110251.

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42

Fisher, M., D. Asboe, and B. G. Gazzard. "Pulmonary diseases and HIV infection." Thorax 51, no. 2 (February 1, 1996): 228. http://dx.doi.org/10.1136/thx.51.2.228-a.

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Muqeetadnan, Mohammed, Ambreen Rahman, Syed Amer, Salman Nusrat, Syed Hassan, and Syed Hashmi. "Pulmonary Mucormycosis: An Emerging Infection." Case Reports in Pulmonology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/120809.

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Abstract:
Mucormycosis is a rare, but emerging, life-threatening, rapidly progressive, angioinvasive fungal infection that usually occurs in immunocompromised patients. We present a case of pulmonary mucormycosis in a diabetic patient who was on chronic steroid therapy for ulcerative colitis. Early recognition of this diagnosis, along with aggressive management, is critical to effective therapy and patient survival. The delay in diagnosis of this rapidly progressive infection can result in mortality.
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44

Murray, M. D, John F. "PULMONARY COMPLICATIONS OF HIV INFECTION." Annual Review of Medicine 47, no. 1 (February 1996): 117–26. http://dx.doi.org/10.1146/annurev.med.47.1.117.

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BECK, JAMES M, MARK J ROSEN, and HANNAH H PEAVY. "Pulmonary Complications of HIV Infection." American Journal of Respiratory and Critical Care Medicine 164, no. 11 (December 2001): 2120–26. http://dx.doi.org/10.1164/ajrccm.164.11.2102047.

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Oshima, Kengo, Hiroshi Yokouchi, Hiroyuki Minemura, Junpei Saito, Yoshinori Tanino, and Mitsuru Munakata. "Pulmonary Infection Caused byMycobacterium shinjukuense." Annals of the American Thoracic Society 12, no. 6 (June 2015): 958–59. http://dx.doi.org/10.1513/annalsats.201503-124le.

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Contreras, M. A., O. T. Cheung, D. E. Sanders, and R. S. Goldstein. "Pulmonary Infection with Nontuberculous Mycobacteria." American Review of Respiratory Disease 137, no. 1 (January 1988): 149–52. http://dx.doi.org/10.1164/ajrccm/137.1.149.

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48

Snow, Norman J., Jacques Kpodonu, Cimenga Tshibaka, Malek G. Massad, and Alexander S. Geha. "Pulmonary Resection for Parenchymal Infection." Chest 126, no. 4 (October 2004): 802S. http://dx.doi.org/10.1378/chest.126.4_meetingabstracts.802s.

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Morris, Alison, Kristina Crothers, and Laurence Huang. "Pulmonary Complications of HIV Infection." Seminars in Respiratory and Critical Care Medicine 37, no. 02 (March 14, 2016): 145–46. http://dx.doi.org/10.1055/s-0036-1579582.

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Schneider, Roslyn F., and Mark J. Rosen. "Pulmonary complications of HIV infection." Current Opinion in Pulmonary Medicine 3, no. 2 (March 1997): 151–58. http://dx.doi.org/10.1097/00063198-199703000-00012.

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