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

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

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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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

Akamine M, Higa F, Arakaki N, Kawakami K, Takeda K, Akira S, Saito A. 2005. Differential roles of Toll-like receptors 2 and 4 in in vitro responses of macrophages to Legionella pneumophila. Infect. Immun. 73(1): 352-361 CrossRef, Medline.Araki N, Yanagihara K, Morinaga Y, Yamada K, Nakamura S, Yamada Y, et al.. 2010. Azithromycin inhibits nontypeable Haemophilus influenzae-induced MUC5AC expression and secretion via inhibition of activator protein-1 in human airway epithelial cells. Eur. J. Pharmacol. 644(1–3): 209-214 CrossRef, Medline.Bitar DM, Molmeret M, Abu Kwaik Y. 2004. Molecular and cell biology of Legionella pneumophila. Int. J. Med. Microbiol. 293(7–8): 519-527 CrossRef, Medline.Chang B, Amemura-Maekawa J, Kura F, Kawamura I, Watanabe H. 2004. Expression of IL-6 and TNF-a in human alveolar epithelial cells is induced by invading, but not by adhering, Legionella pneumophila. Microb. Pathog. 37(6): 295-302 CrossRef, Medline.Chen R, Lim JH, Jono H, Gu XX, Kim YS, Basbaum CB, et al.. 2004. Nontypeable Haemophilus influenzae lipoprotein P6 induces MUC5AC mucin transcription via TLR2–TAK1-dependent p38 MAPK-AP1 and IKKß-I?Ba-NF-?B signaling pathways. Biochem. Biophys. Res. Commun. 324(3): 1087-1094 CrossRef, Medline.DeFife KM, Jenney CR, Colton E, Anderson JM. 1999. Disruption of filamentous actin inhibits human macrophage fusion. FASEB J. 13(8): 823-832 Medline.Friedman H, Yamamoto Y, Klein TW. 2002. Legionella pneumophila pathogenesis and immunity. Semin. Pediatr. Infect. Dis. 13(4): 273-279 CrossRef, Medline.Horwitz MA. 1983. Formation of a novel phagosome by the Legionnaires’ disease bacterium (Legionella pneumophila) in human monocytes. J. Exp. Med. 158(4): 1319-1331 CrossRef, Medline.Imamura Y, Yanagihara K, Mizuta Y, Seki M, Ohno H, Higashiyama Y, et al.. 2004. Azithromycin inhibits MUC5AC production induced by the Pseudomonas aeruginosa autoinducer N-(3-oxododecanoyl) homoserine lactone in NCI-H292 cells. Antimicrob. Agents Chemother. 48(9): 3457-3461 CrossRef, Medline.Inoue D, Yamaya M, Kubo H, Sasaki T, Hosoda M, Numasaki M, et al.. 2006. Mechanisms of mucin production by rhinovirus infection in cultured human airway epithelial cells. Respir. Physiol. Neurobiol. 154(3): 484-499 CrossRef, Medline.Kraft M, Adler KB, Ingram JL, Crews AL, Atkinson TP, Cairns CB, et al.. 2008. Mycoplasma pneumoniae induces airway epithelial cell expression of MUC5AC in asthma. Eur. Respir. J. 31(1): 43-46 CrossRef, Medline.Lewinsohn DM, Alderson MR, Briden AL, Riddell SR, Reed SG, Grabstein KH. 1998. Characterization of human CD8+ T cells reactive with Mycobacterium tuberculosis-infected antigen-presenting cells. J. Exp. Med. 187(10): 1633-1640 CrossRef, Medline.Li D, Gallup M, Fan N, Szymkowski DE, Basbaum CB. 1998. Cloning of the amino-terminal and 5'-flanking region of the human MUC5AC mucin gene and transcriptional up-regulation by bacterial exoproducts. J. Biol. Chem. 273(12): 6812-6820 CrossRef, Medline.Lorenz J, Zahlten J, Pollok I, Lippmann J, Scharf S, N’Guessan PD, et al.. 2010. Legionella pneumophila induced i?b?-dependent expression of il-6 in lung epithelium. Eur. Respir. J. 37(3): 648-657 CrossRef, Medline.Morinaga Y, Yanagihara K, Miyashita N, Seki M, Izumikawa K, Kakeya H, et al.. 2009. Azithromycin, clarithromycin and telithromycin inhibit MUC5AC induction by Chlamydophila pneumoniae in airway epithelial cells. Pulm. Pharmacol. Ther. 22(6): 580-586 CrossRef, Medline.N’Guessan PD, Etouem MO, Schmeck B, Hocke AC, Scharf S, Vardarova K, et al.. 2007. Legionella pneumophila-induced PKCa-, MAPK-, and NF-?B-dependent COX-2 expression in human lung epithelium. Am. J. Physiol. Lung Cell. Mol. Physiol. 292(1): L267-L277 CrossRef, Medline.Opitz B, Vinzing M, van Laak V, Schmeck B, Heine G, Gunther S, et al.. 2006. Legionella pneumophila induces IFNß in lung epithelial cells via IPS-1 and IRF3, which also control bacterial replication. J. Biol. Chem. 281(47): 36?173-36?179 CrossRef, Medline.Rose MC, Voynow JA. 2006. Respiratory tract mucin genes and mucin glycoproteins in health and disease. Physiol. Rev. 86(1): 245-278 CrossRef, Medline.Saijo T, Izumikawa K, Takazono T, Kosai K, Kurihara S, Nakamura S, et al.. 2008. A case of Legionella pneumophila pneumonia followed by invasive aspergillosis. Jpn. J. Infect. Dis. 61(5): 379-381 Medline.Scharf S, Hippenstiel S, Flieger A, Suttorp N, N’Guessan PD. 2010. Induction of human ß-defensin-2 in pulmonary epithelial cells by Legionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-?B and AP-1. Am. J. Physiol. Lung Cell. Mol. Physiol. 298(5): L687-L695 CrossRef, Medline.Schmeck B, N’Guessan PD, Ollomang M, Lorenz J, Zahlten J, Opitz B, et al.. 2007. Legionella pneumophila-induced NF-?B- and MAPK-dependent cytokine release by lung epithelial cells. Eur. Respir. J. 29(1): 25-33 CrossRef, Medline.Shao MX, Nadel JA. 2005. Neutrophil elastase induces MUC5AC mucin production in human airway epithelial cells via a cascade involving protein kinase C, reactive oxygen species, and TNF-a-converting enzyme. J. Immunol. 175(6): 4009-4016 Medline.Shao MX, Nakanaga T, Nadel JA. 2004. Cigarette smoke induces MUC5AC mucin overproduction via tumor necrosis factor-a-converting enzyme in human airway epithelial (NCI-H292) cells. Am. J. Physiol. Lung Cell. Mol. Physiol. 287(2): L420-L427 CrossRef, Medline.Song KS, Lee WJ, Chung KC, Koo JS, Yang EJ, Choi JY, Yoon JH. 2003. Interleukin-1 ß and tumor necrosis factor-a induce MUC5AC overexpression through a mechanism involving ERK/p38 mitogen-activated protein kinases-MSK1-CREB activation in human airway epithelial cells. J. Biol. Chem. 278(26): 23243-23250 CrossRef, Medline.Teruya H, Higa F, Akamine M, Ishikawa C, Okudaira T, Tomimori K, et al.. 2007. Mechanisms of Legionella pneumophila-induced interleukin-8 expression in human lung epithelial cells. BMC Microbiol. 7(1): 102 CrossRef, Medline.Ünal C, Schwedhelm KF, Thiele A, Weiwad M, Schweimer K, Frese F, et al.. 2011. Collagen IV-derived peptide binds hydrophobic cavity of Legionella pneumophila Mip and interferes with bacterial epithelial transmigration. Cell. Microbiol. 13(10): 1558-1572 CrossRef, Medline.Wagner C, Khan AS, Kamphausen T, Schmausser B, Unal C, Lorenz U, et al.. 2007. Collagen binding protein Mip enables Legionella pneumophila to transmigrate through a barrier of NCI-H292 lung epithelial cells and extracellular matrix. Cell. Microbiol. 9(2): 450-462 CrossRef, Medline.Welsh CT, Summersgill JT, Miller RD. 2004. Increases in c-Jun N-terminal kinase/stress-activated protein kinase and p38 activity in monocyte-derived macrophages following the uptake of Legionella pneumophila. Infect. Immun. 72(3): 1512-1518 CrossRef, Medline.Williams OW, Sharafkhaneh A, Kim V, Dickey BF, Evans CM. 2006. Airway mucus: from production to secretion. Am. J. Respir. Cell Mol. Biol. 34(5): 527-536 CrossRef, Medline.Yanagihara K, Seki M, Cheng PW. 2001. Lipopolysaccharide induces mucus cell metaplasia in mouse lung. Am. J. Respir. Cell Mol. Biol. 24(1): 66-73 Medline.

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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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Cellular MicrobiologyEarly View (Online Version of Record published before inclusion in an issue)

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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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Correction for O'Connor et al., Minimization of the Legionella pneumophila genome reveals chromosomal regions involved in host range expansion [Correction]

MICROBIOLOGY Correction for “Minimization of the Legionella pneumophila genome reveals chromosomal regions involved in host …

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Legionella secreted effectors and innate immune responses

Legionella secreted effectors and innate immune responses - Luo - 2011 - 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 Virology Virtual Special IssueFaculty of 1000PostersWiley Job NetworkParasitology Virtual Special Issue You have free access to this contentLegionella secreted effectors and innate immune responsesZhao-Qing LuoArticle first published online: 10 NOV 2011

DOI: 10.1111/j.1462-5822.2011.01713.x

© 2011 Blackwell Publishing Ltd

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Cellular MicrobiologyEarly View (Online Version of Record published before inclusion in an issue)

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How to CiteLuo, Z.-Q. (2011), Legionella secreted effectors and innate immune responses. Cellular Microbiology. doi: 10.1111/j.1462-5822.2011.01713.x

Author Information

Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, IN 47907, USA

*Correspondence: Zhao-Qing Luo,

*Correspondence: E-mail luoz@purdue.edu; Tel. (+1) 765 496 6697; Fax (+1) 765 494 0876.

Publication HistoryArticle first published online: 10 NOV 2011Accepted manuscript online: 11 OCT 2011 03:50AM ESTReceived 1 August, 2011; revised 3 October, 2011; accepted 5 October, 2011. SEARCH Search Scope All contentPublication titlesIn this journalIn this issue Search String Advanced >Saved Searches > SEARCH BY CITATION Volume: Issue: Page: ARTICLE TOOLSGet PDF (300K)Save to My ProfileE-mail Link to this ArticleExport Citation for this ArticleGet Citation AlertsRequest Permissions AbstractArticleReferencesCited By View Full Article (HTML) Get PDF (300K) Summary

Legionella pneumophila is a facultative intracellular pathogen capable of replicating in a wide spectrum of cells. Successful infection by Legionella requires the Dot/Icm type IV secretion system, which translocates a large number of effector proteins into infected cells. By co-opting numerous host cellular processes, these proteins function to establish a specialized organelle that allows bacterial survival and proliferation. Even within the vacuole, L. pneumophila triggers robust immune responses. Recent studies reveal that a subset of Legionella effectors directly target some basic components of the host innate immunity systems such as phagosome maturation. Others play essential roles in engaging the host innate immune surveillance system. This review will highlight recent progress in our understanding of these interactions and discuss implications for the study of the immune detection mechanisms.

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Tumor Necrosis Factor-alpha (TNFα) Blockers: Label Change - Boxed Warning Updated for Risk of Infection from Legionella and Listeria

including Remicade (infliximab), Enbrel (etanercept), Humira (adalimumab), Cimzia (certolizumab pegol), and Simponi (golimumab)

AUDIENCE: Rheumatology, Gastroenterology, Oncology

ISSUE: FDA notified healthcare professionals that the Boxed Warning for the entire class of Tumor Necrosis Factor-alpha (TNFa) blockers has been updated to include the risk of infection from two bacterial pathogens, Legionella and Listeria. In addition, the Boxed Warning and Warnings and Precautions sections of the labels for all of the TNFa blockers have been revised so that they contain consistent information about the risk for serious infections and the associated disease-causing pathogens.

Patients treated with TNFa blockers are at increased risk for developing serious infections involving multiple organ systems and sites that may lead to hospitalization or death due to bacterial, mycobacterial, fungal, viral, parasitic, and other opportunistic pathogens.

BACKGROUND: The class of TNFa blockers are used to treat Crohn's disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, plaque psoriasis, and/or juvenile idiopathic arthritis.

RECOMMENDATION: The risks and the benefits of TNFa blockers should be considered prior to initiating therapy in patients with chronic or recurrent infection and patients with underlying conditions that may predispose them to infection. See the Drug Safety Communication for a listing of recommendations for healthcare professionals and patients, as well as a data summary.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program:

Complete and submit the report Online: www.fda.gov/MedWatch/report.htm
Download form or call 1-800-332-1088 to request a reporting form, then complete and return to the address on the pre-addressed form, or submit by fax to 1-800-FDA-0178
Read the MedWatch safety alert, including a link to the FDA Drug Safety Communication, at:

http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm270977.htm

Posted: September 2011

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Recovery of Legionella species from water samples using an internal method based on ISO 11731: suggestions for revision and implementation

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The htpAB operon of Legionella pneumophila cannot be deleted in the presence of the groE chaperonin operon of Escherichia coli

Gheyath K. Nasrallah,a Elizabeth Gagnon,a,* Dennis J. Orton,a,† Rafael A. Garduñoa,b aDepartment of Microbiology and Immunology, Dalhousie University, Sir Charles Tupper Medical Building, 7th Floor, 5850 College Street, Halifax, NS B3H 1X5, Canada.

bDepartment of Medicine — Division of Infectious Diseases, Dalhousie University, Dickson Building, 1276 South Park Street, Halifax, NS B3H 2Y9, Canada.

*Present address: Department of Microbiology and Immunology, The University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z4, Canada

†Present address: Department of Pathology, Dalhousie University, Sir Charles Tupper Medical Building, NS B3H 1X5, Canada

Published on the web 27 October 2011.

Canadian Journal of Microbiology, 2011, 57:(11) 943-952, 10.1139/w11-086

Allan, D.S. 2002. Secretion of Hsp60 chaperonin (GroEL) homologs by Legionella pneumophila. M.Sc. thesis, Dalhousie University, Nova Scotia, Canada. Berger KH, Isberg RR. 1993. Two distinct defects in intracellular growth complemented by a single genetic locus in Legionella pneumophila. Mol. Microbiol. 7(1): 7-19 .Bethke K, Staib F, Distler M, Schmitt U, Jonuleit H, Enk AH, et al.. 2002. Different efficiency of heat shock proteins (HSP) to activate human monocytes and dendritic cells: superiority of Hsp60. J. Immunol. 169(11): 6141-6148 .Blander SJ, Horwitz MA. 1993. Major cytoplasmic membrane protein of Legionella pneumophila, a genus common antigen and member of the hsp60 family of heat shock proteins, induces protective immunity in a guinea pig model of Legionnaires’ disease. J. Clin. Invest. 91(2): 717-723 .Brassinga, A.K., Mathew, A.C., Hoemaker, C.J., Morash, M.G., LeBlanc, J.J., and Hoffman, P.S. 2006. Novel use of Helicobacter pylori nitroreductase(rdxA) as a counterselectable marker in allelic vector exchange to create Legionella pneumophila Philadelphia-1 mutants. InLegionella — state of the art 30 years after its recognition. Edited by N.P. Cianciotto, Y. AbuKwaik, P.H. Edelstein, B.S. Fields, D.F. Geary, T.G. Harrison, C.A. Joseph, R.M. Ratcliff, J.E. Stout, and M.S. Swanson. ASM Press, Washington, D.C. pp. 339–342. Buchmeier NA, Heffron F. 1990. Induction of Salmonella stress proteins upon infection of macrophages. Science 248(4956): 730-732 .Carreiro MM, Laux DC, Nelson DR. 1990. Characterization of the heat shock response and identification of heat shock protein antigens of Borrelia burgdorferi. Infect. Immun. 58(7): 2186-2191 .Cazalet C, Rusniok C, Brüggemann H, Zidane N, Magnier A, Ma L, et al.. 2004. Evidence in the Legionella pneumophila genome for exploitation of host cell functions and high genome plasticity. Nat. Genet. 36(11): 1165-1173 .Chien M, Morozova I, Shi S, Sheng H, Chen J, Gomez SM, et al.. 2004. The genomic sequence of the accidental pathogen Legionella pneumophila. Science 305(5692): 1966-1968 .Chong A, Lima CA, Allan DS, Nasrallah GK, Garduno RA. 2009. The purified and recombinant Legionella pneumophila chaperonin alters mitochondrial trafficking and microfilament organization. Infect. Immun. 77(11): 4724-4739 .D’Auria G, Jimenez-Hernandez N, Peris-Bondia F, Moya A, Latorre A. 2010. Legionella pneumophila pangenome reveals strain-specific virulence factors. BMC Genomics 11(1) .Ewann, F., and Hoffman, P.S. 2006. Antisense strategy. InLegionella — state of the art 30 years after its recognition. Edited by N.P. Cianciotto, Y. AbuKwaik, P.H. Edelstein, B.S. Fields, D.F. Geary, T.G. Harrison, C.A. Joseph, R.M. Ratcliff, J.E. Stout, and M.S. Swanson. ASM Press, Washington, DC. pp. 336–338. Fernandez RC, Logan SM, Lee SH, Hoffman PS. 1996. Elevated levels of Legionella pneumophila stress protein Hsp60 early in infection of human monocytes and L929 cells correlate with virulence. Infect. Immun. 64(6): 1968-1976 .Fields BS. 1996. The molecular ecology of legionellae. Trends Microbiol. 4(7): 286-290 .Fields BS, Benson RF, Besser RE. 2002. Legionella and Legionnaires’ disease: 25 years of investigation. Clin. Microbiol. Rev. 15(3): 506-526 .Fujiwara K, Ishihama Y, Nakahigashi K, Soga T, Taguchi H. 2010. A systematic survey of in vivo obligate chaperonin-dependent substrates. EMBO J. 29(9): 1552-1564 .Gabay JE, Horwitz MA. 1985. Isolation and characterization of the cytoplasmic and outer membranes of the Legionnaires’ disease bacterium (Legionella pneumophila). J. Exp. Med. 161(2): 409-422 .Garduño RA, Faulkner G, Trevors MA, Vats N, Hoffman PS. 1998a. Immunolocalization of Hsp60 in Legionella pneumophila. J. Bacteriol. 180(3): 505-513 .Garduño RA, Garduño E, Hoffman PS. 1998b. Surface-associated Hsp60 chaperonin of Legionella pneumophila mediates invasion in a HeLa cell model. Infect. Immun. 66(10): 4602-4610 .Garduño RA, Chong A, Nasrallah GK, Allan DS. 2011. The Legionella pneumophila chaperonin — an unusual multifunctional protein in unusual locations. Front. Microbiol. 2 .Glöckner G, Albert-Weissenberger C, Weinmann E, Jacobi S, Schunder E, Steinert M, et al.. 2008. Identification and characterization of a new conjugation/type IVA secretion system (trb/tra) of Legionella pneumophila Corby localized on two mobile genomic islands. Int. J. Med. Microbiol. 298(5–6): 411-428 .Gupta RS. 1995. Evolution of the chaperonin families (Hsp60, Hsp10 and Tcp-1) of proteins and the origin of eukaryotic cells. Mol. Microbiol. 15(1): 1-11 .Helsel LO, Bibb WF, Butler CA, Hoffman PS, Mckinney RM. 1988. Recognition of a genus-wide antigen of Legionella by a monoclonal antibody. Curr. Microbiol. 16(4): 201-208 .Hirsch PR, Beringer JE. 1984. A physical map of pPH1JI and pJB4JI. Plasmid 12(2): 139-141 .Hoffman PS, Butler CA, Quinn FD. 1989. Cloning and temperature-dependent expression in Escherichia coli of a Legionella pneumophila gene coding for a genus-common 60-kilodalton antigen. Infect. Immun. 57(6): 1731-1739 .Hoffman PS, Houston L, Butler CA. 1990. Legionella pneumophila htpAB heat shock operon: nucleotide sequence and expression of the 60-kilodalton antigen in L. pneumophila-infected HeLa cells. Infect. Immun. 58(10): 3380-3387 .Horwich AL, Fenton WA, Chapman E, Farr GW. 2007. Two families of chaperonin: physiology and mechanism. Annu. Rev. Cell Dev. Biol. 23(1): 115-145 .Karlin S, Brocchieri L. 2000. Heat shock protein 60 sequence comparisons: duplications, lateral transfer, and mitochondrial evolution. Proc. Natl. Acad. Sci. U.S.A. 97(21): 11348-11353 .Karunakaran KP, Noguchi Y, Read TD, Cherkasov A, Kwee J, Shen C, et al.. 2003. Molecular analysis of the multiple GroEL proteins of Chlamydia. J. Bacteriol. 185(6): 1958-1966 .Kaufmann SH. 1990. Heat shock proteins and the immune response. Immunol. Today 11(4): 129-136 .Kaufmann SHE, Schoel B, v. Embden JDA, Koga T, Wand-Württenberger A, Munk ME, Steinhoff U. 1991. Heat-shock protein 60: implications for pathogenesis of and protection against bacterial infections. Immunol. Rev. 121(1): 67-90 .Laemmli UK. 1970. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227(5259): 680-685 .Lathigra RB, Butcher PD, Garbe TR, Young DB. 1991. Heat shock proteins as virulence factors of pathogens. Curr. Top. Microbiol. Immunol. 167: 125-143 .LeBlanc JJ, Davidson RJ, Hoffman PS. 2006. Compensatory functions of two alkyl hydroperoxide reductases in the oxidative defense system of Legionella pneumophila. J. Bacteriol. 188(17): 6235-6244 .Lema MW, Brown A. 1995. Legionella pneumophila has two 60-kilodalton heat-shock proteins. Curr. Microbiol. 31(6): 332-335 .Lund PA. 2009. Multiple chaperonins in bacteria — Why so many? FEMS Microbiol. Rev. 33(4): 785-800 .Macellaro A, Tujulin E, Hjalmarsson K, Norlander L. 1998. Identification of a 71-kilodalton surface-associated Hsp70 homologue in Coxiella burnetii. Infect. Immun. 66(12): 5882-5888 .Maguire M, Coates ARM, Henderson B. 2002. Chaperonin 60 unfolds its secrets of cellular communication. Cell Stress Chaperones 7(4): 317-329 .Morash MG, Brassinga AK, Warthan M, Gourabathini P, Garduño RA, Goodman SD, Hoffman PS. 2009. Reciprocal expression of integration host factor and HU in the developmental cycle and infectivity of Legionella pneumophila. Appl. Environ. Microbiol. 75(7): 1826-1837 .Nasrallah GK, Riveroll AL, Chong A, Murray LE, Lewis PJ, Garduño RA. 2011. Legionella pneumophila requires polyamines for optimal intracellular growth. J. Bacteriol. 193(17): 4346-4360 .Pasculle AW, Feeley JC, Gibson RJ, Cordes LG, Myerowitz RL, Patton CM, et al.. 1980. Pittsburgh pneumonia agent: direct isolation from human lung tissue. J. Infect. Dis. 141(6): 727-732 .Sadosky AB, Wiater LA, Shuman HA. 1993. Identification of Legionella pneumophila genes required for growth within and killing of human macrophages. Infect. Immun. 61(12): 5361-5373 .Sambrook, J., and Russell, D.W. 2001. Molecular cloning: a laboratory manual. 3rd ed. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y. Sandegren L, Andersson DI. 2009. Bacterial gene amplification: implications for the evolution of antibiotic resistance. Nat. Rev. Microbiol. 7(8): 578-588 .Sigler PB, Xu Z, Rye HS, Burston SG, Fenton WA, Horwich AL. 1998. Structure and function in GroEL-mediated protein folding. Annu. Rev. Biochem. 67(1): 581-608 .Singh B, Gupta RS. 2009. Conserved inserts in the Hsp60 (GroEL) and Hsp70 (DnaK) proteins are essential for cellular growth. Mol. Genet. Genomics 281(4): 361-373 .Taylor JS, Raes J. 2004. Duplication and divergence: the evolution of new genes and old ideas. Annu. Rev. Genet. 38(1): 615-643 .Towbin H, Staehelin T, Gordon J. 1979. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc. Natl. Acad. Sci. U.S.A. 76(9): 4350-4354 .Viswanathan, V.K., and Cianciotto, N.P. 2001. Electroporation of Legionella species. In Electro-transformation of bacteria. Edited by N. Eynard and J. Teissie. Springer-Verlag Publications, Heidelberg, Germany. pp. 203–211. Young RA, Elliott TJ. 1989. Stress proteins, infection, and immune surveillance. Cell 59(1): 5-8 .Zhang J. 2003. Evolution by gene duplication: an update. Trends Ecol. Evol. 18(6): 292-298 .

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Legionella - Every Infection Preventionist's Dream—Or Is It?

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[Interdisciplinary management of a large Legionella outbreak in Germany].

Landratsamt Alb-Donau-Kreis, Alb-Donau-Kreis, Deutschland.

Between December 2009 and the end of January 2010, the largest hitherto known outbreak of Legionella in Germany took place in the cities of Ulm and Neu-Ulm. Of a total of 64 patients involved, 60 patients had to be hospitalized, and 5 patients died from the infection. This event was caused by a wet cooling tower of a large air conditioning system in the city center of Ulm. The search for the source of the Legionella emission was extremely difficult, since these plants are neither notifiable nor subject to authorization in Germany. We report about the search for the source and the measures to control the outbreak. We also discuss communication and coordination during these investigations. Regulatory measures as proposed by the World Health Organization (WHO) and the European Network for Legionellosis (EWGLI) and already implemented in numerous other European countries would be desirable to prevent such outbreaks in the future.

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Detection of Legionella by quantitative-Polymerase Chain Reaction (qPCR) for monitoring and risk assessment

Research article Louise H Krojgaard, Karen A Krogfelt, Hans-Jorgen Albrechtsen and Soren A Uldum

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BMC Microbiology 2011, 11:254 doi:10.1186/1471-2180-11-254

Published: 21 November 2011

Background Culture and quantitative polymerase chain reaction (qPCR) assays for the detection of Legionella were compared on samples from a residential area before and after two interventions. A total of 84 samples were collected from shower hoses and taps as first flush samples and at constant temperature. Samples were grouped according to the origin of the sample, a) circulation water b) water from empty apartments c) water from shower hoses. The aims were to investigate the usefulness of qPCR compared to culture for monitoring remedial actions for elimination of Legionella bacteria and as a tool for risk assessment.

In water collected from the apartments Legionella spp were detected by qPCR in the concentration range from LOQ to 9.6*105GU/L while L. pneumophila were detected in a range from LOQ to 6.8 *105 GU/L. By culturing, the legionellae were detected in the range from below detection limit (> 10 CFU/L) to 1.6 * 106 CFU/L. In circulating water and in first flush water from shower hoses, culture and qPCR showed the same tendencies. The overall correlation between the bacteria number detected by culture and the two developed qPCR assays (L. spp and L. pneumophila) was relatively poor (r2 =0.31 for culture and Legionella spp. assay, r2 = 0.20 for culture and L. pneumophila assay).

Detection by qPCR was suitable for monitoring changes in the concentration of Legionella but the precise determination of bacteria is difficult. Risk assessment by qPCR only on samples without any background information regarding treatment, timing, etc is dubious. However, the rapid detection by qPCR of high concentrations of Legionella - especially Legionella pneumophila - is valuable as an indicator of risk, although it may be false positive compared to culture results. On the other hand, the detection of a low number of bacteria by qPCR is a strong indication for the absence of risk.

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Identification of Legionella pneumophila serogroups and other Legionella species by mip gene sequencing

Journal Article

PCR methods for the rapid detection and identification of four pathogenic Legionella spp. and two Legionella pneumophila subspecies based on the gene amplification of gyrB

Guangpeng Zhou, Boyang Cao, Yan Dou, Yanwei Liu and Lu Feng, et al.

Applied Microbiology and Biotechnology, 2011, Volume 91, Number 3, Pages 777-787

Journal Article

Legionella pneumophila DNA in serum samples during Legionnaires’ disease in relation to C-reactive protein levels

F. L. van de Veerdonk, C. P. C. de Jager, J. J. A. Schellekens, C. J. J. Huijsmans and F. Beaumont, et al.

European Journal of Clinical Microbiology & Infectious Diseases, 2009, Volume 28, Number 4, Pages 371-376

Journal Article

LAMP-based method for a rapid identification of Legionella spp. and Legionella pneumophila

Xi Lu, Zi-Yao Mo, Hong-Bo Zhao, He Yan and Lei Shi

Applied Microbiology and Biotechnology, 2011, Volume 92, Number 1, Pages 179-187

Journal Article

Profiling of environmental Legionella pneumophila strains by randomly amplified polymorphic DNA method isolated from geographically nearby buildings

Zuhal Zeybek, Irfan Türetgen, Ayten Kimiran Erdem, Gönül Filoglu and Aysin Çotuk

Environmental Monitoring and Assessment, 2009, Volume 149, Numbers 1-4, Pages 323-327

Journal Article

Anin vitro evaluation of the interactions ofLegionella pneumophila serogroups 2 to 14 strains with other bacteria in the same habitat

Ayten Kimiran Erdem and Aysegül Yazici

Annals of Microbiology, 2008, Volume 58, Number 3, Pages 395-401

Reference Work Entry

Legionella Species and Legionnaires’ Disease

Paul Edelstein and Nicholas Cianciotto

2006, The Prokaryotes, PART 3, SECTION 3.3, Pages 988-1033

Journal Article

Screening-level assays for potentially human-infectious environmental Legionella spp.

Helen Y. Buse, Abby Brehm, Jorge W. Santo Domingo and Nicholas J. Ashbolt

The Journal of Microbiology, 2011, Volume 49, Number 2, Pages 200-207

Journal Article

Online First™ Efficacy of Colloidal Silver-Hydrogen Peroxide and 2-Bromo-2-nitroporopane-1,3-diol Compounds Against Different Serogroups of Legionella pneumophila Strains

N. O. Sanli-Yurudu, A. Kimiran-Erdem, E. O. Arslan-Aydogdu, Z. Zeybek and S. Gurun

Indian Journal of Microbiology, Online First™, 28 June 2011

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Scald risk in social housing can be reduced through thermostatic control system without increasing Legionella risk: a cluster randomised trial

An international peer-reviewed journal for health professionals and researchers covering conception to adolescence Arch Dis Child 2011;96:1097-1102 doi:10.1136/archdischild-2011-300606 P Edwards1, MA Durand2, M Hollister3, J Green2, S Lutchmun4, A Kessel5, I Roberts1

1Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK

2Faculty of Public Health and Policy, London School of Hygiene & Tropical Medicine, London, UK

3Department of Housing & Adult Social Care, London Borough of Camden, London, UK

4Public Health Department, NHS Camden, St Pancras Hospital, London, UK

5Department of Social and Environmental Health Research, London School of Hygiene & Tropical Medicine, London, UK Correspondence to Dr Phil Edwards, NPHIR, Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, UK; phil.edwards{at}LSHTM.ac.ukContributors PE, IR, JG, MAD, MH, SL and AK designed the study. MAD managed the data collection and fieldwork. PE conducted the data analyses. PE, MAD, IR and JG interpreted the results. PE and MAD wrote the first draft of the manuscript. IR, JG, AK, SL and MH commented on the draft and contributed to the final manuscript.

Accepted 10 August 2011 Published Online First 20 September 2011 Objective To quantify the effects of a thermostatic control system in social (public) housing on the prevalence of dangerous (>60°C) water temperatures and on fuel consumption.

Design Pair-matched double-blind cluster randomised controlled trial.

Setting Social housing in a deprived inner-London borough.

Participants 150 households recruited as clusters from 22 social housing estates. Four small estates were combined into two clusters (resulting in a total of 10 pairs of clusters).

Intervention Social housing estate boiler houses were randomised to a thermostatic control sterilisation programme (heating water to 65°C during 00:00–06:00 h and to 50°C from 06:00 to 00:00 h daily) or to standard control (constant temperature 65°C).

Main outcome measures Water temperature over 60°C (‘dangerous’) after running taps for 1 min and daily fuel consumption (cubic feet of gas).

Results 10 clusters (80 households) were allocated to the sterilisation programme and 10 clusters (70 households) to control, of which 73 and 67 households, respectively, were analysed. Prevalence of dangerous (>60°C) hot water temperatures at 1 min was significantly reduced with the sterilisation programme (mean of cluster prevalence 1% in sterilisation programme group vs 34% in control group; absolute difference 33%, 95% CI 12% to 54%; p=0.006). Prevalence of high (>55°C) hot water temperatures at 1 min was significantly reduced (31% sterilisation vs 59% control; absolute difference 28%, 95% CI 9% to 47%; p=0.009). Gas consumption per day reduced more in the control group than in the sterilisation programme group, although not statistically significantly (p=0.125).

Conclusions The thermostatic control with daily sterilisation was effective in capping hot water temperatures and therefore reduced scald risk. Although expected to save energy, fuel consumption was increased relative to the control group.

Funding This work was undertaken by the London School of Hygiene & Tropical Medicine who received funding from Camden Primary Care Trust (PCT). AK was Director of Public Health at Camden PCT at inception of the study and assisted with study design and writing of the report. He is currently employed by the Health Protection Agency as Director of Public Health Strategy. The views expressed in the paper are those of the authors and do not necessarily represent those of Camden PCT or the Health Protection Agency. Camden PCT had no role in data collection, data analysis, or data interpretation.

Competing interests None.

Ethics approval Ethical approval for the study was obtained from the London School of Hygiene & Tropical Medicine Research Ethics Committee.

Provenance and peer review Not commissioned; externally peer reviewed.

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Community-acquired versus nosocomial Legionella pneumonia: Lessons learned from an epidemiologic investigation

Epidemiologically, the peak incidence of legionella community-acquired pneumonia (CAP) is in the summer/fall, but cases may occur anytime during the year. The peak age incidence of Legionnaire’s disease is in the elderly population, but Legionella CAP occurs in all age groups. The incubation period for Legionnaire’s disease is 2 to 10 days. Typically, legionella CAP occurs sporadically. Clinical presentation of Legionnaire’s disease is independent of legionella species and Legionella nosocomial pneumonia (NP) is indistinguishable clinically from legionella CAP. (Source: American Journal of Infection Control)

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Population variation in NAIP functional copy number confers increased cell death upon Legionella pneumophila infection.

Authors: Boniotto M, Tailleux L, Lomma M, Gicquel B, Buchrieser C, Garcia S, Quintana-Murci L Abstract The NAIP gene encodes an intracellular innate immunity receptor that senses flagellin. The genomic region containing NAIP presents a complex genomic organization and includes various NAIP paralogs. Here, we assessed the degree of copy number variation of the complete NAIP gene (NAIPFull) in various human populations and studied the functional impact of such variation on host cell fate using Legionella pneumophila as an infection model. We determined that African populations have a NAIPFull duplication at a higher frequency than Europeans and Asians, with an increased transcription of the gene. In addition, we demonstrated that a higher amount of the NAIPFull protein dramatically i...

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Detection of Legionella by quantitative-Polymerase Chain Reaction (qPCR) for monitoring and risk assessment

Conclusion:Detection by qPCR was suitable for monitoring changes in the concentration of Legionella but the precise determination of bacteria is difficult. Risk assessment by qPCR only on samples without any background information regarding treatment, timing, etc is dubious. However, the rapid detection by qPCR of high concentrations of Legionella - especially Legionella pneumophila - is valuable as an indicator of risk, although it may be false positive compared to culture results. On the other hand, the detection of a low number of bacteria by qPCR is a strong indication for the absence of risk. (Source: BMC Microbiology - Latest articles)

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Legionella pneumophila urinary antigen subtyping using monoclonal antibodies as a tool for epidemiological investigations

Abstract  Legionnaires’ disease is diagnosed predominantly by urinary antigen detection, and patient isolates are rarely available. The lipopolysaccharide (LPS) epitope pattern of isolates detected by monoclonal antibodies is an accepted marker for the phenotyping of L. pneumophila serogroup 1 strains into monoclonal subgroups. L. pneumophila LPS is the dominant antigen in patients’ urinary specimens. By using commercially available microtiter wells coated with rabbit anti-Legionella serogroup 1 IgG as the catching antibody, LPS components in urine specimens were bound and detected separately by corresponding monoclonal antibodies of the Dresden Panel. The subtyping of LPS on urinary antigen molecules by using enzyme-linked immunosorbent assay (ELISA) allows deducing of ...

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