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Books on the topic 'Associated bacteria'

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Published: 25 May 2024

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1

S, Gnanamanickam S., ed. Plant-associated bacteria. Dordrecht: Springer, 2006.

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2

Gnanamanickam, Samuel S., ed. Plant-Associated Bacteria. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/978-1-4020-4538-7.

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3

Gnanamanickam, Samuel S., ed. Plant-Associated Bacteria. Dordrecht: Kluwer Academic Publishers, 2006. http://dx.doi.org/10.1007/1-4020-4538-7.

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4

S, Gnanamanickam S., ed. Plant-associated bacteria. Dordrecht: Springer, 2006.

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5

Gross, Dennis C., Ann Lichens-Park, and Chittaranjan Kole, eds. Genomics of Plant-Associated Bacteria. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-55378-3.

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6

Manipulative tenants: Bacteria associated with arthropods. Boca Raton: Taylor & Francis, 2012.

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7

P, Spaink Herman, Kondorosi A, and Hooykaas Paul J. J, eds. The rhizobiaceae: Molecular biology of model plant-associated bacteria. Dordrecht: Kluwer Academic, 1998.

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8

Luan, Xiujie. Study of the bacteria associated with exacerbation of late-onset asthma. [Derby: University of Derby], 2000.

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9

1963-, Fernando A., and Pacific Forestry Centre, eds. Index of plant pathogens, plant-associated microorganisms, and forest fungi of British Columbia. Victoria: Pacific Forestry Centre, 1999.

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10

Peter, Whalley. The proteolytic and saccharolytic activity of some natural waters and their associated bacteria. [s.l.]: typescript, 1987.

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11

L, Garland Jay, Lim Daniel V, and United States. National Aeronautics and Space Administration., eds. Survival of potentially pathogenic human-associated bacteria in the rhizosphere of hydroponically grown wheat. [Washington, D.C: National Aeronautics and Space Administration, 1996.

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12

Song, Young-Ho. The targeting of phospholipid liposomes to oral and skin-associated bacteria and their use forbactericide delivery. Manchester: University of Manchester, 1994.

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13

Sanderson, Neil Michael. Interaction of cationic liposomes with the skin-associated bacteria Staphylococcus epidermis for the delivery of antibacterial agents. Manchester: University of Manchester, 1996.

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14

Chittaranjan, Kole, and SpringerLink (Online service), eds. Genome Mapping and Genomics in Animal-Associated Microbes. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009.

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15

Wahyudi, Aris Tri. Sponge-associated bacteria producing bioactive compounds, screening, analysis of antimicrobial compounds, and its genetic study: Competitive grant of overseas research collaboration and international publication : research report. Bogor: Lembaga Penelitian dan Pengabdian Kepada Masyarakat, Bogor Agricultural University, 2010.

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16

Sayers, Nicola Macdonald. Bacterial toxins associated with cot death. Manchester: University of Manchester, 1996.

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17

David, Davidson. The microbial ecology of bacterial biofilms associated with copper solvency in domestic water systems. Ottawa: National Library of Canada, 1995.

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18

Moriarty, T. Fintan. Biomaterials Associated Infection: Immunological Aspects and Antimicrobial Strategies. New York, NY: Springer New York, 2013.

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19

Anderson, Annette C. Comparison of the bacterial composition and structure in symptomatic and asymptomatic endodontic infections associated with root-filled teeth using pyrosequencing. Freiburg: Universität, 2013.

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20

Choquet, Chritian G. Bacterial glucose mineralization and statistical considerations associated with the use of the heterotrophic activity method in an acid-stressed lake. [s.l: s.n.], 1985.

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21

L, Yu Victor, Merigan Thomas C. 1934-, and Barriere Steven L, eds. Antimicrobial therapy and vaccines: Editors, Victor L. Yu, Thomas C. Merigan, Steven L. Barriere ; associate editors, Alan M. Sugar ... [et al.]. Baltimore: Williams & Wilkins, 1999.

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22

Kolmos, Hans Jørn. Hygenic problems in dialysis: Factors determining bacterial contamination of fluids and equipment used for haemo- and peritoneal dialysis, associated health risks, and methods of prevention. København: Lægeforeningen, 1985.

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23

Gnanamanickam, Samuel S. Plant-Associated Bacteria. Springer, 2006.

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24

Gnanamanickam, Samuel S. Plant-Associated Bacteria. Springer, 2007.

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25

Kole, Chittaranjan, Dennis C. Gross, and Ann Lichens-Park. Genomics of Plant-Associated Bacteria. Springer, 2016.

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26

Kole, Chittaranjan, Dennis C. Gross, and Ann Lichens-Park. Genomics of Plant-Associated Bacteria. Springer, 2014.

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27

Kole, Chittaranjan, Dennis C. Gross, and Ann Lichens-Park. Genomics of Plant-Associated Bacteria. Springer, 2014.

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28

Kole, Chittaranjan, Dennis C. Gross, and Ann Lichens-Park. Genomics of Plant-Associated Bacteria. Springer, 2014.

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29

GROSS, DENNIS C. Genomics of Plant-Associated Bacteria. Springer, 2018.

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30

Bourtzis, Kostas, and Einat Zchori-Fein. Manipulative Tenants: Bacteria Associated with Arthropods. Taylor & Francis Group, 2011.

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31

Bourtzis, Kostas, and Einat Zchori-Fein. Manipulative Tenants: Bacteria Associated with Arthropods. Taylor & Francis Group, 2013.

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32

Bourtzis, Kostas, and Einat Zchori-Fein. Manipulative Tenants: Bacteria Associated with Arthropods. Taylor & Francis Group, 2018.

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33

Bourtzis, Kostas, and Einat Zchori-Fein. Manipulative Tenants: Bacteria Associated with Arthropods. Taylor & Francis Group, 2011.

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34

Spaink, Herman P., Paul J. J. Hooykaas, and Adam Kondorosi. Rhizobiaceae: Molecular Biology of Model Plant-Associated Bacteria. Springer London, Limited, 2012.

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35

Steinhaus, Edward Arthur. Catalogue of Bacteria Associated Extracellularly with Insects and Ticks. Creative Media Partners, LLC, 2015.

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36

(Editor), H. P. Spaink, A. Kondorosi (Editor), and Paul J.J. Hooykaas (Editor), eds. The Rhizobiaceae: Molecular Biology of Model Plant-Associated Bacteria. Springer, 1998.

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37

(Editor), H. P. Spaink, A. Kondorosi (Editor), and Paul J.J. Hooykaas (Editor), eds. The Rhizobiaceae - Molecular Biology of Model Plant-Associated Bacteria. Springer, 1998.

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38

Bertaccini, Assunta, Govind Pratap Rao, Phyllis G. Weintraub, and Nicola Mori. Phytoplasmas : Plant Pathogenic Bacteria - II: Transmission and Management of Phytoplasma - Associated Diseases. Springer, 2019.

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39

Bertaccini, Assunta, Govind Pratap Rao, and Nicola Fiore. Phytoplasmas : Plant Pathogenic Bacteria - I: Characterisation and Epidemiology of Phytoplasma - Associated Diseases. Springer, 2018.

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40

Bertaccini, Assunta, Govind Pratap Rao, Nicola Fiore, and Lia W. Liefting. Phytoplasmas : Plant Pathogenic Bacteria - I: Characterisation and Epidemiology of Phytoplasma - Associated Diseases. Springer, 2018.

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41

Phytoplasmas : Plant Pathogenic Bacteria - I: Characterisation and Epidemiology of Phytoplasma - Associated Diseases. Springer, 2019.

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42

Haddad, Michael Alexander. Phylogenetic characterization of the epibiotic bacteria associated with the hydrothermal vent polychaete Alvinella pompejana. 1994.

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43

Sirová, Dagmara, Jiří Bárta, Jakub Borovec, and Jaroslav Vrba. The Utricularia-associated microbiome: composition, function, and ecology. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779841.003.0025.

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This chapter reviews current advances regarding plant–microbe interactions in aquatic Utricularia. New findings on the composition and function of trap commensals, based mainly on the advances in molecular methods, are presented in the context of the ecological role of Utricularia-associated microorganisms. Bacteria, fungi, algae, and protozoa colonize the Utricularia trap lumen and form diverse, interactive communities. The involvement of these microbial food webs in the regeneration of nutrients from complex organic matter is explained and their potential contribution to the nutrient acquisition in aquatic Utricularia is discussed. The Utricularia–commensal system is suggested to be a suitable model system for studying plant-microbe and microbe-microbe interactions and related ecological questions.
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44

Ali, Ased. Pathogenesis of urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0001.

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The realization of the harms resulting from indiscriminate use of antibiotics for minor infection has added impetus to the need to understand better the interaction between urogenital tract epithelium and invading bacteria during the initial stages of urinary tract infection (UTI). It is thought that uropathogenic Escherichia coli clones develop in the gut and migrate across the perineum to the urethra and up into the bladder. The response of the epithelium to bacterial adherence and the evolution of the invading bacteria will then govern the clinical consequences. These can vary between rapid invasion and further migration to produce systemic sepsis to tolerance of the bacteria in a planktonic state in asymptomatic bacteriuria. The key to these differences is the activation of epithelial pathogen-associated molecular pattern receptors by expressed proteins on the bacterial cell wall. Increased understanding of these interactions will lead to non-antibiotic-based strategies for clinical management of urinary infection.
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45

Rodriguez-Iturbe, Bernardo, and Mark Haas. Glomerulonephritis associated with endocarditis, deep-seated infections, and shunt nephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0079_update_001.

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Endocarditis is a cause of glomerulonephritis. Healthcare interventions (prosthetic valves, indwelling catheters, pacemaker wires) and intravenous drug abuse are presently the most common causes of endocarditis and Staphylococcus aureus is frequently the infecting bacteria. Shunt nephritis is a form of glomerulonephritis associated with infection of ventriculoatrial shunts implanted to relieve hydrocephalus and, typically, are caused by prolonged infections of low-pathogenicity microorganisms. This complication led to the replacement of the technique by ventriculoperitoneal shunts. Deep-seated infections such as chronic abscesses and osteomyelitis can sometimes cause a similar syndrome. In all cases, treatment of the infection is the key strategy. The nature of the glomerulonephritis tends in subacute infection to be a lobular membranoproliferative glomerulonephritis type I pattern associated with low C3 levels. However, an acute post-infectious pattern may also be seen, and a third pattern is focal necrotizing and crescentic glomerulonephritis, which tends to be pauci-immune as seen in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, but usually without positive fluorescence or solid phase assays for ANCA antigens.
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46

Keshav, Satish, and Alexandra Kent. Immunology and genetics in gastrointestinal and hepatic medicine. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0196.

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The gut has a pivotal role in immune homeostasis. It is constantly exposed to a wide array of antigens in food, and resident and consumed microorganisms. It is estimated that the number of bacterial cells in the gastrointestinal tract is tenfold greater than the number of cells in the human body. The gut needs to recognize harmful bacteria, and consequently contains the largest number of immune cells in the body. However, it must remain tolerant to commensal bacteria. Bacteria express antigens that stimulate an immunological response via the gut-associated lymphoid tissue (GALT). The GALT includes the appendix, tonsils, Peyer’s patches, and mesenteric lymph nodes. Therefore, the intestinal immune system is finely balanced between tolerance and reactivity. An example of an abnormal response that generally the individual should be tolerant to is gliadin peptides in coeliac disease. An example of excessive tolerance to an otherwise controllable infection is cryptosporidiosis, which causes diarrhoea in patients with HIV infection. The understanding of genetics in disease has progressed rapidly with the introduction of genome-wide association studies. The Welcome Trust Case Control Consortium has performed extensive research on the genetics of many illnesses, including Crohn’s disease, ulcerative colitis, Barrett’s oesophagus, oesophageal adenocarcinoma, and primary biliary cholangitis. Although these studies have increased our understanding of the molecular basis of disease, they have had little impact on clinical management. This may change as studies associate genotype and phenotype. Several gastrointestinal diseases have an etiology based on immunological or genetic aberrations, and these immunological mechanisms and genetic mutations can be utilized for diagnostic purposes. However, there is no genetic or immunological marker that is 100% specific to a disease and, consequently, the markers are used to support clinical, histological, and/or radiological findings.
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47

Balhara, Kamna S., Basem F. Khishfe, and Jamil D. Bayram. Sepsis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0004.

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Sepsis is a clinical syndrome characterized by systemic inflammation in the presence of infection. The source of infection may be occult. One must be aware of the epidemiology, presenting features and complications, diagnostic considerations and tests, and the organisms involved. Bacteria (gram positive and negative) are most commonly associated with sepsis, although fungi, viruses, and parasites can cause sepsis. Infections in the lungs, urinary tract, abdomen, skin, brain, and other areas can cause bacteremia and lead to sepsis. Treatment includes airway, breathing, and circulation (ABCs) management; aggressive fluid resuscitation; early administration of broad-spectrum antibiotics; and early goal-directed therapy and severe sepsis resuscitation bundle. Diagnosis can be challenging in pediatric and geriatric populations.
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48

Rello, Jordi, and Bárbara Borgatta. Pathophysiology of pneumonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0115.

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Airway colonization, ventilator-associated tracheobronchitis (VAT), and hospital-acquired (HAP) and ventilator-associated pneumonia (VAP) are three manifestations having the presence of micro-organisms in airways in common. Newer definitions have to consider worsening of oxygenation, in addition to purulent respiratory secretions, chest-X rays opacities, and biomarkers of inflammation. Bacteria are the main causes of HAP/VAP. During hospitalization there’s a shift of airway’s colonizing flora from core organisms to enteric and non-fermentative ones. Macro- and micro-aspiration is the most important source of pneumonia. Endotracheal tube secretion leakage is an important source, serving biofilm as a reservoir. Exogenous colonization is infrequent, but it may contribute to cross-infection with resistant species. Prevention of VAP can be achieved by implementing multidisciplinary care bundles focusing on oral/hand hygiene and control of sedation. Pneumonia develops when micro-organisms overwhelm host defences, resulting in a multifocal process. Risk and severity of pneumonia is determined by bacterial burden, organism virulence and host defences. Innate and adaptive immune responses are altered, decreasing clearing of pathogens. Some deficits of the complement pathway in intubated patients are associated with increased risk for VAP and higher mortality. Micro-arrays have demonstrated specific different immunological signatures for VAP and VAT. Early antibiotic therapy is associated with a decrease in early HAP/VAP incidence, but selects for MDR organisms. Attributable mortality is lower than 10%, but HAP/VAP prolongs length of stay, and dramatically increase costs and use of health care resources.
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49

Bayston, Roger. Hospital-acquired urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0003.

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Urinary tract infections (UTIs) account for the majority of hospital-acquired infections (HAI), and most of these occur in catheterized patients. However, for most the presence of bacteria in the urine (bacteriuria) is asymptomatic, yet in many institutional and national surveillance studies it is still attributed as ‘infection’. Although guidance is that only symptomatic UTI should be treated, except in pregnancy, bacteriuria in catheterized patients is frequently overinvestigated and antibiotics overused. Most infections are caused by enteric bacteria such as Escherichia coli, but other bacteria such as Proteus mirabilis and staphylococci are more prominent in HAI. Aseptic technique for catheter insertion and during subsequent catheter care together with minimizing catheter duration are very important to prevent catheter-associated UTI (CAUTI). Prophylactic antibiotics should be avoided. National and international action to adopt evidence-based consensus protocols for management of catheterized patients and judicial use of antimicrobial chemotherapy promise to be of greatest benefit.
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50

Donelli, Gianfranco. Biofilm-Based Healthcare-Associated Infections. Springer International Publishing AG, 2014.

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