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Books on the topic 'Streptococcus pneumoniae'

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Published: 4 June 2021
Last updated: 31 July 2024

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1

Iovino, Federico, ed. Streptococcus pneumoniae. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9199-0.

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2

Brenwald, Nigel Peter. Characterisation of a multidrug efflux system in Streptococcus pneumoniae. Birmingham: University of Birmingham, 2000.

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3

Nuorti, J. Pekka. Prevention of pneumococcal disease among infants and children: Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine : recommendations of the Advisory Committee on Immunization Practices (ACIP). Atlanta, GA: Dept. of Health and Human Services, Centers for Disease Control and Prevention, 2010.

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4

Doherty, Neil Christopher. A molecular analysis of hyaluronate lyase production in Streptococcus pneumoniae. [s.l.]: typescript, 2000.

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5

Boost, Maureen Valerie. Carriage and antibiotic resistance of Streptococcus pneumoniae in Hong Kong. [S.l: The Author], 2004.

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6

Kanclerski, Krzysztof. Streptococcus pneumoniae haemolysin (pneumolysin): Production, purification and use as antigen for diagnosis of pneumococcal pneumonia. [s.l.]: [s.n.], 1987.

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7

I, Tuomanen Elaine, ed. The pneumococcus. Washington, DC: ASM Press, 2004.

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8

Kragsbjerg, Peter. Cytokines in infection: Clinical and experimental studies with special reference to Streptococcus pneumoniae. Uppsala: Uppsala universitet, 1996.

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9

Johnston, Nicole J. Prevalence and characterization of the mechanisms of macrolide, lincosamide, and streptogramin resistance among isolates of Streptococcus pneumoniae and viridans streptococci. Ottawa: National Library of Canada, 1999.

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10

File, Thomas. New insights in the treatment of severe infections in the multiple-drug resistant situation: Proceedings of a satellite symposium to the 11th International Congress on Infectious Diseases, Cancun, Mexico, March 5, 2004. Basel, Switzerland: Karger, 2004.

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11

Rankin, Barbara Anne. The development of a dot immunobinding assay for the detection of streptococcus pneumoniae in sputum. [s.l: The Author], 1990.

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12

Mohammadi, Maryam Khan. Vergleichende Untersuchung der bakteriziden Aktivität von Moxifloxacin und Ciprofloxacin gegenüber Escherichia coli, Staphylococcus aureus, Enterococcus faecalis, Enterococcus faecium und Streptococcus pneumoniae. [s.l.]: [s.n.], 1999.

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13

Berlin, Freie Universität, ed. Molekulargenetische Untersuchung des Penicillin-bindenden Proteins (PBP) 1a von Streptococcus pneumoniae: Verwandtschaft von PBP 1a Mosaikgenen in Penicillin-resistenten klinischen Stämmen. [s.l.]: [s.n.], 1992.

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14

Streptococcus Pneumoniae. Elsevier, 2015. http://dx.doi.org/10.1016/c2012-0-00722-3.

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15

Gillespie. Streptococcus Pneumoniae. John Wiley & Sons, 2002.

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16

Iovino, Federico. Streptococcus Pneumoniae: Methods and Protocols. Springer New York, 2019.

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17

Lydyard, Peter, Michael Cole, John Holton, Will Irving, Nino Porakishvili, Pradhib Venkatesan, and Kate Ward. Case Studies in Infectious Disease: Streptococcus pneumoniae. Garland Science, 2009. http://dx.doi.org/10.4324/9780203854075.

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18

Tomasz, Alexander, ed. Streptococcus Pneumoniae: Molecular Biology & Mechanisms of Disease. MARY ANN LIEBERT PUBLISHING, 2000.

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19

Brown, Jeremy, Sven Hammerschmidt, and Carlos Orihuela. Streptococcus Pneumoniae: Molecular Mechanisms of Host-Pathogen Interactions. Elsevier Science & Technology Books, 2015.

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20

Ana María Del Carmen Martín Rodríguez. Biología Molecular Del Bacteriófago Cp1 de Streptococcus Pneumoniae. Universidad Complutense de Madrid, Servicio de Publicaciones, 2006.

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21

Parker, James N., and ICON Health Publications. The Official Patient's Sourcebook on Streptococcus Pneumoniae Infections. Icon Health Publications, 2002.

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22

Brown, Jeremy M., Sven Hammerschmidt, and Carlos Orihuela. Streptococcus Pneumoniae: Molecular Mechanisms of Host-Pathogen Interactions. Elsevier Science & Technology Books, 2015.

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23

Austrian, Robert, and Lewis Thomas. Life with the Pneumococcus: Notes from the Bedside, Laboratory, and Library. University of Pennsylvania Press, 2016.

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24

Life with the pneumococcus: Notes from the bedside, laboratory, and library. Philadelphia: University of Pennsylvania Press, 1985.

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25

Harrison, Mark. Streptococci and staphylococci. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0013.

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This chapter describes the microbiology of streptococci and staphylococci as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the methods of spread and clinical features of Streptococcus pneumoniae, Streptococcus pyogenes, alpha-haemolytic streptococci, Staphylococcus aureus, MRSA, and Staphylococcus epidermidis. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
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26

Ortiz, Laura Lagartera. Estructura y Función de Las Fosforilcolín Esterasa de Streptococcus Pneumoniae. Universidad Complutense de Madrid, Servicio de Publicaciones, 2008.

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27

Kröger, Alexa. Einfluss der Desinfektion mit Isopropanol auf die Virulenz von Streptococcus pneumoniae. [s.l.], 1985.

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28

Spratt, Brian G., Donald Morrison, Elaine I. Tuomanen, and Timothy J. Mitchell. Pneumococcus. Wiley & Sons, Limited, John, 2014.

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29

(Editor), Elaine I. Tuomanen, Timothy J. Mitchell (Editor), Donald Morrison (Editor), and Brian G. Spratt (Editor), eds. The Pneumococcus. ASM Press, 2004.

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30

Fernández, Eduardo Díaz. Estudio Mediante Ingeniería de Proteínas de la Autolisina Lyta de Streptococcus Pneumoniae. Universidad Complutense de Madrid, Servicio de Publicaciones, 2005.

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31

The pneumococcus. Washington, DC: ASM Press, 2004.

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32

Streptococcus pneumoniae in child care centres: A point prevalence survey of nasopharyngeal carriage, antibiotic resistance and risk factors for resistance. Ottawa: National Library of Canada, 1998.

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33

Albers, Cordula. Einfluss des Zeitpunktes der Gabe von Moxifloxacin und Azithromycin auf die Überlebensfähigkeit humaner respiratorischer Epithelzellen nach Infektion mit Streptococcus Pneumoniae in vitro. 2006.

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34

Kühn, Günter Georg. Untersuchung über den Einfluss von Humanm Vollblut auf Escherichia coli, Streptococcus Paecalis, Klebstella Pneumoniae Staphylococcus Aureus und Pseudomonas Aeruginosa bei Expostion mit Subinhibitorischen Konzentrationen von Penicillinen. 1985.

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35

Informe regional de SIREVA II, 2017. Organización Panamericana de la Salud, 2020. http://dx.doi.org/10.37774/9789275323076.

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La vigilancia pasiva por laboratorio de Streptococcus pneumoniae se realiza en los países de la Región de las Américas desde 1993 bajo la denominación de Sistema Regional de Vacunas (SIREVA), con el apoyo de la Organización Panamericana de la Salud. En 1997, los países de la Región propusieron introducir las pruebas de laboratorio para Haemophilus influenzae, y en el 2000, para Neisseria meningitidis. Así se amplió la vigilancia por laboratorio de las enfermedades bacterianas invasivas con los tres patógenos anteriores, esta vez bajo la denominación de SIREVA II. La red está compuesta por 19 laboratorios nacionales de referencia situados en varios países. Durante los últimos años se han ido incorporando nuevos ensayos, entre ellos pruebas de biología molecular, que facilitan la detección de estos patógenos en muestras biológicas. Los datos de la vigilancia por laboratorio de los países de la Región se recopilan y se presentan desde el 2005 en el Informe regional de SIREVA II. El objetivo principal de esta publicación es compartir información sobre la identificación de estos patógenos en la vigilancia pasiva por laboratorio que realizan los países durante un año calendario, dar seguimiento a la distribución de sus serotipos o serogrupos y correlacionarlos con los presentes en las vacunas disponibles. Esta publicación proporciona información actualizada sobre los aislamientos invasivos de Streptococcus pneumoniae, Haemophilus influenzae y Neisseria meningitidis de muestras biológicas recogidas durante el 2017 y realizadas en laboratorios de países de las Américas. Los datos de la vigilancia por laboratorio de este informe conservan el esquema de presentación que la red definió hace varios años, pues son necesarios para mantener informados a los programas de salud pública, al personal de laboratorio y a la comunidad científica, así como para facilitar información útil a las decisiones basadas en la evidencia. Estos datos pueden servir para promover estudios adicionales que generen nuevo conocimiento y faciliten la comprensión de estos eventos.
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36

García, Yolanda García. Estudio de la Actividad de Amoxicilina/ Clavulanico y Ciprofloxacino in Vitro y en un Modelo Experimental de Neumonía Por Cepas de Streptococcus Pneumoniae de Diferente Serotipo y Sensibilidad a Penicilina. Universidad Complutense de Madrid, Servicio de Publicaciones, 2006.

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37

Informe regional de SIREVA II, 2018. Pan American Health Organization, 2021. http://dx.doi.org/10.37774/9789275324035.

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En esta nueva edición del Informe regional de SIREVA II correspondiente al 2018 se presenta información sobre los serotipos o serogrupos de los tres agentes asociados con las enfermedades bacterianas invasivas que son objeto de vigilancia pasiva por laboratorio —Streptococcus pneumoniae, Haemophilus influenzae y Neisseria meningitidis—, los cuales se identificaron en muestras obtenidas durante el 2018 de pacientes que presentaron algunas de esas enfermedades. Estos datos se presentan de forma agrupada en cuadros y no han sido objeto de ningún tipo de análisis estadístico. En algunas ocasiones, los organismos no lograron identificar los serotipos o serogrupos porque los laboratorios no disponían de todos los reactivos requeridos para la completa caracterización del agente o porque los cultivos perdieron viabilidad y no fue posible remitirlos a un laboratorio de referencia regional para complementar la tipificación. A pesar de estas limitaciones, los datos notificados por los laboratorios de la red SIREVA II son de gran relevancia para la comunidad.
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38

Rajakrishna, Premil, Stewart Cameron, and Neil Turner. Nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0052.

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Nephrotic syndrome is the constellation of manifestations seen in patients with such severe proteinuria that serum albumin falls below normal levels. Its severity and the risk of complications are graded by the severity of the protein loss. The risks of some complications begin to rise at levels of proteinuria below those conventionally associated with nephrotic syndrome. The main manifestation, oedema, is characterized by avid sodium retention and managed by sodium restriction and diuretics. A pronounced thrombotic tendency is particularly apparent within the first 6 months of diagnosis and in patients with the most severe proteinuria. Venous thromboembolism may be a presenting feature. Prophylactic full anticoagulation may be considered for those at highest risk. Hyperlipidaemia is severe and justifies lipid-lowering therapy in patients with sustained nephrotic syndrome. There is a marked increased risk of bacterial infection, particularly from Streptococcus pneumoniae. The causes of nephrotic syndrome are diseases affecting the podocyte, either directly or through an effect on glomerular matrix (e.g. through scarring). Identification of a cause is important for management and often requires a renal biopsy.
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39

Informe regional de SIREVA II, 2016. Organización Panamericana de la Salud, 2019. http://dx.doi.org/10.37774/9789275321850.

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[Prefacio, español]. La red SIREVA (Sistema Regional de Vacunas), conocida en toda la Región, completa sus 25 años de existencia y, en todos esos años, viene prestando un trabajo relevante en la vigilancia de laboratorio de enfermedades bacterianas invasivas, especialmente aquellas causadas por el Streptococcus pneumoniae (neumococo), Haemophilus influenzae (Hi) y la Neisseria meningitidis (meningococo), con reconocido nivel de excelencia. La red también caracteriza los respectivos serotipos/serogrupos y la susceptibilidad a los antimicrobianos de las mencionadas bacterias. Desde el 2005, los laboratorios de la red SIREVA empezaron a contribuir con la red centinela de vigilancia de neumonías y meningitis bacteriana en menores de 5 años, de la cual forman parte nueve países y 21 hospitales. En el 2014, esta red centinela pasó a integrar la red global, coordinada por la OMS, compartiendo mundialmente la información que es generada en la Región. La continuidad y el fortalecimiento de la red de laboratorios son fundamentales para la vigilancia de esas enfermedades. Es primordial que los países garanticen el financiamiento de las actividades de los laboratorios de la red SIREVA. Por otro lado, la Organización Panamericana de la Salud seguirá ofreciendo cooperación técnica a los países y a sus programas nacionales de inmunización de manera de contribuir en la continua mejoría de esta red de vigilancia para mantenerse generando información de calidad que pueda subsidiar a los gestores en la toma de decisiones basadas en evidencia. En este volumen están siendo presentados los datos del 2016 generados por los países que forman parte de la red SIREVA II. [Prefácio, português]. A rede SIREVA (Sistema Regional de Vacinas), conhecida em toda a Região, completa seus 25 años de existência e, em todos esses anos, vem prestando um trabalho relevante na vigilância de laboratório de doenças bacterianas invasivas, especialmente aquelas causadas pelo Streptococcus pneumoníae (pneumococo), Haemophilus influenzae (Hi), e pela Neisseria meningitidis (meningococo), com reconhecido nível de excelência. A rede também caracteriza os respectivos sorotipos/sorogrupos e a suscetibilidade aos antimicrobianos das mencionadas bactérias. A partir de 2005, os laboratórios da rede SIREVA começaram a contribuir com a rede sentinel de vigilância de pneumonias e meningites bacterianas em menores de 5 anos, da qual fazem parte atualmente nove países e 21 hospitais. Em 2014, esta rede sentinela passou a integrar à rede global, coordenada pela OMS, compartilhando mundialmente a informação que é gerada na Região. A continuidade e o fortalecimento da rede de laboratórios são fundamentais para a vigilância epidemiológica dessas doenças. É primordial que os países garantam o financiamento das atividades dos laboratórios da rede SIREVA. Por outro lado, a OPAS continuará oferecendo cooperação técnica aos países e aos seus programas nacionais de imunização de maneira a contribuir no contínuo aprimoramento dessa rede de vigilância, para que se mantenha gerando informação de qualidade que possa subsidiar os gestores para tomar decisões baseadas em evidência. Neste volume estão sendo apresentados os dados de 2016 gerados pelos 19 países que fazem parte da rede SIREVA II.
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40

Pery, Xavier. Coloring Book - You Will Get Better - Streptococcus Pneumonia. Independently Published, 2021.

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41

Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.

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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
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42

Lupton, Joshua. Hospital Acquired Pneumonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0023.

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Pneumonia consists of inflammation of the pulmonary parenchyma, typically resulting from a microbial infection. Hospital-acquired pneumonia (HAP) occurs in (typically elderly) patients in long-term care facilities, with regular IV therapy, with immunosuppression, or with a history of recent treatment at a hospital. It is associated with high mortality. The majority HAP patients present with some constellation of cough, fever, sputum production, and pleuritic chest pain. Patients with chronic obstructive pulmonary disease (COPD) and cystic fibrosis are at increased risk for pneumonia. The Infectious Disease Society of America requires infiltrates on chest x-ray or other imaging for the diagnosis of pneumonia. For hospitalized patients, empiric antimicrobial therapy for HAP should be given as soon as pneumonia is highly suspected. There is currently a vaccine available against Streptococcus pneumonia that all patients should be offered before discharge from the hospital. The elderly are already more susceptible to HAP due to decreased mobility and increased comorbidities.
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43

Rodriguez-Iturbe, Bernardo, and Mark Haas. Post-infectious glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0076.

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Post-infectious glomerulonephritis (GN) defines an inflammatory lesion involving exclusively or predominantly the glomeruli that is a consequence of an infectious disease. There are numerous bacterial, viral, and fungal infections associated with GN. This chapter acts as an overview of the following chapters that discuss only post-streptococcal GN, immunoglobulin A-dominant GN associated with staphylococcal infections, GN associated with bacterial endocarditis, with infected ventriculoatrial shunts (‘shunt nephritis’), and GN associated with deep-seated infections (osteomyelitis, visceral abscesses, pleural suppuration, pneumonia).
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