Quantifying Nonvertical Inheritance in the Evolution of Legionella
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Legionnaires' Disease, Pontiac Fever, Legionellosis and Legionella
Legionnaires’ Disease, Pontiac Fever, Legionellosis and Legionella Q: What is Legionellosis and who is at risk? Legionellosis is an infection caused by Legionella bacteria. Legionellosis can present as two distinct illnesses: Pontiac fever (a self-limited flu-like mild respiratory illness), and Legionnaires’ Disease (a more severe illness involving pneumonia). People of any age can get Legionellosis, but the disease occurs most frequently in persons over 50 years of age. The disease most often affects those who smoke heavily, have chronic lung disease, or have underlying medical conditions that lower their immune system, such as diabetes, cancer, or renal dysfunction. Persons taking certain drugs that lower their immune system, such as steroids, have an increased risk of being affected by Legionellosis. Many people may be infected with Legionella bacteria without developing any symptoms, and others may be treated without having to be hospitalized. Q: What is Legionella? Legionella bacteria are found naturally in freshwater environments such as creeks, ponds and lakes, as well as manmade structures such as plumbing systems and cooling towers. Legionella can multiply in warm water (77°F to 113°F). Legionella pneumophila is responsible for over 90 percent of Legionnaires’ Disease cases and several different species of Legionella are responsible for Pontiac Fever. Q: How is Legionella spread and how does someone acquire Legionellosis (Legionnaires’ Disease/Pontiac Fever)? Legionella bacteria become a health concern when they grow and spread in manmade structures such as plumbing systems, hot water tanks, cooling towers, hot tubs, decorative fountains, showers and faucets. Legionellosis is acquired after inhaling mists from a contaminated water source containing Legionella bacteria. -
Each of 3,323 Metabolic Innovations in the Evolution of E. Coli Arose Through the Horizontal Transfer of a Single DNA Segment
Each of 3,323 metabolic innovations in the evolution of E. coli arose through the horizontal transfer of a single DNA segment Tin Yau Panga,b and Martin J. Lerchera,b,1 aInstitute for Computer Science, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany; and bDepartment of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany Edited by W. Ford Doolittle, Dalhousie University, Halifax, Nova Scotia, Canada, and approved November 15, 2018 (received for review October 31, 2017) Even closely related prokaryotes often show an astounding to efficiently metabolize nutrient sources is an essential determi- diversity in their ability to grow in different nutritional environ- nant of bacterial fitness (12), and flux balance analysis (FBA) has ments. It has been hypothesized that complex metabolic adapta- been established as a robust and reliable modeling framework for tions—those requiring the independent acquisition of multiple the prediction of this ability (13, 14). new genes—can evolve via selectively neutral intermediates. A computational analysis of approximate metabolic models However, it is unclear whether this neutral exploration of pheno- generated automatically from genome sequences suggested that type space occurs in nature, or what fraction of metabolic adap- within-species phenotypic divergence is almost instantaneous, tations is indeed complex. Here, we reconstruct metabolic models whereas divergence between genera is gradual or “clock-like” for the ancestors of a phylogeny of 53 Escherichia coli strains, (12). Accordingly, the genetic distance calculated from multi- linking genotypes to phenotypes on a genome-wide, macroevolu- tionary scale. Based on the ancestral and extant metabolic models, locus sequence typing data is a weak indicator of how similar two we identify 3,323 phenotypic innovations in the history of the E. -
Microbial Evolution and Diversity
PART V Microbial Evolution and Diversity This material cannot be copied, disseminated, or used in any way without the express written permission of the publisher. Copyright 2007 Sinauer Associates Inc. The objectives of this chapter are to: N Provide information on how bacteria are named and what is meant by a validly named species. N Discuss the classification of Bacteria and Archaea and the recent move toward an evolutionarily based, phylogenetic classification. N Describe the ways in which the Bacteria and Archaea are identified in the laboratory. This material cannot be copied, disseminated, or used in any way without the express written permission of the publisher. Copyright 2007 Sinauer Associates Inc. 17 Taxonomy of Bacteria and Archaea It’s just astounding to see how constant, how conserved, certain sequence motifs—proteins, genes—have been over enormous expanses of time. You can see sequence patterns that have per- sisted probably for over three billion years. That’s far longer than mountain ranges last, than continents retain their shape. —Carl Woese, 1997 (in Perry and Staley, Microbiology) his part of the book discusses the variety of microorganisms that exist on Earth and what is known about their characteris- Ttics and evolution. Most of the material pertains to the Bacteria and Archaea because there is a special chapter dedicated to eukaryotic microorganisms. Therefore, this first chapter discusses how the Bacte- ria and Archaea are named and classified and is followed by several chapters (Chapters 18–22) that discuss the properties and diversity of the Bacteria and Archaea. When scientists encounter a large number of related items—such as the chemical elements, plants, or animals—they characterize, name, and organize them into groups. -
Antibiotic Resistance and the Evolution of Bacteria Is There a Human Tit Locus?
21 1 57 _N~_~___ v_o_L._m __ -~--~_L_ ~-----------------------NEWSANDVIEWS-------------------------------------'- Microbiology species exhibiting resistance, as the use of the agent continued. It became clear that two processes are in Antibiotic resistance and the volved in the evolution of resistant popula tions: the 'invention' of the resistance genes themselves, and their multiplication evolution of bacteria and spread. Relatively little is known even from Mark Richmond now about the first of the two stages, though there are some clues. As for these A PAPER by Victoria Hughes and Naomi within the population and capable of being cond, the mechanisms of genetic exchange Datta in this week's issue of Nature (p.725) transferred within the members of the discussed above, coupled with selection, fills a gap in our knowledge of the population. Furthermore, that integration can provide a complete explanation. emergence of antibiotic resistance in and excision ofplasmids into and from the One part of this story has, however, bacteria. The study makes use of a chromosome sometimes transferred blocks always been taken for granted, and it is remarkable collection of bacteria made of information from the chromosomal to here that the paper appearing in this week's between 1917 and 1954-before the use of the extrachromosomal state underlined the issue of Nature finally provides definitive antibiotics became widespread and at a fact that a bacterial population as a whole evidence. For the scenario outlined above time when little was known of bacterial had considerably genetic fluidity even if, to be correct, bacterial strains isolated genetics - and kept in sealed vessels since under normal circumstances, this fluidity before the advent of large-scale use of anti that period. -
Burkholderia Cenocepacia Intracellular Activation of the Pyrin
Activation of the Pyrin Inflammasome by Intracellular Burkholderia cenocepacia Mikhail A. Gavrilin, Dalia H. A. Abdelaziz, Mahmoud Mostafa, Basant A. Abdulrahman, Jaykumar Grandhi, This information is current as Anwari Akhter, Arwa Abu Khweek, Daniel F. Aubert, of September 29, 2021. Miguel A. Valvano, Mark D. Wewers and Amal O. Amer J Immunol 2012; 188:3469-3477; Prepublished online 24 February 2012; doi: 10.4049/jimmunol.1102272 Downloaded from http://www.jimmunol.org/content/188/7/3469 Supplementary http://www.jimmunol.org/content/suppl/2012/02/24/jimmunol.110227 Material 2.DC1 http://www.jimmunol.org/ References This article cites 71 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/188/7/3469.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 29, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Activation of the Pyrin Inflammasome by Intracellular Burkholderia cenocepacia Mikhail A. -
Multiple Legionella Pneumophila Effector Virulence Phenotypes
Multiple Legionella pneumophila effector virulence PNAS PLUS phenotypes revealed through high-throughput analysis of targeted mutant libraries Stephanie R. Shamesa,1, Luying Liua, James C. Haveya, Whitman B. Schofielda,b, Andrew L. Goodmana,b, and Craig R. Roya,2 aDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06519; and bMicrobial Sciences Institute, Yale University School of Medicine, New Haven, CT 06519 Edited by Ralph R. Isberg, Howard Hughes Medical Institute/Tufts University School of Medicine, Boston, MA, and approved October 20, 2017 (received for review May 23, 2017) Legionella pneumophila is the causative agent of a severe pneu- poorly understood. Initial forward genetic screens aimed at identi- monia called Legionnaires’ disease. A single strain of L. pneumo- fying avirulent mutants of L. pneumophila were successful in identi- phila encodes a repertoire of over 300 different effector proteins fying essential components of the Dot/Icm system, but these screens that are delivered into host cells by the Dot/Icm type IV secretion did not identify effector proteins translocated by the Dot/Icm system system during infection. The large number of L. pneumophila ef- (10, 11). It is appreciated that most effectors are not essential for fectors has been a limiting factor in assessing the importance of intracellular replication (12), which is why the genes encoding ef- individual effectors for virulence. Here, a transposon insertion se- fector proteins that are important for virulence were difficult to quencing technology called INSeq was used to analyze replication identify by standard screening strategies that assess intracellular of a pool of effector mutants in parallel both in a mouse model of replication using binary assays that measure plaque formation or infection and in cultured host cells. -
Legionella Pneumophila Lifecycle Critical Review Part I Uptake Into Host Cells
water Review Knowledge to Predict Pathogens: Legionella pneumophila Lifecycle Critical Review Part I Uptake into Host Cells Alexis L. Mraz 1 and Mark H. Weir 1,2,* 1 Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH 43210, USA; [email protected] 2 Risk Modeling Division, Applied Research Center, NSF International, Ann Arbor, MI 48105, USA * Correspondence: [email protected]; Tel.: +1-614-292-4066 Received: 16 December 2017; Accepted: 29 January 2018; Published: 31 January 2018 Abstract: Legionella pneumophila (L. pneumophila) is an infectious disease agent of increasing concern due to its ability to cause Legionnaires’ Disease, a severe community pneumonia, and the difficulty in controlling it within water systems. L. pneumophila thrives within the biofilm of premise plumbing systems, utilizing protozoan hosts for protection from disinfectants and other environmental stressors. While there is a great deal of information regarding how L. pneumophila interacts with protozoa and human macrophages (host for human infection), the ability to use this data in a model to attempt to predict a concentration of L. pneumophila in a water system is not known. The lifecycle of L. pneumophila within host cells involves three processes: uptake, growth, and egression from the host cell. The complexity of these three processes would risk conflation of the concepts; therefore, this review details the available information regarding how L. pneumophila invades host cells (uptake) within the context of data needed to model this process, while a second review will focus on growth and egression. The overall intent of both reviews is to detail how the steps in L. -
Legionnaires' Disease
Prevention Port Waterborne Disease Management in Healthcare Settings Healthcare-associated Infections and Emerging Infectious Diseases Workshops January 28, 2020: Metairie February 4, 2020: Bossier City February 5, 2020: Lafayette “ The speaker does not have a financial or non-financial relationship with a commercial interest that would create a conflict of interest with this presentation. ” Disclosure Statement Objectives By the end of this presentation, attendees will be able to: Describe transmission, burden, and prevention measures Legionella pneumophila and Pseudomonas aeruginosa Describe a Water Management Plan Legionella pneumophila Gram-negative rod-shaped bacteria found naturally in the environment worldwide, usually in aquatic environments at least 60 different species, ~20 implicated in human disease Natural Habitat Occurs worldwide Prefers WARM WATERS with scale, sediment, metallic ions, and commensal flora Max multiplication from 25ºC to 45ºC (77-113F) Reduction at >50ºC (122F) No growth above 58.8ºC (138F) Found in 1-30% of home hot water systems Transmission Generally is not present in sufficient numbers in environment to cause disease Inhalation of water contaminated with Legionella aerosols generated by cooling towers, showers, faucets, spas, respiratory therapy equipment, and fountains Aspiration of contaminated potable water also proposed NO Person-to-person transmission Burden of Disease CDC estimates: 8,000 –18,000 cases in the U.S. annually 130-300 in LA Many infections not diagnosed or reported ~50 cases/year reported -
Experimental Microbial Evolution of Extremophiles Paul H
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by DigitalCommons@University of Nebraska University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Faculty Publications in the Biological Sciences Papers in the Biological Sciences 2016 Experimental Microbial Evolution of Extremophiles Paul H. Blum University of Nebraska-Lincoln, [email protected] Deepak Rudrappa University of Nebraska–Lincoln, [email protected] Raghuveer Singh University of Nebraska - Lincoln, [email protected] Samuel McCarthy University of Nebraska-Lincoln, [email protected] Benjamin J. Pavlik University of Nebraska- Lincoln, [email protected] Follow this and additional works at: http://digitalcommons.unl.edu/bioscifacpub Part of the Biology Commons Blum, Paul H.; Rudrappa, Deepak; Singh, Raghuveer; McCarthy, Samuel; and Pavlik, Benjamin J., "Experimental Microbial Evolution of Extremophiles" (2016). Faculty Publications in the Biological Sciences. 623. http://digitalcommons.unl.edu/bioscifacpub/623 This Article is brought to you for free and open access by the Papers in the Biological Sciences at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Faculty Publications in the Biological Sciences by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Published (as Chapter 22) in P. H. Rampelotto (ed.), Biotechnology of Extremophiles, Grand Challenges in Biology and Biotechnology 1, pp. 619–636. DOI 10.1007/978-3-319-13521-2_22 Copyright © 2016 Springer International Publishing Switzerland. digitalcommons.unl.edu Used by permission. Experimental Microbial Evolution of Extremophiles Paul Blum,1 Deepak Rudrappa,1 Raghuveer Singh,1 Samuel McCarthy,1 and Benjamin Pavlik2 1 School of Biological Science, University of Nebraska–Lincoln, Lincoln, NE, USA 2 Department of Chemical and Biomolecular Engineering, University of Nebraska–Lincoln, Lincoln, NE, USA Corresponding author — P. -
EVALUATION of the P45 MOBILE INTEGRATIVE ELEMENT and ITS ROLE IN
EVALUATION OF THE p45 MOBILE INTEGRATIVE ELEMENT AND ITS ROLE IN Legionella pneumophila VIRULENCE A Dissertation by LANETTE M. CHRISTENSEN Submitted to the Office of Graduate and Professional Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Chair of Committee, Jeffrey D. Cirillo Committee Members, James Samuel Jon Skare Farida Sohrabji Head of Program, Warren Zimmer May 2018 Major Subject: Medical Sciences Copyright 2018 Lanette Christensen ABSTRACT Legionella pneumophila are aqueous environmental bacilli that live within protozoal species and cause a potentially fatal form of pneumonia called Legionnaires’ disease. Not all L. pneumophila strains have the same capacity to cause disease in humans. The majority of strains that cause clinically relevant Legionnaires’ disease harbor the p45 mobile integrative genomic element. Contribution of the p45 element to L. pneumophila virulence and ability to withstand environmental stress were addressed in this study. The L. pneumophila Philadelphia-1 (Phil-1) mobile integrative element, p45, was transferred into the attenuated strain Lp01 via conjugation, designating p45 an integrative conjugative element (ICE). The resulting trans-conjugate, Lp01+p45, was compared with strains Phil-1 and Lp01 to assess p45 in virulence using a guinea pig model infected via aerosol. The p45 element partially recovered the loss of virulence in Lp01 compared to that of Phil-1 evident in morbidity, mortality, and bacterial burden in the lungs at the time of death. This phenotype was accompanied by enhanced expression of type II interferon in the lungs and spleens 48 hours after infection, independent of bacterial burden. -
Legionellosis Investigation Form
LEGIONELLOSIS INVESTIGATION FORM BASIC DEMOGRAPHIC DATA Last Name:________________________________ First Name:_______________________________ Middle Name:________________________ DOB: __ __ / __ __ /__ __ __ __ Age: _______ years months Current Sex: Female Male Unknown Is the patient deceased? No Unknown Yes Date of Death: __ __ / __ __ /__ __ __ __ Street Address 1:_____________________________________________________________ Street Address 2:______________________________ City:_______________________________________ State:_______ Zip Code:_______________ County:_______________________________ Home Phone: (__ __ __) ‐ __ __ __ ‐ __ __ __ __ Cell Phone: (__ __ __) ‐ __ __ __ ‐ __ __ __ __ Work Phone: (__ __ __) ‐ __ __ __ ‐ __ __ __ __ Ext. _______ Ethnicity: Hispanic or Latino Not Hispanic or Latino Unknown Race: American Indian/Alaska Native Asian Black/African American Native Hawaiian/Other Pacific Islander White Unknown INVESTIGATION SUMMARY Investigation Start Date: __ __ / __ __ /__ __ __ __ Investigation Status: Open Closed Investigator:__________________________________ REPORTING SOURCE Date of Report: __ __ / __ __ /__ __ __ __ Reporting Source:_______________________________________________________________________ CLINICAL Physician’s Name:_______________________________________________________ Phone Number: (__ __ __) ‐ __ __ __ ‐ __ __ __ __ Ext. _______ Was patient hospitalized for this illness? No Unknown Yes If yes: Hospital Name:_______________________________________________ Admission Date: __ __ -
Center for Food Safety to the 2021 New York Joint Legislative Budget Hearing on Higher Education February 4, 2021
“The Fire Next Time” Testimony of Jean Halloran, Policy Advisor Center for Food Safety To the 2021 New York Joint Legislative Budget Hearing on Higher Education February 4, 2021 Thank you for the opportunity to submit testimony to the Joint Legislative Budget Hearing on Higher Education. I represent the Center for Food Safety, a national organization dedicated to assuring safe food and a safe environment, through legal, scientific and grassroots action. The COVID-19 pandemic has graphically brought home to all of us how a previously unknown disease can wreak havoc not just on our lives in New York, but on human life around the world. One of the key lessons of the pandemic is the importance of prioritizing public health measures. I am testifying today with regard to a public health measure that must be prioritized in New York, and elsewhere, namely preserving the continued effectiveness of antibiotics. If we do not take action now to end antibiotic overuse, which is causing these lifesaving drugs to become ineffective, we will almost certainly face a new public health crisis, the impact of which could equal or even exceed that of the current pandemic. The Higher Ed Committee has a critical role to play in preserving the efficacy of antibiotics by virtue of its role regulating the practices of veterinarians. Veterinarians, especially those who deal with food animals, are key stewards of antibiotics. Two-thirds of all medically important antibiotics are sold for use in animals. Following guidelines established by the US Food and Drug Administration, veterinarians prescribe when and where antibiotic drugs can be administered or fed.