Sunday 26 February 2012

Vegas Luxor guest dies of Legionnaires

Published: Jan. 31, 2012 at 4:35 PM Legionella

LAS VEGAS, Jan. 31 (UPI) -- A guest who stayed at the Luxor Hotel and Casino in Las Vegas in December and contracted Legionnaires' disease has died, Nevada health officials said.

Brian Labus, a senior epidemiologist at the Southern Nevada Health District, said the Centers for Disease Control and Prevention has not released the patient's name or when he or she died, the Las Vegas Sun reported Tuesday.

Health officials found Luxor water samples tested positive for Legionlla bacteria.

Gordon Absher, vice president of public affairs for MGM Resorts International, said super-heating and super-chlorinating water was used to kill the bacteria in the area where the deceased guest stayed, within a day the test results were confirmed, Absher said.

Within 10 days the hotel will undertake a voluntary remediation for the rest of the hotel, Absher said.

"We take this very seriously," Absher told the Sun said. "Health of our guests and our employees is of paramount importance to MGM Resorts."

The Luxor also developed a monitoring plan to prevent this from occurring, Labus said.

Last spring, two guests staying at the Luxor also became ill with Legionnaires' disease, but both recovered.

At the time, the health district collected bulk water samples for an environmental assessment, but no Legionella bacteria were detected, officials said.


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Plasma‐activated carbon nanotube‐based high sensitivity immunosensors for monitoring Legionella pneumophila by direct detection of maltose binding protein peptidoglycan‐associated lipoprotein (MBP‐PAL)

Saturday 25 February 2012

Application of Legionella pneumophila-specific quantitative real-time PCR combined with direct amplification and sequence-based typing in the diagnosis and epidemiological investigation of Legionnaires’ disease

Immunosuppressants/tumour necrosis factor inhibitors: Legionnaires' disease: 24 case reports

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Keywords: Adalimumab, adverse reactions - serious; Azathioprine, adverse reactions - serious; Elderly; Etanercept, adverse reactions - serious; Hydroxychloroquine, adverse reactions - serious; Infliximab, adverse reactions - serious; Leflunomide, adverse reactions - serious; Legionnaires'-disease, drug-induced; Mercaptopurine, adverse reactions - serious; Methotrexate, adverse reactions - serious; Methylprednisolone, adverse reactions - serious; Prednisone, adverse reactions - serious

Document Type: Short communication

Publication date: 2012-01-01


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Outbreak of Legionnaires' Disease Traced to Hospital Fountain

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WEDNESDAY, Jan. 11 (HealthDay News) -- A decorative fountain in a hospital lobby was the cause of a 2010 Legionnaires' disease outbreak in Wisconsin, a new study says.

Legionnaires' disease is a severe and potentially deadly form of pneumonia caused by the bacteria Legionella, which can be inhaled from contaminated water sources.

State and local health officials launched an investigation after eight people in southeast Wisconsin developed Legionnaires' disease. After interviewing the patients, investigators identified one hospital as the origin of the outbreak.

Environmental testing within the hospital found notable amounts of Legionella in samples collected from the "water wall" decorative fountain in the hospital's main lobby. All eight patients had spent time in the lobby, the study said.

The fountain was shut down when it was first suspected as a source of the outbreak and hospital officials alerted staff and about 4,000 potentially exposed patients and visitors. All eight patients recovered and no further cases of Legionnaires' disease occurred after the fountain was shut down.

Before the outbreak, the fountain had undergone routine cleaning and maintenance, the researchers said.

"Since our investigation, the Wisconsin Division of Public Health has developed interim guidelines advising health-care facilities with decorative fountains to establish strict maintenance procedures and conduct periodic bacteriologic monitoring for Legionella," study lead author Thomas Haupt, an epidemiologist with the Wisconsin Division of Public Health, said in a journal news release.

"The guidelines stress that until additional data are available that demonstrate effective maintenance procedures for eliminating the risk of Legionella transmission from indoor decorative water fountains in health-care settings, water fountains of any type should be considered at risk of becoming contaminated with Legionella bacteria," he added.

The study appears in the February issue of the journal Infection Control and Hospital Epidemiology.


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[Case Report] Pneumonia associated with a dental unit waterline

Pneumonia associated with a dental unit waterline : The Lancet Skip Main Navigation The LancetRSS Feeds RSS
Subscribe|Register|CloseUsername:Password:Forgotten Username or Password?Remember me on this computer until I logoutSearch for in All FieldsArticle Title, Abstract, KeywordsAuthorsArticle TitleAbstractAdvanced SearchHome|JournalsThe LancetThe Lancet Infectious DiseasesThe Lancet NeurologyThe Lancet Oncology|Specialties|Clinical|Global Health|Audio|ConferencesThe Lancet ConferencesConference CollaborationsMeet the Editors at Conferences|Information forAuthorsAdvertisersPress|Healthcare Jobs outline goes here The Lancet, Volume 379, Issue 9816, Page 684, 18 February 2012 Cite or Link Using DOI Pneumonia associated with a dental unit waterlineOriginal TextDr Maria Luisa Ricci BiolD a Corresponding AuthorEmail Address, Stefano Fontana PhD a, Federica Pinci BiolD a, Emanuela Fiumana MD b, Maria Federica Pedna BiolD c, Paolo Farolfi MD e, Maria Antonietta Bucci Sabattini BiolD d, Maria Scaturro PhD aIn February, 2011, an 82-year-old woman was admitted to the intensive care unit with fever and respiratory distress. She was conscious and responsive. Chest radiography showed several areas of lung consolidation. She had no underlying disease. Legionnaires' disease was promptly diagnosed by Legionella pneumophila urinary antigen test; a bronchial aspirate was taken for microbiological examination. Oral ciprofloxacin (750 mg every 12 h) was started immediately. Nevertheless, the patient developed f ... To read this article in full you will need to login or make a paymentAlready Registered?  Please LoginUsername:Password: Forgotten Username or Password?Remember me on this computer until I logout Payment Options Purchase this article for $31.50 Online access for 24 hours. The PDF version can be downloaded as your permanent record. Subscribe to The Lancet
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Renew your print subscriptionHave a Free Trial Code?Activate your free trial a Department of Infectious Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Rome, Italyb Azienda Unità Sanitaria Locale, Forlì, Italyc Azienda Unità Sanitaria Locale, Cesena, Italyd Agenzia Regionale Prevenzione e Ambiente, Bologna, Italye “G B Morgagni-Pierantoni” Hospital, Department of Emergency Anaesthesia and Intensive Care Unit, Forlì, ItalyCorresponding Author Information Correspondence to: Dr Maria Luisa Ricci, Department of Infectious Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Viale Regina Elena 299, Roma, 00161, Italy Access this article on SciVerse ScienceDirect Visit SciVerse ScienceDirect to see if you have access via your institution. Article OptionsFull TextPDF (48 KB)Printer Friendly VersionRequest permissionExport CitationCreate Citation AlertClosePlease login above or register to use this functionality. Registration is free, takes no more than two minutes, and offers you many benefits. Other Articles of InterestReviewHospital-acquired legionellosis: solutions for a preventable infectionmore information Miguel Sabria,Victor L Yu.The Lancet Infectious Diseases 1 June 2002; Volume 2, Issue 6: Page 368ReviewProblem pathogens: paediatric legionellosis—implications for improved diagnosismore information David Greenberg,Christine C Chiou,Ronald Famigilleti,Tzielan C Lee,Victor L Yu.The Lancet Infectious Diseases 1 August 2006; Volume 6, Issue 8: Page 529LEGIONELLACEAE IN THE HOSPITAL WATER-SUPPLYmore information Michele Best,Janet Stout,RobertR. Muder,VictorL. Yu,Angella Goetz,Floyd Taylor.The Lancet 6 August 1983; Volume 322, Issue 8345: Page 307SUBTYPES OF LEGIONELLA PNEUMOPHILA SEROGROUP 1 ASSOCIATED WITH DIFFERENT ATTACK RATESmore information J.F. Plouffe,W.E. Maher,M.F. Para,B. Hackman,L. Webster.The Lancet 17 September 1983; Volume 322, Issue 8351: Page 649EFFECT OF RUBBERS AND THEIR CONSTITUENTS ON PROLIFERATION OF LEGIONELLA PNEUMOPHILA IN NATURALLY CONTAMINATED HOT WATERmore information CorJ. Niedeveld,FredM. Pet,PieterL. Meenhorst.The Lancet 26 July 1986; Volume 328, Issue 8500: Page 180 BookmarkDeliciousDiggredditFacebookStumbleUpon Privacy Policy |Terms and Conditions |Contact Us | About UsCopyright © 2012 Elsevier Limited. All rights reserved. The Lancet® is a registered trademark of Elsevier Properties S.A., used under licence.
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Characteristic morphology of intracellular microcolonies of Legionella oakridgensis OR-10

Yuta Takekawa,a,* Mitsumasa Saito,a Changle Wang,a Tian Qin,b Midori Ogawa,c Takaaki Kanemaru,d Shin-ichi Yoshidaa aDepartment of Bacteriology, Faculty of Medical Sciences, Kyushu University, Fukuoka, 812 - 8582, Japan.

bNational Institute for Communicable Disease Control and Prevention and State Key Laboratory for Infectious Disease Prevention and Control, Chinese Center for Disease Control and Prevention, P.O. Box 5, Changping, Beijing 102206, People’s Republic of China.

cDepartment of Microbiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Fukuoka, 807 - 8555, Japan.

dDepartment of Morphology Core Unit, Kyushu University Hospital, Fukuoka, 812 - 8582, Japan.

*Present address: Mie Prefecture Health and Environment Research Institute, 3684-11 Sakura-machi, Yokkaichi, Mie 512-1211, Japan

Published on the web 20 January 2012.

Canadian Journal of Microbiology, 2012, 58:(2) 179-183, 10.1139/w11-126

Barysheva OV, Fujii J, Takaesu G, Yoshida S. 2008. Application of unstable Gfp variants to the kinetic study of Legionella pneumophilaicm gene expression during infection. Microbiology 154(4): 1015-1025 CrossRef, Medline.Daisy JA, Benson CE, McKitrick J, Friedman HM. 1981. Intracellular replication of Legionella pneumophila. J. Infect. Dis. 143(3): 460-464 CrossRef, Medline.Fields BS, Shotts EB Jr, Feeley JC, Gorman GW, Martin WT. 1984. Proliferation of Legionella pneumophila as an intracellular parasite of ciliated protozoan Tetrahymena pyriformis. Appl. Environ. Microbiol. 47(3): 467-471 Medline.Gress FM, Myerowitz RL, Pasculle AW, Rinaldo CR Jr, Dowling JN. 1980. The ultrastructural morphologic features of Pittsburgh pneumonia agent. Am. J. Pathol. 101(1): 63-77 Medline.Izu K, Yoshida S, Miyamoto H, Chang B, Ogawa M, Yamamoto H, et al.. 1999. Grouping of 20 reference strains of Legionella species by the growth ability within mouse and guinea pig macrophages. FEMS Immunol. Med. Microbiol. 26(1): 61-68 CrossRef, Medline.Kuroki H, Miyamoto H, Fukuda K, Iihara H, Kawamura Y, Ogawa M, et al.. 2007. Legionella impletisoli sp. nov., and Legionella yabuuchiae sp. nov., isolated from soils contaminated with industrial wastes in Japan. Syst. Appl. Microbiol. 30(4): 273-279 CrossRef, Medline.Lo Presti F, Riffard S, Jarraud S, Le Gallou F, Richet H, Vandenesch F, Etienne J. 2000. Isolation of Legionella oakridgensis from two patients with pleural effusion living in the same geographical area. J. Clin. Microbiol. 38(8): 3128-3130 Medline.Maruta K, Miyamoto H, Hamada T, Ogawa M, Taniguchi H, Yoshida S. 1998a. Entry and intracellular growth of Legionella dumoffii in alveolar epithelial cells. Am. J. Respir. Crit. Care Med. 157(6): 1967-1974 Medline.Maruta K, Ogawa M, Miyamoto H, Izu K, Yoshida S. 1998b. Entry and intracellular localization of Legionella dumoffii in Vero cells. Microb. Pathog. 24(2): 65-73 CrossRef, Medline.Middlebrook G, Dubos RJ, Pierce C. 1947. Virulence and morphological characteristics of mammalian tubercle bacilli. J. Exp. Med. 86(2): 175-184 CrossRef, Medline.Ogawa M, Takade A, Miyamoto H, Taniguchi H, Yoshida S. 2001. Morphological variety of intracellular microcolonies of Legionella species in Vero cells. Microbiol. Immunol. 45(7): 557-562 Medline.Oldham LJ, Rodgers FG. 1985. Adhesion, penetration and intracellular replication of Legionella pneumophila: an in vitro model of pathogenesis. J. Gen. Microbiol. 131(4): 697-706 Medline.Orrison LH, Cherry WB, Tyndall RL, Fliermans CB, Gough SB, Lambert MA, et al.. 1983. Legionella oakridgensis: Unusual new species isolated from cooling tower water. Appl. Environ. Microbiol. 45(2): 536-545 Medline.Staropoli JF, Branda JA. 2008. Cord formation in a clinical isolate of Mycobacterium marinum. J. Clin. Microbiol. 46(8): 2814-2816 CrossRef, Medline.Tang PW, Toma S, MacMillan LG. 1985. Legionella oakridgensis: Laboratory diagnosis of a human infection. J. Clin. Microbiol. 21(3): 462-463 Medline.

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Officials: Harmful Bacteria At Playboy Mansion


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Friday 24 February 2012

Respiratory syncytial virus (RSV) community-acquired pneumonia (CAP) in a hospitalized adult with human immunodeficiency virus (HIV) mimicking influenza A and Pneumocystis (carinii) jiroveci pneumonia (PCP)

Contaminated Dental Surgery Equipment Source of Legionnaire's Disease Death

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Academic Journal
Main Category: Dentistry
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 17 Feb 2012 - 5:00 PST

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This week's issue of The Lancet describes a case report of an 82-year-old woman in Italy who died of Legionnaires disease after becoming infected with L pneumophila at her dentist. This case has prompted the authors - led by Dr Maria Luisa Ricci at the Istituto Superiore di Sanita, Rome, Italy, to call for various control measures at dental surgeries to prevent similar incidents.

Suffering with fever and respiratory distress, the woman who was conscious and responsive and had no underlying disease, was admitted in February, 2011, to the intensive care unit of the "G.B. Morgagni-Pierantoni" Hospital, Department of emergency Anaesthesia and Intensive Care Unit, Forlì, Italy.

Results from a chest radiography showed multiple areas of lung consolidation. A Legionella pneumophila urinary antigen test quickly diagnosed the woman with Legionnaires' disease and she was immediately given oral antibiotics (ciprofloxacin) every 12 hours. However, she sadly died two days later after developing rapid and irreversible septic shock, prompting an investigation to find the source of L pneumophila.

The patient had been at home for the majority of the time during the 2 to 10 day incubation period, leaving only twice to attend dentist appointments.

The investigators took water samples from the dental practice's tap, the tap and the high-speed turbine of the dental unit waterlines, as well as from the woman's home (shower and taps) in order to investigate possible L pneumophila contamination. They found that samples from her home tested negative for L pneumophila, but samples from the dental practice tested positive. After laboratory experiments were conducted, results showed genomic matching between L pneumphila in the dental unit waterline and in the women's respiratory secretion.

L pneumophila is a Gram-negative bacterium found in man-made water systems and is ubiquitous in natural water environments. The bacteria can infect individuals by inhalation or microaspiration of aerosolized water causing Pontiac fever (a flu-like disease) or Legionnaires' disease (severe pneumonia), mostly affecting immune-compromised patients and the elderly.

Spas, fountains, air-conditioning systems, and hot-water systems, have been demonstrated to be leading sources of infection.

It has been widely documented that dental waterlines are substantially contaminated with Legionella and studies have also demonstrated that the blood of dentists and dental practice staff has a higher prevalence of antibodies to L pneumophila, which indicates that people working in a dental practice environment are potentially at risk. However, prior to this case, the researchers knew no other cases in which Legionnaires' disease had been linked to this source of infection.

The authors explain:

"The case here shows that the disease can be acquired from a dental unit waterline during routine dental treatment. Aerosolized water from high-speed turbine instruments was most likely the source of the infection. Legionella contamination in dental unit waterlines must be minimized to prevent exposure of patients and staff to the bacterium.

We suggest several control measures: use of anti-stagnation and continuous-circulation water systems; use of sterile water instead of the main water supply in the dental unit waterline; application of discontinuous or continuous disinfecting treatment; daily flushing of all outlets and before each dental treatment; use of filters upstream of the instruments; and annual monitoring of the waterline. Further useful procedures to prevent legionellosis within dental surgeries can be obtained from [already available] dedicated guidelines."

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our dentistry section for the latest news on this subject. “Pneumonia associated with a dental unit waterline” Maria Luisa Ricci et al.
The Lancet, Volume 379, Issue 9816, Page 684, 18 February 2012, doi:10.1016/S0140-6736(12)60074-9 Please use one of the following formats to cite this article in your essay, paper or report:

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Grace Rattue. "Contaminated Dental Surgery Equipment Source of Legionnaire's Disease Death." Medical News Today. MediLexicon, Intl., 17 Feb. 2012. Web.
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Las Vegas' Luxor guests had Legionnaires': officials

Home : Health : Las Vegas' Luxor guests had Legionnaires': officials

In this June 5, 2004 file photo, the Mandalay Bay towers, left and center rear, and the Luxor hotel, are seen in Las Vegas. (AP Photo/Las Vegas Sun, R. Marsh Starks, File) SLIDES.showHideViewT();The Associated Press

Date: Tuesday Jan. 31, 2012 9:25 AM ET

LAS VEGAS — Health officials in Las Vegas said Monday that the bacteria that causes Legionnaires' disease was found in water samples at the Luxor hotel-casino this month after a guest died of the form of pneumonia.

The Southern Nevada Health District said the Centers for Disease Control and Prevention national surveillance program reported three cases in the past year of Luxor guests being diagnosed with the disease caused by Legionella bacteria.

The Las Vegas Strip resort's water was tested after the first two cases were reported during the spring of last year, but no Legionella bacteria was detected, district officials said. Those guests recovered.

Officials say the Luxor, owned by MGM Resorts International, immediately began a remediation process once the bacteria was found.

MGM Resorts spokesman Gordon Absher said treatment procedures include superheating and super-chlorination of the water system.

"We are confident in the integrity of our systems and the safety protocols we follow at all our hotels. Guest and employee safety is always a top priority at our company," Absher said. "Even before last summer, MGM Resorts led the industry with aggressive and stringent programs to control Legionella issues common to all large buildings."

Absher said the company's resorts regularly test for Legionella and treat water systems preventatively, before bacteria are detected.

The new cases come as the company is already facing a civil lawsuit from guests who said they were infected with Legionella at the Aria Resort & Casino, part of the CityCenter complex that is half-owned by MGM Resorts.

MGM Resorts notified guests that they might have been exposed to the bacteria between June 21 and July 4 after the district reported six cases of Legionnaires' disease in July. The district said those guests recovered after treatment.

Eight guests sued in August, seeking $337.5 million in damages from the resort and its builders. An MGM Resorts spokesman at the time denied negligence, saying hotel officials carefully communicated with its guests and reimbursed them fairly for legitimate medical expenses. The case is still pending in federal court in Las Vegas.

Most people who are exposed to the bacteria don't get sick, according to the CDC. Smokers, people over age 50 and those who have chronic lung disease or weak immune systems are most susceptible, the CDC said.

The bacteria isn't spread between people. It grows most often in warm water, infecting people when they breathe in mist or vapor that has been contaminated.

The disease takes its name from an outbreak at the Pennsylvania American Legion convention held at the Bellevue-Stratford Hotel in Philadelphia in 1976.

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Live Legionella pneumophila induces MUC5AC production by airway epithelial cells independently of intracellular invasion

Yoshitomo Morinaga,a Katsunori Yanagihara,a Nobuko Araki,a Yohei Migiyama,a,b Kentaro Nagaoka,a,b Yosuke Harada,a,b Koichi Yamada,a,b Hiroo Hasegawa,a Tomoya Nishino,b Koichi Izumikawa,b Hiroshi Kakeya,b Yoshihiro Yamamoto,b Shigeru Kohno,b,c Shimeru Kamihiraa aDepartment of Laboratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1, Sakamoto, Nagasaki, 852-8501, Japan.

bSecond Department of Internal Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

cGlobal COE Program, Nagasaki University, Nagasaki, Japan.

Published on the web 20 January 2012.

Canadian Journal of Microbiology, 2012, 58:(2) 151-157, 10.1139/w11-123

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Health board fined after patient contracts Legionnaires'

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Thursday 23 February 2012

Study Links Hospital Water Wall, Legionnaires' Disease


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An Outbreak of Legionnaires Disease Associated with a Decorative Water Wall Fountain in a Hospital

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Innate Immune Pathways Triggered by Listeria monocytogenes and Their Role in the Induction of Cell-Mediated Immunity.

Graduate Group in Microbiology, University of California, Berkeley, Berkeley, California, USA.

Acquired cell-mediated immunity to Listeria monocytogenes is induced by infection with live, replicating bacteria that grow in the host cell cytosol, whereas killed bacteria, or those trapped in a phagosome, fail to induce protective immunity. In this chapter, we focus on how L. monocytogenes is sensed by the innate immune system, with the presumption that innate immunity affects the development of acquired immunity. Infection by L. monocytogenes induces three innate immune pathways: an MyD88-dependent pathway emanating from a phagosome leading to expression of inflammatory cytokines; a STING/IRF3-dependent pathway emanating from the cytosol leading to the expression of IFN-ß and coregulated genes; and very low levels of a Caspase-1-dependent, AIM2-dependent inflammasome pathway resulting in proteolytic activation and secretion of IL-1ß and IL-18 and pyroptotic cell death. Using a combination of genetics and biochemistry, we identified the listerial ligand that activates the STING/IRF3 pathway as secreted cyclic diadenosine monophosphate, a newly discovered conserved bacterial signaling molecule. We also identified L. monocytogenes mutants that caused robust inflammasome activation due to bacteriolysis in the cytosol, release of DNA, and activation of the AIM2 inflammasome. A strain was constructed that ectopically expressed and secreted a fusion protein containing Legionella pneumophila flagellin that robustly activated the Nlrc4-dependent inflammasome and was highly attenuated in mice, also in an Nlrc4-dependent manner. Surprisingly, this strain was a poor inducer of adaptive immunity, suggesting that inflammasome activation is not necessary to induce cell-mediated immunity and may even be detrimental under some conditions. To the best of our knowledge, no single innate immune pathway is necessary to mount a robust acquired immune response to L. monocytogenes infection.

Copyright © 2012 Elsevier Inc. All rights reserved.


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Environmental surveillance and molecular characterization of Legionella in tropical Singapore.

Environmental Health Institute, National Environment Agency, Singapore, 11 Biopolis Way #06-05/08 Helios Block Singapore 138667.

Legionnaires' disease is often acquired by inhalation of legionellae from a contaminated environmental source. In recent years, Singapore has seen an increase in the use of aerosol-generating fixtures such as mist fans and spa pools. Poorly maintained and designed water fixtures could pose a public health threat to the community. In this study, we provided an update on the prevalence of Legionella in mist fans (N=28), household water heaters with storage tanks (N=19) and instantaneous heaters (N=30); and extended the survey to spa pools (N=29) and aerosol-generating fixtures in nursing homes (N=116). The prevalence of Legionella were 21.1% in water heaters with storage tanks, 24.1% in spa pools, 14.2% in mist fans and 3.3% in instantaneous heaters. Legionella was not detected in nursing homes. A total of 37 isolates were subjected to molecular characterization using Sequence-Based Typing (SBT) protocol from the European Working Group on Legionella Infections (EWGLI). This is the first study on the use of SBT protocol on environmental strains isolated from tropical South East Asia. The Legionella flora was very heterogenous. The overall diversity of the allelic profile was found to be 0.970 (95% CI 0.946 - 0.994). All known STs of our isolates have been associated with clinical cases in EWGLI database. The phylogenetic analysis showed that our novel environmental isolates were clustered with clinical STs that were previously reported in Europe, Japan, United Kingdom and United States etc. (in EWGLI database), suggesting that Legionella found in the environment of Singapore may potentially cause human disease.


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Domain organization of Legionella effector SetA

Domain organization of Legionella effector SetA - Jank - 2012 - Cellular Microbiology - Wiley Online LibrarySkip to Main Content

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PUBLICATIONSBROWSE BY SUBJECTRESOURCESABOUT US LOGIN Enter e-mail address Enter password REMEMBER ME NOT REGISTERED ?FORGOTTEN PASSWORD ?INSTITUTIONAL LOGIN > Home > Microbiology & Virology > Microbiology & Virology > Journal Home > Early View > Abstract JOURNAL TOOLS Get New Content Alerts Get RSS feed Save to My Profile Get Sample Copy Recommend to Your Librarian JOURNAL MENUJournal HomeFIND ISSUESCurrent IssueAll Issues FIND ARTICLES Early ViewAccepted Articles GET ACCESS Subscribe / Renew FOR CONTRIBUTORS Author GuidelinesSubmit an Article ABOUT THIS JOURNAL NewsOverviewEditorial BoardPermissionsAdvertiseContact SPECIAL FEATURES Faculty of 1000Parasitology Virtual Special IssuePostersVirology Virtual Special IssueWiley Job Network Domain organization of Legionella effector SetAThomas Jank1, Kira E. Böhmer1, Tina Tzivelekidis1, Carsten Schwan1, Yury Belyi2, Klaus Aktories1,*Article first published online: 21 FEB 2012

DOI: 10.1111/j.1462-5822.2012.01761.x

© 2012 Blackwell Publishing Ltd

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How to CiteJank, T., Böhmer, K. E., Tzivelekidis, T., Schwan, C., Belyi, Y. and Aktories, K. (2012), Domain organization of Legionella effector SetA. Cellular Microbiology. doi: 10.1111/j.1462-5822.2012.01761.x

Author Information1

Institut für Experimentelle und Klinische Pharmakologie und Toxikologie, Albert-Ludwigs-Universität Freiburg, Albertstr. 25, Freiburg D-79104, Germany

2

Gamaleya Research Institute, Ulitsa Gamalei 18, Moscow 123098, Russia

* E-mail klaus.aktories@pharmakol.uni-freiburg.de; Tel. (+49) 761 203 5301; Fax (+49) 761 203 5311.

Publication HistoryArticle first published online: 21 FEB 2012Accepted manuscript online: 31 JAN 2012 04:43AM ESTReceived 25 November, 2011; revised 13 January, 2012; accepted 17 January, 2012. SEARCH Search Scope All contentPublication titlesIn this journalIn this issue Search String Advanced >Saved Searches > SEARCH BY CITATION Volume: Issue: Page: ARTICLE TOOLSGet PDF (2198K)Save to My ProfileE-mail Link to this ArticleExport Citation for this ArticleGet Citation AlertsRequest Permissions AbstractArticleReferencesSupporting InformationCited By View Full Article with Supporting Information (HTML) Get PDF (2198K) Summary

Legionella pneumophila is a human pathogen causing severe pneumonia called Legionnaires' disease. Multiple Legionella effectors are type IV-secreted into the host cell to establish a specific vesicular compartment for pathogen replication. Recently, it has been reported that the Legionella effector SetA shares sequence similarity with glycosyltransferases and interferes with vesicular trafficking of host cells. Here we show that SetA possesses glycohydrolase and mono-O-glucosyltransferase activity by using UDP-glucose as a donor substrate. Whereas the catalytic activity is located at the N terminus of SetA, the C terminus (amino acids 401–644) is essential for guidance of SetA to vesicular compartments of host cells. EGFP-SetA expressed in HeLa cells localizes to early endosomes by interacting with phosphatidylinositol 3-phosphate. EGFP-SetA, transiently expressed in RAW 264.7 macrophages, associates with early phagosomes after infection with Escherichia coli and L. pneumophila. Only the combined expression of the C- and N-terminal domains induces growth defects in yeast similar to full-length SetA. The data indicate that SetA is a multidomain protein with an N-terminal glucosyltransferase domain and a C-terminal phosphatidylinositol 3-phosphate-binding domain, which guides the Legionella effector to the surface of the Legionella-containing vacuole. Both, the localization and the glucosyltransferase domains of SetA are crucial for cellular functions.

View Full Article with Supporting Information (HTML) Get PDF (2198K) More content like this Find more content: like this article Find more content written by:Thomas JankKira E. BöhmerTina TzivelekidisCarsten SchwanYury BelyiKlaus AktoriesAll Authors ABOUT USHELPCONTACT USAGENTSADVERTISERSMEDIAPRIVACYTERMS & CONDITIONSSITE MAP

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Purdue scientists reveal how bacteria build homes inside healthy cells

[ Back to EurekAlert! ] Public release date: 20-Dec-2011
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Contact: Elizabeth K. Gardner
ekgardner@purdue.edu
765-494-2081
Purdue University

WEST LAFAYETTE, Ind. - Bacteria are able to build camouflaged homes for themselves inside healthy cells - and cause disease - by manipulating a natural cellular process.

Purdue University biologists led a team that revealed how a pair of proteins from the bacteria Legionella pneumophila, which causes Legionnaires disease, alters a host protein in order to divert raw materials within the cell for use in building and disguising a large structure that houses the bacteria as it replicates.

Zhao-Qing Luo, the associate professor of biological sciences who headed the study, said the modification of the host protein creates a dam, blocking proteins that would be used as bricks in cellular construction from reaching their destination. The protein "bricks" are then diverted and incorporated into a bacterial structure called a vacuole that houses bacteria as it replicates within the cell. Because the vacuole contains materials natural to the cell, it goes unrecognized as a foreign structure.

"The bacterial proteins use the cellular membrane proteins to build their house, which is sort of like a balloon," Luo said. "It needs to stretch and grow bigger as more bacterial replication occurs. The membrane material helps the vacuole be more rubbery and stretchy, and it also camouflages the structure. The bacteria is stealing material from the cell to build their own house and then disguising it so it blends in with the neighborhood."

The method by which the bacteria achieve this theft is what was most surprising to Luo.

The bacterial proteins, named AnkX and Lem3, modify the host protein through a biochemical process called phosphorylcholination that is used by healthy cells to regulate immune response. Phosphorylcholination is known to happen in many organisms and involves adding a small chemical group, called the phosphorylcholine moiety, to a target molecule, he said.

The team discovered that AnkX adds the phosphorylcholine moiety to a host protein involved in moving proteins from the cell's endoplasmic reticulum to their cellular destinations. The modification effectively shuts down this process and creates a dam that blocks the proteins from reaching their destination.

The bacterial protein Lem3 is positioned outside the vacuole and reverses the modification of the host protein to ensure that the protein "bricks" are free to be used in creation of the bacterial structure.

This study was the first to identify proteins that directly add and remove the phosphorylcholine moiety, Luo said.

"We were surprised to find that the bacterial proteins use the phosphorylcholination process and to discover that this process is reversible," he said. "This is evidence of a new way signals are relayed within cells, and we are eager to investigate it."

The team also found that the phosphorylcholination reaction is carried out at a specific site on the protein called the Fic domain. Previous studies had shown this site induced a different reaction called AMPylation.

It is rare for a domain to catalyze more than one reaction, and it was thought this site's only responsibility was to transfer the chemical group necessary for AMPylation, Luo said.

"Revealing that this domain has dual roles is very important to identify or screen for compounds to inhibit its activity and fight disease," he said. "This domain has a much broader involvement in biochemical reactions than we thought and may be a promising target for effective treatments."

During infection bacteria deliver hundreds of proteins into healthy cells that alter cellular processes to turn the hostile environment into one hospitable to bacterial replication, but the specific roles of only about 20 proteins are known, Luo said.

"In order to pinpoint proteins that would be good targets for new antibiotics, we need to determine their roles and importance to the success of infection," he said. "We need to understand at the biochemical level exactly what these proteins do and how they take over natural cellular processes. Then we can work on finding ways to block these activities, stop the infection and save lives."

A paper detailing their National Institutes of Health-funded work is published in the current issue of the Proceedings of National Academy of Sciences. In addition to Luo, Purdue graduate student Yunhao Tan and Randy Ronald of Indiana University co-authored the paper. Luo next plans to use the bacterial proteins as a tool to learn more about the complex cellular processes controlled by phosphorylcholination and to determine the biochemical processes role in cell signaling.

Writer: Elizabeth K. Gardner, 765-494-2081, ekgardner@purdue.edu Source: Zhao-Wing Luo, 765-496-6697, luoz@purdue.edu

Related website:
Luo lab: http://bilbo.bio.purdue.edu/luolab/

Related news release:
Purdue biologists identify new strategy used by bacteria during infection: http://www.purdue.edu/newsroom/research/2011/110712LuoNature.html

PHOTO CAPTION:
Purdue associate professor of biological sciences Zhao-Qing Luo, at right, and graduate student Yunhao Tan look at the growth of Legionella pneumophila bacteria in a petri dish. (Purdue University photo provided by Laurie Iten and Rodney McPhail)

A publication-quality photo is available at http://news.uns.purdue.edu/images/2011/luo-legionella.jpg

Abstract on the research in this release can be found at: http://www.purdue.edu/newsroom/research/2011/111220LuoPNAS.html


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Wednesday 22 February 2012

3rd Briton dies of Legionnaires' disease in Spanish hotel

Home : Health : 3rd Briton dies of Legionnaires' disease in Spanish hotel

Hearing test SLIDES.showHideViewT();The Associated Press

Date: Friday Feb. 3, 2012 6:22 AM ET

MADRID, Spain — Spanish health officials say a third British national has died from Legionnaires' disease while vacationing in Spain.

A Valencia regional government statement Friday said the three, aged between 73 and 78, had contracted the disease at a hotel in the eastern town of Calpe.

The Valencia statement said a further 10 Britons and four Spaniards are being treated for the disease.

The U.K.-based company Saga Holidays reported the first two deaths Thursday, saying the Britons had stayed at the Diamante Beach Hotel in Calpe.

The names of the three victims were not released.

The regional government said authorities have taken measures to control the outbreak, including closing the hotel.

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